S2HY SlideHandouts

Allergy & Immunology
Anaphylaxis
Angioedema
Urticaria
Allergic Rhinitis
Primary Immunodeficiency
Disorders
Allergy & Immunology

Niket Sonpal, MD
Chief Resident
Lenox Hill Hospital NSLIJ
Assistant Clinical Professor Touro College of Medicine
Anaphylaxis
Anaphylaxis
Worst form of acute allergic reaction
Sensitization
Re-exposure Anaphylaxis
DEATH
Synonymous with immediate hypersensitivity

Pathogenesis
Initial sensitization to antigen with subsequent reexposure
Initial
sensitization
to antigen
Upon re-exposure, IgE binds to mast cells leading to

release of their granules (e.g., histamine,
prostaglandins, and leukotrienes)
HISTAMINE
Results in abnormalities that essentially define

anaphylaxis
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No presensitization
to antigen
Non-IgE related
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Hives
Itching
Constriction of
airways
Swollen tongue
Wheezing
Dyspnea
Tachycardia
Nausea, vomiting,
or diarrhea
Dizziness or
fainting
Hypotension
Anaphylaxis/Etiology
Anaphylactoid Reactions
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LEUKOTRIENES
PROSTAGLANDINS
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Anaphylaxis
Upon re-exposure,
IgE binds to mast
cells leading to
release of their
granules
Identical Tx
Causes of anaphylaxis = causes of any

allergic event
Insect bites and stings
Medications: penicillin, phenytoin, lamotrigine,
quinidine, rifampin, and sulfa
Foods
Latex is a very important cause of anaphylaxis in
healthcare workers
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Anaphylaxis/Presentation
Anaphylaxis/Treatment
Characterized by
Hypotension
Tachycardia
Respiratory: stridor
Rash
The best initial treatment is

A Airway Protection
Intubation
Cricothyroidodotomy
B Breathing
g
C - Circulation
Source: Fashad Bagheri. MD
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Epinephrine
Antihistamines H1 and H2
Glucocorticoids
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Angioedema
Angioedema/Presentation
Angioedema is sudden swelling of
Hereditary
angioedema is a
genetic disorder
Face
Tongue
Eyes
Airway
Look for recent start of ACE inhibitors

preceding symptoms
This can be from deficiency of C1 esterase inhibitor

Characteristic association of onset with minor
physical trauma
Angioedema often idiopathic
Glucocorticoids
dont work
Source: commons.wikimedia.org
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Angioedema/Tests
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Angioedema/Treatment
The best initial test...

C2 and C4 levels in complement pathway
Airway
Acute Tx
Long Term Tx
Will be decreased
C1 esterase inhibitor
Also decreased
3 types of hereditary angioedema

Type I - decreased levels of C1INH (85%)
Type II - normal levels but decreased function of
C1INH (15%)
Type III - no detectable abnormality in C1INH
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Ensure
airway
protection
first
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Fresh frozen
plasma
Ecallantide
E ll tid
Androgens
Danazole
And
Stanazole
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Urticaria
Urticaria/Treatment
Form of allergic
reaction that causes
sudden swelling of
superficial skin layers
Can be caused by
1. Antihistamines
Insects
Medications
Pressure
Cold
Vibration
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Hydroxyzine,
diphenhydramine,
fexofenadine,
loratidine, cetirizine,
or ranitidine
2 L
2.
Leukotriene
k ti
receptor
t
antagonists
p. 43
Montelukast or
zafirlukast
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Allergic Rhinitis
Allergic Rhinitis/Diagnostic Tests
IgE-dependent triggering of mast cells

Seasonal allergies such as hay fever are
common
Presents with recurrent episodes of
Watery
y eyes,
y , sneezing,
g, itchyy nose,, and
itchy eyes
Inflamed, boggy nasal mucosa
Pale or violaceous turbinates
Nasal polyps
Diagnosed
clinically
Skin testing and
blood testing
IgE levels may be
elevated
Nasal smear with
eosinophils
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Allergic Rhinitis/Treatment
Common Variable Immunodeficiency (CVID)
1. Prevention & avoidance

2. Intranasal corticosteroid sprays
3. Antihistamines H1 blockers
4. Intranasal anticholinergic medications
5. Desensitization to allergens
B cells are present but decreased Igs

Decrease in all Ig subtypes
IgG, IgM, and IgA
LOW B cells output, normal T cells
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Recurrent sinopulmonary infections

Frequent episodes of
Bronchitis
Pneumonia
Sinusitis
And
Otitis media
Other manifestations are

Giardiasis
Sprue-like intestinal malabsorption
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Clue to CVID is a decrease in the

output of B lymphocytes with a normal
number of B cells as well as normal
amounts of lymphoid tissue (e.g., nodes,
adenoids, and tonsils)
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Immunoglobulin levels
Treatment
Antibiotics are used for each infection
as it develops
Chronic maintenance
Decreased
Antigen Stimulation
Decreased response
Normal Number of B Cells
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Regular
Reg lar inf
infusions
sions of IVIG
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X linked (Bruton) Agammaglobulinemia
Severe Combined Immunodeficiency
Low B, normal T in males

Male children with increased sinopulmonary
infections
B cells and lymphoid tissues are diminished
T cells are normal
Treatment: Abx for infections as they arise
Long-term regular administration of IVIG keeps
children healthier
LOW B AND LOW T

The word combined in severe combined
immunodeficiency (SCID) means that there is
deficiency in both B and T cells
Results in infections related to both deficiencies
LOW B cells and LOW T cells. Analogous to HIV

LOW B cells, normal T cells in young male children
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Severe Combined Immunodeficiency
IgA Deficiency
B cells
Decreased Ig production
These patients present with recurrent

sinopulmonary infections
The difference with this syndrome is:
Atopic diseases
Anaphylaxis to blood transfusion when blood donor
has normal levels of IgA
Sprue-like condition with fat malabsorption
Increase in risk of vitiligo, thyroiditis, and
rheumatoid arthritis
T cells
Markedly decreased numbers of T cells
Long-Term Treatment
Bone marrow transplant
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IgA Deficiency
Hyper IgE Syndrome
Treat infections as they arise

Washed blood transfusions otherwise
anaphylaxis
IVIG injections will not work
The
Th ttrace amounts
t off IIgA
A iin IVIG may
provoke anaphylaxis
Presents with
recurrent skin
infections due to
Staphylococcus
Treat infections as
they arise
Consider prophylactic
antibiotics (e.g.,
dicloxacillin or
cephalexin)
Source: wikimedia commons
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Wiskott Aldrich Syndrome
Chronic Granulomatous Disease (CGD)
Normal T cells normal B cells decline with age

Immunodeficiency combined with
thrombocytopenia and eczema
T lymphocytes markedly deficient in blood and
lymph nodes
Bone marrow transplantation is only definitive
treatment
CGD is genetic disease resulting in

extensive inflammatory reactions
Leads to lymph nodes with purulent
material leaking out
Normal T cells normal B cells decline with age
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Aphthous ulcers
Granulomas may become obstructive in

the GI or urinary tract
Look for infections with odd combination
of:
And
Staphylococcus
Burkholderia
Nocardia
Aspergillus
Inflammation of
nares is
common
Source:commons.wikimedia.org
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Abnormal nitroblue tetrazolium testing

This is a decrease in NADPH oxidase,
which generates superoxide
CGD test is negative
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Primary Immunodeficiency Disorders

CVID
X-linked (Bruton)
Agammaglobulinemia
SCID
IgA
Deficiency
LOW B
cell
output
Normal
T cells
LOW B cells
normal T
cells in young
male children
LOW B & T
cells
Analogous
to HIV
Atopic
Anaphylaxis
Hyper IgE
Syndrome
Skin infections
Staphylococcus
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Wiskott-Aldrich
Syndrome
Normal T cells
Normal B cells
Low Platelets
Eczema
CGD
Lymph nodes with
purulent material
Infections, combined with
Staphylococcus
Burkholderia
Nocardia
Aspergillus
Coronary Artery
Disease Part 1
The Cardiovascular System
Definition
D
fi iti
Risk Factors
Clinical Presentation
Conrad Fischer, MD
Associate Professor of Medicine
Touro College of Medicine
New York City
Coronary Artery Disease (CAD)/Definition
Can be used interchangeably with:

Atherosclerotic heart disease
Ischemic heart disease
All imply insufficient perfusion of

coronary arteries
Abnormal narrowing of vessels
Insufficient oxygen delivery to
myocardial tissue
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48-year-old woman in office with chest pain for

several weeks. Pain isn't reliably related to exertion.
No pain now. The pain is retrosternal and sometimes
associated with nausea. No SOB and no radiation
beyond chest. She has no past medical history.
What is the most likely diagnosis?
a. Gastroesophageal reflux disease (GERD)
b. Unstable angina Acute, severe pain in ED
c. Pericarditis Pain worse with lying down, better when sitting up
d. Pneumothorax Sharp, pleuritic pain, tracheal deviation
e. Prinzmetal angina Nonexertional chest pain,
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early in morning, ST
segment elevation
Risk Factors for CAD

Menstruating women virtually never have MIs
Which of the following is most likely to benefit a

patients risk of coronary disease?
Estrogen simply does NOT help CAD
Risk factors are most important with

equivocal or uncertain histories
a. Administration of estrogen replacement at time of

menopause
b Stopping tamoxifen Tamoxifen unrelated to CAD
b.
c. Stopping aromatase inhibitors Zero relationship to CAD
d. Regular exercise
e. Relaxation methods (e.g., meditation) Good, but
immeasurable,
no evidence of
proven benefit
Women > men eventually die of heart disease

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Clear ones:
Diabetes (worst risk)

HTN
Defined as > 140/90
More common than diabetes
20% of total population (60 million
people) with HTN
50% unaware theyre hypertensive
Diabetes mellitus
Tobacco smoking
HTN
Hyperlipidemia
Family history of premature CAD
Age > 45 men; > 55 women
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Family history not a risk if

CAD developed in elderly relatives
Relatives were grandparents, cousins, or
aunts and uncles
Family
y history
y is a risk ONLY if
First-degree relatives (siblings/parents)
Premature disease:
Defined as:
Which of the following is the most dangerous to a

patient in terms of risk for CAD?
Triglycerides not as dangerous as elevated LDL
a. Elevated triglycerides
b. Elevated total cholesterol Its not the TOTAL cholesterol
or low
l
HDL
HDL, it
its LDL!
c. Decreased
D
d HDL
d. Elevated LDL
e. Obesity The danger of obesity is from its association
with high LDL, DM, and HTN
Male relative < 55

Female relative < 65
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Less clear
Physical inactivity
Excess alcohol
Insufficient fruits & vegetables
Emotional stress
CT scan calcium scores
Positron emission tomography (PET)
scanning
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Postmenopausal woman develops chest pain immediately on

hearing news of her sons death. She develops chest pain, dyspnea,
and ST segment elevation in leads V2 to V4. Troponin levels rise
with MI. Coronary angiography is normal including an absence of
vasospasm.
Echocardiography: Apical LV ballooning
Whats the presumed mechanism of this disorder?
a. Absence of estrogen
g
Its not absent estrogen
g only
y causing
g MI
b. Massive catecholamine discharge
c. Plaque rupture There were no plaques on angiography
d. Platelet activation Platelets cause MI from CAD, not emotions
e. Emboli to coronary arteries
It wouldve been seen
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Unreliable (Unproven) Risk Factors for CAD

Homocysteine
Chlamydia infection
C-reactive protein
No clear benefit in therapeutic intervention on
these factors
Theyre the wrong answers
The Most Common Wrong Answer

If risk factor question involves:
Family history
Mistaking CAD in elderly relatives as a
risk for patient
Frequently used wrong

answers are just as important
to learn as right answers
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Chest Pain/Presentation
Correcting which of the following risk factors for CAD
results in the most immediate benefit?
a.
b.
c
c.
d.
e.
Diabetes mellitus
Tobacco smoking
Hypertension
Hyperlipidemia
Weight loss
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What Is the Most Likely Diagnosis?

Ischemic pain
Dull /Sore
Squeezing (Pressure-like)
Fixing all of them is good.

But
Not as fast as smoking cessation!
p. 53
Like any muscle thats starved for oxygen

Produces sore-muscle type pain when ischemic
Qualities that go against ischemia
Sharp (knifelike) or pointlike
Lasts for few seconds
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Three features help tell whether or not the

pain is ischemic in nature:
< 10% with chest pain in ED end up having

an MI
50% have no cardiac disease at all
1. Changes with respiration (pleuritic)

2. Changes with position of body
3. Changes with touch of chest wall
(tenderness)
MCC of chest pain that isnt

isn t
ischemic in nature is GI related
Each (pleuritic, positional, tender) excludes

ischemia with 95% negative predictive value
(NPV)
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Causes of Chest Pain
Characteristics of Ischemic Pain
Duration
Stable angina: > 2 - < 10 min
ACS: > 10 - 30 min
Provoking factors
Physical activity,
activity cold
cold,
emotional stress
NOT tender
NOT positional
NOT pleuritic
Quality
Squeezing, tightness,
heaviness, pressure,
burning, aching
NOT: sharp, pins,
stabbing, or knifelike
Associated
symptoms
SOB, nausea,
diaphoresis,
dizziness,
lightheadedness,
fatigue
Location
Substernal
Alleviating factors
Rest
Radiation
Neck, lower jaw and teeth,
arms, shoulders
If the case
describes.
Answer as most
likely diagnosis
Answer as most
accurate test
Chest wall tenderness
Costochondritis
Physical examination
Radiation to back,
unequal blood
pressure between
arms
Aortic dissection
Chest X ray
with widened
mediastinum, chest
CTA, MRA, or TEE
confirms disease
Pain worse with lying

flat, better when
sitting up
Pericarditis
EKG with ST elevation

everywhere, PR
depression
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If the case
describes.
Answer as most
likely diagnosis
Answer as most
accurate test
If the case
describes.
Answer as most
likely diagnosis
Answer as most
accurate test
Epigastric discomfort,
pain related to eating
Duodenal ulcer
disease
Endoscopy
Sudden onset, SOB,

tachycardia, hypoxia
Pulmonary embolus
Spiral CT, V/Q scan
Chest X ray
p g
Gastroesophageal
reflux
Response
p
to PPIs;; or
liquid antacids
Sharp, pleuritic pain,

tracheal deviation
Pneumothorax
g ,
Bad taste,, cough,
hoarseness
Cough, sputum,
hemoptysis
Pneumonia
Chest X ray
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Features that DONT help answer the

diagnosis question
Nausea
Fever
SOB (d
(dyspnea))
Sweating (diaphoresis)
Anxiety
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Coronary Artery
Disease Part 2
Diagnosis
p. 54
Diagnostic Tests/Electrocardiogram
Diagnostic Tests/Enzymes (CK MB/Troponin)
The best initial test for all forms of

chest pain is certainly an
electrocardiogram (EKG)
In office-based setting:
Cardiac enzymes are not the answer in

Office/ambulatory case
Chronic or stable chest pain
Expect normal EKG
But
You cant do other testing until you
know the EKG
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If the patient has acute chest pain then the

answer is:
Transfer
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Diagnostic Tests/Enzymes (CK MB/Troponin)
Diagnostic Tests/Stress Testing
Enzymes are the answer when:

Acute cases of chest pain
Emergency department
Exercise tolerance testing (ETT) is the answer when:

Etiology is unclear and
EKG is not diagnostic
Answer Stress test
ETT without nuclear isotopes: when: Etiology
1. Read EKG
2 Exercise
2.
uncertain &
EKG not diagnostic
Exercise means heart rate > 80% of maximum

Maximum heart rate = 220 patient age
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Thallium (Nuclear) Stress
Normal myocardium picks up thallium like
potassium via Na/K-ATPase
Myocardium alive & perfused?
Nuclear isotopes will be picked up
Abnormalities/Ischemia or Infarction?
Decreased thallium or nuclear uptake
Stress or Dobutamine Echo
Normal myocardium moves on echo
Abnormalities decrease wall motion
Dyskinesis, Akinesis, or Hypokinesis
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Ischemia versus infarction:

Ischemia = Reversible decreased perfusion
Reversal of decrease in thallium uptake or
wall motion
It returns to normal after a period of rest
Infarction = Irreversible
Ischemia is reversible wall motion or
thallium uptake between rest and exercise.
Infarction is irreversible or fixed.
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Use of Exercise Tolerance Testing
Cant exercise?
Test
Indication
Persantine (dipyridamole) or adenosine with nuclear

isotopes (e.g., thallium or sestamibi)
Or
Exercise tolerance
Determine presence ST segment depression

of ischemia
Exercise thallium
Cant read EKG
Decreased uptake of
p
nuclear isotope
Exercise echo
Cant read EKG
Decreased wall motion
Dobutamine in combination with echocardiography

Dobutamine increases myocardial oxygen consumption
Dobutamine provokes ischemia
Ischemia decreases wall motion on echocardiogram
Ischemia detected
Dipyridamole thallium Cant exercise
Dipyridamole may provoke bronchospasm.

Avoid in asthmatics.
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Cant exercise
Dobutamine echo
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Decreased uptake of
nuclear isotope
Decreased wall motion
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Chest pain (likelihood of CHD is high)

Resting EKG abnormalities?
Nuclear and Echo:
No
Sensitivity = Specificity
Able to exercise?
Yes
No
Yes
Exercise Thallium = Exercise Echo

Dipyridamole Thallium = Dobutamine Echo
Exercise stress
test
Chemical stress test

(dipyridamole thallium or
dobutamine echo)
p. 56
ANGIOGRAPHY
1 or 2 vessel disease
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Stress
echocardiogram or
nuclear stress test
3 vessel disease, left main or

2 vessel disease in diabetics
Stent placement
CABG
Diagnostic Tests/Coronary Angiography
Diagnostic Tests/Coronary Angiography
Detects anatomic location of disease

Determines surgery, angioplasty, or
other methods of revascularization
Sometimes used if noninvasive tests
are equivocal
Stenosis (narrowing) < 50% of diameter

is insignificant
Surgery or angioplasty is done for at
least 70% stenosis
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Diagnostic Tests/Holter Monitoring
Continuous ambulatory EKG monitor

Records rhythm
Usually for 24-hour period
May be for 48 to 72 hours
Holter monitor detects rhythm disorders:
A-fib, atrial flutter
Ectopy (e.g., premature beats)
V-tach
Holter monitor does not detect ischemia
Not accurate for evaluating the ST segment
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48-year-old woman comes to office with chest pain occurring over

several weeks. Pain isnt reliably related to exertion. Shes
comfortable now. The pain is retrosternal. Past medical history and
the EKG is normal.
What is the most appropriate next step in management?
a. CK-MB Cardiac enzymes evaluate ACS

b. Troponin
Evaluate valve function,
function wall motion
motion, EF
c. Echocardiogram
E h
di
d. Exercise tolerance testing
Detect the anatomic location of stenosis;
e. Angiography
f. CT angiography determines method of revascularization
CT Angiogram and MRI not accurate enough
g. Cardiac MRI
h. Holter monitor
Used for rhythm evaluation
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CAD/Treatment
USMLE Step 2 CK is most concerned that you know:
Coronary Artery
Disease Part 3
Treatment
Medications that lower

mortality
Chronic angina (not an acute coronary syndrome)
Aspirin
Beta blockers
Nitroglycerin
Step 2 will not test dosing

Route of administration is tested
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CAD/Treatment
Nitroglycerin:
Chronic Stable Angina
Oral
Transdermal patch
Acute Coronary Syndrome
Sublingual
Paste
Intravenous
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CAD/Treatment
Nonspecific beta blockers (e.g.. propranolol)

are not used routinely in cardiology
Clopidogrel
Acute MI (all forms)
Aspirin intolerance (e.g., allergy)
Recent angioplasty with stenting
Adverse effect
Rare thrombotic thrombocytopenic purpura
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Treatment/Prasugrel
Treatment/ACE Inhibitors
Thienopyridine - same class as

clopidogrel and ticlopidine
Prasugrel: Antiplatelet medication for
use in:
Angioplasty & stenting
All acute MI
Intolerant of aspirin
75 increased hemorrhagic stroke
Low EF/systolic dysfunction (best

mortality benefit)
Regurgitant valvular disease
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Mostt common adverse

M
d
effect:
ff t
Cough
7% of patients
Switch to ARBs
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Treatment/Lipid Management
64-year-old man starts lisinopril for CAD with EF of 24%, and
symptoms of breathlessness. He sometimes has rales, but is
asymptomatic today. Physical reveals minimal edema of lower
extremities. Potassium level is elevated and its present on a
repeat measurement. EKG is unchanged.
How would you best manage the patient?
Statins (HMG-CoA reductase inhibitors)
CAD with LDL > 100 mg/dL
Remove K from the body;You

y;
should eliminate the cause
a.
b.
c.
d.
e.
Add kayexalate (potassium-binding resin)

Insulin and glucose Drive K into the cell, given in acute situation
He should get an alternative drug
Stop lisinopril
Switch lisinopril to candesartan ARBs lead to hyperkalemia
Switch lisinopril to hydralazine and nitrates
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Treatment/Lipid Management
LDL > 70: Treat when patient has

Coronary disease AND diabetes
Youre tested on national guidelines from
nonbiased federal organizations
g
Not private organizations (e.g., ACC)
Everyone will agree:
With CAD, goal of LDL at least < 100 mg/dL
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CAD Equivalents
CAD equivalents
Statins to bring LDL down if > 100:
Peripheral artery disease (PAD)
Carotid disease (not stroke)
Aortic disease (aortic artery, not valve)
Diabetes mellitus
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Other Lipid Lowering Therapies

Which is the most common adverse effect of statin
medications?
a. Rhabdomyolysis
b. Liver dysfunction
c Renal failure
c.
d. Encephalopathy
e. Hyperkalemia
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The most common wrong answer
They arent adverse effects of statins
p. 60
Niacin, gemfibrozil, cholestyramine, and ezetimibe

all have beneficial effects on lipid profiles
None is Best initial therapy
None has clear mortality benefit statins provide
Niacin and fibric acid derivatives such as
gemfibrozil have some mortality benefit
benefit, but not as
much as statins
Statins:
Antioxidant effect on endothelial lining of
coronary arteries
Gives benefit transcending lowering LDL number
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Niacin
Gemfibrozil
Associated with:
Glucose intolerance
Elevation of uric acid
Uncomfortable itchiness from histamine
Niacin is excellent to add to statins if full lipid
control not achieved with statins
Although statins, exercise, and cessation of
tobacco use will all raise HDL level, niacin
will raise HDL somewhat more
Fibric acid derivatives:

Lower triglyceride levels > statins
Benefit of lowering triglycerides alone not
proven as useful as straightforward mortality
benefit of statins
Use caution combining fibrates with statins
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Fibrates + Statins= Increased myositis
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Cholestyramine
Ezetimibe
Bile acid sequestrant

Significant interactions with
medications in gut
Potentially blocking their absorption
Cholestyramine
Ch l t
i associated
i t d with
ith
uncomfortable GI complaints
Constipation & flatus
Definitely lowers LDL
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No clear benefit to patient

LDL levels are an imperfect marker of benefit
with cholesterol-lowering therapies
Ezetimibe: No better than placebo
No Change in MI, stroke, or death
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Lipid Lowering Therapy
Lipid Lowering Meds and Adverse Effects
Lipid-lowering therapy: What is clear?

Statins lower mortality the most
Questions about adverse effects
Besides the benefit of statins in CAD with
LDL levels > 100 mg/dL, the only truly clear
aspectt off other
th therapies
th
i iis th
their
i adverse
d
effects
Agent
Adverse effect
Statins
Elevations of transaminases (LFTs),

myositis
Niacin
Elevation in glucose and uric acid level,

Pruritus
Fibric acid
derivatives
Increased risk of myositis when combined

with statins
Cholestyramine
Flatus and abdominal cramping
Ezetimibe
Well tolerated and nearly useless
Check AST & ALT

with statins
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Calcium Channel Blockers (CCBs)
Dihydropyridine CCBs:
CCBs are:
Negative inotropes
Should decrease myocardial oxygen
consumption
Increased heart rate in the aggregate
gg g
will
increase myocardial oxygen consumption
Bottom line:
Nifedipine
Nitrendipine
Nicardipine
Nimodipine
Ni di i
May increase mortality with CAD

because of raising heart rate
Do not routinely use CCBs in CAD

None of the calcium-channel blockers have
been shown to lower morality in CAD
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p. 61
MTB S2CK
p. 61
Verapamil and diltiazem, which do not

increase heart rate, are used in those
who cannot tolerate beta blockers
because of severe asthma
70% with reactive airway diseases (e
(e.g.,
g
asthma) still tolerate beta-1 specific BBs
Use CCBs (verapamil/diltiazem) in CAD only

with:
Severe asthma precluding the use of beta
blockers
Prinzmetal variant angina
Cocaine-induced chest pain
Adverse Effects of CCBs
Edema
You must know adverse effects
Constipation
Heart block (rare)
MTB S2CK
p. 61
MTB S2CK
p. 61 62
10
Revascularization
Coronary Artery Bypass Grafting (CABG)
Angiography:
Evaluates possibility of
revascularization
Either coronary bypass surgery or
angioplasty
Symptoms alone cannot tell the
number of vessels involved
Lowers mortality only with:

Three vessels with > 70% stenosis in
each
Left main occlusion
Two-vessel
T
l di
disease with
ith di
diabetes
b t
Persistent symptoms despite maximal
medical therapy
MTB S2CK
p. 62
MTB S2CK
p. 62
Coronary Artery Bypass Grafting (CABG)
Percutaneous Coronary Intervention (PCI)
Benefit greatest with left ventricular

dysfunction
Internal mammary artery grafts last 10
years
Saphenous vein grafts last 5 years
Percutaneous coronary intervention (PCI)

(angioplasty)
Intervention best therapy in acute
coronary syndromes
Particularly those with ST segment
elevation
Mortality benefit of PCI
Much harder to demonstrate in chronic stable
angina
MTB S2CK
p. 62
MTB S2CK
p. 62
Percutaneous Coronary Intervention (PCI)
Max medical therapy with aspirin, beta

blockers, ACEi/ ARBs, and statins has
proven benefit thats PCI in stable CAD
PCI decreases dependence on medication
Decreasing frequency of angina episodes
PCI: Best in acute coronary syndromes,
particularly with ST segment elevation.
PCI doesnt provide clear mortality
benefit for stable patients.
MTB S2CK
Acute Coronary
Syndromes Part 1
Definition
Presentation
Diagnosis
p. 62
11
Acute Coronary Syndromes (ACS)
Definition
Impossible to determine precise
etiology of (ACS) from history & physical
alone
Risk factors (e
(e.g.,
g hypertension
hypertension, diabetes
mellitus, tobacco) same for CAD
Acute Coronary Syndrome

EKG
ST elevation
No ST elevation
Cardiac Biomarkers
+
STEMI
MTB S2CK
p. 62
NSTEMI (Ischemia)
MTB S2CK
NSTEMI
UA
p. 62
STEMI
S4 Gallop
70-year-old woman in ED with crushing substernal
chest pain for last hour. Pain radiates to left arm and
is associated with anxiety, diaphoresis, and nausea.
Pain is sore and dull and clenches fist in front of
chest. History of hypertension.
Pulsus paradoxus,
Which is most likely in this patient? tamponade
p
a. >10 mmHg decrease in BP on inhalation
b. Increase in jugular venous pressure on inhalation
Kussmaul sign: constrictive
friction rub: pericarditis
c. Triphasic scratchy sound Pericardial
pericarditis
d. Continuous machinery murmur PDA (patent ductus)
e. S4 gallop
LVH/dilated cardiomyopathy
f. Point of maximal impulse displaced to axilla
MTB S2CK
p. 63
12
Acute Coronary Syndromes

Increased jugulovenous pressure on inhalation
Kussmaul sign
Constrictive pericarditis
Triphasic scratchy sound:
Pericardial friction rub
Dressler syndrome:
Not until several days after MI
Much rarer
Everyone is on aspirin already!
MTB S2CK
p. 63
Benign compared to LBBB
p. 63 64
Continuous machinery murmur

Patent ductus arteriosus
Displaced point of maximal impulse (PMI)
LVH as well as dilated cardiomyopathy
Displaced
p
PMI is an anatomic abnormality
y
Could not occur with ACS
Dont walk into Step 2
without knowing when
you will expect each
cardiac physical findings
MTB S2CK
70-year-old woman in ED with crushing substernal

chest pain for the last hour.
Which EKG finding gives the worst prognosis?
a. ST elevation in leads II, III, aVF IWMI better prognosis
than AWMI
b. PR interval >200 milliseconds First degree AV block
c ST elevation in leads V2-V4
c.
V2 V4
d. Frequent premature ventricular complexes (PVCs)
e. ST depression in leads V1 and V2 Posterior MI
f. Right bundle branch block (RBBB)
MTB S2CK
PVCs should not be treated,

even with acute infarction
No specific physical finding

allows you to answer a most
likely diagnosis question in
terms of ST elevation or
depression without an EKG
p. 63
70-year-old woman comes to ED with crushing substernal chest pain for

the last hour. EKG shows ST segment elevation in V2 to V4.
What is the next step in management?
a. CK-MB level Neither of them would be elevated
b. Oxygen
All of them should be given,
c. Nitroglycerin sublingual
but neither lowers mortality
d. Aspirin
e. Thrombolytics All will be done, but first aspirin
f. Metoprolol
Sh ld b
Should
be given,
i
titime d
doesntt matter
tt
g. Atorvostatin Not in acute settings
h. Angioplasty
Never the right answer
i. Consult cardiology
j. Transfer patient to intensive care unit
Start treatment first
k. Troponin level
l. Morphine
m. Angiography
MTB S2CK
p. 64 65
Learn the order in which to do things.

You must know what is first.
MTB S2CK
p. 65
70-year-old woman comes to ED with crushing substernal chest

pain for last hour. EKG shows ST segment elevation in V2 to V4.
Aspirin has been given to chew.
What is next step in this patient?
a. CK-MB level Neither of them would be elevated
b. Oxygen
All of them should be given,
c. Nitroglycerin sublingual but none lowers mortality
d. Morphine
Angioplasty is superior to thrombolytics
e. Thrombolytics
BBs and statins should be given, but they are
f. Metoprolol
not critically dependent upon time
g. Atorvostatin
h. Angioplasty
i. Troponin level
j. Lisinopril
MTB S2CK
p. 65
13
ACS/Diagnostic Tests
On USMLE Step 2 CK, consultation is

almost never the correct choice.
Do everything yourself.
In ACS:
Does the treatment lower
mortality?
first?
Which is most important to do
MTB S2CK
p. 65
Test
Time to being
abnormal
Duration of abnormality
EKG
Immediately at
onset of pain
ST elevation progresses
to Q waves over days
to a week
Myoglobin
1 4 hours
1 2 days
CK MB
4 6 hours
1 2 days
Troponin
4 6 hours
10 14 days
MTB S2CK
p. 66
ACS/Diagnostic Tests
Diagnostic Tests/Reinfarction
Troponin
Cant distinguish reinfarction several
days after the first event
Renal insufficiency gives false positive
tests
Troponin: excreted through the kidney
New episode of pain within a few days of the

first?
EKG detects new ST segment abnormalities
Check CK-MB levels
After 2 days,
y , the CK-MB level from the initial
infarction returns to normal
CK-MB elevated several days after initial MI
indicates a new ischemic event
MTB S2CK
p. 66
MTB S2CK
p. 66
Intensive Care Unit Monitoring
After initial management patient should be in

ICU
Continuous rhythm monitoring is essential
Monitoring and rapid cardioversion improves
survival
Most common cause of death first several
days after myocardial infarction is ventricular
arrhythmia (ventricular tachycardia,
ventricular fibrillation)
Rapid electrical cardioversion or defibrillation
MTB S2CK
Acute Coronary
Syndromes Part 2
Treatment
p. 66
14
Treatment/STEMI
Treatment/STEMI
Angioplasty versus Thrombolytics

Angioplasty (PCI) superior to thrombolytics
Complications of PCI
Rupture of coronary artery
Restenosis
Hematoma at entry site into artery
Better survival and mortality

Less bleeding
Complications of MI decreased
Less arrhythmia, less CHF, fewer ruptures of
septum, free wall [tamponade] and papillary muscles
[valve rupture]
Standard of care:
PCI within 90 minutes of arriving in emergency
department with chest pain
Door to balloon time:
under 90 minutes
MTB S2CK
p. 67
Only 20% of U.S. hospitals can do primary

angioplasty
Important to have ability to perform
emergency cardiac surgery to repair the
vessel
MTB S2CK
p. 67
Treatment/STEMI
Which is most important in decreasing the risk of
restenosis of the coronary artery after PCI?
Doesnt change risk with each vessel done
a. Multistage procedure (i.e., doing 1 vessel at a time,

with multiple procedures)
Used only at procedure
b Use of heparin for 36
b.
3 6 months after the procedure
c. Warfarin use after the procedure For DVT and PE not
coronary disease
d. Placement of bare metal stent
e. Placement of drug-eluting stent (paclitaxel,
sirolimus)
Restenosis within 6 Months of PCI

No stent: 30% 40%
Bare metal stent:15% 30%
Drug-eluting stent:10%
Cant use thrombolytics?
Transfer to a facility performing PCI
Has much more risk for restenosis than drug-eluting stent
MTB S2CK
p. 67
MTB S2CK
p. 67
Treatment/STEMI
Absolute Contraindications to
Thrombolytics
Major bleeding:
Bowel (melena), brain
Recent surgery (within the last 2 weeks)

Severe hypertension (>180/110)
Nonhemorrhagic stroke within the last 6
months
Heme-positive brown stool is
not an absolute contraindication
to the use of thrombolytics
MTB S2CK
p. 67 68
Patient comes to small rural hospital without

catheterization lab with chest pain and ST segment
elevation.
a. Transfer for angioplasty Should be done within 90 minutes
b. Administer thrombolytics now
c. Consult cardiology Never the right answer
Time is muscle. Delay = Death
Door to needle time: under 30 minutes
MTB S2CK
p. 68
15
Treatment Indications and Benefits
Treatment Indications and Benefits
Therapy
Therapy
In what cases is effect greatest?
In what cases is effect greatest?
Aspirin
Everyone, best initial therapy
Statins
Everyone, best with LDL > 100 mg/dL
Clopidogrel
All MIs, undergoing angioplasty and

stenting
Oxygen, nitrates
No clear mortality benefit
Heparin
Beta blockers
Everyone, effect not dependent on

time; started any time during
admission
After thrombolytics/PCI to prevent

restenosis, initial therapy with NSTEMI
and unstable angina
ACEI/ARBs
Everyone, benefit best with ejection

fraction < 40%
Calcium channel
blockers
Cant use beta blockers, cocaine

induced pain, Prinzmetal angina
MTB S2CK
p. 68
MTB S2CK
p. 68
Treatment/ST Segment Depression ACS

A man comes to the ED with chest pain for the last hour that is
crushing in quality and does not change with respiration or
position of his body.
EKG: ST segment depression, V2 to V4.
Aspirin has been given.
What is the next step in this patient?
a. Low molecular-weight heparin
b. Thrombolytics Benefit only with STEMI
c. Glycoprotein IIb/IIIa inhibitor (abciximab) PCI with stenting
d.
e.
f.
g.
Nitroglycerin No clear benefit

Morphine
Angioplasty Heparin first
Metoprolol Should be given, but not urgent
MTB S2CK
p. 69
Glycoprotein IIb/IIIa Inhibitors (Abciximab,

Tirofiban, Eptifibitide)
Used in acute coronary syndromes
Those who undergo angioplasty and stenting
Not beneficial in acute ST elevation infarctions
Inhibits
I hibi platelet
l l aggregation
i
Reduction in mortality with ST depression,
particularly in patients whose troponin or CK-MB
levels rise and then develop an MI requiring PCI
with stenting
MTB S2CK
Summary of Treatment Differences between

Cardiac Events
Stable angina
UA/NSTEMI
STEMI
Aspirin
Yes
Yes
Yes
Beta blockers
Yes
Yes
Yes
Nitrates
Yes
Yes
Yes
Heparin
No
Yes
Yes, only after

thrombolytics
GPIIb/IIIa meds No
MTB S2CK
p. 70
Yes
p. 69
Summary of Treatment Differences between

Cardiac Events
Stable angina
UA/NSTEMI
STEMI
Thrombolytics No
No
Yes, but not as

good as PCI
CCBs
No
No
No
Warfarin
No
No
No
No
MTB S2CK
p. 70
16
Acute Coronary Syndromes/Treatment
Treatment/ST Segment Depression ACS
Bottom line:
1. tPA (thrombolytics) are beneficial only with STEMI
2. Heparin is best for NSTEMI
3. GPIIb/IIIa inhibitors are best for NSTEMI and those
undergoing PCI and stenting
Calcium-channel blockers & warfarin:

No mortality benefit in ACS
In non-ST elevation ACS, when all medications have been

given and the patient is not better, urgent angiography and
possibly angioplasty (PCI) should be done.
Not better means:
Persistent pain
S3 gallop or CHF developing
Worse EKG changes
Rising troponin levels
LMW heparin superior to unfractionated heparin for

mortality benefit
MTB S2CK
p. 70
MTB S2CK
Complications of Acute MI

STEMI
Non-STEMI/UA
Aspirin/Clopidogrel
Beta Blockers
Statin
ACE
Morphine
p
Nitrates
PCI
If available <90 min
after patient arrives
1.
2.
Emergency CABG
Failed PCI
Ischemia refractory ALL
therapy
MTB S2CK
p. 70
Heparin
Early PCI
Thrombolytics
If PCI not available.
Use within 12 hrs from
start of chest pain
p. 70
Absolute contraindications to
thrombolytics
Major bleeding (bowel/brain)
Recent surgery (within last 2
weeks)
Severe hypertension (>180/110)
Nonhemorrhagic stroke last 6
months
Excellent source of:

What is the most likely diagnosis? questions,
(most common question on Step 2)
All MI complications can result in low BP
Hypotension: Not help determine diagnosis
MTB S2CK
p. 71
Complications of Acute MI/Bradycardia
Heart rate:
Key to establishing diagnosis
Third-degree (complete) AV block:
Sinus bradycardia:
Very common with MI
From ischemia of sinoatrial (SA) node
MTB S2CK
p. 71
Cannon a waves
Distinguishes 3rd degree block from sinus
bradycardia before EKG
From atrial systole against closed tricuspid
Tricuspid valve closed because essence of
third-degree block is atria and ventricles
contracting separately
Atria/ventricles out of coordination with each
other
MTB S2CK
p. 71
17
Complications of Acute MI/Tachycardia
Cannon is jugulovenous wave

bouncing up into the neck
Look for: right ventricular infarction and
third-degree AV block
All symptomatic bradycardias:
1. Treated first with atropine
2. Then place pacemaker if the atropine
is not effective
3. Pace all permanent 3rd degree blocks
Right Ventricular Infarction

Look for:
New inferior wall MI & clear lungs on
auscultation
Cant g
get blood into lungs
g if blood cant enter
heart
Flip EKG leads from left side to right side of
chest
Most specific finding:
ST elevation in right lead 4 (RV4)
MTB S2CK
p. 71
MTB S2CK
p. 71
Right coronary supplies:
Tamponade/Free Wall Rupture

Usually takes several days after infarction for
wall to scar & weaken enough for rupture
Look for sudden loss of pulse
Lungs: Clear
Cause of Pulseless Electrical Activity (PEA)
Test: Echocardiography
Treat: Pericardiocentesis is done on way into
operating room for repair
Right ventricle (RV)

AV node
Inferior wall of the heart
Up to 40% with inferior wall myocardial
infarctions (IWMI) have right ventricular
infarction
Treat RV infarct with high-volume fluid
Avoid nitroglycerin (markedly worsens filling)
MTB S2CK
p. 71
MTB S2CK
p. 72
Ventricular Tachycardia/Ventricular
Fibrillation
Both can cause sudden death
No way to distinguish without EKG if no
pulse
Cardiovert/ Defibrillate
Valve or Septal Rupture

Both present with new onset murmur and
pulmonary congestion
Mitral regurgitation best heard at apex with
radiation to axilla
Ventricular septal rupture best heard at lower left
sternal border
These complications are the reason patients

with acute MI are monitored in an ICU for the
first several days after the infarction
MTB S2CK
p. 72
Look for a step-up in oxygen saturation as you

go from the right atrium to the right ventricle to
hand you the diagnosis of septal rupture
MTB S2CK
p. 72
18
Most accurate test: Echocardiogram for both

You cant always depend on buzzwords like
step-up for oxygenation
Often, only numbers are presented:
42% oxygen saturation found on blood from
right atrium and 85% saturation found in right
ventricular sample
MTB S2CK
p. 72
Intraaortic Balloon Pump
Intraaortic balloon pump (IABP):

Answer for pump failure from anatomic
problem that can be fixed in operating room
IABP contracts & relaxes in sync with natural
heartbeat
Helps give a push forward to blood
IABP is never a permanent device (bridge to
surgery)
MTB S2CK
p. 72
Extension of the Infarction/Reinfarction
Aneurysm/Mural Thrombus
Second event infarct

Look for:
Recurrence of pain
New rales
Bump up in CK-MBs
Sudden onset pulmonary edema
Actions:
Repeat EKG
Re-treat with angioplasty or thrombolytics
Detected with echocardiography

Most aneurysms dont need specific
therapy
Mural thrombi are treated with heparin
followed by warfarin
Continue: aspirin, metoprolol, nitrates, ACE, statins

MTB S2CK
p. 72 73
MTB S2CK
What is the Most Likely Diagnosis?
p. 73
Diagnosis
Key feature
Diagnosis
Key feature
Third degree AV
Block
Bradycardia, cannon a
Waves
Valve rupture
New murmur,
rales/congestion
Sinus bradycardia
No cannon a waves
Septal rupture
Tamponade/wall
Rupture
Sudden loss of pulse, JVD
New murmur, increase in

oxygen saturation on
entering the right ventricle
RV infarction
IWMI in history, clear lungs,

hypotension
Ventricular
fibrillation
Loss of pulse, need EKG to

answer question
MTB S2CK
p. 73
MTB S2CK
p. 73
19
Preparation for Discharge from Hospital
Detection of Persistent Ischemia

Stress test prior to discharge
Stress test determines if
angiography needed
Angiography
A i
h d
determines
t
i
need
d ffor
revascularization (angioplasty or bypass
surgery)
Everyone should go home on:

Aspirin
Clopidogrel
Beta blockers (metoprolol)
Statins
ACE inhibitors
Best for anterior wall infarctions because
of high likelihood of developing systolic
dysfunction
Dipyridamole is never the right

choice for coronary artery disease
MTB S2CK
p. 73
MTB S2CK
p. 74
Sexual Issues Postinfarction
Clopidogrel: All MIs, or intolerant of

aspirin, or post-stenting
ARBs: those with cough to ACE inhibitor
Ticlopidine: for rare person intolerant of both
aspirin and clopidogrel
The most commonly tested facts are:

Dont combine nitrates with
sildenafil; hypotension can result
because theyre both vasodilators
Erectile dysfunction postinfarction is
most commonly from anxiety
Most common medication is beta
blocker
Prophylactic antiarrhythmic medications:

Do not use amiodarone, flecainide, or any rhythmcontrolling medication to prevent the development of
ventricular tachycardia or fibrillation. Do not be fooled
by the question describing frequent PVCs and
ectopy. Prophylactic antiarrhythmics increase
mortality.
MTB S2CK
p. 74
MTB S2CK
p. 74
Sexual Issues Postinfarction
Wait after MI for sexual activity

2-6 weeks
If post-MI stress test is normal, any form

of exercise program can be started
including sex
MTB S2CK
Congestive Heart Failure

Definition
Presentation
Diagnosis
Treatment
p. 74
20
Congestive Heart Failure (CHF)/Definition
CHF/Causes of Systolic Dysfunction
Shortness of breath (dyspnea) - essential

feature of congestive heart failure (CHF)
Dysfunction of heart as a pump of blood
Insufficient oxygen delivery and fluid in lungs
Either from:
S t li d
Systolic
dysfunction:
f
ti
Low Ejection Fraction (EF) and dilation of heart
Diastolic dysfunction:
EF is preserved
Heart cant relax and receive blood
Most Common:
Hypertension resulting in
cardiomyopathy
Initially theres preservation of EF
Over time
time, the heart dilates resulting in
systolic dysfunction and low EF
Valvular heart disease of all types
results in CHF
MTB S2CK
p. 74 75
MTB S2CK
p. 75
Myocardial infarction (MI) is a very common cause

of dilated cardiomyopathy and decreased EF
Dead or infarcted heart wont pump
CHF most common cause of hospital admission
in USA
MI death rate down from:
Infarction
Dilation
Thrombolytics
Beta blockers
Angioplasty
Aspirin, clopidogrel
Regurgitation
Many are normal, are living with CHF

MTB S2CK
p. 75
CHF
MTB S2CK
p. 75
CHF/Presentation
Less common causes are:

Alcohol
Postviral (idiopathic) myocarditis
Radiation
Adriamycin (doxorubicin) use
Chagas
Ch
di
disease
and
d other
th iinfections
f ti
Hemochromatosis (also causes restrictive
cardiomyopathy)
Thyroid disease
Peripartum cardiomyopathy
Thiamine deficiency
In addition to dyspnea on exertion look for:

Orthopnea (worse when lying flat, relieved when
sitting up or standing)
Peripheral edema
Rales on lung exam
Jugulovenous distention (JVD)
Paroxysmal nocturnal dyspnea (PND)(sudden
worsening at night, during sleep)
S3 gallop rhythm
(Be prepared to identify the sound on Step 2. It
may be played.)
MTB S2CK
p. 75
MTB S2CK
p. 76 77
21
Heart Sounds Timing in the Cardiac Cycle
CHF/Presentation
The most frequently asked USMLE Step

2 CK question is:
MTB S2CK
p. 76
MTB S2CK

for Dyspnea
p. 76

for Dyspnea
Key feature
Most likely diagnosis is
Key feature
Most likely diagnosis is
Sudden onset, clear lungs
Pulmonary embolus
Circumoral numbness, caffeine

use, history of anxiety
Panic attack
Sudden onset, wheezing,

increased expiratory phase
Asthma
Pallor, gradual over days to
weeks
k
Anemia
Slower, fever, sputum, unilateral

rales/rhonchi
Pneumonia
Pulsus paradoxus, decreased
heart sounds, JVD
Tamponade
Decreased breath sounds

unilaterally, tracheal deviation
Pneumothorax
Palpitations, syncope
Arrhythmia
(of almost any kind)
MTB S2CK
p. 77
MTB S2CK
p. 77

for Dyspnea

for Dyspnea
Key feature
Most Likely diagnosis is
Dullness to percussion at base
Pleural effusion
Long smoking history, barrel chest
COPD
All of these will lack:

Orthopnea/PND
S3 gallop
Recent anesthetic use,, brown blood

not improved with oxygen, clear
lungs on auscultation, cyanosis
g
Methemoglobinemia
Burning building or car, wood

burning stove in winter, suicide
attempt
Carbon monoxide poisoning
MTB S2CK
p. 77
MTB S2CK
p. 77
22
CHF/Diagnostic Tests
CHF/Ejection Fraction
Echocardiography
Most important test of CHF
There is no OTHER way to distinguish
What is the best initial test?

Transthoracic echo
Systolic vs. Diastolic dysfunction

Will NOT distinguish by:
History
Physical
Tests (e.g., EKG, chest X-ray, or BNP)
MTB S2CK
p. 77
Whats the most accurate test?

Multiple
Multiple-gated
gated acquisition scan (MUGA) or
nuclear ventriculography
Transesophageal echocardiography (TEE):
More accurate for valves
MTB S2CK
p. 78
When should you answer nuclear

ventriculography?
Rarely needed
Person receiving chemotherapy with
doxorubicin
Trying to give max dose to cure
lymphoma
But not cause cardiomyopathy
When should you answer BNP?

Acute SOB
Etiology unclear
You cant wait for echo
Normal BNP excludes CHF
MTB S2CK
p. 78
MTB S2CK
Tests Used to Determine Etiology of CHF
Test
Etiology of CHF
EKG
MI, heart block
Chest X ray
Dilated cardiomyopathy
Holter monitor
Paroxysmal arrhythmias
Cardiac
catheterization
Precise valve diameters,

septal defects
CBC
Anemia
MTB S2CK
p. 78
p. 78
Tests Used to Determine Etiology of CHF

Test
Etiology of CHF
T4/TSH
Both high and low thyroid levels

cause CHF
Myocardial biopsy
Excludes sarcoid, amyloid

Rarely needed
Can biopsy other sites
Swan Ganz right heart

catheterization
Distinguishes CHF from ARDS; not

routine
MTB S2CK
p. 78
23
CHF/Treatment
CHF/Treatment
Systolic Dysfunction (Low EF)

ACE inhibitors or angiotensin receptor
blockers (ARBs)
Beta blockers
Spironolactone,
S i
l t
E l
Eplerenone
Diuretics
Digoxin
ACE/ARBs
All patients with systolic dysfunction
All stages of disease
Beneficial effects: any drug in class
When are ARBs Next best step?
ACE induced cough
MTB S2CK
p. 79
MTB S2CK
p. 79
CHF/Treatment
CHF/Treatment
Beta Blockers
Not clearly any drug in class
Evidence only for:
Beta Blockers are:

Anti-ischemic
Decrease heart rate
Decrease O2 consumption
Antiarrhythmic
Metoprolol
Bisoprolol
Carvedilol
MTB S2CK
p. 79
MTB S2CK
p. 79
CHF/Treatment
Which of the following is the MCC of death from
CHF?
a.
b.
c
c.
d.
e.
Pulmonary edema We can fix this almost all the time

Myocardial infarction CHF doesnt cause MI
Arrhythmia/sudden death
Emboli Clots rare in CHF unless AFib
Myocardial rupture This from MI, not CHF
MTB S2CK
p. 79
Spironolactone
Benefit from inhibition of aldosterone
Only proven for more advanced CHF
(class III and IV) with dyspnea on
minimal exertion or at rest
What is the most common adverse
effect?
Hyperkalemia
Gynecomastia
MTB S2CK
p. 79 80
24
CHF/Treatment
When is eplerenone the answer?

When spironolactone leads to
antiandrogenic effects (e.g.,
gynecomastia)
CHF/Treatment
Diuretics
ED: Acute pulmonary edema
Office: Combination with ACEi or ARB
Furosemide, torsemide, or bumetanide equal
Spironolactone, although a diuretic, is not
used at doses where it has a diuretic effect
Diuretics control symptoms of CHF.
They do not lower mortality.
MTB S2CK
p. 80
CHF/Treatment
Digoxin
Digoxin does NOT lower mortality in CHF
This is often the single most important
question concerning CHF on USMLE
Digoxin will:
Control symptoms
Decrease frequency of hospitalizations
No positive inotropic agent (digoxin,
milrinone, amrinone, dobutamine) has
been proven to lower mortality
MTB S2CK
p. 80
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CHF/Treatment
Devices with mortality benefit
1. Implantable defibrillator: Ischemic CM

& EF < 35%. Remember: Arrhythmia and
sudden death are MCC of death in CHF
2. Biventricular pacemaker: EF < 35% &
wide QRS > 120 ms with persistent
symptoms
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p. 80 81
CHF/Treatment
CHF/Treatment
Biventricular pacemaker is NOT a dualchamber pacemaker

Dual-chamber pacer has wire in right
ATRIUM and right VENTRICLE
Biventricular pacemaker resynchronizes the
heart when theres a conduction defect
Defers/delays need for cardiac
transplantation
Symptoms markedly improved
Transplantation
Symptoms despite maximal medical
therapy (ACE, BB, spironolactone,
diuretics, digoxin) and possibly
biventricular pacemaker
Warfarin
Always wrong in absence of clot in
heart
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25
CHF/Treatment
Mortality Benefit in Systolic Dysfunction

ACEi/ARBs
Beta blockers
Spironolactone
Hydralazine/nitrates
Implantable defibrillator
Calcium-channel blockers (CCBs)
can actually raise mortality
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p. 81
CHF/Treatment
Diastolic Dysfunction
(CHF with preserved EF)
Less clear
Beta blockers have clear benefit
No mortality benefit in diastolic
dysfunction
Digoxin clearly has no benefit
MTB S2CK
p. 81
CHF/Treatment
Diuretics control symptoms of fluid

overload
Do not confuse diastolic dysfunction
from hypertrophic CM with hypertrophic
obstructive cardiomyopathy (HOCM)
Diuretics are contraindicated in HOCM
because they increase obstruction
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Acute Pulmonary Edema

Definition
Presentation
Diagnosis
Treatment
p. 81
Acute Pulmonary Edema
Acute Pulmonary Edema/Presentation
Definition
Worst (most severe) form of CHF
Rapid fluid accumulation in lungs
How do I answer What is the most likely diagnosis?

Acute shortness of breath with:
Rales
JVD
S3 gallop
Edema
Ed
Orthopnea
MAY be:
Ascites & enlargement of liver/spleen from chronic
passive congestion of right side of heart
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p. 82
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p. 82
26
S3 Gallop Rhythm
JVD
Pitting Edema
Wet Crackles
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Pulmonary edema
with cephalization
of flow and
engorged
pulmonary veins
Source: Saba Ansari, MD.
Brain Natriuretic Peptide (BNP) is the answer if:

Diagnosis not clear
Normal BNP excludes CHF
Chest X-ray shows:
Vascular congestion
Filling
Filli off bl
blood
d vessels
l ttoward
dh
head
d ((cephalization
h li ti
of flow)
Flow mostly at base because of gravity
Enlargement of heart
Effusion
Pulmonary Edema
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p. 83
27
Acute Pulmonary Edema/Diagnostic Tests
Oximetry/Arterial Blood Gas (ABG)

Hypoxia expected
Respiratory alkalosis from
hyperventilation
CO2 leaves
l
more easily
il than
th oxygen
enters
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p. 83
Acute Pulmonary Edema/

Which Test is most likely to alter acute management?
Answer!!!
EKG
A-fib, Atrial flutter, or V-tach
What to do first?
Synchronized cardioversion
Restore atrial systole = Return atrial
contribution to cardiac output
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p. 83
EKG
Diseased hearts need atrial systole more than
normal hearts
Up from 10% to 30 - 40% of cardiac output
Diseased hearts means:
Echocardiography
MUST be done on all patients
ONLY WAY to determine systolic or
diastolic dysfunction
No difference in initial therapy
Huge difference in chronic therapy
Dil
Dilated
t d cardiomyopathy
di
th
Valvular heart disease
If acute pulmonary edema is from arrhythmia

fix it fast with..
Cardioversion!!!!!
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p. 83
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Acute Pulmonary Edema/Treatment

74-woman comes to ED with the acute onset of SOB,
RR of 38/minute, rales to apices, S3 gallop, and JVD.
What is the best initial step in management?
Will be done, but first you have to treat
a. Oximeter
Should be done, but not urgently
b. Echocardiography
c. Intravenous furosemide
d. Ramipril
Although they are used in CHF, they are not
e. Metoprolol
Part of the treatment of acute setting
f. Nesiritide
No mortality benefit. Not better than nitrates
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p. 84
Preload Reduction
Initial therapy:
Oxygen
Loop diuretics (e.g., furosemide or
b
bumetinide)
ti id )
Morphine
Nitrates
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28
The majority in acute pulmonary edema

can be managed with preload reduction
Removing 1 to 2 liters of fluid is best
Nesiritide does NOT work better than
other agents
What do you do if the questions say:

Preload reduction hasnt been effective?
Positive Inotropic Agents
Dobutamine in ICU
Amrinone and milrinone
Phosphodiesterase inhibitors that perform
the same role
Increase contractility
Decrease afterload
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Positive Inotropic Agents

Digoxin too slow!
Increases contractility, but
Needs several weeks to work
No benefit of digoxin in acute setting
Afterload Reduction
ACEi and ARBs:
Used on discharge
Long-term use with systolic dysfunction (low
EF)
Nitroprusside in ICU
Hydralazine alternate for ACE/ARB
Heparin is always wrong for acute
pulmonary edema, use for clots
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p. 85
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p. 85
Valvular Heart Disease/Definition
Valvular Heart Disease

Definition
Presentation
Diagnosis
Treatment
All can be congenital in nature

Rheumatic fever can lead to any form
and mitral stenosis is most common
Aging = Aortic stenosis
Regurgitant
R
it t via
i HTN & iischemia
h i
Infarction regurgitation
Regurgitation
dilation
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p. 85
29
Valvular Heart Disease/Presentation
Valvular Heart Disease/Diagnostic Tests
All forms associated with SOB and CHF

Only murmurs are specific for presentation
Right-sided heart lesions (tricuspid and
pulmonic valve) increase with inhalation
Inhalation venous return to right side
Left-sided lesions (mitral and aortic valve)
with exhalation
Exhalation squeezes blood out of lungs into
left side
Best initial test: Echocardiogram

Transesophageal: more sensitive &
specific than transthoracic echo
Most accurate test: Catheterization
C th t i ti
Catheterization:
Most precise valvular diameter
Most exact pressure gradient across
valve
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p. 85
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Valvular Heart Disease/Diagnostic Tests
Valvular Heart Disease/Treatment
EKG:
Not specific with valvular heart disease
Shows hypertrophy of chambers
Cannot confirm diagnosis from EKG
Chest X
X-ray:
ray:
Shows enlargement chambers
Precise anatomic correlation poor
X-ray is neither the most accurate
test nor the best initial test
All forms associated with fluid overload

All benefit from diuretics
Meds alone cant improve stenotic
lesions
Mitral
Mit l stenosis:
t
i Dilated
Dil t d with
ith balloon
b ll
Aortic stenosis: Surgical replacement
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p. 85
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p. 86
Regurgitant lesions
Respond best to vasodilators
ACEi/ARBs, nifedipine, or hydralazine
Surgical replacement must be done before
heart dilates too much
If heart dilates excessively valve replacement
will not be able to correct decrease in
systolic function
If myocardium stretches too much it wont
return to normal size and shape
Assess ventricular size based on:

End-systolic diameter
Ejection fraction
Expansion of end-systolic diameter (must
replace
p
the valve))
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p. 86
Endocarditis prophylaxis is not

indicated for any of these valve lesions.
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p. 86
30
Mitral Stenosis (MS)
Mitral Stenosis
Definition/Etiology
Most often from rheumatic fever
Extremely uncommon in US
Low incidence of acute rheumatic fever
Treatment if symptomatic
Do not treat asymptomatic MS
MTB S2CK
p. 86
Look for: Pregnancy and Immigrant

Pregnancy:
50% increase in plasma volume
Contraction of uterus squeezes
squeezes 500 mL
extra into central circulation
Most with MS are immigrants to the US
Come from places where acute rheumatic
fever is still common
MTB S2CK
p. 86
Mitral Stenosis
Mitral Stenosis/Presentation
Presentation
SOB and CHF
AND!
Unique features of presentation:
Enlarged left atrium in

mitral stenosis compresses
the esophagus causing
dysphagia
young adult patients
MTB S2CK
p. 86 87
Mitral Stenosis
MTB S2CK
p. 87
Source: Andrew Peredo
Dysphagia: Left atrium (LA) presses on

esophagus
Hoarseness: LA presses on laryngeal nerve
Atrial fibrillation & stroke from enormous
LA
MS: Look for
Hemoptysis
Mitral Stenosis headphones required
Physical findings
Diastolic murmur after opening snap
Squatting & leg raising increase it!
Increased venous return increases
murmur
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p. 87
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31
Mitral Stenosis
Diagnostic tests
Echo
TTE: Best initial test
TEE more accurate than TTE
Catheterization: Most accurate test
EKG
Atrial rhythm disturbance, particularly atrial
fibrillation, very common
LA hypertrophy: Biphasic P wave: V1 and V2
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p. 87
Mitral Stenosis/Treatment
Diagnostic tests
Chest X-ray: Left
Atrial Hypertrophy
Straightening of left
heart border
Elevation of left main
mainstem bronchus
Second bubble
behind heart
Diuretics & sodium restriction:

When fluid overload present
Balloon valvuloplasty
With a catheter
Valve replacement
Only
O l when
h a catheter
h
procedure
d
cannot be
b done
d
or fails
Warfarin
A-fib to INR 2 to 3
Rate control: Digoxin, beta blockers, or diltiazem/
verapamil
MTB S2CK
p. 87 88
Source : Andrew Peredo
Mitral Stenosis/Diagnostic Tests
MTB S2CK
p. 88
Aortic Stenosis
Aortic Stenosis
Definition/Etiology
Congenital bicuspid valve
Increasing calcification with age
Presentation
Angina (most common)
Syncope
CHF:
Murmur
Systolic, crescendo-decrescendo
Peaks in diamond-shape mid-systole
Heard best at 2nd right intercostal
space
Radiates to carotids
Poorest prognosis
2-year average survival
Source: Shwan Christian
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p. 88
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32
Aortic Stenosis
Aortic Stenosis headphones required
Murmur
Valsalva & standing
Decrease intensity of murmur
Less venous return = Less Murmur
Handgrip
Softens murmur
Less blood ejected = Less murmur
MTB S2CK
p. 88
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p. 88
Aortic Stenosis/Diagnostic Tests
Aortic Stenosis/Treatment
TTE, then TEE,

then catheterization
Chest X-ray
Replacement:
Only truly effective therapy for AS
Diuretics CHF but dont tolerate volume
depletion well
Balloon valvuloplasty
p
y
Not routine for AS
AS calcification doesnt improve well with
balloon valvuloplasty
Only if surgery isnt an option
Unstable/fragile patients
Left ventricular
hypertrophy
EKG
LV hypertrophy (LVH)
Source: Nihar Shah, MD.
S V1 + R V5 > 35 mm
MTB S2CK
p. 89
Cardiac enlargement is defined as a heart greater in

diameter than 50% of the total transthoracic diameter
MTB S2CK
p. 89
Mitral Regurgitation
Definition/Etiology
MR is abnormal backward flow of
blood through mitral valve that doesnt
fit together
Hypertension
Endocarditis
Myocardial infarction
Papillary muscle rupture
Any heart dilation leads to MR
Presentation
Signs/Symptoms of CHF
Unique finding:
Pansystolic (holosystolic) murmur
Obscures S1 and S2
Radiates to axilla
Handgrip worsens murmur of MR
Handgrip increases afterload
Pushes blood backwards
Handgrip worsens AR and MR
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p. 89
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p. 90
33
Mitral Regurgitation/Presentation
Mitral Regurgitation headphones required
Squatting & leg raising worsen MR

Increase venous return to heart
All left-sided murmurs except mitral
valve prolapse (MVP) and hypertrophic
obstructive cardiomyopathy will
increase with expiration
MR diagnosed with echo
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p. 90
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p. 90
Mitral Regurgitation/Treatment
Treatment
Vasodilators:
ACE or ARBs are best
Decrease rate of progression
Digoxin & diuretics for symptomatic
CHF
Valve replacement:
Indicated when heart dilates
Dont wait for left ventricular end systolic
diameter (LVESD) to become large
Replace
R l
when:
h
LVESD > 40 mm or EF
< 60%
Valve repair:
Placing a clip or sutures across valve to
tighten
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p. 90
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p. 90
Aortic Regurgitation
Definition/Etiology
AR caused by:
Anything that makes the heart or aorta dilate:
MI
HTN
Endocarditis
Marfan syndrome or cystic medial necrosis
Inflammatory disorders (e.g., Ankylosing
spondylitis, Reiter syndrome)
Syphilis
Presentation
Besides CHF unique physical findings are:
Wide pulse pressure
Water-hammer (wide, bounding) pulse
Quincke pulse (pulsations in nail bed)
Hill sign (BP in legs as much as 40 mmHg
above arm BP)
Head bobbing (de Musset sign)
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p. 90 91
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p. 91
34
Aortic Regurgitation headphones required
Murmur
Diastolic, decrescendo murmur
Heard best: Lower left sternal border
Valsalva & Standing: Softer
Handgrip (increases afterload): Worse
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p. 91
Diagnostic tests
EKG & Chest X-ray: LVH
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p. 91
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p. 91
Treatment
ACEi/ARBs or nifedipine:
Vasodilators
Increase forward flow of blood
Delay progression
Digoxin & Diuretics: Little benefit
Surgical valve replacement:
Acute valve rupture (MI)
Replace valve before LV dilates excessively
EF < 55%
LVESD > 55 mm
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p. 91
Mitral Valve Prolapse (MVP)
Mitral Valve Prolapse
Presentation
Most often asymptomatic
When symptoms do occur:
Symptoms of CHF usually absent
Most common is:
Common
Considered normal anatomic variant
2% to 5% of population
Particularly in women
Marfan or Ehlers-Danlos syndrome
Atypical chest pain

Palpitations
Panic attack
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p. 91
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35
Mitral Valve Prolapse headphones required
Murmur
Presents with:
Midsystolic click
When severe associated with murmur
Mitral regurgitation
Valsalva & Standing worsen MVP
Squatting & Handgrip improve
(diminish) MVP
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p. 92
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Redundant mitral
valve leaflet doesnt
seal allowing
regurgitation
Diagnostic tests
Echocardiography: Best choice
Catheterization: Rarely, if ever, done
Valve replacement: Rarely needed
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p. 92
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Treatment
Beta blockers:
When symptomatic
Valve repair
With catheter
Place clip to tighten valve
Stitches valve to tighten leaflets
Surgical repair rarely necessary
Endocarditis prophylaxis not recommended
MTB S2CK
Cardiomyopathy &
Pericardial Disease
Dilated Cardiomyopathy
Hypertrophic
h Cardiomyopathy
d
h
Restrictive Cardiomyopathy
Acute Pericarditis
Pericardial Tamponade
Constrictive Pericarditis
p. 92
36
Cardiomyopathy/Definition
Cardiomyopathy/Etiology
Abnormal function of heart muscle

Frequent valve or auscultory
abnormalities
But!
It originates
i i t from
f
an abnormally
b
ll
contracting or relaxing myocardium
Can be dilated, hypertrophic, or restrictive

The terms dilated cardiomyopathy, systolic
dysfunction, and low EF are often used
interchangeably
Hypertrophic cardiomyopathy
interchangeable with diastolic dysfunction
Or!!
Cardiac failure with preserved EF
MTB S2CK
p. 92
MTB S2CK
p. 93
Cardiomyopathy/Presentation
Cardiomyopathy/Diagnostic Tests
All forms give:

SOB, particularly worsened by exertion
Edema
Rales
JVD
Echocardiography:
Best initial test
Often Most accurate test used
EKG & Chest X-ray:
Should be performed
Nothing specific on them confirm the
diagnosis
Murmurs not increasing
with expiration:
HOCM
MVP
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p. 93
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Cardiomyopathy/Treatment
All treated with diuretics

Other treatments based on type of
cardiomyopathy
The only real functional difference in
management and answers to questions
is: TREATMENT
In addition to previous MI and ischemia,

dilated cardiomyopathy can be from:
MTB S2CK
p. 93
Alcohol
Postviral myocarditis
Radiation
Toxins (e.g., doxorubicin)
Chagas disease
MTB S2CK
p. 93
37
Dilated Cardiomyopathy/Treatment
Dyspnea, gallop, edema, testing same

as section on CHF
MTB S2CK
Multiple meds mortality

ACEi (or ARBs)
Beta blockers (metoprolol, carvedilol)
Spironolactone (or eplerenone)
Symptom Control ONLY:
Diuretics & Digoxin
p. 93
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p. 93
Dilated Cardiomyopathy/Treatment
Hypertrophic Cardiomyopathy
QRS wide (> 120 ms)

Biventricular pacemaker
Improve both symptoms and survival
Automated implantable
cardioverter/defibrillator
di
t /d fib ill t has
h mortality
t lit
benefit
HTN - MCC
MUST distinguish between hypertrophic
cardiomyopathy (HCM) and HOCM
HCM: Reaction to BP
Heart hypertrophies
yp
p
to carry
y load
Develops difficulty relaxing in diastole
Cant relax = Cant receive blood
Patient becomes short of breath
MTB S2CK
p. 93 94
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Hypertrophic Obstructive Cardiomyopathy
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p. 94 95
Hypertrophic Cardiomyopathy
Genetic disorder
Abnormal shape of
septum
Asymmetrically
hypertrophied septum
and valve leaflet blocks
blood leaving the heart
p. 94
S4 gallop
Fewer signs of right heart failure
Less ascites
Less enlargement of liver and spleen
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p. 94
38
HOCM/Diagnostic Tests
HOCM/Presentation
Dyspnea
Chest pain
Syncope & lightheadedness
Sudden death, particularly in healthy athletes
Worsened by heart rate
(e.g., exercise, dehydration, and diuretics)
Worsened by
size
Systolic anterior motion

(SAM) of mitral valve is
classic for HOCM. It
contributes
t ib t tto obstruction.
b t ti
Catheterization is most
accurate test to
determine precise
gradients of pressure
across the chamber.
in left ventricular chamber
(e.g., ACEi, ARBs, digoxin, hydralazine, valsalva,

and standing suddenly)
MTB S2CK
Echo (best initial test)

Septum 1.5x thickness of posterior wall
p. 94
EKG: Nonspecific ST and

T wave changes are
common. LVH is
common. EKG can be
normal in a quarter
MTB S2CK
Septal Q waves in the

inferior and lateral
leads are common in
HOCM.
p. 95
Hypertrophic Cardiomyopathy/Treatment
HOCM/Specific Therapy
Beta blockers:
Best initial therapy both HOCM &
HCM
Diuretics help HCM
Implantable defibrillator:
HOCM with syncope
Ablation of septum:
Catheter placing absolute alcohol in muscle
Causes small infarctions
If symptoms
t
persist:
i t Surgical
S i l myomectomy
t
Diuretics harm HOCM

Digoxin and spironolactone are
definitely always wrong in
hypertrophic cardiomyopathy.
MTB S2CK
p. 95
Surgical myomectomy
is the therapy only if all
medical and catheter
procedures fail.
MTB S2CK
In HOCM, ACEi and

diuretics definitely dont
help. This is the major
difference between
HOCM and HCM
p. 95
Hypertrophic versus Dilated Cardiomyopathy
Hypertrophic
Dilated
Beta Blockers
Yes
Yes
Diuretics
Yes
Yes
ACEi/ARB
Unclear benefit
Yes
Spironolactone
No
Yes
Digoxin
No
Yes
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p. 95
Combines worst aspects of dilated and

hypertrophic cardiomyopathy
Heart neither contracts nor relaxes
Infiltrated with substances creating
immobility
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p. 96
39
Causes are:
Sarcoidosis
Amyloid
Hemochromatosis
Endomyocardial fibrosis
Scleroderma
Presentation
Dyspnea: Most common
Right heart failure
Ascites, edema, JVD
Enlargement
g
of liver & spleen
p
Pulmonary hypertension: Common
Kussmaul sign:
jugulovenous pressure on inhalation
MTB S2CK
p. 96
MTB S2CK
Diagnosis
Echocardiography: Initial test
EF normal or elevated
EKG: Low voltage
Amyloid: Speckling of septum on echo or
cardiac MRI
Most accurate test:
Endomyocardial biopsy
Rarely done
Diagnosis made from biopsies elsewhere
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p. 96
Squatting/Leg raising
Standing/Valsalva
Increases both
Decreases both
Mitral and aortic

regurgitation
Increases both
Decreases both
Mitral valve
prolapse
Decrease
Increase
HOCM
Decrease
Increase
p. 96
p. 96
Murmurs and the Effects of Maneuvers
Mitral and aortic

stenosis
MTB S2CK
Treat underlying cause

Diuretics relieve some pulmonary HTN
and signs of right heart failure
No other clear therapy
MTB S2CK
Murmurs and the Effects of Maneuvers
Lesion
p. 96
More blood increases all

murmurs except MVP and
HOCM.
Less blood decreases all

murmurs except MVP and
HOCM.
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40
Effects of Maneuvers
Standing from a squatting position:

Opens vessels of legs
Decreases venous return to heart
Valsalva:
Exhalation against a closed glottis
Increases intrathoracic pressure
Decreases venous return to heart
MTB S2CK
p. 97
MVP & HOCM: Worsen with diuretics

Diuretics decrease LV size
Diuretics worsen MVP and obstruction
of HOCM
Standing
St di and
d valsalva
l l worsens them
th
MTB S2CK
p. 97
Amyl nitrate:
Direct arteriolar vasodilator
Decreases afterload
Simulates ACE inhibitors or ARBs on heart
Valvular disease treated with ACEi/ARB will
improve with amyl nitrate
Improves AR and MR
Handgrip = Fuller left ventricle
Amyl nitrate = ACEi = Emptier left ventricle
MTB S2CK
p. 97
Standing or Valsalva = Diuretic use

Stenotic & regurgitant murmurs all
treated with diuretics and salt restriction
Standing
St di & Valsalva
V l l will
ill improve
i
th
them
MTB S2CK
p. 97
Handgrip
Handgrip increases afterload
Contraction of arm muscles compresses
arteries
Decreases emptying of heart
Opposite of ACE inhibitor
Worsens AR and MR
MTB S2CK
p. 97
Effect of Maneuvers on
Intensity (loudness) of Murmurs
Lesion
Handgrip
Amyl nitrate
Aortic stenosis
Decreases
Increases
Mitral stenosis
No effect
No effect
A i regurgitation
Aortic
i i
I
Increases
D
Decreases
Mitral regurgitation
Increases
Decreases
Mitral valve prolapse
Decreases
Increases
HOCM
Decreases
Increases
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p. 97
41
Effect of Maneuvers on
Intensity (loudness) of Murmurs
Handgrip and amyl nitrate have no

meaningful effect on mitral
stenosis in the same way ACEi
stenosis,
has no meaningful effect on MS
MTB S2CK
p. 97
Pericardial Disease
Causes of pericarditis, pericardial tamponade

& constrictive pericarditis overlap
If the etiology of pericarditis extravasates
fluid, then tamponade can occur
If the cause of pericarditis is chronic, fibrosis
and calcification of pericardium lead to
constrictive pericarditis
MTB S2CK
p. 98
Pericarditis/Etiology
Pericarditis/Etiology
Any
Infection
Inflammatory disorder
Connective tissue disorder
Chest trauma or cancer near the heart
can cause pericarditis
Systemic lupus erythematosus:

Most common connective tissue disorder
But
Wegener granulomatosis
Goodpasture syndrome
Rheumatoid arthritis
Polyarteritis nodosa and others
can cause pericarditis
Most common infection is viral

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p. 98
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p. 98
Pericarditis/Presentation
Pericarditis/Diagnostic Tests

Sharp chest pain
Changes with respiration
Changes with position of body
Worsened by lying flat
Improved by sitting up
EKG shows ST segment elevation in all leads, but

the most specific finding is PR segment depression
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p. 98
MTB S2CK
p. 98 99
42
Pericarditis/Treatment
Pericardial Tamponade/Etiology
Treat cause
Majority: Idiopathic
Any cause of pericarditis can extravasate

enough fluid to cause tamponade
Compression heart starts on right side
Walls are thinner
50 mL acutely
y cause tamponade
p
Over weeks to months, pericardium stretches
for 2 L of fluid
Can also be from trauma
Bleed requires emergent thoracotomy
Idiopathic presumed viral

Coxsackie B virus
T
Treated
t d with
ith NSAIDs
NSAID (e.g.,
(
ibuprofen,
ib
f
naproxen)
Colchisine - recurrences
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p. 99
Pericardial Tamponade/Presentation
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p. 99

Hypotension
Tachycardia
Distended neck veins
Clear lungs
Which of the following physical findings is
most likely to be associated with this patient?
Pulsus paradoxus
Decrease of more than 10 mmHg in
systolic blood pressure on inhalation
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p. 99
EKG:
Electrical alternans (different heights of QRS
complexes between beats)
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Chest X-ray:
Enlarged cardiac shadow expanding in both
directions (globular heart)
Echocardiogram:
Right atrial and ventricular diastolic collapse
Right heart catheterization:
Equalization of pressures in diastole
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43
78-year-old man with lung cancer experiences several days of
increasing SOB. Hes lightheaded today. BP 106/70; pulse
112; JVD present; lungs: clear, BP drops to 92/58 on
inhalation.
Which is most appropriate to confirm the diagnosis?
a.
b
b.
c.
d.
e.
EKG Low voltage non-specific. Rare alternans

y; globular
g
heart later
Chest X-ray
X ray Normal acutely;
Echocardiogram
Most accurate;
Right heart catheterization should do echo first
Cardiac MRI Not clearly right for
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Treatment
Pericardiocentesis
Needle rapidly reexpands the heart
IV fluids
A hole or window recurrent cases
Diuretics will decrease intracardiac
filling pressure and may markedly
worsen collapse of right side of heart
ANYTHING at this time
p. 100
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Constrictive Disease
Any cause of pericarditis with

calcification and fibrosis
Prevents filling of right side of heart
Tuberculosis

Signs of right heart failure such as:
Edema
Ascites
Enlargement of liver and spleen
JVD
Constrictive pericarditis is a combination of

physical findings described above with
calcification on chest X-ray
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Pericardial Knock headphones required
Which physical findings is most likely

associated with this patient?
Kussmaul sign:
Increase in JVD on inhalation
Normally neck veins go down on inhalation
Knock:
Extra heart sound in diastole
From ventricular filling
Heart fills to its maximum, it hits the stiff, rigid
pericardium with a knock
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44
Best initial test

Chest X-ray: Calcification & fibrosis
CT scan or MRI more accurate, not 1st

Echocardiogram: Excludes RV
hypertrophy or cardiomyopathy as
cause
Myocardium moves normally with
constrictive pericarditis
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Commons.wikimedia.org.
Used with permission
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Treatment
Diuretics:
Decompress filling of heart
Relieves edema and organomegaly
Surgical removal of pericardium
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Peripheral Artery Disease, Aortic

Disease, & Heart Disease
in Pregnancy
Definition
Etiology
Presentation
Diagnosis
Treatment
p. 101
Peripheral Artery Disease (PAD)/Etiology
Peripheral Artery Disease/Presentation
Stenosis of peripheral arteries from:

Diabetes mellitus
Hyperlipidemia
Hypertension
Tobacco smoking

Pain in calves on exertion
Relieved by rest
Walking up or down hills
Severe disease causes loss of:
Same causes as Coronary Disease!!
Hair
H i ffollicles
lli l
Sweat glands
Sebaceous glands
The skin becomes smooth and shiny

Spinal stenosis pain is worse when walking
down hills because of leaning back
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45
Peripheral Artery Disease

Diagnostic tests
Best initial test = Ankle-brachial index (ABI)
ABI: Ratio of BP in ankles to brachial arteries
Normally equal or slightly greater in ankles
because of gravity
If difference between them is > 10% (ABI < 0
0.9),
9)
disease is present
Most accurate test = angiogram
Angiogram not necessary unless revascularization
will be done
Peripheral Artery Disease
Treatment
The best initial therapy is:
Aspirin
Smoking cessation
Cilostazol
Single most effective medication: Cilostazol

Surgery or angioplasty if medical therapy not
effective
In all major vascular disease
control the following:
BP
LDL < 100
Diabetes
There is no routine screening for PAD since

there is no mortality benefit to be obtained
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Aortic Dissection
67-year-old man in ED with sudden onset chest pain
is also felt between his scapulae. He has a history of
HTN and tobacco smoking. BP 169/108.
a.
b.
c.
d.
e.
f.
g.
Chest X-ray
Chest CT Dont show specific changes
MRA, TEE, and CTA
MRA
have same accuracy;
Transesophageal echocardiogram
not most accurate,
Transthoracic echocardiogram
neither best initial
CT angiogram
Angiography Most accurate, but not best initial test
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Aortic Disease
Most frequently tested points in aortic disease

Diagnosis & treatment of acute dissection
Screening recommendations
Key points for presence of aortic dissection
Pain in between the scapulae
Difference in blood pressure between the arms
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Author: J. Heuser; commons.wikimedia.org

p. 103
p. 103
Aortic Disease/Treatment
For dissection, Most important step is: Control BP
This can be done with:
Beta blockers
Nitroprusside
Beta blockade decreases shearing forces that

worsens dissection
Beta blockers must start before nitroprusside to
protect against reflex tachycardia of nitroprusside,
which worsens shearing forces
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46
Abdominal Aortic Aneurysm

Which of the following is the most appropriate
screening for aortic aneurysm?
a.
b.
c.
d
d.
e.
Everyone > 50 with CT angiography

Men who ever smoked > 65 with ultrasound
Everyone > 50 with ultrasound
Everyone > 65 with ultrasound
Men > 65 with ultrasound
Incidence of AAA is less in both nonsmokers
and in women, so there is no recommendation
for screening in those groups
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p. 104
Peripartum Cardiomyopathy
Which of the following is most dangerous to a
pregnant woman?
a.
b.
c.
d.
e.
Mitral stenosis
Peripartum cardiomyopathy
Choose this if p
peripartum
p
Ei
Eisenmenger
phenomenon
h
cardiomyopathy is not one of
the choices
Mitral valve prolapse
Atrial septal defect
Not as dangerous as choices b and c
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p. 104
Unknown why antibodies are made

against the myocardium in some
pregnant women
LV dysfunction often reversible and
short term
If LV dysfunction does not improve, then
must undergo cardiac transplantation
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Peripartum Cardiomyopathy
Eisenmenger Syndrome
Therapy the same as for dilated cardiomyopathy of

any cause:
From right-to-left shunt from pulmonary

HTN
Develops in person with ventricular septal
defect with left-to-right shunt that eventually
develops pulmonary HTN
When pulmonary HTN becomes very severe
shunt reverses
Right-to-left shunting develops
ACEi/ARB
Beta blockers
Spironolactone
Diuretics
Digoxin
Repeat pregnancy with peripartum cardiomyopathy

will kill 50-70% of women!!
Peripartum cardiomyopathy develops
after delivery in most cases;
ACEi/ARBs must be used
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47
Large left-to-right shunt

(congenital heart defect)
If peripartum cardiomyopathy is not one of

the choices in asking, What is the worst
cardiac disease in pregnant women? then
Look for Eisenmenger in the choices
P l
Pulmonary
HTN
Pregnancy increases plasma volume by 50%.

Mitral stenosis will worsen in pregnancy,
But not as much as peripartum cardiomyopathy
or Eisenmenger
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Reverse of the shunt:

right-to-left shunt
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48
Dermatology Part 1
Dermatology Part 1
Cutaneous Malignancies
Atopic Dermatitis (Eczema)
Psoriasis
Pityriasis Rosea
Seborrheic Dermatitis (Dandruff)
Blistering Diseases
Conrad Fischer, MD
New York City
Cutaneous malignancies
Malignant Melanoma
More frequent in sun-exposed areas

But!
Not exclusive to those areas
Benign vs. Malignant
Melanoma clinically ABCDE:
A: Asymmetry
B: Border irregularity
C: Color irregularities
D: Diameter > 6 mm
E: Evolution (changing over time)
Greater with pale skin

More sun-exposed areas
Diagnosis: Biopsy
Treatment: Surgical removal
No truly effective chemotherapy
Skin Cancer
More sun, more cancer
Biopsy
Remove
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Malignant Melanoma
Distinction Between Benign and Malignant
Diagnosis?
Suspicious?
Benign
Malignant
Round
Asymmetric
Even borders
Borders uneven
Color evenly spread
Color uneven
Diameter constant
Diameter increases
Biopsy!
Include entire thickness of lesion if
possible
ibl
Worst prognosis!!
Growing lesions
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Malignant Melanoma
Benign Lesion
Diagnostic Test
Full thickness biopsy: indispensible
Dont perform shave biopsy
Treatment/Prognosis
Surgical removal
Must include normal skin surrounding lesion
Interferon injection helpful in widespread
disease
Melanoma has strong tendency to metastasize
to brain
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p. 364
Squamous Cell Cancer
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Squamous Cell Cancer
Sunlight
Organ transplant!!!!
Immunosuppressive drugs!
Squamous starts looking like ulcer
Doesnt heal, grows
Biopsy and remove
Source: James Heilman MD
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p. 364
Basal Cell Carcinoma
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Basal Cell Carcinoma
Most common skin cancer

Question describes:
Waxy lesion
Shiny like a pearl

U
Unlike
lik melanoma,
l
wide
id margins
i nott
necessary
Shave biopsy fine! (diagnostic)
Recurrence < 5%
Basal cell: use Mohs microsurgery
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Basal Cell Carcinoma/

Mohs Micrographic Surgery
Remove skin cancer under dissecting

microscope
Very thin slices of skin
Immediate frozen section
VERY precise way to treat skin cancer
Mohs:
Basal Cell Carcinoma/

Mohs Micrographic Surgery
Stop resecting when margin is cancerfree

No removal of wide margins
Mohs Best:
Delicate areas
Eyelid & Ear
Remove cancer
Keep normal
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Kaposi Sarcoma (KS)
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Kaposi Sarcoma (KS)
In past, KS seen only in older men of

Mediterranean origin
Now: AIDS
From HHV-8, which is oncogenic
Reddish/purplish
R ddi h/
li h
More vascular than others
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Kaposi Sarcoma (KS)
Kaposi Sarcoma/Treatment
Also in GI tract and lung

Only from AIDS via sexual contact
associated with KS
IDU AIDS rarely associated with KS
Unlike other skin cancers, KS not

routinely removed surgically
1. Treat AIDS with antiretrovirals
2. Majority disappear as CD4 improves
3 Intralesional
3.
I t l i
l iinjections
j ti
off vincristine
i i ti or
interferon
4. If these fail, use chemotherapy with
liposomal doxorubicin
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Actinic Keratoses
Actinic Keratoses
Premalignant
From high-intensity sun exposure in fairskinned people
Very small risk of SCC for each
individual lesion
Richard Usatine, M.D.

Used with permission.
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Actinic Keratoses
Actinic Keratoses
Many occur in a single person

Risk is cumulative
Like cervical dysplasia and cervical cancer
Slow to progress
Remove with:
Curettage
Cryotherapy
Laser
Topical 5-fluorouracil
Imiquimod

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p. 366
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Actinic Keratoses
Seborrheic Keratoses
Imiquimod
Local immunostimulant
Also for molluscum contagiosum
Condyloma acuminatum
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p. 366
Extremely common in elderly

Hyperpigmented lesions
Commonly referred to as liver spots
Stuck on appearance
May look like melanoma to some people
Seborrheic keratoses = Zero malignant
potential
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p. 366
Removed with:
Cryotherapy
Surgery
Laser
Removal (cosmetic reasons)
Source: James Heilman MD
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p. 366
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Atopic Dermatitis (Eczema)
Atopic Dermatitis (Eczema)/Presentation
Common skin disorder

Associated with overactivity of mast cells &
immune system
Look for history of:
Asthma
Allergic rhinitis
Family history of atopic disorders
Onset < age 5, very rare to start > 30
From premature and idiosyncratic release

of transmitters (e.g., histamine)
Pruritus & scratching is most common
presentation
Scratching leads to scaly rough areas of
thickened skin
On face, neck & skin folds
Popliteal area behind knee
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p. 366

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Atopic Dermatitis (Eczema)/Skin Care
Itching
scratching
Scratching
more itching
Superficial skin infections from Staphylococcus are
common
Microorganisms driven under epidermis by
scratching
This, in turn,
more itching
1. Stay moisturized: dry skin is more itchy

2. Use a humidifier, especially in winter
3. Avoid bathing, soap, and washcloths (skin
hyperirritable)
4. Avoid brushes,, washcloths,, hot water,, and
anything that rubs on skin
5. Cotton less irritating than wool
Skin thickened because of

scratching and drying =
lichenified
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Food allergies dont

exacerbate atopic
dermatitis
p. 367
IgE levels: Elevated in

atopic dermatitis
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p. 367
Atopic Dermatitis (Eczema)/Medical Therapy
Atopic Dermatitis (Eczema)/Medical Therapy
1. Topical corticosteroids: used in flares of

disease (oral steroids only in most severe
acute flares)
2. Tacrolimus and pimecrolimus
3. Antihistamines:
T cellinhibiting agents
L
Longer-term
t
control
t l
Help get patient off steroids
Used systemically in organ transplant
recipients
Prevent organ rejection
Used topically for atopic dermatitis
MTB S2CK
p. 367
Psoriasis/Definition/Presentation
Mild disease: nonsedating drugs

(cetirizine, fexofenadine, loratadine)
Severe disease: hydroxyzine,
diphenhydramine, doxepine
4. Antibiotics (e.g., cephalexin, mupirocin,

retapamulin) when impetigo occurs
5. UV light (phototherapy) for severe
recalcitrant disease
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p. 367
Psoriasis/Definition/Presentation
Incredibly common
2 million in US
Characterized by silvery, scaly plaques
Not itchy most of the time
Arthritis < 10%
Extensive disease associated with
depression
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p. 367
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Psoriasis/Treatment
Local Disease
1. Topical high-potency steroids: fluocinonide,
amcinolone, betamethasone, clobetasol
2. Vitamin A & Vitamin D ointment
Helps get patient off steroids
Vitamin D agent is calcipotriene
Steroids cause skin atrophy
3. Coal tar preparation
4. Pimecrolimus and tacrolimus
Used in delicate areas (e.g., face & penis)
Alternative to steroids
Less deforming
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p. 368
Psoriasis/Treatment
Steroids cause atrophy

Inhibit collagen formation and growth
Convert AAs
glucose
Gluconeogenesis
MTB S2CK
p. 368
Psoriasis/Treatment
Extensive Disease
1.UV light
2.Antitumor necrosis factor (TNF) inhibitors
Etanercept
Adalimumab
Infliximab
Miraculous for severe disease
3.Methotrexate:
Last because of effects on liver & lung
First for psoriatic arthritis
MTB S2CK
p. 368
Pityriasis Rosea
TNF inhibitors reactivate TB

Screen with PPD prior to use
MTB S2CK
p. 368
Pityriasis Rosea
Idiopathic, transient dermatitis

Starts with a single lesion (herald patch)
Then disseminates
Can look like secondary syphilis
But spares palms & soles
Transient
If symptomatic: treat with steroids or UV
light
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Increased in:
Hypersensitivity reaction
Dermal infection
Noninvasive dermatophyte organisms
Both topical steroids and antifungal
agents
t (e.g.,
(
kketoconazole)
t
l ) are useful
f l
AIDS
Parkinsons disease
Seborrheic = Benign
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p. 369
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Pemphigus Vulgaris
Pemphigus Vulgaris
Both idiopathic/autoimmune form and

Drug induced form
Associated with:
ACE inhibitors
Penicillamine
Phenobarbital
Penicillin
Autoantibodies split epidermis, resulting

in:
Bullae that easily rupture
Thin-walled
Involvement
I
l
t off mouth
th
Fluid loss & infection
Widespread (acts like burn)
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Pemphigus Vulgaris
p. 369
Pemphigus Vulgaris
Source: phil.cdc.gov
Pemphigus Vulgaris
Pemphigus Vulgaris
Characteristic finding: Nikolsky sign

Loss or denuding of skin from mild
pressure
Most accurate test = biopsy

Biopsy shows: autoantibodies on
immunofluorescent (IF) studies
Nikolsky
y sign:
g
Removal of superficial layer of skin
Single sheet while pulling on it
Fingers worth of pressure
MTB S2CK - p. 370
Without treatment,
pemphigus is fatal
MTB S2CK
p. 370
Pemphigus Vulgaris/Treatment
Bullous Pemphigoid
1. Systemic steroids (prednisone)

2. Azathioprine or mycophenolate to wean
patient off steroids
3. Rituximab (anti-CD20 antibodies) or IVIG
in refractory cases
Much milder than pemphigus:

Bullae stay intact
Less loss of fluid
Less infection
Mouth involvement uncommon
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Bullous Pemphigoid
p. 370
Bullous Pemphigoid
Biopsy with IF stains is Most accurate test

Best initial therapy: Prednisone
To get patients off steroids, use azathioprine,
cyclophosphamide, or mycophenolate
Mild bullous p
pemphigoid
p g
responds
p
to
erythromycin, dapsone, and nicotinamide
(not niacin)
Nikolsky sign absent in
bullous pemphigoid
MTB S2CK
p. 370
Porphyria Cutanea Tarda
Blistering skin disease

Sun-exposed areas
With history of:
Liver disease
Hepatitis C
Alcoholism
Estrogen use
Iron overload (hemochromatosis)
MTB S2CK
p. 370
Porphyria Cutanea Tarda
Hepatitis C:
Most frequently tested association with
PCT
Look for involvement of:
backs of hands & face
MTB S2CK
p. 370
Porphyria Cutanea Tarda/

Diagnostic Tests/Treatment
Most accurate test

Increased uroporphyrins on 24-hr urine
Deficiency of uroporphyrin decarboxylase
activity
Treatment
Correct underlying cause
Stop alcohol
Stop estrogens
Remove iron with phlebotomy
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Dermatology Part 2
Skin Infections
Drug Reactions
Staphylococcal Scalded Skin Syndrome and
Toxic Shock Syndrome
Acne
p. 370
Impetigo
Impetigo/Treatment
Most superficial bacterial skin infection

Staphylococcus and Streptococcus
invade epidermis
Results in weeping, crusting, oozing, &
draining of skin
Mild disease with topical agents:

Mupirocin
Bacitracin
Retapamulin
Severe disease with oral agents:
Dicloxacillin or cephalexin
Community-acquired MRSA with:
Doxycycline
Clindamycin
Trimethoprim/sulfamethoxazole (TMP/SMZ)
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10
Erysipelas
Erysipelas/Presentation
Much more severe than impetigo

Occurs at deeper level in skin
Streptococcus > Staphylococcus
Invades dermal lymphatics
Causes bacteremia,
bacteremia leukocytosis
leukocytosis, fever
fever, and
chills
Fatal, if untreated
Bright, red, hot swollen

Lesion on face
Leukocytosis
Often systemic disease
Skin infections can cause glomerulonephritis,

but not rheumatic fever.
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p. 371
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Erysipelas/Presentation
p. 371
Erysipelas/Treatment
Although erysipelas is more often from
Streptococci, you must treat for Staphylococcus
as well unless you have a definitive diagnostic test
such as blood cultures.
Treatment of all skin infections is similar
Same answers as for:
Source: Thomas F Sellers
Cellulitis
Folliculitis
Furuncles
Carbuncles
MTB S2CK
p. 371
Mild disease - oral medications:

Dicloxacillin, cephalexin, cefadroxyl
Penicillin allergic: erythromycin,
clarithromycin, or clindamycin
Severe disease (e.g., fever):

IV medications:
Oxacillin, nafcillin, cefazolin
Penicillin allergic: Clindamycin, vancomycin
MRSA:
Vancomycin, linezolid, daptomycin,
tigecycline, ceftaroline
MRSA:
Doxycycline, clindamycin, or TMP/SMX
Cross reaction
Between penicillin and cephalosporins
unusual (< 5%)
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p. 372
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11
Step 2 CK tests:
Route of administration
(O l vs Intravenous)
(Oral
I t
)
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p. 372
Cellulitis
Cellulitis
Soft tissue infection of skin

Extends from dermis into subcutaneous
tissue
Skin: Warm, red, swollen, and tender
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p. 372
Cellulitis
Involves legs > arms
Doesnt have collections of walled-off infection,
which is an abscess
Cellulitis isnt only at hair follicle; that's folliculitis,
furuncles, and carbuncles
Skin infection: Caused by S. aureus
NOT S. epidermidis
S. epidermidis lives on skin as normal flora
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Cellulitis/Diagnostic Tests
Cellulitis/Treatment
No diagnostic testing needed

Most accurate test
Same as for erysipelas

Topical antibiotics will not cover
cellulitis
Below dermal/epidermal junction
Topical
T i l antibiotics
tibi ti wontt reach
h
Inject sterile saline into skin & aspirate

for culture
Yield only 20%
Staphylococcus > Streptococcus
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Folliculitis, Furuncles, Carbuncles
Originate around hair follicles

Different terms dont have precise
definitions
Indistinguishable, no cutoff in size
Folliculitis, Furuncles, Carbuncles/

Size of the Infection
Folliculitis: Earliest & mildest

Furuncle: Small abscess or collection of
infected material
Carbuncle: Collection of furuncles
Folliculitis < Furuncle < Carbuncle
Severe disease =
fever, chills, bacteremia
Treat: Ox/Clox/Diclox/Naf
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Source: cdc.gov

Penicillin Allergy
Reaction - Rash
Use cephalosporins
Reaction - Anaphylaxis
Mild infection: Macrolides, clindamycin,
doxycycline, or TMP/SMZ
Severe infection: Vancomycin, linezolid,
daptomycin, or tigecycline
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13

Other Antistaphylococcal Medications
Fungal Infections
Beta-lactam/beta-lactamase combinations
Amoxicillin/clavulanate
Ticarcillin/clavulanate
Ampicillin/sulbactam
Piperacillin/tazobactam
Carbapenems (imipenem, meropenem)
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p. 373 374
Dermatophyte = superficial fungal

infection = tinea
For example:
Tinea corporis
p
= body
y
Tinea manum = hand
Tinea pedis = foot
Tinea cruris = groin (jock itch)
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Fungal Infections
p. 374
Fungal Infections/Diagnostic Tests/Treatment
Best initial test

KOH (potassium hydroxide)
Dissolves epidermal skin cells
Leaves fungi intact
Most accurate test
Fungal culture

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p. 374
Fungal Infections/Diagnostic Tests/Treatment
Fungal Infections/Treatment
Best initial therapy

Topical antifungal agent if no hair or
nails involved
For hair (tinea capitis) and nail (tinea
unguium)
Topical antifungal agents:

Clotrimazole
Ketoconazole
Oral ketoconazole
Econazole
causes gynecomastia
Miconazole
Mi
l
Nystatin
Ciclopirox
Terbinafine
Itraconazole
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14
Fungal Infections/Oral and Vaginal Candidiasis
Drug Reactions
Hypersensitivity reactions to medications vary in

severity
When severity of reaction changes, the name of
reaction changes
Drugs causing hypersensitivity reactions:
Penicillins
Sulfa drugs (including thiazides, furosemide, and
sulfonylureas)
Allopurinol
Phenytoin
Lamotrigine
NSAIDs
Same answers for both

KOH: Best initial test
Fungal culture: Most accurate test
With clear presentation: Treat
Topical antifungal from previous list
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Drug Reactions
Morbilliform Rash
Drugs that cause hypersensitivity

reactions of the skin are the same
that cause:
Hemolysis
Interstitial
I t titi l nephritis
h iti
Thrombocytopenia
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p. 375
Mildest reaction
Skin stays intact
No mucous membrane involvement
No specific therapy
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Morbilliform Rash
p. 375
Erythema Multiforme
Widespread
Target lesions
Mostly on trunk
Mucous membrane uninvolved
From herpes or mycoplasma
Prednisone may benefit
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15
Erythema Multiforme
Stevens Johnson Syndrome
Erythema multiforme
is characterized by
multiple small
target-shaped
l i
lesions
that
th t can b
be
confluent
MTB S2CK
p. 375
Toxic Epidermal Necrolysis
Mucous membrane involvement

Nikolsky sign
Steroids definitely dont help
Treat with IVIG
MTB S2CK
p. 375
Very severe
Involves mucous membranes
Sloughs off respiratory epithelium
May lead to respiratory failure
Steroids not beneficial
Use intravenous immunoglobulins
(IVIG)
MTB S2CK
p. 375
Toxic Epidermal Necrolysis
The skin comes

off in a sheet,
simulating a
burn.
MTB S2CK
p. 376
Source: Conrad Fischer, MD
Staphylococcal Scalded Skin Syndrome (SSSS)

and Toxic Shock Syndrome (TSS)
Staphylococcal Scalded Skin Syndrome and

Toxic Shock Syndrome
Different severities of same event

Reaction to toxin in surface of Staphylococcus
SSSS looks similar to TEN, including Nikolsky
sign
life
TSS has skin involvement as well as lifethreatening multi-organ involvement:
Both treated with:

Antistaphylococcal medications
Oxacillin or nafcillin are most effective
Cefazolin is essentially equal
Antibiotics dont reverse disease
Kills Staphylococcus that produces toxin
Hypotension
Renal dysfunction ( BUN and creatinine)
Liver dysfunction
CNS involvement (delirium)
MTB S2CK
p. 377
MTB S2CK
p. 377
16
Acne/Treatment
Acne/Treatment
Mild acne
Topical antibacterials: Benzoyl peroxide
If ineffective add topical antibiotics
(e.g., clindamycin or erythromycin)
Moderate acne
Add topical vitamin A derivatives:
tretinoin, adapalene, or tazarotene to
topical antibiotics
If no response to topical vitamin A
derivatives and antibiotics, use oral
antibiotics (e.g., minocycline or
doxycycline)
MTB S2CK
p. 377
MTB S2CK
p. 377
Acne/Treatment
Severe acne
Add oral vitamin A, isotretinoin to oral
antibiotics
Isotretinoin causes hyperlipidemia
Vitamin A derivatives
extremely teratogenic
MTB S2CK
p. 377
17
Toxicology, Poisoning, &

Overdose
EMERGENCY MEDICINE
Niket Sonpal, MD
Chief Resident
Treatment of Overdose
32-year-old woman with a history of depression comes to ED
30 minutes after taking a bottle of pills in a suicide attempt. BP
118/70, pulse 90, and respirations normal. She refuses to tell
you what she took.
What is the next step?
Gastric Lavage
OVERDOSE
TREATMENTS
It could be caustic and injure on
a. Induce emesis with ipecac

p
th way up
the
b. Gastric lavage
c. Psychiatric consultation Consultations are 99% wrong on USMLE
Takes too long
d. Serum chemistry
e. Urine toxicology screen Urine wont show up yet
Pills will not make that transit time
f. Cathartics/laxatives
g. Whole bowel irrigation Doesnt change outcomes
We dont know if its opiates
h. Naloxone
We dont know if its benzos
i. Flumazenil
MTB S2CK
p. 533
Initial Management of Poisoning
Bowel
Irrigation
MTB S2CK
p. 534
Ipecac
Fluids and Diuresis
MTB S2CK
p. 534
Gastrointestinal Emptying
Gastric lavage
Gastric emptying of any kind is
always wrong with
Caustics (acids and alkali)
Altered mental status
Cathartics
Gastric lavage is rarely done.

Removes 50% of pills at 1 hour
Removes 15% of pills at 2 hours
Ipecac is always a wrong answer in ED
MTB S2CK
p. 534
Ipecac
No inpatient benefit
15-20 minutes onset
Hinders antidotes
Cathartics
Cathartic agents WRONG answer
Prokinetics WRONG answer
MTB S2CK
p. 534
MTB S2CK
p. 534
Forced Diuresis
Fluids and diuretics is always a
wrong answer
Risk of PE > benefit
Whole Bowel Irrigation
NGT with polyethylene glycol-electrolyte

solution is almost always wrong
Only for:
Iron ingestion
Lithium
Drug-filled packets
MTB S2CK
p. 534
MTB S2CK
p. 534
When answer is unclear and cause of

overdose is asked say:
Acetaminophen 1st Most Common
Aspirin 2nd Most Common
What to do is often unclear. What is useless

or dangerous (ipecac, forced diuresis,
cathartics) is very clear.
MTB S2CK
p. 535
Woman comes to ED one hour after taking a bottle of

pills. BP 118/70, pulse 90/min, and respirations
14/min. She is confused, disoriented, and lethargic.
What is the next step in the management?
Seizure risk too high 2 line
a. Flumazenil
Dangerous in AMS
b. Gastric lavage
c. Psychiatric consultation Never get a consult youre an MD
d. Naloxone and dextrose
Not the first step
e. Intubation
nd
MTB S2CK
p. 535
Opiate overdose is fatal:

Give naloxone immediately
Psychiatric consultation is
indicated for suicide attempt, but
is a wrong answer on USMLE S2
CK when specific antidotes and
diagnostic tests are needed.
MTB S2CK
p. 535
Benzodiazepine overdose by
itself is not fatal and acute
withdrawal causes seizures
Dont give flumazenil
MTB S2CK
p. 535
Acetaminophen
Charcoal
Charcoal is benign
Charcoal is not dangerous
Charcoal is superior to lavage and
ipecac
Legal drugs kill more people in the United

States than illegal drugs because theyre
less expensive and more available
Toxicity of acetaminophen with ingestion
> 8 to 10 g
Fatality with ingestions > 12 to 15 g
When you dont know what to do

in toxicology, give charcoal
MTB S2CK
p. 535 536
MTB S2CK
p. 536
Acetaminophen
Acetaminophen
Four Most Common Acetaminophen Overdose

Questions:
3. Amount of ingestion unclear?
1. If a clearly toxic amount of acetaminophen has

been ingested (> 810 g)
Ans er N-acetylcysteine
Answer:
N acet lc steine
2. If the overdose was > 24 hours ago
No therapy
MTB S2CK
p. 536
Drug level
4. Charcoal does not make N-acetylcysteine
ineffective
Charcoal isnt contraindicated with Nacetylcysteine
MTB S2CK
p. 536
Aspirin Overdose
Aspirin Overdose
Aspirin causes diffuse, multisystem toxicity
Renal Toxicity
Tinnitus
Altered
Mental
Status
Aspirin Overdose
Increased Anion
Gap
Hyperventilation
MTB S2CK
Increased PT
Respiratory
Alkalosis
Metabolic
Acidosis
p. 536
ARDS
Aspirin Overdose
Respiratory
Failure
Increased
PTT
Lactic Acidosis
MTB S2CK
p. 536
Aspirin Overdose
Treatment is alkalinizing urine, which

increases rate of aspirin excretion
Know blood gas in aspirin overdose
Tinnitus, respiratory alkalosis,
and metabolic acidosis are
the key to diagnosing aspirin
overdose.
MTB S2CK
p. 536
Depressed patient presents with altered mental status

from ingesting multiple toxic substances. You know
for certain that he took some lorazepam only today,
for the first time. There is no response to naloxone
or dextrose. The patient is given flumazenil and
immediately seizes.
What is the most likely cause of the seizure?
a. Cocaine withdrawal Cocaine toxicity causes seizures, not withdrawal
Doesnt cause seizures
b. Opiate withdrawal
c. Tricyclic antidepressants
d. SSRIs
SSRIs toxicity causes serotonin syndrome (SS)
Causes tinnitus and hyperventilation, not seizures
e. Aspirin
MTB S2CK
p. 537
Which of the following is most likely to be found in

aspirin overdose?
(Normal values: pH 7.40, pCO2 40, HCO3 24)
a. pH 7.55 pCO2 50 HCO3 24

b. p
pH 7.25 p
pCO2 62 HCO3 38
c. pH 7.46 pCO2 22 HCO3 16
d. pH 7.35 pCO2 32 HCO3 20
MTB S2CK
This is a distracter
p
overdose never g
gives
Aspirin
respiratory acidosis
Metabolic acidosis with
respiratory compensation
p. 536 537
What is the best initial test for the patient

previously described?
a. Urine toxicology
b. Electroencephalogram
c. EKG
Wont show the cause of the seizure
d. Head CT
in this patient
e. Potassium level
MTB S2CK
p. 537
Tricyclic Antidepressant Toxicity
Tricyclic Antidepressants
Seizures
Widened
QRS
Complex
Arrhythmia
TCA Toxicity
Urinary
retention
Dry mouth
Constipation
MTB S2CK
p. 537
MTB S2CK
p. 538
Tricyclic Antidepressants
Caustics
The best initial treatment of TCA

overdose is with sodium bicarbonate
Caustic ingestion of acids and alkalis

(e.g., drain cleaner) causes
Bicarbonate will protect the heart

against arrhythmia
Bicarbonate does not increase urinary
y
excretion of TCAs as it does for aspirin
MTB S2CK
p. 538
Mechanical damage to oropharynx

Esophageal perforation
Stomach perforation
Dont give alkali to reverse acids
MTB S2CK
p. 538
Caustics
Carbon Monoxide Poisoning
Flush out caustics

Use water in high volumes
Endoscopy is performed to assess
degree of damage
Carbon monoxide (CO) poisoning is the

MCC of death in fires
Thermal injury is always

the wrong answer
Steroids dont prevent

injury from caustics
MTB S2CK
p. 538
MTB S2CK
p. 538
CO binds oxygen to Hb so tightly that

carboxyhemoglobin will not release oxygen
to tissues
Carboxyhemoglobin acts functionally like
anemia
Myocardial
infarction
Functional Anemia
Carbon
Monoxide
Confusion
Seizures
Dyspnea
Lightheadedness
Source: cdc.gov
MTB S2CK
p. 538
MTB S2CK
p. 538
No functional difference between absence of

blood and carboxyhemoglobin; 60%
carboxyhemoglobin = loss of 60% of blood
The left ventricle cant
can t
distinguish between anemia,
carboxyhemoglobin, and
stenosis of coronary arteries.
MTB S2CK
p. 538
Which of the following blood gas results would you

find in carbon monoxide poisoning?
a.
b.
c.
d.
pH 7.55 pCO 50 HCO 24

pH 7.25 pCO 62 HCO 38
pH 7.46 pCO 22 HCO 16
pH 7.35 pCO 26 HCO 18
MTB S2CK
Distracter
Respiratory acidosis with metabolic
alkalosis
Respiratory alkalosis with metabolic
acidosis
p. 538
Diagnostic tests
gives normal pO2 because
oxygen doesnt detach
from hemoglobin
Routine oximetry will be falsely normal

Most accurate test is a level of
carboxyhemoglobin
Treatment
Remove patient from exposure
Give 100% oxygen
MTB S2CK
p. 538
MTB S2CK
p. 539
Methemoglobinemia
Treatment
Severe disease is treated with hyperbaric
oxygen
Severe symptoms are defined as:
CNS symptoms
Cardiac symptoms
Metabolic acidosis
MTB S2CK
Wikimedia
p. 539
Methemoglobin is oxidized Hb
Ferric
3+
Ferric = Fe
Ferrous = Fe2+
Oxidized hemoglobin is brown and
will
ill nott carry oxygen
Chocolate-brown blood
MTB S2CK
p. 539
Methemoglobinemia
Methemoglobinemia/Presentation
Methemoglobinemia from idiosyncratic

reaction of hemoglobin to drugs such as:
Benzocaine and anesthetics
Nitrites and nitroglycerin
Dapsone
p
The effects of methemoglobinemia are similar to

carboxyhemoglobin
Oxygen isnt delivered to tissues
Functional Anemia
Metabolic
Acidosis
Methemoglobinemia
Ferrous
Hemoglobin
MTB S2CK
Benzocaine
Nitrites
Dapsone
Dyspnea
Cyanosis
Methemoglobinemia
Ferric Hemoglobin
p. 539
Confusion
Seizures
Headache
MTB S2CK
Methemoglobinemia/Presentation
Carbon monoxide:
blood abnormally red
Methemoglobinemia:
blood abnormally brown
Lightheadness
p. 539
Methemoglobinemia/Diagnostic Tests/
Treatment
Both methemoglobinemia and

carboxyhemoglobin give normal pO2 on blood
gas
Most accurate test is methemoglobin level
Best initial therapy is 100% oxygen
Most effective therapy is methylene blue,
which half-life of methemoglobin
Cyanosis + normal pO2 =

methemoglobinemia
MTB S2CK
p. 539
MTB S2CK
p. 539 540
Organophosphate (Insecticide) Poisoning and

Nerve Gas
Organophosphates and nerve gas

identical in their effects
Nerve gas faster and more severe
Massive increase in acetylcholine by
i hibiti metabolism
inhibiting
t b li

Nerve Gas
Bronchospasm
Bronchorrhea
Organophosphate
g
p
p
Poisoning
Salivation
MTB S2CK
p. 540

Nerve Gas
Acetylcholine constricts bronchi

and increases bronchial secretions
MTB S2CK
p. 540

Nerve Gas
Nerve gas and

organophosphates
g
p
p
are
absorbed through the skin
MTB S2CK
p. 540
Polyuria
y
Lacrimation
p. 540
56-year-old military commander attacked with nerve

gas. Presents with salivation, lacrimation, urination,
defecation, and SOB. Pupils are constricted.
What is the first step in management?
a. Atropine
p
b. Decontaminate (wash) the patient Stabilize first
c. Remove his clothing
Stabilize first
d. Pralidoxime
Takes too long
e. No therapy is effective Never the right answer
MTB S2CK
p. 540
Digoxin Toxicity/Etiology
Hypokalemia predisposes to digoxin

toxicity because potassium and digoxin
compete for same site on the Na+/K+ATPase
Less potassium is bound, more
digoxin is bound
K+
MTB S2CK
Respiratory arrest
MTB S2CK
Increased
Digoxin Binding
p. 540
Digoxin Toxicity/Presentation
Digoxin Toxicity/Presentation
Yellow Halo Vision
Confusion
Hypokalemia
Digoxin
g
Toxicity
Hyperkalemia
MTB S2CK
Arrhythmias
y
Digoxin toxicity
Digoxin toxicity
Hyperkalemia
Nausea
Vomiting
Abdominal Pain
p. 540 541
Digoxin Toxicity/Diagnostic Tests
MTB S2CK
p. 541
Digoxin Toxicity/Diagnostic Tests
Most accurate test: digoxin level

Best initial tests: potassium level and EKG
EKG: downsloping of ST segment in all
leads
Atrial tachycardia with variable AV block is
the most common digoxin toxic arrhythmia
Digoxin can produce

any arrhythmia
MTB S2CK
p. 541
Digoxin Toxicity/Treatment
Control potassium and give digoxinspecific antibodies

Digoxin-binding antibodies rapidly
remove digoxin from circulation
Strongest indication for
digoxin-binding antibodies:
CNS and cardiac involvement.
MTB S2CK
p. 541
Lead Poisoning
Renal Tubule
Toxicity (ATN)
Abdominal pain
lead colic
Lead
Toxicity
Sideroblastic
Anemia
MTB S2CK
Memory
y loss
confusion
Peripheral
Neuropathy
wrist drop
p. 541
Lead Poisoning
Lead Poisoning/Treatment
Best initial test: level of free

erythrocyte protoporphyrin
Most accurate test: lead level
Chelating agents remove lead from

body
Most accurate test for sideroblastic

anemia: Prussian blue stain
MTB S2CK
p. 541
MTB S2CK
Mercury Poisoning
Neurological
problems
Nervous, jittery,
twitchy, and
sometimes
hallucinatory
Theres no therapy to reverse pulmonary

toxicity
Chelating agents such as dimercaprol and
succimer are effective in removing mercury
from body and decreasing neurological
t i it
toxicity
Lung
toxicity & interstitial
fibrosis
Inhaled
p. 541
Toxic Alcohols/Methanol and Ethylene Glycol

Methanol
Ethylene glycol
1. Intoxication
1
2. Metabolic Acidosis
3. Increased Anion
Gap
4. Osmolar Gap
MTB S2CK
p. 541
Mercury Poisoning
Oral ingested
MTB S2CK
Succimer: only oral

Ethylenediaminetetraacetic acid
(EDTA) and dimercaprol (BAL) are
parenteral
p. 542
Treated w/
1. Fomepizole
2. Dialysis
Differences between Methanol and

Ethylene Glycol
Methanol
Ethylene glycol
Source
Wood alcohol, cleaning

solutions, paint thinner
Antifreeze
Toxic
metabolite
Formic acid/formaldehyde Oxalic acid/oxalate
Presentation
Ocular toxicity
Initial diagnostic Retinal inflammation

abnormality
MTB S2CK
p. 542
Renal toxicity
Hypocalcemia,
envelope shaped
oxalate crystals in
urine
10

Osmolar Gap
Osmolar gap =
measured serum osmolality - calculated osmolality
Serum osmolality =
2(Na+) + BUN/2.8 + Glucose/18
Ex: Measurement 350 - Calculated 300 = gap of 50 osmoles
Treatment
Best initial therapy: fomepizole,
which inhibits alcohol dehydrogenase
and prevents production of toxic
metabolite
Only dialysis removes methanol and
ethylene glycol
Ordinary alcohol (ethanol) also

osmolar gap
MTB S2CK
p. 542
MTB S2CK
p. 542
Snake Bites
Snake Bites/Treatment
Most common injury from snake bites is

local wound
Death from snake bites:
Ineffective or dangerous
treatment
Beneficial therapy
Tourniquets blocking
arterial flow
Pressure
Ice
Immobilization decreases
movement of venom
Incision and suction,

especially by mouth
Antivenin
Hemolytic toxin: hemolysis, DIC, and

damage to endothelial lining of tissues
Neurotoxin: can result in respiratory
paralysis, ptosis, dysphagia, and diplopia
MTB S2CK
p. 542 543
Spider Bites/Presentation
All spider bites present with a sudden,

sharp pain that patient may describe as:
1.I stepped on a nail
2. A piece of glass was in my shoe.
MTB S2CK
p. 543
MTB S2CK
p. 543
Differences between Types of Spider Bites

Black widow
Brown recluse
Presentation
Abdominal
pain,
muscle pain
Local skin
necrosis
Lab test
abnormalities
Hypocalcemia
None
Treatment
Calcium,
antivenin
Debridement,
steroids,
dapsone
MTB S2CK
p. 543
11
Dog, Cat, and Human Bites
Dog, Cat, and Human Bites
Management of dog, cat, and human bites is

essentially identical
Theyre managed with:
Rabies vaccine only if:

Animal has altered mental
status/bizarre behavior
Attack was unprovoked, by a
stray dog that cannot be
observed or diagnosed
Tetanus vaccination booster if > 5 years since
last injection
Dog and Cats: Pasteurella multocida

Humans: Eikenella corrodens
Human bites are more damaging
than dog and cat bites
MTB S2CK
p. 543
MTB S2CK
p. 544
Rabies and Bats
Head Trauma
If a bat was noted to be in the
room and the patient was
asleep VACCINATE!
MTB S2CK
p. 544
Head Trauma
Any head trauma resulting in altered mental

status or loss of consciousness (LOC) is
managed first with a head CT
Head CT without contrast is best initial test to
detect blood
Contrast detects mass lesions such as cancer
and abscess, not blood
Head Trauma
LOC = CT
Concussion:
No focal neurological abnormalities
Normal CT scan
Contusion:
Occasionally (rarely) has focal findings
Ecchymoses found on CT (blood mixed in
with brain parenchyma)
MTB S2CK
p. 544
MTB S2CK
p. 544
12
Contusion
Head trauma
Subdural and epidural hematomas: usually

associated with more severe trauma than a
concussion
Impossible to distinguish without head CT,
epidural hematoma more frequently with
skull
k ll ffracture
t
MTB S2CK
p. 544
MTB S2CK
Epidural Hematoma
MTB S2CK
p. 544
Subdural Hematoma
p. 545
Source: Brendan T. Doherty
Lucid Interval
Treatment
Lucid interval is a second loss of

consciousness occurring several minutes to
several hours after initial loss of
consciousness
Concussion: no specific therapy
Patient wakes up after initial LOC, but loses

consciousness a second time due to
accumulation of blood
Wait at least 24 hours before returning

to sports
Contusion: vast majority need no

specific treatment
Rarely need surgical debridement
Time between first and second episodes

of LOC is lucid interval
Those with concussion safe to go

home. Hospitalization isnt
necessary. Observe at home for
altered mental status.
Both epidural and subdural hematomas

are associated with a lucid interval.
MTB S2CK
p. 545
MTB S2CK
p. 545
13
Treatment
Definition of a Large Intracranial hemorrhage
Subdural and epidural hematoma:

Treatment is based on size and signs
of compression of brain
Small ones are left alone
Large
L
h
hematomas
t
are managed
d with:
ith
Compression of ventricles or sulci

Herniation with abnormal breathing and
unilateral dilation of pupil
Worsening mental status or focal
findings
1. Intubation and hyperventilation

2. Mannitol
3. Drainage
MTB S2CK
p. 545
MTB S2CK
Summary of Severe Head Trauma
p. 546
Summary of Severe Head Trauma
Concussion
Contusion
Subdural
Epidural
Concussion
Contusion
Subdural
Epidural
No focal
findings
Rarely focal
+/ focal
findings
+/ focal
findings
Normal CT
Ecchymoses
Venous,
crescent
No lucid
Interval
No lucid
Interval
+/ lucid
Interval
+/ lucid
interval
Arterial,
biconvex or
lens shaped
hematoma
No specific
treatment;
observe at
home
No specific
treatment;
observe in
hospital
Drain large
ones
Drain large
ones
MTB S2CK
p. 546
MTB S2CK
p. 546
Head Trauma
25-year-old man sustains head trauma in MVA. A
large epidural hematoma is found. Immediately after
intubation and mannitol, surgical evacuation is
successfully performed.
Which of the following will benefit the patient?
Steroids dont benefit intracranial

bleeding. They decrease edema
around mass lesions.
a. Repeated doses of mannitol Doesnt reduce mortality

Doesnt always work
b. Continued hyperventilation
c. Proton pump inhibitor (PPI)
For SAH only
d. Nimodipine
e. Dexamethasone Doesnt change outcomes
MTB S2CK
p. 546
MTB S2CK
p. 546
14
Burns
Burns & Hypothermia
Best initial therapy for those caught in

a fire is 100% oxygen to treat smoke
inhalation and CO poisoning
Airway burn is 2nd MCC of death from
burns only if theres been airway
injury
MTB S2CK
Burns
Burns
Burns inside mouth
Stridor
Burn Victim
Indications for
Intubation
Hoarseness
MTB S2CK
p. 547
Burns inside
nasopharynx
If airway burn is not present, the 2nd

MCC of death is volume loss
Fluid replacement is based on
percentage of body surface area (BSA)
burned
Wheezing
p. 547
MTB S2CK
p. 547
Volume of Fluid Replacement
Volume of Fluid Replacement
Replace with Ringer lactate

Give one-half in first 8 hours, a quarter in
second 8 hours, and a quarter in the third 8
hours
Give 4 mL for each percentage of BSA
burned (including 2nd and 3rd degree burns)
for each kilogram of body weight
Patchy burns that arent continuous make

the percentage of BSA burned hard to
assess. Use the width of patients hand to
make an estimate
Each hand width is 1% of BSA
The short answer is: give the largest amount
of Ringer lactate or normal saline listed as a
choice; its probably the right answer
Head: 9% BSA
Arms: 9% BSA each
Legs: 18% BSA each
Chest or back: 18% BSA each
MTB S2CK
p. 547
Fluid replacement:
(4 mL) (% BSA burned) weight (kg)
MTB S2CK
p. 547
15
Heat Disorders
What is the MCC of death several days to weeks after
a burn?
a. Infection
Rhabdomyolysis causes renal failure
b. Renal failure
c. Cardiomyopathy Not affected so quickly
Most common immediate cause of death
d Lung injury
d.
Fluid loss doesnt mean malnutrition
e. Malnutrition
MTB S2CK
p. 547
Malignant
hyperthermia
Risk
Antipsychotic
medications
Anesthetics
administered
systemically
Body temp
Elevated
Elevated
CPK and K+ level
Elevated
Elevated
Treatment
Dantrolene or
dopamine agonists:
bromocriptine, cabergoline
Dantrolene
Hypothermia
Risk
Exertion; high
outside temp
Exertion; high
outside temp
Body temp
Normal
Elevated
CPK and K+
level
Normal
Elevated
Treatment
Oral fluids and

electrolytes
IV fluids;
evaporation
p. 548
Hypothermia
Neuroleptic
malignant syndrome
p. 548
Heatstroke
MTB S2CK
Heat Disorders
MTB S2CK
Heat cramps/
exhaustion
Look for intoxicated person with

hypothermia
MCC of death: cardiac arrhythmia
Best initial step: EKG
MTB S2CK
p. 548
Drowning
Manage with airway and administer positive

pressure ventilation
Steroids and antibiotics are not beneficial
Salt water drowning: acts like CHF with wet,
heavy lungs
Wrong answers for drowning include:

Steroids
Antibiotics
MTB S2CK
p. 548
MTB S2CK
p. 549
16
Drowning
Fresh water drowning: causes hemolysis

from absorption of hypotonic fluid into
vasculature
RBC
RBC
Cardiac Rhythm Disorders
RBC
Fresh H20
Hemolysis
MTB S2CK
p. 549
Initial Management of Cardiac Arrest
First step :
After patient has been shown to be

unresponsive, and EMS activated, the
next step is:
Make sure patient is truly unresponsive

Call for help: call 911/activate Emergency
Medical Services (EMS)
Truly unresponsive
Chest compressions
Rescue breaths
MTB S2CK
p. 549
When is a precordial thump the

answer?
Very recent onset of arrest (<10
minutes) with no defibrillator available
You know its recent because you saw it
happen (witnessed)
MTB S2CK
p. 549
1. Open airway: head tilt, chin lift, jaw thrust

p
and start chest compressions
p
if
2. Check pulse
pulseless
3. Give rescue breaths if not breathing
CPR doesnt restart the
heart; CPR keeps patient alive until
cardioversion can be performed.
MTB S2CK
p. 549
Pulselessness
Sudden loss of a pulse can be caused

by:
Asystole
Ventricular fibrillation (VF)
Ventricular tachycardia (VT)
Pulseless electrical activity (PEA)
Best initial management of all forms of

pulselessness is CPR
MTB S2CK
p. 549 550
17
Pulselessness
Pulselessness
Asystole
Besides CPR, therapy for asystole is
with epinephrine
Vasopressin is alternative to
epinephrine
They both constrict blood vessels in
tissues (e.g., skin)
Shunts blood into critical central areas
(e.g., heart and brain)
Ventricular Fibrillation
Best initial therapy for VF is an immediate,
unsynchronized cardioversion followed
by CPR
Unsynchronized = defibrillation
All electrical cardioversions synchronized
except VF and pulseless VT
MTB S2CK
p. 550
MTB S2CK
Pulselessness
p. 550
Ventricular fibrillation
Only VF and VT without a

pulse
l gett unsynchronized
h i d
cardioversion.
MTB S2CK
p. 550
MTB S2CK
p. 550
Pulselessness
Pulselessness
After defibrillation, then is epinephrine

or vasopressin followed by another
electrical shock
Amiodarone or lidocaine
Magnesium
Ventricular Tachycardia (VT)

Wide complex tachycardia with regular rate
Management entirely based on
hemodynamic status
Bretylium is always a wrong answer

MTB S2CK
p. 550 551
Pulseless VT: manage exactly same way as

VF
Hemodynamically stable VT: Amiodarone,
then lidocaine, then procainamide. If all
medical therapy fails, then cardiovert patient
MTB S2CK
p. 551
18
Pulselessness
Ventricular Tachycardia
Ventricular Tachycardia
Hemodynamically unstable VT:
Perform electrical cardioversion several
times followed by medications (e.g.,
amiodarone or lidocaine)
VT is managed with shock, drugs,
and CPR at all times in between
the shocks.
MTB S2CK
p. 551
Pulselessness
Hemodynamic instability is defined as:

Chest pain
Dyspnea/CHF
Hypotension
Confusion
MTB S2CK
p. 551
Pulselessness
Pulseless Electrical Activity (PEA)

PEA = electrically normal, but no
motor contraction
PEA = no cardiac output
These qualities of instability are the same for

all rhythm disturbances
Direct intracardiac medication administration
is always a wrong answer
MTB S2CK
p. 551
Pulselessness
MTB S2CK
p. 551
Pulselessness/Treatment
PEA treated by correcting underlying cause

We synchronize delivery of
electricity in cardioversion of VT
to prevent worsening of
arrhythmia into ventricular
fibrillation or asystole.
asystole
PEA: look for patient with a normal EKG and

no pulse
MTB S2CK
p. 551 552
Tamponade
Tension Pneumothorax
Causes of PEA
Massive PE
MTB S2CK
p. 552
HYPOvolemia
HYPOglycemia
HYPO
l
i
HYPOxia
HYPOthermia
Metabolic acidosis
HYPERkalemia
HYPOkalemia
19
Atrial Arrhythmias
Atrial rhythm disturbances rarely

associated with hemodynamic
compromise
Look for :
Palpitations,
p
, dizziness,, or lightheadedness
g
Exercise intolerance or dyspnea
Embolic stroke
MTB S2CK
p. 552
Atrial Arrhythmias
Atrial Arrhythmias
Irregularly irregular rhythm suggests Afib as the most likely diagnosis even
before EKG is done
A-fib:
A fib: most common arrhythmia in the
United States
MTB S2CK
p. 552
Atrial Fibrillation
Atrial Fibrillation and Atrial Flutter

Two disorders with nearly identical
management
Major points of difference are:
Flutter
Fl tt is
i a regular
l rhythm
h th vs.
fibrillation is irregular
Flutter changes to sinus rhythm or
deteriorates into fibrillation
MTB S2CK
p. 552
Atrial Flutter
MTB S2CK
p. 553
Source: Abhay Vakil, MD.
Atrial Arrhythmias/Treatment
Hemodynamically unstable atrial

arrhythmias = synchronized
cardioversion
Synchronization prevents electricity
from being delivered during refractory
period (ST-T wave)
Synchronization prevents change
into VT or VF
MTB S2CK
p. 553
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20
Chronic Atrial Fibrillation

A-fib > 2 days
> 7 days risk of clot formation
Routine cardioversion is not
i di t d
indicated
Chronic is usually secondary atrial or
valvular anatomic change
Chronic Atrial Fibrillation

Shocking doesnt correct a dilated left atrium
causing A-fib
Over 90% will revert to fibrillation
Rate control and warfarin is standard of care
f A-fib
for
A fib
MTB S2CK
p. 553 554
Chronic A-fib should be anticoagulated

before cardioversion. Unstable, acute
disease doesnt need anticoagulation.
MTB S2CK
p. 553 554
Best initial therapy for fibrillation and

flutter is to control the rate
1. Goal HR < 100/minute
2. INR between 2-3
Calcium-channel blockers used to

control HR with atrial arrhythmias are
diltiazem and verapamil
1.
1 Slow rate
2. Anticoagulate
Reliably block AV node

Other calcium-channel blockers control
BP
No matter how much you might think it
better to shock every patient into sinus, it
just doesnt work in long run.
Rate control drugs do not

convert patient into sinus
rhythm.
MTB S2CK
p. 554
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p. 554
Warfarin
Without anticoagulation 6% a year
stroke risk
INR 2-3, rate: 2-3% stroke risk
Dabigatran and Rivaroxaban
Alternatives to warfarin
For non-valvular A-Fib
No INR monitoring
A-fib is caused by anatomic cardiac

defects dilating atrium
Thats why vast majority revert
Acute disease normalizes spontaneously;
dont force it
Chronic disease reverts into arrhythmia;
dont force it either
MTB S2CK
p. 554
MTB S2CK
p. 554
21
Atrial rhythm problems

can cause acute PE from
loss of atrial kick
kick in those
with cardiomyopathy.
MTB S2CK
p. 554
MTB S2CK
p. 554
Major bleeding from warfarin is

defined as:
Intracranial
I t
i lh
hemorrhage
h
Requires transfusion
MTB S2CK
Lone Atrial Fibrillation

Patients with low risk of stroke can use
ASA
2-3% per year vs. 1% per year bleeding
Scoring
S
i is
i called
ll d CHADS score
CHADS 2 = warfarin, dabigatran,
rivaroxiban
p. 554
Definition/Criteria for Low Risk of Stroke from A-fib

No cardiomyopathy/CHF/atherosclerosis
No HTN
Age 75
No diabetes
No stroke in past
The answer for management of lone atrial fibrillation is:
Rate control
Aspirin
No warfarin or dabigatran
MTB S2CK
Supraventricular Tachycardia
p. 555
SVT
Vagal Maneuvers
Carotid Massage
Valsalva
Dive Reflex
Ice immersion
Adenosine
Beta Blockers
CCBs
Digoxin
MTB S2CK
p. 555
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p. 555
22
Wolff-Parkinson-White Syndrome (WPW)

WPW is an anatomic abnormality in cardiac
conduction pathway
Answer most likely diagnosis question by
looking for:
SVT alternating with ventricular tachycardia
SVT gets worse after diltiazem or digoxin
Observing delta wave on EKG
Vagal maneuvers slow and convert SVT.
They dont convert atrial fibrillation.
MTB S2CK
p. 556
Most accurate test for WPW is cardiac

electrophysiology (EP) studies
MTB S2CK
p. 556
Atrial Arrhythmias
Acute therapy: Procainamide or

amiodarone
Chronic therapy: Radiofrequency catheter
ablation is curative for WPW
EP studies tell you where the anatomic
defect is
Digoxin and calcium-channel blockers are
dangerous in WPW
Multifocal Atrial Tachycardia

Multifocal atrial tachycardia (MAT) is
associated with chronic lung disease
such as COPD
Treat underlying lung disease
Treat MAT as you would A-fib, but
avoid beta blockers because of lung
disease
MTB S2CK
p. 556
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p. 556
Atrial Arrhythmias
Woman comes to office for routine evaluation. Shes
found to have a pulse of 40 and an otherwise
completely normal history and physical examination.
What is the most appropriate next step in the
management of this patient?
a. Atropine
You dont know the rhythm
y
yet
y
b. Pacemaker
Too invasive
c. EKG
Too invasive
d. Electrophysiology studies
Can result in ischemia
e. Epinephrine
f. Isoproterenol
Old and no longer used; always wrong
g. Nothing; reassurance Without EKG cannot say
MTB S2CK
p. 557
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p. 557
23
Bradycardia and AV block
Sinus Bradycardia
Isoproterenol is never the right answer
to anything
Sinus
Bradycardia
Asymptomatic
No Treatment
Symptomatic
Atropine 1st
Pacemaker Long Term
MTB S2CK
p. 557
MTB S2CK
p. 558
First-Degree AV block
Use same management as sinus
bradycardia
Second-Degree AV block
Mobitz I or Wenckebach block: progressively
lengthening PR interval results in a dropped
beat
Mobitz I is most often a sign of normal aging of
conduction system.
y
If there are no symptoms,
y p
, its
managed the same way as sinus bradycardia
Dont treat if asymptomatic
Atropine
p
and p
pacemaker are used
for sinus bradycardia only if
symptomatic.
MTB S2CK
p. 558
MTB S2CK
p. 558
Second-Degree AV block
Mobitz II block: far more pathologic than Mobitz I
Mobitz II just drops a beat without progressive
lengthening of PR interval. Mobitz II progresses or
deteriorates into third-degree AV block. Treat it like
third-degree AV block. Everyone with Mobitz II
block gets a pacemaker even if they are
asymptomatic
MTB S2CK
p. 558
MTB S2CK
p. 558
24
58-year-old woman is admitted to hospital with an

acute MI. On the second hospital day she develops
sustained VT even though she is on aspirin, heparin,
lisinopril, and metoprolol.
What is the most appropriate next step in
management?
a. Increase the dose of metoprolol Wont treat ischemia
b. Add diltiazem Will not affect rhythm
c. Angiography for angioplasty or bypass
d. Implantable defibrillator Underlying cause can be fixed
e. EP studies Not ectopy, but rather from ischemia
MTB S2CK
p. 559
73-year-old man has his third syncopal episode in last

6 months. An EKG done in the field shows VT. His
stress test is normal.
a. Metoprolol
Not enough
g to p
prevent death
b. Diltiazem
Have no affect in VT
c. Angiography Normal stress therefore no need for angio
d. Implantable defibrillator
e. EP studies
EKG shows cause so need for EP
MTB S2CK
p. 559 560
Which of the following tests would you do for this

patient to determine a risk of recurrence?
For unexplained syncope
a. EP studies
b. Echocardiography
c. MUGA scan (nuclear ventriculography) For perfusion
d. Ventilation/perfusion
p
scan
For PE study
e. Tilt-table testing For syncope
MTB S2CK
p. 559
46-year-old man has intermittent episodes of

palpitations, lightheadedness, and near-syncope. His
EKG is normal. The echo shows an EF of 42%. Holter
monitor shows several runs of wide complex
tachycardia lasting 5-10 seconds.
Which of the following is most likely to benefit
this patient?
a. Pacemaker placement Dont know underlying cause yet
b. Digoxin
Does nothing for vent arrhythmias
c. Warfarin
Low risk for clot
d. EP studies
e. Swan-Ganz catheter
Swan if for diagnosing SHOCK
MTB S2CK
p. 560
25
Pituitary Disorders
Panhypopituitarism
Diabetes Insipidus
p
Acromegaly
Hyperprolactinemia
Endocrinology
Dr. Conrad Fischer, MD
New York City
Panhypopituitarism/Etiology
The Pituitary Gland
Compression or damage of the pituitary

gland
Tumors, cancer, adenomas, cysts,
meningiomas, craniopharyngiomas, or
lymphoma
Trauma and radiation are damaging
MTB S2CK
p. 107
MTB S2CK
p. 107
Panhypopituitarism/Etiology
Panhypopituitarism/Presentation
Conditions such as:

Hemochromatosis
Sarcoidosis
Histiocytosis X
Infection with fungi
fungi, TB
TB, or parasites
Autoimmune and lymphocytic infiltration
damages gland
Prolactin deficiency
Men
MTB S2CK
p. 107
No symptoms
Women:
Prolactin = In favor of or pro
p
lactation
If deficient, the patient cannot lactate normally
after childbirth
MTB S2CK
p. 107
Luteinizing hormone (LH) and follicle-stimulating

hormone (FSH) deficiency
Both genders will have decreased libido and
decreased axillary, pubic, and body hair
Men
Growth hormone (GH) deficiency

Adults
Unable to produce testosterone or sperm

Erectile dysfunction and decreased muscle mass
Women
Unable to ovulate or menstruate normally and
become amenorrheic
MTB S2CK
p. 107
Few symptoms
Children
Dwarfism
Catecholamines, glucagon, and cortisol

act as stress hormones
MTB S2CK
p. 108
Panhypopituitarism/Diagnostic Tests
Kallman Syndrome
Decreased FSH and LH
Decreased GnRH
Anosmia
Hyponatremia from:
Hypothyroidism
Glucocorticoid underproduction
Potassium levels remain normal
MTB S2CK
p. 108
Aldosterone is unaffected and aldosterone

excretes potassium
MTB S2CK
p. 108
MRI detects compressing mass lesions on pituitary
Growth Hormone (GH)

IGF level
Arginine Stimulation: increases GH
GHRH stimulation: increases GH
ACTH and Cortisol levels
High
Hi h or normall levels
l
l excludes
l d panhypopituitarism
h
it it i
Sex Hormones
LH, FSH level
Testosterone level
Thyroid
TSH
MTB S2CK
p. 108
Source: James G. Smirniotopoulos, MD
MTB S2CK
p. 108
Panhypopituitarism/Treatment
Older, Less Useful Tests
Replace deficient hormones with...
Metyrapone
Inhibits 11-beta hydroxylase and decreases cortisol
Normal: ACTH and 11deoxycortisol levels rise
I
Insulin
li stimulation
ti
l ti
Normal: decreased glucose levels raise GH
Failure of GH to rise in response to insulin
indicates pituitary insufficiency
MTB S2CK
p. 109
Thyroxine
Cortisone
Testosterone and estrogen
Recombinant human growth hormone
Antidiuretic hormone (ADH) and oxytocin (Posterior Pituitary)
Note: No deficiency disease described for oxytocin

Oxytocin helps uterine contraction during delivery, but delivery
still occurs even if its absent
ADH deficiency also known as central diabetes insipidus
MTB S2CK
p. 109
Diabetes Insipidus/Etiology
Diabetes Insipidus/Etiology
Decrease in amount of ADH from pituitary (central DI)

or its effect on kidney (nephrogenic DI)
Nephrogenic DI (NDI):
Chronic pyelonephritis
Amyloidosis
Myeloma
Sickle cell disease
Lithium
Hypercalcemia or hypokalemia inhibits
ADH effect
Central Diabetes Insipidus (CDI)

Damage to brain:
Stroke
Tumor
Trauma
Hypoxia
Infiltration (sarcoidosis, hemochromatosis)
Infection
MTB S2CK
p. 109
MTB S2CK
p. 109
Diabetes Insipidus/Presentation
Diabetes Insipidus/Diagnostic Tests
Excessive thirst
Extremely high-volume urine
Volume depletion
Urine osmolality: Low
Severe Hypernatremia
Neurological symptoms
Confusion,
C f i
disorientation,
di i t ti
llethargy,
th
and
d eventually
t ll
seizures and coma
Only when volume losses are unmatched by fluid
intake
MTB S2CK
p. 109
Urine sodium: Low

Serum osmolality: High
Urine volume: Enormous
MTB S2CK
p. 110
Diabetes Insipidus/Diagnostic Tests
Diabetes Insipidus/Treatment
Difference between central and nephrogenic DI is:
Central DI:
Long-term vasopressin (desmopressin)
Response to vasopressin
Central DI:
Urine volume decrease & urine osmolality increase
Nephrogenic DI:
No effect of vasopressin use on urine volume or
osmolality
MTB S2CK
p. 110
Nephrogenic DI:
1. Correct the cause (hypokalemia or
hypercalcemia)
2. Hydrochlorothiazide, NSAIDs,
amiloride
MTB S2CK
Diabetes Insipidus/Evaluation
High-volume urine, plus
excessive thirst
Serum:
Osmolality: Elevated
Sodium: Elevated
p. 110
Diabetes Insipidus/Evaluation
Vasopressin
(Desmopressin)
stimulation test
Volume depletion, plus

hypernatremia
Urine:
Volume: HIGH
Osmolality: Decreased
Sodium: Decreased
Effect
Urine:
Volume decrease +
osmolality increase
Diagnosis
Proceed with
vasopressin
(desmopressin)
stimulation test
MTB S2CK
p. 109
Treatment
MTB S2CK
Central
diabetes insipidus
Vasopressin
Urine:
No effect
Nephrogenic diabetes
insipidus
Treat underlying cause,

hydrochlorothiazide,
amiloride, NSAIDs
p. 110
Acromegaly
Acromegaly/Etiology
Soft tissue overgrowth

throughout the body
Pituitary adenoma
Part of Multiple Endocrine Neoplasias
(MEN)
Combined with parathyroid and
pancreatic disorders (e
(e.g.,
g gastrinoma
or insulinoma)
Rarely caused by ectopic GH or GHRH
production
MTB S2CK
p. 110
Copyright Richard Usatine, M.D.

MTB S2CK
p. 110
Acromegaly/Presentation
Increased hat, ring, and
shoe size
Carpal tunnel syndrome
Obstructive sleep apnea
from soft tissues enlarging
Body odor from sweat
gland hypertrophy
Teeth widening from jaw
growth
Deep voice and
macroglossia (big tongue)
MTB S2CK
Acromegaly/Diagnostic Tests
Colonic polyps
Arthralgias from joints
growing out of
alignment
Hypertension for
unclear reasons in 50%
Cardiomegaly, CHF,
and erectile
dysfunction from
increased prolactin
cosecreted with
pituitary adenoma
p. 110 111
Hyperglycemia
Glucose intolerance
Hyperlipidemia
Best initial test...
Insulin-like growth factor (IGF)
M t accurate
Most
t ttest...
t
Glucose suppression test
Normal: Glucose should suppress growth hormone
MRI?
Only after the laboratory identification of
acromegaly
MTB S2CK
p. 111
Acromegaly/Treatment
Hyperprolactinemia/Etiology
1. Surgery
Many causes not associated with pituitary

adenoma
Transphenoidal resection of pituitary

Cures 70%
2. Medications
Cabergoline: Dopamine agonist inhibits GH release
Octreotide or lanreotide: Somatostatin inhibits GH
release
Pegvisomant: GH receptor antagonist
Prolactin increases via:

Cosecretion with GH in acromegaly
g y
Hypothyroidism with pathologically high TRH
levels
3. Radiotherapy
Only when not responsive to surgery or medications
MTB S2CK
p. 111
MTB S2CK
p. 111
Hyperprolactinemia/Etiology
Hyperprolactinemia/Presentation
Women
Galactorrhea
Amenorrhea
Infertility
Men
Erectile dysfunction
Decreased libido
Galactorrhea (very rare in men)
Pregnancy
Chest wall stimulation
Cutting pituitary stalk
Antipsychotic medications, tricyclic
antidepressants,
p
, and SSRIs
Methyldopa
Metoclopromide
Opioids
MTB S2CK
p. 111
MTB S2CK
p. 111
Hyperprolactinemia/Diagnostic Tests
Hyperprolactinemia/Treatment
After the prolactin level is found to be high, perform:

Thyroid function tests
Pregnancy test
BUN/creatinine (kidney disease elevates prolactin)
Liver function tests (cirrhosis elevates prolactin)
1. Dopamine agonists
MRI is done after...

High prolactin level is confirmed AND
Secondary causes like medications are excluded
AND
Patient is not pregnant
MTB S2CK
p. 112
Cabergoline is better tolerated than

bromocriptine
2 Transphenoidal surgery when NOT

2.
responding to medications
3. Radiation is rarely needed
MTB S2CK
p. 112
What to look for...
Thyroid Disorders
Hypothyroidism
Hyperthyroidism
Hypothyroidism
Hyperthyroidism
Bradycardia
Tachycardia, palpitations,
arrhythmia (A fib)
Diarrhea (hyperdefecation)
Weight loss
Anxiety, nervousness,
restlessness
Hyperreflexia
Heat intolerance
Fever
Constipation
Weight gain
Fatigue, lethargy, coma
Thyroid Nodules
Decreased reflexes
Cold intolerance
Hypothermia (hair loss,
edema)
MTB S2CK
p. 113
Hypothyroidism
Hypothyroidism
Etiology
Most from failure of thyroid gland from burnt-out
Hashimoto thyroiditis
Diagnostic tests
Best initial test for all thyroid disorders is...
Acute phase is rarely perceived
Dietary deficiency of iodine

Amiodarone
What to look for...
Hypothyroidism: Everything is SLOW!
Except menstrual flow, which is increased
MTB S2CK
p. 112
TSH
TSH levels are markedly elevated if gland has failed
If the TSH level is suppressed, measure...

T4
Treatment
Replace thyroxine (synthroid)
MTB S2CK
p. 113
Hyperthyroidism/Findings
Diagnosis
Myxedema
Unique feature
Graves disease
Eye proptosis (20 40%)

Skin findings (5%)
Subacute thyroiditis
Tender thyroid
Painless silent
silent thyroiditis Nontender,
Nontender normal P/E
Involuted gland isnt
Exogenous thyroid
palpable
hormone use
High TSH level
Pituitary adenoma
MTB S2CK
p. 113
Multinodular Goiter
Thyroid Bruit
Hyperthyroidism/Diagnostic Tests
Hyperthyroidism/Treatment
T4 (thyroxine) level
Elevated in all forms of hyperthyroidism
TSH level
Pituitary release of TSH is inhibited in all forms
EXCEPT...
Pituitary adenomas, will have high TSH level
Graves disease (unique features):
Eye and skin abnormalities
Elevated radioactive iodine uptake
TSH receptor antibodies
MTB S2CK
p. 113 114
Graves Ophthalmopathy
Best initial therapy...
Steroids
For those unresponsive

to steroids...
Radiation
What if unresponsive to
other therapy...
Source: Jonathan Trobe, MD
Decompressive
surgery
MTB S2CK
p. 114
Hyperthyroidism/Treatment
Acute Hyperthyroidism/Thyroid Storm
Diagnosis
Treatment
Treatment:
Graves disease
Radioactive iodine
Subacute thyroiditis
Aspirin
y
Painless silent thyroiditis
None
Propranolol
Blocks target organ effect
Inhibits peripheral conversion of T4 T3
Exogenous thyroid
hormone use
Stop use
Pituitary adenoma
Surgery
MTB S2CK
p. 114
Thiourea drugs
Methimazole and propylthiouracil
Block hormone production
MTB S2CK
p. 114
Acute Hyperthyroidism/Thyroid Storm
Thyroid Nodules
Treatment:
5% women
1% men
95% benign
Iodinated contrast material

Blocks peripheral conversion of T4 to T3
Blocks release of existing hormone
Steroids (hydrocortisone)
Role in treating hyperthyroidism?
Adenoma, colloid nodule, cyst
Thyroid nodules rarely hyperfunctioning
Radioactive iodine
Ablates gland for permanent cure
MTB S2CK
p. 114
MTB S2CK
p. 114
Thyroid Nodules/Diagnostic Tests

46-year-old woman with a small mass on palpation of
thyroid. No tenderness and otherwise asymptomatic.
What is the most appropriate next step?
a. Fine-needle aspiration Done if TFTs are normal
b Radionuclide iodine uptake scan Determines etiology
b.
of hyperfunctionality
c. T4 and TSH levels
Guides biopsy
d. Thyroid ultrasound
e. Surgical removal (excisional biopsy)
Biopsy with a fine-needle aspirate if theres

normal thyroid function (T4/TSH)
Ultrasound or radionuclide scanning not
required (tests cannot exclude cancer)
Follicular adenoma
when you cant be sure
MTB S2CK
p. 115
MTB S2CK
p. 115
46-year-old woman with thyroid nodule and normal

thyroid function testing has a biopsy showing
indeterminate for follicular adenoma.
Calcium Disorders
Hypercalcemia
g
, determines extent
a. Neck CT Doesnt make a diagnosis,
a
b. Surgical removal (excisional biopsy)
c. Ultrasound Cant excluded cancer, still need biopsy
d. Calcitonin levels Suggests extent of medullary
Hyperparathyroidism
Hypocalcemia
carcinoma only
MTB S2CK
p. 115
Hypercalcemia/Etiology
Hypercalcemia/Etiology
Vitamin D intoxication
Sarcoidosis and other granulomatous
diseases
Thiazide diuretics
Hyperthyroidism
yp
y
Metastases to bone and multiple myeloma
Most common cause is...
MTB S2CK
p. 116
Primary hyperparathyroidism (PTH)

Most cases are asymptomatic
Severe, acute symptomatic hypercalcemia
a high prevalence of cancer
MTB S2CK
p. 116
Hypercalcemia/Presentation
Hypercalcemia/Treatment
Acute, symptomatic hypercalcemia
Acute hypercalcemia, treat with...

Saline hydration at high volume
Bisphosphonates: pamidronate, zoledronic
acid
Calcitonin
Confusion, stupor, lethargy

Constipation
Bone lesions: Osteoporosis
Renal: Nephrolithiasis,
Nephrolithiasis DI,
DI renal insufficiency
Cardiovascular: Short QT syndrome
MTB S2CK
p. 116
Prednisone:
ONLY for sarcoidosis and granulomatous
disease
MTB S2CK
p. 116
Hyperparathyroidism
75-year-old man with history of malignancy admitted with
lethargy, confusion, and abdominal pain. Found to have a
markedly elevated calcium level. After 3L normal saline
and pamidronate, his calcium level is still markedly
elevated the following day.
a Calcitonin
a.
Doesnt add to pamidronate
b. Zolendronic acid
c. Plicamycin Less efficacy than pamidronate. Always wrong
d. Gallium Less efficacy than pamidronate. Always wrong
e. Dialysis Not needed. Renal failure has low Ca++
Primary hyperparathyroidism:
Solitary adenoma (80%85%)
Hyperplasia of all 4 glands (15%20%)
Parathyroid malignancy (1%)
f. Cinacalcet Inhibits PTH

MTB S2CK
p. 116 117
MTB S2CK
p. 117
Hyperparathyroidism
Hyperparathyroidism
Elevation in calcium levels often asymptomatic

When symptomatic:
Osteoporosis
Nephrolithiasis and renal insufficiency
Muscle weakness
Anorexia, nausea, vomiting, and abdominal
pain
Peptic ulcer disease (calcium stimulates
gastrin)
Besides high calcium and PTH levels,

you also find:
Low phosphate level
Short QT on EKG
Sometimes an elevated BUN and creatinine
Alkaline phosphatase elevated from effect of
PTH on bone
MTB S2CK
p. 117
MTB S2CK
p. 117
Hyperparathyroidism/Management
Hyperparathyroidism/Treatment
Bone X-ray is NOT a good test for bone

effects of PTH
Surgical removal of involved

parathyroid glands
DEXA densitometry is better

Preoperative imaging of neck with
sonography or nuclear scanning may be
helpful in determining the surgical approach
MTB S2CK
p. 117
MTB S2CK
p. 117 118
10
Hypocalcemia
Hypocalcemia/Presentation
Low calcium =
twitchy, hyperexcitable
Neural hyperexcitability:
Chvostek sign (facial
nerve hyperexcitability)
Carpopedal spasm
Perioral numbness
Mental irritability
Seizures
Trousseau sign (tetany)
High calcium =
lethargic, slow
Souce: nih.gov
MTB S2CK
p. 118
MTB S2CK
p. 118
Hypocalcemia/Diagnosis & Treatment

EKG:
Prolonged QT
May cause arrhythmia
Adrenal Disorders
Ventricular tachycardia
Hypercortisolism
Treatment
Replace calcium and vitamin D
Hyperparathyroidism
Hypocalcemia
MTB S2CK
p. 118
Pituitary Adrenal Axis
Hypercortisolism
Cushing disease
Pituitary overproduction of ACTH
Cushings syndrome
Due to ectopic production of ACTH
C
Carcinoid
i id ((mostt common iis smallll cellll carcinoma
i
off
the lung)
Overproduction autonomously in adrenal gland
Prednisone (glucocorticoid use) causes same

manifestations of hypercortisolism
Source: nih.gov
MTB S2CK
p. 119
11
Hypercortisolism/Etiology
Hypercortisolism/Presentation
Cause of Hypercortisolism
Frequency
Pituitary ACTH
(Cushing disease)
70%
Adrenals
15%
EEctopic
i ACTH
(carcinoid)
10%
Unknown source of ACTH
5%
MTB S2CK
Fat redistribution
HTN
Moon face, truncal

obesity, buffalo hump,
thin extremities,
increased abdominal fat
Skin
MTB S2CK
p. 119
Hypercortisolism/Diagnostic Evaluation
Always confirm the source of

hypercortisolism with biochemical tests
before you perform imaging studies
10% of population has an abnormality of pituitary

on MRI
If you start with a scan, you may remove the
pituitary when the source is in the adrenals
CC: I feel weak and tired, and I notice hair growth

on my face and strange marks on my stomach
24-hour urine
cortisol
Low-dose (1mg)
dexamethasone
suppression test
Increased
High?
ACTH-dependent
Cushings syndrome
p. 120
MTB S2CK
Hypercortisolism/Diagnostic Evaluation
ACTH-dependent
Cushings syndrome
ACTH-independent
Cushings syndrome
Pituitary vs. Ectopic

ACTH production?
Adrenal
Mass?
Supression
of cortisol?
Pituitary adenoma
(Cushing disease)
MTB S2CK
p. 120
From hyperglycemia and

increased free water
clearance
Osteoporosis
p. 119
High-dose
dexamethasone
suppression
i ttestt
Menstrual disorders
Polyuria
Striae, easy bruising,

decreased wound
healing, thinning of skin
Hypercortisolism/Diagnostic Tests
MTB S2CK
From increased sodium

reabsorption in kidney
and increased vascular
reactivity
Late-night salivary
cortisol
Decreased =
Disease
Excluded
Serum
ACTH
Increased
Low?
ACTH-independent
Cushings syndrome
p. 119 120
Confirmatory Laboratory Findings in

Adrenal Disorders
Adrenal
Pituitary
Ectopic
ACTH level
Low
High
High
Petrosal sinus
ACTH
Not done
High
g ACTH
Low ACTH
Suppresses
Cortisol
No suppression
CT Adrenals
Increased
ACTH &
cortisol?
Ectopic ACTHsecreting tumor
Chest
CT
High dose
No suppression
dexamethasone
Pituitary
Mass?
Pituitary
MRI
No mass
seen?
Petrosal sinus
sampling for
ACTH
MTB S2CK
p. 121
12
Hypercortisolism/Other Findings
Hypercortisolism/Treatment
Cortisol - anti-insulin stress hormone

Hyperglycemia
Hyperlipidemia
Surgically remove source of

hypercortisolism
Transsphenoidal surgery for pituitary sources
Laparoscopic removal for adrenal sources
Theres some aldosterone-like effect of cortisol

Hypokalemia
H
k l i
Metabolic alkalosis
Leukocytosis from demargination of WBCs
MTB S2CK
p. 120
MTB S2CK
p. 121
Evaluation of Adrenal Incidentaloma
Hypoadrenalism (Addisons)/Etiology
How far should you go in the evaluation of an

unexpected, asymptomatic adrenal lesion found on
CT?
1. Metanephrines of blood or urine to exclude
pheochromocytoma
2 Renin and aldosterone levels to exclude
2.
hyperaldosteronism
3. 1 mg overnight dexamethasone suppression test
Addisons disease
Chronic
hypoadrenalism
Etiology
MTB S2CK
p. 121
Autoimmune
destruction ((80%))
Infection (TB)
Adrenoleukodystrophy
Metastatic cancer to
adrenal gland
MTB S2CK
Adrenal crisis
Acute adrenal
insufficiency
Etiology
Hemorrhage, surgery,
hypotension,
yp
, trauma
Suddenly stopping
chronic high-dose
prednisone
p. 121
Hypoadrenalism/Presentation
Hypoadrenalism/Diagnostic Tests
Weakness, fatigue
Acute adrenal crisis
can also present with
profound hypotension,
Nausea, vomiting,
fever, confusion, and
anorexia, hypotension
coma
Hyperpigmentation from
chronic adrenal
insufficiency
Pituitary failure:
Hypoglycemia
ACTH is low
Hyperkalemia
Metabolic acidosis
Adrenal failure:
Hyponatremia
ACTH is high
High BUN
Eosinophilia is
common in
hypoadrenalism
MTB S2CK
p. 121 122
Copyright Richard Usatine, MD

MTB S2CK
p. 122
13
Hypoadrenalism
Hypoadrenalism/Treatment
Signs & Symptoms

Weakness
Hypotension
Weight Loss
Hyperpigmentation
Cosyntropin Stimulation Test

Plasma cortisol before & after 250 ug cosyntropin IM or IV
Cortisol fails to rise

High ACTH
Aldosterone Low too
Primary adrenal
insufficiency
MTB S2CK
p. 121 122
Low ACTH
Aldosterone an increase
Secondary adrenal insufficiency

Adrenal atrophy from pituitary
insufficiency
Treatment is more important than testing in

acute adrenal crisis
Replace
p
steroids with hydrocortisone
y
Fludrocortisone
For postural instability
A steroid hormone particularly high in
mineralocorticoid or aldosterone-like effect
MTB S2CK
p. 122
Primary Hyperaldosteronism
Patient brought to ED after sustaining severe abdominal
trauma in MVA. On second hospital day, he becomes
markedly hypotensive without evidence of bleeding. Theres
fever, high eosinophil count, hyperkalemia, hyponatremia, and
hypoglycemia.
a.
b.
c.
d.
e.
Norepinephrine will constrict

CT scan of the adrenals
vessels more effectively
Draw cortisol level and administer hydrocortisone
Treating severe hypotension
Cosyntropin stimulation testing
more important than finding
ACTH level
etiology
Dexamethasone suppression testing
MTB S2CK
p. 122 123
The autonomous overproduction of

aldosterone despite a high pressure
with a low renin activity
Solitary adenoma: 80%

Bilateral hyperplasia:15-20%
Malignant: 1%
MTB S2CK
p. 123
Primary Hyperaldosteronism
Primary Hyperaldosteronism/Diagnostic Tests
All forms of secondary HTN are more likely in those

whose onset is...

Plasma aldosterone to plasma renin ratio
A low plasma renin with high aldosterone =
Primary hyperaldosteronism
< 30 or > 60 years

Uncontrolled by 2 antihypertensive medications
Has a characteristic finding on the history, physical,

or labs
Primary hyperaldosteronism =
High BP + Low K+
MTB S2CK
p. 123
Most accurate test...

Adrenal venous blood sampling
high aldosterone!
CT Scan?
Only after laboratory testing reveals...
Low potassium, low plasma renin, and
high aldosterone despite a high-salt diet
MTB S2CK
p. 123
14
Primary Hyperaldosteronism/Treatment
Pheochromocytoma
Unilateral adenoma
Resected by laparoscopy
Nonmalignant lesion of adrenal medulla

Autonomous overproduction of catecholamines
despite high BP
Bilateral hyperplasia
Eplerenone or spironolactone
Pheochromocytoma is the answer when theres:

Episodic HTN
Headache
Sweating
Palpitations and tremor
Spironolactone causes...
Gynecomastia
Decreased libido
Anti-androgenic
MTB S2CK
p. 124
MTB S2CK
p. 124
Pheochromocytoma/Diagnostic Tests
Imaging of adrenal glands (CT or MRI)

Done only after biochemical testing
Plasma catecholamines
Confirmed with...
24-hour urine metanephrines and catecholamines
MIBG scanning
Nuclear isotope scan
Detects
D t t location
l
ti off pheochromocytoma
h
h
t
that
th t
originates outside adrenal gland
More accurate than VMA level
MTB S2CK
p. 124
MTB S2CK
p. 124
Pheochromocytoma/Treatment
MIBG scan showing unilateral pheochromocytoma
Source: Laura N Modzelewski
1.
2.
3.
4.
Phenoxybenzamine: (IV alpha blocker)

Propranolol
Calcium-channel blocker (possible)
Laparoscopic removal
MTB S2CK
p. 124
15
Diabetes Mellitus (DM)
Diabetes Mellitus
Presentation
Diagnosis
Treatment
Diabetic Ketoacidosis
Health Maintenance
Complications
Persistently fasting blood glucose levels > 125

on at least 2 separate occasions
Type 1 DM
Type 2 DM
Onset in childhood
Insulin dependent from
early age
Not related to obesity
Insulin deficiency
MTB S2CK
Onset in adulthood
Directly related to
obesity
Insulin resistance
p. 124 125
Diabetes Mellitus/Presentation
Diabetes Mellitus/Diagnostic Tests
Polyuria, polyphagia, and polydipsia
2 FBG measurements > 125 mg/dL
Type 1 DM: thinner than Type 2 diabetics
One glucose level about 200 mg/dL with

symptoms
Type 2 DM: more resistant to diabetic

ketoacidosis (DKA)
Abnormal oral glucose tolerance testing
Both types:
Hemoglobin A1c > 6.5%
MTB S2CK
wound healing
p. 125
MTB S2CK
p. 125
Diabetes Mellitus/Treatment
Best initial treatment...
Oral Hypoglycemic Medications

Best initial drug: metformin
Metformin blocks gluconeogenesis
Sulfonylureas insulin release from pancreas
weight gain
Diet, exercise, and weight loss

Weight loss controls as much as 25% of
cases of type
yp 2 DM without medications,,
Exercising muscle doesnt need insulin
MTB S2CK
p. 125
Dipeptidyl Peptidase Inhibitors

Increase insulin
Decrease glucagon
Sitagliptin, Saxagliptin, Linagliptin
MTB S2CK
p. 125
16
Thiazoladinediones (glitazones)
Rosiglitazone, Pioglitazone
Relatively contraindicated in CHF
Increase fluid overload
Incretins (exenatide, liraglutide)

Raise insulin
Decrease glucagon levels
Decrease gastric motility
Helps in weight loss
Nateglinide and repaglinide

Stimulates insulin release
Similar to sulfonylureas
No additional therapeutic benefit to
sulfonylureas
MTB S2CK
p. 125 126
MTB S2CK
p. 126
Alpha-glucosidase inhibitors (acarbose, miglitol)

Block glucose absorption in bowel
Cause flatus, diarrhea, and abdominal pain
Insulin
Added if patient isnt controlled with oral
hypoglycemic agents
Insulin glargine gives steady state of insulin for
entire day
Dosing isnt
isn t tested
Glargine provides much more steady blood levels
than NPH insulin
Combined with short-acting insulin (e.g., lispro,
aspart, or glulisine)
Pramlintide
Analog
A l off protein
t i called
ll d amylin
li thats
th t secreted
t d
normally with insulin
Amylin
decreases gastric emptying
decreases glucagon levels
decreases appetite
MTB S2CK
p. 125 126
Diabetes Mellitus
MTB S2CK
p. 126
Pharmacokinetics of insulin formulations
MTB S2CK
p. 126
Drug
Type
Onset (hr)
Peak (hr)
Duration (hr)
Aspart
Glulisine
Lispro
Rapid-acting
0.20.5
0.52
34
Regular
Short-acting
0.51
23
68
NPH
Intermediate
1.5
410
1624
Lente
Intermediate
1.53
715
1624
Ultralente
Long-acting
34
915
2228
Glargine
Long-acting
No peak
2436
MTB S2CK
p. 126
17
Diabetic Ketoacidosis (DKA)
Diabetic Ketoacidosis/Treatment
More common with type 1 diabetes

Can definitely present in type 2 diabetes
Presents with...
Hyperventilation
Metabolic
M t b li acidosis
id i with
ith increased
i
d anion
i gap
Hyperkalemia in blood, but decreased total body
potassium because of urinary spillage
Increased anion gap on blood testing
Serum is positive for ketones
Treat with...
1. Large-volume saline and insulin replacement
2. Replace potassium when potassium level
approaches normal
3. Correct the underlying
y g cause
MTB S2CK
p. 126
Noncompliance with medications

Infection
Any serious illness
MTB S2CK
p. 127
Diabetes Mellitus/Health Maintenance

57-year-old man admitted to ICU with altered mental
status, hyperventilation, and markedly elevated
glucose level.
Which of the following is the most accurate measure
of the severity of his condition?
a. Glucose level Can be elevated without DKA
If very low, theres risk of death
b. Serum bicarbonate
Mean
very
little
c. Urine ketones
Not
all
blood
ketones are detected
d. Blood ketones
e. pH level on blood gas Need to know whats
All patients with DM should receive...

Pneumococcal vaccine
Yearly eye exam to check for proliferative
retinopathy, which needs laser therapy
Statins to g
get LDL < 100 mg/dL
g
ACEi or ARBs to get BP < 130/80 mmHg
ACEi or ARB if urine tests positive for
microalbuminuria
Foot exam for neuropathy and ulcers
responsible for pH level

MTB S2CK
p. 127
MTB S2CK
p. 127
Complications of Diabetes
Gastroparesis
Immobility of bowels
Bloating, constipation
Early satiety, vomiting
Abdominal discomfort
Treat with metoclopramide or
erythromycin
Non-proliferative retinopathy
Tighter control of glucose
Aspirin doesnt help retinopathy
MTB S2CK
p. 128
Proliferative retinopathy
Neovascularization and vitreous
hemorrhages
Treated with laser photocoagulation
MTB S2CK
p. 128
18
Neuropathy
Decreased sensation in feet
Main cause of skin ulcers
Leads to osteomyelitis
Treatment pain with
Pregabalin
Gabapentin
Tricyclic antidepressants
MTB S2CK
p. 128
19
Autonomy
Advance Directives
Minors
Brain
i Death
h
Ethics
New York City
Ethics
Ethics
Every human being of adult years and sound mind

has the right to determine what shall be done with his
own body; and a surgeon who performs an operation
without his patients consent commits an assault, for
which he is liable in damages except in cases of
emergency where the patient is unconscious and
where
h
it iis necessary tto operate
t before
b f
consentt can
be obtained.
This states the premise underlying half

the ethics questions on S2 CK of USMLE:
1. Autonomy
2. Adult
3 Capacity
3.
C
it tto understand
d t d
Justice Benjamin Cardozo, Schloendorff v. Society of New York Hospital,

211 NY 125, 105 NE 92 (1914)
MTB S2CK
MTB S2CK
p. 561
p. 561
Autonomy
Patients have sole right to determine what

treatment they shall and shall not accept
Autonomy beats Beneficence
Beneficence: trying to do good for others
Trying
y g to help
p not as important
p
as following
g
wishes
Patients have the right
to refuse treatments
that are good for them if
they dont want them.
MTB S2CK
p. 561
A man has an ugly house you offer to paint free in his favorite
color. Everyone in neighborhood agrees the house is ugly
& what you offer is clearly superior. He understands everything
you are offering, including the clear benefit to him. The man
Cost and benefit and the
still refuses.
common good arent as
What do you do?
important as the autonomy
have to just do
a. Honor the mans
man s wishes: no paint job individuals
what
h t they
th wantt with
ith th
their
i
own property.
b. Paint his house against his will
c. Ask the neighborhood council to consent to the paint job
d. Get a psychiatric evaluation on the man
e. Get a court order to allow the paint job
f. Ask his family for consent to the paint job
g. Wait until he is out of town, then paint his house
MTB S2CK
p. 561 562
Advance Directives
Man comes to ED after MVA that causes a ruptured spleen. Hes
fully conscious. He understands that hell die without splenectomy,
and that hell live if he has the splenectomy. He refuses the repair
and blood transfusion. Entire family including brother who is
healthcare proxy and document completed only a few weeks ago
clearly state, Everything possible should be done, including
surgery.
What do y
you do?
a. Honor his current wishes, no surgery
b. Wait until he loses consciousness, then perform the surgery
You must follow the last known wishes of the
c. Psychiatric consult
patient, even if they are verbal, and even if they
contradict the written proxy. You cannot wait until
d. Ethics committee
his consciousness is lost, then go against his
e. Emergency court order wishes.
f. Follow what is written in the documented health-care proxy
g. See if there is consensus from the family
MTB S2CK
p. 562
Tell caregivers parameters of care the

patient wanted
Agent = person designated by patient to
carry out patients wishes
Term Agent sometimes used
interchangeably with healthcare proxy
Healthcare proxy is written document
outlining parameters of care
Major problem with proxy is details of care
often unclear
MTB S2CK
p. 562
Advance Directives
Advance Directives
Not helpful to just say, No heroic measures

To be useful, document must specifically
state, No intubation, no CPR, no
chemotherapy, no dialysis
Can also specifically state wishes about fluid
and nutrition
If proxy says, No NG tube, no artificial
feeding, then its useful
Proxy takes effect only when patient has lost
capacity to make decisions
Order of Decision Making
MTB S2CK
p. 561 562
1. Patient with capacity supersedes all

else
2 Healthcare
2.
H lth
proxy: an agentt ((person))
to carry out wishes
MTB S2CK
p. 563
Advance Directives
Advance Directives

3. Living will

4. Persons clearly familiar with the
patients wishes
Document outlining patients wishes

Stating, I never want dialysis is more valid than a
family member or friend saying, From what I know
about
b t hi
him, h
he wouldnt
ld t wantt dialysis,
di l i or He
H ttold
ld me
he never wants dialysis.
Documentation!
Written living will with concrete statements I never
want blood transfusion or chemotherapy is valid
MTB S2CK
p. 563
Problem with documentation

Difficult for friends to document they knew the
patients wishes
If case clearly states friend knows and can
prove that she knew the patients wishes,
then this is the plan of care thats followed
MTB S2CK
p. 563
Advance Directives
Advance Directives

5. Family
Ethics Committee
The answer when:
General order of decision making

1.
2
2.
3.
4.
Spouse
Adult children
Parents
Siblings
Unlike life, USMLE S2 CK must be clear

If family is split, then answer is:
Ethics committee or court order
MTB S2CK
p. 563
1. Patient has lost capacity to make decisions

2 Advance directive is missing or unclear
2.
Critically important for medical futility
E.g. when the patient or proxy asking for
tests and treatments that may have no
benefit
MTB S2CK
p. 563
Advance Directives
Advance Directives
Court order is right answer when:

Theres no advance directive and
1. Patient has no capacity
2. Family in disagreement
Psychiatric Evaluation of Patient

The answer when...
It is not clear if patient has capacity
Like a house being

g left equally
q
y to four children
who cannot agree what to do with it
Caregivers want to withdraw care and ethics

committee cannot reach a conclusion
MTB S2CK
p. 563
Question clearly states patient has capacity?

Not necessary!
Clearly delirious or psychotic?
Not necessary!
MTB S2CK
p. 563
Minor
Minor
Minors do not have decision-making capacity

Cannot consent to or refuse medical treatments
Only parents or legal guardian can consent and
refuse
Exceptions are:
Contraception
Prenatal care
Substance abuse treatment
Sexually transmitted diseases (STDs) including
HIV/AIDS
Abortion
States are split on parental notification
laws
Some require it, some dont
Your
Y
answer is:
i
Tell the minor patient to notify her
parents.
MTB S2CK
p. 564
MTB S2CK
p. 564
Brain Death
Brain death = death in our legal system

If brain dead, you dont need consent to stop
therapy such as mechanical ventilation or
antibiotics
Court order and ethics committee arent
correct answers
Consent
Do Not Resuscitate Orders
Physician Assisted Suicide
Euthanasia
Terminal Sedation and
Law of Double Effect
Futile Care
Organ and Tissue Donation
USMLE S2 CK will want you to

discuss, educate, explain, and
confer before everything else.
MTB S2CK
p. 564
Consent
Consent
Patient signs consent for ovarian biopsy on left

side. At surgery you find cancer of right side.
What do you do?
Wake patient up & obtain consent to remove
ovary on right side.
Only adults can consent to procedures

Each procedure needs individual consent
Consent implied in emergency
Person doing procedure must obtain consent
Adverse effects of procedure must be explained to
make consent valid
Consequences of refusing procedure must be
explained to make consent valid
Pregnant women can refuse procedures and
treatments for their unborn children
Telephone consent is valid
MTB S2CK
p. 564
MTB S2CK
p. 564
Consent
Patient needs colonoscopy. Gastroenterologist asks

you to obtain consent for procedure.
What do you do?
DNR orders refer only to withholding

CPR
They dont refer to withholding any other
form of therapy
The gastroenterologist who will perform the

procedure needs to obtain consent.
Do you know all complications of the procedure and
alternatives?
If you dont explain the possibility of perforation
because you are unfamiliar with it, the consent isnt
valid
If patients colon perforates and you didnt explain
alternate procedures, the consent isnt valid
MTB S2CK
p. 564
MTB S2CK
p. 565
Patient with capacity consents to DNR before

losing consciousness. She needs a surgical
procedure, but the surgeon refuses because
the patient is DNR.
What do you do?
Perform the surgery
DNR doesnt mean withholding antibiotics,
chemotherapy, or surgery
DNR means only that, if the patient dies, you
wont attempt resuscitation
MTB S2CK
p. 565
Physician-administered treatment
intended to end or shorten patients life
Always
y wrong
g
p. 565

The question is one of intent:

If the meds are given with intent to
relieve pain, and as an adverse effect
they shorten life, its ethical
If the primary intent is to shorten life, its
unethical
MTB S2CK
p. 565
Always a wrong answer!

This includes states in which its legal
Ethical requirements for physicians
supersede legality
Physician
Physician-assisted
assisted suicide is administered by
the patient, but this is still unethical for
physicians
Physician ethics come before legal
requirements. You cannot do something
unethical even if its legal at the moment.
MTB S2CK
Euthanasia
MTB S2CK
Physician Assisted Suicide
p. 565

Is it acceptable to administer pain medication

even if theres the possibility treatment
shortens life?
For example, its acceptable to give pain
medications to a person with COPD who has
metastatic cancer even if the only way to
relieve pain is to give enough opiates that
breathing may be impaired, causing the
patient to die earlier
MTB S2CK
p. 565
Futile Care
Physician not obligated to render care

thats futile even if the family or patient
wants it
If brain dead & family insists on
continued mechanical ventilation
ventilation, you
are under no obligation to do so
You are under no obligation to perform
tests and treatments you consider
worthless
MTB S2CK
p. 565
Organ and Tissue Donation
Consent for Organ Donation
Payment for ORGANS is unacceptable
Only organ donor network should ask for

consent for organs
Ethical conflict of interest for physician to ask
for consent for organ donation
Organ donor network has fewer refusals than
physician
Organ donor cards give an indication of
patients wishes, but family can refuse organ
donation even if patient has organ donor
card
Payment for RENEWABLE tissues

(sperm & eggs) is acceptable
MTB S2CK
p. 565
MTB S2CK
p. 566
Confidentiality
Physician
Responsibilities
Confidentiality
Doctor/Patient Relationship
Gifts from Industry
Abuse
Impaired Drivers
Execution of Prisoners
Torture
Confidentiality
Right to confidentiality cannot be broken

for:
Employers
Coworkers
Government agencies
Family
Confidentiality is
Friends
important, but not as
important as protecting
others from harm.
MTB S2CK
p. 566
Patients right to confidentiality can be

broken when theres danger to others
STDs
HIV/AIDS
Airborne
Ai b
communicable
i bl diseases
di
((e.g.,
tuberculosis)
Court order demanding information
MTB S2CK
p. 566
Patient with HIV/AIDS has repeatedly refused to

disclose his HIV status to his sexual partner. The
partner accompanies the patient to the office visits
and is in the waiting room. The patient insists you not
tell the partner.
What do you do?
a.
b.
c.
d.
The confidentiality of the patient
Honor the patients wishes is not as important as protecting

the health of the partner.
Obtain a court order
Consult the ethics committee
Either the physician or the department of health
can notify the partner
MTB S2CK
p. 566
Confidentiality
Woman comes to your office with valid identification
from a law enforcement/government agency. She
requests a copy of your patients medical records.
What do you do?
Provide health-related protected records to
government agencies, including those from law
enforcement,
f
t only
l if:
if
Confidentiality
HIV-positive healthcare workers do

not have to disclose their status to
their patients or their employers.
Valid warrant or subpoena from courts

Otherwise violates the constitutional protection against
illegal search and seizure of property
This violates HIPAA, which protects health information
MTB S2CK
p. 566
Doctor/Patient Relationship
Physicians arent obligated to accept

everyone coming to him or her as a patient
You have the right to end the doctor/patient
relationship but must give the patient
sufficient time to obtain another caregiver
Small
S ll gifts
ift ffrom patients
ti t are acceptable
t bl as
long as they arent tied to a specific
treatment request
Romantic or sexual contact between
patients and their current physicians is never
acceptable
MTB S2CK
p. 566 567
MTB S2CK
p. 566
Gifts from Industry
Never acceptable!
Even pens, penlights, pads, and cups
are unacceptable
Meals in direct association with
educational activities arent considered
gifts
MTB S2CK
p. 567
Elder Abuse
Domestic Violence and Spousal Abuse
You can report elder abuse against

the consent of patient
Abused older adults may be too weak,
fragile, or vulnerable to protect
themselves
Elder abuse is treated ethically like
child abuse
Unlike child abuse, domestic abuse

cannot be reported against the
patients wishes
You can report and intervene only with
patients
patient
s consent
MTB S2CK
p. 567
MTB S2CK
p. 567
Impaired Drivers
(Seizure Disorders and Driving)
Least clear area nationally

No uniformity of laws between states
Answer suggest that the patient find another
means of transportation
Wrong answers would be:
a. Confiscating car keys and reporting to law
enforcement
b. Hospitalizing patient
c. Refusing to let the patient get in car
MTB S2CK
p. 567
Torture
Execution of Prisoners
Never ethical for a physician to

participate in executions at any level
You cannot ethically formulate a lethal
injection or even do so much as
pronounce a prisoner dead
Even if state law makes execution
legal, physicians should never
participate at any level
MTB S2CK
Torture
Physicians are never to participate in torture

of prisoners or detainees
Even if the question states that youre in the
military, your ethical obligation as a
physician supersedes your obligation to the
military
ilit
This would include:
Torture is the ethical

equivalent of child abuse.
Your p
participation
p
is never
acceptable; youre obligated
only to report it.
a. Refusing orders from military superiors to

participate in torture
b. Keeping the torture safe so that its not fatal
or damaging
MTB S2CK
p. 567
p. 567 568
MTB S2CK
p. 568
Esophagus
Achalasia
Esophageal Cancer
Esophageal Spasm
Esophagitis
Rings and Webs
Zenkers Diverticulum
Scleroderma
Mallory Weiss Tear
Boerhaaves Syndrome
Gastroenterology
Niket Sonpal, MD
Chief Resident
Esophageal Disorders/Definitions
Esophageal Disorders/Presentation
Dysphagia
Difficulty swallowing
Odynophagia
Pain while swallowing
Both can lead to weight loss

Hence, weight loss cannot be used to answer
MTB S2CK
p. 237
With the symptoms

Weight loss
Anemia
Heme-positive stool
MTB S2CK
Endoscopy!
p. 237
Achalasia/Diagnosis
Achalasia/Diagnosis
Inability of lower esophageal sphincter (LES) to

relax due to a loss of nerve plexus within
lower esophagus
Etiology unclear
Aperistalsis of esophageal body
Look for...
Young patient (< 50)
Progressive worsening dysphagia to both
solids and liquids at the same time
No association with alcohol and tobacco
use
Complain of...
Regurgitation and halitosis
Chagas Disease = recent travel to

South America and new onset dysphagia
MTB S2CK
p. 237
MTB S2CK
p. 237
Achalasia/Diagnostic Tests
Marked Dilation of the Esophagus
Barium esophagram
Will show a birds beak
Source: commons.wikimedia.com
MTB S2CK
Source: Niket Sonpal, MD
p. 238
Most accurate test is

Manometry
Chest X-ray
May show abnormal widening of esophagus,
but is neither very sensitive nor very specific
Chest X-ray is never the right

answer to diagnose achalasia
MTB S2CK
p. 238
MTB S2CK
p. 238
Achalasia/Treatment
Upper endoscopy
Shows normal
mucosa in achalasia
Cannot exactly be cured

All treatment is based on simple
mechanical dilation of esophagus
MTB S2CK
p. 238
MTB S2CK
p. 238
Achalasia/Treatment
Achalasia/Treatment
Pneumatic dilation
Botulinum toxin injection

Will relax LES, but effects wear off in about
3-6 months, requiring reinjection
Effective > 80% to

85% of patients
Repeat sessions
are necessaryy
Site of
Botulinum
Injection
Freedictionary.com
MTB S2CK
p. 238
MTB S2CK
p. 238
Achalasia/Treatment
Esophageal Cancer/Diagnosis
Surgical sectioning
or myotomy can help
to alleviate
symptoms
Known as Heller
M t
Myotomy
Look for:
Age 50 or older
Dysphagia with solids first then progresses to
liquids
Association with p
prolonged
g alcohol and
tobacco use
> 5 years of GERD symptoms
Niket Sonpal MD
MTB S2CK
p. 238
MTB S2CK
Esophageal Cancer/Diagnostic Tests
p. 239
Esophageal Cancer/Diagnostic Tests
Endoscopy is indispensible, since only a

biopsy can diagnose cancer
NO TISSUE, NO ISSUE
CT and MRI scans

Only shows extent of tissue
PET scan
Gives information about other anatomic
lesions
Barium cannot
diagnose cancer
MTB S2CK
p. 239
MTB S2CK
p. 239
Esophageal Cancer/Treatment
Esophageal Cancer/Treatment
Surgical resection is always the thing to try

No resection (removal) = no cure
Stent placement
Purely palliative
Chemotherapy and radiation
MTB S2CK
p. 239
MTB S2CK
p. 239
Esophageal Spasm/Background
Esophageal Spasm/Diagnosis
Diffuse esophageal spasm (DES) and nutcracker esophagus are clinically

indistinguishable
Both present
EKG and stress
Sudden onset of chest pain

Not related to exertion
MTB S2CK
p. 239
Esophageal Spasm/Treatment
Normal
Esophagram best initial test

Normal
Manometry
y most accurate test
Abnormal contraction in various section of the
esophagus
MTB S2CK
p. 239
Esophageal Spasm/Barium Study
Treated with:
Nitrates
Relax smooth muscle
Calcium-channel blockers
No Ca+2= no smooth muscle contraction
MTB S2CK
p. 240
MTB S2CK
p. 240
Infectious Esophagitis/Management
43-year-old man recently diagnosed with AIDS comes to
ED with pain on swallowing thats become progressively
worse over the last several weeks. Theres no pain when
not swallowing. His CD4 count is 43 mm3. The patient
isnt currently taking any medications.
Doesntt diagnose candida
a Esophagram Doesn
a.
b. Upper endoscopy Too invasive
c. Oral nystatin swish and swallow Only for oral candida
d. Intravenous amphotericin Too big gun
e. Oral fluconazole
MTB S2CK
Dysphagia with
HIV CD4 < 100
Yes
Empirically start
fluconazole
Yes
Improvement
No
Perform upper
endoscopy with
biopsy
Continue therapy
and HAART
CMV large
ulcerations. Tx:
ganciclovir or
foscarnet
HSV small
ulcerations. Tx:
acyclovir
p. 240
Infectious Esophagitis
Rings and Webs

Schatzki ring
Schatzki rings and Plummer-Vinson syndrome both
cause dysphagia
Source: Aaron Cho
MTB S2CK
p. 241
Rings and Webs
Rings and Webs
Schatzki ring
Associated with
intermittent dysphagia
Plummer-Vinson syndrome
Triad of:
1.
Dysphagia due to Esophageal Webs
2.
Iron Deficiency Anemia
3.
Glossitis
More
M
proximal
i l than
th Schatzki
S h t ki rings
i
Diagnosis
Barium esophagram
Treatment
Iron replacement
MTB S2CK
p. 241
Source: Azmeena Laila, MD
MTB S2CK
p. 241
Outpocketing of
posterior pharyngeal
constrictor muscles
Best test for diagnosis is

Esophogram
No medical treatment and

surgical intervention is
best
Stanford Hospital Media
MTB S2CK
p. 241
MTB S2CK
p. 241
Scleroderma
Mallory Weiss Syndrome/Presentation
Presentation
Upper GI bleed
secondary to repetitive
retching
Self-limited
Dx: endoscopy
Symptoms of reflux
Scleroderma or progressive systemic sclerosis
Diagnosis
Manometry
Treatment
PPIs
Screening for Barretts esophagus
MTB S2CK
p. 242
MTB S2CK
p. 242
Mallory Weiss Syndrome/Treatment
Boerhaaves Syndrome
No specific therapy and will resolve

spontaneously
Severe cases with persistent bleeding are
managed with injection of epinephrine or
electrocautery to stop bleeding
Esophageal rupture
due to prolonged
retching
A full thickness tear
Physical exam
Hammens sign crepitus
Subcutaneous air =
snap crackle and
pop
EMERGENCY!
MTB S2CK
p. 242
Stomach
Epigastric Pain
Gastroesophageal Reflux Disease
Barretts Esophagus
Gastritis
Peptic Ulcer Disease
Non ulcer Dyspepsia
Gastrinoma
Diabetic Gastroparesis
44-year-old woman comes to see you because of

epigastric pain for several months. She denies
nausea, vomiting, weight loss, or blood in her stool.
On physical examination you find no abnormalities.
a.
b.
c.
d.
e.
f.
Duodenal ulcer disease No anemia or heme (+) stools

Gastric ulcer disease Heme (+) stools
Gastritis Need EGD to diagnose
Pancreatitis Acute not chronic
Non-ulcer dyspepsia
Pancreatic cancer No painless jaundice
MTB S2CK
Abdominal Pain/Causes of Pain by Location
p. 242 243
Epigastric Pain/Most Likely Diagnosis

If this is in the history:
Right Upper
Quadrant
Left Upper
Quadrant
Cholecystitis
Biliary colic
Cholangitis
Perforated
duodenal ulcer
Right Lower
Quadrant
Splenic rupture
IBS Splenic
flexure syndrome
Mid-Epigastrium
Pancreatitis
Aortic dissection
Peptic ulcer disease
Appendicitis
Ovarian torsion
Ectopic pregnancy
Cecal diverticulitis
Left Lower
Quadrant
Sigmoid volvulus
Sigmoid diverticulitis
Ovarian torsion
Ectopic pregnancy
Pain worse with food

Pain better with food
Weight loss
Tenderness
Bad taste, cough, hoarse
Diabetes, bloating
Nothing
MTB S2CK
Epigastric Pain/Treatment
Endoscopy
Only way to truly
understand the etiology
of epigastric pain from
ulcer disease
Only
y way
y to g
give a
precise diagnosis
Proton pump inhibitors

(PPIs)
First line therapy
Empiric
Minimum 4 weeks
MTB S2CK
p. 243
H2 blockers
Ranitidine, nizatidine,
cimetidine, famotidine
Not as effective, but will
work in about 70% of
patients
MTB S2CK
Gastric ulcer
Duodenal ulcer
Cancer, gastric ulcer
Pancreatitis
Gatroesophageal reflux
Gastroparesis
Non ulcer dyspepsia
p. 243
Epigastric Pain/Diagnostic Tests
Wikimedia
The most likely diagnosis is:
Liquid antacids
Roughly the same
efficacy as H2 blockers
Misoprostol
Artificial prostaglandin
analogue
Used to treat NSAIDinduced gastric damage
When PPIs arrived,
misoprostol became
wrong answer
p. 243
Gastroesophageal Reflux Disease (GERD)

Inappropriate relaxation of LES
Results in acid contents of stomach coming up into
esophagus
Patient complains of...
Heartburn
Metallic taste
Cough
MTB S2CK
p. 244
42-year-old man comes to office with epigastric pain

radiating up under his chest, which becomes worse
after lying flat for an hour. He also has a brackish
taste in his mouth.
a. Ranitidine
Not as effective
b. Liquid antacid Not as effective
c. Lansoprazole
Not the first step must fail 1st
d. Endoscopy
e. Barium swallow Not an anatomic disease
f. 24-hour pH monitoring Too invasive
MTB S2CK
p. 244
GERD/Diagnostic Tests
GERD/Treatment
Most often diagnosed using patient history

When not clear, the most accurate test is...
All patients should try lifestyle changes
24-hour pH monitoring
Endoscopy when:
Dysphagia or odynophagia
Weight loss
Anemia or heme-positive stools
> 5 years of symptoms to exclude Barretts
esophagus
MTB S2CK
p. 244 245
Lose weight, avoid alcohol, nicotine and

certain foods, eat within 3 hours of bedtime
Elevate head 6-8 inches
Mild or Intermittent Symptoms

May be treated with liquid antacids or H2
blockers
Persistent Symptoms or Erosive Esophagitis
PPIs for 4-6 weeks
MTB S2CK
p. 245
GERD/Treatment
Barretts Esophagus
5% will not respond to PPIs

Patients require surgery to tighten LES:
Due to long-standing GERD

Change to columnar metaplasia
Typically takes 5 years
Nissen fundoplication
Stomach wrapped around LES
Endocinch
Scope used to place a suture around LES
Local heat or radiation of LES

Causes scarring to tighten LES
Last resort
MTB S2CK
p. 245
Diagnosis
Biopsy via endoscopy
Only way to assess presence of Barretts
esophagus
MTB S2CK
p. 245
Barretts Esophagus/Treatment
Gastritis
Finding
Barretts alone
(metaplasia)
Low grade dysplasia
Inflammation or erosion of gastric lining

Sometimes called gastropathy
High grade dysplasia
Management
PPIs and rescope every 2
3 years
PPIs and rescope every
6 12 months
Ablation with endoscopy,
photodynamic therapy,
radiofrequency ablation,
or surgical removal
3 levels: mild, moderate and severe

With or without hemorrhage
Many causes
Alcohol
NSAIDs
Helicobacter pylori
Portal HTN
Stress
Burns, trauma, sepsis, multiorgan failure
MTB S2CK
p. 246
MTB S2CK
p. 246
Gastritis/Presentation
Gastritis/Diagnosis
Often with GI bleeding without pain

Severe, erosive gastritis can present with
epigastric pain
Look for NSAIDs or alcoholism in history
No unique
q p
physical
y
findings
g
The most accurate

test is...
EGD
You cannot answer the most likely diagnosis

question from history and physical alone
MTB S2CK
p. 246
What is good
about this test?
Test
Endoscopic
biopsy
Serology
H. py
pylori testing
g
Treated if associated
with gastritis
MTB S2CK
Testing for Helicobacter pylori

Invasive test
(endoscopy)
Inexpensive,
excludes infection
if negative
Lacks specificity,
cant distinguish
current/previous
infection
Urea C13 or C14 Positive only in

breath testing active infection,
Requires expensive
equipment
H. Pylori
stool antigen
Requires stool
sample
Treat with PPIs

H2 blockers, sucralfate, and liquid antacids
arent effective as PPIs
Sucralfate is an inert substance (aluminum

hydroxide complex) that coats the stomach.
If sucralfate is presented as a choice, its
nearly always the wrong answer.
noninvasive
MTB S2CK
p. 246 247
p. 246
Gastritis/Treatment
What is bad
about this test?
Most accurate of
all tests
Positive only in
active infection,
noninvasive
Capsule endoscopy is
not appropriate for upper
GI bleeding if endoscopy
is one of the choices
MTB S2CK
p. 247
Gastritis
Peptic Ulcer Disease (PUD)
Stress ulcer prophylaxis is indicated in:

Mechanical ventilation
Burns Curlings ulcers
Head trauma Cushings ulcers
Coagulopathy
PUD refers to both duodenal ulcer and

gastric ulcer disease
Endoscopy is key to diagnosis and
treatment
MCCs H. pylori and NSAIDs
MTB S2CK
p. 247
Note: Alcohol and tobacco dont cause ulcers.

They delay healing of ulcers
MTB S2CK
p. 247 248
Peptic Ulcer Disease/Presentation
PUD presents with recurrent episodes of

epigastric pain
Abdominal Pain
(dull, sore, gnawing)
Pain that is improved
with eating
Pain that is worsened

by eating
Duodenal Ulcer
MTB S2CK
p. 248
Peptic Ulcer Disease/Diagnosis
Peptic Ulcer Disease/Treatment
Upper endoscopy: most accurate test

Allows for intervention and biopsy
PUD responds to PPIs...

But must treat for H. pylori
Ulcer on endoscopy
Biopsy positive for H. pylori
Duodenal Ulcer
Clip or epinephrine
injection
Radiologic Testing
Poor sensitivity and no histology testing
MTB S2CK
p. 248
Gastric Ulcer
Bleeding ulcer
H. pylori in more than 80%

to 90% of cases
Antibiotic treatment
Gastric Ulcer
H. pylori in 50% to
70% of cases
Cancer is present in 4% of those with GU but

in none of those with DU.
MTB S2CK
p. 248 249
10
H. pylori Treatment
56-year-old woman comes to clinic with epigastric pain from

endoscopically confirmed duodenal ulcer, which is
unresponsive to several weeks of PPI, clarithromycin, and
amoxicillin.
Biopsy positive for H. Pylori

PCN allergy?
PPI combined with

clarithromycin and amoxicillin
Replace amoxicillin
with metronidazole
30-60 day post therapy

testing for eradication
MTB S2CK
p. 243

Treatment of Refractory Ulcers
If initial therapy doesnt resolve the DU then
detecting persistent H. pylori and switching the
antibiotics to metronidazole and tetracycline is
appropriate or adding bismuth
For those with refractory
y GU,, a repeat
p
endoscopy is done to exclude cancer
a.
b.
c.
d.
e.
f.
g.
Refer for surgery

g y Too invasive
Switch the PPI to ranitidine PPI is superior to ranitidine
Abdominal CT scan CT cant detect H. pylori
Capsule endoscopy Cant detect H. pylori
Urea breath testing
Vagotomy Not necessary and too invasive
Add sucralfate Always the wrong answer
MTB S2CK
p. 249
Gastric Ulcers vs. Duodenal Ulcers
GU is routinely biopsied
Routinely
repeating the
endoscopy to
confirm healing is
standard with GU
GU vs. DU
GU is associated
with cancer in
4%
GU pain is more often

worsened by food
MTB S2CK
p. 249
MTB S2CK
p. 250
Non ulcer Dyspepsia
Non ulcer Dyspepsia
Non-ulcer (functional) dyspepsia is epigastric

pain that has no identified etiology
MCC of epigastric pain in U.S.
The best initial therapy is with PPIs

NUD < 45-55 years
NUD > 45-55 years
Empiric PPI therapy
PPIs and EGD to r/o

cancer
Symptoms persist and H.

Pylori is present =
treat for H. pylori
MTB S2CK
p. 250
MTB S2CK
p. 250
11
Gastrinoma (Zollinger Ellison Syndrome)
Gastrinoma/Diagnostic Tests
Look for patient with ulcers

that are:
1. Large > 1 cm
2. Multiple
3. Past 3rd portion of
duodenum
4. Presents with:
Diarrhea
Abdominal pain
Anemia
Heme-positive stools
After endoscopy confirms an ulcer, diagnosis made using

one of the following three:
1. High gastrin levels after antisecretory therapy (PPIs/H2)
2. High gastrin levels despite a high gastric acid output
3. Persistent high gastrin levels despite injecting secretin
(most accurate)
MTB S2CK
p. 251
MTB S2CK
p. 251
Source: Niket Sonpal MD
Gastrinoma/Diagnostic Tests
Gastrinoma/Treatment
What is the next best step after diagnosing ZE?

Exclude metastatic disease
Local disease is removed surgically
Somatostatin receptor scintigraphy +

Endoscopic ultrasound
Metastatic disease requires lifelong

PPIs to block acid production
Ultrasound, CT, and MRI of abdomen have

poor sensitivity and are never the most
accurate test for diagnosing ZE
MTB S2CK
p. 251
MTB S2CK
p. 251
64-year-old patient with diabetes for 20 years comes to
the office with several months of abdominal fullness,
intermittent nausea, constipation, and a sense of
bloating. On physical examination, a splash is heard
over the stomach.
a. Abdominal CT scan Can only diagnose static conditions
b. Colonoscopy Wrong end!
c. Erythromycin
d. Upper endoscopy Wouldnt reveal anything
e. Nuclear gastric emptying study Most accurate test for
MTB S2CK
p. 252
diabetic gastroparesis,
but rarely used
Long standing diabetes
Autonomic neuropathy
from high glycemic
index
+
Resultant dysmotility
from an inability to
sense stretch in the GI
tract
=
Diabetic
gastroparesis
MTB S2CK
Nausea, vomiting, and

early satiety
p. 252
12
The patients most common complaint is abdominal
discomfort with eating large or small meals
Nausea &
vomiting
Bloating &
constipation
Upper and Lower

Symptoms
Anorexia
Early satiety
Neurologic Symptoms
Endoscopy - large
amount of retained
food
Succussion
splash
Signs elicited by exam
Colon
Gastrointestinal Bleeding
Diarrhea
Irritable Bowel Syndrome
Inflammatory Bowel Disease
Diverticular Disorders
Colon Cancer Screening
69-year-old woman comes to ED with multiple red/black stools. Past
medical history significant for aortic stenosis. Pulse 115/ minute.
BP 94/62 mmHg. Examination otherwise normal.
a.
b.
c.
d.
e.
f.
g.
h.
Colonoscopy
Nasogastric tube placement
Upper endoscopy
Patient is unstable,
Bolus of normal saline
Stablized first, THEN
CBC
diagnose
Bolus of 5% dextrose in water
Consult gastroenterology
D5w doesnt stay intravascular
Check for orthostasis
MTB S2CK
p. 252 253
Esophagitis
Upper GI
bl di
bleeding
Gastritis
Varices
Duodenitis
Cancer
MTB S2CK
p. 253
Gastrointestinal Bleeding/Physical Findings

Severity of Blood Loss Based on Hemodynamics
Most
common:
Diverticulosis
Lower GI
bl di
bleeding
Polyps
Most
common:
Ulcer disease
Physical Finding
Hemorrhoids
Orthostasis
Pulse > 100/minute
Systolic BP < 100 mmHg
Percentage of blood loss

15 20%
30%
30%
Remember: orthostasis is defined as...

IBD
UGIB
Cancer
MTB S2CK
p. 253
>10-point rise in pulse when going from supine to

sitting or standing up or BP drop of 20 points or
more when sitting up
MTB S2CK
p. 253
13
Variceal Bleeding
Gastrointestinal Bleeding/Diagnostic Tests
For acute severe bleeding
Vomiting
blood +/
black stool
Cirrhosis
Spider
angiomata
and caput
medusa
MTB S2CK
Variceal
bleeding
Replace fluids and check Hct, platelet count, and

coagulation tests (PT or INR)
Asterixis
For variceal bleeding

Octreotide and urgent endoscopy to control the
bleed by banding
Palmar
erythema
Splenomegaly
p. 253 254
MTB S2CK
p. 254
Additional Diagnostic Tests for GI Bleeding
Gastrointestinal Bleeding/Treatment
Test
Indication
Stabilization Treatment
Nuclear bleeding scan
Endoscopy unrevealing in a massive

acute hemorrhage
Specific site of bleeding needs
to be identified prior to surgery or
embolization of vessel; used onlyy in
massive, nonresponsive bleeding
Small bowel bleeding when upper and
lower endoscopy dont show etiology
Not useful in GI bleeding
Shows ischemia in severe bleeding
Fluid replacement
Angiography
Capsule endoscopy
CT or MRI of abdomen
EKG
MTB S2CK
p. 254
1-2 liters an hour
Packed RBCs
Hct < 30 in those who are older or suffer from CAD
MTB S2CK
p. 255
Stabilization Treatment
Treat Underlying Cause

Endoscopy to determine diagnosis and
administer treatment (band varices,
cauterize ulcers, inject epinephrine into
bleeding gastric vessels)
IV PPI for upper GI bleeding
Surgery to remove site of bleeding if fluids,
blood, platelets, and plasma will not control
bleed
Fresh frozen plasma

INR > 1.3
Platelets
< 50,000 when bleeding
MTB S2CK
p. 255
MTB S2CK
p. 255
14
Esophageal and Gastric Varices

Octreotide (somatostatin)
Banding
Transjugular intrahepatic portosystemic
shunting
h ti (TIPS)
Propranolol
Diarrhea/Types
Lactose
intolerance
Carcinoid
syndrome
Diarrhea
Antibioticassociated
diarrhea
MTB S2CK
Chronic
pancreatitis
Malabsorption
p. 255
Diarrhea/Antibiotic Associated
Clindamycin associated with highest

incidence of antibiotic-associated diarrhea
and Clostridium difficile
Blood and white cells may be present in stool
Presents several days or weeks after start of
antibiotics
ANY antibiotic can potentially cause diarrhea
Best initial test is...

Stool C. diff. toxin
Most accurate test is...

C. diff. PCR
Best initial therapy is...

Metronidazole
If theres no response to metronidazole, next step

in management is to...
Switch to oral vancomycin or fidaxomicin
IV vancomycin is always wrong for
antibiotic-associated diarrhea since it
will not pass bowel wall.
MTB S2CK
p. 255
MTB S2CK
p. 255 256
75-year-old man is admitted to hospital with pneumonia.
Several days after start of antibiotics, he has diarrhea. Stool C.
diff toxin is positive, and hes started on metronidazole, which
leads to resolution of diarrhea over a few days. Two weeks
later diarrhea recurs and C. diff toxin is positive again.
a.
b.
c.
d.
e.
Retreat with metronidazole orally

Use vancomycin orally Repeat metronidazole before switching
Sigmoidoscopy and treat only if pseudomembranes are found
Not necessary
Intravenous metronidazole Only if patient
cannot
take
orally
Wait for stool culture
C. diff. doesnt grow in culture
f. Intravenous vancomycin
Repeat metronidazole before switching /
IV vancomycin does not work
MTB S2CK
Diarrhea after
antibiotic Use
Yes
C. difficile
positive?
No
Consider
alternative causes
Yes
T t with
Treat
ith
metronidazole
No
Switch to oral
vancomycin or
fidaxomicin
Improvement?
Yes
Continue
metronidazole
until end of
course
p. 256
15
Diarrhea/Malabsorption
All present with steatorrhea:

Oily
Greasy
Stools
Floating
Foul smelling
All forms of fat malabsorption present with

deficiency of fat-soluble vitamins (A, D, E, and K)
Hence, they can all present with...
Causes:
Celiac disease
Whipples disease
Chronic pancreatitis
MTB S2CK
Deficiency
Manifestation
Vitamin D
Vitamin K
Vitamin B12
Hypocalcemia
Bleeding, easy bruising
Anemia, hypersegmented
neutrophils, neuropathy
Vitamin B12 needs an intact bowel wall
and pancreatic enzymes to be absorbed
p. 256
MTB S2CK
p. 256 257
Diarrhea/Diagnostic Tests
Celiac disease
Whipples Disease
Arthralgias
Ocular findings
Neurologic abnormalities (dementia, seizures)
Fever
Lymphadenopathy
L
h d
th
Anti-tissue transglutaminase
Most accurate diagnostic test is...

Small bowel biopsy
Flattening of villi
Can exclude lymphoma
Other tests
IgA antigliadin antibody
Antiendomysial antibody
MTB S2CK
p. 257
MTB S2CK
p. 257
Chronic Pancreatitis/Diagnostic Tests
Whipples disease and

tropical sprue
Most accurate
diagnostic test is...
Abdominal X-ray
50% to 60% sensitive
for calcification of
pancreas and very
specific when test is
abnormal
Bowel wall biopsy

showing specific
organism
Treat with ceftriaxone
or TMP/SMZ
MTB S2CK
p. 257
MTB S2CK
p. 257 258
16
Abdominal CT scan
80% to 90% sensitive
for pancreatic
calcification
Secretin stimulation testing

Most accurate diagnostic test
Place NG tube; normal pancreas releases large
volume of bicarbonate-rich fluids after IV secretin
D-xylose testing
Old test to distinguish pancreatitis from bowel wall
abnormalities
D-xylose normal in pancreatic disorders
MTB S2CK
p. 257 258
MTB S2CK
Malabsorption/Treatment
p. 257 258
Carcinoid Syndrome
Disease
Specific Treatment
Chronic pancreatitis
Enzyme replacement
Celiac disease
Avoid gluten containing

foods (wheat, oats, rye,
barley)
Whipples disease
Ceftriaxone, TMP/SMX
Tropical sprue
TMP/SMX, tetracycline
Presentation
Flushing
Wheezing
CV murmurs tricuspid regurgitation
Diarrhea
Best initial diagnostic test is...
Urinary 5-hydroxyindoleacetic acid (5-HIAA) test
Treatment
Octreotide
MTB S2CK
p. 258
MTB S2CK
p. 258 259
Lactose Intolerance
Irritable Bowel Syndrome (IBS)
Presents like malabsorptive diarrhea, except...
Pain syndrome with either diarrhea, constipation, or

both
Pain of IBS is...
Intermittently
No weight loss
Normal vitamin levels
Best initial diagnostic test is...

Stool osmolality test

Cessation of symptoms after diet change
Best treatment is...

Stop eating milk products and consider exogenous
lactase therapy
MTB S2CK
p. 259
Relieved by BM
Less at night
Relieved by a change in bowel habit (e.g., diarrhea)
No specific diagnostic test

Diagnosis of exclusion in association with complex of
symptoms
Not associated with...

Weight loss
Blood or white cells in stool
MTB S2CK
p. 259
17
Irritable Bowel Syndrome/Treatment
Fiber in diet
Antispasmodic agents
Crohns disease (CD) and ulcerative colitis

(UC) present with...
Diarrhea and abdominal pain
Blood in stool
anemia
Weight
g loss
Fever
Hyoscyamine
Dicyclomine
Tricyclic
y
antidepressants
p
Amitriptyline
Antimotility agents
Loperamide for diarrhea
Lubiprostone (chloride-channel activator)
Increases BM frequency
MTB S2CK
p. 259
MTB S2CK
p. 259
Extraintestinal manifestations in both CD and UC

Arthralgias
Uveitis, iritis
Skin manifestation (erythema nodosum, pyoderma
gangrenosum)
Sclerosing cholangitis (more frequent in UC)
Erythema Nodosum
Risk of cancer associated with CD and UC

Both forms of IBD can lead to colon cancer
Cancer risk with duration
CD involving colon has same cancer risk as UC
MTB S2CK
Pyoderma Gangrenosum
p. 259 260
Inflammatory Bowel Disease/Differences
Inflammatory Bowel Disease/Diagnostic Tests
Crohns disease
Ulcerative colitis
Skip lesions
Transmural granulomas
Fistulas and granulomas
Masses and obstruction
Perianal disease
Curable by surgery
Entirely mucosal
No fistulas, no abscesses
No obstruction
No perianal disease
Endoscopy
Frequent question: When should screening occur?

Answer: After 8 to 10 years of colonic involvement,

with colonoscopy every 1 to 2 years.
MTB S2CK
p. 260
CD thats mainly in small bowel, radiologic tests

such as barium studies will detect lesions
MTB S2CK
p. 260
18
Inflammatory Bowel Disease/Diagnostic Tests
ANCA and ASCA Results in IBD

Test
Crohns disease Ulcerative colitis
Antineutrophil cytoplasmic
antibody (ANCA)
Negative
Positive
Antisaccharomyces
cerevesiae antibody (ASCA)
Positive
Negative
Inflammatory Bowel Disease/Treatment
Acute exacerbations of either CD or UC are

treated with steroids
Chronic maintenance of remission is with 5ASA derivatives (mesalamine)
Asacol for UC
Pentasa for CD
Perianal CD
Ciprofloxacin and metronidazole
MTB S2CK
p. 260
MTB S2CK
p. 260 261
Inflammatory Bowel Disease/Treatment
Diverticulosis
Azathioprine and 6-mercaptopurine are used to

wean patients off steroids
Fistulae and severe unresponsive disease
Anti-tumor necrosis factor (TNF) agents (infliximab)
Surgery only if theres no response to anti-TNF
agents
NOTE
Neither form of IBD is routinely treated with surgery
UC can be cured, however, with colectomy
In CD, surgery is used exclusively for bowel
obstruction as it recurs at surgical site
Outpocketings of colon
Where arteries meet mucosa
Vegetarians
At risk?
Asymptomatic
Infection?
MTB S2CK
p. 261
MTB S2CK
p. 261
Diverticulosis
Diverticulitis

Colonoscopy
Barium studies
Fiber Fiber Fiber
Diagnosis
LLQ pain and tenderness
Fever
Leukocytosis
Palpable mass sometimes occurs
Symptoms such as nausea, constipation,
and bleeding can be present, but are
nonspecific
MTB S2CK
p. 261
MTB S2CK
p. 261
19
Diverticulitis
Diverticulitis

CT scan of the abdomen
98% accuracy
Colonoscopy and barium enema are
dangerous
g
in acute diverticulitis
Increased risk of perforation because
infection weakens colonic wall
MTB S2CK
p. 261
Diverticulitis/Treatment
Treatment
Antibiotics that cover E. coli and anaerobes that
are present in bowel such as...
Ciprofloxacin combined with metronidazole

Surgery is for those with...

No response to medical therapy
Frequent recurrences of infection
Perforation, fistula formation, abscess, strictures, or
obstruction
MTB S2CK
261 262
Which of the following is the most effective method of

screening for colon cancer?
a. Colonoscopy
b. Sigmoidoscopy
All less sensitive
c. Fecal occult blood testing (FOBT) than colonoscopy
d Barium enema
d.
e. Virtual colonoscopy with CT scanning Low sensitivity;
misses small
f. Capsule endoscopy
For small bowel bleeding
MTB S2CK
polyps
p. 262
Colon Cancer/Frequency of Screening
Routine testing
Patients should have a colonoscopy every 10
years beginning at age 50
Hereditary nonpolyposis colon cancer

syndrome (HNPCC) comprises...
3 family members
2 generations
1p
premature ((< 50))
Single
g family
y member with colon cancer?
Begin 10 years earlier than the age at which
the family member developed their cancer or
age 40, whichever is younger
Screen every 10 years if relative > 60 or
every 5 years if relative < 60
MTB S2CK
p. 262
Start screening at age 25 with colonoscopy

every 1 to 2 years
MTB S2CK
p. 262
20
Familial adenomatous polyposis (FAP)

Presence of thousands of polyps with
abnormal genetic test known as
adenomatous polyposis coli (APC) test
Start screening with sigmoidoscopy at age
12 every year
Previous adenomatous polyp

Patient should have colonoscopy...
Every 3 to 5 years
Previous history of colon cancer

Patient should have colonoscopy...
1 year after resection
Then at 3 years
Then every 5 years
MTB S2CK
p. 263
MTB S2CK
p. 263
Other Polyposis Syndromes

Peutz-Jeghers syndrome
Multiple hamartomatous polyps, melanotic spots on
lips and skin, frequency of breast cancer, gonadal
and pancreatic cancer
Pancreas & Liver
Gardner syndrome
Colon cancer associated with: osteomas, desmoid
tumors, and other soft tissue tumors
Turcot syndrome
Colon cancer in association with CNS malignancy
Juvenile polyposis
Colon cancer in association with multiple
hamartomatous polyps
MTB S2CK
p. 263
Acute Pancreatitis
Drug allergy
Acute Pancreatitis/Presentation
Most
common
1. GB stones
2. ETOH
Ductal
obstruction
Pancreatitis
Trauma
Hypertriglyceridemia
Hypercalcemia
MTB S2CK
p. 263 264
Drug toxicity
Scorpion
sting
Acute epigastric pain + tenderness + nausea/vomiting

=
Pancreatitis
Pain intensity is subjective and doesnt correlate
with degree of organ damage
In severe cases theres hypotension and fever
The pain of pancreatitis goes straight through to
the back like a spear stabbed into the abdomen.
Cholecystitis pain goes around the side to the
back.
Infection
MTB S2CK
p. 264
21
Acute Pancreatitis/Diagnostic Tests

Which of the following is associated with the worst
prognosis in pancreatitis?
a. Elevated amylase
Levels do not correlate
with severity
b. Elevated lipase
c. Intensity of the pain Pain doesnt predict
d Low calcium
d.
e. C-reactive protein (CRP) rising
Elevated with all inflammation
MTB S2CK
p. 264
Best initial tests are...

Amylase and lipase
Most specific diagnostic test is
CT scan
Labs
CBC: leukocytosis, drop in Hct over time with
rehydration
Elevated LDH and AST
Hypoxia
Hypocalcemia
Elevated urinary trypsinogen activation peptide
MTB S2CK
p. 264 265
Imaging
CT or MRI scan are best
Also detect pseudocysts
ERCP
Can help determine etiology (stones, stricture, tumor)
Plain X
X-ray
ray
Sentinel loop of bowel (air-filled piece of small bowel
in LUQ)
Limited utility
Ultrasound has very poor accuracy

Overlying bowel blocks precise imaging
MTB S2CK
NOTE: Abdominal CT scan is always performed with IV and

oral contrast to better define and outline abdominal structures.
p. 265
Acute Pancreatitis/Treatment
Acute Pancreatitis/Treatment
> 30% necrosis on CT or MRI, add antibiotics

(e.g., imipenem)
Infected, necrotic pancreatitis should be
resected with surgical debridement to
prevent ARDS and death
Pseudocysts are drained with a needle if
they are enlarging or painful
NPO (no food)

IV hydration
Analgesia
PPIs pancreatic stimulation from acid
entering
g duodenum
MTB S2CK
p. 265
MTB S2CK
p. 265
22
Acute Pancreatitis/Complication
Liver Disease
Spider
angiomata and
palmar
erythema
Hepatorenal
syndrome
Hepatopulmonary
syndrome
Portal hypertension
leading to varices
Chronic
Li
Liver
Disease
Thrombocytopenia
Coagulopathy
Asterixis and
encephalopathy
h l
th
Hypoalbuminemia &
edema and ascites
MTB S2CK
Ascites
p. 265
Ascites
Paracentesis is performed with...

New-onset ascites
Abdominal pain and tenderness
Fever
Low albumin
L
lb i iin th
the ascitic
iti fluid?
fl id?
Portal HTN from cirrhosis is the etiology
SAAG: Correlating Level with Specific Diseases

< 1.1 g/dL
> 1.1 g/dL
Infections
Cancer
Nephrotic syndrome
Portal HTN
CHF
Hepatic vein thrombosis
Constrictive pericarditis
Serum ascites albumin gradient (SAAG)

The difference or gradient of albumin between
serum and ascitic fluid
MTB S2CK
p. 266
MTB S2CK
p. 266
Spontaneous Bacterial Peritonitis
Spontaneous Bacterial Peritonitis
Infection without perforation of bowel

Cell count with > 250 neutrophils
Causative organisms
E. coli (most common)

Other gram-negative bacilli
Pneumococcus
Anaerobes (rare)

Fluid culture, but takes too long for results
Gram
G
stain
t i iis negative/LDH
ti /LDH nonspecific
ifi
Treatment: cefotaxime or ceftriaxone
NOTE: SBP frequently recurs. When the ascites
fluid albumin level is quite low, use prophylactic
norfloxacin or TMP/SMX.
MTB S2CK
p. 266
MTB S2CK
p. 266
23
Treatment of Specific Features of Cirrhosis
Alcoholic Liver Disease
Feature
Treatment
Ascites and edema
Spironolactone and other diuretics. Serial

pericentesis for large volume ascites.
FFP and/or platelets only if bleeding occurs
Diagnosis of exclusion
No specific therapy
Coagulopathy and
thrombocytopenia
Encephalopathy
Hypoalbuminemia
lb
Spider angiomata and palmar
erythema
Varices
Hepatorenal syndrome
Hepatopulmonary syndrome
Liver biopsy
Lactulose, neomycin, or rifaximin

f therapy
h
No specific
No specific therapy
Alcohol and drugs causing liver disease give a
Propranolol and banding via endoscopy

Somatostatin (octreotide), midodrine
No specific therapy
greater elevation in AST compared to ALT.

Viral hepatitis: Higher ALT than AST.
Binge drinking: Sudden rise in GGTP.
MTB S2CK
p. 267
MTB S2CK
p. 267
Primary Biliary Cirrhosis (PBC)
PBC is most likely diagnosis with...

Woman in 40s or 50s
Fatigue and itching
Normal bilirubin
Elevated alkaline phosphatase
Most unique features of PBC are...

Xanthelasma/xanthoma
Osteoporosis
Liver biopsy
Most accurate blood test:
Antimitochondrial antibody
Treatment with...
Ursodeoxycholic acid
MTB S2CK
p. 267
MTB S2CK
p. 267 268
Primary Sclerosing Cholangitis

Pruritus
Elevated alkaline
phosphatase
GGTP
Elevated bilirubin level
Treatment
Cholestyramine
Ursodeoxycholic acid

ERCP, not liver biopsy
Shows beading, narrowing,
or strictures in biliary
system
MTB S2CK
p. 268
24
Primary Sclerosing Cholangitis
Alpha 1 Antitrypsin Deficiency

Look for...
Combination of...
PSC doesnt improve or resolve with

resolution of IBD.
Even after a colectomy in UC, patient may
still progress to needing a liver
transplantation.
Liver disease
Emphysema (COPD)
Young patient (< 40)

Nonsmoker
Treatment
Replace enzyme exogenously
MTB S2CK
p. 268
MTB S2CK
Hemochromatosis
p. 268
Hemochromatosis
Genetic disorder leading to overabsorption of

iron in duodenum
Amenorrhea
Skin
Darkening
Mutation: C282y gene

Erectile
dysfunction
Presentation
Patient in their 50s with mild increases in AST
and alkaline phosphatase
MTB S2CK
p. 268

Iron studies
Increased serum iron
and ferritin
Decreased iron binding
capacity

Liver biopsy
Increased iron
MTB S2CK
p. 269
Cardiomegaly
Fatigue and joint
pain (pseudogout)
MTB S2CK
Hemochromatosis
Hemochromatosis
Diabetes
p. 268 269
Chronic Hepatitis B and C

EKG
Conduction defects
Echocardiogram
Dilated or restrictive
cardiomyopathy
Both are associated with...

Cirrhosis
Liver cancer
PAN
Best therapy
Phlebotomy
MTB S2CK
p. 269
25
Chronic Hepatitis B and C

Chronic hepatitis B
Surface antigen
positive > 6 months
Hepatitis B DNA PCR
is the best way to
determine viral
replication activity
Liver biopsy for fibrosis
Biopsy tracks progress
MTB S2CK
Chronic Hepatitis B and C/Treatment

Chronic hepatitis C
80% have chronic
infection
Never symptomatic
when illness contracted
Hepatitis C DNA PCR
Determines disease
activity
p. 270
Chronic hepatitis B
Adefovir
Lamivudine
Telbivudine
Entecavir
Tenofovir
T
f i
Interferon
MTB S2CK
Chronic hepatitis C
Combination of...
Interferon +
Ribavirin +
Telapavir
( Boceprevir)
(or
B
i)
p. 270
Hepatitis Treatment Side Effects
Wilson Disease/Presentation
Drug
Adverse Effects
Interferon
Arthralgias, thrombocytopenia,
depression, leukopenia
Ribavarin
Anemia
Adefovir
Renal dysfunction
Lamivudine
None
Bocepevir
Anemia
Decrease in ceruloplasmin causes buildup of

copper
Psychosis, tremor, dysarthria, ataxia, or
seizures
Coombs negative hemolytic anemia
Renal tubular acidosis or nephrolithiasis
Telaprevir
Rash
MTB S2CK
p. 270
Wilson Disease/Diagnosis
MTB S2CK
p. 270 271
Wilson Disease

Slit-lamp examination for Kayser-Fleischer
rings
Most accurate diagnostic
g
test is...
Abnormally increased amount of copper
excretion into urine after giving penicillamine
MTB S2CK
p. 271
MTB S2CK
p. 271
26
Wilson Disease/Treatment
Autoimmune Hepatitis
Penicillamine chelates copper and removes it

Additional therapies are...
Zinc: interferes with intestinal copper absorption
Trientine: alternate copper-chelating compound
Look for...
Young women
Signs of liver
inflammation
Positive ANA
Decreased ceruloplasmin level is not the most

accurate test. This is the most common wrong
answer. All plasma proteins can be decreased in those
with liver dysfunction and cirrhosis.
More specific tests:

Liver-kidney
microsomal antibodies
Anti-smooth muscle
antibodies
MTB S2CK
p. 271
MTB S2CK
Autoimmune Hepatitis
Most accurate test:

Liver biopsy
Treatment
Prednisone and/or
azathioprine
p. 271
Nonalcoholic Steatohepatitis
Nonalcoholic Fatty Liver Disease
Extremely common cause of mildly abnormal liver
function tests
Disorder is associated with:

Obesity
Diabetes
Hyperlipidemia
Corticosteroid use
Most accurate test: biopsy
Management: weight loss
MTB S2CK
p. 272
Nonalcoholic Steatohepatitis
27
Anemia
Presentation
Diagnostic Tests
y p
Symptoms
Mean Corpuscular Volume
Microcytic Anemia
Macrocytic Anemia
Normocytic Anemia
Treatment
Hematology
New York City
Anemia
Hematocrit and Symptoms
Presentation
All forms of anemia present with identical
symptoms if they have the same hematocrit (Hct)
Symptoms based on severity, not etiology
Hematocrit
Expected Symptoms
> 30 35%
None
25 30%
Dyspnea (worse on
exertion),
), fatigue
g
20 25%
Lightheadedness, angina
< 20 25%
Syncope, chest pain
Cannot be answered using symptoms alone
Diagnostic Tests
Best initial test to evaluate anemia?
Always a complete blood count (CBC)
MTB S2CK
p. 203
Anemia/Diagnostic Tests
Ultimately, cardiac ischemia from

anemia proves fatal. Myocytes cant
distinguish between:
Anemia
Hypoxia
CAD
MTB S2CK
p. 203
Mean Corpuscular Volume
Mean corpuscular volume (MCV)

First clue to knowing etiology
Mean Corpuscular
Volume
(Normal 80100 fL)
Smaller?
Larger?
Microcytosis
Macrocytosis
All of these conditions result in decreased

oxygen delivery to tissues
MTB S2CK
p. 203 204
MTB S2CK
p. 204
Microcytosis
Microcytosis
Causes of low MCV:

Iron deficiency
Thalassemia
Sideroblastic anemia
Anemia of chronic disease
Similarities among microcytic anemias

Low reticulocyte count
Only alpha thalassemia has 3 genes deleted
elevated reticulocyte count
Microcytic anemias are due to production
problems
MTB S2CK
p. 204
Microcytosis
Routine blood smear

Not effective in telling the difference between
types of microcytosis
All hypochromic
All potentially give target cells
MTB S2CK
p. 204
Nearly synonymous with
MTB S2CK
reticulocyte counts
p. 204
Macrocytic Anemia/Etiology
Causes of high MCV
B12 & folate deficiency
Alcoholism
Liver disease or hypothyroidism
Medications
M di ti
(
(e.g.,
zidovudine
id
di or phenytoin)
h
t i )
Antimetabolite medications: azathioprine, 6mercaptopurine, hydroxyurea
Myelodysplastic syndrome (MDS)
MTB S2CK
p. 204
Normocytic Anemia
Anemia/Treatment
Acute blood loss & hemolysis

rapid drop in
Hct (no time for MCV change)
Blood loss leads to iron deficiency & microcytosis
Hemolysis increases reticulocyte count
Treatment
If severe: give packed RBCs
Answering the question At what Hct do I
transfuse a patient? depends on the following
factors:
Reticulocytes raise the MCV

Reticulocytes slightly larger than normal cells
MTB S2CK
p. 204
1. Symptomatic? Transfuse.
2. Hct very low in elderly person? Heart disease?
Transfuse.
MTB S2CK
p. 205
Anemia/Treatment
Blood Products
Symptomatic from anemia means:

SOB
Lightheaded, confused, and sometimes
syncope
Hypotension and tachycardia
Chest pain
Remember:
No transfusion if young & asymptomatic
MTB S2CK
p. 205
Packed Red Blood Cells (PRBCs)

Concentrated form of blood
Whole blood - 150 mL plasma = PRBCs

Hct of PRBCs: 70% - 80%
Removal of plasma doubles Hct
Each unit PRBCs raises Hct by 3 points/unit
MTB S2CK
p. 205
Blood Products
Blood Products
Fresh Frozen Plasma (FFP)

Replaces clotting factors for elevated prothrombin
time, aPTT, or INR
Most important if actively bleeding
FFP used as replacement with plasmapheresis
Cryoprecipitate
Used to replace fibrinogen
Some utility in disseminated intravascular
coagulation (DIC)
Provides high amounts of clotting factors in small
plasma volume
Whole blood is never correct

Whole blood is divided into either PRBCs or FFP
MTB S2CK
p. 205
MTB S2CK
p. 205
Microcytic Anemia
Microcytosis = MCV < 80 fL
Microcytic Anemia
Etiology
Presentation
Diagnostic Tests
Treatment
Microcytic, hypochromic anemia seen on blood smear.

MTB S2CK
p. 206
Copyright James Van Rhee.

Microcytic Anemia/Etiology
Iron deficiency
Blood loss
One teaspoon (5 mL/day) blood loss leads to iron
deficiency over time
Body only needs very tiny amount of iron
Chronic disease
Initially MCV is normal, then decreases
Unclear etiology
Any cancer or chronic infection
Clear mechanism only in renal failure deficiency of
erythropoietin
Hemoglobin synthesis will not occur because iron
does not move forward
Iron is locked in storage or trapped in macrophages
or in ferritin
1 to 2 mg/day
Menstruating women need a little more

2-3 mg/day
Pregnant women need 5-6 mg/day

Duodenum absorbs only about 4 mg/day
MTB S2CK
p. 206
MTB S2CK
p. 206
Can be macrocytic when associated with
myelodysplasia (MDS)
Most common cause: Alcohol effect on marrow
Less common causes...
Thalassemia
Extremely common cause of microcytosis
Most with thalassemia trait are asymptomatic
Lead poisoning
Isoniazid
Vitamin B6 deficiency
MTB S2CK
p. 206
MTB S2CK
p. 206
Microcytic Anemia/Presentation
Microcytic Anemia/Presentation
You cant distinguish these anemias

based on symptoms
Might have a suggestion from history
How to answer What is the most likely

diagnosis? for anemia
Feature in the History
Most likely diagnosis?
Blood loss (GI bleeding)
Menstruation
Cancer or chronic infection
Alcoholic
Asymptomatic
MTB S2CK
p. 206
MTB S2CK
Iron deficiency
Iron deficiency
Chronic disease
Chronic disease
Sideroblastic
Thalassemia
p. 206
Microcytic Anemia/Diagnostic Tests
Microcytic Anemia/Diagnostic Tests
Peripheral smear not useful!

All hypochromic
All can be associated with target cells
Target cells: most common with

thalassemia
MTB S2CK
p. 207
MTB S2CK
p. 207
Microcytic Anemia/Iron Studies
Unique features and diagnoses of iron studies
Iron deficiency
Unique Feature
Low ferritin
High iron
Normal iron studies
MTB S2CK
Diagnosis
Iron deficiency
Thalassemia
p. 207
Copyright James Van Rhee.

Low ferritin = Iron deficiency

However, one third of patients with iron deficiency
will have normal or increased ferritin
Ferritin is an acute phase reactant
This means any infection or inflammation can
raise the ferritin level
MTB S2CK
p. 207
Both iron deficiency and anemia of chronic disease

are associated with low serum iron
Iron deficiency: increase in total iron binding
capacity (TIBC)
TIBC measures unbound sites on transferrin
Open sites on transferrin = increased capacity
capacity or
number of unbound sites
Chronic disease
Serum iron: low in circulation
Iron trapped in storage
Ferritin (stored iron): elevated or normal
Circulating iron: decreased
Major
M j diff
difference iis TIBC is
i low
l
MTB S2CK
p. 207
MTB S2CK
p. 207
Unique Laboratory Features
Only microcytic anemia elevated circulating iron
level
Iron deficiency
Red cell distribution of width (RDW) increased
Thalassemia
Genetic disease with normal iron studies
Newer cells are more iron deficient

Newer cells are smaller in iron deficiency
As body runs out of iron, newer cells have less Hb &
get p
g
progressively
g
y smaller
Elevated platelet count common

Single most accurate test is...
Bone marrow biopsy for stainable iron (decreased)
Rarely done, but most accurate
MTB S2CK
p. 207
MTB S2CK
p. 207
The most accurate test is...
Prussian blue staining
for ringed sideroblasts
Basophilic stippling can
occur in any cause of
sideroblastic anemia
Thalassemia
MTB S2CK
p. 207 208
Hb electrophoresis!
MTB S2CK
p. 208
Electrophoresis Findings
Thalassemia
Most accurate test for alpha thalassemia
Alpha thalassemia
Beta thalassemia
One gene deleted: normal

Two genes deleted: mild anemia,
normal electrophoresis
Three genes deleted: moderate
anemia with Hb H (beta 4
tetrads), increased reticulocytes
Four genes deleted: gamma 4
tetrads or hemoglobin Bart; CHF
causes death in utero
Inc. Hb F and A2
N/A
Genetic studies
3-gene deletion alpha thalassemia
Hb H (beta-4 tetrads)
Increased reticulocyte count
All thalassemia types have normal RDW
MTB S2CK
p. 208
MTB S2CK
Beta thalassemia intermedia

Normal Hb F
No transfusion dependence
N/A
p. 208
Microcytic Anemia/Treatment
Microcytic Anemia/Treatment
Iron deficiency
Replace iron with oral ferrous sulfate
If insufficient, patients get IM iron
Chronic disease
Correct underlying disease
Only
O l end-stage
d t
renall ffailure
il
responds
d tto
erythropoietin
Correct the cause
Some respond to vitamin B6 (pyridoxine)
Thalassemia
Trait not treated
MTB S2CK
p. 208
Beta thalassemia major (Cooley anemia)

Chronic transfusion lifelong
Iron
I
overload
l d managed
d with
ith d
deferasirox
f
i
((orall iiron
chelator)
Deferoxamine is parenteral
MTB S2CK
Macrocytic Anemia
Etiology
Presentation
Diagnostic Tests
Treatment
p. 209
73-year-old man in office with fatigue progressively worse over

several months. He is short of breath when he walks up one
flight of stairs. He drinks 4 vodka martinis a day. He complains
of numbness and tingling in his feet.
Physical: decreased sensation in feet.
Hct: 28%
MCV: 114 fL (elevated)
What is the next step? 1st is peripheral smear
Once hypersegmented neutrophils are seen,
a. Vitamin B12 level
THEN get B12 & folate levels
b. Folate level
c. Peripheral blood smear
d. Schilling test To see if B12 deficiency is due to pernicious anemia
e. Methylmalonic acid level
Confirms diagnosis of B12 deficiency
when B12 levels are equivocal
MTB S2CK
p. 209
Macrocytic Anemia
Megaloblastic
Hypersegmented neutrophils
Vitamin B12 deficiency is caused by...

Pernicious anemia
Pancreatic insufficiency
Dietary deficiency (vegan/strict vegetarian)
Crohns disease damaging terminal ileum
Blind loop syndrome (gastrectomy or gastric
bypass for weight loss)
Diphyllobothrium latum
Many factors raise MCV

Only B12 & folate
deficiency &
antimetabolite
medications cause
hypersegmentation
Source: Alireza Eghtedar, MD
MTB S2CK
p. 209 210
MTB S2CK
p. 209
Macrocytic Anemia/Presentation
Folate deficiency
Dietary deficiency (goats milk has no folate
and limited iron/B12)
Psoriasis & skin loss or turnover
Drugs:
g p
phenytoin,
y
, sulfa
Alcohol
Gives macrocytosis & neurological problems
Will not give hypersegmented neutrophils
MTB S2CK
p. 209
MTB S2CK
p. 209
Macrocytic Anemia/Presentation
Macrocytic Anemia/Diagnostic Tests
B12 deficiency
Can give any neurological abnormality
Peripheral neuropathy most common
Dementia least common
Posterior column damage to position & vibratory
sensation or subacute
subacute combined degeneration
degeneration of
cord is classic
Look for ataxia
Labs common to both B12 & folate deficiency

Megaloblastic anemia
Increased LDH & indirect bilirubin levels
Decreased reticulocyte count
Hypercellular bone marrow
Macroovalocytes
M
l
t
Increased homocysteine levels
Only B12 deficiency is associated with increased
methylmalonic acid level
MTB S2CK
p. 210
MTB S2CK
p. 210

B12 & folate deficiency
Identical hematologically on blood smear
73-year-old woman with decreased position & vibratory

sensation of lower extremities. Hct: 28%, MCV: 114 fL,
and hypersegmented neutrophils.
B12 level decreased, but near the borderline of normal.
a.
b.
c.
d.
e.
f.
Methylmalonic acid level

Confirms cause as pernicious
Anti-intrinsic factor antibodies anemia after B12 deficiency
confirmed
Anti-parietal cell antibodies
Schillings test Rare test of etiology; premature
Folate level Folate doesnt give neurological deficits
Homocysteine level Doesnt add anything
Source: Alireza Eghtedar, MD
MTB S2CK
p. 210
MTB S2CK
p. 210 211
Tested facts about macrocytic anemia

Schilling test is never the right answer
Pernicious anemia is confirmed with antiintrinsic factor and anti-parietal cell
antibodies
Red cells are destroyed as they leave the
marrow, so reticulocyte count is low
Tested facts about macrocytic anemia

B12 & folate deficiency can cause
pancytopenia as well as macrocytic anemia
Pancreatic enzymes are needed to absorb B12
MTB S2CK
p. 211
They free it from carrier (R) protein
Neurological abnormalities will improve as long as

they are minor (e.g., peripheral) and short duration
MTB S2CK
p. 211
Macrocytic Anemia/Treatment
Replace what is deficient

Folate replacement corrects hematologic
problems of B12 deficiency, but not the
neurological problems
Which of the following is a complication of B12 or

folate replacement?
a. Seizures Not associated with treatment
b. Hemolysis Cells are produced rapidly, not hemolyzed
c Hypokalemia
c.
High K+ from massive tissue or
d. Hyperkalemia
cellular breakdown
e. Diarrhea
Cause hypokalemia, but not associated
with B12 or folate replacement therapy
MTB S2CK
p. 211
MTB S2CK
p. 211
Hemolytic Anemia
Hemolytic Anemia Part 1

Sickle Cell Disease
Hereditary Spherocytosis
Autoimmune Hemolysis
y
All forms lead to:

Sudden in Hct
Increased LDH, indirect bilirubin & reticulocytes
Decreased haptoglobin
Slight increase in MCV
Reticulocytes
R ti l
t > normall cells
ll
Hyperkalemia
MTB S2CK
p. 211 212
Sickle Cell Disease
Sickle Cell Disease/Presentation
Chronic, well-compensated hemolytic anemia

Reticulocyte count always high
Acute painful vaso-occlusive crisis is caused by...
Hypoxia
Dehydration
I f ti
Infection
Cold temperatures
Look for...
African American
Sudden, severe pain in chest, back & thighs
May have fever
MTB S2CK
p. 212
Rare for adult to present with acute crisis

without clear history of sickle cell disease
MTB S2CK
p. 212
Sickle Cell Disease/Manifestations
Sickle Cell Disease/Diagnostic Tests
Bilirubin gallstones
Increased infection
from autosplenectomy

- Peripheral smear
Encapsulated
organisms
Osteomyelitis
y
Most commonly from
Salmonella
Stroke
Enlarged heart with
hyperdynamic features
and systolic murmur
Skin ulcers
Avascular necrosis of
femoral head
Retinopathy
MTB S2CK
p. 212
Most accurate test..

- Hemoglobin
electrophoresis
Trait (AS disease) does
not give sickled cells
MTB S2CK
p. 212 213
Sickle Cell Disease/Treatment

Which is found on smear in sickle cell disease?
a.
b.
c.
d
d.
e.
Basophilic stippling Associated with lead poisoning

Howell-Jolly bodies
Bite cells Seen with G6PD deficiency
Fragmented red cells seen with
S hi t
Schistocytes
t
intravascular hemolysis
Morulae
1. Oxygen/hydration/analgesia
2. Fever or white cell count higher than usual?
Antibiotics given! Ceftriaxone, levofloxacin, or
moxifloxacin
3. Folic acid in everyone
4. Pneumococcal vaccine: autosplenectomy
5. Hydroxyurea: prevent recurrences, increases Hb F
Seen inside neutrophils in Ehrlichia infections
Dont wait for results of testing!

Start antibiotics with fever.
No spleen = Overwhelming infection = Death!!
MTB S2CK
p. 213
MTB S2CK
p. 213
10
Sickle Cell Disease/Treatment
Exchange transfusion for severe vasoocclusive crisis with:

Acute chest syndrome
Priapism
Stroke
Visual disturbance from retinal
infarction
43-year-old man with sickle cell disease admitted with

acute pain crisis. Only med is folic acid. Hct on
admission: 34%. On 3rd hospital day, hematocrit
drops to 22%.
What is the initial test?
y count Not best way to gauge severity of
a. Reticulocyte
b. Peripheral smear hemolysis
Causes aplastic crisis which freezes growth of
c. Folate level marrow
d. Parvovirus B-19 IgM level
Most accurate test for parvovirus B-19 is
e. Bone marrow
PCR for DNA. IVIG is best initial therapy.
Marrow shows giant pronormoblasts, but this isnt better than
reticulocyte count at measuring severity of hemolysis
MTB S2CK
p. 214
MTB S2CK
p. 214
Sickle Cell Trait
Hereditary Spherocytosis
Patient is heterozygous for sickle gene (AS)

Only manifestation is inability to
concentrate urine (isosthenuria)
Clinically asymptomatic
Normal CBC
Normal smear
Hematuria sometimes occurs
No treatment for sickle cell trait
Genetic defect in
cytoskeleton of RBCs
Leads to abnormal
round shape
Loss of normal flexibility
characteristic of
biconcave disc that
allows red cells to bend
in spleen
MTB S2CK
p. 214
MTB S2CK
p. 214 215
Hereditary Spherocytosis/Presentation
Hereditary Spherocytosis/Diagnosis
Look for...
Recurrent episodes of hemolysis in a
young child or newborn
Intermittent jaundice
Splenomegaly
S l
l
Family history of anemia or hemolysis
Bilirubin gallstones
Low MCV
Increased mean corpuscular
hemoglobin concentration (MCHC)
Negative Coombs test
MTB S2CK
p. 214 215
Most acc
accurate
rate test:
test Osmotic fragility
fragilit
Cells are placed in slightly hypotonic solution
Increased swelling leads to hemolysis
MTB S2CK
p. 215
11
Hereditary Spherocytosis/Treatment
Autoimmune Hemolysis
1. Chronic folic acid replacement supports red

cell production
2. Splenectomy stops hemolysis but doesnt
eliminate spherocytes
Also known as warm or IgG hemolysis

Idiopathic in 50%
Clear causes are...
MTB S2CK
p. 215
Chronic lymphocytic leukemia (CLL)

Lymphoma
Systemic lupus erythematosus (SLE)
Drugs: penicillin, alpha-methyldopa, rifampin,
phenytoin
MTB S2CK
p. 215
Autoimmune Hemolysis/Diagnostic Tests
Autoimmune Hemolysis/Diagnostic Tests
Most accurate diagnostic test is...

Coombs test
Autoantibodies remove small amounts of red cell

membrane and lead to smaller membrane
Forces cell to become round
Biconcave discs have greater surface than sphere
Detects IgG on surface of red cells

Direct & indirect tests tell basically the same
thing
Indirect associated with greater amount of
antibody
Smear doesnt show fragmented cells because

destruction occurs inside spleen or liver, not in
blood vessel
MTB S2CK
p. 215 216
Autoimmune Hemolysis/Treatment
MTB S2CK
Autoimmune Hemolysis/Treatment
1. Glucocorticoids (prednisone) best initial

therapy
2. Recurrent episodes: splenectomy
3. Severe, acute hemolysis not responding to
prednisone can be controlled with intravenous
immunoglobulin
g
((IVIG))
4. Rituximab when splenectomy doesnt control
hemolysis
MTB S2CK
p. 216
p. 215 216
Alternate treatments to
diminish need for steroids:
Cyclophosphamide
Cyclosporine
Azathioprine
Mycophenolate mofetil
MTB S2CK
p. 216
12
Cold Agglutinin Disease
Hemolytic Anemia Part 2

G6PD Deficiency
HUS and TTP
PNH
IgM antibodies against red cells in association with

Epstein-Barr virus, Waldenstrm macroglobulinemia, or
Mycoplasma pneumoniae
Presentation
Symptoms in colder parts of body
Numbness or mottling of nose, ears, fingers, and toes
Symptoms resolve on warming body part
Diagnosis
Direct Coombs test positive only for complement
Smear normal in most
May show spherocytes
MTB S2CK
p. 216
Cold Agglutinin Disease/Treatment
Treatment
1. Stay warm
2. Administer rituximab
3. Cyclophosphamide, cyclosporine, or other
immunosuppressive agents stop production of
antibody
4. Plasmapheresis in some
Cryoglobulins often mixed up with cold agglutinins.

Both are IgM and dont respond to steroids.
Cryoglobulins are associated with:
Hepatitis C
Joint pain
Glomerulonephritis
Steroids and splenectomy

usually dont work
MTB S2CK
p. 216 217
MTB S2CK
p. 217
G6PD Deficiency
G6PD Deficiency/Presentation
X-linked recessive
Inability to generate glutathione reductase and
protect red cells from oxidant stress
Most common oxidant stress is infection
Other causes: dapsone, quinidine, sulfa drugs,
primaquine nitrofurantoin
primaquine,
nitrofurantoin, and fava beans
Look for...
African American or Mediterranean males

Sudden anemia & jaundice
Normal-sized spleen
With infection
i f ti or drug
d
G6PD deficiency is X-linked recessive,

it manifests almost exclusively in males
MTB S2CK
p. 217
MTB S2CK
p. 217
13
G6PD Deficiency/Diagnosis
G6PD Deficiency

Peripheral smear
Treatment
Avoid oxidant stress
Nothing reverses hemolysis
Look for Heinz bodies

and bite cells

G6PD level
1 to 2 months after
acute episode of
hemolysis
MTB S2CK
p. 217
MTB S2CK
p. 218
HUS and TTP
HUS and TTP
Hemolytic uremic syndrome (HUS) and thrombotic

thrombocytopenic purpura (TTP) are different
versions of the same basic disease
Both characterized by:
HUS
Associated with E. coli
0157:H7
More frequent in children
TTP
Associated with
ticlopidine clopidogrel
ticlopidine,
clopidogrel,
cyclosporine, and AIDS
Neurological disorders
(confusion and seizures)
Fever
More common in adults
Intravascular
hemolysis with
fragmented red cells
(schistocytes)
Thrombocytopenia
Renal insufficiency
MTB S2CK
p. 218
MTB S2CK
p. 218
HUS and TTP
Paroxysmal Nocturnal Hemoglobinuria
Diagnosis
No one specific test diagnoses either disorder
Normal PT/aPTT
Negative Coombs test
Clonal stem cell defect with increased sensitivity to

complement in acidosis
Treatment
Severe cases treated with plasmapheresis or plasma
exchange
MTB S2CK
p. 218
Etiology
Deficiency of complement regulatory proteins CD 55 and
59, also known as decay accelerating factor (DAF)
Gene for phosphatidylinositol glycan class A (PIG
(PIG-A)
A) is
defective
overactivation of complement system
During sleep, relative hypoventilation leads to pCO2
and acidosis
This does nothing to an unaffected person
In PNH it leads to hemolysis and thrombosis
MTB S2CK
p. 218
14
Presentation
Episodic dark urine with first urination of day from
hemoglobin
Pancytopenia and iron deficiency anemia
Pancytopenia
Decreased CD55 & CD59
Ham test and sucrose hemolysis are never

the correct answer
Flow cytometry is another way of saying
CD55/CD59 testing
Thrombosis MCC of death

MTB S2CK
p. 218
MTB S2CK
p. 218 219
1. Prednisone
2. Allogeneic bone marrow transplant is the
only method of cure
3. Eculizumab inactivates C5 in complement
pathway and decreases red cell destruction;
its a complement inhibitor
4. Folic acid and iron replacement with
transfusions as needed
MTB S2CK
Hematologic Malignancies
Aplastic Anemia
Polycythemia Vera
Essential Thrombocytosis
Myelofibrosis
p. 219
Aplastic Anemia
Aplastic Anemia
Pancytopenia of unclear etiology

Any infection or cancer can invade marrow causing
decreased production or hypoplasia
Other causes:
Fatigue of anemia
Infections from low white cell counts
Bleeding from thrombocytopenia
Radiation and toxins (e.g., toluene, insecticides (DDT),

and benzene)
Drug effect: sulfa, phenytoin, carbamazepine,
chloramphenicol, alcohol, chemotherapy
SLE
PNH
Infection: HIV, hepatitis, CMV, EBV
B12 and folate deficiency
Thyroid-inhibiting medications (e.g., propylthiouracil
(PTU) and methimazole)
MTB S2CK
p. 219

is
Bone marrow biopsy
Aplastic anemia is confirmed by excluding all
causes of pancytopenia
MTB S2CK
p. 219
15
Aplastic Anemia/Treatment
Aplastic Anemia/Treatment
Treat any underlying cause thats identified

THEN...
Blood transfusion, antibiotics for infection, and
platelets for bleeding
True aplastic anemia treated with allogeneic bone

marrow transplantation (BMT) if young enough
and matched
Aplastic anemia acts as autoimmune disorder

T cells attack patients own marrow
Cyclosporine inhibits T cells
This brings the marrow back to life!
MTB S2CK
p. 219
When too old for BMT (> 50) or no matched donor

y
y g
globulin ((ATG)) and
treatment is anti-thymocyte
cyclosporine
Tacrolimus is alternative to cyclosporine
MTB S2CK
p. 219 220
Polycythemia Vera
Polycythemia Vera
Unregulated overproduction of all 3 cell lines

Red cell overproduction is most prominent
Mutation in JAK2 protein which regulates marrow
production
Red cells grow wildly despite low erythropoietin
Symptoms of hyperviscosity from increased red cell

mass such as:
Headache, blurred vision, and tinnitus
Hypertension
Fatigue
Splenomegaly
Bleeding from engorged blood vessels
Thrombosis from hyperviscosity
MTB S2CK
p. 220
MTB S2CK
Polycythemia Vera
Hematocrit markedly
elevated > 60%
Platelets and WBC count
Erythropoietin
Total red cell mass
MTB S2CK
p. 220
p. 220
Polycythemia Vera
You must exclude hypoxia
as cause of erythrocytosis
Oxygen levels: normal
Vitamin B12 levels are
elevated for unclear
reasons
it s
Iron levels because its
been used to make red cells

JAK2 mutation (95%)
Increased basophils
All myeloproliferative disorders
Small number converted to AML
MTB S2CK
p. 220
16
Essential Thrombocytosis (ET)
Essential Thrombocytosis (ET)
Markedly elevated platelet count > 1 million

Leads to both thrombosis & bleeding
Very difficult to distinguish from an elevated platelet
count as a reaction to another stress (e.g.,
infection, cancer, or iron deficiency)
< 60 & asymptomatic

with platelets < 1.5
million
MTB S2CK
p. 221

Hydroxyurea
Anagrelide with red cell

No treatment necessary suppression from
hydroxyurea
> 60 & thromoboses or
platelet count > 1.5
Aspirin for
million
erythromelalgia (painful,
Begin treatment
red hands in ET)
MTB S2CK
p. 221
Myelofibrosis
Older persons with pancytopenia
Bone marrow shows marked fibrosis
Blood production shifts to spleen & liver, which become
markedly enlarged
Look for teardrop-shaped cells and nucleated red
blood cells on smear
Thalidomide and lenalidomide: tumor necrosis factor
inhibitors that increase bone marrow production
Occasional patient < 50-55, allogeneic bone marrow
transplantation is attempted
MTB S2CK
Leukemia
Acute Leukemia
Chronic Myelogenous Leukemia
Leukostasis Reaction
Myelodysplastic Syndrome
Chronic Lymphocytic Leukemia
Hairy Cell Leukemia
p. 221
Acute Leukemia/Presentation
Acute Leukemia/M3
Most frequently tested acute leukemia is M3,

known as acute promyelocytic leukemia (APL)
M3 is associated with disseminated intravascular
coagulation (DIC)
History of myelodysplasia suggests acute leukemia

Signs of pancytopenia (fatigue, infection, bleeding)
Even if WBC is normal or increased
Infection is common presentation
Leukemic cells (blasts) dont function normally
M3
DIC
No distinct clinical presentation bet

between
een the 3
subtypes of acute lymphocytic leukemia (ALL)
MTB S2CK
p. 221
MTB S2CK
p. 221
17
Acute Leukemia/Diagnosis
Acute Leukemia/Diagnosis

Blood smear
Auer rods
Eosinophilic inclusions
Associated with acute
promyelocytic leukemia
(M3)
Shows blasts

Flow cytometry
Distinguishes different subtypes of acute leukemia
Detects specific CD subtypes associated with each
type of leukemia
Myeloperoxidase
Characteristic of acute myelocytic leukemia (AML)
MTB S2CK
p. 221
MTB S2CK
p. 221 222
Acute Leukemia/Treatment
Both AML & ALL treated initially with chemotherapy

to remove blasts from peripheral blood smear
Known as inducing remission
The question is: proceed to BMT after remission or
give more chemotherapy
Prognosis poor? go straight to BMT
Prognosis good? more chemotherapy
The best indicator of prognosis in acute leukemia is...
MTB S2CK
p. 222
1. Add all-trans-retinoic acid (ATRA) to those

with M3 (acute promyelocytic leukemia)
1. Add intrathecal chemotherapy such as
methotrexate to ALL treatment; prevents
relapse of ALL in CNS
MTB S2CK
p. 222
Cytogenetics
Assesses specific chromosomal characteristics
found in each patient
Good cytogenetics = less chance of relapse =
more chemotherapy
Bad cytogenetics = more chance of relapse =
immediate BMT
MTB S2CK
p. 222
Most tested facts for acute leukemia are...

M3 (promyelocytic leukemia) gives DIC
Add ATRA to M3
Auer rods = AML
Add intrathecal methotrexate to ALL
MTB S2CK
p. 222
18
Chronic Myelogenous Leukemia/Presentation
Chronic Myelogenous Leukemia/Diagnosis
Look for...
High WBC count: all neutrophils
Vague symptoms of fatigue, night sweats, and
fever from hypermetabolic syndrome
Splenomegaly: early satiety, abdominal fullness,
and LUQ pain
Pruritus is common after hot baths/showers
Determine if its a reaction to another

infection, stress (leukemoid reaction), or
leukemia
CML may give small numbers of blasts
Should be < 5%
Basophils increased
Histamine release from basophils
MTB S2CK
p. 223
MTB S2CK
p. 223
Chronic Myelogenous Leukemia/Diagnosis
Chronic Myelogenous Leukemia/Treatment
If leukocyte alkaline phosphatase score (LAP) is

a choice, then this is first
Imatinib (Gleevec),
dasatinib, or nilotinib are
the best initial therapy
Only BMT cures CML
Leukemic cells dont have normal amounts of

alkaline phosphatase; LAP score low in CML
If LAP score is not a choice, or the question is

What is the most accurate test? then answer
BCR-ABL
Never the first therapy
Can be done by PCR on peripheral blood
MTB S2CK
p. 223
MTB S2CK
p. 223
Myelodysplastic Syndrome (MDS)

54-year-old man with SOB, blurry vision, confusion, and
priapism. WBC count 225,000/L. Predominantly
neutrophils with about 4% blasts.
What is next step in management of this case?
a.
b.
c.
d.
e.
f.
g.
Leukapheresis
In acute leukostasis reaction,
BCR-ABL
BCR
ABL testing
i
important
t t to
t remove excessive
i
Bone marrow biopsy
white cells from the blood than
Bone marrow transplant
to establish a specific
Consult hematology/oncology diagnosis, no matter what the
etiology
Flow cytometry
Hydroxyurea
Will lower the cell count, but not as
rapidly as leukapheresis
MTB S2CK
p. 223 224
Preleukemic disorder in those > 60

Pancytopenia despite hypercellular bone
marrow
Most never develop AML
Infection & bleeding lead to death before leukemia
occurs
MTB S2CK
p. 224
19
Myelodysplastic Syndrome
Myelodysplastic Syndrome/Diagnosis
Many present with asymptomatic pancytopenia

on routine CBC
Symptoms can be...
Fatigue & weight loss
Infection
Bleeding
Sometimes splenomegaly
No single pathognomonic finding in history or
physical examination
CBC: anemia with increased

MCV, nucleated red cells,
and small number of blasts
Marrow: hypercellular
Prussian blue stain shows
ringed sideroblasts
Severity based on
percentage of blasts
MTB S2CK
p. 224
MTB S2CK
p. 224 225
Myelodysplastic Syndrome/Treatment
Chronic Lymphocytic Leukemia
CLL is a clonal proliferation of normal, mature-appearing B

lymphocytes that function abnormally
Occurs over age 50 in 90% affected
Most asymptomatic at presentation
Most common symptom is fatigue
Other symptoms:
Transfuse blood products as needed

Erythropoietin: about 20% response
Lenalidomide for those with 5q deletion
Decreases transfusion dependence
Lymphadenopathy (80%)
Spleen or liver enlargement (50%)
Infection
No unique physical findings

Richter phenomenon:
Conversion of CLL into
high-grade lymphoma
Occurs in 5%
MTB S2CK
p. 225
MTB S2CK
p. 225
Chronic Lymphocytic Leukemia/Diagnosis
Chronic Lymphocytic Leukemia/Treatment
WBC usually > 20,000/ L

80% to 98% lymphocytes
Half are
hypogammaglobulinemic
Anemia &
thrombocytopenia occur
from marrow infiltration or
autoimmune warm IgG
antibodies
Stage 0 (elevated WBC) & stage I

(lymphadenopathy); no treatment
Stage II (hepatosplenomegaly), stage III (anemia),
and stage IV (thrombocytopenia) treat with
fludarabine
If choices list fludarabine and rituximab,, this is the
best initial therapy for advanced-stage disease (II,
III, IV) or any patient who is symptomatic (severe
fatigue, painful nodes)
PCP prophylaxis is indicated in CLL
MTB S2CK
p. 225
Smudge cell:
Lab artifact
Nucleus crushed by
cover slip
MTB S2CK
p. 226
20
Chronic Lymphocytic Leukemia/Treatment
Hairy Cell Leukemia
Refractory cases: cyclophosphamide

(more efficacy, but more toxic)
Middle-aged men with:
Mild cases: chlorambucil
Severe infection: IVIG
Pancytopenia
Massive splenomegaly
Monocytopenia
Inaspirable dry tap, despite
hypercellularity of marrow

Autoimmune thrombocytopenia
or hemolysis: prednisone
Tartrate resistant acid

phosphatase (TRAP) or
CD11c
Treat with cladribine
MTB S2CK
p. 226
MTB S2CK
p. 226
Non Hodgkin Lymphoma
Lymphoma
Hodgkin Disease
Multiple Myeloma
MGUS
Waldenstrm Macroglobulinemia
Proliferation of lymphocytes in nodes and spleen

NHL most often widespread at presentation
NHL and CLL are extremely similar
NHL is solid mass and CLL is liquid or circulating
MTB S2CK
p. 226
Painless lymphadenopathy
May involve pelvic, retroperitoneal, or mesenteric
structures
Nodes not warm, red, or tender
B symptoms:
Fever,
Fever weight loss
loss, drenching night sweats
Advanced stages in 80% to 90% of cases
MTB S2CK
p. 227
Excisional biopsy
CBC normal in most cases

High LDH correlates with worse severity
Staging determines intensity of therapy
Typical staging procedures are:
CT scan of chest, abdomen, and pelvis
Bone marrow biopsy
MTB S2CK
p. 227
21
Non Hodgkin Lymphoma/Treatment
Staging
Stage I: 1 lymph node group
Stage II: 2+ lymph node groups on same
side of diaphragm
Stage III: both sides of diaphragm
Stage IV: widespread disease
Local disease (Stage Ia and IIa): local radiation

Advanced disease (Stage III and IV, any B
symptoms): combination chemotherapy with
CHOP and rituximab (antibody against CD20)
C = cyclophosphamide
H = adriamycin (doxorubicin or hydroxydaunorubicin)
O = vincristine (oncovin)
P = prednisone
Mucosal Associated Lymphoid Tissue
Most common wrong answer is needle

aspiration of node. Aspiration not enough because
individual lymphocytes appear normal.
MTB S2CK
p. 227
MTB S2CK
Hodgkin Disease
Normal
lymphocyte
Reed Sternberg
cell
p. 228
p. 227
Differences between HD and NHL
Presentation, diagnostic tests, B symptoms, and

staging of Hodgkin disease (HD) are same as NHL
Hodgkin disease has Reed-Sternberg cells on
pathology
MTB S2CK
Lymphoma of stomach is associated with

Helicobacter pylori
Treat with clarithromycin and amoxicillin
Hodgkin Disease
Local, Stage I, and Stage II in

80 90%
Stage III and Stage IV in 80 90%
Centers around cervical area
Disseminated
Reed Sternbergg cells on

pathology
No Reed Sternbergg cells
Pathologic classification:
Lymphocyte predominant has
best prognosis
Lymphocyte depleted has
worst prognosis
Pathologic classification:
Burkitt and immunoblastic
have worst prognosis
MTB S2CK
p. 228
Hodgkin Disease/Treatment
Hodgkin Disease/Treatment
Stage Ia and IIa: local radiation and Chemo

Stage III and IV or anyone with B symptoms:
ABVD
A = adriamycin (doxorubicin)
B = bleomycin
Relapses after radiation
V = vinblastine
therapy are treated with
D = dacarbazine
chemotherapy. Relapses
after chemotherapy are
treated with extra high dose
chemotherapy and bone
marrow transplantation.
Complications of Radiation and Chemotherapy

Radiation increases the risk of solid tumors such
as breast cancer or lung cancer
Screening for breast cancer earlier after treatment
Radiation increases premature coronary
disease
The risk of acute leukemia, MDS, and NHL from
chemotherapy is about 1% per year
MTB S2CK
p. 228
MTB S2CK
p. 228
22
Which of the following is most useful to determine

dosing of chemotherapy in HD?
The other choices arent as
a. Echocardiogram
accurate in determining left
b. Bone marrow biopsy
ventricular function
c. Gender
d MUGA or nuclear ventriculogram
d.
e. Hematocrit
f. Symptoms
MTB S2CK
p. 228 229
Hodgkin Disease/
Adverse Effects of Chemotherapy
Chemotherapeutic Agent
Toxicity
Doxorubicin
Cardiomyopathy
Vincristine
Neuropathy
Bleomycin
Lung fibrosis
Cyclophosphamide
Hemorrhagic cystitis
Cisplatin
Renal and ototoxicity
MTB S2CK
p. 229
Multiple Myeloma
Multiple Myeloma
Most common presentation is...
Abnormal proliferation of plasma cells

Unregulated production of useless immunoglobulin
Usually IgG or IgA
Immunoglobulins dont fight infection, but clog up
the kidney
IgM is a separate disease called Waldenstrm
macroglobulinemia
MTB S2CK
p. 229
Bone pain from pathologic fractures
Pathologic fracture: bone breaks under normal use

Due to osteoclast activating factor (OAF), which
attacks the bone causing lytic lesions
OAF
hypercalcemia
Infection common because abnormal plasma cells
dont make immunoglobulins effective against
infection
MTB S2CK
p. 229
Multiple Myeloma
Multiple Myeloma
Hyperuricemia: increased turnover of nuclear

material of plasma cells
Anemia: from infiltration of marrow with plasma
cells
Renal failure: from immunoglobulins and BenceJones p
protein in kidney;
y; hypercalcemia
yp
and
hyperuricemia also damage the kidney
Renal failure and infection are MCCs of death
First test done is X-ray of affected bone shows

lytic lesions
Serum protein electrophoresis (SPEP) shows an
IgG (60%) or IgA (25%) spike of a single type or
clone.
One clone = Monoclonal or M spike
p
Fifteen percent have light chains or Bence-Jones
protein only
MTB S2CK
p. 229
MTB S2CK
p. 229 230
23
Multiple Myeloma
Additional abnormalities
Hypercalcemia
Bence-Jones protein on urine immunoelectrophoresis
Beta-2 microglobulin levels correspond to severity of
disease
Smear with rouleaux
Elevated BUN and creatinine
Bone marrow biopsy: >10% plasma cells defines
myeloma
Elevated total protein with normal albumin
MTB S2CK
p. 230
Multiple Myeloma
Rouleaux
IgG paraprotein sticks to
red cells causing them
to adhere to each other
in a stack or roll
MTB S2CK
p. 230
Multiple Myeloma
M-spike on SPEP doesnt mean IgM

Myeloma has a decreased anion gap.
IgG is cationic.
Increased cationic substances will
increase chloride and bicarbonate levels.
This decreases the anion gap.
69-year-old woman admitted with severe back pain that

suddenly worsened--pop felt when she coughs and
tenderness over ribs. X-ray: lytic lesions. Calcium is 2
points above normal, Hct 27%, creatinine elevated.
UA: trace protein, but 24-hour urine show 5 grams of
protein.
What do you expect on technetium bone scan?
a. Normal
b. Lytic lesions at site of fractures
c. Increased uptake diffusely
d. Decreased uptake Nuclear bone scan shows increased
uptake with osteoblastic activity,
which is absent in myeloma.
MTB S2CK
p. 230
Why the difference between the protein on urinalysis

and 24-hour urine?
a.
b.
c.
d.
e.
False positive 24-hour urine is common in myeloma

Calcium in urine creates false negative urinalysis
Uric acid creates a false positive 24-hour
24 hour urine
Bence-Jones protein isnt detected by dipstick.
IgG in urine inactivates urine dipstick
MTB S2CK
p. 230
What is the single most accurate test for myeloma?

a. Skull X-rays Will show lytic lesions, but not as specific
b. Bone marrow biopsy Nothing besides myeloma is
associated with > 10% plasma
c. 24-hour urine
Of those with an M-spike
cells on bone marrow biopsy
of immunoglobulins, 99%
d. SPEP
dont have myeloma.
e. Urine
U i immunoelectrophoresis
i
l t h
i
Most IgG spikes are
(Bence-Jones protein)
from monoclonal
gammopathy of
unknown significance
that doesnt progress or
need treatment.
Bence-Jones protein is detected by urine

immunoelectrophoresis. Urine dipstick
detects only albumin.
MTB S2CK
p. 230
MTB S2CK
p. 230 231
24
Multiple Myeloma/Treatment
Best initial therapy is...
Combination of steroids with lenalidomide,
bortezomib, or melphalan
Most effective therapy under age 70 is autologous

bone marrow transplant with stem cell support
Myeloma therapy is in a state of rapid

flux due to numerous advances
MTB S2CK
Monoclonal Gammopathy of
Unknown Significance
IgG or IgA spike on SPEP is common in older
patients
Evaluate with bone marrow biopsy to exclude
myeloma
Monoclonal gammopathy of unknown significance
(MGUS) has small numbers of plasma cells
No therapy for MGUS
1% a year transform into myeloma
The quantity of immunoglobulin in the spike is main
correlate of risk for myeloma:
More MGUS = More myeloma
p. 231
MTB S2CK
p. 231
Overproduction of IgM
Malignant B cells lead to hyperviscosity
Presents with...
Lethargy
Blurry
Bl
vision
i i and
d vertigo
ti
Engorged blood vessels in eye
Mucosal bleeding
Raynaud phenomenon
MTB S2CK
p. 231
Anemia common
IgM spike on SPEP results in hyperviscosity
No bone lesions
Plasmapheresis is best initial therapy
Removes IgM and viscosity
L
Long-term
t
treatment
t t
t with
ith chlorambucil
hl
b il or
fludarabine and prednisone
Control cells that make abnormal Igs
Decrease means of production
MTB S2CK
p. 231
Bleeding Disorders
Bleeding Disorders
ITP
Von Willebrand Disease
Hemophilia
Factor XI Deficiency
DIC
Thrombophilia
Heparin Induced Thrombocytopenia
First step in evaluation is determining if bleeding is

from platelets or clotting factors
Platelet Bleeding
Superficial
Epistaxis, gingival,
petechiae, purpura,
gums, vaginal bleeding
Factor Bleeding
Deep
Joints and muscles
Bleeding in brain or GI system can be from either

platelet or clotting factor deficiency
MTB S2CK
p. 232
25
Immune (Idiopathic) Thrombocytopenic Purpura (ITP)
Look for...
Isolated thrombocytopenia
Normal Hct
Normal
N
l WBC countt
Normal-sized spleen
MTB S2CK
23-year-old woman comes to ED with increased

menstrual bleeding, gum bleeding when she brushes
her teeth, and petechiae.
Platelet count: 17,000/L (low)
What is the next step in therapy?
a. Bone marrow biopsy
b. Intravenous immunoglobulins
c. Prednisone
d. Antiplatelet antibodies
e. Platelet transfusion
p. 232
MTB S2CK
Prednisone is more
important than checking for
increased megakaryocytes
or antiplatelet antibodies,
which is characteristic of
ITP.
p. 232
ITP
ITP/Treatment
Diagnosis of exclusion
Presentation
Management
No bleeding, count > 30,000
No treatment
Occasional tests are:
Mild bleeding, count < 30,000
Glucocorticoids
Antiplatelet antibodies lack specificity, limited

benefit
Ultrasound or CT scan to exclude
hypersplenism
Megakaryocytes are elevated in number
Severe bleeding (GI/CNS),

count < 10,000
IVIG, Anti Rho (anti D)
Recurrent episodes, steroid

dependent
Splenectomy
Romiplostim or eltrombopag for
recurrences after splenectomy
Splenectomy or steroids not

effective
Rituximab, azathioprine,
cyclosporine, mycophenolate
MTB S2CK
p. 232
ITP
p. 233
Von Willebrand Disease (VWD)
Before splenectomy, give vaccination to:

Neisseria meningitidis
Hemophilus influenzae
Pneumococcus
MTB S2CK
MTB S2CK
p. 233
Most common inherited bleeding disorder

Von Willebrand factor (VWF) level or function
Autosomal dominant
Look for bleeding related to platelets (epistaxis,
gingival, gums) with normal platelet count
Markedly worsened after aspirin
aPTT elevated in 50% of patients
MTB S2CK
p. 233
26
Von Willebrand Disease (VWD)
Hemophilia
Diagnosis
Bleeding time: increased duration of bleeding
VWF (antigen) level may be decreased
Ristocetin cofactor assay: detects VWF
dysfunction
Look for...
Delayed joint or muscle
bleeding in male child
Treatment
Initial therapy: DDAVP (desmopressin), which
releases subendothelial stores of VWF
If no response, use factor VIII replacement or VWF
concentrate
MTB S2CK
p. 233
Bleeding delayed
because primary
hemostatic plug is with
platelets
Prothrombin time (PT)

normal
aPTT prolonged
MTB S2CK

Specific assay for
factor VIII or IX
Mixing studies with

normal plasma correct
aPTT to normal
Treat mild cases with
DDAVP
Severe bleeding treated
with replacement of
specific factor
p. 234
Factor XI Deficiency
Disseminated Intravascular Coagulation (DIC)
Most of time, no increase in bleeding with factor

XI deficiency
With trauma or surgery, theres increased bleeding
DIC doesnt occur in otherwise healthy people

Look for a definite risk such as...
Look for...
Normal PT with p
prolonged
g aPTT
Mixing study: corrects aPTT to normal
Treatment
Use FFP to stop bleeding
MTB S2CK
p. 234
Sepsis
Burns
Abruptio placenta or amniotic fluid embolus
Snake bites
Trauma resulting in tissue factor release
Cancer
Theres bleeding related to both clotting factor

deficiency as well as thrombocytopenia
MTB S2CK
p. 234
Diagnostic Tests
Elevated PT and aPTT
Low platelet count
Elevated D-dimer & fibrin split products
Decreased fibrinogen level (has been
consumed)
Treatment
Replace platelets < 50,000/ L as well
as clotting factors with FFP
Heparin has no benefit
Cryoprecipitate
C
i it t may be
b effective
ff ti tto
replace fibrinogen levels if FFP doesnt
control bleeding
MTB S2CK
p. 234
MTB S2CK
p. 235
27
Hypercoaguable States/Thrombophilia
MCC:
HIT more common with unfractionated heparin
Factor V Leiden mutation
No difference in intensity of
anticoagulation
Warfarin to INR of 2
2-3
3 for 6 months
MTB S2CK
p. 235
Can still occur with LMW heparin
Presents 5 to 10 days after start of heparin with a

marked drop in platelet count (> 30%)
Both venous and arterial thromboses occur
Venous clots more common
HIT rarely leads to bleeding

Platelets just precipitate out
Diagnostic Tests
HIT confirmed with ELISA for platelet factor 4
(PF4) antibodies or serotonin release assay
MTB S2CK
p. 235
Antiphospholipid Syndromes
Treatment
Immediately stop all heparin-containing products
Cant just switch unfractionated heparin to LMW
heparin
Direct thrombin inhibitors
Two main syndromes - lupus anticoagulant and

anticardiolipin antibody
Both cause thrombosis
Anticardiolipin antibodies associated with multiple
spontaneous abortions
Antiphospholipid (APL) syndromes specifically
cause thrombophilia with abnormal aPTT
Argatroban,
Argatroban lepirudin,
lepirudin and bivalirudin
After direct thrombin inhibitor is started, use warfarin
MTB S2CK
p. 235
MTB S2CK
p. 235
Antiphospholipid Syndromes
Mixing study
Because its a circulating inhibitor, aPTT remains

elevated after mix
Most accurate test for lupus anticoagulant is...
Russell viper venom test
Treatment
Treat with heparin and warfarin as you would for
any cause of DVT or PE
APL syndrome may require lifelong anticoagulation
MTB S2CK
p. 235
28
Introduction to Antibiotics
Principles of Answering Questions
Beta lactam Antibiotics
Fluoroquinolones
Aminoglycosides
Doxycycline
Trimethoprim/Sulfamethoxazole
Beta lactam/Beta lactamase Combinations
Specific Organism Groups and Their Treatments
Infectious Diseases
Conrad Fischer, MD
New York City
Organisms associated with diseases

dont change
But antibiotics that treat them change
Principles of Answering Infectious

Diseases Questions
The radiologic test is never the most
accurate test
Risk factors for an infection aren
arentt as
important as individual presentation
Beta-lactam antibiotics have greater
efficacy than other classes
M
Mostt iimportant
t t thing
thi
Antibiotics associated with each group
of organisms
MTB S2CK
p. 3
MTB S2CK
p. 3
Beta lactam Antibiotics
Penicillins
Penicillins, Cephalosporins, Carbapenems,

Aztreonam
Ampicillin and amoxicillin
Penicillins
Penicillin ((G,, VK,, benzathine))
Viridans group streptococci
Streptococcus pyogenes
Oral anaerobes
Syphilis
Leptospira
MTB S2CK
p. 3
Cover same organisms as penicillin

And
E. coli
Lyme disease
Gram-negative bacilli (few)
MTB S2CK
p. 3
Penicillins
Penicillins
Answer as Best Initial Therapy for

Gram-negative bacteria
covered by amoxicillin
H. influenzae
E. coli
Listeria
Proteus
Salmonella
MTB S2CK
p. 3
Penicillins
Oxacillin, Cloxacillin, Dicloxacillin, and

Nafcillin
Skin infections: Cellulitis
Endocarditis, meningitis, and bacteremia
from staphylococci
Osteo & Septic arthritis only when proven
sensitive
Not against Methicillin-Resistant
Staphylococcus aureus (MRSA) or
Enterococcus
MTB S2CK
p. 4
Otitis media
Dental infection and endocarditis
prophylaxis
Lyme disease limited to rash, joint, or 7th
CN involvement
UTI in pregnant women
Listeria monocytogenes
Enterococcal infections
MTB S2CK
p. 4
Penicillinase resistant penicillins (PRPs)
Methicillin is never right

Causes allergic interstitial nephritis
Methicillin sensitive or
resistant means oxacillin
sensitive or resistant.
MTB S2CK
p. 4
Penicillins
Piperacillin, Ticarcillin, Azlocillin, Mezlocillin
Piperacillin, Ticarcillin
Gram-negative bacilli (e.g., E. coli, Proteus)
enterobacteriaciae & pseudomonads
Also for: streptococci and anaerobes

BUT
NOT the answer, infection exclusively from
these single organisms
Cholecystitis & ascending cholangitis

Pyelonephritis
Bacteremia
Hospital-acquired and ventilator-associated
pneumonia
Neutropenia and fever
MTB S2CK
p. 4
Use narrower agent

Combined with a beta-lactamase inhibitor
such as tazobactam or clavulanic acid
MTB S2CK
p. 4
Cephalosporins
Cephalosporins
Cross-reaction penicillin & cephalosporins is
Very small (3% to 5%)

All cephalosporins, in every class, will cover group
A, B, and C streptococci, viridans group
streptococci, E. coli, Klebsiella, and Proteus
mirabilis
If the case describes a rash to penicillin

Answer cephalosporins
If the case describes anaphylaxis
You must use a non-beta-lactam
antibiotic
Listeria, MRSA, and Enterococcus

are resistant to all forms of
cephalosporins.
MTB S2CK
p. 4
First Generation
Cefazolin, Cephalexin, Cephradrine,

Cefadroxyl
1st-gen cephalosporins treat
Staphylococci
Methicillin sensitive = oxacillin sensitive =
cephalosporin sensitive
Streptococci (except Enterococcus)

Some gram-negative bacilli such as E. coli, but
not Pseudomonas
Osteomyelitis, septic arthritis, endocarditis,
cellulitis
MTB S2CK
p. 5
MTB S2CK
p. 5
Second Generation
Cefotetan, Cefoxitin, Cefaclor, Cefprozil,

Cefuroxime, Loracarbef
Cover same organisms as 1st-gen
cephalosporins
AND
Add coverage for anaerobes & more
gram-negative bacilli
MTB S2CK
p. 5
Second Generation
Third Generation
Cefotetan, Cefoxitin, Cefaclor, Cefprozil,

Cefuroxime, Loracarbef
Cefotetan or cefoxitin
Best initial therapy for pelvic inflammatory disease
(PID) combined with doxycycline
Warning
Cefotetan and cefoxitin risk of bleeding and give
a disulfiram-like reaction with alcohol
Cefuroxime, loracarbef, cefprozil, cefaclor
Respiratory infections (e.g., bronchitis, otitis media,
and sinusitis)
Ceftriaxone, Cefotaxime, Ceftazidime

Ceftriaxone
First-line for pneumococcus, including
partially insensitive organisms
MTB S2CK
p. 5
Meningitis
Community-acquired pneumonia (in
combination with macrolides)
Gonorrhea
Lyme involving heart or brain
Avoid ceftriaxone in neonates because of
impaired biliary metabolism
MTB S2CK
p. 5
Third Generation
Fourth Generation
Cefotaxime
Cefepime
Better staphylococcal coverage compared
with the 3rd-generation cephalosporins
Ventilator-associated pneumonia
Superior to ceftriaxone in neonates

Spontaneous bacterial peritonitis
C ft idi
Ceftazidime
h
has pseudomonal
d
l coverage
MTB S2CK
p. 5
MTB S2CK
Carbapenems
Ceftaroline: only cephalosporin to cover

MRSA
Imipenem, Meropenem, Ertapenem,

Doripenem
Cover gram-negative bacilli, including many
thatre resistant
Anaerobes
Streptococci and staphylococci
p. 5
Monobactams
Aztreonam
Only monobactam used
Exclusively
Gram-negative bacilli
Including
I l di Pseudomonas
P
d
No cross-reaction with penicillin
Ertapenem differs from other

carbapenems. Ertapenem does
not cover Pseudomonas
MTB S2CK
p. 6
Fluoroquinolones
Ciprofloxacin, Gemifloxacin, Levofloxacin,

Moxifloxacin
Community-acquired pneumonia,
including penicillin-resistant
pneumococcus
Gram-negative bacilli including most
pseudomonads
Cipro: NOT for pneumococcus
MTB S2CK
p. 6
MTB S2CK
p. 6
Fluoroquinolones
Ciprofloxacin: Cystitis and pyelonephritis

Moxifloxacin: Not for urine/cystitis
Diverticulitis and GI infections
Combined with metronidazole
Don
Dontt cover anaerobes except moxifloxacin
Moxifloxacin as single agent for
diverticulitis without metronidazole
MTB S2CK
p. 6
Fluoroquinolones
Fluoroquinolones
Quinolones cause
Bone growth abnormalities in children
and pregnant women
Tendonitis and achilles tendon rupture
Gatifloxacin removed because of
glucose abnormalities
Source: Grook Da Oger, commons.wikimedia.org
MTB S2CK
p. 6
Aminoglycosides
Gentamicin, Tobramycin, Amikacin

Gram-negative bacilli (bowel, urine,
bacteremia)
Synergistic with beta-lactam
beta lactam antibiotics
for enterococci and staphylococci
No effect against anaerobes (need
oxygen to work)
Nephrotoxic and ototoxic
MTB S2CK
p. 6
MTB S2CK
p. 6
Doxycycline
Chlamydia
Lyme
Rash
Joint
7th CN
palsy
MRSA skin
MTB S2CK
p. 7
Target-shaped rash of Lyme disease or erythema migrans. Source: Nishith Patel.
Doxycycline
Trimethoprim/Sulfamethoxazole
Rickettsia
Syphilis: Primary & secondary ONLY if
allergic to penicillin
Borrelia, Ehrlichia, and Mycoplasma
Ad
Adverse
effects
ff t
Tooth discoloration (children)
Fanconi syndrome (Type II RTA
proximal), photosensitivity
Esophagitis
Cystitis
Pneumocystis pneumonia treatment and
prophylaxis
MRSA of skin and soft tissue (cellulitis)
Rash
Hemolysis (G6PD deficiency)
Marrow suppression (folate antagonist)
MTB S2CK
p. 7
Nitrofurantoin has one indication:

Cystitis, especially in pregnant women.
MTB S2CK
p. 7
Beta lactam/Beta lactamase Combinations
Ampicillin/sulbactam
Beta lactamase adds staphylococci effect
Beta-lactamase
Sensitive Staph only
Gram Positive Cocci: Staphylococci and

Streptococci
Best initial therapy:

Oxacillin, cloxacillin, dicloxacillin, nafcillin
First-generation cephalosporins: Cefazolin,
cephalexin
Fluoroquinolones
Macrolides (azithromycin, clarithromycin,
erythromycin) are third-line
Less efficacy than oxacillin or cephalosporins
Erythromycin more toxic
MTB S2CK
p. 7
MTB S2CK
p. 7
Oxacillin (Methicillin) Resistant Staph
Anaerobes
Oral (above diaphragm)

Penicillin (G, VK, ampicillin, amoxicillin)
Clindamycin
Metronidazole (GI)
Vancomycin
Linezolid: Reversible bone marrow toxicity
Daptomycin
Tigecycline
Ceftaroline
Piperacillin, carbapenems, and

2nd-generation cephalosporins
also cover anaerobes
Minor MRSA infections of skin are

treated with:
TMP/SMX
Clindamycin
Doxycycline
MTB S2CK
p. 7
Gram Negative Bacilli (E. coli, Klebsiella,

Proteus, Pseudomonas, Enterobacter, Citrobacter)
Bowel (peritonitis, diverticulitis)

Urinary tract (pyelonephritis)
Cholecystitis or Cholangitis
Quinolones
Aminoglycosides
Carbapenems
Piperacillin, ticarcillin
Aztreonam
Cephalosporins
MTB S2CK
p. 8
MTB S2CK
p. 8
Man admitted with E. coli bacteremia.

Which of the following is the most appropriate
therapy?
a. Vancomycin
b. Linezolid
c. Quinolones, aminoglycosides, carbapenems,
piperacillin, ticarcillin, or aztreonam
d. Doxycycline
They dont cover grame. Clindamycin
negative bacilli.
f. Oxacillin
MTB S2CK
p. 8
Central Nervous System (CNS) Infections
Central Nervous System Infections

Meningitis
g
Encephalitis
All CNS infections give

Fever
Headache
Vomiting
Seizures
MTB S2CK
Meningitis/Definition
Clues to Answering the

Most Likely Diagnosis Question
Symptom
Diagnosis
Stiff neck
Photophobia
Meningismus
Meningitis
Confusion
Encephalitis
Focal neurological
findings
Abscess
MTB S2CK
p. 9
Infection/inflammation of CNS covering
Source: SVG by Mysid, original by SEER

Development Team commons.wikimedia.org
p.
Meningitis/Etiology: 4 bugs 95% of cases
Meningitis/Presentation
Streptococcus pneumonia (60%)

Group B streptococci (14%)
Haemophilus influenzae (7%)
Neisseria meningitidis (15%)
Listeria (2%)
Fever
Headache
Neck stiffness
(nuchal rigidity)
Photophobia
Staphylococcus with recent

neurosurgery
Patient with Neck stiffness. Source: Sophian, Abraham: Epidemic

cerebrospinal meningitis (1913), St. Louis, C.V Mosby ,
commons.wikimedia.org
S. Pneumoniae Source: CDC/Dr. M.S. Mitchell
MTB S2CK
p. 9
MTB S2CK
p. 9
Meningitis/Presentation
Acute bacterial (presents in several hours)

Focal abnormalities: 30%
If confusion occurs, you wont be able to
answer What is the most likely diagnosis?
without a CT and lumbar puncture (LP)
Cryptococcal meningitis: Slow several weeks
AIDS with <100

CD4 cells/ L
p. 9
Camper/hiker
Rash
R h target-like
lik
shape
Joint pain
Facial palsy
Tick remembered
in 20%
MTB S2CK
Meningitis/Diagnostic Tests
p. 10
Camper/hiker
Rash moves
from arms/legs
t trunk
to
t
k
Tick remembered
in 60%
Rocky Mountain
spotted fever
(Rickettsia)
Neisseria
Viral
Pulmonary
TB in 85%
Tuberculosis
p. 9
Cerebrospinal Fluid Evaluation
Best initial test and Most accurate test

Lumbar Puncture
MTB S2CK
Adolescent,
petechial rash
None
Cryptococcus
Lyme disease
MTB S2CK
Stiff Neck
Photophobia
Cryptococcus,
Tuberculosis Viral
Lyme, Rickettsia
10s100s
10s100s
10s100s
1000s,
Lymphocytes Lymphocytes
Neutrophils Lymphocytes
Bacterial
Cell
count
Protein Elevated
level
Possibly
elevated
Markedly
elevated
Usually
normal
Glucose Decreased
level
Possibly
decreased
May be low
Usually
normal
Stain
Stain:
and
5070%;
Culture Culture:
90%
Negative
Negative
Negative
MTB S2CK
p. 10
When Is Head CT the Best Initial Test?

If before the LP, there is
Neuro exam needs patient who

understands and follows instructions
and answers questions
Papilledema
Seizures
Focal
neurological
abnormalities
Confusion
Blurred
disc
margin
You cannot do an
accurate neurologic
exam if the patient is
severely confused.
Papilledema is a blurred, fuzzy disc margin from increased intracranial pressure. Source:
Conrad Fischer, MD
MTB S2CK
p. 10
MTB S2CK
p. 10
Bacterial Antigen Detection

(Latex Agglutination Tests)
If theres a contraindication to immediate LP,

giving antibiotics is best initial step in
management
Better
B
tt to
t treat
t t and
d
decrease the accuracy of a
test than to risk permanent
brain damage.
MTB S2CK
p. 10
Lyme and
Rickettsia
Acid fast stain and culture

on 3 high-volume lumbar
punctures
Centrifuge to concentrate
the organisms
TB has high CSF protein
Uncentrifuged sample of
CSF: 10% sensitivity
MTB S2CK
India ink is
60% to 70%
sensitive
p. 11
Meningitis/Treatment
Cryptococcus
Specific serologic
testing, ELISA,
western blot, PCR
Similar accuracy to Gram stain

If positive, theyre extremely specific
If negative, could still have infection
Not sufficiently sensitive to exclude bacterial
meningitis
i iti
When is a bacterial antigen test indicated?
Those receiving antibiotics prior to LP
Culture may be falsely negative
MTB S2CK
What is the Most Accurate Diagnostic Test?

Tuberculosis
Viral
Diagnosis of
exclusion
Cryptococcal
antigen: > 95%
sensitive and
specific
p. 11
Bacterial: Ceftriaxone, Vancomycin, and Steroids

Base treatment answer on cell count
Culture
Needs 2 to 3 days
Never available when treatment decision is made
G
Gram
stain
t i
Good if positive
False negative: 30% to 50%
Protein & Glucose
Nonspecific
Doesnt allow treatment decision
MTB S2CK
p. 11
Meningitis/Treatment
Listeria Monocytogenes
Steroids (dexamethasone)
Lowers mortality only in S. pneumoniae
Give when thousands of neutrophils present
No culture results for several days
Resistant to cephalosporins
Sensitive to penicillins
Add Ampicillin to Ceftriaxone and Vancomycin if
case describes risk factors for Listeria.
Risks
Thousands of neutrophils on
CSF = ceftriaxone, vancomycin,
and steroids. Add ampicillin if
immunocompromised for
Listeria.
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p. 11
Elderly
Neonates
Steroid use
AIDS or HIV
Immunocompromised (includes alcoholism)
Pregnant
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p. 11
Respiratory isolation
Rifampin or Ciprofloxacin to close contacts
Close contacts
Major respiratory fluid contact
Household contacts
Kissing
Sharing cigarettes or eating utensils
Routine school and work contacts are

not close contacts
Healthcare workers qualify only if they
MTB S2CK
p. 12
Intubate patient
Perform suctioning
Or
Have contact with respiratory secretions
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p. 12
Meningitis
Man comes to emergency department with fever,

severe headache, neck stiffness, and
photophobia. He has weakness in his left arm
and leg.
Whats the next step in management?
a. Ceftriaxone, Vancomycin, and Steroids
b. Head CT Focal neurological deficits,
initiate therapy
c. Ceftriaxone
Almost always
d. Neurology consultation wrong
e. Steroids Not sufficient
MTB S2CK
p. 12
Consultation is almost always a wrong answer on

USMLE Step 2 CK
What is the most common

neurological
l i ld
deficit
fi it off
untreated bacterial
meningitis? Eighth cranial
nerve deficit or deafness.
MTB S2CK
p. 12
Encephalitis
Acute onset
Fever, and
Confusion
Many causes
Herpes simplex
((most common))
Must do head CT
first because of
confusion
What is the most accurate test of herpes

encephalitis?
a.Brain biopsy Less accurate than PCR
b.PCR of CSF
c MRI
c.MRI
The radiologic test is never

the most acc
accurate
rate test
d.Viral culture of CSF Most accurate test for

genital, skin lesions
e.Tzanck prep Best initial test for genital lesion

Useless, 95%
f. Serology for herpes (IgG, IgM) population

MTB S2CK
p. 12
MTB S2CK
p. 13
positive
10
Encephalitis/Treatment
Acyclovir
Best initial therapy (Herpes encephalitis)
Famciclovir & Valacyclovir
IV unavailable
A woman with herpes encephalitis confirmed by PCR

gets 4 days of acyclovir. Her creatinine level rises.
Whats the most appropriate next step in
management?
a. Stop acyclovir Important to treat
a Reduce the dose of acyclovir and hydrate
a.
b. Switch to oral famciclovir or valacyclovir
Foscarnet
Acyclovir-resistant herpes
MTB S2CK
Insufficient for herpes

encephalitis
> Nephrotoxicity than acyclovir
c. Switch to foscarnet
p. 13
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p. 13
Otitis Media
Head and Neck Infections

Otitis Media
Sinusitis
Pharyngitis
Influenza (The Flu)
Redness
Immobility
Bulging
Decreased light
reflex
Pain
Decreased hearing
Fever
Otitis media. Source: www.sharinginhealth.ca

MTB S2CK
p. 13
Otitis Media/Diagnostic Tests/Treatment
Which of the following is the most sensitive

physical finding for otitis media?
a. Redness
b. Immobility
c. Bulging
d. Decreased light reflex
e. Decreased hearing
Theyre less sensitive
MTB S2CK
p. 13 14
Tympanocentesis:
Sample of fluid for culture
Most accurate diagnostic test
Choose tympanocentesis if:
Multiple recurrences
No response to multiple antibiotics
Radiologic tests for otitis are always the

wrong answer
MTB S2CK
p. 14
11
Otitis Media/Treatment
Amoxicillin: Best initial therapy

If no response to amoxicillin or it recurs,
answer:
Azithromycin
A ith
i or clarithromycin
l ith
i
Cefuroxime or loracarbef
Levofloxacin, gemifloxacin, moxifloxacin
Quinolones are relatively
contraindicated in children
MTB S2CK
p. 14
34-year-old woman with facial pain, discolored nasal

discharge, bad taste in mouth, fever and facial
tenderness.
Which of the following is the most accurate diagnostic
test?
a.Sinus
a
Sinus biopsy or aspirate
Radiologic test never the most
b.CT scan
accurate test
c.X-ray
d.Culture of the discharge Always the wrong
answer for sinusitis
e.Transillumination
Doesnt provide precise
microbiological
diagnosis
MTB S2CK p. 14
Sinusitis
Culture of nasal discharge is always

the wrong answer for sinusitis
Use Sinus Biopsy or Aspirate

Infection frequently recurs
No response to different empiric therapies
MTB S2CK
p. 14
34-year-old woman with facial pain, discolored nasal

discharge, bad taste in her mouth, and fever. She has
facial tenderness.
What is the most appropriate next step, action, or
management?
a.
a
b.
c.
d.
e.
Excellent for resistant g

gram-positive,
p
Linezolid doesnt cover Haemophilus

CT scan Diagnosis is clear, radiologic testing
X-ray
unnecessary
Amoxicillin and decongestant
Erythromycin and decongestant
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Poor coverage for

S. pneumoniae
p. 15
Pharyngitis
Pharyngitis/Diagnostic Tests
Pain on swallowing
Enlarged lymph nodes in
neck
Exudate in pharynx
Fever
No cough and no hoarseness
Best initial test: Rapid strep test

An office/clinic-based test
Finds group A beta-hemolytic streptococci in
minutes
Negative test excludes disease and no antibiotics
are needed
Positive rapid strep test = positive pharyngeal
culture
Small vesicles or ulcers: HSV or herpangina
Membranous exudates: Diphtheria, Vincent angina,
or EBV
Streptococcal pharyngitis. Source: James Heilman,

MD
These features make the likelihood of streptococcal

pharyngitis exceed 90%
MTB S2CK
p. 15
MTB S2CK
p. 15
12
Pharyngitis/Treatment
Influenza (The Flu)
1. Penicillin or amoxicillin is best initial therapy

2. Penicillin allergic:
Cephalexin (reaction only rash)
Clindamycin or macrolide (anaphylaxis)
Streptococcal pharyngitis treated to

prevent rheumatic fever
Arthralgias/myalgias
Cough
Fever
Headache
Sore throat
Nausea, vomiting, or
diarrhea, especially
in children
Source: Mikael Hggstrm
MTB S2CK
p. 15
MTB S2CK
p. 16
Influenza (The Flu)
Influenza (The Flu)/Treatment
The most appropriate next step in

management depends on time course
from presentation
Within 48 hours of onset
Perform nasopharyngeal swab or wash
Rapidly detects antigen associated with
influenza
< 48 hours of symptoms:

Oseltamivir, zanamivir
Neuraminidase inhibitors shorten duration of
symptoms
Treats both influenza A and B
> 48 hours of symptoms:
Symptomatic treatment only
Analgesics, rest, antipyretics, hydration
Oseltamivir and zanamivir dont

successfully treat complications of
influenza such as pneumonia.
MTB S2CK
p. 16
MTB S2CK
p. 16
Blood and WBCs in Stool
Infectious Diarrhea
No Blood or WBCs in Stool
When you see...in the history the answer

is.
Poultry
Salmonella
Campylobacter: MCC associated with
Guillain-Barre Syndrome
E. coli 0157:H7Hemolytic Uremic
Syndrome (HUS)
Shigella: 2nd most common association
with HUS
MTB S2CK
p. 16
13
Shellfish and cruise ships

Vibrio parahaemolyticus:
Shellfish, liver & skin disease
Vibrio vulnificus:
Hemochromatosis blood transfusions
Hemochromatosis,
Yersinia: High affinity for iron
Antibiotics, white and red cells in stool
Clostridium difficile
The Best initial test is:

Blood and/or fecal
leukocytes
Wont determine specific
organism
Stool lactoferrin: Greater
sensitivity
iti it & specificity
ifi it
than stool leukocytes
MTB S2CK
p. 16
WBCs in a stool sample (Methylene Blue Stain). Source:

Bobjgalindo
Lactoferrin: Better answer than fecal leukocytes if

one of the choices
Most accurate test is stool culture
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p. 16
No Blood No WBCs in Stool
Treatment
Viral
Giardia:
Mild disease: Oral fluid replacement

Severe disease: Fluid replacement and
ciprofloxacin
Camping/hiking and unfiltered fresh water
Cryptosporidiosis:
AIDS <100 CD4 cells
Test acid fast stain
Bacillus cereus: Vomiting

Staphylococcus: Vomiting
MTB S2CK
p. 16 17
Scombroid
Most rapid onset
Wheezing, flushing, rash
Found in fish
Treat with antihistamines
Severe infectious diarrhea means:

Hypotension
Tachycardia
Fever
Abdominal pain
Bloody diarrhea
Metabolic acidosis
MTB S2CK
p. 17
Disease Specific Treatment

Organism
Treatment
Disease
GiardiaSpecific Treatment
Metronidazole,
Tinidazole
Cryptosporidiosis
Treat underlying AIDS,

Ni
Nitazoxanide
id
Viral
Fluid support as needed
B. cereus,
Staphylococcus
Fluid support as needed
MTB S2CK
Hepatitis
Acute Hepatitis
Chronic Hepatitis
p
p. 17
14
Acute Hepatitis/Definition/Etiology
Acute Hepatitis
Infection or inflammation of liver

Majority of acute cases are viral hepatitis A/B
Hepatitis C
Rarely presents with acute infection
Found on blood tests for liver function
Evaluation of cirrhosis
Hepatitis D
Exclusively as coinfection of hepatitis B
IDUs
MTB S2CK
p. 17
Hepatitis E
Worst in pregnancy
East Asia
S
Sex,
Blood,
Bl d M
Mom: H
Hepatitis
titi B
B, C
C, D
Food and water (enteric): Hepatitis A and E
You Ate hepatitis A & you Eat hepatitis E
MTB S2CK
p. 18
Acute Hepatitis/Presentation
Acute Hepatitis/Diagnostic Tests
No way to detect specific type from

symptoms
All forms present with:
Jaundice
Fever,
F
weight
i ht loss,
l
and
d fatigue
f ti
Dark urine
Hepatosplenomegaly
Nausea, vomiting, abdominal pain
Increased direct bilirubin

Increased ratio of alanine aminotransferase
(ALT) to aspartate aminotransferase (AST)
Increased alkaline phosphatase
MTB S2CK
p. 18
Aplastic anemia is a rare

complication of acute hepatitis
MTB S2CK
p. 18
Disease Specific Diagnostic Tests
Which correlates with increased mortality?

a.
b.
c.
d
d.
e.
Bilirubin
Prothrombin time
ALT
AST
Alkaline phosphatase
MTB S2CK
p. 18
All can be
markedly elevated
and better fast,
except PT
Hepatitis A, C, D, and E: Best initial diagnostic

test
IgM antibody: Acute infection
IgG antibody: Resolution of infection
Hepatitis C: Disease activity
PCR RNA level = Amount of active viral
replication
Hepatitis C PCR level = First thing to change
PCR drop = Improvement with treatment
PCR rises = Treatment failure
MTB S2CK
p. 18
15
Serologic Patterns
Serologic Patterns
Acute or chronic
infection
Resolved, old, past

infection
Surface
antigen
Positive
Negative
e antigen
Positive
Vaccination
Window period
Surface
antigen
Negative
Negative
Negative
e antigen
Negative
Negative
Core antibody Positive IgM or IgG
Positive IgG
Core antibody Negative
Surface
antibody
Positive
Surface
antibody
MTB S2CK
Negative
p. 19
MTB S2CK
Which becomes abnormal first after acquiring

hepatitis B infection?
a.
b.
c.
d.
e.
f.
Bilirubin
Viral replication rises after S Ag
e-antigen
Surface antigen
Measure of bodys
Core IgM antibody response to infection
ALT
Anti-hepatitis B e-antibody Resolution
MTB S2CK
Which of the following is the most direct correlate with

the amount/quantity of active viral replication?
a.
b.
c.
d.
e.
f.
Bilirubin
e-antigen
Doesnt tell quantity
Surface antigen
Core IgM antibody
Measure of bodys
response to infection
ALT
Anti-hepatitis B e-antibody
Will appear prior to

resolution of all DNA
polymerase activity
MTB S2CK
Which indicates you cant transmit infection

(i.e., active infection has resolved)?
a. Bilirubin normalizes
b No e-antigen
b.
e antigen found
Normalize long before viral

replication stops.
No viral replication
c. No surface antigen found

d. No core IgM antibody found
e. ALT normalizes
f. Anti-hepatitis B e-antibody
MTB S2CK
p. 19
starting
p. 19
p. 19 20
No serological
evidence of disease
Will appear prior to
resolution of all DNA
polymerase activity
Positive
Positive IgM, then

IgG
Negative
p. 19
Which is the best indication of the need for treatment

in chronic disease?
a.
b.
c.
d.
e.
f.
Bilirubin
At least some active disease,
e-antigen
it might be on the way to
Surface antigen
spontaneous resolution and
Core IgM antibody wouldnt benefit
ALT
Measure of bodys
Anti-hepatitis B e-antibody response to infection
MTB S2CK
p. 20
16
Acute hepatitis/Treatment
Which of the following is the best indicator that a
pregnant woman will transmit infection to her child?
At least some active disease, it might
a. Bilirubin
be on the way to spontaneous
b. e-antigen
resolution and wouldnt benefit.
c. Surface antigen
Perinatal transmission: 10% if
d. Core IgM antibody positive surface antigen, but eantigen is negative; 90% when
e. ALT
both positive
f. Anti-hepatitis B, e-antibody
Measure of the bodys response to
infection
MTB S2CK
p. 20
Chronic Hepatitis/Treatment
Chronic hepatitis B = Surface antigen > 6 months
e-antigen = Elevated level of DNA polymerase
Treat when BOTH surface and e-antigen are positive
Entecavir, or
Adefovir, or
T
Tenofovir,
f i or
Lamivudine, or
Telbivudine, or
Interferon (joint & muscle pain, depression, the flu)
Interferon is an injection
Interferon has most adverse effects
MTB S2CK
p. 21
Role of Liver Biopsy
Hepatitis A and E:
Resolve spontaneously over weeks
Almost always benign conditions
Only acute hepatitis C
Hepatitis B:
gets medical therapy
Ch i iin 10%
Chronic
No treatment for acute disease
Hepatitis C:
Use interferon, ribavirin and either telaprevir or
boceprevir!!!
Treatment decreases likelihood of chronic infection
MTB S2CK
Chronic Hepatitis/Treatment
Adverse effects of interferon:
Arthralgia/myalgia
Leukopenia & thrombocytopenia
Depression & flu-like symptoms
Goal of hepatitis therapy:

Reduce DNA polymerase
Convert e-antigen to anti-hepatitis e-antibody
MTB S2CK
p. 21
p. 21
Chronic Hepatitis
Fibrosis is a strong indication to begin

therapy for either hepatitis B or C right away
Fibrosis + Active Viral replication will
progress to cirrhosis
Cirrhosis: Irreversible
Who will progress?
Old terms chronic active or chronic
persistent hepatitis are unhelpful
DNA polymerase level is helpful
MTB S2CK
p. 21
ALT levels arent a good

indication of chronic
hepatitis activity. You can
have significant infection
with normal transaminase
levels.
MTB S2CK
p. 21
17
Treatment of Chronic Hepatitis C
Treatment of Chronic Hepatitis C
Theres no way to determine the duration

of infection with hepatitis C, since theres
no equivalent of surface antigen test
Most patients dont have acute symptoms
PCR RNA viral load is elevated, patients
If PCR-RNA
should be treated with interferon and
ribavirin and either boceprevir or telaprevir
Three Drugs!
80% resolution with 3 drugs
Interferon AND Ribavirin
AND either
Telaprevir OR Boceprevir
Ribavirin causes anemia

MTB S2CK
p. 21
MTB S2CK
p. 21 22
Urethritis
Sexually Transmitted Diseases

Urethritis
Cervicitis
Pelvic Inflammatory Disease (PID)
Syphilis
Genital Warts (Condylomata Acuminata)
Pediculosis (Crabs)
Scabies
Urethritis/Diagnostic Tests
Best initial test
Men: Urethral swab for Gram stain & WBCs
Intracellular gram-negative diplococci = Neisseria
gonorrhoeae
Urine for nucleic acid amplification test (NAAT)
detects gonorrhea and Chlamydia
NAAT or DNA probe: Most accurate test
Other causes of urethritis:
Mycoplasma genitalium
Ureaplasma
Women: Self-administered vaginal swab
MTB S2CK
p. 22
Look for urethral discharge to answer

Both urethritis & cystitis give:
Dysuria
Frequency
Burning
Cystitis: No discharge
MTB S2CK
p. 22
Urethritis/Treatment
Combine:
One drug for gonorrhea & one for Chlamydia
Quinolones arent the best initial therapy
because of resistance
MTB S2CK
Gonorrhea
Chlamydia
Cefixime
Ceftriaxone
Azithromycin
Doxycycline
p. 22
18
Cervicitis
PID/Presentation
Cervical discharge
Inflamed strawberry cervix
Testing & treatment are identical to
previous description for urethritis
Except
E
t self-administered
lf d i i t d vaginal
i l swab
b
for NAAT
Lower abdominal tenderness

Lower abdominal pain
Fever
Cervical motion tenderness
Leukocytosis
Always to exclude pregnancy first!!
MTB S2CK
p. 22
MTB S2CK
p. 22 23
PID/Diagnostic Tests
Laparoscopy in PID
Cervical swab for:

Culture
DNA probe or nucleic acid amplification
(NAAT)
Tests clarifyy need for treating
gp
partner
Culture preferred to determine resistance
The most accurate test for PID

Only rarely needed
Laparoscopy is answer if:
Diagnosis is unclear
Symptoms persist despite therapy
Recurrent episodes for unclear reasons
Cervical testing isnt

the most accurate
test for PID.
MTB S2CK
p. 23
PID/Treatment
Combination of medications for gonorrhea

and Chlamydia
Inpatient: Cefoxitin or cefotetan combined
with doxycycline
Outpatient: Ceftriaxone and doxycycline
(possibly with metronidazole)
Anaphylaxis to penicillin?:
Levofloxacin and metronidazole (outpatient)
Clindamycin and gentamicin (inpatient)
MTB S2CK
p. 23
MTB S2CK
p. 23
Ulcerative Genital Disease/

Often impossible to determine specific
diagnostic, visual characteristics
Question must have sufficient
evidence to g
give answer
All genital ulcers can have inguinal

adenopathy
MTB S2CK
p. 23
19
Presentation of STDs
Diagnostic Tests
History and physical findings
Most likely diagnosis
Diagnosis
Diagnostic Test
Painless ulcer
Syphilis
Syphilis
Painful ulcer
Chancroid (Haemophilus
ducreyi)
Dark field microscopy (Best in primary)

VDRL or RPR (75% sensitive in primary)
FTA or MHA TP (confirmatory)
Chancroid (Haemophilus
ducreyi)
Stain & culture (special media)
Lymph nodes tender and

suppurating
Lymphogranuloma
venereum
Lymphogranuloma
venereum
Complement fixation titers in blood

Nucleic acid amplification testing on
swab
Vesicles prior to ulcer

and painful
Herpes simplex
Herpes simplex
Tzanck prep: Best initial test

Viral culture: Most accurate test
MTB S2CK
p. 23
MTB S2CK
Diagnostic Tests
p. 24
Treatment
Diagnosis
If dark-field is positive for

spirochetes no further
testing for syphilis is
necessary
necessary.
Treatment
Syphilis
One dose IM benzathine penicillin

Doxycycline, if penicillin allergic
Chancroid
Azithromycin (single dose)
(Haemophilus ducreyi)
Lymphogranuloma
venereum
Herpes simplex
MTB S2CK
p. 24
MTB S2CK
Doxycycline
Acyclovir, valacyclovir, famciclovir
Foscarnet for acyclovir resistant
herpes
p. 24
Syphilis/Presentation
Woman comes to clinic with multiple painful genital
vesicles.
a. Acyclovir orally
y
topically
p
y Worthless
b. Acyclovir
If the presentation is diagnostic testing is
c. Tzanck prep not necessary
Most accurate test, but not necessary, if
Primary Syphilis
Painless genital ulcer
with heaped-up
indurated edges (it
becomes painful if it
becomes secondarily
infected with bacteria)
Painless adenopathy
d. Viral culture vesicles are clear
Chancres heal spontaneously even

without treatment. Penicillin
prevents later stages.
e. Serology Cant distinguish genital infection from oral

infection in the past
f. PCR
MTB S2CK
p. 24
Richard Usatine, M.D. Used with permission
PCR encephalitis, not genital

MTB S2CK
p. 25
20
Secondary Syphilis
Rash (palms and
soles)
Alopecia areata
Mucous patches
Condylomata lata
Tertiary Syphilis
Neurosyphilis
Meningovascular (stroke from vasculitis)
Tabes dorsalis (loss of position and vibratory sense,
incontinence, cranial nerve)
Tabes Dorsalis . Source: CDC/Susan Lindsley
MTB S2CK
p. 25
phil.cdc.gov
Tertiary Syphilis
Neurosyphilis
General paresis (memory and personality
changes)
Argyll Robertson pupil
Aortitis (aortic regurgitation, aortic

aneurysm)
Gummas (skin and bone lesions)
MTB S2CK
p. 25
Syphilis
p. 25
Sensitivity of Diagnostic Tests by Stage

Test
VDRL or RPR
FTA ABS
Primary
75%85%
95%
Secondary
99%
100%
Tertiary
95%
98%
MTB S2CK
p. 25
Syphilis/Treatment
False positive VDRL/RPR

Infection, older age, injection drug
use, AIDS, malaria, antiphospholipid
syndrome, and endocarditis
Titers of VDRL or RPR are
reliable at > 1:8
Lower titer is more often falsely
positive
High titers (> 1:32) are rarely
false positive
MTB S2CK
MTB S2CK
p. 25
Primary & secondary syphilis:

Single IM injection of penicillin
Oral doxycycline: Penicillin allergy
Tertiary syphilis:
IV penicillin
Desensitize to penicillin if allergic
MTB S2CK
p. 25
21
Syphilis
Genital Warts (Condylomata Acuminata)/

Diagnosis
Jarisch-Herxheimer reaction
Fever, headache, myalgias after treatment
Give aspirin & antipyretics (itll pass)
Desensitization the answer for

neurosyphilis and pregnant women
MTB S2CK
p. 26
MTB S2CK
Genital Warts (Condylomata Acuminata)/

Treatment
Remove by physical means:

Cryotherapy with liquid nitrogen
Surgery for large ones
Laser
Melt with podophyllin or trichloroacetic
acid
Imiquimod: Apply locally
(immunostimulant leads to sloughing off of
lesion)
MTB S2CK
Papillomavirus
Diagnose based on
the visual
appearance
Wrong answers:
Biopsy
Serology
Stain, smear, or
Condylomata acuminata (genital warts). Source: Farshad
culture
Bagheri, MD.
p. 26
p. 26
Pediculosis (Crabs)
Hair-bearing areas
(axilla, pubis)
Itchy
Visible on surface
Treat with permethrin;
li d
lindane
iis equall iin
efficacy, but more toxic
MTB S2CK
Pediculosis pubis. Source: commons.wikimedia.

p. 26
Scabies
Scabies/Treatment
Web spaces between

fingers and toes or at
elbows
Around nipples near
the genitals
Burrows visible (they
dig) but smaller than
pediculosis
Scrape & magnify
Permethrin
Widespread disease: Oral Ivermectin
Severe disease needs repeat dosing
MTB S2CK
p. 27
Scabies burrow under the skin and must be scraped out to

establish a diagnosis. Source: Conrad Fischer, MD.
MTB S2CK
p. 27
22
Urinary Tract Infections (UTI)
Urinary Tract Infections

Cystitis
Pyelonephritis
y
p
Acute Prostatitis
Perinephric Abscess
Present with dysuria (frequency, urgency,

burning), maybe fever
Urinalysis shows WBCs
E. coli MCC
Quinolones Best initial therapy
Anatomic defects lead to UTIs:
Stones
Strictures
Tumor or prostate hypertrophy
Diabetes
MTB S2CK
p. 27
Urinary Tract Infections
Cystitis
Foley catheter is a foreign body

Neurogenic bladder is an obstruction
Presents with dysuria and:

Suprapubic pain/discomfort
Mild/absent fever
Frequency = Multiple episodes of micturation

Polyuria = Increase in volume of urine
Men have anatomic abnormalities

Women most often dont
Best initial test: Urinalysis with > 10 WBCs
Most accurate test: Urine culture
MTB S2CK
p. 27
MTB S2CK
p. 27 28
Cystitis/Treatment
Trimethoprim/sulfamethoxazole (TMP/SMZ)
if local resistance is low
Ciprofloxacin
Cephalexin
Nitrofurantoin ((Pregnant
g
women))
All beta-lactam antibiotics are
considered safe in pregnancy
MTB S2CK
p. 28
36 year old generally healthy woman comes with

urinary frequency and burning.
UA: > 50 WBC
a.
b.
c.
d.
e.
TMP/SMZ for 3 days

TMP/SMZ for 7 days With anatomic abnormality
Urine culture
No need of culture
Ultrasound of urinary system or imaging when
symptoms of cystitis
CT scan of urinary system
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p. 28
are clear & WBCs in

urine
23
Pyelonephritis
Pyelonephritis
Dysuria with:
Flank or CVA tenderness
High fever
Occasional abdominal pain
UA with high WBCs
Imaging studies (CT or sonogram) look
for anatomic abnormalities causing
infection
Treat with:
Ampicillin & gentamicin
Ciprofloxacin
Change based on culture/sensitivity
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p. 28
Any drugs for gram-negative

bacilli would be effective for
pyelonephritis
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Acute Prostatitis
Perinephric Abscess
Dysuria with:
Perineal pain
Tender prostate on examination
Diagnostic yield of urine culture greatly
increased with p
prostate massage
g
Treat same as you would for pyelonephritis
Longer duration
TMP/SMZ or ciprofloxacin for 6 to 8 weeks
for chronic prostatitis
Look for:
Pyelonephritis not resolving with appropriate
therapy
When drug choice & dose are correct failure
of infection to resolve is an anatomic problem
Do sonogram or CT scan
Drainage of fluid collection is mandatory
Culture of infected fluid is essential to guide
therapy
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Endocarditis/Definition
Endocarditis
Heart valve infection

Leads to fever & murmur
Diagnosis:
Positive blood cultures
Vegetations on echocardiogram
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24
Endocarditis/Etiology
Endocarditis/Etiology
Rare on normal heart valves (except

IDUs)
Risk proportional to degree of damage
of valves
Regurgitant & stenotic lesions have
increased risk
Prosthetic valves: Highest risk
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Endocarditis/
Fever
New murmur or
change in a murmur
Complications of
endocarditis
Source: Splarka
http://en.wikipedia.org/wiki/Splinter_hemorrhages
p. 29 30
p. 29
Endocarditis/Presentation/
Splinter hemorrhages
Janeway lesions (flat
and painless)
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Can develop on normal valves if:

Severe bacteremia
Highly pathogenic organisms
(Staphylococcus aureus)
Dental procedures with blood confer a small
risk of endocarditis
Surgery of mouth & respiratory tract confers
no risk unless severe valve disease is
present
Artificial valve or cyanotic heart disease
Endoscopy confers no risk even with biopsy
Osler nodes (raised and painful)

Roth spots in eyes
Brain (mycotic aneurysm)
Kidney (hematuria, glomerulonephritis)
Conjunctival petechiae
Splenomegaly
Septic emboli to lungs
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Endocarditis/Diagnostic Tests
Best initial test Blood culture (95%99%

sensitive)
If positive do an Echo
Transthoracic echo (60% sensitive, but 95%
specific)
Transesophageal
T
h
l echo
h (95% sensitive
iti and
d
specific)
EKG rarely shows atrioventricular (AV) block if
dissection of conduction system occurs (5%
10%)
A man comes into the ED with fever and a murmur.

Blood cultures grow Streptococcus bovis.
Transthoracic echocardiography shows vegetation.
What is the next step in the management?
a.
b
b.
c.
d.
e.
Transthoracic showed
Colonoscopy
vegetation.
Transesophageal echocardiogram
Will not show diverticuli
CT of the abdomen
Repeat the blood cultures No point, already positive
Surgical valve replacement Premature
Fever + murmur =
endocarditis
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25
How to Diagnose
Culture Negative Endocarditis
Endocarditis/Treatment
1. Oscillating vegetation on echocardiography

2. Three minor criteria:
Fever
Risk: IDU or prosthetic valve
Embolic phenomena
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Empiric:
Vancomycin and gentamicin
When culture results are available
Treat based on sensitivities
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Organism
Treatment
Organism
Viridans streptococci
Ceftriaxone for 4 weeks
Vancomycin
Staphylococcus aureus
(sensitive)
Oxacillin, nafcillin, or
cefazolin
Staphylococcus
epidermidis or resistant
Staphylococcus
Enterococci
Ampicillin & gentamicin
Fungal
Amphotericin and valve

replacement
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Endocarditis
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p. 31
Endocarditis
Treatment of Resistant Organisms

Add aminoglycoside & extend duration of
treatment
When Is Surgery the Answer?
CHF or ruptured valve or chordae tendineae
Prosthetic valves
Fungal endocarditis
Abscess
AV block
Recurrent emboli while on antibiotics
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Treatment
Add rifampin for prosthetic

valve endocarditis with
Staphylococcus.
The single strongest indication
for surgery is acute valve
rupture and CHF.
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26
Treatment of Culture Negative Endocarditis
Prophylaxis for Endocarditis
Most common culture negative = Coxiella

HACEK: Acronym for organisms difficult to
culture causing endocarditis
Use prophylaxis if theres BOTH:

1. Significant cardiac defect
Haemophilus aphrophilus
Haemophilus parainfluenza
Actinobacillus
Cardiobacterium
Eikenella
Kingella
Prosthetic valve
Previous endocarditis
Cardiac transplant recipient with valvulopathy
Unrepaired cyanotic heart disease
AND!
2. Risk of bacteremia
Dental work with blood
Respiratory tract surgery that produces
bacteremia
Use ceftriaxone for HACEK group

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Amoxicillin prior to procedure

If penicillin allergic use clindamycin,
azithromycin, or clarithromycin
Procedures and anatomic abnormalities
that do not need prophylaxis are:
Flexible endoscopy, even with biopsy,
ERCP
Obstetrical and gynecologic procedures
Urology procedures (including prostate

biopsy)
Mitral valve prolapse, even with murmur
Mitral regurgitation, mitral stenosis,
aortic regurgitation
regurgitation, aortic stenosis
stenosis,
hypertrophic obstructive
cardiomyopathy (HOCM), atrial septal
defect (ASD)
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Lyme Disease/Definition
Lyme Disease
Arthropod-borne
Spirochete: Borrelia burgdorferi
What is the most common manifestation?
Fever & Rash
What is the most common manifestation if
untreated?
Joint pain
Also: Cardiac or neurologic disease
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27
Lyme Disease/Etiology
Transmitted by deer
tick (Ixodes
scapularis)
Tick very small
Only 20% patients
recall bite
Patients recall being outdoors

Hiking or camping
Experimental models:
Tick must be attached for at least 24
hours in order to transmit organism
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Lyme Disease/Presentation
Ixodes tick
Northeast states:
Connecticut (where the town of Lyme gave
the disease its name)
Massachusetts
New York
New Jersey
Rash:
Most common manifestation (85% - 90%)
Occurs 5-14 days after bite
Fever often present
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cdc.gov
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Erythema migrans
Round, red
Pale center
Target or bulls-eye
Joint pain 60% without treatment

Oligoarthritis = few joints
Joint fluid: ~ 25,000 WBCs/ L
Similar number to gout, pseudogout and
many infections
i f ti
The knee is the most commonly
affected joint in Lyme disease.
Target-shaped rash of Lyme disease or erythema migrans.

Source: Nishith Patel.
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28
Neurological manifestations 10% 15%

CNS or peripheral
Meningitis, encephalitis, or CN palsy
Cardiac: 4% - 10%
Any part of myocardium or pericardium
Myocarditis or ventricular arrhythmia
Transient AV block is the most

common cardiac manifestation in
Lyme disease.
Bells palsy or 7th CN is most

common neurological
manifestation of Lyme disease.
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Lyme Disease/Diagnostic Tests
Lyme Disease/Treatment
Typical rash doesnt need serologic testing to

start treatment
Serologic testing for Lyme is essential for:
Joint
Neurologic
g
Cardiac manifestations
Most 7th CN palsy, arthralgia & AV block are
not caused by Lyme
Testing is with IgM, IgG, ELISA, Western
blot, and PCR testing
Manifestation
Treatment
Asymptomatic tick bite
No treatment
routinely
Rash
Doxycycline
Amoxicillin
Joint, 7th CN palsy
Doxycycline
Amoxicillin
Cardiac and neurologic

manifestations other than 7th CN
palsy
IV ceftriaxone
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Asymptomatic Tick Bite
Bites without symptoms rarely need

treatment
Who DOES need treatment?
Single dose of doxycycline
Within 72 hours of tick bite when:
HIV/AIDS
Ixodes scapularis clearly identified as tick

Tick attached for > 24-48 hours
Engorged nymph-stage tick
Endemic area
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29
HIV/AIDS/Definition
A retrovirus infecting CD4 (T-helper)

cells
CD4 cells drop from normal (600-1000)
at a rate of 50 to 100/year untreated
5 and 10 years before clinical
manifestations
Not HIV itself that leads to death
Low CD4 leads to illness
HIV life cycle
Source: nih.gov
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HIV/AIDS/Etiology
Transmitted by:
IDU
Sex, particularly men who have sex with men
Transfusion (extremely rare since 1985)
Perinatal
Needle stick or blood-contaminated sharp
instrument injury
Kissing is not proven to
transmit HIV.
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Risk of Transmission of HIV

Without Prophylactic Treatment
Mode of
transmission
Vaginal transmission
Percentage of risk with each event

1:30001:10,000 for insertive intercourse
1:1000 for receptive intercourse
Oral sex
1:1000 for receptive fellatio with ejaculation

Unclear for insertive fellatio or cunnilingus
Needle stick injury
1:300
Anal sex
1:100 for receptive anal intercourse
Mother to child
25%30% perinatal transmission without

medication
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HIV/AIDS/Presentation
HIV/AIDS/Diagnostic Tests
Best initial test: ELISA test

Confirmed with Western blot
Infected infants:
Diagnose with PCR or viral culture
ELISA testing is unreliable in infants
Maternal HIV antibodies are present for
up to 6 months after delivery
Infections when CD4 drops < 50/ L

PCP < 200/ L
CD4 > 200/ L (few infections occur)
Infections > 200/ L are:
Varicella zoster (shingles)
Herpes simplex
TB
Oral and vaginal candidiasis
Bacterial pneumonia
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30
Viral Load Testing (PCR RNA level)
Viral Load Testing (PCR RNA level)
The goal of therapy is to drive down

viral load
Undetectable levels (< 50/ L): CD4 will
rise
CD4 rises = Opportunistic infections
stop
Life expectancy when viral load is
undetectable by PCR-RNA is equal in
duration to HIV-negative person
Measures response to therapy

Decreasing levels good
Detect treatment failure
Rising levels bad
Diagnoses HIV in babies
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Viral Resistance Testing (Genotyping)
HIV/AIDS/Treatment
Perform prior to initiating antiretroviral

medications
Decreases likelihood of starting
medication to which patients virus is
resistant
Resistance testing: Evaluates treatment
failure
Guides choice of medications
Select 3 drugs from 2 different classes to
which patients virus is susceptible
For HIV: Treatment is initiated when:

CD4 < 500/ L
or
Viral load is very high (>100,000/ L)
or
Opportunistic infection occurs
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HIV/AIDS/Treatment
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Choice of Initial Antiretroviral Medication

Initial drug regimen:
Treatment failure first

manifests with rising PCRRNA viral load
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Emtricitabine, Tenofovir, and

Efavirenz
USMLE Step 2 CK doesnt
doesn t test
dosing
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31
Choice of Initial Antiretroviral Medication
Antiretroviral First line Medications by Class
Treatment failure:
Rising viral load
CD4 count decreases or fails to rise
CD4 changes are slower than changes in
viral load
Alternate Drug Regimens
If emtricitabine/tenofovir/efavirenz cannot be
used because of resistance alternate
regimens are based on combination of 3
drugs from at least 2 different classes
Nucleoside and
nucleotide reverse
transcriptase
inhibitors (RTIs)
Non
nucleoside
RTIs
Protease inhibitors
Zidovudine
Didanosine
Stavudine
Lamivudine
Emtricitabine
Abacavir
Tenofovir
Efavirenz
Etravirine
Nevirapine
Ritonavir
Saquinavir
Nelfinavir
Amprenavir
Fosamprenavir
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Additional Classes of Second line Agents
Postexposure Prophylaxis
Used with drug resistance to multiple classes of

first-line agents
Entry inhibitors:
Enfuvirtide
Maraviroc
Integrase inhibitor:
Raltegravir
Lopinavir
Atazanavir
Indinavir
Tipranavir
Darunavir
All significant needle stick injuries

Sexual exposures
Bites
Give 4 weeks of combination therapy
Urine & stool arent an indication for
postexposure prophylaxis (PEP)
USMLE Step 2 CK wont require you to

know details of efficacy differences
between classes.
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Postexposure Prophylaxis
Postexposure prophylaxis
isnt routinely indicated for
needle stick injury if HIV
status of needle is unknown
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p. 37
Adverse Effects of HIV Medications

Drug
Adverse effect
Zidovudine
Anemia
Stavudine and didanosine
Peripheral neuropathy and pancreatitis
Abacavir
Hypersensitivity, Stevens Johnson

Reaction
Protease inhibitors
Hyperlipidemia, hyperglycemia
Indinavir
Nephrolithiasis
Tenofovir
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Renal insufficiency
p. 38
32
Prevention of Perinatal Transmission
Prevention of Perinatal Transmission
Pregnant Patients
If already on antiretroviral medications
Continue same treatment
If pregnant and not already on
medications
di ti
Start combination antiretrovirals
Only Efavirenz is NOT used in
pregnancy
After Delivery for Mother

CD4 > 500 and she doesnt need them
Stop after delivery
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Indications for Antiretrovirals

During Pregnancy
Action
Patient on antiretrovirals at
the time of pregnancy
Continue same medications,

except switch efavirenz to
protease inhibitor
Not on antiretrovirals,
CD4 low or viral load high
Initiate antiretrovirals
immediately. Continue after
delivery
Not on antiretrovirals,
CD4 high and viral load low
Antiretrovirals immediately,
stop them in mother after
birth
p. 38
p. 38
Cesarean Delivery for HIV Positive Mothers
Condition
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CD4 < 500 or viral load high

Continue after delivery
Baby
Zidovudine during delivery (intrapartum) AND
For 6 weeks after to help prevent transmission
Viral load >1000 L: Perform Cesarean

delivery
Everyone: Intrapartum zidovudine
Fully controlled HIV (viral load
undetectable) gives <1%
transmission.
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33
Diagnostic Tests
in Nephrology
Nephrology
Emma Holliday,
Holliday MD
Resident Physician
Radiation Oncology
University of Texas MD Anderson Cancer Center
Urinalysis
White Blood Cells
Hematuria
Cytoscopy
Casts
Urinalysis
Dipstick vs. Urinalysis
Measures:
Both give some quantitative values

Dipstick described as direct (e.g., 300 mg protein)
or scale number: 0, 1+, 2+, 3+, or 4+
Microscopic urinalysis reports number of cells/highpowered field
Protein
WBCs or leukocyte esterase
RBCs
Specific gravity and pH
Nitrites
Pyuria with positive nitrites = UTI
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p. 299
Dont worry about the precise scale

Every USMLE Step 2 CK test comes with a range
of normal values attached to assess severity
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Urinalysis/Protein
Urinalysis/Protein
Renal tubules secrete slight amounts of TammHorsfall protein
2 - 10% of population has transient proteinuria

Benign reasons for proteinuria:
Should be < 30 to 50 mg/24 hours
Greater amounts of protein associated with either

tubular disease or glomerular disease
Very large amounts of protein excreted with
glomerular disease
1+ proteinuria ~ 1g/day
2+ proteinura ~ 2g/day
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Orthostatic proteinura or physical exertion

If symptoms of
proteinuria - best
initial test?
Urinalysis/Dipstick
If positive, order urine

protein to creatinine ratio
or 24 hour urine collection
Most accurate for
determining
etiology?
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Renal biopsy
p. 300
Urinalysis/Proteinuria
Urinalysis/Microalbuminuria
Limitations of dipstick for proteinuria:

Only detects albumin
Cant detect Bence Jones protein
Microalbuminuria
Present in multiple myeloma

Best test for Bence Jones proteinuria is UPEP (urine
protein electrophoresis)
Cant detect very low amounts of protein
Tiny amounts of protein too small to

detect on UA
An important screening test in diabetic

patients
Should be performed yearly
Long-term microalbuminuria
Leads to worsening renal function in
diabetic patient and should be treated
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Pyuria
Diabetic patient is evaluated, UA shows no protein.
Microalbuminuria is detected (level between 50 - 300
mg/24 hours).
Whats the next best step in management?
a. Enalapril
b Kidney biopsy Extreme! We know the etiology already
b.
c. Hydralazine Less effective & with more adverse effects
d. Renal consultation NEVER consult on Step 2
e. Low-protein diet Bad for glycemic control
f. Repeat UA annually and treat when trace protein is
Starting early will delay disease progression
detected
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p. 301
White blood cells in urine:

Inflammation
Infection
Allergic interstitial nephritis
Neutrophils cant be distinguished from eosinophils

on UA
Neutrophils indicate infection (UTI or urethritis)
Eosinophils indicate allergic or acute interstitial
nephritis (NOT NSAID-induced renal disease)
Wright and Hansel
stains detect
eosinophils in the urine.
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p. 301
Hematuria
Etiology:
Stones
Coagulopathy
Infection (cystitis, pyelonephritis)
Cancer
Cancer
C
T
Treatments
t
t (cyclophosphamide)
( l h
h id )
Trauma
Glomerulonephritis
False positive = hemoglobinuria or myoglobinuria
Woman is admitted with trauma and dark urine. The

dipstick is markedly positive for blood.
a. Microscopic examination of urine
Overkill - best test to look for bladder mass
b. Cystoscopy
Best test for hydronephrosis
c Renal ultrasound
c.
d. Renal/bladder CT scan Most accurate test for stones
e. Abdominal X-ray Best test for ileus or to detect free air
f. Intravenous pyelogram Never the right answer - slow
test uses nephrotoxic contrast
Dysmorphic RBCs = glomerulonephritis

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When Is Cystoscopy the Answer?
Casts
When theres hematuria without

infection or prior trauma and:
Microscopic collections of material clogging up the

tubules and being excreted in urine
The renal ultrasound or CT doesnt

show etiology
Bladder sonography shows mass for
possible biopsy
Hyaline
Broad, waxy
Granular, muddybrown
Cystoscopy is the most

accurate test of the
bladder.
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Type of cast
Red cell
White cell
Eosinophil
p. 302
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p. 302 303
Association
Glomerulonephritis
Pyelonephritis
Acute interstitial
nephritis
Dehydration
Chronic renal disease
Acute tubular necrosis
(are dead tubular
casts)
Acute Kidney Injury
Acute kidney injury (AKI)
Acute Kidney Injury

Acute Tubular Necrosis
Hepatorenal
p
Syndrome
y
Atheroemboli
Acute (Allergic) Interstitial Nephritis
Analgesic Nephropathy
Decrease in creatinine clearance

Results in sudden rise in BUN and creatinine
The definition is not based on specific values

of BUN and creatinine
Categories:
Prerenal azotemia (decreased perfusion)
Postrenal azotemia (obstruction)
Intrinsic renal disease (ischemia and toxins)
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Acute Kidney Injury/Presentation
Acute Kidney Injury

Prerenal
Intrinsic Renal
ATN
Hypotension
- Toxins
- Sepsis
NSAIDs
- Anaphylaxis
AG, ampho
Cis,
Cis cyclosporine
- Bleeding
- Prolonged ischemia
- Dehydration AIN
Hypovolemia
- PCN, sulfa
Rhabdo/hemoglobinuria
- Diuretics
Contrast
- Burns
Crystals
- Pancreatitis Bence-Jones proteins
Post-strep infection
- pump fxn
- Low albumin
- Cirrhosis
MTB S2CK p. 303 304
artery stenosis
Renal
p. 303
Post Renal
BPH/Prostate cancer
Ureteral stone
Cervical cancer
Urethral stone
Neurogenic bladder
Retroperitoneal
fibrosis (chemo or
XRT)
AKI usually = asymptomatic rise in BUN and

creatinine; when symptomatic:
Nausea and vomiting
Fatigue/malaise
Weakness
SOB, edema (fluid overload)
Very severe disease presents with:

Confusion
Arrhythmia from hyperkalemia and acidosis
Sharp, pleuritic chest pain from pericarditis
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p. 304 305
Acute Kidney Injury/Diagnostic Tests
The best initial test is...
What is the best initial imaging test?
BUN and creatinine
Nonfunctional kidneys creatinine rises

~ 1 point/day (1 mg/dL)
If the BUN:creatinine
BUN creatinine ratio is > 20
20:1
1 the
etiology is either prerenal or postrenal
damage
Intrinsic renal disease ratio closer to
10:1
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Renal sonogram because it isnt invasive and

doesnt need contrast
Kidney biopsy is rarely the right answer for

AKI
MTB S2CK
p. 305
When cause is unclear next best diagnostic step

is:
Urine Sodium and Fractional Excretion of Sodium

Normal kidney:
Urinalysis
Urine sodium (UNa)
Fractional excretion of sodium (FENa) or urea
(FEUrea)
Urine osmolality
If all of these are choices always go with

urinalysis first
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p. 306
blood pressure
aldosterone
aldosterone
sodium reabsorption
in the urine (< 20)
sodium
Damaged kidney (e.g., ATN):

Kidneys cant reabsorb Na appropriately (> 20)
Prerenal azotemia:
low UNa (below 20) =
low FENa (less than 1%)
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You can answer all the

questions on USMLE Step
2 CK without knowing the
mathematical formula for
FENa.
p. 306
Urine Osmolality
Normal kidney:
intravascular volume
ADH
ADH
water reabsorption at
collecting duct
urine osmolarity
Damaged kidney (e.g., ATN):

Kidneys cant concentrate urine
appropriately - will see Osm similar to
blood (~300mOsm)
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20-year-old African-American man has screening test

for sickle cell. Hes found to be heterozygous (trait or
AS) for sickle cell.
Sickle cell trait rarely
What is the best advice for him?experience pain crises
a.
b.
c.
d.
e.
Nothing needed until he has a painful crisis

Avoid dehydration
y
Hydroxyurea Only if > 4 pain crises per year.
Folic acid supplementation Indicated if hemolysis
Pneumococcal vaccination present (high RBC
Indicated if functionally
asplenic
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p. 307
Classification of Acute Renal Failure

Test
Prerenal
azotemia
Acute tubular
necrosis
BUN:Creatinine
> 20:1
< 20:1
Urine Sodium (UNa)
< 20 mEq/L
> 20 mEq/L
FFractional
ti
l excretion
ti
of sodium (FENa)
< 1%
> 1%
Urine osmolality
(UOsm)
> 500
mOsm/kg
< 300
mOsm/kg
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Patient presents with fever and acute LLQ abdominal

pain. Blood cultures grow E. coli and Candida albicans.
Patient started on vancomycin, metronidazole,
gentamicin, and amphotericin. CT scan reveals
diverticulitis. After 36 hours, her creatinine rises
dramatically.
Which of the following is most likely the cause of her renal
insufficiency?
a. Vancomycin Need 5-10 days exposure
b. Gentamicin Need 5-10 days exposure
c. Contrast media
d. Metronidazole Hepatically excreted
e. Amphotericin Need 5-10 days exposure
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Acute Tubular Necrosis/Definition
Injury to kidneys from ischemia and/or toxins

result in sloughing of tubular cells into urine
Proteinuria isnt significant since protein, not
tubules, spill into urine when glomeruli are
damaged
Acute renal failure and a toxin in history are

your clues to What is the most likely
diagnosis? question for ATN
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74-year-old blind man admitted with obstructive uropathy

and chest pain. History of hypertension and diabetes.
Creatinine drops from 10 mg/dL to 1.2 mg/dL 3 days after
catheter placement. The stress test shows reversible
ischemia.
This is still
What is the most appropriate management? considered
a. Coronary artery calcium score on CT scan experimental

a
b. One to two liters of normal saline hydration prior and
during angiography
Evidence not as strong
c. N-acetylcysteine prior to angiography
d. Mannitol during angiography Doesnt help
e. Furosemide during angiography Loop diuretics are dangero
worsen it
f. Intravenous sodium bicarbonate before and during
angiography Evidence not as strong
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Extra Difficult Question
A patient with mild renal insufficiency undergoes

angiography and develops 2 mg/dL rise in creatinine
from ATN despite the use of saline hydration before
and after procedure.
What do you expect to find on laboratory testing?
A patient with extremely severe myeloma with a

plasmacytoma is admitted for combination
chemotherapy. Two days later creatinine rises.
What is the most likely cause?
a.
b.
c.
d.
Urine sodium
FENa
Urine specific gravity
8 (low)
>1%
1.035 (high)
58 (high)
>1%
1.005 (low)
5 (very low)
<1%
1.040 (very high)
45 (high)
>1%
1.005 (low)
Spasm of afferent arteriole leads to reabsorption of Na
(and thus water)
very concentrated urine ( specific
gravity)
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a.
b
b.
c.
d.
e.
Cisplatin Takes 5-10 days

Hyperuricemia
Can cause renal insufficiency
Bence-Jones proteinuria but would not get worse with
treatment
Hypercalcemia
Hyperoxaluria Oxalate crystals can be present in
urine in cases of bowel resection
MTB S2CK
p. 309
What wouldve prevented this event?

Allopurinol, hydration, and rasburicase
Given prior to chemotherapy to prevent
renal failure from tumor lysis syndrome
Suicidal patient ingests an unknown substance and

develops renal failure 3 days later. Her calcium level
is low and urinalysis shows an abnormality.
What did she take?
MTB S2CK
p. 309
a.
b.
c.
d.
e.
f.
Aspirin Doesnt affect Ca levels or cause crystals

p
Hepatotoxic
Acetaminophen
p
Ethylene glycol
Constrict afferent arteriole
ATN and
Ibuprofen
papillary necrosis
Opiates Can cause FSGS, but not AKI
Methanol Affects retinal inflammation not AKI
MTB S2CK
p. 310
Acute Tubular Necrosis/Toxins
3 things increase risk of toxic/insult ATN:

Hypoperfusion of kidney
Underlying renal insufficiency
Hypertension
Diabetes
Older age
Summary of Causes:
Slow onset (5 - 10 days)
We lose 1% of renal
function every year past
age of 40.
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p. 310
Mag
Contrast
Best prevented with saline hydration

N-acetylcysteine and sodium bicarbonate arent
consistently proven as beneficial
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p. 310
Rhabdomyolysis
Summary of Causes:
Hemoglobin and myoglobin
Hyperuricemia
Ethylene Glycol
Multiple Myeloma
NSAIDs
Etiology?
p. 310
risk for aminoglycoside and cisplatin
Immediate toxicity (24 48 hrs)

media
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Drug-related injury
Aminoglycosides, amphotericin, cisplatin,

vancomycin, acyclovir, cyclosporine
Dose dependent
Trauma, prolonged immobility, snake

bites, seizures, and crush injuries
The best initial test?

UA (dipstick AND microscopic analysis)
Characteristic findings?
Blood is positive on dipstick but NO
RBCs are seen on microscopic exam
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p. 311
Rhabdomyolysis
Rhabdomyolysis
Most specific lab test?
Treat with:
Saline hydration
Mannitol
Bicarbonate
Urine myoglobin
Abnormal lab findings?

Creatine phosphokinase (CPK)
Hyperkalemia
H
k l i
Hyperuricemia
Hyperphosphatemia
Hypocalcemia
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p. 311
Dont treat hypocalcemia

in rhabdomyolysis if
asymptomatic. In recovery, the
calcium will come back
out of muscles.
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p. 311
Acute Tubular Necrosis/Treatment

A man comes to the ED after a triathlon followed by
status epilepticus. He takes simvastatin at triple the
recommended dose. His muscles are tender and
urine is dark. IV fluids are started.
What is the next best step in management?
a.
b.
c.
d.
e.
CPK level Would suggest

gg
rhabdo as cause,, but not life
threatening complications.
EKG
Potassium replacement Would be fatal
Urine dipstick Same reason as A
Urine myoglobin Same reason as A
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p. 311 312
No therapy proven to benefit ATN

Patients should be managed with
Hydration, if theyre volume depleted and
correction of electrolyte abnormalities
Diuretics increase urine output, but dont

change overall outcome
More urine output with
diuretics doesnt mean
renal failure is reversing.
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p. 312
Answering treatment questions for ATN is

based on recognizing the most common
wrong answers:
When Is Dialysis the Answer?

Dialysis is initiated if theres:
Fluid overload
Encephalopathy
Pericarditis
Metabolic acidosis
A- acidosis
E- electrolytes
Hyperkalemia
Low-dose dopamine
Diuretics
Mannitol
Steroids
All these are ineffective in reversing ATN
I- intoxications
O- overload of
volume
U-uremia
Correct underlying cause

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Acute Tubular Necrosis/Rhabdomyolysis
Hepatorenal Syndrome
Patient develops ATN from gentamicin. Shes

vigorously hydrated and treated with high doses of
diuretic, low-dose dopamine, and calcium acetate as
a phosphate binder. Urine output increases, but she
still progresses to end-stage renal failure. She also
becomes deaf.
What caused her hearing loss?
Renal failure developing secondary to liver

disease
Kidneys normal
Look for:
a.
b.
c.
d.
e.
Hydrochlorothiazide No otoxicity
Dopamine No ototoxicity
Furosemide
Chlorthalidone No ototoxicity
Calcium acetate No ototoxicity
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Severe liver disease (cirrhosis)

New-onset renal failure with no other explanation
Very low urine sodium (> 10 15 mEq/dL)
FeNa < 1%
Elevated BUN:creatinine ratio (> 20:1)
Treat with:
Albumin, midodrine, octreotide
p. 313
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Atheroemboli/Etiology
p. 313
Atheroemboli/Etiology
Livedo reticularis
Can occur during catheter procedures:

Cardiac catheterization, angiogram
Emboli can go to:

Kidney, leading to AKI
Eye
Cutaneous vessles
livedo reticularis
Lab findings:
Eosinophilia/Eosinophiluria,
compliment,
ESR
Most accurate test:

Biopsy
Peripheral pulses
are normal in
atheroemboli
atheroemboli.
Theyre too small to
occlude vessels
such as the radial or
brachial artery.
cholesterol crystals
Source: Farshad Bagheri, MD
MTB S2CK
p. 313 314
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p. 314
Antibodies and eosinophils attack cells lining

tubules
Reaction to drugs (70%), infection, and
autoimmune disorders
Presentation: What Is the Most Likely Diagnosis?

Look for acute renal failure (rising BUN and
creatinine) with:
Fever (80%)
Rash (50%)
Arthralgias
Eosinophilia and eosinophiluria (80%)
BUN/Cr ratio < 20:1
WBC and RBC in urine
What is the most accurate test?
Wright/Hansel stain to identify eosinophiluria
Penicillins and cephalosporins

Sulfa drugs (including diuretics like furosemide and
thiazides which are sulfa derivatives)
thiazides,
Phenytoin
The medications that cause AIN
Rifampin
are the same as those that cause:
Quinolones
Drug allergy and rash
Allopurinol
Stevens-Johnson syndrome
PPI
Toxic epidermal necrolysis
Hemolysis
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Treatment
AIN usually resolves spontaneously with
stopping drugs or controlling infection
Severe disease is managed with dialysis,
which may be temporary
When creatinine continues to rise after
stopping the drug, giving glucocorticoids
(prednisone, hydrocortisone,
methylprednisolone) is the answer
MTB S2CK
p. 316
Analgesic nephropathy presents with:

ATN from direct toxicity to tubules
AIN
Membranous glomerulonephritis
Papillary necrosis
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p. 316
Papillary Necrosis
Presentation
Vascular insufficiency of kidney from inhibiting
prostaglandins
Sloughing off renal papillae

Etiology
NSAIDs or sudden vascular insufficiency
Prostaglandins dilate the afferent arteriole

NSAIDs constrict the afferent arteriole and
decrease renal perfusion
p
Asymptomatic in healthy patients
When patients are older and have underlying
renal insufficiency from diabetes and/or
hypertension, NSAIDs can tip them over into
clinically apparent renal insufficiency due to
direct toxicity to tubules
MTB S2CK
p. 316
Papillary Necrosis
Clinical presentation:
Fever, hematuria, and sudden onset flank
pain
Looks like pyelonephritis
Best initial test:

UA
Most accurate test:

CT scan
Death of cells in papillae and their dropping

off the internal structure of kidney
Occurs with underlying kidney damage:

Sickle Cell
DM
Urinary obstruction
Chronic pyelonephritis
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p. 316
Differences between Pyelonephritis

and Papillary Necrosis
Pyelonephritis
Papillary necrosis
Onset
Symptoms
Few days
Dysuria
Urine culture
CT scan
Positive
Diffuse
swollen kidney
Antibiotics, such as
ampicillin/gentamicin
or fluoroquinolones
Few hours
Necrotic material
in urine
Negative
Bumpy contour
of kidney interior
No treatment
Treatment
Treatment:
No specific therapy
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p. 317
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Glomerular Diseases
Goodpasture Syndrome
IgA Nephropathy
Postinfectious Glomerulonephritis
Alport Syndrome
Polyarteritis Nodosa
Lupus Nephritis
Amyloidosis
Nephrotic Syndrome
Tubular Disease
Glomerular Diseases
Acute
Caused by toxins
Not nephrotic
No biopsy
No steroids
or immunosuppressives
MTB S2CK
Chronic
Immune mediated
All nephrotic
Need biopsy
Often steroids,
cyclophosphamide,
mycophenolate
p. 318
Glomerular Diseases/Diagnostic Tests
All forms of glomerulonephritis have:

UA with hematuria
Dysmorphic red cells (deformed as they
squeeze through an abnormal glomerulus)
Red cell casts
Urine sodium and FENa are low
Proteinuria
The amount of
Lung + kidney involvement

No upper respiratory tract involvement
Diagnosis
Best initial test:
proteinuria is the
main difference between
glomerulonephritis and
nephrotic syndrome.
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Antiglomerular basement membrane

antibodies
Kidney biopsy in
Most accurate test:

Lung or kidney biopsy
MTB S2CK
p. 318
Goodpasture syndrome
shows linear deposits.
p. 319
Diagnosis
Anemia from hemoptysis
CXR abnormal, but not diagnostic
Treatment
Plasmapheresis
Steroids
Cyclophosphamide
MTB S2CK
p. 319
Commons.wikimedia. Used with permission
MTB S2CK
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10
IgA nephropathy (Berger disease)
MCC of acute glomerulonephritis in U.S.

Presentation: Gross hematuria 1 to 2 days
after an upper respiratory tract infection
IgA levels in 50%
Most accurate test = kidneyy biopsy
p y
No treatment: will resolve, progress to
ESRD
Steroids and ACE-inhibitors may help severe
proteinuria
Most common infection is Streptococcus

Follows throat infection or skin infection
(impetigo) by 1 to 3 weeks
Presentation
MTB S2CK
p. 319 320
Cola-colored urine
Edema (periorbital)
HTN
Oliguria
MTB S2CK
p. 320
Diagnostic Tests
1st - UA
glomerulonephritis
nd
2 - Antistreptolysin O (ASO) titers and
anti-DNAse antibody titers
Most
M t accurate
t - Biopsy
Bi
Commons.wikimedia, James Heilman, MD.

MTB S2CK
p. 320
Treatment
Management of strep infection does not
reverse glomerulonephritis
Use supportive therapies such as:
Antibiotics
A tibi ti
Diuretics to control fluid overload
<5% of those with PSGN
will progress.
MTB S2CK
p. 320
Commons.wikimedia. Used with permission
MTB S2CK
p. 320
11
Alport Syndrome
Congenital defect of collagen

Results in glomerular disease combined
with:
Definition
Systemic vasculitis of small and
medium-sized arteries
Spares lungs
Associated
A
i t d with
ith hepatitis
h
titi B
Sensorineural hearing loss

Visual disturbance from loss of collagen
fibers that hold lens of eye in place
PAN is nonspecific.
Theres no single finding
that allows you to
answer the most likely
diagnosis question.
Theres no specific therapy to reverse

this defect of type IV collagen
MTB S2CK
p. 320
MTB S2CK
p. 321
Polyarteritis Nodosa/Presentation
Polyarteritis Nodosa/Diagnostic Tests
The most common organ systems involved are:

GI
Blood tests will show:

Anemia and leukocytosis
ESR and C-reactive protein
ANCA: Not present in most cases
ANA and rheumatoid factor: Sometimes present in
low titer
Angiography
Renal, mesenteric, or hepatic artery showing
aneurysmal dilation
Biopsy
Most accurate if at symptomatic site
Abdominal pain, bleeding, nausea, and vomiting

occur
Neuro
Peripheral neuropathy or mononeuritis
mononeuritis multiplex.
multiplex.
Skin
Petechiae, purpura, ulcers, livedo reticularis
Cardiac
Stroke or MI, particularly in young person
MTB S2CK
p. 321
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p. 321
Lupus Nephritis
Treatment
Prednisone and cyclophosphamide
mortality
Treat hepatitis B when its found
SLE can give any degree of renal involvement

Normal
Mild, asymptomatic proteinuria
Membranous glomerulonephritis
Glomerulosclerosis
scars kidneys without
inflammation leading to ESRD requiring dialysis
Diagnosis
Biopsy (tells severity)
Treatment
Steroids, cyclophosphamide, mycophenolyate
MTB S2CK
p. 321 322
MTB S2CK
p. 322
12
Amyloidosis
Amyloidosis
Amyloid is an abnormal protein produced in

association with:
Myeloma
Chronic inflammatory diseases
Inflammatory bowel disease
Chronic infections
Amyloid, HIV
Most accurate test = biopsy

Apple-green birefringence with Congo
red staining
Best treatment = control underlying
disease
2nd line Treatment = melphalan and
prednisone
nephropathy,
polycystic kidneys, and
diabetes give large
kidneys on sonogram
and CT scan.
MTB S2CK
p. 322
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Amyloidosis
p. 322
Nephrotic Syndrome/Definition
Measure of the severity of proteinuria in association
with any form of glomerular disease
> 3.5 g/24 hrs
Liver can no longer increase the production of

albumin to compensate for urinary losses
Massive proteinuria leads to:
Edema (periorbital)
Hyperlipidemia
Thrombosis:
From urinary loss of natural anticoagulants protein C,
protein S, and antithrombin
MTB S2CK
p. 322
Katsumi M. Miyai, MD, PhD. Regents of the

University of California. Used with permission
MTB S2CK
p. 322
Nephrotic Syndrome/Etiology
Nephrotic Syndrome/Diagnostic Tests
MCC = diabetes and hypertension

Any of the glomerular diseases just described
Other associations are:
Cancer (solid organ): membranous
Children: minimal change disease
Injection drug use and AIDS: focal-segmental
NSAIDs: minimal change disease and
membranous
SLE: Any of them
Best initial test = urinalysis

Next best test = albumin/creatinine ratio or
24-hour urine protein collection
Most accurate test = biopsy:
MTB S2CK
p. 323
Focal-segmental
Focal segmental
Membranous
Membranoproliferative
Minimal change
Mesangial
MTB S2CK
p. 323
13
Nephrotic Syndrome/Diagnostic Tests
Nephrotic Syndrome/Treatment
By definition, nephrotic syndrome is:

Hyperproteinuria (> 3.5 g/24 hours)
Hypoproteinemia
Hyperlipidemia
Edema
Treatment
Best 1st therapy = glucocorticoids
2nd line = cyclophosphamide
ACE inhibitors or ARBs to control proteinuria
Edema managed with salt restriction and
diuretics
Hyperlipidemia is managed with statins as
you would any form of hyperlipidemia
MTB S2CK
p. 324
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End Stage Renal Disease/Definition
End Stage Renal Disease

Etiology
Presentation
Manifestations
Treatment
Kidney Transplantation
Not defined as a particular BUN or creatinine

Loss of renal function
symptoms and
laboratory abnormalities known as uremia
Uremia is defined as the presence of:
Metabolic acidosis
Fluid overload
Encephalopathy
Hyperkalemia
Pericarditis
Peritoneal dialysis and

hemodialysis are equally
effective at removing
wastes from the body.
Acute indications for dialysis

MTB S2CK
p. 324 325
Manifestations of Renal Failure

Anemia: Normocytic, normochromic
Manifestations of Renal Failure (contd)

Bleeding:
Loss of EPO
No degranulation
Hypocalcemia: Cant absorb Ca from GI tract

25-hydroxy-vitamin D
1,25-dihydroxy-vitamin D
Osteodystophy: Demineralized bones, soft/weak

Secondary hyperparathyroidism
Hyperphosphatemia: Cant excrete

PTH
release of PO4 from bones
Hypermagnesemia: Cant excrete

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p. 325
cant aggregate
Infection:
No degranulation
cant fight infection
Accelerated atherosclerosis:
Abnormal WBCs cannot clear lipid accumulation
from arteries
Pruritus:
Unclear reasoning; urea accumulating in skin
causes itching
MTB S2CK
p. 325
14
Treatment of ESRD Manifestations
Manifestations of Renal Failure (contd)

Endocrinopathy:
Manifestation
Treatment
Anemia
Erythropoietin replacement and

iron supplementation
Replace vitamin D and calcium
DDAVP increases platelet function
Dialysis and ultraviolet light
Oral binders, see Hyperphos Rx
Restriction of high Mg foods, laxatives,
and antacids
Dialysis
Dialysis, estrogen & testosterone
replacement
Women are anovulatory

Men have testosterone
erectile
dysfunction
Hyperinsulinemia and insulin resistance
Either hyper- or hypoglycemic
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Hypocalcemia
Bleeding
Pruritus
Hyperphosphatemia
Hypermagnesemia
Atherosclerosis
Endocrinopathy
p. 325
MTB S2CK
p. 325
Treatment of Hyperphosphatemia
Medications:
Calcium acetate
Calcium carbonate
Use sevelamer and
Sevelamer
lanthanum when calcium
level is high.
Lanthanum
Kidney Transplantation
Only 50% of ESRD patients will be
suitable for transplantation
The donor doesnt have to be alive or
related although these are both better
related,
HLA-identical, related donor
kidneys last 24 years on average.
Never use aluminum containing

phosphate binders. Aluminum
causes dementia.
MTB S2CK
p. 326
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Thrombotic thromobocytopenic purpura

and Hemolytic Syndrome
Survival by Method
1 year
3 years
5 years
Living, related donor
95%
88%
72%
Deceased donor
90%
78%
58%
Dialysis alone
Variable
Variable
30 40%
Diabetics on dialysis
Variable
Variable
20%
MTB S2CK
p. 326
p. 326
Different variants, same disease

TTP is associated with HIV, cancer, and
drugs (e.g., cyclosporine, ticlopidine, and
clopidogrel)
HUS is MC in children and the most
frequently tested association is E. coli
0157:H7 and Shigella
MTB S2CK
p. 326
15


Both TTP and HUS are associated with:

Intravascular hemolysis
Renal insufficiency
Thrombocytopenia
TTP also
l is
i associated
i d with:
ih
Fever
The hemolysis is visible on smear with

schistocytes, helmet cells, and fragmented
red cells
MTB S2CK
p. 326
MTB S2CK
p. 327
Thrombotic thromobocytopenic purpura and

Hemolytic Syndrome
Most cases of HUS from E. coli will resolve
spontaneously
Plasmapheresis is generally urgent in TTP
Severe HUS also needs urgent plasmapheresis
If plasmapheresis is not one of the choices
choices, use
infusions of fresh frozen plasma (FFP)
Steroids dont help
Cystic Disease
Simple versus Complex Cysts
Polycystic
y y
Kidneyy Disease
Platelet transfusion is never

the correct choice for TTP or
HUS
MTB S2CK
p. 327
Benign (Simple) vs. Malignant (Complex) Cysts

Simple Cyst
Complex Cysts
Echogenicity
Echo free
Mixed echogenicity
Walls
Smooth, thin
Irregular, thick
Demarcation
Sharp
Transmission
Good through
to back
Lower density
on back wall
Debris in cyst
MTB S2CK
p. 326
Polycystic Kidney Disease
Polycystic kidney disease (PCKD)

presents with:
Pain
Hematuria
Stones
No therapy exists to
Infection
prevent or reverse cysts
of any type.
HTN
MTB S2CK
p. 328
16
What is the MCC of death from PCKD?

a.
b.
c.
d
d.
e.
Sodium & Potassium

Disorders
Only 10-15% have cerebral
Intracerebral hemorrhage aneurysms

Stones Can occur but do not lead to death
Infection Pyelo is more common but rarely fatal
potential. Doesnt
Doesn t progress
Malignancy No malignant potential
Renal failure to RCC
MTB S2CK
Hypernatremia
Hyponatremia
Hyperkalemia
Hypokalemia
p. 328
Hypernatremia/Etiology
Hypernatremia/Etiology
Loss of free water

Examples are:
Diabetes Insipidus (DI)

High urinary volume water loss
Insufficient or ineffective ADH
Symptoms
Sweating
Burns
Fever
F
Pneumonia (insensible losses from
hyperventilation)
Diarrhea
Diuretics
MTB S2CK
p. 328
p. 328
Hypernatremia/Diagnostic Tests
Central DI
Nephrogenic DI
Definition
Loss of ADH
production
Loss of ADH
effect
Etiology
CNS disorders:
Stroke
Tumor
Trauma
Hypoxia
Infection
Lithium
Demeclocycline
Chronic kidney
disease
Hypokalemia
Hypercalcemia
p. 328 329
Sodium disorders
cause CNS problems
If uncorrected, severe hypernatremia causes

coma and irreversible brain damage
MTB S2CK
Diabetes Insipidus (DI)
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Confusion
Disorientation
Lethargy
Seizures
To distinguish DI from other causes of

hypernatremia look for:
Increased urine volume
Decreased urine osmolality
Decreased
D
d urine
i sodium
di
Increased urine volume
despite dehydration and
hyperosmolality of
blood suggests DI
MTB S2CK
p. 329
17
Diagnosing DI
Central DI vs. Nephrogenic DI

Water deprivation test
Best initial test?

Continued
high volume
dilute urine
urine volume
osmolality
Diabetes
Insipidus
Psychogenic
Polydipsia
Next best test?
ADH administration test

urine volume
osmolality
Central DI
MTB S2CK
Continued high
volume dilute urine
Nephrogenic DI
**Most
accurate test
= ADH level
NDI
CDI
p. 329
CDI
NDI
Polyuria and nocturia
Yes
Yes
Urine osmolality and sodium
Low
Low
Positive water deprivation test
Yes
Yes
Response to ADH
Yes
No
ADH level
Low
High
MTB S2CK
p. 329
Hypernatremia/Treatment
Hypernatremia/Treatment
Fluid loss:
Complications of Therapy
Cerebral edema: sodium levels brought
down too rapidly
Cerebral edema presents with
worsening confusion and seizures
Correct underlying cause of fluid loss
CDI:
Replace ADH (vasopressin also known as
DDAVP)
NDI:
Correct potassium and calcium
Stop lithium or demeclocycline
Give hydrochlorothiazide or NSAIDs for those
still having NDI despite these interventions
MTB S2CK
p. 330
Hyponatremia/Etiology
MTB S2CK
p. 330
Hypervolemia
MCC of hyponatremia with
hypervolemic state are:
Intravascular volume depletion

CHF, nephrotic syndrome, cirrhosis
CHF
Nephrotic syndrome
Cirrhosis
Increased ADH levels

Stimulated by baroreceptors
in atria and carotids
Free water reabsorption

Sodium concentration drops
MTB S2CK
p. 330
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18
Hypovolemia
Sweating
Burns
Fever
Pneumonia
Diarrhea
Diuretics
Addisons disease
Loss of adrenal function
loss of
aldosterone
Aldosterone causes Na+ reabsorption
If the body
y loses aldosterone,, it loses Na+
MTB S2CK
p. 330
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p. 331
Hyponatremia/Presentation
Euvolemic Hyponatremia
MCCs:
Hyponatremia presents entirely with CNS

symptoms:
Confusion
Lethargy
Disorientation
Seizures
Symptoms of hyponatremia
Coma
Pseudohyponatremia (hyperglycemia)
Psychogenic polydipsia
Hypothyroidism
H
th idi
Syndrome of inappropriate ADH (SIADH)
release
MTB S2CK
p. 331
Hyponatremia/Diagnostic Tests
SIADH
High urine osmolality
High urine sodium
Low uric acid level and BUN
Most accurate test is a high ADH level
MTB S2CK
p. 332
are dependent on how fast

it occurs.
MTB S2CK
p. 331
Response to Hyponatremia
Normal levels
SIADH
Urine
osmolality
Low
(< 100 mOsm/kg)
High
Urine
sodium
Low (< 20 mEq/L)
High (> 40 mEq/L)
MTB S2CK
p. 332
19
Hyponatremia/Treatment
The treatment answer isnt

based on sodium level;; its
based on the symptoms.
MTB S2CK
p. 332
Hyponatremia/Treatment
Clinical Manifestations of Hyponatremia by Severity

Degree of
hyponatremia
Specific
manifestation
Management
Mild
hyponatremia
No symptoms
Restrict fluids
Moderate
Minimal confusion
Saline and loop

diuretics
Severe
Lethargy, seizures,
coma
Hypertonic saline,
conivaptan,
tolvaptan
MTB S2CK
p. 332
Central Pontine Myelinolysis
Complications of Treatment
Goal: increase in Na is 0.5 to 1 mEq/hour (12
to 24 mEq/day)
If the sodium level is brought up to normal
too rapidly
central pontine myelinolysis
(osmotic demyelinization occurs)
MTB S2CK
p. 332
Hyperkalemia
MTB S2CK
p. 332
Hyperkalemia/Etiology
Typically defined as [K+] > 5mEq/L
Severe hyperkalemia can

stop the heart in seconds if
the level is high enough.
K > 5mEq/L
Pseudohyperkalemia
Hemolysis
Leukocytosis
Thrombocytosis
Repeat the blood
sample
MTB S2CK
p. 332
MTB S2CK
Decreased
Excretion
Renal failure
Acute or chronic
Low aldosterone state
ACE
inhibitors/ARBs
RTA IV
Drugs
Addison disease
Increased
Release from
Tissues
Cell lysis
Low insulin
Acidosis
Drugs
Beta blockers
Digoxin
Heparin
p. 333
20
Hyperkalemia/Presentation
Hyperkalemia/Diagnostic Tests
Potassium disorders interfere with muscle

contraction and cardiac conductance
Look for:
If hyperkalemia is suspected
Most urgent test:
Weakness
Paralysis when severe
Ileus (paralyzes gut muscles)
Cardiac rhythm disorders
EKG
The EKG in severe hyperkalemia shows:

Peaked T waves
Wide QRS
PR interval prolongation
Hyperkalemia does not

cause seizures.
MTB S2CK
p. 333
MTB S2CK
Hyperkalemia/Treatment
Hyperkalemia/Treatment
K > 5mEq/L
Pseudohyperkalemia?
When theres hyperkalemia and an

abnormal EKG, the most appropriate
next step is clearly calcium chloride or
gluconate.
EKG
Changes?
Yes
No treatment needed
MTB S2CK
No
Calcium chloride or
calcium gluconate
Insulin and glucose,
inhaled beta agonist
Give bicarbonate if
acidosis is the cause
Consider hemodialysis
MTB S2CK
Hypokalemia/Etiology
MTB S2CK
Shift into cells
Alkalosis
Insulin
agonists
(stimulate Na/K
ATPase
pump)
p. 334 335
p. 334
Hypokalemia/Presentation
K < 3.5 mEq/L
Very Rare
Kidney can
adjust excretion
Sodium = CNS symptoms

Hyperkalemia = muscular
and cardiac symptoms
Kayexalate
Loop diuretics
p. 334
Decreased
Intake
p. 333 334
Renal Losses
aldosterone
Conns
Volume
Cushings
Bartters
Licorice
Hypomagnesemia
RTA I and II
GI
Losses
Vomiting
Diarrhea
Laxatives
Hypokalemia leads to problems with

muscular contraction and cardiac
conduction
Potassium is essential for proper
neuromuscular contraction
Hypokalemia presents with:
Weakness
Paralysis
Loss of reflexes
MTB S2CK
Muscular abnormalities may

be so severe as to cause
rhabdomyolysis.
p. 335
21
Hypokalemia/Presentation
Hypokalemia/Treatment
EKG findings
U waves are the most characteristic finding
of hypokalemia
Other findings are ventricular ectopy (PVCs),
flattened T waves, and ST depression
No maximum rate of oral potassium

replacement
GI tract cannot absorb potassium faster than the
kidneys can excrete it
IV potassium replacement, however, can cause

a fatal arrhythmia if its
it s done too fast
You must allow time for potassium to equilibrate
into cells
Hypokalemia does not

cause seizures.
MTB S2CK
p. 335
MTB S2CK
Patient is admitted with vomiting and diarrhea from

gastroenteritis. His volume status is corrected with IV
fluids and diarrhea resolves. His pH is 7.40 and
serum bicarbonate has normalized. Despite vigorous
oral and IV replacement, his potassium level fails to
rise.
What should you do?
a.
b.
c.
d.
e.
Consult nephrology Dont consult except for procedures!

Magnesium level
Parathyroid hormone level Mg needed for PTH release
Intracellular pH level Not MCC
24-hour urine potassium level Doesnt tell you
MTB S2CK
IV potassium replacement
must be very slow.
p. 335 336
underlying cause or
change tx
p. 335
Woman with ESRD and G6PD deficiency skips dialysis

for a few weeks. She experiences a crush injury during a
MVA. She is taking dapsone and has recently eaten fava
beans.
What is the most urgent step?
a.
b
b.
c.
d.
e.
f.
g.
h.
Initiate dialysis
Must look for EKG changes 1st
EKG
Bicarbonate administration
Take 15-20min to work
Insulin administration
Kayexalate Take hours to work
Urine dipstick
Doesnt address life threatening
CPK levels
complications
Urine myoglobin
MTB S2CK
p. 336
Non anion gap metabolic acidosis (NAGMA)
Acid Base Disturbances

Renal Tubular Acidosis
Urine Anion Gap
p
Metabolic Acidosis
Metabolic Alkalosis
Respiratory Acidosis and Alkalosis
The anion gap is:

Na+ - (Cl- + HCO3- )
Normal anion gap is 6 12
The difference in + & is due to negative
charges
g on albumin
Elevated gaps means increased acids
(negatively changed) present
MTB S2CK
p. 336
22
Non anion gap metabolic acidosis
Renal Tubular Acidosis (RTA)
What causes NAGMA?
Distal RTA (Type I)

Pathology in distal tubule
Inability to generate enough bicarbonate
RTA
Diarrhea
Why is the gap normal in these?

They
y have elevated Cl ((hyperchloremic
yp
metabolic acidosis)
The anion gap increases from ingested

substances (e.g., ethylene glycol or
methanol), or organic acids (e.g., lactate) that
are anionic and drives chloride levels down
MTB S2CK
Inadequate bicarb
acid cannot be excreted
p
pH of urine is high,
g ,p
pH of blood is low
Caused by factors damaging distal tubule

Amphotericin
SLE or Sjgren syndrome
MTB S2CK
p. 336 337
p. 337
Distal RTA (Type I)/Diagnostic Tests
Distal RTA (Type I)

Symptoms to look out for?
Best initial test
Calcium oxalate kidney stones

Due to alkaline urine
Distal RTA calcifies

kidney parenchyma
(nephrocalcinosis)
MTB S2CK
No acid into the

tubule makes the
urine basic
p. 337
Urine pH (> 5.5)
Most accurate test

Infuse ammonium chloride (acid)
Normal person
excretes acid
urine pH
decreases
Distal RTA
cannot excrete acid
urine pH
remains high
Treatment
Replace HCO3
MTB S2CK
p. 337
RTA Type II/Diagnostic Tests
Proximal RTA (Type II)

Pathology in proximal tubule
Inability to absorb filtered bicarb
Caused by factors damaging proximal tubule:
Proximal RTA (Type II)

Urine pH: Low (< 5.5)
Amyloidosis
Myeloma
Fanconi syndrome
Acetazolamide
Heavy metals
MTB S2CK
p. 337
Because distal tubule absorbs bicarb normally

If you give bicarb: urine pH increases
Osteomalacia
Chronic metabolic acidosis leaches calcium
out of the bones and become soft
MTB S2CK
p. 337
23
RTA Type II/Treatment
RTA Type IV/Definition/Diagnostic Tests
Treatment:
MASSIVE doses of bicarbonate
Hyporeninemic, Hypoaldosteronism (Type IV

RTA)
Pathology in distal nephron
Problem is decreased amount or effect of
aldosterone
Because proximal tubule doesnt absorb

it normally
Thiazide diuretics
Cause volume depletion
reabsorption
MTB S2CK
bicarb
Both proximal and distal

RTA are hypokalemic.
Potassium is lost in the
urine.
p. 338
RTA Type IV/Treatment
Fludrocortisone is the
steroid with the highest
mineralocorticoid or
aldosterone-like effect.
p. 338
Proximal (Type II) Distal (Type I)
Type IV
Variable
High > 5.5
< 5.5
Blood potassium Low

level
Low
High
Nephrolithiasis
No
Yes
No
Diagnostic test
Administer
bicarbonate
Administer acid Urine salt

loss
Treatment
Thiazides
Bicarbonate
MTB S2CK
p. 338
Urine Anion Gap/Definition
Fludrocortisone
p. 338
Metabolic Acidosis
Normal anion gap (612):
NAGMA
RTA and diarrhea
Elevated anion gap (>12):
UAG
RTA
MTB S2CK
Urine pH
To promote Na+ reabsorption, K+ and H+

secretion
Positive
Caused by diabetes
Best test
High urine Na even after Na-restricted diet
Hyperkalemia
Types of Renal Tubular Acidosis (RTA)
Treatment:
Fludrocortisone
MTB S2CK
Loss of Na+, retention of K+ and H+
Negative
The anion gap is increased if there are

unmeasured anions driving bicarbonate
level down
Respiratory alkalosis from
hyperventilation
compensates for all forms
of metabolic acidosis.
Diarrhea
MTB S2CK
p. 339
24
Causes of Metabolic Acidosis with

an Increased Anion Gap
Cause
Test
Treatment
Lactate
Hypotension or
hypoperfusion
Blood lactate
level
Correct
hypoperfusion
Ketoacids
DKA, starvation
Acetone level
Oxalic acid
Ethylene glycol
overdose
Crystals on UA
MTB S2CK
Causes of Metabolic Acidosis with

an Increased Anion Gap
Cause
Test
Treatment
Formic acid
Methanol
overdose
Inflamed retina
Fomepizole,
dialysis
Insulin & fluids
Uremia
Renal failure
BUN, creatinine Dialysis
Fomepizole,
dialysis
Salicylates
Aspirin overdose Aspirin level
MTB S2CK
p. 339
Metabolic Acidosis
Alkalinize urine
p. 339
You cannot determine the etiology of metabolic

acidosis from the ABG.
Metabolic problems
always show
compensation.
Metabolic Alkalosis
Key laboratory finding?
Elevated serum bicarbonate level
Respiratory compensation?
Decreased respiratory rate
CO2 retention
respiratory acidosis
Etiology
GI loss: vomiting or nasogastric suction
aldosterone: primary, Cushing, ACTH, volume
contraction, licorice
Diuretics
Milk-alkali syndrome
Hypokalemia
Metabolic Alkalosis/Etiology
Respiratory Acidosis and Alkalosis
Arterial Blood Gas in Metabolic Alkalosis

The ABG in metabolic alkalosis will always
have:
Minute ventilation is a more precise

measure of respiratory status than
respiratory rate
Minute ventilation = RR x TV
Arterial Blood Gas in Metabolic Acidosis

The arterial blood gas (ABG) in metabolic acidosis
will always have:
Decreased pH < 7.4
Decreased pCO2 indicating respiratory alkalosis as
compensation
p
Decreased bicarbonate
MTB S2CK
p. 339
Increased pH > 7.40

Increased pCO2 (compensatory respiratory
acidosis)
Increased bicarbonate
MTB S2CK
p. 339 340
Hyperventilation may occur

with a tiny tidal volume.This
does not increase minute
ventilation.
Metabolic derangements
kill patients with cardiac
arrhythmia. They also alter
potassium levels.
MTB S2CK
p. 340
MTB S2CK
p. 340
25
Causes of Respiratory Acidosis and Alkalosis

Respiratory alkalosis
Respiratory acidosis
Decreased pCO2
Increased pCO2
Increased minute ventilation
Decreased minute ventilation
Metabolic acidosis as
Metabolic alkalosis as
Compensation
Compensation
Anemia
COPD/emphysema
Anxiety
Drowning
Pain
Opiate overdose
Fever
Interstitial lung disease
Kyphoscoliosis
Pulmonary emboli
Sleep apnea/morbid obesity
MTB S2CK
Nephrolithiasis
Etiology
Treatment
Long term Management
Metabolic Acidosis and Stone Formation
1 antitrypsin deficiency
p. 340
Nephrolithiasis/Pearls
Most common stone?

Calcium oxalate
Forms more frequently in?

Alkaline urine
Most
M t common risk
i k ffactor?
t ?
Overexcretion of calcium in urine
MTB S2CK
p. 340
46-year-old man comes to the ED with excruciating

left flank pain radiating to groin. He has some blood in
urine.
a.
b.
c.
d.
e.
Ketorolac
X-ray
Sonography Provide pain relief before diagnostic tests
Urinalysis
Serum calcium level
MTB S2CK
p. 341
Nephrolithiasis/Treatment
What is the most accurate diagnostic test for
nephrolithiasis?
a.
b.
c.
d.
e.
CT scan
X-ray 10-20% false negative. Misses uric acid stones
Sonography Less accurate
Urinalysis
y
May
ay show
s o hematuria,
e a u a, not
o spec
specific
c to
o cause
Intravenous pyelogram Requires contrast, takes hours
The best initial therapy for acute renal

colic is with:
Analgesics
Hydration
Imaging
I
i
CT noncontrast
t t
Cystine stones are
managed with surgical
removal, alkalinizing urine.
Uric acid stones are not

detectable on X-ray, but
visualized on CT.
MTB S2CK
p. 341
MTB S2CK
p. 341
26
Nephrolithiasis/Treatment
Etiology of the stone determined with:

Stone analysis
Serum calcium, sodium, uric acid, PTH,
magnesium, and phosphate levels
24-hour
24 h
urine
i ffor volume,
l
calcium,
l i
oxalate, citrate, cystine, pH, uric acid,
phosphate, and magnesium
Fat malabsorption increases
stone formation.
MTB S2CK
p. 341
Woman with her first episode of renal colic has a 1.8

cm stone in the left renal pelvis. No obstruction.
Normal BUN and creatinine.
a.
a
b.
c.
d.
e.
Wait for it to pass; hydrate and observe If < 5mm

Lithotripsy
Surgical removal If > 2cm
Hydrochlorothiazide Decreases calcium in urine
Stent placement Only releives hydronephrosis
MTB S2CK
p. 342
Nephrolithiasis
50% with kidney stones will recur over

the next 5 years
UTI gives struvite stones
(magnesium/ammonium/pho
sphate). Remove them
surgically.
MTB S2CK
p. 342
A man with a calcium oxalate stone is managed with

lithotripsy. Stone is destroyed and passes. Urinary
calcium level is increased.
Besides increasing hydration, which is most likely to
benefit this patient?
a.
b.
c.
d.
e.
Calcium restriction Can rate of oxalate stones

Hydrochlorothiazide
Furosemide Increases urinary calcium
Stent placement Only relieves obstruction
Increased dietary oxalate Can rate of oxalate stones
MTB S2CK
p. 342
Nephrolithiasis
Metabolic acidosis removes calcium

from bones and increases stone
formation
In addition, metabolic acidosis
decreases citrate levels
Citrate binds calcium, making it
unavailable for stone formation
MTB S2CK
p. 342
Urinary Incontinence
Stress incontinence
Urge incontinence
Symptoms
Older woman with

painless leakage with
coughing, laughing, or
lifting heavy objects
Sudden pain in bladder

followed immediately by
the overwhelming urge
to urinate
Test
Have patient stand

and cough; observe
for leakage
Pressure measurement
in half full bladder;
manometry
MTB S2CK
p. 343
27
Urinary Incontinence
Treatment
Stress incontinence
Urge incontinence
1. Kegel exercises
1. Bladder training
exercises
2. Local anticholinergic
therapy
1. Oxybutynin
y
y
2. Tolterodine
3. Solifenacin
4. Dariferancin
3. Surgical tightening of
urethra
2. Local estrogen
cream
3. Surgical
tightening of
urethra
MTB S2CK
Hypertension
Definition
Etiology
gy
Presentation
Diagnostic Tests
Treatment
Hypertensive Crisis
p. 343
Hypertension/Definition
Hypertension/Etiology
Systolic pressure > 140 mmHg

Diastolic pressure > 90 mmHg
Most common etiology? (95%)
Special population with lower threshold?

Diabetics
Definition of hypertension?
> 130/80
MTB S2CK
p. 343
Essential hypertension
Common secondary causes?
Renal artery stenosis

Glomerulonephritis
Coarctation of aorta
Acromegaly
Pheochromocytoma
Hyperaldosteronism
Cushing syndrome or any cause of hypercortisolism
including therapeutic use of glucocorticoids
Congenital adrenal hyperplasia
MTB S2CK
p. 343 344
Hypertension/Presentation
Typically asymptomatic
Symptoms of end organ damage:
Presentation of Secondary Hypertension

Renal artery stenosis:
Coronary artery disease

Cerebrovascular disease
CHF
Visual disturbance
Renal insufficiency
Peripheral artery disease
MTB S2CK
p. 344
Bruit is auscultated at flank and is

continuous throughout systole and diastole
Glomerulonephritis
p
Coarctation of aorta:
Upper extremity > lower extremity BP
MTB S2CK
p. 344
28
Hypertension/Diagnostic Tests
Acromegaly
Pheochromocytoma: Episodic
hypertension with flushing
Hyperaldosteronism: Weakness from
hypokalemia
Other tests to perform in hypertensive

patients
EKG
Urinalysis
Glucose
Gl
measurements
t to
t exclude
l d
concomitant diabetes
Cholesterol screening
MTB S2CK
MTB S2CK
p. 344
p. 344
Hypertension/Treatment
Hypertension/Drug Therapy
Best initial therapy?

Lifestyle modifications:
Best first drug? (all-comers)
Weight loss (*most effective*)

Sodium restriction
Dietary modification
Exercise
Tobacco cessation
Hydrochlorothiazide
If BP > 160/100?
Defines Stage 2 HTN
Start 2 medications immediately
Lifestyle modifications are

tried for 3 to 6 months
before medications are started.
MTB S2CK
p. 344 345
MTB S2CK
p. 345
Hypertension
Hypertension
If diuretics dont control BP, the most

appropriate next step in management is:
Medications for refractory hypertension:

Central-acting alpha agonists
ACE inhibitor
Angiotensin receptor blocker (ARB)
Beta blocker (BB)
Calcium-channel blocker (CCB)
Alpha methyldopa, clonidine
Peripheral-acting alpha antagonists

Prazosin, terazosin, doxazosin
Direct-acting vasodilators
Hydralazine, minoxidil
MTB S2CK
p. 345
MTB S2CK
p. 345
29
Hypertension/Compelling Indications
Hypertensive Crisis
If this is in the history
This is the best initial therapy
Coronary artery disease
BB, ACE, ARB
Diabetes mellitus
ACE, ARB
Benign prostatic
Alpha blockers
Defined as HTN with SYMPTOMS

Confusion
Blurry vision
Dyspnea
Chest
Ch t pain
i
hypertrophy
Depression and asthma
Avoid BBs
Hyperthyroidism
BB first
Osteoporosis
Thiazides
MTB S2CK
p. 345
MTB S2CK
p. 345 346
Hypertensive Crisis
The best initial therapy?

Labetolol or nitroprusside
2nd line agents?
Enalapril
CCBs:
Diltiazem
Verapamil
Esmolol
MTB S2CK
p. 346
30
Stroke
Definition
Etiology
Presentation
Diagnostic Tests
Treatment
Neurology
Conrad Fischer, MD
New York City
Stroke/Definition
Stroke/Etiology
Sudden onset neurological deficit

Death of brain tissue
3rd most common cause of death in the
USA
Risk
Ri k ffactors
t
Bleeding (15%)
Blockage of flow (85%)
Hypertension
Diabetes
Hyperlipidemia
Tobacco
MTB S2CK
Thrombosis
Embolus
Heart
H t
Atrial fibrillation
Valvular heart disease
DVT via Patent foramen ovale
Carotid stenosis
p. 273
MTB S2CK
Stroke/Presentation
p. 273
Stroke/Presentation
Middle cerebral artery (MCA)

>90% of all strokes
Weakness or sensory loss
Opposite (contralateral) side from stroke
Contralateral homonymous hemianopsia

Eyes look toward the side of lesion
Aphasia
If stroke on same side as speech center
On left in 90%
MTB S2CK
p. 273
MTB S2CK
p. 273
Stroke/Presentation
Stroke/Diagnostic Tests
Anterior cerebral artery (ACA)
Best initial test for stroke is...

CT scan of the head
With or without contrast?...
Without contrast
Most accurate test for stroke is...
MRI
Personality/cognitive defects (e.g., confusion)

Urinary incontinence
Leg > arm weakness
Posterior cerebral arteryy (PCA)

(
)
Loss of consciousness
Ipsilateral (same side) sensory loss of face, 9th,
and 10th CNs
Contralateral sensory loss of limbs
Limb ataxia
MTB S2CK
p. 274
MTB S2CK
p. 274
Stroke/Diagnostic Tests
Stroke/Treatment
CT
Done first
Excludes
hemorrhage
Prior to treatment
Nonhemorrhagic
Best initial therapy when LESS than 3 hours since
onset...
Thrombolytics
More than 3 hours since onset...

Aspirin
If the patient is already on aspirin...

ADD dipyridamole
OR
SWITCH to clopidogrel
Source: Mohammad Maruf, MD
MTB S2CK
p. 274
MTB S2CK
p. 274 275
Stroke/Treatment
Stroke/Evaluation of Causes & Treatment
Hemorrhagic
Best initial
treatment...
Nothing
Echocardiogram
Damaged valves?
Surgical replacement
Thrombi?
Heparin followed by warfarin to INR of
2-3
MTB S2CK
p. 275
MTB S2CK
p. 275
Electrocardiogram
Atrial fibrillation or atrial flutter
Warfarin as long as arrhythmia persists
no P wave
A fib
P wave
NSR
Source: J Heuser
Source: Kjetil Lenes
Holter monitor
Holter monitor
Detect arrhythmias
If initial EKG is normal: Do Holter monitor
Detect atrial arrhythmias
G t sensitivity
Greater
iti it th
than EKG
MTB S2CK
Source: Macro987
p. 275
Carotid duplex ultrasound

Carotid stenosis is a frequent cause of
emboli
Surgery?
Symptomatic
S
t
ti and
d >70%
70% stenosis
t
i
Endarterectomy superior to carotid
angioplasty
Stroke
Patient presents with:
Sudden onset unilateral weakness
Facial droop
+/- Speech deficits
Best Initial Test:

Head CT without contrast
No acute process
Likely ischemic stroke

MTB S2CK
Acute hemorrhage
Likely hemorrhagic stroke
p. 275
Stroke
< 3 hours from

onset of
symptoms
Treatment:
Consider TPA, if
no hx of bleeding
MTB S2CK
Stroke
Likely ischemic stroke
p. 274 275
> 3 hours from

onset of
symptoms
Likely hemorrhagic stroke

Symptoms last
< 24 hours,
then resolve
Treatment:
Aspirin
ADD dipyridamole or
switch to clopidogrel
if already on aspirin
Transient
ischemic
attack
Treatment:
Control blood pressure
Optimal systolic BP is between 140-160 mmHg
If > 170 mmHg,
mmHg use nicardipine,
nicardipine enalaprilat,
enalaprilat or labetalol
Reverse anticoagulation
If patient is on warfarin
fresh frozen plasma, vitamin K
If patient is on heparin
protamine sulfate
Perform further studies

to asses etiology
Stroke
Goals!
Diabetes
Headache
Hemoglobin A1C <7%
Types
Physical
y
Examination
Diagnostic Tests
Treatment
Trigeminal & Postherpetic Neuralgia
Hypertension
BP <140/90 mmHg
LDL
<100 mg/dL if carotid stenosis is the cause
Tobacco smoking
Must stop!
MTB S2CK
p. 276
Headache
Headache/Tension Headache
Types
Tension
Migraine
Cluster
Giant cell (temporal) arteritis
Pseudotumor cerebri
Constant pressure
Mild to moderate pain, mainly bilateral
Lasts 4-6 hours
Physical exam
Nothing!
Diagnostic tests
None (all normal)
Treatment
NSAIDs and other analgesics
MTB S2CK
p. 276
MTB S2CK
p. 276
Headache/Migraine
Headache/Migraine
Visual disturbance
Photophobia aura
May be related to:
Food/menses
Precipitated by emotions
Ph i l exam
Physical
Rare cases: aphasia, numbness, dysarthria,
weakness
Diagnostic tests
All normal
Scan head the first time, then stop
Treatment
Abortive
MTB S2CK
p. 276
Triptans or ergotamine
Prophylactic (preventive)
> 3 migraines/month
Propranolol
Other preventive medications:

SSRIs
Botulinum toxin injections
MTB S2CK
p. 277
Headache/Cluster Headache
Headache/Cluster Headache
Symptoms
Treatment
Abortive
Triptans
Ergotamine
100% oxygen
Preventive
Verapamil
Lithium
Prednisone
Frequent, short duration, high intensity
Men 10X MORE than women!!!

Red,, tearing
g eye
y with rhinorrhea
Horner syndrome occasionally
Diagnostic tests
Scan head first time
No need for subsequent imaging with recurrences
MTB S2CK
p. 276
MTB S2CK
Headache/Giant Cell (Temporal) Arteritis
p. 277
Headache
Headache
Symptoms
Visual disturbance, jaw claudication
Muscle pain, fatigue, and weakness
Physical exam
Visual loss, temporal area tenderness
Diagnostic tests
Elevated ESR
Most accurate test?
Biopsy!
Bilateral band-like
pressure
Lasts 4-6 hours
Normal P/E
Tension
Headache
H
d h
Treatment
NSAIDs
Acetaminophen
Treatment
p. 276
Migraine
Treatment
Avoid triggers
NSAIDs
5-HT1 agonists
3 attacks/month
Prednisone
MTB S2CK
+/- Aura, photophobia

Related to
food/emotions/menses
Rare: aphasia,
numbness, dysarthria
MTB S2CK
p. 389.4
Prophylaxis
Propranolol
Sodium valproate
Episodic pain
Unilateral periorbital
intense pain
Lacrimation
Eye-reddening
Nasal stuffiness
Lid ptosis
Cluster
Headache
Acute Treatment
Sumitriptan
Octreotide
Oxygen
Prophylaxis
Verapamil
Prednisone
Sodium valproate
Headache/Pseudotumor Cerebri
Cranial Nerve 6 Palsy
Associated with
Obesity
Oral contraceptives
Vitamin A toxicity
Mimics brain tumor: nausea & vomiting
Physical exam
Papilledema
Diplopia: 6th CN (abducens) palsy
MTB S2CK
p. 276
Diagnostic tests
CT or MRI
Normal
Done to exclude intracranial mass
Lumbar puncture
Increased pressure
CSF
Normal
Treatment
Acetazolamide +/- furosemide
Weight loss
Steroids
Repeated lumbar puncture
Ventriculoperitoneal shunt
MTB S2CK
p. 277
MTB S2CK
p. 277
Headache/Trigeminal Neuralgia
Headache/Trigeminal Neuralgia
Idiopathic
5th CN
Severe, overwhelming knife-like facial pain
Precipitated by
Chewing
Touching the face
Pronouncing words in which the tongue
strikes the back of front teeth
Treatment
Carbamazepine or oxcarbazepine
Baclofen
Lamotrigine
Surgical decompression when failing
medications
MTB S2CK
p. 278
MTB S2CK
p. 278
Headache/Postherpetic Neuralgia
Residual pain
following resolution
of herpes zoster
(shingles) vesicular
lesions
Shingles
Shi l iis a painful
i f l
dermatomal rash
that occurs in 15%
with prior varicella
zoster (chickenpox)
infection
Acute Treatment:
Acyclovir, famciclovir, or valacyclovir
reduce the incidence of pain
Steroids do not help
MTB S2CK
p. 278
Shingles rash caused by herpes zoster virus. Source: NIAID
MTB S2CK
p. 278
Prevention of Herpes Zoster (Shingles)
Treatment
Zoster vaccine
Everyone > 60
High dose varicella vaccine
Decreases reactivation of varicella into
zoster
t
Tricyclic antidepressants (amitriptyline)

Gabapentin or pregabalin
Carbamazepine
Phenytoin
Topical capsaicin
Antiepileptic medications
Have some beneficial effect in neuropathic pain
(e.g., postherpetic neuralgia or peripheral
neuropathy)
None work in > 50% to 70%

MTB S2CK
p. 278
MTB S2CK
p. 278
Classification of Seizures
Seizures
Classification
Diagnostic Tests
Treatment
Management
Partial
Absence (petit mal)
Generalized (tonic-clonic)
Status
S
a us epilepticus
ep ep cus
MTB S2CK
p. 279
Partial Seizures
Absence Seizures
Focal to one part of the body
Also referred to as petit mal

Consciousness briefly impaired
Patient often remains upright and often
appears normal or stares into space
Absence
Ab
seizures
i
occur more often
ft in
i
children
Limited to arm or leg
Partial seizures can be:

Simple
Intact consciousness
Complex
MTB S2CK
p. 279
MTB S2CK
p. 280
Generalized Seizures
Generalized Seizures/Causes
Also referred to as tonic-clonic

Generalized seizure
Varying phases
Muscular rigidity (tonic)
Followed by jerking of muscles for
several minutes (clonic)
MTB S2CK
p. 280
Hyponatremia or hypernatremia
Hypoxia
Hypoglycemia
Any CNS infection
Encephalitis, meningitis, abscess
Any CNS anatomic abnormality
Trauma, stroke, tumor
MTB S2CK
p. 278
Generalized Seizures/Causes
Seizures/Diagnostic Tests
Electroencephalogram (EEG)
The right answer after the other tests
are done
If CT or MRI are normal
No
N point
i t iin EEG if there
th
is
i a clear
l
metabolic, toxic, or anatomic defect
causing the seizure
Hypocalcemia
Uremia (elevated creatinine)
Hepatic failure
Withdrawal
Alcohol, barbiturate, and
benzodiazepine
Cocaine toxicity
Hypomagnesemia
(rare)
MTB S2CK
p. 278
MTB S2CK
p. 279
Delerium, Stupor, and Coma
Treatment of Status Epilepticus
Altered consciousness
Unresponsiveness to stimuli
From metabolic, toxic, and CNS infections
Also called
Confusion
Difficulty
Diffi lt with
ith arousal
l
Obtundation
When severe enough, a seizure occurs
Confusion is to coma and seizure,
as angina is to myocardial infarction
The only seizure treatment that is clear

Benzodiazepine
Lorazepam
Diazepam intravenously
MTB S2CK
p. 279
MTB S2CK
p. 279
If seizure persists...
Phenytoin or fosphenytoin
Fosphenytoin = phenytoin efficacy
Fosphenytoin has fewer adverse effects
1. Benzodiazepines did NOT work

2. Fosphenytoin did NOT work
3. Use phenobarbital
Ph
Phenytoin
t i
Hypotension and AV block
Fosphenytoin
No BP or cardiac effect
Can be given more rapidly
MTB S2CK
p. 279
MTB S2CK
p. 279
What if barbiturates do NOT work?
To summarize...
1. Benzodiazepine
2. Fosphenytoin
3. Phenobarbital
4. General anesthesia
1. Neuromuscular blocking agents allow intubation:

Succinylcholine
Vecuronium
Pancuronium
2. General anesthesia
Midazolam or propofol
Place on ventilator before propofol, which can
stop breathing
MTB S2CK
p. 278
MTB S2CK
p. 280
Epilepsy Treatment/Indications
Choice of Antiepileptic Drugs
Antiepileptic drugs
Not long term for single seizure
When should you start after a single
seizure?
Presentation
P
t ti in
i status
t t epilepticus
il ti
Abnormal EEG
Family history of seizures
MTB S2CK
p. 280
Status epilepticus treatment is clear

Epilepsy long-term treatment is not clear
No medication is clearly superior to the others
Phenytoin, valproic acid, and carbamazepine all
have nearly equal efficacy
Gabapentin,
Gabapentin topiramate,
topiramate lamotrigine,
lamotrigine
oxcarbazepine, or levetiracetam
Ethosuximide is the best therapy for absence
seizures
You cannot be asked to choose between them
based on efficacy
MTB S2CK
p. 280
Choice of Antiepileptic Drugs
Discontinuance of Antiepileptic Medication
If not controlled with single agent, an

alternate medication should be tried
If still not controlled, add a second drug
If multiple medications do not work:
Surgery!
Wait until seizure-free for 2 years
MTB S2CK
p. 280
38-year-old man evaluated for seizures achieves partial

control with second medication. He drives to work daily.
What do you do about his ability to drive?
a. Confiscate his license Rules vary state to state
Cannot
b. Allow him to drive if he is seizure-free for 1 year prevent
c. Allow him to drive as long as his seizure history is
noted
t d on hi
his lilicense Rules vary state to state
d. Recommend that he find an alternate means of
transportation
e. Do not let him leave the office unless he is picked up by
someone; no further driving Cannot incarcerate
f. Allow him to drive as long as he is accompanied
Being accompanied does not prevent seizures
MTB S2CK
Sleep deprivation EEG:

The best way to detect possibility of
recurrence
Elicits abnormal activity with more
sensitivity
This is NOT a 100% sensitive test!
MTB S2CK
p. 281
Subarachnoid
Hemorrhage
Definition/Etiology
Diagnostic Tests
Treatment
p. 281
10
Subarachnoid Hemorrhage
Circle of Willis
Rupture of aneurysm
Usually in Circle of
Willis (anterior)
Aneurysms found in
2% of autopsies
Majority never
rupture
Cause of rupture not
clear
MTB S2CK
p. 281
MTB S2CK
p. 281
Subarachnoid Hemorrhage/Diagnosis

Look for...
How does SAH differs from meningitis?

Very sudden in onset
Sudden onset of severe headache with

meningeal irritation (stiff neck, photophobia)
and fever!
Loss of consciousness in 50%

Sudden increase in intracranial pressure
Focal neurological complications occur in 30%
MTB S2CK
p. 281
MTB S2CK
p. 281

CT without contrast
(95% sensitive)
Lumbar puncture
showing blood
LP necessary only for 5% with falsely

negative CT
CSF in SAH has both increased WBCs and
RBCs
WBC can mimic meningitis
Ratio of WBCs to RBCs will be normal in
SAH
Source: Saba Ansari, MD
MTB S2CK
p. 282
MTB S2CK
p. 282
11
WBC count > normal 1:500?
Angiography
Determines site of aneurysm
Guides lesion repair
MRA
Diagnosis based on...
CT and sometimes LP
Only angiography can tell location
Suspect meningitis
Xanthochromia
Yellow CSF
From breakdown red cells in CSF
EKG
May show large or inverted T waves

Suggestive of myocardial ischemia
Cerebral T waves
From excessive sympathetic activity
MTB S2CK
p. 282
MTB S2CK
p. 282
Subarachnoid Hemorrhage/Treatment
Nothing reverses hemorrhage

Nimodipine (calcium-channel blocker)
prevents subsequent ischemic stroke
MTB S2CK
p. 282
MTB S2CK
p. 283
Embolization (coiling)
Catheter clogs up site of bleeding
Prevents repeated hemorrhage
Interventional neuroradiologist places
platinum wire
p
Embolization superior to surgical clipping for
survival and complications
Ventriculoperitoneal shunt
SAH associated with hydrocephalus
Shunt only if hydrocephalus develops
MTB S2CK
p. 283
MTB S2CK
p. 283
12
Seizure prophylaxis
Phenytoin is not routine
If the question asks Which of the
following is most likely to decrease
mortality? ...
mortality?
Consultation is only right when you want

to do a procedure that isnt given as a
choice.
Phenytoin is not the answer
MTB S2CK
p. 283
MTB S2CK
A woman in the ED with a severe headache one day

prior to admission. Temp 103 F, nuchal rigidity &
photophobia. Head CT is normal.
LP CSF WBCs: 1,250 RBCs: 50,000
Whats the next step?
Spine Disorders
Anterior Spinal Artery Infarction
Subacute Combined Degeneration of the Cord
Spinal Trauma
Brown Squard Syndrome
Syringomyelia
Angiography
g g p y For location of SAH, this is not SAH
50 000 RBC should
50,000
h ld only
l
Ceftriaxone and vancomycin
give 50-100 WBCs
Nimodipine Prevent SAH stroke 1,250 WBCs is infection
Embolization Permanent SAH fix
Surgical clipping Worse alternative to embolization
Useless for blood
Repeat CT scan with contrast
Neurosurgical consultation Dont consult unless you
REALLY want a procedure
MTB S2CK p. 283
not listed
a.
b.
c.
d.
e.
f.
g.
Anterior Spinal Artery Infarction
Loss of all function except posterior column

Position and vibratory sensation intact
Flaccid paralysis below the level of infarction
Loss of deep tendon reflexes (DTRs) at level of
infarction
Evolves into spastic paraplegia several weeks later
Loss of pain and temperature
Extensor plantar response
p. 284
Subacute Combined Degeneration

of the Cord
B12 deficiency or neurosyphilis

Position & vibratory sensation lost
Everything else intact
No specific therapy
MTB S2CK
p. 284
MTB S2CK
p. 284
13
Spinal Trauma
Brown Squard Syndrome
Acute limb weakness and/or sensory

disturbance
Below level of injury
Severity in proportion to degree of injury
Sphincter
p
function impaired
p
Loss of DTRs at level of injury
Followed by hyperreflexia below level of
trauma
Treat with glucocorticoids
Unilateral hemisection of spinal cord

Due to injury
Knife cutting half the cord
On physical exam...
MTB S2CK
p. 284
Ipsilateral
Motor
Position
Vibration
Contralateral
Pain
Temperature
No treatment
MTB S2CK
p. 284
Syringomyelia
Syringomyelia
Fluid-filled, dilated central canal of spinal

cord
Widening bubble or cavitation damages
neural fibers passing near center of spine
Caused by tumor or severe trauma to spine

Look for:
Loss of pain & temperature bilaterally
Across the upper back and both arms
Look for the phrase capelike
capelike distribution
distribution
Loss of reflexes
Muscle atrophy
MTB S2CK
p. 285
MTB S2CK
p. 285
Syringomyelia
The most accurate
test is...
MRI
CNS Abscess & Disease

Brain abscess
Neurocutaneous diseases
The best treatment

is...
Surgical
Removal of tumor
Drain cavity
Source: Mohammad Maruf, MD.
MTB S2CK
p. 285
14
Brain Abscess/Definition & Etiology
Brain Abscess/Presentation
Collection of infected material in brain

parenchyma
Acts as space-occupying lesion
Spreads from contiguous infection
Starts in sinuses,, mastoid air cells,, or otitis
media
Any bacteremia
Headache, nausea, vomiting, fever,

seizures, and focal neurological findings
No way to distinguish brain abscess
from cancer without a biopsy
Cancer gives fever
fever, too
Pneumonia and endocarditis cause bacteremia,

which can lead to a brain abscess
MTB S2CK
p. 285
MTB S2CK
p. 286
Brain Abscess/Diagnostic Tests
Brain Abscess/Diagnostic Tests

Head CT or MRI
Brain biopsy
Scan shows a ring or

contrast-enhancing
lesion
Surrounding edema
Mass effect
Cancer and infection
are indistinguishable
based on imaging
study alone
Source: Nishith Patel
MTB S2CK
p. 286
Source: Nishith Patel
MTB S2CK
p. 286
Brain Abscess/Microbiology
Brain Abscess/Treatment
Biopsy is essential
Only biopsy distinguishes abscess from cancer
Only way to know sensitivity of organism
Abscesses can be...
Staphylococci, streptococci, Gram-negative bacilli,
and anaerobes
Frequently mixed (polymicrobial)
Treat for...
6 to 8 weeks intravenously
Followed by 2 to 3 more months orally
Empiric therapy
Penicillin + metronidazole +
ceftriaxone (or cefepime)
Vancomycin (alternative to penicillin)
Use vancomycin if theres been recent
neurosurgery
MTB S2CK
p. 286
MTB S2CK
p. 287
15
Neurocutaneous Diseases
Tuberous Sclerosis
Tuberous sclerosis
Neurofibromatosis (von Recklinghausen
Disease)
Sturge-Weber Syndrome
Neurological abnormalities
Seizures, slowly progressive mental deterioration
Skin
Adenoma sebaceum (reddened facial nodules)
Shagreen patches (leathery plaques on trunk)
Ash leaf (hypopigmented) patches
MTB S2CK
p. 287
Retinal lesions
Cardiac rhabdomyomas
No specific treatment
Control seizures
MTB S2CK
p. 287
Neurofibromatosis
(von Recklinghausen Disease)
Neurofibromatosis
(von Recklinghausen Disease)
Neurofibromas: soft,
flesh-colored lesions
attached to peripheral
nerves
8th CN tumors
Cutaneous
hyperpigmented lesions
(caf au lait spots)
Meningioma and gliomas
No specific treatment
Lesions affecting 8th CN may require
surgical decompression to preserve
hearing
Source: Mohammad Maruf, MD.
MTB S2CK
p. 287
MTB S2CK
p. 287
Sturge Weber Syndrome

Port-wine stain of face
Seizures
CNS
Homonymous hemianopsia
Hemiparesis
Mental subnormality
Skull X-ray
Calcification of angiomas
No treatment
Control seizures
MTB S2CK
Movement Disorders Part 1

Essential Tremor
Parkinsonism
Restless Leg Syndrome
Huntington Disease
Tourette Disorder
Multiple Sclerosis
p. 288
16
Essential Tremor
Essential Tremor
Occurs at both rest and intention (i.e., reaching for

things)
Tremor greatest in hands, but can affect head
Affects some manual skills
Handwriting or use of computer keyboard
Caffeine makes it worse

Treat with propranolol
Tremor at rest and exertion improved with a drink of

alcohol is key to diagnosis
MTB S2CK
p. 288
Parkinsonism/Definition
Parkinsonism/Etiology
Head trauma from boxing

Use of antipsychotic medications
Loss of substantia nigra

Decrease in dopamine
Movement disorder
Tremor and gait disturbance
Thorazine
Encephalitis
Reserpine
Metoclopromide
No test for parkinsonism

Diagnosis is entirely on clinical presentation
MTB S2CK
p. 288
Parkinsonism/Presentation
MTB S2CK
p. 288
Pill Rolling Tremor
Look for 50-60 (or older) with...

Tremor
Muscular rigidity
Bradykinesia (slow movements)
Shuffling gait with unsteadiness on turning
Tendency
T d
to
t fall
f ll
Cogwheel rigidity (slowing of movement on passive
flexion or extension of extremity)
Facial expression limited (hypomimia)
Writing is small (micrographia)
MTB S2CK
p. 289
17
Parkinson Facies
Parkinsonism/Presentation
Postural instability or orthostatic hypotension
Inability of pulse and BP to reset
Lightheadedness when getting up from
seated position
The most frequent Parkinsonism question is:

Treatment
Know the drugs!
MTB S2CK
p. 289
Parkinsonism/Treatment
Mild disease
Anticholinergic medications relieve tremor
and rigidity
Benztropine and trihexyphenidyl
Adverse effects
Dry mouth
Worsening prostate hypertrophy
Constipation
More frequent in older patients
Mild disease
Amantadine
Increases release of dopamine from
substantia nigra
Definitely
y the answer in older patients
p
((> 60))
intolerant of anticholinergic medications
MTB S2CK
p. 289
MTB S2CK
p. 289
Severe disease
Inability to care for themselves, orthostatic
Dopamine agonists
Pramipexole
Ropinirole
Bromocriptine and cabergoline are older
agents
Infrequent use because of adverse effects
Severe disease
Levodopa/carbidopa
Single most effective medication
Associated with on/off phenomena
Episodes of insufficient dopamine (off)
( off )
characterized by bradykinesia
The on effect is too much dopamine
resulting in dyskinesia
MTB S2CK
p. 289
MTB S2CK
p. 289
18
Severe disease
COMT inhibitors (tolcapone, entacapone)
Extends duration of levodopa/carbidopa
Blocks metabolism of dopamine
Used only with levodopa/carbidopa
Use when there are on/off phenomena to
even out dopamine level
When response to therapy is inadequate
Severe disease
MAO inhibitors (rasagiline, selegiline)
MTB S2CK
p. 289
As single agent or an adjunct to levodopa/carbidopa

Block metabolism of dopamine
Deep brain stimulation

Electrical stimulation
Highly effective in some patients
MTB S2CK
p. 289
Spasticity
70-year-old man with extremely severe
parkinsonism comes to ED with psychosis and
confusion developing at home. Hes maintained on
levodopa/carbidopa, ropinirole, and tolcapone.
Whats the most appropriate next step in
management?
a.
b.
c.
d.
e.
MTB S2CK
Dontt stop meds!

Don
Stop levodopa/carbidopa Severe Parkinsonism

Start clozapine
Stop ropinirole Dont stop meds severe parkinsonism
Stop tolcapone Dont stop meds severe parkinsonism
Start haloperidol More adverse effects than clozapine
p. 290
Painful, contracted muscles

From damage to CNS
Often associated with MS
No single treatment always effective
Baclofen and tizanadine (central-acting
alpha agonist) may work
MTB S2CK
p. 290
Restless Legs Syndrome
Huntington Disease (HD)
Hereditary disease
CAG trinucleotide repeat sequences on
chromosome 4
Uncomfortable sensation in legs

Creepy and crawly at night
Bed partner who is being kicked at night
Discomfort worsened by caffeine
Relieved by moving legs
Treat with dopamine agonists (e.g.,
pramipexole)
MTB S2CK
p. 290
MTB S2CK
p. 291
19
Huntington Disease/Presentation
Huntington Disease

HD is the answer when you see...
Choreaform movement disorder (dyskinesia)
Dementia
Behavior changes
Irritability, moodiness, antisocial behavior
Onset between 30 - 50
Often with family history of HD
Diagnosis
Symptom triad
Movement
Memory
Mood
MTB S2CK
p. 291
Genetic testing >99% accurate
MTB S2CK
p. 291
Huntington Disease
Tourette Disorder
Treatment
No treatment can reverse HD
Dyskinesia treated with tetrabenazine
Psychosis treated with haloperidol or
quetiapine
ti i
Idiopathic disorder
Vocal tics, grunts, and coprolalia
Motor tics (sniffing, blinking, frowning)
Obsessive-compulsive behavior
Treat with neuroleptics
e.g. Fluphenazine, clonazepam, pimozide
ADHD drugs
Methylphenidate
MTB S2CK
p. 291
MTB S2CK
p. 291
Multiple Sclerosis
Multiple Sclerosis/Presentation
Idiopathic disorder
Exclusively CNS (brain and spinal cord)
More common in white women living in
colder climates

Look for:
Multiple neurological deficits of CNS
Affects any aspect of CNS
Most common
presentation:
Blurry vision
Visual disturbance
from optic neuritis
MTB S2CK
p. 291
MTB S2CK
p. 291
NEUR_02_19
20
Multiple Sclerosis/Presentation
Multiple Sclerosis/Diagnostic Tests
After optic neuritis, the most common abnormalities

are motor and sensory
Other findings
MRI: Best initial AND Most accurate test
Fatigue
Spasticity and hyperreflexia
Cerebellar deficits
Least common findings

Cognitive defects
Dementia
Sexual dysfunction
Source: Saba Ansari, MD
MTB S2CK
p. 292
MTB S2CK
p. 292
Multiple Sclerosis/Diagnostic Tests
Multiple Sclerosis/Treatment
Lumbar puncture: CSF

Mild elevation in protein
< 50 - 100 WBCs
The best initial therapy for acute

exacerbations of MS...
High-dose steroids
Oligoclonal bands: Found in 85% of MS

Oligoclonal bands: Not specific to MS
Oligoclonal bands are the answer in 3% - 5% with

equivocal (nondiagnostic) MRI
MTB S2CK
p. 292
MTB S2CK
p. 292
Drugs that prevent relapse and progression

Glatiramer (copolymer1)
Beta-interferon
Natalizumab
Mitoxantrone
Fingolimod
Dalfampridine
Azathioprine and cyclophosphamide (rarely
used)
A new MS treatment is started.

MRI shows new, multiple white matter
hypodense lesions.
What is it?
Progressive
g
multifocal
leukoencephalopathy (PML)
What is the cause?
Natalizumab
MTB S2CK
p. 292
MTB S2CK
p. 293
21
Amyotrophic Lateral Sclerosis (ALS)
Movement Disorders Part 2

Amyotrophic Lateral Sclerosis
Charcot Marie Tooth Disease
Peripheral Neuropathy
Facial Nerve Palsy
Guillain Barr Syndrome
Myasthenia Gravis
Exclusively a loss of upper and lower

motor neurons
Idiopathic
MTB S2CK
p. 293
Amyotrophic Lateral Sclerosis (ALS)

Look for...
Weakness starting in 20s to 40s
Combination of upper and lower motor neuron loss
Initial presentation...
Difficulty
Diffi lt chewing
h i and
d swallowing
ll i
Decrease in gag reflex
Pooling of saliva in pharynx and weak cough
Frequent episodes of aspiration
Death in patients within 3 to 5 years after diagnosis
Most commonly due to respiratory failure
MTB S2CK
p. 293
Kinetic Tremor
Presentation of Amyotrophic Lateral Sclerosis

Upper Motor Neurons
Lower Motor Neurons
Weakness
Weakness
Spasticity
Wasting
Hyperreflexia
Fasciculations
Extensor plantar responses
MTB S2CK
p. 293
Fasciculations
22
Amyotrophic Lateral Sclerosis/Diagnostic Tests
Amyotrophic Lateral Sclerosis/Treatment
Electromyography
Riluzole
Reduces glutamate buildup in neurons
Delays progression
Baclofen
Treats spasticity
CPAP and
d BiPAP
Help respiratory difficulties secondary to muscle
weakness
Tracheostomy
Maintenance on ventilator necessary when disease
advances
Loss of neural innervation in multiple

muscle groups
CPK levels
MTB S2CK
p. 293
MTB S2CK
p. 293
Charcot Marie Tooth Disease
Peripheral Neuropathy
Genetic disorder
Lose both motor and sensory innervation
MCC: Diabetes mellitus

Other causes: uremia, alcoholism, and
paraproteinemias (e.g., MGUS)
Distal weakness & sensory loss

Wasting in legs
Decreased DTRs
Tremor
Pregabalin, gabapentin
Foot deformity with high arch common (pes cavus)

Legs look like inverted champagne bottles
Most accurate test: Electromyography
No treatment
MTB S2CK
p. 294
Most seizure medications effective in some people
Phenytoin
Carbamazepine
Lamotrigine
MTB S2CK
p. 294
Specific Peripheral Nerve Neuropathies
Specific Peripheral Nerve Neuropathies
Nerve
Precipitating event
Presentation
Nerve
Precipitating event
Presentation
Ulnar nerve
Biker, pressure on palms of

hands, medial elbow trauma
Tibial
nerve
Worsens with walking
Pain/numbness in
ankle & sole of foot
Radial nerve
pp arm,
Pressure on inner/upper
use of crutches, Saturday night
palsy (falling asleep on arm)
Wasting of
hypothenar
eminence,
4th/5th digit pain
p
Wrist drop
Peroneal
nerve
High boots, pressure on the

back of knee
Weak foot with

decreased
dorsiflexion and
eversion
Lateral
cutaneous n.
of the thigh
Obesity, pregnancy, sitting with

crossed legs
Pain/numbness
of outer aspect
of thigh
Median
nerve
Typists, carpenters,
working with hands
Thenar eminince,
pain/numbness
in 1st 3 fingers
MTB S2CK
p. 294
MTB S2CK
p. 294
23
Facial (Seventh Cranial) Nerve Palsy
Also known as Bells palsy

Mostly idiopathic
Some identified causes
Paralysis of entire side of face

Stroke paralyzes only lower half of face
Upper half of face innervate from both cerebral
hemispheres
Lyme, sarcoidosis, herpes zoster, and

tumors
Look for statement the face feels stiff

or pulled to one side
MTB S2CK
p. 294
Difficulty closing eye

If they can wrinkle forehead on affected side worry
about stroke
Cannot wrinkle forehead = Bell's palsy!
MTB S2CK
p. 295
Hyperacusis
Sounds are extra loud
7th CN supplies stapedius muscle
Acts as a shock absorber on ossicles of
middle ear

Electromyography and nerve
conduction studies
But...no test is usually done
Taste disturbance
7th CN supplies sensation of taste to anterior
two-thirds of tongue
MTB S2CK
p. 295
MTB S2CK
p. 295
The best initial therapy is...

Prednisone
But...
60% of patients have full recovery even
without treatment
Acyclovir does not help
MTB S2CK
p. 278
38-year-old with pain near his ear followed by

weakness of one side of his face. Both upper and
lower parts of face are weak. Sensation is intact.
What is the most common complication?
a.
b.
c.
d.
e.
f.
Corneal ulceration
Aspiration pneumonia Gag reflex and cough are normal
Sinusitis Nasal discharge & face pain
Otitis media Ear pain, decreased hearing
Deafness Sounds are actually extra loud
Dental caries Cavities do not paralyze your face!
MTB S2CK
p. 295
24
Acute inflammatory polyneuropathy

Autoimmune damage of multiple peripheral nerves

Look for:
Weakness of legs that ascends from feet
Moves toward chest
Loss of DTRs
Some
S
have
h
mild
ild sensory di
disturbance
t b
Respiratory muscle weakness
No CNS involvement
Circulating antibody attacks myelin sheaths of
peripheral nerves
Associated with Campylobacter jejuni
GBS hits diaphragm!

Autonomic dysfunction with hypotension, HTN, or
tachycardia can occur
MTB S2CK
p. 296
MTB S2CK
p. 296
CSF = increased protein + normal cell count
Tests of respiratory muscle involvement

Inspiration is the active part of breathing
and the patient loses the strength to inhale
Most specific diagnostic test

Nerve conduction studies/electromyography
Decrease in propagation of electrical impulses along
nerves
Decrease in FVC
Decrease in peak inspiratory pressure
PFTs tell who might die from GBS
MTB S2CK
p. 296
MTB S2CK
p. 296
Treatment
Intravenous immunoglobulin (IVIG) or
plasmapheresis are equal in efficacy
Prednisone is a wrong answer for GBS,

doesnt help
Combining IVIG and plasmapheresis is
incorrect
MTB S2CK
p. 296
Woman comes with bilateral leg weakness over last

few days. No knee jerk or ankle jerk reflexes.
Weakness started in feet and progressed up to calves
and thighs.
Which of the following is the most urgent step?
a.
b.
c.
d.
e.
Pulmonary function testing

Arterial blood gas Dont wait for inc CO2 on ABG
Nerve conduction study Most accurate, but not next
Lumbar puncture For Dx, not severity assessment
Peak flow meter Assesses expiratory flow
MTB S2CK
p. 296
25
Myasthenia Gravis
Myasthenia Gravis/Presentation
Muscular weakness from antibodies

against acetylcholine receptors at the
NMJ

Look for...
Double vision and difficulty chewing

Weakness of limb muscles worse at end of the day
Ptosis
Weakness with sustained activity
Normal pupillary responses
Extraocular muscles & mastication (masseter) are

often the only 2 muscular activities universally done
by people (e.g., watching TV and eating)
MTB S2CK
p. 297
MTB S2CK
p. 297
Myasthenia Gravis/Diagnostic Tests
Myasthenia Gravis/Diagnostic Tests

Acetylcholine receptor antibodies
(80% 90% sensitive)
Better answer than edrophonium testing
Edrophonium

Electromyography
Short-acting inhibitor of acetylcholinesterase

Temporary bump up in acetylcholine levels
Associated with a clear improvement in motor
function that lasts for a few minutes
MTB S2CK
p. 297
Shows decreased strength with repetitive stimulation
Questions often ask What

What imaging test should be
done?
Answer...
Chest something!
Chest X-ray, CT, or MRI are done to look for
thymoma or thymic hyperplasia
MTB S2CK
p. 297
Myasthenia Gravis/Treatment
Best initial treatment is...

Neostigmine or pyridostigmine
Longer acting versions of edrophonium
If meds dont control disease, the most

appropriate next step in management is...
Thymectomy if < 60
If > 60 prednisone is used
Azothioprine,
p
, cyclophosphamide,
y p
p
, or
mycophenolate are used in order to get
patient off steroids
MTB S2CK
p. 297
MTB S2CK
p. 298
26
Acute myasthenic crisis

Severe, overwhelming disease
Profound weakness
Respiratory involvement
Treated with IVIG or plasmapheresis
MTB S2CK
p. 298
27
Pregnancy
Obstetrics and
Gynecology
Definitions
Signs and Diagnosis of Pregnancy
Ph i l i Ch
Physiologic
Changes iin P
Pregnancy
Jason M. Franasiak, MD
Chief Resident Physician
Obstetrics & Gynecology
University of North Carolina
Pregnancy
27-year-old woman with nausea and vomiting for 2 weeks.
Symptoms worsen in the morning, but occur at any time during
the day. She has a decrease in appetite. Her last menstrual
period (LMP) was 6 weeks ago. Physical examination is
unremarkable.
Which is the best next step?
Pregnancy Symptoms
Amenorrhea
Breast tenderness
Nausea and vomiting
Fatigue
The surge in estrogen, progesterone, and betahuman chorionic gonadotropin (beta-HCG) leads to
many symptoms of pregnancy
p for anemia,, but

a. Complete
p
blood count Helpful
not next step
b. Beta-HCG
c. HIDA scan Not initial work-up for nausea/vomitting
d. Comprehensive metabolic panel Important, but must
diagnose cause
e. Urinalysis Important, but must
diagnose cause
MTB S2CK
p. 441
MTB S2CK
Definitions
p. 441
Dating Methods
Developmental age (DA): Days since fertilization
Gestational age (GA): Days/weeks since the LMP
Embryo
Fetus
On average, 2 weeks longer than DA
Infant
Ngele rule: Estimate day of delivery

Take the first day of LMP, subtract 3 months then
add 7 days
Bi th
Birth
8 weeks
gestation
1 year
Example: LMP = 7 / 1 / 2010

-3 +7
Fertilization
EDD = 4 / 8 / 2011
MTB S2CK
p. 441
MTB S2CK
p. 442
Trimester Breakdown
1st Trimester
2nd Trimester
Fertilization
3rd Trimester
Delivery
24 weeks DA
26 weeks GA
12 weeks DA
14 weeks GA
Genetic triple or
quad screen
Fetal movement at
16-20 weeks GA
Anatomic ultrasound
at 18-20 weeks GA
FIRST screening
Fetal heart tones
with doppler
MTB S2CK
Term Lengths
Frequent visits
Monitoring for
labor
p. 442
Previable
Preterm
Term
Fertilization
24 weeks
GA
MTB S2CK
37 weeks
GA
Postterm
42 weeks
GA
p. 442
Gravidity/Parity
G6P2124
Living
Children
Gravity
Abortions
Number of
Pregnancies
Parity
Full-term
birth
Preterm
birth
F-PAL = Full-term (F); Preterm (P);

Abortions (A); Living Children (L)
MTB S2CK
p. 442 443
Sign
Physical Finding
Goodell sign
Ladin sign
Softening of cervix
Softening of uterine
midline
Blue discoloration of
vagina and cervix
Small blood vessels/
reddening of palms
Hyperpigmentation of
the face, worse with sun
Hyperpigmentation
down abdomen midline
Telangiectasias/
palmar erythema
Chloasma
Linea nigra
MTB S2CK
p. 444
a. Quickening
b. Goodell sign
c. Ladin sign
d. Linea nigra
e. Chloasma
MTB S2CK
Signs of Pregnancy
Chadwick sign
20-year-old woman presents to the office because

she believes shes pregnant. Her sexual partner
usually wears a condom, but didnt 2 weeks ago. She
is now 4 weeks late for her menstruation.
Which of the following is a first sign of pregnancy?
Not felt until second trimester
Seen at 6 weeks gestation
Seen in second trimester
Seen at 16 weeks gestation
p. 443
Diagnostic Evaluation
Time from Conception
4 6 weeks
6 weeks
6 8 weeks
1st trimester
16 weeks
2nd trimester
Beta-hCG
Urine and serum testing
all highly sensitive
Produced by cytotrophoblast or syncytiotrophoblast
in placenta
First trimester
Doubling every 48 hours for first 4 weeks
Urine pregnancy tests are positive 4 weeks
following the first day of LMP
Peak levels at 10 weeks gestation
Levels drop in 2nd trimester
MTB S2CK
p. 444
Diagnostic Evaluation
Physiologic Changes in Pregnancy
Step 2 Key Points
Cardiovascular changes
Cardiac output increases 30-50%
Lower blood pressure
Ultrasound confirms
intrauterine
pregnancy
At 5 weeks, or a
beta-HCG of 1500
IU/L, a gestational
sac should be seen
on ultrasound
Decreased afterload
Increased blood volume
Gestational
Sac
Yolk Sac
Image: X.Compagnion , commons.wikimedia.org
MTB S2CK
p. 444
MTB S2CK
p. 444
Gastrointestinal changes
Morning sickness
Genitourinary and Renal Changes
Caused by increase in estrogen, progesterone,

and HCG made by placenta
Gastroesophageal reflux
Lower
L
esophageal
h
l sphincter
hi t h
has d
decreased
d ttone
Displacement of stomach by uterus
Constipation
Motility in large intestine decreased
MTB S2CK
p. 445
Increase in the size of

kidney and ureters
Increased risk of
pyelonephritis
Increased incidence of
stress urinary
incontinence
Increase in GFR
Decrease in
BUN/creatinine
MTB S2CK
Image: Nevit Dilmen, WikiCommons
p. 445
Hematology Changes
Increased...
Hematology Changes
Hypercoagulable state
RBCs
Plasma
Coagulation factors
Anemia
Physiologic
hydronephrosis
in pregnancy
Fibrinogen (Factor I) increases 50% along with fibrin

split products (Factors VII, VIII, IX, X)
Protein C and S (inhibitors of coagulation) decrease
No increase in PT,, PTT,, or INR
Recall: Virchow triad
Hypercoagulation
Plasma volume > RBCs
Endothelial Damage
MTB S2CK
p. 445
MTB S2CK
Stasis
p. 445
Prenatal Care/First Trimester
Prenatal Care
First Trimester
Second Trimester
Third Trimester
Other Screening Tests
Visits every 4 to 6 weeks

Between 11 and 14 weeks
Ultrasound confirms gestational age and check for
nuchal translucency
A thickened or enlarged
nuchal translucency is
an indication of Down
syndrome.
MTB S2CK
Image: Dr. Wolfgang Moroder WikiCommons
p. 445
Prenatal Care/Second Trimester

17-year-old woman presents for routine prenatal
checkup at 12 weeks.
Which of the following is the most accurate method to
establish gestational age?
a. Ultrasound
b. Beta-HCG
c. Pelvic exam
d. Fundal height
e. LMP
MTB S2CK
Levels varyy widely

y
May change with multiple gestations
May change with multiple gestations
May be unreliable
p. 445 446
Genetic Screening: Risk of chromosomal anomalies

15-20 weeks gestation
Triple screen
Maternal serum alpha-fetoprotein (MSAFP)
beta-HCG
Estriol
Quad screen
Inhibin A added to triple screen
Banana Sign
MTB S2CK
p. 446
Increased MSAFP may indicate dating error, neural

tube defect, or abdominal wall defect
Landmarks in 2nd trimester:

Auscultation of fetal heart rate
Ultrasound at 16 weeks
showing banana sign
created by compression
of cerebellum in
posterior fossa due to
neural tube defect.
16 to 20 weeks: Quickening
Fetal movement first detected by mother
Multiparous
M lti
may experience
i
earlier
li
Banana Sign
Anatomic ultrasound
18 to 20 weeks
Image: Dr. W. Moroder, WikiCommons
MTB S2CK
p. 446
MTB S2CK
p. 446
Prenatal Care/Third Trimester
Third Trimester Testing
Visits are every 2 to 3 weeks until 36 weeks
Week
27
Weekly visits after 36 weeks

Braxton-Hicks Contractions
Oft
Often occur during
d i 3rd trimester
ti
t
Sporadic and dont cause cervical dilation
If they become regular, the cervix should be checked
to rule out preterm labor before 37 weeks
MTB S2CK
p. 446
Test
Complete blood
count
24 28 Glucose challenge
36
MTB S2CK
Action
If hemoglobin < 11,
replace iron orally
* with stool softener
If glucose > 140 at one
hour perform oral
hour,
glucose challenge test
Treat if positive
Cervical cultures for

Chlamydia and gonorrhea
Prophylactic antibiotics
Rectovaginal culture for
during labor
group B Streptococcus
p. 446
Prenatal Care/Third Trimester
Prenatal Care/Other Screening Tests
Glucose challenge test: Fasting or nonfasting

ingestion of 50 g of glucose and serum glucose
check 1 hour later
Chorionic Villus Sampling

Done at 10 to 13 weeks
Obtains fetal karyotype
Catheter into intrauterine cavity to aspirate
chorionic villi from placenta
Glucose challenge test: Fasting serum glucose,

ingestion of 100 g of glucose
Serum glucose checks at 1, 2, and 3 hours
Elevated glucose during any two of these tests is
abnormal
MTB S2CK
p. 447
MTB S2CK
p. 447
Image: National Human Genome

Research Institute, WikiCommons
Amniocentesis
Done after 15-20 weeks
Obtains fetal karyotype
Needle placed transabdominally into
amniotic
i ti sac and
d withdraw
ithd
amniotic
i ti
fluid
Percutaneous umbilical blood sample

In cases of Rh isoimmunization and
when a fetal CBC is needed
Needle placed transabdominally into
uterus to get blood from umbilical cord
MTB S2CK
p. 447
MTB S2CK
p. 447
Ectopic Pregnancy
Risk Factors
Presentation
Diagnosis
Management
29-year-old woman with history of chlamydia and

abnormal vaginal bleeding presents with left lower
quadrant abdominal pain for the past eight hours. Her
LMP was 6 weeks ago. Her temperature is 99 F, heart
rate is 100 bpm, blood pressure is 130/80 mmHg, and
respiratory rate is 13 breaths/minute.
Which of the following is the most likely diagnosis?
a. Ectopic pregnancy
b. Menstrual cramps Altered menstrual pattern present
c. Diverticulitis Does not cause vaginal bleeding
d. Ovarian torsion
e. Ovarian cyst
MTB S2CK
p. 447 448
Ectopic Pregnancy
Ectopic Pregnancy/Risk Factors
Pregnancy implants outside the uterus

Most commonly occurs in ampulla of fallopian tube
Risk Factors
Previous ectopic pregnancies (strongest risk factor)
Pelvic inflammatory disease (PID)
Intrauterine devices (IUD)
70-80%
Source: Kaplan Lecture Notes
MTB S2CK
p. 448
Source: Nevit Dilmen, wikimedia commons
MTB S2CK
p. 448
Ectopic Pregnancy
Ectopic Pregnancy
Presentation
Differential diagnosis
Abortion
Acute appendicitis
Adnexal torsion
Corpus luteum cyst
rupture
Period of amenorrhea
Unilateral lower abdominal or pelvic pain
Vaginal bleeding
If ruptured
ruptured, can be hypotensive with
peritoneal irritation
MTB S2CK
Source: Gloecknerd, wikimedia commons
Diverticulitis
Endometriosis
Gastroenteritis
PID
UTI
p. 448
Ectopic Pregnancy
Ectopic Pregnancy/Transvaginal Ultrasound
Diagnostic Tests
Beta-hCG
Confirms pregnancy
Bladder
Uterus
Ultrasound
Locates implantation
p
site
Laparoscopy:
Invasive test and treatment to visualize and
remove the ectopic pregnancy
MTB S2CK
Image: Courtesy of Jason Franasiak, MD
p. 448
Ectopic Pregnancy/Treatment
Ectopic Pregnancy/Medical Treatment
Ectopic
Confirmed
Not
Ruptured
Ruptured
Medical
Treatment
Stable
Surgery
(Laparoscopy)
MTB S2CK
Surgical
Treatment
Unstable
IV fluids,
blood products,
dopamine
p. 448
Ectopic Pregnancy
Exclusion Criteria for Methotrexate
Hemodynamically unstable patients
Signs of impending or ongoing ectopic mass rupture
Clinically important abnormalities in baseline hematologic,
renal, or hepatic laboratory values
Immunodeficiency, active pulmonary disease, or peptic ulcer
disease
Hypersensitivity to Methotrexate
Coexistent viable intrauterine pregnancy
Breastfeeding
Unwilling or unable to be compliant with post-therapeutic
monitoring
Do not have timely access to a medical institution
MTB S2CK
Ectopic
pregnancy
p. 449
Baseline labs:
CBC
LFTs
Kidney function
-hCG
Methotrexate given,
-hCG checked 4 & 7 days later
< 15% drop

in -hCG
2nd dose of methotrexate,

-hCG checked day 4 & 7
Persistently
high -hCG
MTB S2CK
p. 449
> 15% drop

in -hCG
> 15% drop

in -hCG
Observe for
side effects,
no other Rx
necessary
Surgical
treatment
Ectopic Pregnancy/Surgical Treatment

Surgical
Treatment
Salpingostomy
Salpingectomy
ostomy = cut
ectomy = remove
Images: Courtesy of Jason Franasiak, MD
MTB S2CK
p. 449 450
Ectopic Pregnancy
Mothers who are Rh negative should receive anti-D
Rh immunoglobulin (RhoGAM) to prevent hemolytic
disease
MTB S2CK
Abortion
p. 450
Abortion
20-year-old woman presents to ED for vaginal bleeding and
lower abdominal pain for one day. She states that shes 15
weeks pregnant. T 99.0 F, HR 100 bpm, BP 110/75 mmHg,
and RR 12/min. Pelvic exam, blood present in vault.
Ultrasound shows intrauterine bleeding, products of
conception, and dilated cervix.
Which is the most likely diagnosis?
a. Complete abortion
b. Incomplete abortion
c. Inevitable abortion
d. Threatened abortion
e. Septic abortion
MTB S2CK
A pregnancy that ends < 20 weeks

gestation or fetus weighs 500g
80% of spontaneous abortions occur prior
to 12 weeks gestation
We are going to review

the definitions in this
section
p. 450
MTB S2CK
Abortion
p. 450
Abortion
Maternal factors that increase risk of abortion

Maternal age
Anatomic abnormalities
MTB S2CK
p. 450
Source: Ed Uthman, MD., commons.wikimedia.org
Source: RadsWiki, commons.wikimedia.org
Abortion
Abortion
Maternal factors that increase risk of

abortion
5
6
3
1.
2.
3.
4.
5.
6.
Dye injector
Cervix
Uterus
Adhesions
Right Tube
Left Tube
Maternal Age
Anatomic abnormalities
Infections
Immunological factors (e.g. Anti-phospholipid
syndrome or SLE)
Endocrinological factors
Malnutrition
Trauma
Source: Floranerolia, commons.wikimedia.org
MTB S2CK
p. 450
Abortion/Presentation
Abortion/Diagnostic Tests
Signs/Symptoms
Cramping abdominal pain
Vaginal bleeding
Hypotension
Tachycardia
CBC
Blood type and Rh screen
Pelvic ultrasound
MTB S2CK
You cannot answer the most

likely diagnosis question about
abortion without an ultrasound
p. 450
MTB S2CK
Abortion/Types
Complete
Abortion
Incomplete
No products
of conception
Follow up
in office
p. 451
Inevitable
Threatened
Products of conception
intact, but intrauterine
bleeding present and
dilation of cervix
Missed
Septic
Death of fetus,
but all products
of conception
present in the
uterus
Mothers whore Rh negative should also

receive anti-D Rh immunoglobulin at this
time
D&C/Medical
Some
products of
conception
Dilation &
Curettage
(D&C) / Medical
MTB S2CK
p. 451
Products of
conception
intact, intrauterine
bleeding, No
dilation
of cervix
Bed rest,
pelvic rest
D&C/M di l
D&C/Medical
Infection of
uterus and
surrounding
areas
D&C and IV
Antibiotics
(levofloxacin &
metronidazole)
MTB S2CK
p. 451
Multiple Gestations/Presentation
Multiple Gestations
Signs/Symptoms
Exponential growth of uterus
Rapid weight gain by mother
Elevated beta-HCG and Maternal
S
Serum
Al
Alpha-Fetoprotein
h F t
t i (MSAFP)
Fertility drugs increase
multiple gestations
MTB S2CK
Multiple Gestations/Diagnostic Tests
p. 451
Multiple Gestations
Ultrasound visualizes fetus

Monozygotic 1 egg and Identical twins
1 sperm
Same gender
that splits Same physical characteristics
Same blood type
Fingerprints differ
Dizygotic
MTB S2CK
2 eggs and Fraternal twins

2 sperm
Different or same sex
They resemble each other
As any siblings would
p. 452
Multiple Gestations/Diagnostic Tests
Source:Trlkly , commons.wikimedia.org
Multiple Gestations
For monozygotic twins, amnionicity and

chorionicity depend on timing of
cleavage
10
Multiple Gestations
Multiple Gestations
Complications
Source: Kevin Dufendach, commons.wikimedia.org
Preterm Labor
Spontaneous abortion of one fetus

Premature labor and delivery
Placenta previa
Anemia
MTB S2CK
p. 452
28-year-old woman 28th week of pregnancy with

severe lower back pain. The pain is cyclical and is
increasing in intensity. On physical examination she
seems to be in pain. T 98.9 F, HR 104 bpm, BP
135/80 mmHg, RR 15/min. Cervix is 3 cm dilated.
a. Premature rupture of membranes Membranes intact
b. Preterm labor
c. Cervical incompetence Presents with contractions
d. Preterm contractions Cervical dilation present
MTB S2CK
p. 452
Preterm Labor
Preterm Labor/Risk Factors
Preterm births occur < 37 weeks gestation
Spontaneous: preterm labor

Indicated: maternal or fetal
Preterm labor
Activation of hypothalamic-pituitary-adrenal
yp
p
y
(HPA) axis
Decidual hemorrhage
Inflammation
Uterine distension
Premature rupture of membranes

Multiple gestation
Previous history of preterm labor
Placental abruption
Maternal factors
Uterine anatomical abnormalities
Infections
MTB S2CK
p. 452 453
11
MTB S2CK
Source: RadsWiki, commons.wikimedia.org
p. 453
Preterm Labor/Presentation
Contractions
MTB S2CK
Source: Ed Uthman, , commons.wikimedia.org
p. 453
Preterm Labor/Evaluation
Cervical
change
Initial evaluation
Gestational age
Fetal weight
Presenting fetal part
Occurring between 20 and 37 weeks

gestation
MTB S2CK
p. 453
Preterm Labor/Evaluation
MTS2CK
p. 453
Preterm Labor
Preterm labor
Indications for delivery
Maternal severe HTN

Maternal cardiac disease
Maternal cervical dilation > 4 cm
Maternal hemorrhage (abruptio placenta, DIC)
Fetal death
Chorioamnionitis
Preterm rupture of membranes (34 weeks)
Fetal distress
Intrauterine growth restriction with reverse diastolic flow
When any of these is present, answer delivery

MTS2CK
p. 453
Stop delivery if
Delivery if
EGA 24-33 wks
EGA 34-37 wks
EFW 600-2,500
600-2 500 g EFW > 2,500
2 500 g
Betamethasone
& Tocolytics
MTS2CK
p. 453
12
Preterm Labor/Corticosteroids
Preterm Labor/Tocolytics
Corticosteroids
Betamethasone or dexamethasone
Effects of betamethasone begin within 24 hours
and peak at 48 hours
Goal
Delay preterm labor
Allows time for steroids to work
Transport to specialist unit
Goal
Decrease risk of RDS and neonatal mortality
Agents
Magnesium sulfate
Corticosteriods increase surfactant and

thus mature fetal lungs
MTS2CK
p. 453
MTS2CK
Preterm Labor
Magnesium toxicity leads to

respiratory depression &
cardiac arrest, check deep
tendon reflexes often!
Toxicity: Give calcium gluconate
MTS2CK
p. 454
p. 454
Goal
Decrease contractions
Given to allow time for steroids to work
Agents
Magnesium sulfate
-adrenergic agents
Prostaglandin synthetase inhibitors
MTS2CK
p. 454
Premature Rupture of
Membranes
Ductus
Arteriosus
Source:
13
Premature Rupture of Membranes (PROM)
Premature Rupture of Membranes
The rupture of chorioamniotic membrane

before onset of labor
Diagnosis
Sterile speculum examination
Fluid pools in posterior fornix
Fluid turns nitrazine paper blue
When dry, fluid has ferning pattern
Source: Elizabeth August, MD
MTS2CK
p. 454
MTS2CK
p. 454
Premature Rupture of Membranes
Premature Rupture of Membranes/Treatment
PROM can lead to

Preterm labor
Cord prolapse
Placental
ace a ab
abruption
up o
Chorioamnionitis
Before 32 weeks gestation

Corticosteroids
Antibiotics
>37 weeks gestation, unknown GBS, > 18 hours rupture

Penicillin administered for prophylaxis
34-37
34
37 weeks gestation, unknown GBS
Initiate Penicillin
Known GBS negative

NO Antibiotics
PROM = Do fewer exams!
<34 weeks gestation, unknown GBS

Erythromycin and Penicillin initiated
MTS2CK
p. 454 455
MTS2CK
p. 455
Third Trimester Bleeding
DDx
Vulva (trauma, varicose veins)

Vagina (lacerations)
Cervix (polyp, cervicitis, carcinoma)
Ut i
Uterine
Uterine rupture
Placenta previa
Vasa previa
Placental abruption
14
Third Trimester Bleeding/Previa
Placenta previa
Abnormal implantation of placenta over
internal cevical os
24-year-old woman in her 32nd week of pregnancy

presents to ED. She woke up in bed in a pool of
blood. Denies contractions or pain. HR 105 bpm, BP
110/70 mmHg.
Which is the next step?
Never do digital exam w/o
Risk
Ri k F
Factors
t
Previous uterine scar
Multiple gestations
Previous placenta previa
MTS2CK
p. 456
a. Digital vaginal exam

knowing placental location
b. Transabdominal ultrasound
c. Immediate vaginal delivery
Gather information first
d. Immediate cesarean delivery
e. Transvaginal ultrasound Abdominal US is safer
MTS2CK
p. 455
Digital vaginal exam contraindicated in

third trimester vaginal bleeding
Can cause
Separation between placenta and uterus
Severe hemorrhage
Source: Jason Franasiak, MD
Presentation
PAINLESS vaginal bleeding
Usually presents > 28 weeks
MTS2CK
Third Trimester Bleeding/Previa Types
MTS2CK
p. 456
Vasa
Previa
Partial
Complete
Marginal
Partial covering
of the internal
cervical os, but
covers more than
th
the marginal
Diagnosis
Transabdominal ultrasound
Placenta location
p. 455
Complete
covering of
the internal
cervical os
MTS2CK
Marginal
covering of
the internal
cervical os
Lowlying
Placenta
Fetal vessel
present over
cervical os
Placenta thats
implanted in lower
segments of uterus
but not covering
internal cervical os
p. 456
15

Full
moon
Half
moon
Crescent
moon
Umbilical
cord
Placenta
Fetal
vessels
Internal os
Source: Sigrid de Rooij, comons.wikimedia.org
MTS2CK
p. 456
MTS2CK
p. 457
Third Trimester Bleeding/Treatment
Third Trimester Bleeding/Accreta
Treatment of placenta previa

Strict pelvic rest
Type and screen, CBC
Fetal considerations
Delivery by C-section
Placental invasion (based on depth)

Accreta
Increta
Percreta
Labor
Severe hemorrhage
Fetal distress
MTS2CK
p. 457
MTS2CK
p. 457 458
Third Trimester Bleeding/Accreta
Placental invasion (based on depth)

Accreta
Increta
Percreta
Risk Factors
Placenta previa
Prior uterine scars
MTS2CK
p. 458
MTS2CK
p. 457
16
Third Trimester Bleeding/Abruption
Placental Abruption
Placental abruption
Abnormal, premature separation of placenta from
uterus
Effects
Complete
Partial
Life-threatening
g
bleeding
Premature delivery
Uterine tetany
DIC
And
Hypovolemic shock
MTS2CK
Minor bleed
No clinical
signs/symptoms
p. 458
Placental Abruption/Etiology
Placental Abruption/Presentation
Risk factors
Maternal HTN (chronic, preeclampsia,
eclampsia)
Prior placental abruption
Tobacco
T b
and/or
d/ cocaine
i use
Trauma
Clinical presentation
Vaginal bleeding
Severe abdominal PAIN (uterine
tenderness)
Contractions
C t ti
Possible fetal distress
MTS2CK
p. 458
MTS2CK
Placental Abruption/Presentation
p. 458
Placental Abruption/Diagnostic Tests
Diagnosis
Transabdominal ultrasound
Clinical scenario
Late Decelerations
Placenta previa = painLESS vaginal bleeding

Placental abruption = painFUL vaginal bleeding

MTS2CK
p. 459
17
Placental Abruption/Diagnostic Tests
Source: Nevit Dilman commons.wikimedia.org
Placental Abruption/Treatment
Delivery plan
Cesarean delivery
Uncontrollable hemorrhage
Fetal distress
Placental Abruption
Type
Description
Complications
Concealed
Blood within uterine

cavity
Placenta more likely
to be completely
detached
Serious complications:
DIC
Uterine tetany
Fetal hypoxia
Fetal death
Sheehan syndrome
(postpartum
hypopituitarism)
External
Blood drains through Usually smaller with minimal

cervix
complications
Placenta more likely
to be partially
detached
MTS2CK
p. 459
Placental Abruption/Treatment
Mothers who are Rh negative should also

receive anti-D Rh immunoglobulin at
this time
Vaginal delivery
Placental separation is limited
Fetal heart tracing is assuring
Fetal death prior to presentation
MTS2CK
p. 459
MTB S2CK
p. 451
Uterine Rupture
Uterine Rupture
Spontaneous complete transection of uterus from

endometrium to serosa
Usually occurs during labor
Life threatening to mother and baby

Life-threatening
Immediate delivery!
MTS2CK
p. 459
18
Uterine Rupture/Risk Factors
Uterine Rupture
Risk factors
Previous C-section
Classical: higher risk of uterine rupture
Low transverse
Trauma
Uterine myomectomy
Uterine overdistention
Polyhydramnios
Multiple gestations
Types of cesarean scars. Source: Elizabeth August, MD.
Placenta percreta
MTS2CK
p. 460
MTS2CK
p. 460
Uterine Rupture/Presentation
Uterine Rupture/Treatment
Clinical presentation:
Extreme abdominal pain
Abnormal bump in abdomen
Lack of uterine contractions
Regression of fetus
Treatment
Emergent laparotomy and delivery
Repair of uterus or hysterectomy
Future management
Early delivery via C
C-section
section
Uterine rupture requires
immediate laparotomy and
delivery of the fetus
MTS2CK
p. 460
MTS2CK
p. 461
Rh Incompatibility
Rh incompatibility
Rh Incompatability
Mother RhD negative

Baby RhD positive
Leads to isoimmunization
Rh isoimmunization
Fetal RBCs cross placenta
Maternal antibodies to RhD antigen are
made
MTS2CK
p. 461
19
Rh Incompatibility
Rh Incompatibility
Clinical significance
1st pregnancy: mild anemia/hyperbilirubinemia
2nd pregnancy: maternal antibodies attack the
second Rh positive baby
Hemolytic Disease of Newborn

Fetal anemia
Extramedullary production of fetal RBCs
Hemolysis
Neurotoxicity from hyperbilirubinemia
Leads to hemolysis of fetal RBCs
High output cardiac failure
Hemolytic disease of newborn
MTS2CK
heme and bilirubin levels
p. 461
MTS2CK
Rh Incompatibility
Hydrops fetalis
p. 461
Rh Incompatibility
Rh Antibody Screening
Rh Negative
Antibody titer
Sensitized
Further
Monitoring
MTS2CK
Unsensitized
Rh Positive
No further
screening
Antibody screen: if mother is Rh or Rh+

Antibody titer: how many maternal
antibodies to Rh+ blood
Repeat at 28 weeks
and give Rhogam as
indicated
p. 461
MTS2CK
p. 461
Rh Incompatibility
Rh Incompatibility
Rhogam indications for Rh unsensitized

patients
28 weeks gestation
Delivery
Procedures (amniocentesis)
(
)
Bleeding (abortion, abruption)
Antibody Screen Positive

Antibody titer
Titer 1:4
Sensitized
Titer 1:16
consider treatment
algorithm
l ith
Unsensitized = no anti-Rh antibodies present
MTS2CK
p. 461 462
MTS2CK
p. 462
20
Rh Incompatibility
Rh Incompatibility
Antibody titer
Antibody titer 1:16

Fetus is Rh Antigen Positive
1:16
Determine paternal Rhesus type
Homozygote
Positive
Middle Cerebral Artery Dopplers
Homozygote
g
Negative
Heterozygote
or unsure
paternity
Treatment
algorithm
Peak MCA Velocity is

>1 5 MOM
>1.5
(Multiples of median)
No Treatment
Fetal genotyping
performed on samples
of chorionic villi,
amniocytes or fetal
blood
MTS2CK
Cordocentesis with
transfusion if fetal Hct
is <30%
p. 462
MTS2CK
Rh Incompatibility
p. 462.3
Rh Incompatibility
Source: Jason Franasiak, M.D.

Rh Incompatibility
Antibody titer 1:16
No MCA Doppler Capability
Amniocentesis for fetal cells to be evaluated under

spectrophotometer (evaluated bilirubin)
Indeterminate
Repeat
amniocentesis
2-3 weeks
Affected
Repeat
amniocentesis
1-2 weeks
Hypertension
Transfusion
zone
Fetus probably is anemic
Do percutaneous umbilical blood
sample (fetal hematocrit)
Fetal Hct is <30%
Perform an intrauterine transfusion
MTS2CK
p. 462.3
21
Hypertension/Chronic
29-year-old woman G2P1 in her 30th week of pregnancy
presents for routine prenatal visit. Her wedding ring is
getting too tight. BP 150/100 mmHg, HR 92 bpm, RR 12,
T 99 F. Urine 1+ protein. LFTs: normal.
a. Chronic hypertension
b. Gestational hypertension No proteinuria
c. HELLP syndrome No laboratory abnormalities
d. Preeclampsia
e. Eclampsia Pre-eclampsia + seizures
Chronic HTN
BP 140/90 mmHg before 20 weeks
gestation
Treatment
Labetalol, nifedipine, or methyldopa
ACE inhibitors and ARBs cause fetal
malformations
Dont use during pregnancy
MTS2CK
p. 463
Hypertension/Gestational
Gestational HTN
BP 140/90 mmHg after 20 weeks
gestation
No proteinuria
Treatment
T t
t
Labetalol, nifedipine, or methyldopa
Only during pregnancy
MTS2CK
p. 463
MTS2CK
p. 463
Hypertension/Preeclampsia
Mild preeclampsia Severe preeclampsia
Hypertension
Proteinuria
Edema
Mentall status
changes
Vision changes
Impaired liver
function
MTS2CK
Generalized
Yes
No
No
Yes
Yes
p. 463
Preeclampsia Risk Factors

Nulliparity
Multiple gestation
Advanced maternal age
Chronic HTN
Renal disease
History of preeclampsia
Mild
BP > 140/90 mmHg
Proteinuria 1+ to 2 +
MTS2CK
p. 463
At term
Preeclampsia
Severe
BP > 160/110
Proteinuria 3+ to 4+
Preterm
IInduce
d
delivery
MTS2CK
> 160/110
Dipstick 3+; 24 hour
urine > 5 g
> 140/90
Dipstick 1+ to
2+; 24 hour
urine > 300 mg
Hands, feet, face
No
1. Betamethasone
a. Mature fetus
lungs
2. Magnesium sulfate
a. Seizure
prophylaxis
1. Prevent Eclampsia
p
a. Magnesium
sulfate
2. Control BP
a. Hydralazine
3. Delivery
a. Preterm
b. Term
p. 464
22
The only definitive treatment

in preeclampsia is delivery
Hypertension/Eclampsia
Eclampsia
Tonic-clonic seizures occurring in
patient with preeclampsia
Treatment
Stabilize
St bili mother
th
Seizure control: magnesium
BP control: hydralazine and labetalol
Deliver baby
MTS2CK
p. 464
MTS2CK
p. 464
Hypertension HELLP
HELLP Syndrome
Hemolysis, Elevated Liver enzymes,
Low Platelets
Gestational Diabetes
Treatment
Stabilize mother
BP control: hydralazine and labetalol
Deliver baby
MTS2CK
p. 464
Pregestational Diabetes
28-year-old woman in her 27th week of gestation
presents for routine prenatal visit. No complaints. T 99 F,
BP 120/80 mmHg, HR 87 bpm. The patient is given 50
mg of glucose. An hour later, blood glucose 145 mg/dL.
Which is the best next step?
a. Treat with insulin The 1h GTT is a screening test
b. Treat with sulfonylurea
c. Do a fasting blood glucose level A 3h GTT is needed
d. Perform oral glucose tolerance test
MTS2CK
p. 464 465
Pregestational diabetes
Diabetes before pregnancy
Either Type 1 or Type 2 DM
MTS2CK
p. 465
23
Maternal Complications
Preeclampsia
Spontaneous abortion
Increased rate of infection
Increased postpartum hemorrhage
Fetal Complications
Congenital anomalies
Macrosomia
MTS2CK
p. 465
Shoulder dystocia
Preterm
P t
labor
l b
MTS2CK
p. 465
Pregestational Diabetes/Evaluation
Additional prenatal testing

EKG
24-hour urine for baseline renal function
HbA1C
Ophthalmological exam
DM type
Route of administration
Insulin type
Type 1
Type 2
Insulin pump
Subcutaneous insulin
NPH
NPH, lispro
MTS2CK
p. 465
MTS2CK
Pregestational Diabetes/Fetal Testing

Age (weeks)
32-36
>36
37
38-39
Lecithin/sphingomyelin
ratio (L/S ratio)
NST: fetal well-being

Ultrasound: fetal size
L/S ratio: assess fetal

lung maturity test
(if mat
mature
re
delivery)
deli er )
Twice-weekly testing; one

NST and one biophysical
prole (BPP)
NST: fetal well-being
BPP: amount of amniotic uid
and fetal well- being
p. 466
p. 465
Gestational Diabetes/Complications
Weekly nonstress test

(NST) and ultrasound
MTS2CK
Oral Medications
Metformin and glyburide
Continue
testing, IOL at
39 weeks
Gestational diabetes (GDM)

Glucose intolerance identified during pregnancy
Complications
Preterm birth
Fetal
F t l macrosomia
i
Birth injuries from fetal macrosomia
Neonatal hypoglycemia
Development of overt Type 2 DM postpartum
MTS2CK
p. 466
24
Gestational Diabetes/Evaluation
Erbs
Palsy
Diagnosis
Routine screening between 24 and 28
weeks GA
1-hour glucose tolerance test
Positive
Positi e if > 140 mg/dL
3-hour glucose tolerance test

Klumpkes Palsy
MTS2CK
Gestational Diabetes
Diabetes/Treatment
Glucose load test

Non-fasting ingestion of 50g glucose
followed by
No
serum measurement one hour later
< 140 mg/dL
NO gestational
diabetes
All glucose levels

are normal
No further test
p. 466
> 140 mg/dL

Oral glucose tolerance test
Fasting ingestion of 100 mg of glucose
followed by serum glucose measurements at
1, 2, and 3 hours after ingestion
Elevation of serum glucose
at 1, 2, or 3 hours
Treatment
Diabetic diet and exercise (walking)
Medical management
Insulin
Oral hypoglycemics
Dont tell pregnant patients to lose weight. Its the

most common wrong answer. Once patients are put
on insulin they should follow fetal testing schedule
starting at 32 weeks.
Gestational diabetes
MTS2CK
p. 467
MTS2CK
p. 467
Diabetes/Treatment
Gestational diabetes needs formal 2-hour

GTT postpartum to screen Type 2 DM
MTS2CK
Fetal Growth Abnormalities

Intrauterine Growth Restriction
Macrosomia
p. 467
25
Intrauterine Growth Restriction/Etiology
Fetuses with intrauterine growth restriction (IUGR)

weigh in bottom 10% for gestational age
Types of IUGR
Type
Symmetric
Characteristic
Brain in proportion with rest of body
Occurs < 20 weeks gestation
Asymmetric Brain weight isnt decreased

Abdomen is smaller than head
Occurs > 20 weeks
MTS2CK
p. 467 468
Chromosomal abnormalities
Neural tube defects
Infections (viral, protozoans)
Multiple gestations
Maternal disease
HTN or renal disease
Malnutrition
Substance abuse
Hemoglobinopathies
MTS2CK
p. 468
Fundal height = gestational age in weeks
Example: a patients fundal height at
28 weeks should be 28 cm
Diagnosis
Ultrasound done to confirm gestational age and
fetal weight
MTS2CK
p. 468
26
Complications
Premature labor
Stillbirth
Fetal hypoxia
Lower IQ
Seizures
Mental retardation
Treatment/Prevention
Quit smoking
Prevent maternal infection with
immunizations
Determine
D t
i optimal
ti l d
delivery
li
titime
MTS2CK
p. 468
MTS2CK
p. 468
Macrosomia/Risk Factors
Macrosomia/Diagnostic Tests
Macrosomia
Estimated birth weight > 4500 g
Risk factors
Maternal
M t
l diabetes
di b t or obesity
b it
Advanced maternal age
Post term pregnancy
Fetal genetic syndromes
MTS2CK
Example: a patients fundal height at

28 weeks should be 28 cm
Macrosomia
Fundal height
p. 468
MTS2CK
Macrosomia/Diagnostic Tests
Physical Examination
Fundal height 3 cm than GA
Fundal height = gestational age in weeks
3 cm greater than GA
p. 469
Ultrasound
Ultrasound confirms the estimated weight by

Femur length
Abdominal circumference
Head circumference and biparietal diameter
MTS2CK
p. 469
27
Macrosomia
Shoulder Dystocia/ Clavicle Fracture
Complications
Shoulder dystocia
Birth injuries
Low Apgar scores
Hypoglycemia
MTS2CK
Source: Nevit Dilman, commons.wikimedia.org
p. 469
Macrosomia
Treatment
Induction of labor
Erbs
Palsy
Lungs mature
EFW < 4500 grams
Cesarean deli
delivery
er
EFW > 5000 grams
Klumpkes Palsy
MTS2CK
p. 469
28
Nonstress Test
Allows for evaluation of fetal well-being in utero
Labor and Delivery

Fetal Testing
Electronic Fetal Monitoringg
Physiologic Changes Before Labor
Induction of Labor
MTS2CK
Nonstress Test
p. 469
Biophysical Profile
Biophysical profile (BPP)

Test
NST
Fetal Breathingg
Fetal Movement
Tone
Amniotic Fluid
Score
0 or 2
0 or 2
0 or 2
0 or 2
0 or 2
MTS2CK
p. 469
MTS2CK
Electronic Fetal Monitoring
p. 470
MTS2CK
p. 470
MTS2CK
p. 470
29
Type
Description
Cause
Early
decelerations
Decrease in heart rate that

occurs with contractions
Head
compression
Variable
decelerations
Decrease in heart rate and

return to baseline with no
relationship to contractions
Umbilical cord
compression
Late
decelerations
(most serious
and dangerous)
Decrease in heart rate after

contraction started. No
return to baseline until
contraction ends
Fetal hypoxia
MTS2CK
p. 470
MTS2CK
p. 471
Physiological Changes Before Labor
Labor & Delivery
Early Changes
Lightening
Braxton-Hicks contractions
Bloody show
Stages of Labor
Stage 1
Onset of labor
full
dilation of cervix
Primipara: 618 h
p
210 h
Multipara:
Latent
phase
p. 471
MTS2CK
Stage 3
Full dilation of
cervix
delivery
of neonate
Primipara:
p
2h
Multipara: 1 h
Delivery of
neonate
delivery of
placenta
30 min
Active phase
Onset of labor
4 cm dilation
Primipara: 67 h
Multipara: 45 h
MTS2CK
Stage 2
4 cm dilation
full dilation
Primipara: 1.2 cm/h (minimum)
Multipara: 1.5 cm/h (minimum)
p. 471
30
Labor & Delivery
Labor & Delivery
Monitoring (Stage 1)
Maternal BP and pulse
Electronic fetal monitor: fetal HR and
uterine contractions
Examine
E
i cervix
i (every
(
2 hours)
h
)
Cervical dilation
Cervical effacement
Fetal station
MTS2CK
NOT
effaced
NO
dilation
Fully
effaced
1 cm
dilated
5 cm
dilation
Fully
dilated
at
10 cm
Source: Fred the Oyster, commons.sikimedia.org
p. 471
Labor & Delivery
Labor & Delivery
Stage 2
Cervix fully dilated to delivery
Internal vs. External Fetal Monitoring
MTS2CK
p. 472
Stages of fetal head descent. Source: Elizabeth August, MD.
Labor & Delivery
Labor & Delivery

31
Labor & Delivery
Labor & Delivery
Stage 2
Cervix fully dilated to delivery
Stage 2: Cervix is fully dilated to delivery

Cardinal Movements of Labor

Rupture of amniotic membranes
Spontaneous or artificial
Meconium
1.
2.
3
3.
4.
5.
6.
7.
MTS2CK
Engagement
Descent
Flexion
Internal Rotation
Extension
External Rotation
Expulsion
p. 472 473
Labor & Delivery
Operative Delivery
Stage 3
From delivery of neonate to placenta
Operative Vaginal Delivery

Forceps
Vacuum
Immediately after delivery

Repair lacerations of vagina
Signs of placental separation include:
Fresh bleeding from vagina
Umbilical cord lengthening
Uterine fundus rising
Uterus becoming firm
MTS2CK
C-section
p. 473
Operative Delivery
Induction of Labor/Medications
Induction of labor
Initiating labor via medical means
Medications
PGE2 used for cervical ripening
Oxytocin
Types of cesarean scars. Source: Elizabeth August, MD.
MTS2CK
p. 460
MTS2CK
p. 473
32
Induction of Labor/Medications
Mechanical means
Amniotomy
Foley Balloon
Complications of Labor
and Delivery
Prolonged Latent Stage
Protracted Cervical Dilation
Arrest Disorders
Malpresentation
Shoulder Dystocia
Postpartum Hemorrhage
Inspect for a prolapsed umbilical cord

after puncturing amniotic sac
MTS2CK
p. 473

22-year-old primipara in 39th week of pregnancy, with
intense abdominal pain thats intermittent. Gush of fluid
felt 3 hours ago. Cervix 3 cm dilated, 50% effaced, and
fetus head is felt at 2 station. The next 3 hours she
progresses, her cervix is 5 cm dilated, 60% effaced, and
fetal head at 1 station. Six hours after presentation, her
cervix is 5 cm dilated and 60% effaced, fetal head at 0
station.
a. Prolonged latent stage Cervix has not dilated
b. Protracted cervical dilation Cervix has not dilated
c. Arrest of descent Fetal head has descended
d. Arrest of cervical dilation
MTS2CK
p. 474
Prolonged latent stage

Latent phase 20 hours for primipara
Latent phase 14 hours for multipara
Etiology
Sedation
Unfavorable cervix
Uterine dysfunction with irregular/weak
contractions
MTS2CK
p. 474
Treatment of Prolonged Latent Phase

Rest
Hydration
Stage 1 of labor
< 1.2 cm/hour in primipara
< 1.5 cm/hour in multipara
Most will convert to spontaneous

delivery in 6 to 12 hours
MTS2CK
p. 474
Etiology: 3 Ps
Power: strength and frequency of contractions
Passenger: size and position of fetus
Passage: size of pelvis
MTS2CK
p. 474 475
33
Arrest Disorders/Types
Treatment of protracted cervical

dilation
Power
Arrest of Cervical Dilation

No cervical dilation for 2 hours
Pitocin
Amniotomy
Passenger/Pelvis
Arrest of Fetal Descent

No fetal descent for 1 hour
C-section
MTS2CK
p. 475
MTS2CK
p. 475
Arrest Disorders/Etiology
Etiology
Cephalopelvic disproportion
Cesarean delivery
Excessive sedation/anesthesia
Rest or reversal
Malposition
Time
Operative delivery (forceps)
Cesarean delivery
MTS2CK
p. 475
25-year-old woman in 35th week of gestation

presents for routine prenatal checkup. T 98 F, BP
130/90, HR 87, and RR 12. Her abdomen is gravid. A
hard circular surface is felt in proximal part of the
uterus.
Which is the next step?
a. External cephalic version Perform ultrasound first
b. Ultrasound
c. CT scan Ultrasound is used to determine position
d. X-ray
MTS2CK
p. 475
Malpresentation/Presentation
Presenting Part
Part of fetal body thats closest to
vaginal canal and will be engaged when
labor starts
Cephalic
Diagnosis
Leopold maneuvers
Vaginal exam
Ultrasound
Ultraso nd
Head
Should always confirm suspected

diagnosis on physical examination
with ultrasound
Malpresentation
Foot or buttock
MTS2CK
p. 476
MTS2CK
p. 476.
34
Types of Breech Presentation
Type
Description
Frank breech Fetus hips are flexed with extended

knees bilaterally
Complete
b
breech
h
Fetus hips and knees are flexed

bil
bilaterally
ll
Footling
breech
Fetus feet are first

one leg (single footling)
or
both legs (double footling)
MTS2CK
p. 476
MTS2CK
MTS2CK
p. 477
p. 476
Source: Elizabeth August, MD.
MTS2CK
p. 477
Malpresentation/Treatment
Shoulder Dystocia
Treatment
External cephalic version
C-section
Shoulder dystocia
Entrapment of anterior shoulder behind
pubic symphisis after delivery of fetal
head
MTS2CK
p. 477
MTS2CK
p. 477
35
Shoulder Dystocia
Shoulder Dystocia/Risk Factors
Risk Factors
Maternal diabetes
Maternal obesity
Post-term pregnancy
History of prior shoulder dystocia
Any factor that indicates fetus is too big or
the pelvis is too small is a risk factor for
shoulder dystocia
MTS2CK
p. 478
Shoulder Dystocia/Treatment
MTS2CK
p. 478
Treatment
1. McRoberts Maneuver
McRoberts maneuver. Source: Elizabeth August, MD.
MTS2CK
p. 478 479
MTS2CK
p. 478
Postpartum Hemorrhage/Etiology
Treatment
Postpartum hemorrhage
More than 500 mL after delivery
Early vs. late postpartum bleeding
1. McRoberts maneuver
2. Rubin maneuver
3. Woods maneuver
4. Delivery of posterior arm
5. Deliberate fracture of fetal clavicle
6. Zavanelli maneuver
MTS2CK
p. 478
Etiology
gy
a = without
Uterine atony
tony = contractions
Laceration
Retained products of conception
Coagulopathy
MTS2CK
p. 479
36
Postpartum Hemorrhage/Risk Factors
Risk factors for atony

Anesthesia
Uterine overdistention
Prolonged/rapid labor
Augmented labor
Uterine leiomyoma
Preeclampsia with magnesium therapy
MTS2CK
p. 479
Postpartum Hemorrhage/Treatment
Evaluation/Treatment
Examination of perineum, vagina, and cervix
Bimanual examination of uterus (+/- compression/massage)
Administer uterotonics (oxytocin, methylergonovine maleate,
15 methyl-PGF2alpha/Hemabate, misoprostol)
Operative management
Uterine arteryy embolization
D&C
Bakri balloon placement
Collapsed silicone ballon inserted in uterus, later filled with fluid
B-Lynch stitch
Uterine artery ligation
Hysterectomy
MTS2CK
p. 479
B-Lynch Suture
Evaluation/Treatment
Examination of perineum, vagina, and cervix
Bimanual examination of uterus
Administer uterotonics
Operative management
Uterine Artery Ligation
Blood products
PRBCs, FFP, Cryoprecipitate
Source: Niels Olson, commons.wikimedia.org

Modified: Jason Franasiak, MD
Product
Contents
Packed RBCs
RBCs, WBCs, plasma
FFP
Soluble plasma
proteins
p
Cryoprecipitate Factors VIII and XIII,

fibrinogen,
fibronectin, vWF
Platelets
Platelets, RBCs,
WBCs, plasma
Effect
Hct 3%
Hgb 1g/dL
fibrinogen 10
mg/dL
g/
fibrinogen 10
mg/dL
The Uterus
Premenstrual Syndrome
Menopause
AUB/DUB
Contraception
5000
10,000/mm3 per
unit
37
PMS/PMDD
PMS/PMDD
Premenstrual syndrome (PMS)

Physical, mood-related, and behavioral
changes
Over 200 symptoms attributed to PMS
Premenstrual Dysphoric Disorder (PMDD)

Severe form of PMS
MTB S2CK
p. 481
Common symptoms
Headache
Breast
B
t ttenderness
d
(mastodynia)
(
t d i )
Pelvic pain, bloating
Irritability, lack of energy
MTB S2CK
p. 481
PMS/PMDD
PMS/PMDD
Diagnostic criteria
Present for 2 consecutive cycles
Symptom-free in first part of cycle
Symptoms present in second half of cycle
Dysfunction in social or economic
performance
Treatment of PMS/PMDD
Lifestyle
Limit caffeine, alcohol, cigarettes, and chocolate
Aerobic exercise
Increase calcium and magnesium
Pharmacologic
NSAIDs
Severe: SSRIs
MTB S2CK
p. 481
MTB S2CK
p. 481
Menopause
Menopause
Menopause
Permanent cessation of menses
Due to permanent cessation of estrogen
production
Median
M di age off onset:
t 51
Physiology
Early
MTB S2CK
The oocytes
produce less
estrogen and
progesterone
t
LH and FSH start
to rise
Shortening of
menstrual cycles
Late
Changes in sex
hormones
Testosterone
Androstenedione
Estrone
Estradiol
p. 482
38
Menopause
Menopause
Symptoms
Menstrual irregularity
Sweats and hot flashes
Mood changes
Dyspareunia (pain during sexual intercourse)
Decrease in breast size
Vaginal/cervical atrophy
Uterovaginal prolapse
Women are symptomatic for an average

of 12 months, but some experience
symptoms for years
MTB S2CK
p. 482
Atrophic vaginitis: vaginal epithelium is

estrogen dependent. The absence of
estrogen causes thinning, presents as
itching, burning, and/or dyspareunia.
MTB S2CK
Menopause/Osteoporosis
p. 482
Menopause
Hormone replacement therapy (HRT)
Estrogen +/- progesterone
Contraindications
Estrogen-dependent carcinoma
History of PE or DVT
HRT associated with endometrial

hyperplasia, can lead to endometrial
carcinoma
Vertebral body fractures. Source: Dr Robert CARLIER, CHU

Raymond Poincar, Garches, France, commons.wikimedia.org
Abnormal Uterine Bleeding

Menorrhagia
Hypomenorrhea
Heavy, prolonged
menstrual bleeding
Gushing of blood
Clots may be seen
Endometrial
hyperplasia
Uterine fibroids
Dysfunctional
uterine bleeding
Intrauterine device
MTB S2CK
p. 482 483
MTB S2CK
p. 482

Metrorrhagia
Menometrorrhagia
Intermenstrual bleeding
Light menstrual
flow
May only have
spotting
Obstruction
(hymen, cervical
stenosis)
OCPs
Endometrial polyps
Endometrial/cervical
cancer
Exogenous estrogen
administration
d i i t ti
Postcoital
bleeding
Oligomenorrhea
Menstrual cycles > 35 days long
Irregular bleeding
Time intervals
Duration
u at o
Amount of bleeding
Pregnancy
Menopause
Significant weight loss
(anorexia)
Tumor
T
secreting
ti estrogen
t
Endometrial polyps
Endometrial/cervical cancer
Exogenous estrogen
administration
Malignant tumors
MTB S2CK
Bleeding after
intercourse
Cervical cancer
Cervical polyps
Atrophic vaginitis
p. 483
39

Uterine fibroid
Postcoital bleeding is cervical cancer until

proven otherwise
Any patient > 35 with abnormal bleeding

should undergo endometrial biopsy to
rule out endometrial carcinoma
Source: James Heilman, MD, commons.wikimedia.org
MTB S2CK

Normal squamous cells
p. 482 483

HPV infects cells causing
mild dysplasia
Anovulatory Uterine Bleeding

Estrogen produced
No progesterone
No ovulation
no corpus luteum
progesterone
Prevents withdrawal bleeding
no
Source: Ed Uthman MD, commons.wikimedia.org
Dysfunctional Uterine Bleeding
Diagnosis/Evaluation
CBC
Pregnancy test
PT/PTT
Pelvic ultrasound
Endometrial biopsy
Pap smear
Thyroid studies
Prolactin levels
Dysfunctional uterine bleeding

(DUB)
Unexplained abnormal bleeding
Theres no specific test for DUB

Diagnosis by exclusion
MTB S2CK
p. 483
40
Treatment of DUB
Oral contraceptive
pills (OCP)
Cyclic progesterone
Long-term
Endometrial
ablation
Hysterectomy
Acute hemorrhage
D&C
IV estrogen
MTB S2CK
Source: Hic et nunc, commons.wikimedia.org
p. 484
Contraception/Female Condoms
Advantages
Offer some protection against HIV and STDs
Under female control
Disadvantages
Not as effective as other methods
They are larger and bulkier than male
condoms
Contraception/Female Condoms
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p. 484
Contraception/Vaginal Diaphragm
Source: : ka Grzywacz, commos.wikimedia.org
MTB S2CK
p. 484
Source: Axefan2, commons.wikimedia.org
MTB S2CK
p. 484
41
Contraception/Cervical Cap
Contraception/Vaginal Diaphragm
Advantages
Under female control
Disadvantages
Need to be fitted properly
Requires advance preparation
Improper placement or dislodging reduces
efficacy
Source: Ceridwen, commons.wikimedia.org

Source: Dake, commons.wikimedia.org
MTB S2CK
Contraception/Oral Contraceptive Pills
p. 484
Hormones
Combination of both estrogen and progestin
Progestin only
Use
21 days of active pill
7 days placebo
Menses occurs during 7 days of placebo pills
Source; Matthew Bowden, commons.wikimedia.org
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p. 484
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p. 484
Contraception/Vaginal Ring
Advantages
Effective with perfect use
Reduces rates of ovarian and endometrial
cancer
Easily
y reversible
A flexible vaginal ring inserted in vagina
Disadvantages
User dependent
Risk of thromboembolism
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p. 484
Releases both estrogen and progesterone

Remains in place for 3 weeks
The vaginal
aginal ring has similar side effects
and efficacy to OCPs
MTB S2CK
p. 485
42
Contraception/Transdermal Patch
Contraception/Transdermal Patch
Transdermal patch
Combination of estrogen and progesterone
Placed on skin for 7 days
Patches shouldnt
sho ldnt be placed on breast
Side effects and efficacy = OCPs
Source : Keitei, commons.wikimedia.org
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p. 485
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Contraception/Injectable
Contraception/Implantable
Depo-Medroxyprogesterone Acetate
(DMPA)
Implant contraceptive system

Releases progestin daily
Inhibits ovulation and thickens cervical
mucus
IM injection
Every 3 months
Contraception/Intrauterine Device
Intrauterine device (IUD)

Copper device
Levonorgestrel device
Most commonly used worldwide

Most effective aside from sterilization
Source: Gloecknerd, commons.wikimedia.org
MTB S2CK
p. 485
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43
Contraception/Sterilization
Tubal Ligation/Occlusion
Vasectomy
Source: Nevit Dilmen ,commons.wikimedia.org
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p. 485
Vulva and Vagina/Labial Fusion
Vulva and Vagina
Fusion
Occurs when excess androgens are present
Exogenous
Endogenous
MCC of labial fusion is 21-B

hydroxylase deficiency
Treatment
Conservative
Reconstructive surgery
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Vulva and Vagina/Epithelial Abnormalities

Abnormality
Lichen
sclerosus
Age group
affected
Any age
If postmenopausal,
increased concern
for cancer
Description
White, thin skin
from labia to
perianal area,
parchment
q
g p
patients
Squamous
Anyy age;
Patients with
cell
whove had chronic chronic irritation
hyperplasia vulvar pruritus
develop hyper
keratosis (raised
white lesion)
Lichen
planus
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30s60s
p. 486
p. 485
Vulva and Vagina/Bartholin Gland Cyst

Treatment
Topical
steroids
Sitz baths or
lubricants
(relieve
pruritus)
Pruritic, polygonal, Topical

papular and
steroids
Purple
Bartholin Glands
Location: lateral sides of vulva
Function: secrete mucus
Bartholin Gland Cyst/Abscess
y
Presents with pain, tenderness, and
dyspareunia
Edema and inflammation with deep fluctuant
mass
MTB S2CK
p. 486
44

Clitoris
Labia Minora
Urethra
Skenes glands
g
Vagina
Bartholins glands
Source: Nicholasolan, commons.wikimedia.org
Bartholin Abscess
Simple incision and drainage (I&D)
Word catheter placement
4-6 weeks duration
Small rubber catheter, inflatable balloon tip is
inserted into cyst incision,
incision after the contents of
the cyst have been drained
Recurrence: marsupialization or excision
During I&D, fluid released should be
cultured for STDs (e.g., Neisseria gonorrhea
and Chlamydia trachomatis)
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p. 486
Vaginitis/Risk Factors
19-year-old woman with vaginal pruritus and
discharge for one week. Discharge is green and
profuse. Shes had multiple sexual partners in past 2
months. LMP 2 weeks ago. Wet mount: motile
flagellates.
a. Chlamydia Dx w/ culture or DNA probe
b. Bacterial vaginosis Clue cells on wet mount
c. Neisseria gonorrhoeae
d. Candidiasis Hyphae on wet mount
e. Trichomonas vaginalis
MTB S2CK
p. 486 487
Antibiotic use (Lactobacillus normally

keeps vaginal pH < 4
4.5)
5)
Diabetes
Overgrowth of normal flora
p. 487
Vaginitis
Bacterial vaginosis
Candidiasis
Gardnerella
Vaginal
discharge with
fishy odor;
gray white
Saline prep:
clue cells
Metronidazole
or clindamycin
Candida albicans
White, cheesy
vaginal discharge
Potassium
hydroxide (KOH):
pseudohyphae;
vaginal culture is
most specific
Miconazole or
clotrimazole,
econazole, or
nystatin
p. 487
Risk factors
MTB S2CK
Types of Vaginitis
MTB S2CK
Vaginitis: spectrum of conditions
Trichomonas (most
common nonviral STD)
Trichomonas: partners need

to be treated
Trichomonas
vaginalis
Profuse, green,
frothy vaginal
discharge
Saline prep:
motile
flagellates
Treat both
patient and
partner with
metronidazole
MTB S2CK
p. 487
45
Vaginitis/Gardnerella
Vaginitis/Candida albicans
Clue cells. Source: Per Grinsted, commos.wikimedia.org
Vaginitis/Trichomonas vaginalis
Source: Nephron, commons.wikimedia.org
Vulva/Malignant Disorders
Paget Disease
Intraepithelial neoplasia
Most common in postmenopausal Caucasians
Presentation
Vulvar soreness and pruritus
Appears as a red lesion with superficial white
coating
Trichomonas. Source: cdc.gov
Trichomonas. Source: Alex Brollo,

MTB S2CK
p. 487
Large cells with clear
cytoplasm in epidermis
Biopsy is needed for definitive diagnosis

Treatment
Wide local excision or vulvectomy
2 cm margin is optimal
Source: Nephron, commons.wikimedia.org
MTB S2CK
p. 487
46
Staging of Squamous Cell Carcinoma
Squamous Cell Carcinoma

Most common type of vulvar cancer
Stage
Findings
0
I
II
III
Carcinoma in situ
Limited to vaginal wall < 2 cm
Limited to vulva or perineum > 2 cm
Tumor spreading to lower urethra or anus,
unilateral
il
l lymph
l
h nodes
d present
Tumor invasion into bladder, rectum, or
bilateral lymph nodes
Distant metastasis
Presentation
Pruritus, bloody vaginal discharge, and
postmenopausal bleeding
Exam: ranges from a small ulcerated lesion to large
cauliflower-like lesion
A biopsy is essential for diagnosis
MTB S2CK
p. 488
IV
IVa
MTB S2CK
p. 488
Treatment
Unilateral: modified radical vulvectomy
Bilateral: radical vulvectomy
Uterine Abnormalities
Lymph nodes thatre involved must

undergo lymphadenectomy
MTB S2CK
p. 488
Uterine Abnormalities/Adenomyosis
Adenomyosis
Invasion of endometrial glands into myometrium
Typically between ages of 35 and 50
Diagnosis
Clinical diagnosis
Risk factors
Endometriosis
Uterine fibroids
Presentation
Dysmenorrhea and menorrhagia
MTB S2CK
p. 488
Uterus is large, globular, boggy
MRI
Treatment
Hysterectomy - only definitive treatment
MTB S2CK
p. 488
47
Uterine Abnormalities/Endometriosis
Endometriosis
Endometrial tissue outside of endometrial cavity
Most common sites are ovary and pelvic
peritoneum
Presentation
Cyclical pelvic pain
Abnormal bleeding
Infertility
Endometriosis occurs in women of reproductive

age
More common if first-degree relative has
endometriosis
MTB S2CK
p. 488
Dysmenorrhea and dyspareunia

are common in endometriosis
MTB S2CK
Nodular uterus
Adnexal mass
p. 488 489
Uterine Abnormalities/Treatment
Mild disease
NSAIDs
Combined OCPs
Severe disease
Danazole
Leuprolide acetate (leupron)
Surgery
Source: Julie M. Hastings, Asgerally T. Fazleabas, commons.wikimedia.org
MTB S2CK
p. 489 490
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p. 489
48
Uterine Abnormalities/Treatment
Ovarian Abnormalities
Polycystic Ovarian Syndrome/Symptoms
Polycystic Ovarian Syndrome/Diagnosis
Presentation
Amenorrhea or irregular menses
Hirsutism and obesity
Acne
Insulin resistance
Diagnostic test
Pelvic ultrasound
Elevated free testosterone
LH to FSH ratio > 3:1
MCC of androgen excess and

hirsutism
MTB S2CK
p. 489
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Uterus
Ovary
Source: Schomyny, commons.wikimedia.org
49
Polycystic Ovarian Syndrome/Treatment
Treatment
Weight loss
OCPs
Spironolactone (hirsutism)
Metformin (insulin resistance)
Clomiphene (infertility)
MTB S2CK
p. 490
50
Breast Cancer
Oncology
Presentation
Diagnosis
g
Genetic Tests
Treatment
Emma Holliday,
Holliday MD
Resident Physician
Radiation Oncology
University of Texas MD Anderson Cancer Center
Breast Cancer/Presentation
Breast Cancer/Presentation
Most often found by patient

Found in asymptomatic women
- On screening mammography
- By palpation of a mass
Hard immobile
Hard,
immobile, fixed to the chest wall
Painless lump
Skin changes
Nipple retraction
Nipple discharge
Source:http://www.4woman.gov/faq/cancerillustrations-with-t.gif
MTB S2CK
p. 347
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p. 347
Breast Cancer/Diagnostic Tests
Breast Cancer/Diagnostic Tests
Biopsy is the best initial test
Mammography
Screen the general
population starting
at age 50
Different methods are:

Fine needle aspiration (FNA)
Best initial biopsy
Core needle biopsy

Tells receptor status
Open surgical biopsy

Most accurate test
MTB S2CK
p. 347
MTB S2CK
p. 347
When Is Ultrasound the Answer?

A woman finds a hard, nontender breast mass on
self-examination. There is no alteration of the mass
with menstruation. She is scheduled to undergo a
FNA biopsy.
Which of the following is most likely to benefit the
patient?
a. Mammography
b. BRCA testing
c. Ultrasound
d. Bone scan
e. PET scan
MTB S2CK
Confirms an extra risk of cancer
Clinically indeterminate mass lesions. It

tells cysts versus solid lesions
Answer ultrasound if the lesion:
Is painful
Varies in size or pain with menstruation
Tells cystic vs solid

To exclude bone metastases
To look for metastatic disease
p. 348
MTB S2CK
p. 348
When Is PET Scan the Answer?
When Is PET Scan the Answer?
Determines content of abnormal lymph nodes that

are not easily accessible to biopsy. Cancer
increases uptake on PET scan.
For example:
How do you tell the content of

an abnormal, inaccessible lesion
without biopsy? Try PET scan.
MTB S2CK
p. 348
When Is BRCA Testing the Answer?

BRCA associated with increased risk of breast
cancer, particularly within families
BRCA associated with ovarian cancer
80-year-old woman with biopsy-proven breast

cancer has no nodes with cancer in the axilla. The
primary lesion is small and the woman may not
need adjuvant
j
chemotherapy.
py Chest CT shows an
abnormal hilar lymph node.
MTB S2CK
p. 348
When Is Sentinel Lymph Node Biopsy

the Answer?
When you want to know how likely it is that the
breast cancer has spread
What is not clear is what to do when BRCA is

positive BRCA not shown to add mortality benefit
positive.
The precise utility of MRI for breast

cancer is not yet clear.
Source:http://www.cancer.gov/ncicancerbulletin/022211/page2
MTB S2CK
p. 348
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p. 349
When Are Estrogen and Progesterone

Receptors Tested?
Estrogen receptor (ER) and progesterone receptor
(PR) testing is routine for all patients
Hormone manipulation therapy is done if either test
is positive
Breast Cancer/Treatment
Surgery Options
Lumpectomy
Modified Radical Mastectomy
Radical Mastectomy
Radical mastectomy is always the wrong answer

Lumpectomy + Radiation is JUST AS GOOD as
modified radical mastectomy
MTB S2CK
p. 349
MTB S2CK
p. 349
Hormonal Manipulation
All ER or PR positive patients should receive:
Know the differences in side effects:
Tamoxifen
Raloxifene
Aromatase inhibitors (anastrazole, letrozole,
exemestane)
If all are among the answer choices, aromatase
inhibitors are the answer to the most likely to benefit
the patient question
MTB S2CK
p. 349
When Is Trastuzumab the Answer?

All breast cancers should be tested for HER
2/neu. This is an abnormal estrogen receptor
Those who are positive should receive antiHER 2/neu antibodies known as trastuzumab
Trastuzumab decreases the risk of recurrent
disease
Tamoxifen rarely gives endometrial

cancer and clots (tamoxifen is a selective
ER modifier).
)
Aromatase inhibitors give osteoporosis
(aromatase inhibitors inhibit estrogen effect
everywhere, even the good effects, like on
bone density).
MTB S2CK
p. 349
When Is Chemotherapy
the Answer?
Neoadjuvant means therapy given

BEFORE the definitive treatment. Goal is
to decrease cancer burden
Adjuvant means an additional therapy to
clean up presumed microscopic cancer
cells too small in amount to be detected
MTB S2CK
p. 350
MTB S2CK
p. 350
When Is Adjuvant Chemotherapy

the Answer?
Adjuvant chemotherapy is the answer when:
Lesions >1 cm
Positive axillary lymph nodes found
Use tamoxifen when
multiple first-degree
relatives have breast
cancer. It lowers the
risk of breast cancer.
MTB S2CK
All of these definitely lower mortality:

Mammography
ER/PR testing, then tamoxifen/raloxifene
Aromatase inhibitors
Adjuvant chemotherapy
Lumpectomy and radiation
Modified radical mastectomy
Trastuzumab (anti-Her 2/neu)
Prophylaxis with tamoxifen
We do not know what

to do about BRCA
when it is positive.
p. 350
MTB S2CK
p. 350
Prostate Cancer/Presentation
Prostate Cancer
Presentation
Treatment
Screening
Obstructive
symptoms
Palpable mass
Elevated or rising
PSA
Source:http://www.cancer.gov/cancertopics/pdq/treatment/prostate/Patient/page2
MTB S2CK
p. 350
Prostate Cancer
Prostate Cancer/Treatment
Biopsy is the best

initial test and the
most accurate test.
Prostatectomy
Radiation therapy
Brachytherapy
Hormonal therapy
Watchful waiting
Half of men above age

80 have prostate cancer
on autopsy.
MTB S2CK
p. 350
Source:http://kidney.niddk.nih.gov/kudiseases/pubs/i
magingut/
MTB S2CK
p. 350 351
Prostate Cancer/Treatment
Gleason Grading
Prostatectomy has slight benefit over

radiation in terms of survival
Gleason Score =
Tumor Grade
Most common complications of

prostatectomy are:
Urinary incontinence
High Gleason grade

suggests greater
g
benefit of surgical
removal of the
prostate
Source:http://www.training.seer.cancer.gov/prostate/abstract-codestage/morphology.html
Get it out before it metastasizes if the Gleason

grade is high
MTB S2CK
p. 350 351
MTB S2CK
p. 351
Hormonal Manipulation in Prostate Cancer
Management That Is Definitely

Not Beneficial in Prostate Cancer
Flutamide
These answers are ALWAYS wrong:

Screening imaging study like ultrasound
Lumpectomy
Chemotherapy
Hormonal manipulation to prevent recurrences
Competitive inhibitor of testosterone & DHT
Leuprolide, goserelin
GNRH agonists: downregulates LH & FSH
Ketoconazole
K t
l
Suppresses testosterone
Orchiectomy
Stops endogenous production
MTB S2CK
p. 351
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p. 351
Prostate Specific Antigen (PSA)
PSA is controversial:
No mortality benefit with PSA
PSA is not to be routinely offered
Normal PSA does not exclude prostate cancer
High PSA doesnt always mean prostate cancer
If question specifically says, The patient

is requesting PSA to screen for cancer,
then the answer is do the test
The higher the PSA, the

greater the risk of cancer. PSA
corresponds to the volume of cancer.
MTB S2CK
p. 351
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p. 351
Elevated PSA Algorithm

Elevated PSA
Palpable mass
No palpable mass
Biopsy
p y the mass
Transrectal ultrasound
Mass seen
Biopsy the
mass
MTB S2CK
Lung Cancer
No mass seen
Multiple blind
biopsies
p. 351
Lung Cancer
Surgery
Who can get surgery?

Size of the tumor alone does not determine
whether or not it can be resected
Large tumors can be resected with
Demonstration of suffficient residual lung
volume by PFTs
It is solitary and surrounding tissue is healthy
Small tumors cannot be resected if PFTs

indicate poor lung function
MTB S2CK
Source:http://www.cancer.gov/cancertopics/pdq/treatment/non- Source:http://www.cancer.gov/cancertopics/pdq/treatment/non
small-cell-lung/Patient/page4
-small-cell-lung/Patient/page4
Source:http://www.cancer.gov/cancertopics/pdq/treatment/n
on-small-cell-lung/Patient/page4
p. 352
Lung Cancer
Surgery is not possible in these cases:

Bilateral disease
Malignant pleural effusion
Heart, carina, aorta, or vena cava is involved
Small cell cancer is considered unresectable
in 95% of cases because it is metastatic or
spread outside one lung
MTB S2CK
Ovarian Cancer
Screening
Diagnosis
g
Treatment
p. 352
Ovarian Cancer
Ovarian Cancer/Diagnosis
No screening test for ovarian cancer
The initial test is an ultrasound or CT scan
Presentation:
Woman >50 years old
Increasing abdominal girth
No history of liver disease
Weight loss, fatigue

Source:http://www.cancer.gov/cancertopics/pdq/treatment/ovaria
nepithelial/Patient/page1
MTB S2CK
p. 352
MTB S2CK
Source: James Heilman, MD,

http://en.wikipedia.org/wiki/File:POvarianCA.png
p. 352
Ovarian Cancer/Diagnosis
Ovarian Cancer/Treatment
Most accurate test is biopsy
The only cancer in which removing large

amounts of locally metastatic disease
benefits patient
Remove all visible tumor and pelvic
organs and give chemotherapy
Source: http://en.wikipedia.org/wiki/File:Ovarian_carcinoma.JPG
MTB S2CK
p. 352
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p. 352
Testicular Cancer/Presentation
Testicular Cancer
Presentation
Diagnosis
g
Treatment
Young men: 20-40 years old

Painless lump in the scrotum
Next best step?
Transillumination
Scrotal Ultrasound
Differential
ee a d
diagnosis?
ag os s
Epididymitis
Hematocele
Varicocele
MTB S2CK
p. 352
Testicular Cancer/Diagnosis
Testicular Cancer/Diagnosis
Seminoma
Has NORMAL AFP
Can have elevated
bHCG
LDH correlated with
disease burden
Diagnostic Testing
Remove the whole testicle
with inguinal orchiectomy
Do not cut the scrotum,
which
hi h can spread
d the
th
disease
Needle biopsy of the
testicle is always a wrong
answer
MTB S2CK
AFP
Embryonal
AFP and bHCG
AFP and bHCG
Teratoma
AFP and bHCG
Source:Ed Uthman, MD.

http://en.wikipedia.org/wiki/File:Seminoma_of_the_Testis.jpg
p. 352
Testicular Cancer/Treatment
Staging is performed with:
1st- orchiectomy
2nd- radiation
3rd- chemotherapy
CT scan of the abdomen, pelvis, and

chest
Lymphatic channels in the retroperitoneum
spread testicular cancer into the chest
p. 353
Yolk sac or
Endodermal sinus
Choriocarcinoma
Testicular Cancer/Staging
MTB S2CK
Non-seminoma
http://emedicine.medscape.com/article/437966-clinical#a0218
Testicular cancer is one of the only

malignancies in which chemotherapy can
cure widely metastatic disease, including
spread into the brain
MTB S2CK
p. 353
Prevention of Invasive Cervical Cancer
Cervical Cancer
Prevention/early detection
Clinical Presentation
Treatment
Human papillomavirus (HPV)

vaccine is given to all women
between ages 11 and 26
Pap smear is performed
starting at age 21
Everyy 3 yyears,, with
cytology, until 30 years old
After age 30, every 5 years,
if HPV testing added
Stop at age 65 with
adequate screening history
and low risk
MTB S2CK
Source:http://www.cdc.gov/cancer/dcpc/prevention/vaccination.htm
Source: Nephron,
http://en.wikipedia.org/wiki/File:Adenocarcinoma_on_pap_test_1.jpg
p. 353
Detection of Cervical Cancer
Detection of Cervical Cancer
Atypical squamous cells of undetermined

significance (ASCUS)
HPV testing
If positive
If negative
Pap smear does not lower

mortality as much as
mammography or colonoscopy.
colposcopy and biopsy

repeat Pap in 6 mo
Low-grade
g
and high-grade
g g
dysplasia
y p
Colposcopy and biopsy
MTB S2CK
p. 353
MTB S2CK
Cervical Cancer/Presentation
Asymptomatic
Detected on Pap
p. 353
Cervical Cancer
Symptomatic
Abnormal vaginal
bleeding
Post coital bleeding
Abnormal discharge
Pelvic p
pain or fullness
Dysuria
The management of early cervical cancer =

hysterectomy
Source: Hic et nunc, http://en.wikipedia.org/wiki/File:Scheme_hysterectomy-en.svg
Ophthalmology
Conjunctivitis
The Red Eye (Ophthalmologic Emergencies)
Cataracts
Diabetic Retinopathy
Retinal Artery & Vein Occlusion
Retinal Detachment
Macula Degeneration
Ophthalmology
Conrad Fischer, MD
New York City
Comparison of Viral and Bacterial

Conjunctivitis
Viral conjunctivitis
Bacterial conjunctivitis
Bilateral
Watery discharge
Easily transmissible
Normal vision
Itchy
Preauricular adenopathy
No specific therapy
MTB S2CK
Unilateral
Purulent, thick discharge
Poorly transmissible
Normal vision
Not itchy
No adenopathy
Topical antibiotics
Conjunctivitis
Viral conjunctivitis
Bacterial conjunctivitis
Source: phil.cdc.gov
David C Cogan Ophthalmic Pathology Collection
p. 497
Conjunctivitis
Etiologies of The Red Eye

Conjunctivitis
Uveitis
Glaucoma
Abrasion
Autoimmune
diseases
Pain
Trauma
Photophobia
Fixed
midpoint
pupil
Feels like
sand in
eyes
Slit lamp
examination
Tonometry
Fluorescein
stain
Topical
steroids
Acetazolamide
Mannitol
Pilocarpine
Laser
trabeculoplasty
No specific
therapy
Patch not
clearly
beneficial
Presentation
The must know subjects

in ophthalmology are:
The red eye (emergencies)
Diabetic retinopathy
Artery and vein occlusion
Retinal detachment
Discharge
Eye findings
Normal pupils
Most
accurate test
Clinical
diagnosis
Best initial
therapy
Topical
antibiotics
MTB S2CK
p. 497
MTB S2CK
p. 498
Glaucoma/Chronic Glaucoma
Most often asymptomatic

Diagnosed by screening
Confirmation with tonometry
Elevated intraocular pressure
Glaucoma/Chronic Glaucoma
Treat to decrease production of aqueous humor or
increase drainage
Prostaglandin analogues Topical carbonic
Latanaprost
anhydrase
Travoprost
inhibitors
Bimatoprost
Topical
p
beta blockers
Timolol
Carteolol
Metipranolol
Betaxolol
Or
Levobunolol
MTB S2CK
p. 498
Glaucoma/Acute Angle Closure Glaucoma
Look for
Sudden onset
Extremely painful, red eye hard to palpation
Walking into dark room precipitates pain
because of p
pupillary
p
y dilation
Pupil doesnt react to light because its stuck
Cup-to-disc ratio > 0.3
MTB S2CK
Dorzolamide
Brinzolamide
Alpha-2 agonists
Apraclonidine
Pilocarpine
Laser
p. 498

Conjunctival
vessels dilated
at corneal edge
Hazy
cornea
Author:Jonathan Trobe, M.D. Source: commons.wikimedia.org
MTB S2CK
p. 498
Herpes Keratitis
Diagnosis
Confirmed with tonometry
Infection of cornea
Eye is red, swollen, and painful, but
dont use steroids
Steroids markedly increase production
of virus
Treatment
IV acetazolamide
IV mannitol (osmotically draws of fluid out)
Pilocarpine & beta blockers constrict pupil &
enhance drainage
Laser iridotomy
MTB S2CK
p. 498
Fluorescein stain confirms dendritic

pattern
MTB S2CK
p. 499
Herpes Keratitis
Cataracts
Treatment
Oral acyclovir, famciclovir, or valacyclovir
Topical trifluridine or idoxuridine
No medical therapy for cataracts

Surgically remove lens & replace with new
intraocular lens
New lens may automatically have bifocal
capability
Early cataracts are diagnosed with an
ophthalmoscope or slit-lamp exam
Advanced cataracts visible on exam
Beware of steroid use for

herpes keratitis
Steroids worsen condition
MTB S2CK
p. 499
MTB S2CK
Cataracts
p. 499
Annual screening exams INDISPENSIBLE!!!!
Detects retinopathy before visual loss occurs
Nonproliferative or background retinopathy is
managed by controlling glucose level
Most accurate test is
Fluorescein angiography
Proliferative: treated with laser photocoagulation

Vascular endothelial growth factor inhibitors
(VEGF) injected in some patients to control
neovascularization
nih.gov
MTB S2CK
p. 499
Retinal Artery and Vein Occlusion
Vitrectomy may be necessary to remove a vitreal

hemorrhage obstructing vision
Both present with

Sudden onset monocular visual loss
Cant make diagnosis without retinal examination
No conclusive therapy for either condition
MTB S2CK
p. 499
New blood vessel formation obscures vision. Source: Conrad Fischer, MD.
MTB S2CK
p. 500
Retinal Artery Occlusion
Retinal Vein Occlusion
Retinal vein occlusion leads to extravasation of blood into the retina.

Source: Conrad Fischer, MD.
Retinal artery occlusion presents with sudden loss of vision and a pale retina and dark
macula. Source: Conrad Fischer, MD.
MTB S2CK
p. 500
MTB S2CK
p. 500
Retinal Artery and Vein Occlusion
Retinal Detachment
Treatment of artery occlusion attempted with...

100% oxygen
Acetazolamide to intraocular pressure
Thrombolytics
Caused by
Trauma
Extreme myopia (changes shape of eye)
Diabetic retinopathy
Anything that pulls on retina can detach it
Presents with
Sudden onset of painless, unilateral loss
of vision
Described as curtain coming down
Macula
Mac
la is described as
cherry redin artery
occlusion because the
rest of retina is pale
MTB S2CK
p. 500
MTB S2CK
p. 501
Retinal Detachment
Macular Degeneration
Reattachment by mechanical methods

Surgery, laser, cryotherapy
Injection of expansile gas pushes retina back up
against globe of eye
MTB S2CK
p. 501
Sudden painless loss of vision like a courtain coming down.

MCC of blindness in older persons in U.S.

Idiopathic
Atrophic (dry) type and neovascular (wet) type
Far more common in older patients
Bilateral
N
Normal
l external
t
l appearance off eye
Central vision lost
MTB S2CK
p. 501
Neovascular disease
More rapid
More severe
New vessels grow between retina and underlying
Bruchs membrane
Neovascular or wet type causes 90% of permanent
blindness from macular degeneration
Atrophic macular
degeneration has no
proven effective therapy
MTB S2CK
p. 501
MTB S2CK
p. 502
Macular degeneration can be diagnosed only by visualization

of the retina. Source: Conrad Fischer, MD.
Best initial therapy for neovascular disease

VEGF inhibitors
Ranibizumab or bevacizumab
Injected directly into vitreous chamber

every few weeks
Over 90% stop progression
1/3 improve vision
MTB S2CK
p. 502
Routine Management
of the Newborn
Pediatrics
Physical Exam
Apgar Score
Eye Care
Routine Screening and Prevention
Ryan Close, MD MPH

Resident Physician
Internal Medicine Pediatrics
Hospital of the University of Pennsylvania
Apgar Score
Physical Exam
Adults
Physical exams start
with vital signs...Newborns
Heart Rate (HR)
60 100 BPM
120160 BPM
Respiratory Rate
(RR)
12 24 BrPM
40 60 BrPM
Systolic Blood
Pressure (SBP)
120 mmHg
65 mmHg
Diastolic Blood
Pressure (DBP)
80 mmHg
50 mmHg
MTB S2CK p. 403
Apgar Score
Scores calculated at 1 minute and 5 minutes

Score at 1 minute
Represents conditions during labor and
delivery
Indicates need for resuscitation
Score at 5 minutes
Represents effectiveness of resuscitation
efforts
Prognostic of survival
MTB S2CK p. 404
Important part of physical exam

Translates physical exam into a score
Used for management decisions
Provides both short- and long-term

prognostic indicators
MTB S2CK p. 404
Apgar Score
0 points
1 point
2 points
Appearance
Skin color
Blue all over Pink torso/blue

extremities
Pink all over
Pulse
Rate
< 60 bpm or 60 100 bpm

asystole
> 100 bpm
Grimace
G
i
N response Grimace/
No
Gi
/
Reflex & irritability
feeble cry
S
Sneeze,
cough,
h
loud cry
Activity
Muscle tone
None
Some flexion
Active
movement
Respiration
Breathing
Absent
Weak, irregular
Strong
MTB S2CK p. 404
Apgar Score
Low Apgar score isnt predictive of

cerebral palsy
Knowing differences in management if

Apgar score is low
MTB S2CK p. 404
Prevention/Eye Care
A 3.9 kg male infant whose Apgar scores were 9 and
10 at 1 and 5 minutes, respectively, presents five
days after delivery because of red eyes. The delivery
was without any complications.
What is the most likely diagnosis at day 5 of life?
a. Chemical irritation
b. Neisseria gonorrhoeae
c. Chlamydia trachomatis
d. Group-B Streptococci
e. Herpes simplex
A 28-year-old G1PO woman delivers a 3.9 kg male infant

whose Apgar scores are 9 and 10 at 1 and 5 minutes,
respectively. The delivery was uncomplicated, and both
mother and child are in no acute distress.
Whats the most appropriate first step upon delivery of this
patient?
a. Intubate the child No signs of respiratory distress / high Apgar score
b. Send cord blood for arterial blood gas (ABG) Patient is stable
c. Suction the mouth and nose
d. Nasogastric tube (NGT) placement No need for decompression
e. Give prophylactic antibiotics No evidence of infection or sepsis
What we are not told:
- Is this child term, or pre-term?
- Vital signs ?
MTB S2CK p. 403
- Erythromycin ointment
- Tetracycline ointment
- Silver nitrate drops
Chemical
Irritation
Due to
silver
nitrate
Developing
countries
Not an
allergy
Prevention/Eye Care
Chlamydia
trachomatis
Neisseria
gonorrhea
Gram
Gramnegative
diplococci
Prevent with
ointments
Treat with
ceftriaxone
Not effectively
prevented by
prophylaxis
ointments
Herpes
Simplex
Treat with
systemic
acyclovir
and topical
vidarabine
Treat with oral

erythromycin
MTB S2CK p. 404 405
Prevention/Eye Care
Prevention & Screening/Vitamin K Deficiency
A 3.9 kg male infant whose Apgar scores were 9 and

10 at 1 and 5 minutes, respectively, presents five
days after delivery because of red eyes. The delivery
was without any complications.
What is the most likely diagnosis at day 5 of life?
a. Chemical irritation
b. Neisseria gonorrhoeae
c. Chlamydia trachomatis
d. Group-B Streptococci
e. Herpes simplex
Vitamin K deficient bleeding = hemorrhagic disease

of newborn
Neonate colon lacks normal bacterial flora that
produces vitamin K
Vitamin K is responsible for clotting factors II, VII,
IX,, and X as well as proteins
p
C and S
Vit K
Inactive
Clotting
Factors
Active
Clotting
Factors
Treatment: one IM injection of vitamin K

Oral doses will not work
MTB S2CK p. 405
Prevention & Screening/Vitamin K Deficiency

Intrinsic Pathway
Prevention & Screening/Testing
Extrinsic Pathway
XIIa
XI
XIa
IX
VIII
TF
IXa
VIIa
VIIIa
VII
II
Xa
V
Va
Fibrinogen
IIa
Thrombin
Fibrin
Newborns should be screened for:

Phenylketonuria (PKU)
Congenital adrenal hyperplasia (CAH)
Biotinidase
Beta-thalassemia
Galactosemia
G l t
i
Hypothyroidism
Homocysteinuria
G6PD deficiency
Hearing test
MTB S2CK p. 405 406
Transient Conditions of the Newborn
The Big Transient Three
Medical Conditions
of the Newborn
Transient conditions
Polycythemia
Tachypnea
Hyperbilirubinemia
Delivery associated injuries
Newborn infections
Polycythemia
Tachypnea
Hyperbilirubinemia
MTB S2CK
p. 406 407
Transient Polycythemia of the Newborn
Transient Polycythemia of the Newborn
Polycythemia
Transient Polycythemia
Increased RBCs
Benign
Most often related to cord clamping
Epo!
Primary vs. Secondary

Primary: Normal or low EPO levels
Secondary: High EPO levels
Source: James Van Rhee
Hypoxia
Polycythemia of the Newborn

Can be very harmful
EPO!
Hyperviscosity, decreased perfusion, thromboses

LGA, SGA, and IDM
MTB S2CK
p. 406
MTB S2CK
p. 406
Transient Tachypnea of the Newborn (TTN)
Transient Tachypnea of the Newborn (TTN)
Tachypnea
The Takeaway:
Benign condition
Term infants
Delivered via C-section
Oxygen, antibiotics, and watch closely
Watch for
60 BrPM (40 60 is normal)
TTN or Respiratory Distress Syndrome II (RDS II)
Benign condition 1% to 2% of newborns

Causes
Excess remaining lung fluid
Pulmonary immaturity
Surfactant deficiency/insufficiency
Management
Sepsis
Oxygen and antibiotics

Work-Up: CBC and chest radiograph
MTB S2CK
p. 406 407
MTB S2CK
Transient Hyperbilirubinemia
Hyperbilirubinemia
Production > Elimination
p. 406 407
increased TSB
From increased production, decreased elimination,

or both
Indirect = Unconjugated bilirubin

Direct = Conjugated bilirubin
(Total Bili) (Direct Bili) = Indirect Bili
Any hyperbilirubinemia < 24 hr of life

Evaluation
Any conjugated hyperbilirubinemia
Evaluation
Benign and very common (~60% newborns)
Peaks at 2-3 days of life
Increased production of unconjugated bilirubin
MTB S2CK
p. 407
MTB S2CK
p. 407
Transient Conditions of the Newborn
Delivery Associated Injuries
The Big Transient Three
Types of injuries
Subconjunctival hemorrhage
Skull fracture
Scalp injuries
Brachial palsies
Clavicular
Cl i l fracture
f t
Facial nerve palsy
Polycythemia
Tachypnea
Microhemorrhages
Benign
Caput succedaneum
Cephalohematoma
Brief paralysis
of facial nerve
Hyperbilirubinemia
MTB S2CK
p. 406 407
MTB S2CK
p. 407
Brachial Plexus Injuries
Brachial Plexus Injuries
General
Macrosomic infants (e.g., IDM)
Shoulder dystocia
Duchenne-Erb Paralysis
90% of brachial palsies
C5 C6
Waiters tip
Cannot abduct or externally rotate
Klumpke Paralysis
C7 T1
Claw hand +/- Horner syndrome
MTB S2CK
p. 407 408
Clavicular Fracture
Physical Exam
Most common newborn fracture

Usually result of:
Physical exams start with vital signs...
Shoulder dystocia
Systolic
Blood
Pressure
(SBP)
Diastolic
Blood
Pressure
(DBP)
60-100 BPM 16-24 BrPM
120 mmHg
80 mmHg
120-160
BPM
65 mmHg
50 mmHg
Age Group
Heart Rate
(HR)
Adult
Newborns
Respiration
Rate (RR)
Best diagnostic tool:

Radiograph
g p
Most appropriate management:
40-60 BrPM
Immobilize
MTB S2CK
p. 408
Neonatal Sepsis
ToRCH Infections
Early
Late
GBS
E. Coli
Listeria
Staphylococci
E. Coli
GBS
IVF
Cultures
Antibiotics
Ampicillin
Gentamicin
Cefotaxime*
MTB S2CK
p. 433
Ampicillin
Gentamicin
Cefotaxime*
Type
Presentation
Diagnostic tests Treatment
Chorioretinitis, hydrocephalus,
Toxo
plasmosis ring enhancing lesion
Initial: IgM
Most accurate: PCR
Pyrimethamine
and sulfadiazine
Syphilis
Rash on palms/soles, snuffles,

frontal bossing, Hutchinson 8th
n. palsy, saddle nose
Initial: VDRL / RPR

Most accurate: FTA
ABS / Dark Field
Penicillin IV
Rubella
PDA, cataracts, deafness,

hepatosplenomegaly, low plts,
elevated bilirubins
Elevated maternal
rubella IgM with
clinical picture
Supportive
CMV
Periventricular calcifications,
microcephaly, chorioretinitis,
hearing loss
Initial: Urine/saliva
viral titers
Most accurate: PCR
Ganciclovir
Herpes
Week 1: Shock and DIC

Week 2: Vesicular skin lesions
Week 3: Encephalitis
Initial: Tzanck smear

Most accurate: PCR
Acyclovir and
supportive care
MTB S2CK
p. 434
Amniotic Fluid Abnormalities
Common Abnormalities
of the Newborn
Abdominal Abnormalities
Genitourinary Abnormalities
Amniotic Fluid
80% from mother
20% from infant
Problems
Polyhydramnios (too much)
Oligohydramnios (too little)
MTB S2CK
p. 408
Polyhydramnios
Too much fluid
Overproduction / Decreased resorption
CNS malformations
Polyhydramnios
GI malformations
MTB S2CK
p. 408
Esophageal atresia
MTB S2CK
p. 408
Oligohydramnios
Too little fluid (Low AFI)
Under production
Causes
A premature infant born at 28 weeks in respiratory

distress with grunting, nasal flaring, and use of
accessory muscles. Bowel sounds heard upon
auscultation of the back and chest X-ray shows air
fluid levels in the chest.
a. Hydrocele
b. Gastroschisis
c. Diaphragmatic Hernia
d. Hiatal Hernia
e. Omphalocele
Post-term pregnancies
Renal agenesis and renal failure
Cord Compression
ACE-inhibitors
Potters syndrome
MTB S2CK
p. 408
MTB S2CK
p. 409
a.
b.
c.
d
d.
e.
Urological issue not respiratory issue

Hydrocele
Abdominal wall defect
Gastroschisis
Diaphragmatic Hernia
M
More
common iin GERD seen in
i adults
d lt
Hi t l Hernia
Hiatal
H i
Omphalocele Abdominal wall defect
MTB S2CK
p. 409
Diaphragmatic Hernia
Congenital defect in diaphragm
Two types: Bochdalek and Morgagni
LEFT side most common
Key findings:
Respiratory distress
Scaphoid abdomen
Bowel sounds in chest
Abnormal chest radiograph
First step in management
MTB S2CK
p. 409
Omphalocele
Midline wall defect
With sac covering
Associations
Imperforate anus
Congenital heart defects (50%)
Conjoined twins
Trisomy 18 (Edwards
syndrome)
Beckwith Wiedemann
syndrome
Gastroschisis
Lateral wall defect

No sac covering
Atresias
Surgery is necessary
Surgery is necessary
Intubation
MTB S2CK
p. 409
MTB S2CK
p. 410
Abdominal Abnormalities/Tumors
Wilms Tumor
Most common primary renal malignancy in peds
Presents with
An elevated AFP in abdominal wall defects

The MCC of elevated AFP is incorrect dating
Umbilical hernias: Similar to omphaloceles
Asymptomatic flank mass

Hematuria
Hypertension and aniridia
First step in evaluation: Abdominal ultrasound

MC diagnostic test: Computed tomography
Relationships with syndromes
WAGR, Denys-Drash, Beckwith-Wiedemann
Treatment: Surgery + chemotherapy + radiation

MTB S2CK
p. 410
MTB S2CK
p. 410
Abdominal Abnormalities/Tumors
Genitourinary Abnormalities
Neuroblastoma
Very common among children
Often involves adrenal gland
Presents with
Hydrocele
Painless, benign, fluid-filled
Cryptorchidism
Undescended testis, increased cancer risk
Surgical correction after 6 months
Hypospadias
Ventral surface opening, surgery
Epispadias
Dorsal surface opening, surgery
Painful abdominal mass

Neurological findings
Opso(myo)clonus
Diarrhea
Diagnostic keys
Urine catecholamines and their metabolites
Vanillyl Mandelic Acid (VMA)
Homovanillic acid (HVA)
MTB S2CK
p. 411
MTB S2CK
p. 411
Cyanotic Heart Defects
Tetralogy of Fallot
Tetralogy of Fallot
Transposition of the Great Vessels
Hypoplastic Left Heart Syndrome
Truncus Arteriosus
Total Anomalous Pulmonary Venous
Return
Tetralogy of Fallot
The most common cyanotic heart

defect in children
Four aspects
p
Pulmonary stenosis
VSD
Overriding aorta
Right ventricular hypertrophy
MTB S2CK
p. 412
Tetralogy of Fallot/Signs & Symptoms
Tetralogy of Fallot
Cyanosis
Lips and extremities
Squatting
Increases systemic pressure
Shunts blood to pulmonary circulation
Holosystolic
H l
t li murmur
VSD
There are 3 holosystolic murmurs
Mitral regurgitation (MR)
Tricuspid regurgitation (TR)
Ventricular septal defect (VSD)
MTB S2CK
p. 412 413
Tetralogy of Fallot
Two separate circulations

Right heart/systemic circulation
Left heart/pulmonary circulation
Defect dependent
Patent ductus arteriosus (PDA)
VSD
Atrial septal defect (ASD)
Most common cyanotic lesion of neonates
MTB S2CK
p. 413
Treatment
Prostaglandin E1
Surgery
MTB S2CK
p. 413
Syndrome
Absent pulses
Right ventricular heave
Mild cyanosis/gray
MTB S2CK
p. 414
Truncus Arteriosus
Truncus Arteriosus
One Great Vessel

The less common heart defect (2%)
NOT dependent on PDA
Mild cyanosis
Big problem: Pulmonary hypertension
Treat with
Surgery!
MTB S2CK
p. 414
Total Anomalous Pulmonary Venous Return
Abnormal pulmonary venous return

Pulmonary veins
Right atrium
PFO dependent
Right heart overload
Two types:
With obstruction
Without obstruction
MTB S2CK
p. 414 415
TAPVR 2
Sign/Symptoms
Tests
TAPVR with
obstruction
Early in life with

respiratory
distress and
severe cyanosis
CXR shows
pulmonary
edema
Echo is test of
choice
TAPVR without
obstruction
Presents later
Age 1 2 years
with heart
failure
S
Surgery
CXR shows
snowman sign
Echo is test of
choice
MTB S2CK
Treatment
Surgery
p. 415
10

R
L Shunt
PDA dep
VSD
Surgery
TOF
Acyanotic Heart Defects
TGV
Hypoplastic LH
Truncus Art
TAPVR
Acyanotic Heart Defects
Heart murmur in a child
VSD
3-year old female brought in because her parents say

she wont eat anymore. Upon physical examination, a
loud pansystolic murmur is appreciated. The child
appears small for her age, but her records dont show
any maternal or delivery complications.
ASD
Which of the following is the most likely finding on EKG?
PDA
Coarctation of the aorta
a.
b.
c.
d.
e.

RBBB
ST-segment elevation
QT-prolongation
P-wave inversion
MTB S2CK
Ventricular Septal Defect
p. 415
VSD, Murmurs, and Auscultation
There are 3 holosystolic murmurs...

MR
TR
VSD
VSD
VSD is the most common

congenital heart defect
MTB S2CK
p. 415
11

Pathophysiology
Left-to-Right shunt (opposite of cyanotic defects)

Pulmonary hypertension
Presentation
Dyspnea with distress
Loud pulmonic S2
High-pitched holosystolic murmur
Tests
CXR: Findings are not diagnostically helpful
Best initial test is an echocardiogram
Most diagnostic (definitive) test is a cardiac
catheterization
MTB S2CK
p. 416
Heart murmur in a child
VSD

a.
b.
c.
d.
e.

RBBB
ST-segment elevation
QT-prolongation
P-wave inversion
MTB S2CK
p. 415
VSD & Eisenmenger Syndrome

a.
b.
c.
d.
e.

RBBB ASD or ischemic disease
ST-segment elevation Myocardial infarction
Electrolyte disturbances
QT-prolongation
P-wave inversion Atrial arrhythmias
MTB S2CK
p. 415
12
Atrial Septal Defect
Types of ASDs
Primum, secundum, and sinus venosus
2xs common in men
Usually asymptomatic
Fixed wide-splitting S2 vs. Physiologic splitting
Tests
Best initial test is an echocardiogram (bubble study)
Most diagnostic test is a cardiac catheterization
Prognosis
Most close without intervention
MTB S2CK
p. 416 417
Patent Ductus Arteriosus
Without closure
Failure of closure after 12 hours

Left-to-Right shunt
Presentation
Atrial enlargement
Dysrhythmias
Embolic Risk
Treatment
Surgical
Machinery-like murmur
Wide pulse pressures
Bounding pulses
Tests
Best initial test is an echocardiogram
Most diagnostic test is a cardiac catheterization
Treatment
NSAIDS (indomethacin)
MTB S2CK
p. 417
13
!!
!
!
!!
Jaundice,
Hyperbilirubinemia
Gastroenterology,,Part,1,
Jaundice,)
Esophageal,)Duodenal,)Choanal)Atresia)
Pyloric)Stenosis)
Hirschsprungs)Disease)
Production > Elimination
Jaundice very common in newborns

Red flags:
Jaundice < 24 hrs of life ! Evaluation
Direct hyperbilirubinemia ! Evaluation
Hyperbilirubinemia after 3 weeks ! Evaluation
Jaundice never common in children

Physiologic Benign
Primary concern ! Kernicterus
MTB)S2CK))A))p.)419)
The,Approach,to,Jaundice,
Child
or Newborn?
Child
Child
or Newborn?
Evaluate
Newborn
24 hrs
of life?
Evaluate
Newborn
Y
24 hrs
of life?
Evaluate
Evaluate
Direct vs.
Indirect
Direct vs.
Indirect
Direct vs.
Indirect
Direct
Child
Direct vs.
Indirect
Indirect
Direct
Indirect
Direct
Direct
Indirect
Evaluate
Sick
appearing?
N
Y
2 weeks of life
Breast milk
jaundice?
1 2 wks
Transient vs.
Breast feeding
jaundice
< 1 wk
Hepatocyte:
- Infection
- Sepsis
- Endocrine
- Genetic
Obstruction:
- Biliary
atresia
Jaundice,
Kernicterus
Bilirubin encephalopathy
Basal gangalia, hippocampus, subthalamic
nucleus
Multiple neurological abnormalities
InD
Prevention
Phototherapy vs. exchange transfusion
)
Atresias,
Esophageal,Atresia,
Esophageal,Atresia,Types,
Choanal,Atresia,
Duodenal,Atresia,
)Blind)esophagus)
80 90%
of cases
MTB)S2CK))A))p.)420)A)424)
20% of all cases = unimportant
Atresias,
Esophageal,Atresia,
Atresias,
Choanal,Atresia,
Duodenal,Atresia,
)Blind)esophagus)
)Presents)with:)
Esophageal,Atresia,
Choanal,Atresia,
)Blind)esophagus)
)Presents)with:)
)Buccopharyngeal))
)membrane)
)(+))resp)distress)
)Best)iniKal)test:)
Frothing, cough,
cyanosis, and
respiratory distress
with feeds
Frothing, cough,
cyanosis, and
with feeds
No)resp)distress)at,
rest,
)IniKal)test)
)CXR)
rest,
)IniKal)test)
)CXR)
)Concerns)
)AspiraKon)PNA)
)
Treatment of choice for aspiration PNA

is penicillin-like antibiotics (amoxicillinclavulanate, piperacillin-tazobactam) or
clindamycin
MTB)S2CK))A))p.)420))
Atresias,
Choanal,Atresia,
)Blind)esophagus)
)Presents)with:)
)Buccopharyngeal))
)membrane)
)(+))resp)distress)
)Best)iniKal)test:)
rest,
)IniKal)test)
)CXR)
)Concerns)
Newborns are
obligate nose
breathers
Pass NG tube
)Most)diagnosKc:)
CT Scan
CT sees bone
better
)First)step)in))
)management:)
Secure airway!
)AspiraKon)PNA)
)
MTB)S2CK))A))p.)420)A)424)
Duodenal,Atresia,
Esophageal,Atresia,
Frothing, cough,
cyanosis, and
with feeds
)Concerns)
Duodenal,Atresia,
Pass NG tube
)Most)diagnosKc:)
CT Scan
)First)step)in))
)management:)
Secure airway!
Duodenal,Atresia,
)Failed)duodenal))
)canalizaKon)
)NO,resp)distress))
)Bilious,vomiKng))
)IniKal)test)
AXR
Double-Bubble
Double-bubble +
distal gas =
volvulus
)AspiraKon)PNA)
)
Source: James C. Pascual
MTB)S2CK))A))p.)424A425)
Atresias,
Pyloric,Stenosis,
Esophageal,Atresia,
Choanal,Atresia,
)Blind)esophagus)
)Buccophayngeal))
)membrane)
)(+))resp)distress)
)Best)iniKal)step:)
)Presents)with:)
Frothing, cough,
cyanosis, and
with feeds
rest,
)IniKal)test)
)CXR)
)Concerns)
)AspiraKon)PNA)
)
MTB)S2CK))A))p.)424A425)
Pass NG tube
)Most)diagnosKc:)
CT Scan
)First)step)in))
)management:)
Secure airway!
Duodenal,Atresia,
)Failed)duodenal))
)canalizaKon)
)NO,resp)distress))
)Bilious,vomiKng))
)IniKal)test)
AXR
Double-Bubble
Hypertrophy of pyloric sphincter

Not atresia
Presents
3 weeks of age
Nonbilious vomiting ! projectile!
Small olive pit size epigastric mass
Dehydration contraction alkalosis
)TRISOMY)21)
)First)step)in))
)management:)
IVF
Pyloric,Stenosis,
Pyloric,Stenosis,
Contraction Alkalosis
Tests
Loss of ECF
Fluid Loss
Vomiting
Loss of H+
Loss of K+
Loss of Cl-
Ultrasound: more
diagnostic than X-ray
Radiograph is helpful
RAAS
Metabolic Alkalosis
High pH, High Bicarb, High pCO2
Hypochloremic
Hypokalemic
Treatment
IVF
NG Tube
Pyloric myotomy
Source: Gergory J. Hall
Hirschsprung,Disease,
Congenital lack of ganglionic cells in large bowel
KEY clinical feature
Failure or delayed passage of meconium
Progresses to large bowel obstruction (LBO)
Abdominal distention
Best initial diagnostic test: AXR

Most diagnostic test: Rectal suction biopsy
NOT barium study
NOT manometry
Treament
Surgery
MTB)S2CK))A))p.)422A423)
!
!
!
!
!
Bilious Vomiting
Meckels Diverticulum
Rule of 2s
Bilious
Vomiting
Duodenal
Atresia
Within 1st day

Initial test:
AXR
Volvulus
Intussusception
Within 1st year

Initial test:
AXR
Within 1st year

Initial test:
US
Doughnut
First Step
IVF!
Treament
Surgery
First Step:
IVF!
Treatment
Air Enema
Double
bubble
First Step
IVF!
Treament
Surgery
MTB S2CK
p. 424 426
Painless rectal
bleeding
MTB S2CK
Diarrhea and Gastroenteritis
Katsumi M. Miyai, M.D., Ph.D., Regents of the

University of California. Used with permission.
p. 426 427
The most important questions to ask:

Is this chronic or acute?
Infectious or not?
Bloody or not?
How sick is the child?
MTB S2CK
2% prevalence
2 years old
2 ft proximal to
ileocecal valve
2 inches long
2 types of ectopic tissue
Males 2x more affected
2% symptomatic
Infectious
Diarrhea
Viral
Parasites
Fungal
Giardia
Cryptosporidia
Candida spp
Histoplasma
Bacterial
Salmonella
Shigella
C difficile
C.
E. Coli
Campylobacter
Yersinia
p. 427
Infectious
Diarrhea
Viral
Rotavirus
Most
M t common
Winter
Symptoms:
Fever, emesis
NO blood
< 7 days
Viral prodrome
Vaccine
Adenovirus
Endemic
E d i
Year round
Symptoms:
Fever, emesis
NO blood
> 7 days
Viral prodrome
Small, round
Norwalk
N
lk
EPI demic
Symptoms:
Explosive
Cramping, pain
Short lived
1 2 days
Management
Hydration is key
Almost always the answer
Antibiotics for suspected bacterial
i f ti
infection
WBC or blood in stool
NEVER use antidiarrheal meds in
these patients
MTB S2CK
p. 428
15
Large for Gestational Age/Macrosomia
Endocrinology
Infants of Diabetic Mothers
Congenital
g
Adrenal Hyperplasia
yp p
(CAH)
(
)
Vitamin D Deficiencies
A 10.5-pound infant is born to a mother with Type I diabetes. Upon

examination of newborn, he is shaking, and a holosystolic murmur is
heard over precordium. The babys right arm is adducted and
internally rotated. His lab findings show an elevated bilirubin.
Which of the following is the most appropriate next step in
management?
a.
b.
c.
d.
e.
IV insulin
Blood sugar level
Serum calcium levels
Serum TSH
CT head and neck
MTB S2CK
Infants of Diabetic Mothers (IDM)
Maternal
Hyperglycemia
MTB S2CK
Fetal / Infant
Hyperglycemia
Infants of Diabetic Mothers (IDM)
Infant
Hyperinsulinemia
p. 430
IDM/Macrosomia
Macrosomia = weight 4500 g
Large for gestational age (LGA) = top 90th percentile
Causes in IDM
Oversupply of AAs, glucose, etc.
Insulin is a growth factor
Consequences
C
Trauma
Risk of C-section
Treatment
None Prevention!
MTB S2CK
p. 430
p. 429
Four primary issues...

Macrosomia
Hypoglycemia
Electrolyte abnormalities
Jaundice
MTB S2CK
p. 430
IDM/Hypoglycemia
Maternal
Hyperglycemia
Infant
Hyperglycemia
Infant
Hyperinsulinemia
Birth
MTB S2CK
p. 430
16
IDM/Hypoglycemia
IDM/Electroyte abnormalities
Direct consequence of maternal hyperglycemia

Hypertrophied pancreatic beta-cells
Insulin overproduction
Hyperresponsive
After birth:
No
N changes
h
iin iinsulin
li production/activity
d ti / ti it
Consequences
Severe hypoglycemia
Seizures
Treatment
Monitoring + Glucose
Hypocalcemia
Hypomagnesemia / Hyperphosphotemia
Twitching and Tremulousness
Cardiac arrhythmias
Calcium and Magnesium levels linked
Always
Al
check
h kb
both
th
Correct together
MTB S2CK
p. 430
MTB S2CK
p. 430
IDM/Jaundice
One-third of IDMs will develop jaundice
Unconjugated/Indirect hyperbilirubinemia
Overproduction of bilirubin
Resolving hematomas
Polycythemia
Treatment
T t
t
Phototherapy
MTB S2CK
p. 430
A 10.5-pound infant is born to a mother with Type I diabetes. Upon

examination of newborn, he is shaking, and a holosystolic murmur is
heard over precordium. The babys right arm is adducted and
internally rotated. His lab findings show an elevated bilirubin.
Which of the following is the most appropriate next step in
management?
a.
b.
c.
d.
e.
IDMs have hyperinsulinemia
IV insulin
Blood sugar level
Serum calcium levels
Serum TSH
CT head and neck
MTB S2CK
Check, but not most immed.

Good test, but not relevant
No concern trauma or bleed
p. 429
IDM/Other
Congenital Adrenal Hyperplasia (CAH)
Other abnormalities
Small left colon syndrome
Respiratory distress syndrome (RDS)
Cardiac abnormalities
Cholesterol
Pregnenolone
17-OHg
Pregnenolone
DHEA
Androstenediol
17-OHProgesterone
Deoxycortisol
Androstenedione
Estrone
Testosterone
Estradiol
17 -hydroxylase deficiency
Cortisol
21-hydroxylase deficiency
MTB S2CK
p. 430
17
CAH: 17 Hydroxylase Deficiency
Congenital Adrenal Hyperplasia

17 hydroxylase def
Cholesterol
Aldosterone
Cortisol
21 hyroxylase def
Aldosterone
Cortisol
Sex hormones
HYPERtensive
Classic S2CK: teenage girl

presents with delayed puberty
and incidentally found to have
elevated BP
Sex Development
p
Testosterone
Girls: nml at birth

Boys: pseudo
hermaphroditism
Estradiol
11 hydroxylase def
Electrolytes
Hypokalemia
MTB S2CK
p. 430
MTB S2CK
21 Hydroxylase Deficiency
p. 430
Cholesterol
Aldosterone
Cortisol
17 hydroxylase def
21 hyroxylase def
Aldosterone
Cortisol
Sex hormones
HYPERtensive
Aldosterone
Cortisol
Sex hormones
HYPOtensive
Sex Development
p
Testosterone
Girls: nml at birth

Boys: pseudo
hermaphroditism
Estradiol
Electrolytes
Hypokalemia
MTB S2CK
p. 430
MTB S2CK
11 Hydroxylase Deficiency
Cholesterol
11-DOC
Cortisol
Electrolytes
Hyponatremia
Hypochloremia
Hyperkalemia
17 hydroxylase def
21 hyroxylase def
11 hydroxylase def
Aldosterone
Cortisol
Sex hormones
HYPERtensive
Aldosterone
Cortisol
Sex hormones
HYPOtensive
Aldosterone
Cortisol
Sex hormones
11 DOC
HYPERtensive
Estradiol
Girls: nml at birth

Boys: pseudo
hermaphroditism
Electrolytes
Hypokalemia
p. 430
Girls: virilized
Boys: nml at birth
p. 430
Sex Development
p
MTB S2CK
Salt wasting Shock
Sex Development
Aldosterone
Testosterone
11 hydroxylase def
MTB S2CK
Salt wasting Shock
Sex Development
Girls: virilized
Boys: nml at birth
Electrolytes
Hyponatremia
Hypochloremia
Hyperkalemia
Sex Development
Girls: virilized
Boys: nml at birth
Few electrolytes
abnormalities
p. 430
18
Rickets
Cholesterol
Disorder of children
Soft and weak bones
fractures
Vitamin D, calcium, and phosphate
Children are particularly susceptible
Rapidly growing bones
Breast
B
t milk
ilk deficiency
d fi i
in
i vitamin
it i D
Prophylaxis with vitamin D supplements
Pregnenolone
17-OHg
Pregnenolone
DHEA
Androstenediol
17-OHProgesterone
Deoxycortisol
Androstenedione
Estrone
Testosterone
Estradiol
Cortisol
Rickets
Bone Metabolism/Simplified
Bone Metabolism/Simplified
Vitamin D
PTH
Calcium
Phosphate
Rickets
Vitamin D
PTH
Calcium
Phosphate
Source: Paul M Michaud
MTB S2CK
p. 432
19
Rickets
Disorder of children
Soft and weak bones
fractures
Vitamin D, calcium, and phosphate
Children are particularly susceptible
Rapidly growing bones
Breast
B
t milk
ilk deficiency
d fi i
in
i vitamin
it i D
Prophylaxis with vitamin D supplements
Treat with vitamin D and calcium supplements
MTB S2CK
Pulmonary
Croup
Epiglottitis
pg
Whooping Cough
Asthma
p. 431
Croup
Anatomy of upper airway disease
2-year-old brought in by daycare provider for severe cough,

fever, and runny nose. The childs cough sounds like a bark
and shes in obvious respiratory distress. Upon physical
examination, the child refuses to lie flat. A chest X-ray shows a
positive steeple sign.
a.
b.
c.
d.
e.
Intubate
Racemic epinephrine
Empiric antibiotics
Acetaminophen
CT-scan of neck
Not necessary in croup

Not first step in improving airway
Croup
MTB S2CK
commons.wikimedia.org. Used with permission
p.435
Croup
Epiglottitis
Laryngotracheitis or
Laryngotracheobronchitis
Infection of upper airway
Subglottic space
Viral
Parainfluenza or RSV
Presentation
Triad: barking cough,
coryza, and stridor
Respiratory distress:
accessory muscle use
CXR: Steeple sign
MTB S2CK
p. 435
Treatment
Moderate severity:
Steroids
Severe: Racemic
epinephrine and steroids
Think bacterial causes:
(1) older kids or
(2) those unresponsive to
racemic epinephrine
The MOST common

cause of stridor in
children
4-year-old child brought in by daycare provider because hes

extremely irritable and refuses to eat. He refuses to lean back,
speaks in muffled words, looks extremely ill, and is drooling.
Chest radiograph shows a positive thumb-print sign.
a.
b.
c.
d.
e.
Intubate
Racemic epinephrine
Empiric antibiotics
Acetaminophen
CT-scan of the neck
MTB S2CK
Only for croup

Good not most immeidate
Fever is not a concern
Further imaging not warranted
p. 436
20
Anatomy of upper airway disease
Epiglottitis
Upper-airway infection and emergency
MCC: Bacterial
Non-vaccinated: H. influenzae type-B
Vaccinated: Streptococcus species and nontypeable
H. influenzae
Presentation
Fever,
F
drooling,
d li
respiratory
i t
distress
di t
NO coryza, NO prodrome, NO cough
Management
Transfer to O.R.
INTUBATE
Start empiric antibiotics: ceftriaxone or cefuroxime
No imaging required
Epiglottitis
Croup
commons.wikimedia.org. Used with permission
Epiglottitis
MTB S2CK
p. 436
Pertussis
Bordetella pertussis
Whooping Cough
Gram-negative, non-invasive
Causes ciliary paralysis
Three Stages:
Source: MS-4 USU
MTB S2CK
Pertussis/Stages
p. 437
Pertussis
Bordetella pertussis
~ 14 days
14 30 days
~ 14 days
Catarrhal
Paroxysmal
Convalescent
Rhinorrhea,
congestion,
cold sxs
sx s
cold
Most
contagious
time period
Only time abx
helpful to
patient
MTB S2CK
p. 437
Severe coughing
Post-tussive emesis
Usually no fever
Low requirement for
admission
Abx prescribed to
reduce transmissibility
Prolonged
resolution of
symptoms
Coughing fits
remain less
respiratory
distress
Whooping Cough
Gram-negative, noninvasive
Causes ciliary paralysis
Three Stages:
Catarrhal Stage: 14 days
Runny
R
nose, congestion,
ti
URI Symptoms
S
t
Most contagious time period

Paroxysmal Stage: 14-30 days
Severe coughing, posttussive emesis
Convalescent Stage: 14 days
Resolution of symptoms
MTB S2CK
p. 437
21
Pertussis
Viral Infections of Childhood
Diagnosis
Virus
Presentation
Diagnostic tests Treatment
Varicella
Initial: Tzanck smear

Most accurate:
culture
Rubeola
(Measles)
Multiple highly pruritic

vesicular rash; starts on face;
fever/malaise
Cough, Coryza, and
Conjunctivitis; Koplik spots
Fifths
d
disease
Fever and URI symptoms;

l
slapped
d cheeks
h k rash
h
Clinical diagnosis
Supportive
Roseola
Fever and URI progressing Clinical diagnosis

to diffuse rash
Supportive
Mumps
Fever precedes classic

parotid gland swelling with
possible orchitis
Supportive
This is a clinical diagnosis

CXR is helpful
PCR useful where available
Management
Patient:
P ti t Primarily
Pi
il supportive
ti
Supportive
Initial: Clinical
Supportive
Most accurate: IgM
Catarrhal stage azithromycin/erythromycin

Everybody gets treated
Close contacts: Macrolides
The community: Vaccination campaigns
MTB S2CK
p. 437
MTB S2CK
p. 434
Asthma
Asthma
The most common chronic disease in children

Pathophysiology
Reversible obstruction
Hyperresponsiveness
Inflammation
Remodeling
Diagnosis
Decreased FEV1 and
No single available test
FEV1/FVC ratio!
Clinical
Pulmonary Function Tests (PFTs)
Bronchoprovocation
CXR
Treatment
MTB S2CK
p. 129 130
Clinical diagnosis
Avoidance of triggers
Short-acting 2-agonists (SABA)
Inhaled corticosteroids (ICS)
Long-acting 2-agonists (LABA)
Leukotriene
L k ti
antagonists
t
i t ((modifiers)
difi ) (LTRA)
MTB S2CK
p. 131 132
Asthma/Treatment
SABA as
needed
ADD
Low-dose
ICS
ADD
LABA,
LTRA or
LTRA,
move to
mediumdose ICS
High-dose
ICS
and
LABA
High-dose
ICS
and
LABA
and
Oral
steroids
Severity of Symptoms
MTB S2CK
p. 131 132
22
Childhood Disorders
Mental Retardation
Pervasive Developmental Disorders
Attention Deficit Hyperactivity Disorder
Tourette Disorder
Psychiatry
Sam Asgarian, MD/MBA
Class of 2012
Tulane University
Mental Retardation
Types of Mental Retardation
To determine the level of retardation patients must

exhibit deficits in both
Intellectual functioning
Mild
Moderate
IQ range
IQ range
Level of functioning
Cognitive abilities
Social adaptive functioning

Perform daily activities
More frequent in boys

Highest incidence being in school-age children
MTB S2CK
p. 503
Profound
IQ range
IQ range
Little or no speech,
veryy limited abilities to
manage self care
MTB S2CK
p. 503
2nd grade level

May work with
supervision and support
Needs help in mildly
stressful situations
p. 503
Mental Retardation/Treatment
Severe
2025 to 3540
3040 to 5055
6th grade level

Can work and live
independently
Needs help in difficult or
stressful situations
MTB S2CK
Types of Mental Retardation
5055 to 70
< 20
Needs continuous
p
care and supervision
Treatment
Genetic counseling, prenatal care, and safe
environments for expectant mothers
If due to medical condition (e.g., PKU) treat
disorder
Special education to improve level of functioning
Behavioral therapy to reduce negative behaviors
MTB S2CK
p. 503 504
Pervasive Developmental Disorders/Definition
Autistic Disorder
Characterized by
Social, behavioral, and language problems
Incidence: boys > girls

Lacks peer relationships,
poor eye contact, and
social smile
Absent or bizarre speech
Repetitive behaviors
Occurs before age 3
Childhood Developmental Disorders

Autistic disorder
Rett disorder
Childhood disintegrative disorder
Asperger disorder
MTB S2CK
p. 504
Stacking
Injurious behavior to self
or others
MTB S2CK
~18 mo boy with autism, obsessively stacking cans

Source: Andwhatsnext , commons.wikimedia.org
p. 504
Autistic Treatment
Rett disorder
Improve ability to develop relationships, attend

school, and achieve independent living
May benefit from behavioral modification programs
If aggressive, use antipsychotic medications
Greater incidence in girls

Progressive encephalopathy
Microcephaly
Hand-wringing
Loss of speech
Ataxia
At i
Psychomotor retardation
Treatment
Symptomatic
Behavior therapy for self-injurious behavior
Physiotherapy for muscular dysfunction
MTB S2CK
p. 504
MTB S2CK
p. 504
Childhood Disintegrative Disorder
Childhood Disintegrative Disorder/Treatment
Greater incidence in boys

Normal development for 2 years, followed
by marked functional regression in
Improve ability to develop relationships,

attend school, and achieve independent
living
May benefit from behavioral
modification programs
If aggressive, use antipsychotic
medications
Loss of language
Social interaction
Motor function
Bladder function
Repetitive/stereotyped behaviors
MTB S2CK
p. 504
MTB S2CK
p. 504
Asperger Disorder
Greater incidence in
boys
Social and behavioral
problems
No language or
intellectual deficits
Preoccupied with rules
Gabriel is a healthy 2-year-old boy whose parents

have taken him to the pediatrician. His problems
started at 18 months of age, when he did not speak
much. He does not have much attachment to his
parents and seems aggressive toward other children.
a. Deafness
Ruled out
Impaired judgment,
b. Schizophrenia, childhood onset behavior, and reality

Often display intense interests. Source: Poindexter
Propellerhead at the English language, commons.wikimedia.org
Treatment
Improve relationships with others
Progressive encephalopathy, loss of
c. Rett disorder speech, ataxia, and psychomotor

d. Autism
retardation
e. Learning deficit No evidence of learning deficit

MTB S2CK
p. 504
MTB S2CK
p. 504 505
Attention Deficit Hyperactivity Disorder
ADHD
Characterized by
Inattention
Short attention span
Or
Hyperactivity that
interferes with daily
functioning in school,
home, or work
Symptoms must be present in at least 2 areas, such as:

School
Home
Source: cdc.gov
Must be present for > 6 months and usually

appears before age 7
The symptoms may persist into adulthood
MTB S2CK
p. 505
Interrupt others
Fidget in chairs
Run or climb
excessivelyy
Unable to engage in
leisure activities
Talk excessively
MTB S2CK
Unable to pay
attention
Make careless
mistakes in
schoolwork
Do not follow through
with instructions
Difficulties organizing
tasks
Easily distracted
p. 505
Treatment
Disruptive Behavioral Disorders
First-line: methylphenidate and dextroamphetamine
Oppositional Defiant Disorder

Epidemiology
Usually noted by age 8
Boys > girls before puberty
Side effects: insomnia, decreased appetite, and

headache
Second-line: atomoxetine (norepinephrine reuptake

inhibitor)
But equal incidence after puberty

On the USMLE Step 2 CK, atomoxetine is usually
chosen over the first-line treatment, given the side
effect profiles of those treatments
MTB S2CK
p. 505
MTB S2CK
p. 506
Disruptive Behavioral Disorders/

Features
Argues often
Loses temper
Easily annoyed
Blames others for
their mistakes
Tends to have
problems with
authority figures

Justifies behavior as
response to others actions
Treatment
Teach parents appropriate child
management skills and how to lessen
oppositional
iti
lb
behavior
h i
Source: Chris Willia, commons.wikimedia.org
MTB S2CK
p. 506
Disruptive Behavioral Disorders
Conduct Disorder
Epidemiology
Seen more frequently in
Boys whose parents have antisocial
personality disorder and alcohol
dependence
MTB S2CK
p. 506

Conduct Disorder
Features
Persistent behavior where
rules are broken
Behaviors include
aggression toward others:
Bullying
Cruelty to animals
Fighting
Or
Using weapons
Source: Diego Grez, commons.wikimedia.org
Vandalize and destroy property; set fires

Steal items from others or lie to obtain goods from others
Violate rules (truancy, running away from home, breaking
curfew)
MTB S2CK
p. 506

Conduct Disorder
Treatment
Behavioral intervention using rewards
for prosocial and nonaggressive
behavior
If aggressive
Antipsychotic medications have been
used
MTB S2CK
p. 506
A 10-year-old boy is seen by the school counselor after

teachers complained of his behavior. He frequently becomes
angry toward others and loses his temper. His parents report
that he refuses to comply with house rules, stays up past his
bedtime, and frequently talks back to them.
a. Conduct disorder Breaks rules of society or commits
crimes
b. Tourette disorder Multiple tics
c. Adjustment disorder Maladaptive reaction to identifiable
stressor
d. Oppositional Defiant Disorder
e. Learning disorder, not otherwise specified
Needs evidence of a learning problem
MTB S2CK
p. 506
MTB S2CK
p. 506
Tourette Disorder
Tourette Disorder/Treatment
Characterized by onset of multiple tics
Seen more frequently in
Lasting > 1 yr
Occurs before age 18
Boys
Begins at age 7
Motor tics most commonly involve

Facial and neck muscles (e.g., head shaking and
blinking)
The vocal tics include
Dopamine
p
antagonists
g
Antipsychotic medications (e.g., risperidone)
Grunting, coughing, and throat clearing
MTB S2CK
p. 506
MTB S2CK
p. 507
Mood Disorders
Major Depression
Bipolar Disorder
Dysthymia
Cyclothymia
Atypical Depression
Seasonal Affective Disorder
Bereavement (Grief)
Psychiatry
Sam Asgarian, MD/MBA
Class of 2012
Tulane University
Major Depression
Major Depression
Mood disorders present with at least a 2-week

course of symptoms thats a change from the
previous level of functioning
Symptoms
Depressed mood or anhedonia (absence of
pleasure)
And
4 others including
Vincent van Gogh's 1890 painting Sorrowing old man ('At Eternity's Gate') Source: The
Yorck Project, commons.wikimedia.org
MTB S2CK
p. 507
Depressed mood most

of day
Weight changes
Sleep changes
Psychomotor
disturbances
MTB S2CK
Fatigue
Poor concentration
Thoughts of death and
worthlessness
p. 507
Major Depression/Diagnosis and Treatment
Major Depression/Treatment
Diagnosis
Rule out medical causes
SSRIs
Effective and relatively mild side effects
Less toxic in overdose than other antidepressants
If some improvement, but not full response
Increase dose of SSRI
Psychotherapy (e.g., cognitive therapy) proven to be
effective
Goal of cognitive therapy is
Reduce depression by teaching patients to identify
negative cognitions and develop positive ways of
thinking
Most common (hypothyroidism)
Most common neurological associations are

Parkinson disease and dementia
First-line treatment: SSRIs

Fluoxetine
Paroxetine
Sertraline
Citalopram
Escitalopram
MTB S2CK
p. 507
Major Depression
SSRIs should NOT be taken with MAO

inhibitors as they will cause a dramatic
increase in serotonin.
USMLE Step 2 CK wont give you 2 SSRIs

from which to choose
MTB S2CK
p. 507 508
MTB S2CK
p. 507
Exceptions to SSRI Use

Variety of depression
Specific alternative to SSRIs
Patient with depression and

neuropathic pain
Use desvenlafaxine
Approved for both
depression & neuropathy
Patient with depression who

iis ffearful
f l off weight
i h gain
i or
sexual side effects
Bupropion has fewer

sexuall side
id effects
ff
and
d less
l
weight gain than SSRIs
Also used as adjunct
treatment for SSRI
induced sexual side effects
MTB S2CK
p. 507
Major Depression
45-year-old woman was seen by her PCP due to complaints of
depressed mood, lack of pleasure, sleep problems, decreased
appetite and weight, decreased energy, and problems with
concentration. She states that these symptoms started when
she was fired from her job about 4 weeks ago, and that since
then, she has been unable to function.
What is the most indicated treatment at this time?
a. Alprazolam Anxiolytic
b. Paroxetine
c. Bupropion Not 1st line
d. Venlafaxine
When initial therapy doesnt
e. Trazodone
work, or depression more
f. Electroconvulsive therapy severe and associated with
psychotic features
MTB S2CK
p. 508
Choices on USMLE may include an SSRI

and another antidepressant medication
Pick the cleanest: SSRI
MTB S2CK
p. 508
Bipolar Disorder
Bipolar Disorder
Mood disorder
Patient experiences
Manic symptoms
Manic symptoms
that last at least 1
week
Cause significant
distress in level of
functioning
Elevated mood
Increased self-esteem
Distractibility
Pressured speech
Decreased need for
sleep
Increase in goaldirected activity

Racing thoughts
Excessive involvement
pleasurable
in p
activities
MTB S2CK
p. 508
MTB S2CK
p. 508
Bipolar Disorder
Bipolar Disorder
Typically starts with depression
The difference between mania and hypomania

Severity of symptoms
Duration
Diagnosis
Exclude drug use
Cocaine/amphetamine
Obtain history and urine drug screen
MTB S2CK
p. 508
Mania
M i
Hypomania
H
i
> 1 week
Affect functioning
Warrant
hospitalization
MTB S2CK
< 1week
Dont severely affect
functioning
Dont warrant
hospitalization
p. 508
Types of Bipolar Disorders

Bipolar disorder type I
Mania and depression
Bipolar disorder type II
Hypomania and depression
21-year-old college student was taken to the university clinic

after she was noted to be acting bizarrely in class. She is
talking fast and reported that she has not slept for over 4 days.
She appears to be giggling and not paying attention in class.
Her roommate reported that she has been drinking alcohol
excessively over the last few days and has had many sexual
contacts with unknown men.
Wh t iis th
What
the mostt lik
likely
l di
diagnosis?
i ?
a. Alcohol-induced mood disorder No history of alcoholism
b.
c.
d.
e.
MTB S2CK
p. 509
Bipolar disorder type I

Bipolar disorder type II Hypomania
Major depression with psychosis Thoughts of death,
preoccupation with
Cyclothymia Hypomanic
worthlessness,
episodes and
psychomotor
mild
depression
MTB S2CK p. 509
retardation, psychosis
Bipolar Disorder/Treatment
Bipolar Disorder
You must distinguish whether

Acute mania
1st line
Lithium
Valproic acid
Atypical
antipsychotics
Severe
symptoms,
consider
If kidneys are compromised, dont use

lithium
Bipolar depression
Lithium
Lamotrigine
Lithi
Lithium iis th
the correctt answer tto mostt
bipolar questions
Atypical antipsychotics
Shorter onset of action
MTB S2CK
p. 509
MTB S2CK
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Dysthymia
33-year-old man was taken to emergency room by police after
neighbors complained about his behavior. His family informed
the doctor hes been diagnosed with bipolar disorder and was
recently started on lithium. While in the emergency room, he
became combative and punched a nurse on the mouth.
What is the next step in the management of this patient?
a. Obtain lithium level
Symptoms are acute
b. Admit to psychiatric unit > important to treat
c. Refer to psychiatry
Never refer
1st line is an antipsychotic
d. Add valproic acid
e. Olanzapine
MTB S2CK
p. 509 510
Characterized by
Depressed mood that lasts most of the day
and is present almost continuously
Symptoms must be present for: > 2 years
Treatment
Antidepressant medications and
psychotherapy
MTB S2CK
p. 510
Cyclothymia
Atypical Depression
Characterized by
Hypomanic episodes and mild depression
Characterized by
Symptoms must be present for: > 2 years

Treatment
Lithium, valproic acid, or carbamazepine
Psychotherapy
MTB S2CK
p. 510
Reverse vegetative changes

Increased sleep
Increased weight
Increased appetite
Mood tends to be worse in evenings and
patients may complain of extremities
feeling heavy
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p. 510
Atypical Depression/Treatment
Seasonal Affective Disorder
SSRIs or MAOIs
SSRIs have better side-effect profile
If MAOIs and SSRIs are in the same
question, choose SSRIs because of sideeffect profile
Characterized by
Seasonal changes in mood during fall and winter
Usually MAOIs are answer on Step 2 for

atypical depression
Symptoms
Weight gain
Increased sleep
Lethargy
Treat with
Phototherapy and bupropion
MTB S2CK
p. 510
MTB S2CK
Postpartum Disorders
p. 510
Disorder
Postpartum blues or baby blues
Disorder
Postpartum depression
Onset
Symptoms
Mothers feelings
toward baby
Treatment
Immediately after birth up to 2 weeks

Sadness, labile mood, tearfulness
No negative feelings
Onset
Symptoms
Within 13 months after birth

Depressed mood, weight changes, sleep
disturbances, and excessive anxiety
May have negative feelings toward baby
Supportive, usually self limited
Mothers feelings
toward baby
Treatment
Antidepressant medications
MTB S2CK
p. 511
MTB S2CK
Disorder
Within 23 weeks after birth

Depression, delusions, and thoughts
of harm
Mothers feelings toward baby May have thoughts of harming baby
Treatment
Antipsychotic medication, lithium,
and possibly antidepressants
p. 511
Bereavement (Grief)
Postpartum psychosis
Onset
Symptoms
MTB S2CK
p. 511
Bereavement
Major depression
(greater severity than bereavement)
Begins after death of

loved one
Feelings of
Sadness
Worrying
y g
Irritability
Sleep difficulties
Poor concentration
Tearfulness
< 6 months, but can go
on longer
Thoughts of death
Morbid preoccupation with
worthlessness
Marked psychomotor
retardation
Psychosis
Prolonged functional
impairment
> 2 months and adversely
affect functioning
MTB S2CK
p. 511
Bereavement (Grief)
Treatment
Supportive
psychotherapy
Medical therapy is
wrong answer
Source: Bundesarchiv, Bild 146-1996-036-01 /

Unknown / CC-BY-SA, commons.wikimedia.org
A 65-year-old man brought to office by daughter. He has been

hopeless and helpless since his wife died 3 months ago.
Daughter is worried about his isolative behavior and lack of
appetite. He lost over 30 pounds. He doesnt seem interested
in getting better and believes he should have died with his
wife.
a. Bereavement Severe symptoms just to be bereavement
b. Dysthymia Depressed mood, lasts most of the day and
continuously
c. Major depression
Anxiety, depression or
d. Adjustment disorder disturbances of conduct
e. Bipolar disorder
MTB S2CK
p. 511
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p. 511
Mood disorder with manic symptoms,

at least 1 week
Antidepressants, Mood Stabilizers,

Electroconvulsive Therapy

Type of medication
Type of medication
Adverse effects
Tricyclic
antidepressants
Amitriptyline
Nortriptyline
Imipramine
MTB S2CK
Hypotension
Dry mouth
Constipation
Confusion
Arrhythmias
Sexual side effects
Weight gain
GI disturbances
p. 512
Monoamine
oxidase inhibitors
- Phenelzine
- Isocarboxazid
- Tranylcypromine
MTB S2CK
p. 512
Adverse effects
Monitor diet, given that

food rich in tyramine will
produce hypertension
-
Safe foods include white wine

and processed cheese
Unsafe foods include red wine,
aged cheese, and chocolate
Source: Vincent van Gogh, Still life with bottle, two

glasses, cheese and bread. commons.wikimedia.org


Type of medication
Type of medication
Serotonin selective
reuptake inhibitors
-
Fluoxetine
Paroxetine
Sertraline
Citalopram
Escitalopram
Fluvoxamine
MTB S2CK
p. 512
Adverse effects
Headaches
Weight changes
Sexual side effects
GI disturbances
Adverse effects
Serotonin norepinephrine Hypertension

reuptake inhibitors
Blurry vision
- Venlafaxine
Weight changes
- Duloxetine
Sexual side effects
- Desvenlafaxine
GI disturbances
MTB S2CK
p. 512
10


Type of medication
Type of medication
Others
-
Bupropion
Trazodone
Mirtazapine
Adverse effects
Bupropion: seizures
Trazodone: priapism
Mirtazapine: weight gain
and sedation
Lithium
Adverse effects
Tremors, weight gain, GI

disturbance, nephrotoxic,
teratogenic, leukocytosis,
diabetes insipidus
Severe toxicity gives
confusion, ataxia, lethargy,
and abnormal reflexes
MTB S2CK
p. 512
MTB S2CK
p. 512


Type of medication
Type of medication
Valproic acid
Adverse effects
Tremors, weight gain, GI

disturbances, alopecia,
teratogenic, hepatotoxic
Adverse effects
Lamotrigine
Stevens Johnson syndrome
Electroconvulsive
therapy
Headaches, transient memory loss
Must monitor levels; toxicity

causes
-
MTB S2CK
Hyponatremia
Coma
Death
p. 512
MTB S2CK
p. 512
Serotonin Syndrome
What is the single most effective treatment for depression?
a. Electroconvulsive therapy
b. Fluoxetine
Equally efficacious, but the SSRIs
c. Venlafaxine are used more frequently due to
side-effect profiles
d. Imipramine
e. Phenelzine
Potentially life-threatening
From use of SSRIs, often with interactions between
drugs, overdose, or recreational use of drugs that are
serotonergic in origin
Symptoms
Cognitive effects
Agitation, confusion, hallucinations, hypomania
MTB S2CK
p. 513
MTB S2CK
p. 513
11
Serotonin Syndrome
Autonomic effects
Sweating, hyperthermia, tachycardia, nausea,
diarrhea, shivering
Psychotic Disorders
Somatic effects
Schizophrenia
Delusional Disorder
Tremors, myoclonus
Treatment
Stop SSRI medication
Symptomatic treatment of fever, diarrhea,
hypertension
Cyproheptadine (serotonin antagonist)
MTB S2CK
p. 513
Classification of Psychotic Disorders
Brief Psychotic Disorder
Schizophreniform Disorders
Duration of symptoms
> 1 day, but < 1 month
Symptoms
Delusions
Hallucinations
Disorganized speech
Grossly disorganized
Catatonic behavior
Treatment
Antipsychotic
medication
MTB S2CK p. 513
> 1 month, but < 6
months
Symptoms
Delusions
Hallucinations
Disorganized speech
Catatonic behavior
Negative symptoms
Flat affect
Poor grooming
Social withdrawal
Treatment
Antipsychotic
medication
MTB S2CK p. 513
Psychotic Disorders
Schizophrenia
> 6 months
Symptoms
Delusions
Hallucinations
Disorganized speech
Catatonic behavior
Negative symptoms
MTB S2CK p. 513
Severely affects level

of functioning
Treatment
Antipsychotic
medication
Duration of symptoms distinguishes brief

psychosis, schizophreniform, and schizophrenia
If no time is mentioned, always choose
schizophrenia as the correct answer to the What is
the most likelyy diagnosis?
g
question
q
MTB S2CK p. 514
12
Schizophrenia/Definition
Schizophrenia/Definition
Thought disorder: impairs judgment,

behavior, and ability to interpret reality
At least 6 months and must affect
functioning
Incidence: men = women
Affects men at young age
Urine drug screen

Cocaine
Amphetamine
A schizophrenic patient at the Glore Psychiatric Museum made this piece of cloth and it
gives us a peek into her mind. Source: Cometstarmoon, commons.wikimedia.org
MTB S2CK p. 514
Types of Schizophrenia/Diagnostic criteria
Paranoid
Delusions or hallucinations, mostly persecutory
or grandiose type
Most common type of schizophrenia
Later age of onset
Catatonic
Psychomotor disturbances from retardation to
excitation
Disorganized
Marked regression to disinhibited
behavior with little contact with reality
Typically appear disheveled and have
bizarre emotional responses
Worst prognosis and earliest age of
onset
Stupor, rigidity, excitement, or posturing
Mutism is common
MTB S2CK p. 514
MTB S2CK p. 514
Schizophrenia/Treatment
Residual
Lack of positive symptoms
Hospitalize: acutely psychotic

Ensure patient safety, administer atypical
antipsychotic such as
Hallucinations
Delusion
Presence of negative symptoms

Flat affect
Poor grooming
Social withdrawal
Undifferentiated
Characterized by not meeting criteria for other
types
MTB S2CK p. 514
Risperidone, olanzapine, quetiapine,

ziprasidone, aripiprazole, or paliperidone
In emergency situation where intramuscular

medication is needed consider
Olanzapine or ziprazidone
Haloperidol may be used, but has more side
effects
MTB S2CK p. 514 515
13
If noncompliant with medication

Long-acting antipsychotic
Risperidone: first-line
Haloperidol may be used, more side effects
Clozapine
Use when NO response to a trial of typical
or atypical antipsychotics
Know the differences in the side effect

profiles of the atypical antipsychotics
Its common to have 2 appear on the
test; you need to pick the best based on
side effects
Never used as first-line
MTB S2CK p. 515
MTB S2CK p. 515
Adverse Effects of
Atypical Antipsychotic Medications
Olanzapine
Greater incidence of
diabetes and weight gain;
avoid in diabetic & obese
Risperidone
Quetiapine
Greater
incidence of
movement
disorders
Less incidence
of movement
disorders
Ziprasidone
Clozapine
Increased risk of
prolongation of QT
interval; avoid in
conduction defects
High risk of agranulocytosis;

monitor CBC on regular
basis; never used as firstline treatment given sideeffect profile
MTB S2CK p. 515
Acute
dystonia
Hours
to days
Akathisia
Weeks
MTB S2CK p. 516
a.
b.
c.
d.
e.
Aripiprazole
Olanzapine Highest risk of metabolic abnormalities
Quetiapine
Have medium risk
Clozapine
Risperidone
MTB S2CK p. 515
Management of Adverse Effects of

Onset of
symptoms
22-year-old woman with schizophrenia. Shes 30

pounds overweight and suffers from type 2 DM. She
is concerned about her medications and asks for
advice.
Which of the following would be most indicated in this
patient?
Acute dystonia
Symptoms
Muscle spasms
Torticollis
Laryngeal spasms
Occulogyric crisis
Generalized
restlessness
Pacing
Rocking
Inability to relax
Treatment
Muscle
spasms
Benztropine
Trihexyphenidyl
Diphenhydramine
Reduce dose
Beta blockers
Switch to
atypical
14
Management of Adverse Effects of

Onset of
symptoms
Tardive
dyskinesia
Rare
before 6
months
Neuroleptic
malignant
syndrome
Not
time
limited
Symptoms
Treatment
Abnormal involuntary
movements of
Head
Limb
Trunk
Perioral, most
common
Muscular rigidity
Fever
Autonomic changes
Agitation
Obtundation
Switch to
atypical
antipsychotic
Clozapine
has least risk
Dantrolene or
bromocriptine
MTB S2CK p. 516
23-year-old man recently diagnosed with

schizophrenia is started on haloperidol. Within a
few hours he develops muscle stiffness. His eyes
roll upward and he cannot move them down.
a Tardive dyskinesia 6 mo. involuntary, perioral movements
a.
No time, muscular
b. Neuroleptic malignant syndrome rigidity, fever
Weeks. Generalized restlessness,
c. Akathisia pacing, rocking, inability to relax
d. Serotonin syndrome SSRIs
e. Acute dystonic reaction
MTB S2CK p. 516
Delusional Disorder
Delusional Disorder
Characterized by
Non-bizarre delusions
for > 1 month and NO
impairment in level of
functioning
The p
patient may
y believe
the country is about to
be invaded, but he or
she still obeys the law,
goes to work, and pays
bills
Hallucinations arent present

Treatment
Atypical antipsychotic: first-line therapy
Psychotherapy to help promote reality
testing
MTB S2CK p. 516
MTB S2CK p. 516
Panic Disorder/Definition
Anxiety Disorders
Is the experience of intense anxiety along with

feelings of dread and doom
Panic Disorder
Phobias
MTB S2CK p. 517
15
This is accompanied by at least 4 symptoms

of autonomic hyperactivity such as
Last < 30 minutes and may be accompanied

by agoraphobia
Diaphoresis
Trembling
Chest pain
Fear of dying
Chills
Palpitations
SOB
Nausea
Dizziness
Dissociative
symptoms
Paresthesias
MTB S2CK p. 517
Fear of places where escape is felt to be difficult
Typically in women, can occur at any time,

and usually has no specific stressor
R/O thyroid disease, hypoglycemia, and
cardiac disease
MTB S2CK p. 517
Panic Disorder/Treatment
SSRIs, typically
Fluoxetine, paroxetine, and sertraline are indicated
for this disorder
Along with SSRIs, patients may benefit from

benzodiazepines (e.g., alprazolam)
Begin
g with both
Then taper the benzodiazepine (potential abuse)
Behavioral and individual therapy

Helpful
But
Not sufficient as only treatment
MTB S2CK p. 517
a.
b.
c
c.
d.
e.
Alprazolam Panic attack

Buspirone Generalized anxiety
Sertraline
Imipramine Major depression, enuresis
Fluvoxamine Not 1st-line
MTB S2CK p. 517
Phobias Definition
Fear of an object or
situation and the
need to avoid it
Which is the first-line treatment for panic

disorder?
Types of Phobias
Specific phobia
Fear of an object
(e.g., animals,
heights, or cars)
Social phobia
Fear of a situation
Public restrooms
Eating in public
Public speaking
Situations where
something potentially
embarrassing may
happen
May be learned,
involves 2 main
types
Source: Alex.Ramek, commons.wikimedia.org
Source: Kilarin, commons.wikimedia.org
MTB S2CK p. 517 518
MTB S2CK p. 518
16
Phobias/Diagnosis and Treatment
Phobias/Treatment
Diagnosis
History of
Relaxation techniques such as
Anxiety symptoms in specific situations

Or
When in contact with feared objects
Treatment
Behavioral modification techniques such as
Systematic desensitization:
Breathing
Or
Guided imagery
Beta blockers (e
(e.g.,
g atenolol or propanolol) are
used for performance anxiety such as stage
fright. They are given 30 minutes to 1 hour
before performance.
Expose individuals to their feared objects moving from

least
most anxiety-provoking
MTB S2CK p. 518
MTB S2CK p. 518
40-year-old man referred to psychiatrist because he is

too shy. He has problems going to parties, feels anxious
about getting close to others, and stays at home in fear
that others would laugh at him. When confronted by
others, he develops severe anxiety as well as
hyperventilation and increased sweating.
Obsessive Compulsive
Disorder
Intense anxiety, dread and doom, 4
a. Panic disorder
autonomic hyperactivity symptoms
b. Social anxiety
Chronic worrying about things
c. Generalized anxiety disorder that dont merit concern
d. Specific phobia Fear of an object
e. Acute stress disorder Stressor, 2 days to 1 month, relive
the event
MTB S2CK p. 518
Obsessive Compulsive Disorder (OCD)/

Definition
Difference between Obsessions and

Compulsions
Obsessions alone
Or, most commonly
Combination of
obsessions and
compulsions
l i
Typically affect the
individuals level of
functioning
Obsessions
MTB S2CK p. 518
Compulsions
Thoughts that are

intrusive, senseless,
and distressing, thus
increasing anxiety
Includes fear of
contamination
Rituals such as counting

and checking done to
neutralize thoughts
Time consuming and
tends to lower anxiety
Source: Lars Klintwall Malmqvist, commons.wikimedia.org
MTB S2CK p. 519
17
OCD/Diagnosis and Treatment

Diagnosis
More frequent in young patients
Incidence: men = women
OCD can coexist with Tourette disorder
Treatment
SSRIs: treatment of choice
Most common, first-line: fluoxetine, paroxetine,
sertraline, citalopram, or fluvoxamine
Main behavioral therapy used
Exposure and response prevention
Posttraumatic Stress Disorder

and Acute Stress Disorder
MTB S2CK p. 519
Posttraumatic Stress Disorder (PTSD) and

Acute Stress Disorder/Definition
In both, individuals have Usually overwhelming
been exposed to a
(e.g., war, rape,
stressor to which they
hurricanes, or
react with fear and
earthquakes)
helplessness
Patients continually
relive
li the
h event and
d
avoid anything that
reminds them of event
PTSD and Acute Stress Disorder/Definition
Affect the patients level of functioning

Other symptoms
Increased startle response
Hypervigilance
Sleep disturbances
Anger outbursts
Concentration difficulties
Source: Department of Defense visual information (DVIC)

Author: US Army, Office of War Information (OWI)
MTB S2CK p. 519
MTB S2CK p. 519
Difference between PTSD and

Acute Stress Disorder
PTSD
Symptoms last for
> 1 month
MTB S2CK p. 519
PTSD and Acute Stress Disorder/Diagnosis
Acute stress disorder

Symptoms last for
> 2 days and a
maximum of 1
month
th
They occur within
1 month of
traumatic event
Main feature
Determine the time period when traumatic
events occurred in relationship to
symptoms
Rule out
Depression and substance abuse
Both worsen diagnosis
MTB S2CK p. 519 520
18
PTSD and Acute Stress Disorder/Treatment
First-line treatment
Paroxetine and sertraline
Relaxation techniques and hypnosis,

proven helpful
Psychotherapy after traumatic events
will allow
Development of coping techniques and
acceptance of event
MTB S2CK p. 520
35-year-old woman with palpitations, dizziness, and increased

sweating for 8 months. Has visited numerous physicians, none
have been helpful. Her husband is concerned because she
cannot relax and worries about everything. She worries about
her parents health even though they are healthy. She worries
about her finances, although her husband assures her theyre
financially secure.
Wh t iis th
What
the mostt lik
likely
l di
diagnosis?
i ?
a. Generalized anxiety disorder
b. Phobias Fear of an object or a situation
Intense anxiety, dread and doom, 4 autonomic
c. Panic disorder
hyperactivity symptoms
d. Adjustment disorder
Maladaptive reaction to a stressor
e. Social anxiety Anxiety to social interactions, situations
MTB S2CK p. 520
Generalized Anxiety Disorder/Definition
Generalized Anxiety Disorder
Excessive anxiety and worry about most things,

lasting > 6 months
Typically, anxiety is out of proportion to event
Accompanied by
Fatigue
Concentration difficulties
Sleep problems
Muscle tension
Restlessness
Usually women, who complain of feeling anxious

as long as they can remember
MTB S2CK p. 520
Generalized Anxiety Disorder/Treatment
SSRIs
Fluoxetine, paroxetine, sertraline, or
citalopram
Venlafaxine and buspirone have also

been used
Psychotherapy and behavioral therapy
Beneficial
Not considered first-line
Antianxiety Medications and

Their Adverse Effects
Antianxiety medication
Benzodiazepines
Diazepam
Lorazepam
Clonazepam
Alprazolam
Oxazepam
Chlordiazepoxide
Temazepam
Flurazepam
Buspirone
MTB S2CK p. 520
Adverse effects
Sedation
Confusion
Memory deficits
Respiratory depression
And
Addiction potential
Headaches
Nausea
Dizziness
MTB S2CK p. 521
19

Their Specific Indications

Their Specific Indications
Lorazepam
Used frequently in emergency situations
because it can be given intramuscularly
Clonazepam
May be used if addiction is a concern
concern, longer
half-life
Chlordiazepoxide, oxazepam
Used frequently in treatment of alcohol
withdrawal
Alprazolam
Used frequently in panic disorder
MTB S2CK p. 521
Flurazepam, temazepam,
Flurazepam
temazepam triazolam
Approved as hypnotics (rarely used)
MTB S2CK p. 521
Generalized Anxiety Disorder

Flumazenil is a benzodiazepine
antagonist used only when
The overdose is acute
And:
Youre certain that theres no
chronic dependence
Substance Related Disorders
Flumazenil can cause seizures in benzodiazepinedependent patients. It causes acute withdrawal: tremor or
seizures similar to delirium tremens (alcohol withdrawal).
MTB S2CK p. 521
Specific Substance Abuse/Definition
Substance Related Disorders/Definition
Intoxication
Reversible experience - substance leads to either
psychological or physiological changes
Withdrawal
Cessation or reduction of a substance leading to
either psychological or physiological changes
Abuse
Maladaptive pattern - substances that leads
to
MTB S2CK
p. 521
Engaging in hazardous situations

Legal problems
Inability to fulfill obligations
Continued use despite adverse
consequences
MTB S2CK
p. 521
20
Substance Related Disorders/Definition
Intoxication and Withdrawal/Alcohol

Alcohol
Dependence
Maladaptive pattern, substances leads to
Intoxication
Tolerance
Withdrawal when
trying to cut down
Patients spend a great
deal of time engaging in
drug use
Continued use despite
adverse consequences
Talkative
Sullen
Gregarious
Moody
Disinhibited
p. 521
Mechanical
ventilation, if
severe
MTB S2CK
Intoxication and Withdrawal/

Amphetamines & Cocaine
Benzodiazepines
Thiamine
Multivitamins
Folic acid
p. 522
Cannabis
Signs & Symptoms
Withdrawal
Signs & Symptoms
Euphoria
Hypervigilance
Autonomic hyperactivity
Weight loss
Pupillary dilatation
Perceptual disturbances
Anxiety
Tremulousness
Headache
Increased Appetite
Depression
Risk of suicide
Treatment
Treatment
Antipsychotics and/or
benzodiazepines and/or
antihypertensives
MTB S2CK
Bupropion and/or
bromocriptine
Intoxication
Signs &
Symptoms
Impaired motor
coordination
Slowed sense of
time
Social withdrawal
Increased appetite
Conjunctival injection
Treatment
benzodiazepines and/or
talking down
MTB S2CK
p. 522
Source: JonRichfield,
Treatment
None
p. 522
Intoxication and Withdrawal/Inhalants
Hallucinogens
Ideas of reference
Perceptual
disturbances
Impaired judgment
Tremors
Incoordination
Dissociative symptoms
None
Treatment
MTB S2CK
Intoxication and Withdrawal/Hallucinogens
Signs &
Symptoms
Withdrawal
Signs &
Symptoms
None
p. 522
Intoxication
Source: GeographBot,
Intoxication and Withdrawal/Cannabis
Amphetamines & Cocaine
Intoxication
Tremors
Hallucinations
Seizures
Delirium tremens
Treatment
Source: Carlos t . commons.wikimedia.org
MTB S2CK
Withdrawal
Signs &
Symptoms
Hallucinogens
Withdrawal
Intoxication
Signs &
Symptoms
Signs &
Symptoms
None
Treatment
Source: Ksd5
Ksd5, commons
wikimedia org
None
Belligerence
Apathy
Aggression
Impaired judgment
Stupor
Coma
Withdrawal
Signs &
Symptoms
None
Treatment
None
Treatment
Antipsychotics
MTB S2CK
p. 522
21
Intoxication and Withdrawal/Opiates
Intoxication and Withdrawal/

Phencyclidine (PCP)
Opiates
Withdrawal
Intoxication
Signs &
Symptoms
Apathy
Dysphoria
Pupillary
constriction
Drowsiness
Slurred speech
Coma
Death
Source: Eleassar,
Treatment
Belligerence
Psychomotor agitation
Violence
Nystagmus
HTN
Seizures
benzodiazepines and/
or talking down
p. 522
MTB S2CK
Intoxication and Withdrawal/Anabolic Steroids
Withdrawal
Signs &
Symptoms
Source: Jara172,
None
Treatment
Treatment
Clonidine
Methadone
Or
Buprenorphine
Naloxone
MTB S2CK
Signs &
Symptoms
Fever
Chills
Lacrimation
Abdominal cramps
Muscle spasms
Diarrhea
Treatment
PCP
Intoxication
Signs &
Symptoms
None
p. 522
Substance Related Disorders/Treatment
Anabolic Steroids
Intoxication
If you suspect someone is an alcoholic, do CAGE test.

Two positive responses to four questions are
considered a positive test and indicate that further
assessment is warranted.
Withdrawal
Signs &
Symptoms
Signs &
Symptoms
Irritability
Aggression
Mania
Psychosis
Treatment
Depression
Headaches
Anxiety
Increased concern
over bodys
physical state
Antipsychotics
Source: Cristian navas roman

roman,
Treatment
C - Have you ever felt you should cut down on your drinking?
A - Have people annoyed you by criticizing your drinking?
G - Have you ever felt bad or guilty about your drinking?
E - Eye opener: Have you ever had a drink first thing in the
morning to steady your nerves or to get rid of a hangover?
SSRIs
MTB S2CK
p. 522
MTB S2CK
p. 523
Substance Related Disorders/Treatment

Detoxification
Usually 5-10 days
Mostly in hospital settings to assure safe detoxification
Rehabilitation
Usually 28 days or more with a focus on relapse
prevention techniques
Alcoholics Anonymous
Narcotics Anonymous
Pharmacologic treatments often include:
Disulfram (acetaldehyde dehydrogenase inhibitor)
Naltrexone (opioid receptor antagonist)
Acamprosate
MTB S2CK
p. 523
65-year-old engineer suffered femur fracture and some

cuts and bruises after being involved in an MVA. Hes
admitted to the medicine floor and started on oxycodone.
The day after admission, he appears confused with
observable tremors in both extremities. He becomes
concerned about bugs on the walls in his room and
asks for your help.
What is the most likely explanation for his symptoms?
a. Brain concussion Typically after injury
b. Alcohol withdrawal
c. Oxycodone intoxication Constipation, miosis
>1 day but <1 month, delusions,
d. Brief psychotic disorder hallucinations, disorganized speech &

behavior
e. Schizophrenia >6 months, delusions, hallucinations, disorganized

MTB S2CK
p. 523
speech & behavior
22
Somatoform Disorders
Characterized by
Somatoform Disorder,
Factitious Disorder, and
Malingering
Physical symptoms with no medical explanation
Symptoms severe enough to adversely affect

level of functioning
More frequent in young women
Usually has psychological component,
component which the
patient is unaware
Treatment of choice: psychotherapy
Source of symptoms is psychological
MTB S2CK
Types of Somatoform Disorders/

Diagnostic criteria
Somatization disorder
Hypochondriasis
Patients must have at
Patients believe that
least
they have some
specific disease
4 Pain
despite constant
2 GI
reassurance
1 Se
Sexual
al
And
1 Pseudoneurological
symptom
MTB S2CK
MTB S2CK
p. 524

Diagnostic criteria
Conversion
Affects voluntary motor or sensory
functions, indicative of a medical
condition
Usually caused by psychological factors
Associated with la belle indifference
Unconcerned about impairment
p. 524
MTB S2CK

Diagnostic criteria
Body Dysmorphic Disorder
Patients believe that some
part of the body is
abnormal, defective, or
misshapen
Source: elovedfreak,
p. 523
Pain Disorder
Main complaint:
presence of pain
And must have
Psychological
f t
factors
associated
i t d
with pain
p. 524
35-year-old married mother of 3 has frequent complaints

of dizziness, nausea, diarrhea, vomiting, pain during
intercourse, paresthesias, leg pain, stomach pain, food
intolerance, and headaches. She has tried numerous
medications, but none have been beneficial. Neurological
examination: normal.
What is the next step in the management of this patient?
a. Lorazepam Anxiety disorder
b. Sertraline Fibromyalgia & depression
c. Individual psychotherapy
d. Lithium Bipolar disorder
e. Risperidone Psychosis
MTB S2CK
p. 524
23
Factitious Disorder
Factitious Disorder
Individual fakes an illness to get attention

and emotional support in patient role
Either psychological or physical illness
Psychological symptoms
Hallucinations, delusions, depression, and

bizarre behavior
Physical symptoms
Inflict life-threatening injuries on themselves

Behavior may be compulsive at times
Formerly known as Mnchausen syndrome
Factitious disorder by proxy, caretaker fakes signs
and symptoms in another person
Usually a child
child, in order to assume the sick role by
proxy as the caregiver
Abdominal pain, fever, nausea, vomiting, or

hematomas
MTB S2CK
p. 524
MTB S2CK
p. 525
Factitious Disorder
Factitious Disorder/Treatment
Typically, women
with a history of
being employed in
healthcare
Men more often have
physical symptoms
Patients ultimate
goal: admission to
hospital
Always exclude any
medical disorder with
similar symptoms
No specific therapy has been

proven to be effective
When a child is involved in factitious
disorder by proxy
MTB S2CK
Contact child protective services to

ensure childs safety
Factitious disorder cannot
be diagnosed without first
ruling out medical illness
p. 525
MTB S2CK
p. 525
Malingering
Malingering/Diagnosis
Characterized by
Conscious production of signs and symptoms
for an obvious gain, such as
Diagnosis
More frequently in prisoners and military
personnel
Typically diagnosed when theres a
discrepancy between
Avoiding work
Evading criminal prosecution
Or
Achieving financial gain
Not a mental illness
MTB S2CK
p. 525
Patients complaints
And
Actual physical or laboratory findings
MTB S2CK
p. 525
24
Malingering
If medical evaluation reveals malingering

Confront patient with the outcome
Adjustment Disorder
A lack of cooperation from

patients is characteristic of
malingering
MTB S2CK
p. 525
Adjustment Disorder
Characterized by
Maladaptive reaction to
an identifiable stressor
Loss of job
Divorce
Or
Failure in school
Adjustment Disorder/Treatment
Symptoms
Anxiety
Depression
Disturbances of conduct
Severe enough to cause

impairment in functioning
Treatment of choice
Psychotherapy
Both individual and group therapy have
been used effectively
Usually occur within 3

months of stressor and
must remit within 6
months of removal of
stressor
MTB S2CK
p. 525
MTB S2CK
p. 525
Personality Disorders
Personality Disorders
Characterized by
Personality patterns that are:
Pervasive
Inflexible
Maladaptive
Cl t A
Cluster
Cl t B
Cluster
Paranoid
Schizoid
Schizotypal
Histrionic
Antisocial
Borderline
Narcissistic
MTB S2CK
Cl t C
Cluster
Avoidant
Dependent
Obsessive
compulsive
p. 525 526
25
Types of Personality Disorders
Paranoid
Schizoid
Schizotypal
Histrionic
Suspicious
Mistrustful
Secretive
Isolated
A d
And
Questioning
loyalty of
family &
friends
Choice of
solitary activities
Lack of close
friends
Emotional
E
i
l
coldness
No desire for or
enjoyment of close
relationships
Ideas of
reference
Magical
thinking
Odd thinking
thi ki
Eccentric
behavior
Increased social
anxiety
Brief psychotic
episodes
Must be center
of attention
Inappropriate sexual
behavior
Self-dramatization
Use physical
appearance to draw
attention to self
MTB S2CK
p. 526
MTB S2CK

Antisocial
Failure to
conform to
social rules
Deceitful
Lack of remorse
Impulsive
I
l i
Aggressive
towards others
Irresponsible
Must be 18+
MTB S2CK
p. 526
p. 526
Borderline
Narcissistic
Unstable
relationships
Impulsive
Recurrent suicidal
behaviors
Chronic
Ch
i ffeelings
li
of emptiness
Inappropriate
anger
Dissociative
symptoms when
severely stressed
Brief psychotic
episodes
Grandiose
sense of self
Belief that they
are special
Lack empathy
Sense
S
off
entitlement
Require
excessive
admiration
Avoidant
Dependent
Unwilling
to get
involved
with people
Views self
as socially
inept
Reluctant to
take risks
Feelings of
inadequacy
Difficulty making
day-to-day
decisions
Unable to
assume
responsibility
Unable to express
disagreement
Fear of being
alone
Seeks relationship
as source of care
MTB S2CK
Obsessive
compulsive
Preoccupied
with details
Rigid
y
Orderly
Perfectionists
Excessively
devoted to
work
Inflexible
p. 526
Personality Disorders/Treatment
Individual psychotherapy
Medications if mood or anxiety
symptoms are present
MTB S2CK
p. 526
Which of the following personality

disorders has been associated with
positive psychotic symptoms?
a. Borderline & Schizotypal
b Histrionic
b.
Not
c. Schizoid
associated
d. Paranoid
e. Antisocial
MTB S2CK
p. 527
26
Eating Disorders
Anorexia Nervosa
Bulimia Nervosa
Eating Disorder Not
Otherwise Specified
15-year-old girl brought to clinic by her mother,

who found her vomiting in the bathroom. She
vomits daily after each meal and exercises
excessively. She has numerous calluses on her
hands as well as cavities. She is 55 and weighs
90 pounds.
What is her most likely diagnosis?
a. Bulimia nervosa Frequent binge eating, normal
weight, obesity history
Neither
b. Anorexia nervosa
anorexia
c. Eating disorder not otherwise specified nor
bulimia
d. Obesity Increased weight
e. Atypical depression Increased apetite & weight
MTB S2CK
p. 527
Anorexia Nervosa
Anorexia Nervosa/Diagnosis
Characterized by
Lose weight by
Failure to maintain a
normal body weight
Fear and
preoccupation of
gaining weight
Body image
disturbance
Strict caloric control

Excessive exercise
Purging
Laxative & diuretic
Source: http://www.womenshealth.gov/bodyimage/eating-disorders/
Unrealistic self-evaluation as overweight

Amenorrhea is common from low body weight
Deny their emaciated condition
Great concern with appearance and frequently examine
and weigh themselves
MTB S2CK
p. 527
And
Fasting
F ti
Bulimia Nervosa
Hospitalization to prevent
Characterized by
Frequent binge eating in a

discrete amount of time
Lack of control of
overeating episodes
Psychotherapy
Behavioral therapy
SSRIs
Source: girlshealth.gov
p. 528
Accompanied by
compensatory
behavior to prevent
weight gain
Purging
Laxatives &
diuretics
Fasting
And
Excessive exercise
To promote weight gain

MTB S2CK
Arrhythmia MCC of
death
p. 527
Anorexia Nervosa/Treatment
Dehydration
Starvation
Electrolyte imbalances
Death
Potassium deficiency
y
More frequently, teenage

girls 14 -18 years of age
Severe weight loss
Hypotension
MTB S2CK
Bradycardia
Lanugo hair
And
Edema
EKG changes
MTB S2CK
Self-evaluation
influenced by body
shape and weight
p. 528
27
Bulimia Nervosa
Eating Disorder Not Otherwise Specified
Diagnosis
More frequently women and later in adolescence
than anorexia nervosa
Most normal weight, but history of obesity
Doesnt meet criteria for either anorexia

nervosa or bulimia nervosa
Examples
Criteria for anorexia present in girls, but
menstruation is normal
Anorexic patient with normal weight
Use of compensatory behavior after eating
normal amounts of food
Treatment
Doesnt require hospitalization, unless
Severe electrolyte abnormality
Psychotherapy
SSRIs
MTB S2CK
p. 528
MTB S2CK
p. 528
Narcolepsy
Characterized by
Sleep Disorders
Narcolepsy
Insomnia
Excessive daytime
sleepiness
And
Abnormalities of REM
sleep
Most frequently begins

in young adulthood
Sleep studies are
usually indicated in
diagnosis
MTB S2CK
Narcolepsy
No curative therapy
Forced daytime naps
Modafinil
To maintain alertness
MTB S2CK
p. 528 529
Source:http://www.cdc.gov/sleep/
p. 528
Psychiatric & Physical Symptoms

of Narcolepsy (Sleep Disorder)
Specific feature of narcolepsy
Sleep
attacks
Cataplexy
Episodic
irresistible
sleepiness
And
Feeling
refreshed
upon
awakening
MTB S2CK
p. 529
Sudden
muscle tone
loss:
pathognomonic
And
May be
precipitated by
loud noise or
emotions
Hypnogogic
and
hypnopompic
hallucinations
Hallucinations
occur as
patient is
going to sleep
and waking
up
Sleep
paralysis
Awake
but unable
to move
Typically
upon
awakening
28
Insomnia
Insomnia
Characterized by
Sleep hygiene techniques
Inability to initiate or
maintain sleep
Going to bed and waking up at the same time

Avoiding caffeinated beverages
And
Avoiding daytime naps
May be due to anxiety

and depression
g to affect
Severe enough
level of functioning
Typically women who
complain of feeling tired
or have increased
appetite and yawning
MTB S2CK
p. 529
Behavioral modification techniques include

Using the bed only for sleeping (not for reading,
watching TV, or eating)
Medical therapy
Zolpidem, eszopiclone, or zaleplon
Source: nih.gov
MTB S2CK
p. 529
Terminology of Human Sexuality
Human Sexuality
Sexual identity
Based on a persons
secondary sexual
characteristics
Gender identity
Based on a persons
sense of maleness or
femaleness,
established by age 3
MTB S2CK
Human Sexuality
Masturbation
Normal precursor of object-related sexual behavior
All men and women masturbate
Problematic if it interferes with daily functioning
Homosexuality
H
lit
Not considered a mental illness unless it is egodystonic (person not happy with sexual orientation)
May be considered normal experimentation in
teenagers
MTB S2CK
p. 530
Gender role
Based on external
patterns of behavior
that reflect inner sense
of gender identity
Sexual orientation
Based on persons
choice of love object;
may be heterosexual,
homosexual, bisexual,
or asexual
p. 529
Types of Sexual Dysfunction

Impotence
Persistent or recurrent
inability to attain or
maintain an erection
until completion of
sexual
se
ua act
Premature ejaculation
Ejaculation before
penetration or just after
penetration, usually
due to anxiety
Treatment
Treatment
R/O medical causes or

medication
Psychotherapy, couples
sexual therapy
MTB S2CK
Psychotherapy, behavioral
modification techniques
(stop and go, squeeze),
SSRI medication
p. 530
29
Types of Sexual Dysfunction
Paraphilias
Dyspareunia
Vaginismus
Pain associated with

sexual intercourse,
not diagnosed if due
to medical condition
Prolonged and painful

contraction or spasm of
the vagina
Usually severe enough
to prevent intercourse
Treatment
Treatment
Psychotherapy
MTB S2CK
Psychotherapy
Dilator therapy
p. 530
Group of disorders that are recurrent,

sexually arousing, and seen more frequently
in men
Usually focus on humiliation, nonconsenting
partners, or use of nonliving objects
Must occur
> 6 months and cause distress
Affect level of functioning
Dont diagnose if experimentation
MTB S2CK
Types of Paraphilias
p. 530
Exhibitionism
Recurrent urge to
expose oneself to
strangers
Pedophilia
Recurrent urges or
arousal toward
prepubescent
children
Fetishism
Recurrent use of
nonliving objects to
achieve sexual
pleasure
Masochism
Recurrent urge or
behavior involving the
act of humiliation
Sadism
Recurrent urge or behavior involving acts in
which physical or psychological suffering
of victim is exciting
Transvestic fetishism
MTB S2CK
p. 531
Recurrent urge or behavior involving cross

dressing for sexual gratification; usually in
heterosexual males
MTB S2CK
p. 531
Paraphilias/Treatment
Frotteurism
Rubbing ones pelvis or erect penis against a
nonconsenting person for sexual gratification
Behavioral modification techniques
Aversive conditioning
Antiandrogens or SSRIs to reduce

sexual drive
MTB S2CK
p. 531
Source: Dschwen, commons.wikimedia.org
MTB S2CK
p. 531
30
Gender Identity Disorder
Gender Identity Disorder
Characterized by
Patients will take hormones when older to deepen

voice, if female, or soften voice, if male
Women may bind their breasts and men may hide
their penis and testicles
Its seen more frequently in young men
Persistent discomfort and sense of

inappropriateness regarding the patients assigned
sex
Diagnosis
Wearing
g opposite
pp
g
genders clothes
Using toys assigned to opposite sex
Play with opposite-sex children when young
And
Feeling unhappy about ones own sexual
assignment
MTB S2CK
p. 531
Treatment
Sexual reassignment surgery if approved
MTB S2CK
p. 531
Suicide
Suicide
Recent suicide attempt

Complaints of suicidal
thoughts
Admission of suicidal
thoughts
Demonstration of
suicidal behaviors
Source: samhsa.gov
Buying weapons
Giving away
possessions
Writing a will
MTB S2CK
p. 532
Source: samhsa.gov
Suicide
Risk Factors
Men
Older adults
Social isolation
Presence of psychiatric
illness/drug abuse
Perceived
hopelessness
Previous attempts
MTB S2CK
Treatment
Hospitalize patient
Take all threats
seriously
p. 532
31
Asthma/Definition
Asthma or reactive airway disease
Abnormal bronchoconstriction of airways
Asthma
Stephen Bagley, MD
Resident Physician
Internal Medicine
Hospital of the University of Pennsylvania
Characterized by
Reversible airway obstruction secondary to
bronchial smooth muscle hyperactivity
Airway inflammation, mucus plugging, and smooth
muscle hypertrophy
Can lead to chronic, irreversible airway obstruction
MTB S2CK
p. 129
Asthma/Etiology
Asthma/Etiology
Extremely common
Etiology unknown
Associated with atopic disorders and
obesity
Causes acute exacerbations of symptoms

Allergens such as pollen, dust mites, cockroaches,
and cat dander
Infection
Changes in weather (especially cold air)
Exercise
Catamenial (related to menstrual cycle)
Aspirin, NSAIDs, beta blockers, tobacco smoke
Gastroesophageal reflux disease (GERD)
Asthma prevalence,
incidence, and hospitalization
rates are increasing
MTB S2CK
p. 129
MTB S2CK
p. 129
Asthma/Presentation
Asthma/Presentation
Most often presents with
Which of the following is most likely to be found

in an asthmatic patient?
Wheezing
Acute onset of SOB
Cough
And
Chest tightness
Increased sputum production common

Fever is often not present
Remember all that wheezes
is not asthma!
MTB S2CK
p. 129
Symptoms worse at night

Nasal polyps
Eczema or atopic
physical
y
dermatitis on p
examination
Increased length of
expiratory phase of
respiration
Increased use of
accessory
respiratory muscles
(e.g., intercostals)
Hyperresonance to
percussion, pulsus
paradoxus
I/E ratio decreases

(normal is 1:2)
MTB S2CK
p. 129 130
Asthma/Presentation
The answer to the best initial test question

in asthma is based on the severity of
presentation
Asthma/Diagnostic Tests
The best initial test in an acute

exacerbation
Arterial blood gas (ABG) or peak
expiratory flow (PEF)
ABG if mild,
mild early
earl e
exacerbation:
acerbation mild
hypoxia, respiratory alkalosis
ABG if severe, late exacerbation: severe
hypoxia, respiratory acidosis
MTB S2CK
p. 130
MTB S2CK
p. 130
Chest X-ray
Most accurate diagnostic test is

pulmonary function testing (PFTs)
Most often normal in asthma, but may

show hyperinflation
Useful for excluding other disease
processes
You must understand lung volumes!
Pneumonia, CHF, pneumothorax
MTB S2CK
p. 130
MTB S2CK
p. 130
PFTs in asthma show
OBSTRUCTION: FEV1 and FVC with a
FEV1/FVC ratio
HYPERINFLATION: total lung capacity (TLC)
AIR TRAPPING: in residual volume
REVERSIBILITY: in FEV1 > 12% with use of
albuterol
BRONCHIAL HYPERRESONIVENESS: FEV1 >
20% with use of methacholine
MTB S2CK
p. 131
15-year-old boy with occasional SOB every few weeks.
Currently feels well. No medications and denies any other
medical problems. Pulse is 70 and RR is 12. Chest
examination is normal.
Which is the single most accurate diagnostic test at this time?
Acute exacerbation
a. Peak expiratory flow
Less likely in asymptomatic
b. Increase in FEV1 with albuterol
Asymptomatic
c. Diffusion capacity of carbon monoxide
d. > 20% decrease in FEV1 with use of methacholine
e. Increased alveolar-arterial oxygen difference
Asymptomatic
(A-a gradient)
f. Increase in FVC with albuterol Less likely in asymptomatic
g. Flow-volume loop on spirometry Best for fixed obstructions
h. Chest CT scan Shows nothing or hyperinflation
i. Increased pCO2 on ABG Acute exacerbation
MTB S2CK
p. 130
Acetylcholine and histamine provoke

bronchoconstriction and increase in
bronchial secretions
Methacholine is artificial form of
acetylcholine used in diagnostic testing
MTB S2CK
p. 131
Asthma/Treatment
Additional testing options include

CBC may show an increased eosinophil
count
Skin testing to identify specific allergens
that provoke bronchoconstriction
Increased IgE levels suggest allergic
etiology
Chronic management
Stepwise fashion of progressively
adding more types of treatment if no
response
Also seen in allergic bronchopulmonary

aspergillosis
MTB S2CK
p. 131
MTB S2CK
Asthma/Chronic Management
Step 1
Asthma/Treatment
Step 2
Step 3
Step 4
Mild
intermittent:
< 2 days/week
< 2 nights/ month
Mild persistent:
> 2 days/week
> 2 nights/month
Moderate
persistent: daily,
or > 1 night/week
Severe
persistent:
continual,
frequent
Inhaled shortacting
ti beta
b t
agonist SABA
Albuterol
Levalbuterol
Add a long-term
control agent:
Low-dose inhaled
corticosteroids
(ICS) for daily use
Beclomethasone
Budesonide
Flunisolide
Fluticasone
Mometasone
Triamcinolone
MTB S2CK
p. 131 132
p. 131
Add a longg beta

acting
agonist
(LABA) to a
SABA & ICS
Or
Increase
dose of ICS
LABA
Salmeterol
Or
Formoterol
Increase
d
dose
off
ICS to
maximum
in
addition
to LABA &
SABA
Adverse effects of inhaled

steroids are dysphonia and oral
candidiasis
Alternate long-term control agents include
C
Cromolyn
l and
d nedocromil:
d
il inhibit
i hibit mastt cellll mediator
di t
release useful for exercise
Theophylline: phosphodiesterase inhibitor
increasing cAMP levels (cardio- and neurotoxicity)
Leukotriene modifiers: montelukast, zafirlukast, or
zileuton best with atopic patients
MTB S2CK
p. 131
Asthma/Treatment
Zafirlukast is hepatotoxic
and has been associated
with Churg-Strauss
syndrome
MTB S2CK
p. 131
Management of Acute Exacerbation
Step#1: determine severity of asthma

exacerbation, quantified by
Decreased peak expiratory flow (PEF)
ABG with evidence of increased A-a
Aa
gradient or CO2 retention
MTB S2CK
p. 133
Asthma/Treatment
PEF is an approximation of FVC

No precise normal value
Based predominantly on height and age,
not weight
PEF is used in acute assessment byy seeing
g
how much difference theres from patients
usual PEF when stable
Management of Acute Exacerbation

Oxygen
Albuterol (often nebulized to ensure adequate
delivery to lungs) +/- inhaled anticholinergic (e.g.,
ipratropium)
Corticosteroids: need 4-6
4 6 hours to begin to work
work, so
give right away
Epinephrine injections are no more effective
than albuterol and have more adverse systemic
effects
MTB S2CK
p. 133
MTB S2CK
p. 133
Asthma/Treatment
Asthma/Treatment
Anticholinergics
Role of ipratropium and tiotropium in asthma
management unclear
Magnesium
Some modest effect in bronchodilation
Not as effective as albuterol, ipratropium, or
steroids, but it does help
In general, ipratropium should be used, but doesnt

work as rapidly as albuterol
Epinephrine
Rarely used and only as a drug of last resort
MTB S2CK
p. 132 133
Magnesium
g
helps
p bronchospasm.
p
Magnesium is used only in acute,
severe asthma exacerbation not responsive
to several rounds of albuterol while waiting
for steroids to take effect.
MTB S2CK
p. 133
Asthma/Treatment
Asthma/Treatment
Adverse Effects of Chronic Systemic

Corticosteroids
Should be a last resort because of very harsh
adverse effects such as
Osteoporosis
Cataracts
Adrenal suppression and fat redistribution
Hyperlipidemia, hyperglycemia, acne, and
hirsutism (particularly in women)
Thinning of skin, striae, and easy bruising
MTB S2CK
p. 132
High-dose inhaled steroids

rarely lead to adverse effects
associated with prednisone
MTB S2CK
p. 132
Asthma/Treatment
47-year-old man with history of asthma comes to ED
with several days of increasing SOB, cough, and
sputum production. RR is 34. He has diffuse
expiratory wheezing and prolonged expiratory phase.
Which would you use as the best indication of the
severity of his asthma?
a. Respiratory rate
b. Use of accessory muscles Subjective
c. Pulse oximetry Hypoxia, until imminent respiratory failure
d. Pulmonary function testing Short of breath
e. Pulse rate Adds nothing
MTB S2CK
p. 132.4
The following are not effective in

acute exacerbations
Theophylline
Cromolyn and nedocromil (best
with
ith extrinsic
t i i allergies
ll i like
lik h
hay
fever)
Leukotriene modifiers
Omalizumab
Salmeterol
MTB S2CK
p. 133
Asthma/Treatment
If no response to oxygen, albuterol, and

steroids or develops respiratory acidosis
(increased pCO2)
Consider endotracheal intubation and
mechanical ventilation
MTB S2CK
Chronic Obstructive
Pulmonary Disease
p. 133
COPD/Definition
COPD/Definition
Characterized by airflow obstruction

secondary to emphysema and/or
chronic bronchitis
Emphysema
Chronic bronchitis
Terminal airway destruction resulting

in decreased elastic recoil of lungs
Normally, elastin fibers allow passive
exhalation
MTB S2CK
p. 134
Productive cough for > 3 months/year

for 2 consecutive years
Both
Part of COPD spectrum
Results in decrease in FEV1 and FVC
with increase in TLC
MTB S2CK
p. 134
COPD/Etiology
COPD/Presentation
Tobacco smoking
Leads to almost all COPD
Destroys elastin fibers
SOB worsened by exertion

Intermittent exacerbations with cough,
sputum, and SOB often brought on by
infection
Barrel chest from air trapping
Muscle wasting and cachexia
Young and
Y
d a nonsmoker,
k
answer alpha-1 antitrypsin
deficiency as most likely cause
MTB S2CK
p. 134
COPD now thought to have a component of

systemic inflammation
MTB S2CK
p. 134
COPD/Diagnostic Tests
Best initial test:

chest X-ray
Increased
anteriorposterior (AP)
di
diameter
t
Air trapping and
flattened
diaphragms
Most accurate diagnostic test: PFT

Decreased FEV1, FVC, and FEV1/FVC ratio
(< 70%)
Increased TLC due to RV
Decreased DLCO in emphysema
p y
(destruction of alveolar septae where
capillaries are found)
Incomplete improvement with albuterol
Little or no worsening with methacholine
MTB S2CK
p. 134
MTB S2CK
p. 134
Reversibility with Inhaled Bronchodilators

COPD generally associated with IRREVERSIBLE
airway obstruction
But
COPD has a broad response to inhaled
bronchodilators (e
(e.g.,
g albuterol)
Ranges from no reversibility to complete
reversibility
Arterial blood gas (ABG)

Acute exacerbations of COPD are
associated with pCO2 and hypoxia
Reversibility in response to
bronchodilators is: > 12% increase and
200 mL increase in FEV1
MTB S2CK
p. 134
Respiratory acidosis may be present if

theres
there
s insufficient metabolic compensation
and bicarbonate level will be elevated to
compensate
In between exacerbations, not all those
with COPD will retain CO2
MTB S2CK
p. 134
COPD/Treatment
EKG
Right atrial hypertrophy and right ventricular
hypertrophy
A-fib or multifocal atrial tachycardia (MAT)
Improves Mortality and Delays Progression of

Disease: only 2 interventions!
Echocardiography
Right atrial and right ventricular hypertrophy
Pulmonary hypertension
MTB S2CK
p. 135
COPD/Treatment
Definitely Improves Symptoms (But Does Not
Decrease Disease Progression)
Short-acting beta agonists (e.g., albuterol)

Anticholinergic agents: tiotropium, ipratropium
Inhaled steroids
Long-acting beta agonists (e.g., salmeterol)
Pulmonary rehabilitation
Smoking cessation
Oxygen therapy for hypoxia
PaO2 <55 or SaO2 <90%
PaO2 <60 or SaO2 <90%
If patient also has pulmonary hypertension,
cor pulmonale or polycythemia
Mortality benefit from oxygen is directly proportional

to the number of hours that oxygen is used
MTB S2CK
p. 135
COPD/Treatment
Asthmatics not
controlled with albuterol
Inhaled steroid
COPD not controlled

with albuterol
Anticholinergic
(e.g., tiotropium)
Inhaled steroid
Inhaled anticholinergic agents are most

effective in COPD
MTB S2CK
p. 135
MTB S2CK
p. 135
COPD/Treatment
COPD Acute Exacerbations/Treatment
Possibly Improves Symptoms

Theophylline
Lung volume reduction surgery
Combination of bronchodilators and

corticosteroid therapy
No Benefit
Cromolyn
C
l
Leukotriene modifiers (e.g., montelukast)
COPD exacerbation treatment

is identical to asthma
exacerbation treatment, but
with less proven benefit
When all medical therapy is insufficient,

the answer is refer for transplantation
MTB S2CK
p. 135
Antibiotics
For exacerbation of moderate to severe
COPD
Defined as requiring hospitalization or having at
least two of the three cardinal symptoms of a
COPD flare
Dyspnea
Sputum production
Sputum purulence
MTB S2CK
p. 136
MTB S2CK
p. 136
Chronic Bronchitis Acute Exacerbations/

Treatment
Antibiotics
Although viruses cause 20-50% of episodes,
coverage should be provided against
Streptococcus pneumoniae, H. influenzae, and
Moraxella catarrhalis
Macrolides: azithromycin, clarithromycin

Cephalosporins: cefuroxime, cefixime
Amoxicillin/clavulanic acid
Quinolones: levofloxacin, moxifloxacin
Second-line Agents
Doxycycline, TMP/SMX
MTB S2CK
p. 136

Criteria for Oxygen Use in COPD
Although the hypoxic drive elimination concept is
incorrect
Avoid reflexively placing a patient with COPD on
very high-flow 100% nonrebreather mask
Use only as much oxygen necessary to raise pO2
above 90% saturation
Bronchiectasis &
Associated Conditions
The idea of eliminating hypoxic drive is

not accurate. Dyspneic, hypoxic patients
with COPD must get oxygen
MTB S2CK
p. 136
Bronchiectasis/Definition
Bronchiectasis/Etiology
Uncommon disease
from chronic
destruction, remodeling,
and dilation of the
large bronchi
Single MCC
Cystic fibrosis: 50% of cases
Other causes are
Infections
TB ((and non-tuberculous mycobacterium)
y
)
Pneumonia (staph or repeated aspiration)
Permanent anatomic
abnormality that
cannot be reversed or
cured
MTB S2CK
p. 136
Panhypogammaglobulinemia and immune

deficiency
Source: Yale Rosen, commons.wikimedia.org
MTB S2CK
p. 137
Bronchiectasis/Etiology
Bronchiectasis/Diagnostic Tests
Foreign body or tumors

Allergic bronchopulmonary aspergillosis
(ABPA)
Collagen vascular such as RA
Immotile cilia syndrome
y
((Kartagener
g
syndrome)
Best initial test

Chest X-ray shows
These conditions result in repeated and

persistent lung infections
MTB S2CK
p. 137
Dilated, thickened bronchi, sometimes with

tram-tracks, which is thickening of bronchi
Most accurate test

High-resolution CT, general rule of thumb
Sizable airways are larger in diameter than
corresponding adjacent bronchial arteries
MTB S2CK
p. 137
Impossible to diagnose bronchiectasis

without imaging study such as CT
Sputum culture
Only way to determine specific bacterial
etiology
MTB S2CK
p. 137
Source: Thomas P. Eberle
MTB S2CK
p. 137
Bronchiectasis/Treatment
1. Chest physiotherapy (cupping and

clapping) and postural drainage
Essential for dislodging plugged-up bronchi
2. Treat each episode of infection as it

arises
Same antibiotics as for COPD exacerbations
Only difference is inhaled antibiotics seem to
have some efficacy
3. Surgical resection
Hypersensitivity to fungal antigens that

colonize bronchial tree
Almost exclusively with asthma and atopic
disorders
Look for
Asthmatic with recurrent episodes of
brown-flecked sputum and transient
infiltrates on X-ray
Cough, wheezing, hemoptysis, bronchiectasis
Focal lesions
MTB S2CK
Allergic Bronchopulmonary Aspergillosis

(ABPA)
p. 138
MTB S2CK
p. 138

(ABPA)/Diagnostic Tests

(ABPA)/Treatment
Peripheral eosinophilia
Skin test reactivity to aspergillus
antigens
Precipitating
p
g antibodies to aspergillus
p g
on blood test
Elevated serum IgE levels
Pulmonary infiltrates on chest X-ray or
CT
1. Oral steroids (prednisone) for severe cases
MTB S2CK
p. 138
Autosomal recessive from mutation that

codes for chloride transport
Known as CF transmembrane conductance
regulator (CFTR)
Mutations in CFTR g
gene damage
g chloride
and water transport across apical surface of
epithelial cells in exocrine glands throughout
the body
p. 138 139
2. Itraconazole or voriconazole orally for

recurrent episodes
i d
Inhaler cant deliver high enough dose
steroids to be effective in ABPA
MTB S2CK
Cystic Fibrosis (CF)/Etiology
MTB S2CK
Inhaled steroids arent effective for ABPA
Source: Mucoviscidose.PNG:
Mirmillon, commons.wikimedia.org
p. 138
Cystic Fibrosis/Etiology
Leads to abnormally thick mucus in
General
Growth failure (malabsorption)
Vitamin deficiency states
Vitamins A,D,E,K
Nose & Sinuses
Nasal polyps
Sinusitis
Liver
Hepatic steatosis
Portal hypertension
Gallbladder
Biliary cirrhosis
Neonatal
obstructive jaundice
Cholelithiasis
MTB S2CK
p. 139
Lungs
Bronchiectasis
Bronchitis
Broncholitis
Pneumonia
Atelectasis
Hemoptysis
Pneumothorax
Reactive airway
disease
Cor pulmonale
Respiratory failure
Mucoid impaction
of the bronchi
Allergic
bronchopulmonary
aspergillosis
Heart
Right ventricular
hypertrophy
Pulmonary artery
dilation
Source: Maen K Abu Househ, commons .wikimedia.org
10
Bone
Hypertrophic
osteoarthropathy
Clubbing
Arthritis
Osteoporosis
Intestines
Meconium ileus
Meconium peritonitis
Rectal prolapse
Intussusception
Volvulus
Fibrosing colonopathy
(strictures)
Appendicitis
Intestinal atresia
Distal intestinal obstruction
syndrome
Inguinal hernia
MTB S2CK p. 139
Spleen
Hypersplenism
Damaged mucus clearance decreases ability to get

rid of inhaled bacteria
Stomach
GERD
Neutrophils in CF dump tons of

DNA into airway secretions
clogging them up
Pancreas
Pancreatitis
Insulin
I
li d
deficiency
fi i
Symptomatic
hyperglycemia
Diabetes
Reproductive
Infertility
Aspermia, absence
of vas deferens
Amenorrhea
Delayed puberty
Source: Maen K Abu Househ, commons .wikimedia.org
MTB S2CK
p. 139
Cystic Fibrosis/Presentation
Over 1/3 CF patients are adults
Look for
Young adult with chronic lung disease
Cough
Sputum
py
Hemoptysis
Bronchiectasis
Wheezing
Dyspnea
And
Recurrent episodes of infection
Sinus pain and polyps are common

Source: nih.gov
MTB S2CK
p. 139
p. 139
Gastrointestinal Involvement
Meconium ileus:
infants with abdominal
distention
Pancreatic
insufficiency (in 90%)
with steatorrhea and
vitamin A, D, E, and K
malabsorption
MTB S2CK
Recurrent
pancreatitis
Distal intestinal
obstruction
Biliaryy cirrhosis
Islets spared,
beta cell function is
normal until much
later in life
Genitourinary Involvement
Men are often infertile
95% have azoospermia, vas deferens
missing in 20%
Women are infertile because

Chronic lung disease alters menstrual
cycle
And
Thick cervical mucus blocks sperm entry
MTB S2CK
p. 139
11
Cystic Fibrosis/Diagnostic Tests
Cystic Fibrosis/Diagnostic Tests
Most accurate test: increased sweat chloride test

Pilocarpine increases acetylcholine levels
increases sweat production
Sputum Culture
Chloride levels in sweat > 60 mEq/L in CF on

repeated testing establishes diagnosis
Genotyping, not as accurate as increased sweat

chloride level
Nontypable Haemophilus influenzae

Pseudomonas aeruginosa
Burkholderia cepacia
Because there are so many different types of

mutations leading to CF
MTB S2CK
p. 139
MTB S2CK
Cystic Fibrosis/Treatment
p. 140
Cystic Fibrosis/Treatment
1. Antibiotics are routine
Gross hemoptysis
Eliminating colonization: difficult

Sputum culture: essential to guide therapy
Inhaled aminoglycosides: almost exclusively limited to
CF
Rigid bronchoscopy
Unsuccessful
2. Inhaled recombinant human deoxyribonuclease

( hDN
(rhDNase)
)
Embolization
Interventional radiology
Breaks down massive amounts of DNA in respiratory

mucus that clogs up airways
3. Inhaled bronchodilators
Albuterol
4. Lung transplantation
MTB S2CK
Place patient bad lung-side down

Helps prevent bleeding into healthier lung, which is
providing most of oxygen exchange
p. 140
Community Acquired Pneumonia/Definition
Pneumonia Part 1
Community-acquired pneumonia
(CAP)
Pneumonia occurring before
hospitalization
Or
Within 48 hours of hospital admission
MTB S2CK
p. 140
12
CAP/Definition
Most common infectious cause of death

in U.S.
CAP/Etiology
Common Pathogens in CAP & Their Associations
Haemophilus
influenzae
Klebsiella
pneumoniae
COPD
Alcoholism
Diabetes
MCC: Streptococcus pneumoniae
Staphylococcus
aureus
Recent viral
infection
(influenza)
Mycoplasma
pneumoniae
Young
Healthy
patients
Anaerobes
Animals
at time of
giving
birth
Veterinarians
Farmers
Contaminated water
sources
Air
conditioning
Ventilation
systems
Chlamydophila
pneumoniae
Poor
dentition
Aspiration
Coxiella
burnetii
Legionella
Chlamydia
psittaci
Birds
Hoarseness
MTB S2CK
p. 140
MTB S2CK
p. 141
CAP/Presentation
CAP/Presentation
All forms of pneumonia present with

Fever and cough
Severe infection
Associated with dyspnea
Distinguished by abnormalities of
Abdominal pain or diarrhea can occur with infection

in lower lobes irritating intestines through
diaphragm
Vital signs (tachycardia, hypotension, tachypnea)

Or
Mental status
Dyspnea, high fever, and abnormal

chest X-ray are main ways to
distinguish pneumonia from bronchitis
MTB S2CK
p. 141
CAP/Presentation
Legionella is particularly known for causing diarrhea
Chills or rigors are sometimes a sign of

bacteremia
S. pneumo would be most common
Chest pain (often pleuritic) occurs from

inflammation of pleura
Hypothermia is as bad as fever in terms of
pathologic significance
MTB S2CK
p. 141
CAP/Presentation
Organism-specific Associations on Presentation
USMLE S2 may play abnormal breath

sounds as part of multimedia and ask you
to recognize them
Dullness to percussion if theres
effusion
Bronchial breath sounds and
egophony consolidation of air spaces
MTB S2CK
p. 141
Klebsiella
pneumoniae
Mycoplasma
pneumoniae
Pneumocystis
Hemoptysis from
necrotizing disease
disease,
currant jelly
sputum
Dry cough, rarely

severe bullous
severe,
myringitis
AIDS with
<200
CD4 cells
Legionella
Anaerobes
Foul-smelling sputum,
rotten eggs
MTB S2CK
p. 141
Gastrointestinal symptoms
Abdominal pain, diarrhea,
or CNS symptoms
Headache & confusion
13
CAP/Presentation
CAP/Presentation
Dry or non-productive cough

Mycoplasma
Viruses
Coxiella
Pneumocystis
Chlamydia
Preferentially involve interstitial

space
Air spaces of alveoli empty
MTB S2CK
p. 142
Thats why theres less sputum

production!
Specific sputum colors are
useless in determining etiology
MTB S2CK
p. 142
CAP/Diagnostic Tests
Best initial test for all respiratory

infections
Atypical pneumonia
Organism not visible on Gram stain and
not culturable on standard blood agar
Chest X-ray: but cant determine specific

etiology
Sputum Gram stain and sputum

culture
Best ways to first determine specific
etiology
Many organisms wont be detected
MTB S2CK
p. 142
Mycoplasma
Chlamydophila
Legionella
Coxiella
And
Viruses
MTB S2CK
30-50% of cases
of CAP
p. 142
Chest X-ray
Bilateral interstitial Nonproductive
infiltrates with
cough
Mycoplasma
X-rays lag behind
Viruses
clinical findings
Coxiella
Pneumocystis
Chlamydia
1st chest X-ray can

be falsely negative
in 10-20%
Right middle lobe infiltrate characteristic of bacterial pneumonia. Source: Nirav Thakar, MD
MTB S2CK
p. 142
MTB S2CK
p. 143
14
Blood Cultures are positive

5-15% of CAP
Particularly with S. pneumoniae!
Sputum Gram stain is adequate if:
> 25 WBCs and < 10 epithelial cells
MTB S2CK
p. 143
Interstitial infiltrates leave the air space empty. This chest x-ray can be consistent
with PCP, Mycoplasma, viruses, and Chlamydia. Source: Craig Thurm, MD
MTB S2CK
p. 143
Chest CT and MRI show

Greater definition of abnormalities found
on chest X-ray
But
Wont
W t determine
d t
i specific
ifi microbiologic
i bi l i
etiology
Tests Done in Severe Disease with an Unclear

Etiology, or Those Not Responding to Treatment
Thoracentesis
In infectious diseases radiologic test is

never the most accurate test
MTB S2CK
p. 143
Any new large

effusion should be
analyzed
Empyema
Infected pleural
effusion
Acts like abscess
Only improves if
drained with chest
tube
MTB S2CK
Etiology of pleural effusions

Transudative
Secondary to
Increased PCWP
Or
Decreased
intravascular oncotic
pressure
Source: nih.gov
p. 143
Exudative
Secondar to
Secondary
Increased
vascular
permeability
Empyema
LDH > 60% of serum
OR
Protein > 50% of serum
pH < 7.2,
7 2 +gram stain
stain, +culture
+culture, or frank
pus
New, large effusions

secondary to pneumonia
should be tapped
MTB S2CK
p. 143
15
Bronchoscopy
S. pneumo can be tested via urine antigen
Only needed if sputum stain and culture

and blood cultures dont yield an organism
and patients condition is worsening
despite empiric therapy
Exception is pneumocystis pneumonia
MTB S2CK
p. 143 144
Specific Diagnostic Tests by Organism

Mycoplasma
pneumoniae
PCR
Cold
agglutinins
Serology
Special
culture
media
MTB S2CK
CAP/Treatment
p. 144
Rising serologic
titers
Urine antigen,
Culture on charcoalyeast extract
Severity of disease,
not the etiology drives
initial therapy
Mycoplasma & Chlamydophila,

rarely confirmed because they
are simply treated empirically
MTB S2CK
CAP/Treatment
p. 144
CAP/Treatment
Outpatient Treatment
Previously healthy or no
antibiotics in past 3 months
and mild symptoms
Comorbidities or
antibiotics in past 3
months
Macrolide
- Azithromycin
or
clarithromycin
Or
Doxycycline
Respiratory
fluoroquinolone
Levofloxacin
Or
Moxifloxacin
p. 144
Bronchoalveolar
lavage (BAL)
Legionella
p. 144
Determines location in which to place

patient
MTB S2CK
Pneumocystis
jiroveci (PCP)
CAP/Treatment
Rare to have specific organism

identified at time treatment is initiated
If case describes organism on Gram
stain treatment is directed towards that
organism
Most important step is determining
severity of disease.
MTB S2CK
Chlamydophila
pneumoniae,
Chlamydia
psittaci &
Coxiella burnetii
Inpatient Treatment
Respiratory fluoroquinolone: levofloxacin or
moxifloxacin
Or
Ceftriaxone and azithromycin
Almost all infectious diseases are initially treated

empiricallythat is, without a specific etiology
MTB S2CK
p. 144
16
CAP/Treatment
CAP/Treatment
Reasons to Hospitalize
80% safely treated outpatient with oral antibiotics
Severe disease is defined as a combination of
Hypotension (systolic <
90 mmHg)
Respiratory rate >
30/min
pO2 < 60 mmHg, pH <
7.35
Elevated BUN > 30
mg/dL,
Sodium <130 mmol/L
MTB S2CK
Glucose >250 mg/dL

Pulse > 125/min
Confusion
Temperature > 104 F
65 or comorbidities
such as cancer, COPD,
CHF, renal failure, or
liver disease
p. 145
Hypoxia and hypotension as

single factors are a reason to
hospitalize a patient
Chest X-ray does not guide

admission cannot tell severity
of hypoxia
MTB S2CK
p. 145
CAP
CURB 65
Confusion
Uremia
Respiratory Distress
BP low
65-year-old woman is hospitalized with CAP. Sputum Gram

stain: Gram-positive diplococci. Sputum culture doesnt grow a
specific organism. Chest X-ray: lobar infiltrate and large
effusion. Shes placed on ceftriaxone and azithromycin.
Thoracentesis: marked elevated LDH and protein level with
17,000 WBC/ L. Blood cultures grow Streptococcus
pneumoniae with minimal inhibitory concentration (MIC) to
penicillin
i illi < 0
0.1
1 g/mL.
/ L Oxygen
O
saturation
t ti 96% on room air.
i BP
110/70, T 102 F, Pulse 112.
a. Repeated thoracentesis Will add nothing
b. Placement of chest tube for suction
c. Add ampicillin to treatment No benefit
d. Place patient in ICU
No need for chest tube
e. Consult pulmonary Will add nothing
MTB S2CK
CAP/Treatment
MTB S2CK
p. 146
p. 145
CAP/Treatment
Pleural effusion with a large meniscus sign. Only a fluid sample from
thoracentesis can determine the specific cause. Source: Craig Thurm, MD
MTB S2CK
p. 146
Effusion should be freely mobile and from a layer when the patient lies
on her side. Source: Nishith Patel.
17
CAP/Treatment
CAP/Treatment
Pneumococcal Vaccination
Everyone > 65 should receive vaccination with 23
polyvalent vaccine
Chronic heart
Liver
Vaccinated as soon as
Kidney
their underlying disease
is apparent, regardless
Or
of age
Lung disease
Including asthma
MTB S2CK
p. 146
Hydropneumothorax is both abnormal air and fluid (effusion) in the pleural

space. Chest tube drainage is the most effective way to remove this
condition. Source: Albert Takem, MD.
MTB S2CK
p. 146
CAP/Treatment
CAP/Treatment
Other reasons to vaccinate
Generally healthy: single dose at 65
If first vaccination was given before 65
or with other conditions previously
described a second dose should also
described,
be given 5 years after first dose
Functional or anatomic asplenia (e.g., sickle cell

disease)
Hematologic malignancy (leukemia, lymphoma)
Immunosuppression: diabetes mellitus,
alcoholics, corticosteroid users, AIDS or HIV
positive
CSF leak and cochlear implantation recipients
MTB S2CK
p. 146 147
Healthcare workers do not need

pneumococcal vaccine
MTB S2CK
p. 147
Healthcare Associated Pneumonia or

Hospital Acquired Pneumonia (HAP)/Definition
Pneumonia Part 2
Pneumonia developing > 48 hours after

admission
g
incidence of Gram Much higher
negative bacilli such as E. coli or
Pseudomonas
MTB S2CK
p. 147
18
HAP/Treatment
HAP/Treatment
Main difference in management is

Macrolides (azithromycin or clarithromycin) are
unacceptable as empiric therapy
Piperacillin and ticarcillin

always used in combination
with beta-lactamase inhibitor
((e.g.,
g tazobactam or
clavulanic acid)
Centered around therapy for Gram-negative bacilli

Antipseudomonal cephalosporins: cefepime or
ceftazidime
Or
Antipseudomonal penicillin: piperacillin/tazobactam
Or
Carbapenems: imipenem, meropenem, or
doripenem
MTB S2CK
p. 147
MTB S2CK
p. 147
Ventilator Associated Pneumonia/Definition
VAP/Diagnosis
Mechanical ventilation interferes with normal

mucociliary clearance of respiratory tract
(e.g., ability to cough)
Positive pressure is tremendously damaging
to normal ability to clear colonization
Ventilator-associated pneumonia (VAP) has
an incidence as high as 5% per day in first
few days on ventilator
Because of multiple countercurrent

illnesses (e.g., CHF) even a diagnosis
of VAP can be hard to establish
Look for
MTB S2CK
p. 147
VAP/Diagnostic Tests
Sputum culture: nearly worthless

Due to colonization of endotracheal tube
(ET)
Diagnosis of specific etiology is

extremely difficult on ventilator
MTB S2CK
p. 148
Fever and/or rising WBC count

New infiltrate on chest X-ray
Purulent secretions coming from
endotracheal tube
MTB S2CK
p. 147
Least accurate but
easiest to do
Bronchoalveolar
lavage (BAL)
Tracheal
aspirate
Suction catheter
placed
l
d into
i t ET and
d
aspirates contents
below trachea when
catheter is past end
of tube
MTB S2CK
Most accurate but

dangerous
Bronchoscope placed
deeper in lungs
where there arent
supposed to be
organisms
Can be contaminated
when passed through
the nasopharynx
Protected brush
specimen
Tip of
p
bronchoscope
covered when
passed through
nasopharynx,
then uncovered
only inside lungs
Much more
specific,
decreased
contamination
p. 148
19
VAP/Treatment
Combine 3 different drugs
1. Antipseudomonal
beta-lactam
PLUS
Cephalosporin
(ceftazidime or cefepime)
Or
Penicillin
(piperacillin/tazobactam)
Or
Carbapenem (imipenem,
meropenem, or doripenem)
d i
)
2. Second antipseudomonal agent

PLUS
MTB S2CK
p. 148
Subcutaneous emphysema is air abnormally leaking into soft tissue of

the chest wall. Chest tube placement may cause air to leak into soft
tissues of the chest wall. Source: Birju Shah, MD.
3. Methicillin-resistant
antistaphylococcal agent
MTB S2CK
p. 148 149
Aminoglycoside
(gentamicin or
tobramycin or amikacin)
Vancomycin
Or
Linezolid
VAP/Treatment
Change initial therapy for VAP if

specific etiology is identified
MTB S2CK
p. 149
Patient hospitalized for head trauma and subdural hematoma

is intubated for hyperventilation and subsequent craniotomy.
Several days after admission hematemesis ensues and
stomach stress ulcers are found. Lansoprazole is started. VAP
develops, placed on imipenem, linezolid, and gentamicin.
Phenytoin, started prophylactically. Three days later creatinine
rises followed by seizures . Repeat head CT shows no
changes.
h
a. Switch phenytoin to carbamazepine Less likely to cause
renal failure (RF)
b. Stop lansoprazole Not likely to
cause RF
c. Stop imipenem
d. Stop linezolid Not likely to cause RF
e. Perform an electroencephalogram Will add nothing
MTB S2CK
p. 149
Lung Abscess/Etiology
Lung Abscess/Etiology
Rare because of prompt treatment of

aspiration pneumonia
Large-volume aspiration occurs from
Occurs only with

Large-volume
Large ol me aspiration of oral/phar
oral/pharyngeal
ngeal
contents, usually with poor dentition, who
isnt adequately treated
MTB S2CK
p. 149
Stroke with loss of gag reflex

Seizures
Intoxication
Endotracheal intubation
Aspiration pneumonia happens in

the right upper lobe when lying flat
MTB S2CK
p. 149
20
Lung Abscess/Presentation
Lung Abscess/Diagnostic Tests
Look for
Best initial test: chest X-ray
Person with one of these risk factors

presenting a chronic infection developing
over several weeks with large-volume
sputum that is foul smelling because of
anaerobes
Weight loss is common
MTB S2CK
p. 150
Lung Abscess/Diagnostic Tests
Cavity, possibly with air-fluid level
Chest CT is more accurate

Only lung biopsy can establish specific
microbiologic etiology
Sputum culture is the wrong answer for
diagnosing a lung abscess. Everyones
sputum has anaerobes from mouth flora.
MTB S2CK
p. 150
Lung Abscess/Treatment
Clindamycin is best to cover lung

abscess
Cavity consistent with an abscess with a thick wall and an air-fluid level. Source: Alejandro de la Cruz, MD.
MTB S2CK
p. 150
MTB S2CK
p. 150
Pneumocystis Pneumonia (PCP)/Etiology
PCP/Presentation
Agent causing PCP has been renamed

P. jiroveci instead of P. carinii
Almost exclusively in patients with AIDS
whose CD4 cell count is < 200/ L and
who aren
arentt on prophylactic therapy
Look for
Also occurs in chronically

immunosuppressed patients, especially
those on long term high dose steroids
MTB S2CK
p. 150
Patient with AIDS presenting with dyspnea

on exertion, dry cough, and fever
Question will often suggest or directly

state that CD4 count is low (< 200/ L)
and that patient isnt on prophylaxis
MTB S2CK
p. 150
21
PCP/Diagnostic Tests
Best initial test
Sputum stain: quite specific if its positive
Chest X-ray showing bilateral interstitial

infiltrates
Or
ABG looking for hypoxia or an increased
A-a gradient
LDH levels are always elevated

Most accurate test
If positive, there is no need to do further testing

If negative, bronchoscopy as the best
diagnostic test
Normal LDH means DONT answer PCP as

the most likely diagnosis
Bronchoalveolar lavage
MTB S2CK
p. 150
MTB S2CK
p. 150 151
PCP/Treatment
Best initial therapy for both treatment and prophylaxis
S2CK asks what is the most likely diagnosis,

not what is the for sure diagnosis
Cannot distinguish PCP from

Mycoplasma, Chlamydophila, or viruses
by X-ray alone. However, in HIV, PCP is
most likely with interstitial infiltrates
MTB S2CK
p. 151
Trimethoprim/sulfamethoxazole (TMP/SMX)
Add steroids to decrease mortality if PCP is severe

Severe PCP: pO2 < 70 or A-a gradient > 35
Atovoquone
Alternative to TMP/SMX if mild PCP, meaning
g there is
only mild hypoxia
If toxicity from TMP/SMX switch to either

Clindamycin and primaquine
Or
Pentamidine
MTB S2CK
p. 151
PCP/Treatment
HIV-positive African American man is admitted with
dyspnea, dry cough, high LDH, and pO2 of 63 mmHg.
He is started on TMP/SMX and prednisone. On 3rd
hospital day he develops severe neutropenia and
rash. He has anemia and smear shows bite cells.
What is the most appropriate next step in
management?
a. Stop TMP/SMX Need to treat
Will not help acute
b. Begin antiretroviral medications opportunistic infection
c. Switch TMP/SMX to intravenous pentamidine
IV for active
d. Switch TMP/SMX to aerosol pentamidine
disease
e. Switch TMP/SMX to clindamycin and primaquine
MTB S2CK
p. 151
Contraindicated due to G6PD
Often students will see 2 correct

treatments and think theres a mistake in
the question.
question If there are 2 correct
treatments, look for a contraindication to
one of them.
MTB S2CK
p. 152
22
PCP/Prophylaxis
PCP/Treatment
AIDS with CD4 count < 200/ L
1. TMP/SMX
Rash
Or
Neutropenia
2. Atovoquone
or Dapsone
Always choose therapy based first on

efficacy, not adverse effects
Dapsone is contraindicated in
those with G6PD deficiency
Aerosol pentamidine: not used as second-line

therapy for prophylaxis
Due to less efficacy than either atovoquone or
dapsone
MTB S2CK
p. 152
MTB S2CK
p. 152
HIV-positive woman with 22 CD4 cells/ L is admitted with PCP

and is treated successfully with TMP/SMX. Prophylactic
TMP/SMX and azithromycin are started. She is then started on
antiretroviral medication and her CD4 rises to 420 cells for last
6 months.
p TMP/SMX And azithromycin
a. Stop
y
because CD4
b. Stop both TMP/SMX and azithromycin
Cannot stop antiretrovirals;
c. Stop all medications and observe
CD4 will
d. Stop all medications if the PCR-RNA viral load is
undetectable CD4 will ; antiretrovirals maintain CD4
e. Continue all the medications No prophylaxis needed
f. Stop the azithromycin
And TMP/SMX because CD4
MTB S2CK
Tuberculosis
p. 152
Tuberculosis (TB)/Etiology
Tuberculosis/Etiology
Due to Mycobacterium tuberculosis

Initial infection most commonly leads to
latent TB
Most symptomatic cases due to
Almost all patients with TB have 1+ established risk

factors
Reactivation
R
ti ti off latent
l t t infection
i f ti rather
th
than primary exposure
Pulmonary TB most common, but can

affect any organ system
MTB S2CK
p. 152
Recent immigrants (in past 5 years)

Prisoners
HIV positive
Healthcare workers
Close contact of someone with TB
Steroid use
Hematologic malignancy
Alcoholics
Diabetes mellitus
MTB S2CK
p. 153
23
Tuberculosis/Presentation
Tuberculosis/Diagnostic Tests
Look for
Best initial test: chest X-ray as with all

respiratory infections
Sputum stain and culture specifically for acid-fast
bacilli (mycobacteria) must be done 3 times to
fully exclude TB
g
acid-fast stains,, but clinical suspicion
p
If 3 negative
high
Previously listed risk factors presenting with fever,

cough, sputum, weight loss, hemoptysis, and night
sweats
Symptoms are almost always > 3 weeks in

duration
You cannot answer TB as diagnosis
without a clear risk factor, a cavity on
chest X-ray or a positive smear
MTB S2CK
p. 153
Bronchoscopy with BAL or pleural biopsy
PPD skin testing is never best test for TB in

symptomatic patient
MTB S2CK
p. 153 154
Tuberculosis/Diagnostic Tests
Tuberculosis/Treatment
Most common finding: cavitary upper lobe infiltrate
Smear positive: begin therapy with 4 drugs

Rifampin, isoniazid, pyrazinamide, and ethambutol
(RIPE)
Ethambutol not needed if known from start of

therapy that organism is sensitive to all TB
medications
Ethambutol: given as part of 4-drug empiric therapy prior
to knowing sensitivity of organism
After using RIPE for first 2 months

Stop ethambutol and pyrazinamide
And
Continue rifampin and isoniazid for next 4 months
MTB S2CK
p. 153
Chest x-ray with upper lobe disease consistent with TB. Source: Craig Thurm, MD.
MTB S2CK
p. 154
Standard of care: 6 months total of

therapy
Treatment is extended to 9 months for
Toxicity of Therapy
All TB medications cause hepatoxicity
Osteomyelitis
Miliary tuberculosis
Meningitis
Pregnancy or any other time pyrazinamide
isnt used
MTB S2CK
p. 154
Dont stop them unless transaminases

rise
i 3
3-5
5 titimes upper limit
li it off normall
MTB S2CK
p. 154
24
Adverse Effects of Antituberculosis Therapy

Rifampin
Isoniazid
Pyrazinamide
Ethambutol
Peripheral
neuropathy
Hyperuricemia
Optic
neuritis/
color
vision
i i
Toxicity
Red color
to body
secretions
Use of Steroids
Glucocorticoids decrease risk of constrictive
pericarditis in those with pericardial involvement
Decrease neurologic complication in TB meningitis
Treatment
Pregnant patients shouldnt

receive pyrazinamide
None,
benign
finding
MTB S2CK
Use
pyridoxine
to prevent
No treatment
unless
symptomatic
Decrease
dose in
renal
failure
p. 154
MTB S2CK
p. 154
Latent Tuberculosis/PPD Testing
Indications for PPD Testing

Not a general screening test for whole
population
Only those in risk groups previously
described should be screened
PPD testing isnt useful in those who
are symptomatic or those with abnormal
chest X-rays
What Is Considered a Positive Test?

Only induration is counted towards a positive test
Erythema is irrelevant
Induration > 5 mm
MTB S2CK
p. 154
HIV-positive patients
Glucocorticoid users
Close contact with active TB patients
Abnormal calcifications on chest X-ray
Organ transplant recipients
MTB S2CK
p. 155
Induration > 10 mm
Two-Stage Testing
If patient never had a PPD skin test before, a
second test is indicated within 1-2 weeks if first test
is negative
Recent immigrants (past 5 years)

Prisoners
Healthcare workers
Close contacts with TB patients
Hematologic malignancy
malignancy, alcoholics
alcoholics, DM
Induration > 15 mm
1st test maybe falsely negative
If 2nd test is negative: truly negative

If 2nd test is positive: first test was false negative
Those with no risk factors
If the first test is positive, a

second test isnt necessary
Everyone with a reactive PPD test should have

a chest X-ray to exclude active disease
MTB S2CK
p. 155
MTB S2CK
p. 155
25
Latent Tuberculosis/PPD Treatment
Treatment for a Positive PPD

After active TB has been excluded with a
chest X-ray, patients should receive 9 months
of isoniazid
Positive PPD confers a 10% lifetime risk of TB
Isoniazid results in 90% reduction in risk; after
isoniazid lifetime risk of TB goes from 10% to
1%
Those at high risk (e.g., healthcare workers),

should have a PPD annually to screen for
conversion
Majority of risk for developing active TB lies
within first 2 years after conversion
MTB S2CK
p. 155
Once PPD is positive, itll

always be positive in future
MTB S2CK
p. 155

PPD testing is one of the hardest and most
misunderstood tests on USMLE S2 CK. Reread
preceding section and forget what youve learned in
the past.
Solitary Pulmonary Nodule &

Interstitial Lung Disease
Previous BCG has no effect on these

recommendations. If PPD is positive, the
patient must take isoniazid for 9 months
even if he or she had BCG.
MTB S2CK
p. 155
Solitary Pulmonary Nodule
For Step 2, be sure to know when biopsy is

appropriate!
Qualities of Benign and Malignant Pulmonary Nodules
Benign
< 30 years old
No change in size
Nonsmoker
Smooth border
Small, < 1 cm
Normal lung
Adenopathy ( )
Dense, central calcification
Normal PET scan
MTB S2CK
p. 156
Malignant
> 40 years old
Enlarging
Smoker
Spiculated (spikes)
Large, > 2 cm
Atelectasis
Adenopathy (+)
Sparse, eccentric calcification
Abnormal PET scan
Best initial step in all lung lesions is to compare size

with old X-rays
Biopsy all enlarging lung lesions,
particularly
p
y if they
y are rapidly
p y enlarging
g g
However, doubling in size < 30 days more likely to
be infectious than malignant (think about clinical
scenario to decide)
MTB S2CK
p. 156
26
High Probability Lesions/Management
When many features are described under

malignant
Resect (remove) lesion
Sputum cytology, needle biopsy, and PET
scanning shouldnt be done because a
negative
ti ttestt iis lik
likely
l false
f l negative
ti
If resection is one of the choices, then its

the answer
Source: Lange123 at the German language Wikipedia, commons.wikimedia.org
MTB S2CK
p. 156
Intermediate Probability Lesions/

Management

Management
There are some gray or inconclusive

aspects of solitary pulmonary nodule such as
Sputum cytology
Age range gap (between 30 and 40)

Or
Size ((between 1 cm and 2 cm))
Definition of intermediate probability
MTB S2CK
p. 156
If positive, this is highly specific, the most

appropriate next step in management is resection
of lesion
If negative cytology doesnt exclude malignancy
Bronchoscopy or transthoracic needle biopsy

Each is the most appropriate next step in most
patients with intermediate probability of malignancy
Bronchoscopy for central lesions
Transthoracic biopsy for peripheral lesions
MTB S2CK
p. 156

Management

Management
Diagnostic test question in intermediate

lesions; clear answer must be present.
Choice of test may not be clear, but
adverse effects are always clear.
clear Most
common adverse effect of a transthoracic
biopsy is pneumothorax.
Positron emission tomography (PET scan)

Tells whether content of lesion is malignant
without biopsy
Malignancy has increased uptake of tagged
glucose
Sensitivity of PET scan is 85 - 95%
Negative scan points away from malignancy
MTB S2CK
p. 157
MTB S2CK
p. 157
27

Management
Video-assisted thoracic surgery (VATS)

VATS is both more sensitive and more
specific than all other forms of testing
Frozen section in operating room allows for
immediate conversion to an open
thoracoscopy and lobectomy if malignancy is
found
MTB S2CK
Benign pulmonary nodules often

represent scar from previous infection
Immigrant, think TB
SW United States, think
coccidioidomycosis
y
Ohio River Valley, think histoplasmosis
p. 157
Interstitial Lung Disease/Definition
Interstitial Lung Disease/Etiology
Diseases characterized
by inflammation and/or
fibrosis of interalveolar
septum
Specific Causes of Interstitial Lung Disease

Idiopathic pulmonary fibrosis (IPF) and other
idiopathic interstitial pneumonias
Collagen vascular disease
Granulomatous disorders
Hypersensitivity disorders
Pneumoconiosis
Radiation
Drugs: bleomycin, busulfan, amiodarone,
methylsergide, nitrofurantoin, cyclophosphamide
Fibrosis causes
Impaired gas exchange
Increased lung stiffness
And
Decreased lung
compliance & expansion
MTB S2CK
p. 157
Source: Ed Uthman. commons.wikimedia.org
Interstitial Lung Disease/Etiology

Types of Pneumoconioses
Exposure
Coal
Sandblasting, rock
mining, tunneling
Shipyard
py
workers,, p
pipe
p
fitting, insulators
Cotton
Electronic manufacture
Moldy sugar cane
Disease
Coal workers pneumoconiosis
Silicosis
Asbestosis
MTB S2CK
p. 157
Interstitial Lung Disease/Presentation

All forms of pulmonary fibrosis, regardless of
etiology, present with
Dyspnea worsening on exertion

Hypoxia worsening on exertion
Fine rales or crackles on examination
Loud P2 heart sound (if pulmonary HTN present)
Clubbed fingers
Byssinosis
Berylliosis
Bagassosis
Inflammatory infiltration with white

cells is reversible (treatable),
whereas fibrosis is irreversible
Biopsy shows granulomas in berylliosis

MTB S2CK
p. 157
MTB S2CK
p. 158
28
Interstitial Lung Disease/Diagnostic Tests
Interstitial Lung Disease/Diagnostic tests
Best initial test: always chest X-ray

High resolution CT scan is more
accurate than chest X-ray
Most accurate test: lung biopsy
Echocardiography
E h
di
h will
ill often
ft show
h
pulmonary HTN and possibly right
ventricular hypertrophy
MTB S2CK
PCP. Source: commons.wikimedia.org
p. 158
Interstitial Lung Disease/Diagnostic tests
Interstitial Lung Disease/Diagnostic Tests

PFTs
Restrictive lung disease with proportional decrease
FEV1, FVC, TLC, and RV all , but since
everything is decreased, the FEV1/FVC ratio will
be normal
DLCO
Decreased in proportion to severity of alveolar
septal thickening
MTB S2CK
p. 158
Severe, long-standing interstitial fibrosis produces thick walls between alveoli

that give the appearance of honeycombing. Source: Craig Thurm, MD.
Interstitial Lung Disease/Treatment

Most types of interstitial lung diseases are
untreatable
Biopsy shows
White cell or inflammatory infiltrate; prednisone
should be used
Mostlyy fibrosis ((e.g.,
g IPF),
) steroids typically
yp
y NOT
effective
Of all causes of pneumoconioses, berylliosis is

most likely to respond to steroids
Due to granulomas (sign of inflammation)
MTB S2CK
p. 158
MTB S2CK
p. 158
Interstitial Lung Disease/

Hypersensitivity Pneumonitis
Specific type of interstitial lung disease

caused by pulmonary hypersensitivity
reaction to certain environmental
antigens
Inflammation from hypersensitivity
reaction results in alveolar thickening
and granuloma formation
MTB S2CK
p. 158
29


Presentation
Acutely
Most common antigens causing hypersensitivity

pneumonitis include
Fever, dyspnea, severe cough

Within 4-6 hours of antigen exposure
Or
Chronically
Progressive dyspnea on exertion, fine
rales, pulmonary fibrosis
Antigens from feathers (bird fanciers lung)

MAI antigen (hot tub lung)
Spores of actinomyces from moldy hay (farmers
l
lung)
)
Spores of actinomyces from compost (mushroom
workers lung)
Spores of actinomyces from air conditioners (air
conditioner lung)

Treatment
Corticosteroids help to reduce
inflammation
AVOID
O ONGOING
O GO G EXPOSURE
OSU
to
inciting agent
Sarcoidosis &
Thromboembolic Disease
Sarcoidosis/Definition/Etiology
Sarcoidosis/Presentation
More common in African American

women
Look for
Idiopathic inflammatory disorder

predominantly of lungs,
lungs but can affect
most of the body
Young African American woman with SOB on

exertion and occasional fine rales on lung exam, but
without wheezing of asthma
Erythema
y
nodosum and lymphadenopathy
y p
p
y on
chest X-ray hands you diagnosis question
Characterized by noncaseating
granulomas
MTB S2CK
p. 159
MTB S2CK
p. 159
30
Brain complications
Also presents with

Constitutional symptoms: fever, malaise, weight
loss
Arthritis
Parotid gland enlargement
Facial pals
palsy
Heart block and restrictive cardiomyopathy
CNS involvement
Iritis and uveitis
Eye problems (burning,

itching, tearing or pain)
Salivary glands
Enlarged lymph nodes
in neck & chest
Heart complications
Lupus pernio (painful

skin sores on face)
Skin lesions on back, arms,
neck, face, and scalp
Granulomas (inflamed
lumps in lungs)
Liver enlargement
Spleen enlargement
Enlarged lymph
nodes in chest near
windpipe and lungs
Scarring and
granulomas in lung
Erythema nodosum (itchy

and painful rashes) on the
lower legs and ankles
MTB S2CK
p. 159
Source: National Heart, Lung, and Blood Institute, commons.wikimedia.org
Sarcoidosis/Diagnostic Tests
Answer sarcoidosis when chest X-ray or CT shows

hilar adenopathy in generally healthy African
American woman
Although liver and kidney
granulomas are very common
on autopsy, they are rarely
symptomatic
MTB S2CK
p. 159
Chest X-ray: best initial test

Hilar lymphadenopathy > 95% with sarcoidosis
Parenchymal involvement can also be present in
combination with lymphadenopathy
CXR can reveal bilateral hilar lymphadenopathy only
Hilar lymphadenopathy with parenchymal disease
Or
Parenchymal disease alone (depending on stage of
disease)
MTB S2CK
p. 159
Lymph node biopsy: most accurate test

Granulomas are noncaseating
Elevated ACE level: 60%

Hypercalciuria: 20%
Hypercalcemia:
yp
5%
Granulomas in sarcoidosis make vitamin D
PFTs: restrictive lung disease

Decreased FEV1, FVC, and TLC with a normal
FEV1/FVC ratio
Source: Jmh649, commons.wikimedia.org
MTB S2CK
p. 159
31
Sarcoidosis/Treatment
Thromboembolic Disease/Definition
Prednisone: drug of choice
Pulmonary emboli (PE) and deep venous

thrombosis (DVT) are treated as same
disease
Few patients fail to respond
Asymptomatic hilar adenopathy doesnt

need to be treated
MTB S2CK
p. 159
PE
From DVT vessels of legs in 70% of cases
and pelvic veins in 30%, but since risks and
treatment are the same they can be
discussed simultaneously
MTB S2CK
p. 160
Thromboembolic Disease/Etiology
Thromboembolic Disease/Presentation
Virchows triad outlines conditions that predispose

to venous TE
Look for
Sudden onset SOB with clear lungs on examination
and normal chest X-ray
Other findings in PE
Immobility
CHF
Recent surgery
Trauma
T
Surgery
Recent
fracture
MTB S2CK
p. 160
Factor V Leiden mutation

Any malignancy leads to
DVT
Thromboembolic Disease/Diagnostic Tests

Most questions about PE concern diagnostic testing and
treatment
There is no single, uncomplicated diagnostic test

for PE
y, EKG,, and ABG are best initial tests
Chest X-ray,
In PE, the main issue is to know Whats the most
common finding?
And
Whats the most common abnormality when theres
an abnormality?
MTB S2CK
p. 160
Tachypnea, tachycardia, cough, and hemoptysis

Leg pain from DVT
Pleuritic chest pain from lung infarction
Fever can arise from any cause of clot or hematoma
Extremely severe emboli will produce hypotension
MTB S2CK
p. 160

Chest X-ray
Usually normal in PE
Most common
abnormality is
atelectasis
Wedge
Wedge-shaped
shaped
infarction (Hampton
hump), and oligemia of
one lobe (Westermark
sign) are much less
common than simple
atelectasis
MTB S2CK
EKG
Usually shows sinus
tachycardia
Most common
abnormality is
nonspecific
p
ST-T wave
changes
Only 5% will show right
axis deviation, RV
hypertrophy or RBBB
p. 160 161
32

ABG
Hypoxia and respiratory alkalosis ( pH and
CO2) with normal chest X-ray is extremely
suggestive of PE
Frequent wrong answer is to

choose S1, Q3, T3 as the most
common abnormality on EKG
MTB S2CK
p. 161
65-year-old woman with recent hip replacement has acute

onset of SOB and tachycardia. Chest X-ray normal. Hypoxia
on ABG, increased A-a gradient, EKG with sinus tachycardia.
a. Intravenous unfractionated heparin
b. Thrombolytics Hemodynamically unstable & acute RV failure
Anticoagulants contraindicated,
c. Inferior
I f i vena cava filter
filt
recurrent emboli & RV dysfunction
d. Embolectomy If heparin ineffective & persistent
e. Spiral CT scan hypotension, hypoxia, tachycardia
f. Ventilation/perfusion (V/Q) scan If initial labs suggestive, treat!
g. Lower-extremity Doppler studies Dont wait to confirm PE
h. D-dimer Poor specificity
MTB S2CK
p. 161
Spiral CT scan
Also called CT angiogram
Standard of care in diagnostic testing to
confirm presence of PE after X-ray,
EKG and ABG
EKG,
Specificity is excellent (> 95%)
However, sensitivity is 85%, it can miss
15% of clots
MTB S2CK
Chest spiral CT scan with radiocontrast agent showing multiple filling defects both at the bifurcation
and in the pulmonary arteries. Source: James Heilman, MD, commons.wikimedia.org
p. 161
Ventilation/Perfusion (V/Q) scan

May reveal segmental areas of mismatch
High probability scans have no clot (false positive)
in 15%
Low probability scans have a clot (false negative) in
15%
Interpret results in combination with clinical
suspicion
Chest X-ray must be normal for V/Q scan to
have any degree of accuracy. Do a spiral
CT if chest X-ray is abnormal.
MTB S2CK
p. 161 162
V/Q or ventilation perfusion scanning is still very useful in evaluating pulmonary emboli. A
positive test is an area that is ventilated with decreased perfusion. Source: Nishith Patel.
MTB S2CK
p. 161
33
D-dimer
Test is very sensitive (better than 97%
negative predictive value)
Specificity poor. Any clot or bleeding
elevates D-dimer level
Negative test excludes clot
Positive test doesnt mean anything
MTB S2CK
p. 162
D-dimer is answer when pretest probability of PE is

low and you need a simple, noninvasive test to
exclude thromboembolic disease
MTB S2CK
p. 162
Lower extremity (LE) Doppler study

If LE Doppler positive, no further testing needed
Only 70% of PEs originate in legs, so itll miss 30%
of cases
You dont need a spiral CT or V/Q scan to confirm a
PE if there
theress a clot in legs because they wont
won t
change therapy
Patient still needs heparin and 6 months of warfarin
Spiral CT negative
V/Q or LE
Doppler
negative
withhold therapy
with heparin
MTB S2CK
p. 162
LE Dopplers
D
l
are a good
d test if
V/Q and spiral CT do not give
clear diagnosis
MTB S2CK
p. 162
Angiography
Most accurate test
Nearly 100% specificity and a false negative rate
< 1%
Unfortunately, theres 0.5% mortality, which is
high if you consider the tens of thousands of tests
a year that are needed to exclude PE in all cases
When testing for PE, angiography is rarely done
MTB S2CK
p. 162
Thrombus (labeled A) causing a central obstruction in the left main

pulmonary artery. ECG tracing shown at bottom. Source: Aung Myat
and Arif Ahsan, commons.wikimedia.org
34
Thromboembolic Disease/Treatment
Heparin
Warfarin should be started
simultaneously with heparin to
When is an inferior vena cava (IVC) filter the

right answer?
Contraindication to the use of anticoagulants
(e.g., melena, CNS bleeding)
Recurrent emboli while on heparin or fully
therapeutic warfarin (INR of 23)
Right ventricular (RV) dysfunction with an
enlarged RV on echo. In this case, the next
embolus, even if seemingly small, could be
potentially fatal
Achieve
Achie e therapeutic
therape tic INR of 2 to 3 times
normal as quickly as possible
MTB S2CK
p. 162
When are thrombolytics the right answer?

Hemodynamically unstable patients (e.g.,
hypotension and tachycardia)
Acute RV dysfunction
Contraindicated in p
patients with recent
surgery or bleeding
MTB S2CK
p. 162
When are direct-acting thrombin

inhibitors (argatroban, lepirudin) the
answer?
Heparin-induced thrombocytopenia
When is aspirin the answer?
Never
No specific time limit in which to

use thrombolytics as there is in
stroke or MI
MTB S2CK
p. 162
MTB S2CK
p. 162 163
Pulmonary Hypertension/Definition
Pulmonary Hypertension,
Obstructive Sleep Apnea, &
Acute Respiratory
Distress Syndrome
Lung or pulmonary circulation normally

extremely low pressure
Systolic 25 mmHg
Diastolic 8 mmHg
Mean 15 mmHg
MTB S2CK
p. 163
35
Pulmonary Hypertension/Definition
Pulmonary Hypertension/Etiology
Classified as either
Primary
Idiopathic dysfunction of pulmonary arteries
Secondary causes include
Chronic hypoxemia leads to pulmonary

HTN, which results in more hypoxemia
L sided-heart failure (MCC)

(
)
Intracardiac L
R shunting
Hypoxic vasoconstriction from chronic lung
disease (e.g., COPD)
Thromboembolic disease
MTB S2CK
p. 163
MTB S2CK
p. 163
Pulmonary Hypertension/Presentation
Pulmonary Hypertension/Diagnostic Tests
Chest X ray and CT
Dyspnea and fatigue

Syncope (exertional!)
Chest pain (exertional!)
Wide splitting of S2 with loud P2 or tricuspid and
pulmonary valve insufficiency
Sign of right
right-sided
sided heart failure
Its impossible to know that pulmonary
HTN is causing dyspnea without tests
Best initial tests

Showing dilation
of proximal
pulmonary
arteries with
narrowing or
pruning of
distal vessels
Source: tmcr.usuhs.mil
MTB S2CK
p. 163
MTB S2CK
p. 163
Right heart or Swan Ganz catheter

Most accurate
test
And
Most precise
method to
measure
pressures
EKG
Right axis deviation,
right atrial and
ventricular
hypertrophy
Echocardiography
RA and RV
hypertrophy; Doppler
estimates pulmonary
artery (PA) pressure
MTB S2CK
p. 163
MTB S2CK
V/Q scanning
Identifies chronic
PE as cause of
pulmonary HTN
CBC
Shows
polycythemia from
chronic hypoxia
p. 163
36
Pulmonary Hypertension/Treatment
Pulmonary Hypertension/Treatment
1. Correct underlying cause when one is clear

2. Idiopathic disease is treated with
Oxygen slows progression, particularly

with COPD
Inhaled or intravenous prostacyclin analogues

(pulmonary arterial vasodilators): epoprostenol,
treprostinil, iloprost, beraprost
Endothelin antagonists: bosentan
Phosphodiesterase inhibitors: sildenafil
Only lung transplantation is

curative for idiopathic
pulmonary HTN
Only if demonstrated to be responsive to them during

right heart catheterization
MTB S2CK
p. 164
MTB S2CK
p. 164
Obstructive Sleep Apnea (OSA)/Definition
Obstructive Sleep Apnea (OSA)/Presentation
Cessation of
airflow due to
upper airway
obstruction during
sleep
Obesity
Ob it is
i mostt
commonly
identified cause
Patients present with daytime

somnolence and history of loud snoring
Other symptoms include
Headache
Impaired memory and judgment
Depression
HTN
Source: Habib M'henni, commons.wikimedia.org
MTB S2CK
p. 164
MTB S2CK
p. 164
Obstructive Sleep Apnea
Obstructive Sleep Apnea/Treatment
Risk factors include
1. Weight loss and avoidance of alcohol

2. Nasal continuous positive airway
pressure (nasal CPAP)
3. Surgical widening of airway
(uvuloplatopharyngoplasty) if this fails
4. Avoid use of sedatives
Male gender
Obesity
Large uvula/tongue
And
Retrognathia (recession of mandible)
Arrhythmias and erythrocytosis are common

Can lead to pulmonary HTN and RV failure
Most accurate test is polysomnography (sleep
study)
Shows multiple episodes of apnea
MTB S2CK
p. 164
MTB S2CK
p. 164
37
Acute Respiratory Distress Syndrome (ARDS)/

Definition
Acute respiratory failure from overwhelming lung
injury or systemic disease
Characterized by
Severe hypoxia
Poor lung compliance
And
Noncardiogenic pulmonary edema
ARDS is caused by endothelial injury at level of
alveolus, making lung cells leaky so that alveoli fill
up with fluid
MTB S2CK
p. 164 165
ARDS/Diagnostic Tests
ARDS/Etiology
ARDS is idiopathic
Large number of illnesses and injuries are
associated with alveolar epithelial cell and
capillary endothelial cell damage
Illnesses and injuries associated with
developing ARDS include
Sepsis or aspiration
Lung contusion/trauma
Near-drowning
Burns or pancreatitis
MTB S2CK
p. 165
Chest X-ray shows bilateral

infiltrates quickly become confluent
(white out)
Air bronchograms are common
MTB S2CK
p. 165
Source: Samir , commons.wikimedia.org
Defined as having PaO2/FiO2 ratio < 200

The FIO2 is expressed as a decimal (e.g., room
air with 21% oxygen = 0.21)
If pO2 is 105 on room air (21% oxygen or 0.21),
then the ratio of pO2/FIO2 is 500 (i.e., 105/.21)
If pO2 (as measured on ABG) is 70 while
breathing 50% oxygen, the ratio is 70/0.5 or 140
ARDS is associated with normal findings on

right heart catheterization
Wedge pressure is normal (< 18 mmHg)
Air bronchograms are a sign of dense consolidation of the lung air space. This is a case of pneumococcal pneumonia
that left only the air space in the larger bronchi open or air bronchograms. Source: Omid Edrission, MD.
MTB S2CK
p. 165
MTB S2CK
p. 165
38
ARDS/Treatment
ARDS/Treatment
Low tidal volume mechanical

ventilation is the best support while
waiting to see if lungs will recover
Positive end-expiratory pressure (PEEP) is used

when patient is undergoing mechanical ventilation
to FIO2
Levels of FIO2 > 50% are toxic to lungs
Maintain plateau pressure < 30 cm of water
measured on ventilator
Use 6 mL/kg of tidal volume
Steroids aren
arentt clearly beneficial in
most cases
They may help in late-stage disease in
which pulmonary fibrosis develops
MTB S2CK
p. 166
No treatment is proven to reverse ARDS.

Dont forget to treat the underlying cause.
MTB S2CK
p. 166
39
Cancer Screening
Breast Cancer
Cervical Cancer
Colon Cancer
Prostate Cancer
Lung Cancer
Preventative Medicine
Conrad Fischer, MD
New York City
Breast Cancer Screening
Mammography screening tool of choice

Start at 50 years old
When reward is highest
Starting at 40 is controversial
MRI,
MRI CT
CT, and US are adjuvant screening
Self-examination not recommended.
Never the correct answer on S2CK.
MTB S2CK p. 356
TAMOXIFEN
Greater risk:
DVT/PE and endometrial cancer
Less risk: Fractures
Remember!
Better to be ALIVE with a DVT
than DEAD with normal legs
Which of the following is most likely to benefit an

asymptomatic patient with multiple first-degree relatives
with breast cancer?
a.
b.
c
c.
d.
e.
f.
Tamoxifen
Most familial breast ca. NOT BRCA
BRCA testing
Aromatase inhibitors Unproven in prevention
Effective but to lesser degree
Dietary modification
Performed in breast cancer patients
HER-2/neu testing
Estrogen/progesterone Performed in breast cancer patients
receptor testing
MTB S2CK p. 356
Can STOP mammography at age 75
HER-2/neu positive patients treated

with trastuzumab if you HAVE
cancer! Not a prophylactic!
Cervical Cancer Screening
Papanicolaou test =
Pap Smear
Start at age 21
Done every 3 years,
with cytology, until 30
years old
After age 30, if HPV
testing added, then
every 5 years
Stop at age 65 with
adequate screening
history and low risk
MTB S2CK p. 357
Colonoscopy
Katsumi M. Miyai, M.D., Ph.D.,

Regents of the University of California.
The most accepted screening test

Start at 50 years
All other testing
Repeat every 10 years
modalities are
inferior to
Exceptions
colonoscopy
Family history
1st-degree relative 40 or ten years earlier
Whichever is EARLIER!
HNPCC:
3 relatives, 2 generations, 1 premature
Start at 25 and do colonoscopy every 1-2 years
MTB S2CK p. 357
Prostate Cancer Screening
Familial Adenomatous Polyposis
Theres no test that reduces mortality

Doesnt reduce mortality
Useful in tracking current disease
Digital Rectal Exam (DRE)
Doesnt reduce mortality
Sigmoidoscopy at age 12, then every year
Personal History of Polyps

Repeat
p
every
y 3-5 y
years
PSAs require a conversation with the

patient regarding pros and cons
MTB S2CK p. 357 358
Lung Cancer Screening
Summary of Preventive Medicine Key Points
Not recommended at this time

Chest radiograph, CT scan, MRI, PET, etc.
All have their purpose but NOT in
screening
Any question asking who and when to

screen for lung cancer is a trick
MTB S2CK p. 358
Mammography >50 to age 75

Tamoxifen for multiple 1st degree relatives
BRCA is NOT clear!
Pap smear interval to 5 years after age 30,
if combined with HPV testing
No lung or prostate screening clearly
effective
MTB S2CK p. 358
Lipid Screening
Different by age and gender
Non Cancer Screening and

Prevention
Lipid Screening
Hypertension: Diagnosis and Control
Diabetes Mellitus
Other Screenings
Men start at 35 yo
Women start at 45 yo
Frequency depends on CVD status
What is the test?

Cholesterol panel
Total CHL, HDL, LDL
LDL guides therapy usually
We do NOT know what to do with Triglycerides!
MTB S2CK p. 358
Lipid Screening
Lipid Screening
Normal Values?
Goals of Therapy
Determined by whats tolerable given risk
Interventions
HDL Cholesterol > 40
0-1 Risk:
Diet, Exercise, Pharmacology
Goals differ based on comorbidities

Diabetes
HTN
Coronary disease or equivalent
Coronary Artery Disease (CAD) equivalents:
Carotid disease, peripheral arterial disease (PAD),
diabetes mellitus, and aortic disease
MTB S2CK p. 358
Diet at LDL >160

Drugs at LDL >190
2 or more risks
Diet at LDL >130
Drugs at LDL >160
For CAD and Equivalents

LDL Cholesterol < 100 Both diet and drugs
Possibly < 70 for CAD combined with Diabetes!
MTB S2CK p. 358
Hypertension
Diabetes Screening
All adults (>18) should be screened at every visit

At least every two years
HTN
Who is screened?
Elevated BP at 2 separate occasions

Not clear what to do about Pre-hypertension
Those with CHD

Hypertension is the clearest risk to screen for DM
Fasting Blood Glucose (FBG)
Test
Diabetes
126 mg/dL
Oral Glucose
Tolerance Test (OGTT)
200 mg/dL
Hemoglobin A1C
6.5%
MTB S2CK p. 358
MTB S2CK p. 359
Osteoporosis
Other Screenings
Bone density 2.5 SDs below average

Recommendation
Abdominal Aortic Aneurysms
Every woman screened at 65 yo

Dual-Energy X-ray Absorptiometry (DEXA) scan
Osteoporosis
Fractures
Increased Mortality
All men
65 -75
ANY smoking history
Receive abdominal ultrasounds at least once
Tobacco (traditional or smokeless)

Employ the Five-As
Ask, Advise, Attempt, Assist, Arrange
Intimate Partner Violence

Not to be overlooked
MTB S2CK p. 361
MTB S2CK p. 361
Alcohol Dependence
Alcohol
Know difference between dependence and abuse
CAGE Questions
Vaccinations
Do they feel the need Cut down?

Do they feel Annoyed with criticism of drinking?
Influenza and Pneumococcal

Varicella
Hepatitis A & B
Tetanus
Meningococcal
Have they ever felt Guilty by their drinking?

Do they ever need an Eye-opener?
MTB S2CK p. 361 362
Influenza Vaccination
Pneumococcal Vaccine
Influenza A and B
23-valent Pneumococcal Polysaccharide Vaccine

Protects against Streptococcal pneumoniae
Who gets it?
Strains circulating in previous year

Inactivated (killed) injection
Who gets it?
Chronically ill
Everybody Every year

Healthcare workers,
workers pregnant women
women, elders
Respiratory, heart, kidney, and liver diseases
Immunocompromised
Asplenia
INFLUENZA VACCINE
Every person
Every year
MTB S2CK p. 359
Elderly:
65 yo
Revaccination after 5 years
MTB S2CK p. 359
Varicella & Herpes Zoster Vaccination
Varicella Vaccination
Live attenuated vaccine against varicella virus

Who gets Chicken Pox vaccination?
ALL adults seronegative for varicella infection
Who gets Herpes Zoster vaccination?

ALL adults
60 yo
Reduces incidence and severity
Herpes Zoster vaccine
Chicken Pox vaccine
Different strengths and indications

Vaccines given to persons 60 to prevent
zoster have 18 times viral antigens of
pediatric vaccines

MTB S2CK p. 360
Hepatitis Vaccination
Hepatitis A
Fecal oral transmission
Infection related to poor
hygiene and crowding
No carrier state
Low mortality/morbidity
Hepatitis A Vaccine
Chronic liver disease
MSM or IV drug users
Infected close contacts
Travelers
Hepatitis Vaccination
Hepatitis B
Percutaneous, perinatal,
and sexual routes
(+) Carrier state
10% develop chronic
disease
Hepatitis B Vaccine
Hepatitis B Vaccine
DIABETES is an indication!
Chronic Liver disease

MSM or IV drug users
Infected close contacts
Healthcare workers
Dialysis patients
MTB S2CK p. 360
MTB S2CK p. 360
Tetanus Vaccine
Meningococcal Vaccination
Tetanus Toxoid booster every 10 years

One Tdap (Tetanus Acellular Pertussus) should be
one of them
Five years after a dirty wound
Quadrivalent conjugate polysaccharide vaccine

A,C,Y,W
Very efficacious
Who gets it?
ALL children age 11
Adults:
Asplenia or equivalent immunodeficiency
Epidemic settings (military, college dormitories)
MTB S2CK p. 360
MTB S2CK p. 360
Important Definitions
Epidemiology
Prevalence:
Incidence:
Sensitivity (SN):
Sensitivity & Specificity

Positive and Negative Predictive Values
Changing the Cutoff?
Important Formulas
The 2x2 Table
Specificity (SP):
Positive Predictive
Value (PPV):
Total number of diseased patients in the

population.
Number of NEW cases during a specified
period of time.
Probability that person with disease has
a positive test.
Probability that person without disease
has a negative test.
Of those with a positive test, what
proportion have disease?
Negative Predictive Of those with a negative test, what

proportion do not have disease?
Value (NPV):
The 2x2 Table: Sensitivity and Specificity

(+) D
(-) D
(+) Test
((-)) Test
est
(+) D
(-) D
(+) Test
((-)) Test
est
Sensitivity (SN):
Probability that person with disease has

a positive test.
= a / (a+c)
The 2x2 Table: Sensitivity and Specificity

(+) D
(-) D
(+) Test
((-)) Test
est
Specificity (SP):
Probability that person without disease

has a negative test.
= d / (b+d)
The 2x2 Table: PPV and NPV

(+) D
(-) D
(+) Test
((-)) Test
est
Positive Predictive
Value (PPV):
Of those with a positive test, what

proportion have disease?
= a / (a+b)
The 2x2 Table: PPV and NPV
The 2x2 Table: SN, SP, PPV, NPV
(+) D
(-) D
(+) Test
((-)) Test
Negative Predictive Of those with a negative test, what

proportion do not have disease?
Value (NPV):
(+) D
(-) D
(+) Test
PPV
a / (a+b)
((-)) Test
NPV
d / (c+d)
SN
a / (a+c)
SP
d / (b+d)
= d / (c+d)
Formulas List
Epidemiology in Practice
Sensitivity (SN):
a / (a + c)
Specificity (SP):
d / (b + d)
Positive Predictive
Value (PPV):
a / (a + b)
Disease
No disease
Negative
g
Predictive
d / (c + d)
Value (NPV):
False Negative
Ratio:
c / (a + c) or (1 SN)
False Positive
Ratio:
b / (b + d) or (1 SP)
Test
Cutoff
Disease
No disease
Test
Cutoff
Positive Test
Negative Test
Disease
No disease
Test
Cutoff
Moving the Cutoff
Positive Test
Negative Test
Disease
No disease
Disease
Test
Cutoff
Test
Cutoff
Moving the Cutoff
Moving the Cutoff
Positive Test
Negative Test
Disease
No disease
Positive Test
Negative Test
Disease
No disease
Test
Cutoff
Test
Cutoff
How does this affect: SP, SN, PPV, NPV ?

Positive Test
Negative Test
(+)T
Disease
Important Epidemiology Concepts

(+) D
(-) D
Sensitivity and specificity are independent of

disease prevalence
Characteristics of test
No disease
(-)T
Positive Test
No disease
PPV and NPV are dependent on disease

prevalence
Negative Test
SN:
Disease
No disease
SP:
PPV:
NPV:
Important Epidemiology Concepts
Formulas List
When using a particular test:
Sensitivity (SN):
a / (a + c)
Specificity (SP):
d / (b + d)
Positive Predictive Value (PPV):
a / (a + b)
Negative Predictive Value (NPV):
d / (c + d)
False Negative Ratio:
c / (a + c) or (1 SN)
False Positive Ratio:
b / (b + d) or (1 SP)
Positive Likelihood Ratio:
(SN) / (1 SP)
Negative Likelihood Ratio:
(1 SN) / SP
Raising the Cutoff

Increases Sensitivity and NPV
Decreases Specificity and PPV
Lowering the Cutoff

Increases Specificity and PPV
Decreases Sensitivity and NPV
Epidemiology
Sensitivity & Specificity
Positive and Negative Predictive Values
Changing the cutoff?
Important Formulas
X rays
RADIOLOGY
Matthew Kinney, MD
Orthopedic Resident
University of California San Diego
Chest X ray Indications
Chest X ray Indications
Subjective pulmonary complaints
Objective pulmonary
findings
Cough
SOB/dyspnea
Pleuritic chest pain
Hemoptysis
Rales (Crackles)
Rhonchi
Wheezing
Hyperresonance/
yp
dullness to percussion
Chest wall tenderness
Tracheal deviation
SVC syndrome
JVD
Plethora
MTB S2CK
p. 491
MTB S2CK
p. 491
Chest X ray Views
Chest X ray Views
Posterior/anterior (PA) films
Anterior/posterior (AP) films
Standard CXR positioning

Patient must be capable of standing
Necessary for immobile patients

ICU
Paralysis
Source: Mikael Hggstrm
MTB S2CK
p. 491
Source: James Heilman, MD
MTB S2CK
p. 491
Chest X ray Views
Chest X ray Views
Lateral
Lateral decubitus
Useful to localize lesion found on PA films

Most sensitive test for pleural effusion
Patient lies on side

Useful to evaluate
pleural effusions
Source: Nicholas Lange
MTB S2CK
Source: Zachary M Alexander
p. 492
MTB S2CK
p. 491
Chest X ray Findings
Lobar pneumonia
Solitary pulmonary nodule
Source: Zachary M Alexander
Source: Nicholas Lange
MTB S2CK
p. 491
MTB S2CK
p. 491
Pleural effusion
Pneumothorax
Source: Magnus Manske

Source: John Yasmer
MTB S2CK
p. 491
MTB S2CK
p. 491
Abdominal X ray Indications
Free air under diaphragm
Small bowel obstruction

Mechanical obstruction
Ileus
Source: Brian Johnston
MTB S2CK
p. 491
MTB S2CK
p. 492
Abdominal X ray Views
Abdominal X ray Views
Abdominal plain film
Kidneys, ureters, and bladder (KUB)
Erect view of abdomen
Supine view of abdomen
Source: Nevit Dilmen
Source: Nevit Dilmen
MTB S2CK
p. 492
MTB S2CK
p. 492
Abdominal X ray Findings
Bone X ray Indications
Small Bowel Obstruction
Mechanical obstruction
Fracture
Bone tumor evaluation
Osteomyelitis
Skeletal Survey
Trauma
Child abuse
Air fluid levels

Source: Stephanie A Bernard
MTB S2CK
p. 492
MTB S2CK
p. 492
Bone X ray Findings

Osteomyelitis
Periosteal elevation
Osteolysis
Computed Tomography (CT)
Surrounded by ring
of sclerosis
Note: XR findings are

delayed (2 weeks)
MRI is positive
earlier
MTB S2CK
p. 492
CT Basics
Non contrast Head CT Indications
Definition Computed Tomography

Large series of 2D X-rays around a single axis of
rotation to create 3D image
Severe head trauma
Increased detail clarity

Windowing capability
Stroke
Hemorrhagic
Ischemic
Drawbacks
High doses of radiation
Often requires IV contrast
Intracranial bleeding
Subdural hematoma
Epidural hematoma
Anaphylaxis risk
Renal damage
Consider 1-2 liters of fluids, NaHCO3, and/or
NAC if mild renal insufficiency
Medication contraindications (metformin)

MTB S2CK
p. 493
Non contrast Head CT
Non contrast Head CT Findings
Bone - bright white

Blood - bright white
CSF - dark black
Ischemic Stroke
Darkening of brain
parenchyma
Blurred Gray-White
Junction
Mass effect
Source: Andrew Ciscel
MTB S2CK
p. 493
Source: Lucien Monfils
MTB S2CK
p. 493
Hemorrhagic Stroke
Subdural Hematoma
Crescent-shaped, bright
white region
Bright, localized area

corresponding to bleed
Mass effect
Gray-white junction intact
Not confined by skull

sutures
Adjacent
j
to skull
Mass effect
Source: James M. Grimson
MTB S2CK
p. 493
MTB S2CK
p. 493
Contrast Head CT Indications
Epidural Hematoma
Biconvex, bright white
region
Infection
Meningitis
Abscess
Adjacent to skull
Confined by skull
sutures
Tumor
Primary Cancer
Brain Metastasis
Mass effect
Source: Hellerhoff, commons.wikimedia.org
MTB S2CK
p. 493
MTB S2CK
Contrast Head CT Findings
p. 493
Contrast Head CT Findings
Tumor
Tumor
Primary tumor:
Single lesion
Metastasis:
Often multiple lesions
Bright white
Mass effect
Identical to abscess
Bright white
Found mostly at
gray-white junction
Mass effect
MTB S2CK
p. 493
MTB S2CK
p. 493
Abdominal CT Indications
Abdominal CT Views
Retroperitoneal structure pathology

Pancreatitis
Adrenal gland tumors
Appendicitis
Diverticulitis
Nephrolithiasis
Abdominal viscera masses
Liver tumors
Splenic laceration
NOTE: Use both oral and IV contrast
MTB S2CK
p. 493
MTB S2CK
p. 493
Abdominal CT Findings
Pancreatitis
Appendicitis
Irregular pancreatic outline

Pancreatic enlargement
Retroperitoneal fluid
Appendix enlargement (> 6mm)

Wall thickening
Fat stranding
Appendix
dilated to 15
mm that
doesnt fill with
contrast.
Source: James M Grimsom
MTB S2CK
p. 493
MTB S2CK
Diverticulitis
Localized bowel wall
thickening
Fat stranding
p. 493
Source: Andrew Sellers
Evidence of diverticulae
Note: If advanced,
abscess may be present
Nephrolithiasis
Evidence of hydronephrosis
Visible calcification in (if obstructing)
urinary tract
Note: No oral or IV contrast
Source: Phil Kang
MTB S2CK
p. 493
Source: Hellerhoff, commons.wikimedia.org
MTB S2CK
p. 493 494
Chest CT Indications
Normal Chest CT
Mass lesions
Lung
Mediastinum
Lung pathology
Interstitial lung disease

Sarcoidosis
Bronchiectasis
Cavitary lesions
Pulmonary embolism
Source: Brendan T Doherty
MTB S2CK
p. 494
MTB S2CK
p. 494
MRI Basics
Definition Magnetic Resonance Imaging
Magnetic Resonance Imaging,

Ultrasonography, & Nuclear
Medicine
1) Magnetic field aligns H20 molecular dipoles

2) RF waves are applied, which alters proton spin
3) When waves are stopped, the protons relax to their
natural spin -- producing a measurable signal
Upshot: Allows visualization of tissue based on water
content
Best test for evaluating soft tissue
Drawbacks
Long scans requiring complete immobility
Certain metal implants are contraindicated
Small bore tubes claustrophobia + body mass issues
MTB S2CK
p. 494
MRI Indications
MRI Findings
CNS pathology
Primary Brain Tumor

Contrast enhancing
Solitary lesion
Mass effect
Brain/spinal cord tumors

MS
Specific regions of the head
Sinuses
Orbits
Musculoskeletal disease
Osteomyelitis
Soft tissue injury
Nerve compression
Herniated disc disease
Brachial plexus injury
MTB S2CK
p. 494
Source: Steven J. Goldstein
MTB S2CK
p. 494
MRI Findings
MRI Findings
Multiple Sclerosis
Contrast-enhanced
Demyelinated plaques
appear white
Spinal Disc Herniation

Disc extruding from
IV space
Compression of
spinal cord
MTB S2CK
Source: Jeffery Hirsch
p. 494
MTB S2CK
p. 494
US Basics
Definition Ultrasonography
Ultrasonography
Sound waves of a certain frequency emitted

Echoes return based on specific tissue properties
Dense objects (e.g., stones, tissue) reflect waves
better than fluid/air
Scanner measures echoes and creates image based on
differences in object density
Drawbacks
Poor at visualizing structures beyond bone
Poor at visualizing structures beyond air
Body habitus affects image quality
MTB S2CK
p. 494 495
US Indications
US Findings
Gallstone disease
Cholecystitis
Renal disease
Presence of gallstone
Stone in lumen
Silhouette
Gall bladder wall
thickening
Pericholestatic fluid
Sonographic
Murphys sign
PCKD
Hydronephrosis
Note: CT preferred for kidney stones
Gynecologic evaluation
PCOS
Uterine evaluation
Pregnancy evaluation
Ectopic pregnancy
Source: Joseph Lagrew
Pancreatic disease (via endoscopic US)

MTB S2CK
p. 494 495
MTB S2CK
p. 494 495
Nuclear Scans Basics

Definition
Nuclear Medicine
Radiolabeled molecules
localize to specific organs
Emission detected and
allow for visualization of
organ function
PET scan = Glucose
Cholescintigraphy =
HIDA
V/Q scan
Source: Jeffrey Hirsch
MTB S2CK
p. 495
Nuclear Scan Types
Nuclear Scan Types
HIDA (Hepatobiliary) scan
Ventilation/perfusion (V/Q) scanning
Source: Kieran Maher
Source: Jonathan Sexton
MTB S2CK
p. 495
MTB S2CK
p. 495
Nuclear Scan Types

Bone scan
Uptake into osteoblasts
Useful for detecting area of high bone turnover
Occult cancer metastasis
Indium scan
Uptake into WBCs
Useful in detecting fever of unknown origin (FUO)
Gallium scan
Uptake with iron metabolism
Useful for detecting FUO and some cancers
Nuclear Ventriculography
Used to measure cardiac ejection fraction
MTB S2CK
p. 495
Osteoarthritis, Gout, &

Pseudogout
RHEUMATOLOGY
Niket Sonpal, MD
Chief Resident
Osteoarthritis/Definition
Osteoarthritis/Etiology
Osteoarthritis or degenerative joint

disease (DJD)
Chronic, slowly progressive, erosive
damage to joint surfaces
Loss of articular cartilage
Incidence directly proportional to

increasing age and trauma to joint
Contact sports with trauma
Obesity increases DJD

DJD is, by far, the MCC of joint
disease.
MTB S2CK
p. 167
MTB S2CK
p. 167
Osteoarthritis/Presentation
Osteoarthritis/Presentation
Most commonly symptomatic in weightbearing joints

Hand is affected, but isnt as great a
cause of disability
Distal interphalangeal (DIP) joints are >
proximal interphalangeal joints (PIP)
and metacarpophalangeal joints (MCP)
Crepitations of involved joints are

common
Effusion is rare
Stiffness is of short duration (<15 min)
DIP enlargement:
l
t Heberdens
H b d nodes
d
PIP enlargement: Bouchards nodes
MTB S2CK
p. 167
MTB S2CK
p. 167
Osteoarthritis
Osteoarthritis/Diagnostic Tests
Heberdens nodes (DIP joint)
Erythrocyte
sedimentation rate
Bouchards nodes
(PIP joint)
Complete blood
countt
Normal Lab Tests
Antinuclear
antibody
tib d
Rheumatoid
factor
MTB S2CK
p. 167
Osteoarthritis
Dense subchondral
bone
Joint space
narrowing
X-rays
y Show:
Osteophytes
Bone cysts
MTB S2CK
Absence of inflammation,
normal lab tests,
and short duration of stiffness
distinguishes DJD from RA
MTB S2CK
Source: Russell A. Patterson
p. 168
p. 168
Osteoarthritis/Treatment
1. Weight loss and moderate exercise

2. Acetaminophen: best initial analgesic
3. NSAIDs: used if symptoms arent controlled
with acetaminophen; toxicity - GI bleeding
4. Capsaicin
p
cream
5. Hyaluronic acid injections
6. Intra-articular steroids
7. Joint replacement
Glucosamine and
MTB S2CK
p. 168
chondroitin sulfate are

no more effective than
placebo.
Gout/Definition/Etiology
Defect in urate metabolism

90% of cases in men
Can be from:
Overproduction
or
Underexcretion
Gout/Etiology
Idiopathic
Enzyme deficiency
Overproduction
Increased cell turnover

Acidosis
Renal Insufficiency
Underexcretion
Thiazides or ASA
MTB S2CK
p. 168
MTB S2CK
Gout/Presentation
p. 168
Gout
Man who develops sudden, excruciating

pain, redness, and tenderness of big toe at
night after binge drinking with beer
Fever is common
Hard to distinguish initial gouty attack from
infection without arthrocentesis
Metatarsal phalangeal (MTP) joint of great
toe most frequently affected
Also in ankles, feet, and knees
Richard Usatine, M.D. Used with permission.
MTB S2CK
p. 168
Gout/Presentation
Gout/Diagnostic Tests
Chronic Gout
Tophi: tissue deposits of urate crystals with foreign
body reaction
Most often tophi occur in cartilage, subcutaneous
tissues, bone, and kidney
Often take years to develop
Uric acid kidney stones occur in 5% to 10% of
patients
Long asymptomatic periods between attacks are
common
Most accurate test:

Aspiration of joint
Needle-shaped
crystals with
negative
birefringence on
polarized light
microscopy
Commons.Wikimedia.org. used with permission
Tophi can occur anywhere

in the body.
MTB S2CK
p. 169
MTB S2CK
p. 169
WBC joint fluid elevated 2,000 to 50,000/ L

Predominantly neutrophils
Infected joint has redness, warmth, and
tenderness
Its essential to tap joint to exclude infection
Uric acid levels: elevated at some point in

95% of patients
Single level during an acute attack
normal in 25%
Acute attacks = ESR and leukocytosis
Protein and glucose levels in synovial fluid dont

help answer the most likely diagnosis question
MTB S2CK
p. 169
MTB S2CK
p. 169
Gout/Treatment
X-rays:
Acute Attack
NSAIDs superior to colchicine as best initial
therapy
Corticosteroids injection: single joint , oral: multiple
joints
Steroids (e
(e.g.,
g triamcinolone) is answer when:
Normal in early
disease
Erosions of cortical
bone happen later
No response to NSAIDs
Contraindication to NSAIDs such as renal
insufficiency
Contraindication questions are always clear

Source: Wikimedia.org
MTB S2CK
p. 169
MTB S2CK
Chronic Management
p. 169
Gout/Treatment
Management
1) Diet
Colchicine gives diarrhea and

bone marrow suppression
(neutropenia).
Decrease consumption of alcohol, particularly

beer; lose weight
Decrease high-purine foods
2) Stop thiazides, aspirin, and niacin

3) Colchicine is effective at preventing
second attack of gout
Probenecid, NSAIDs, and

sulfinpyrazone are
contraindicated in renal
insufficiency. Allopurinol is safe
with renal injury.
4) Probenecid and sulfinpyrazone increase

the excretion of uric acid in kidney
(uricosuric)
5) Allopurinol decreases production of uric
acid
MTB S2CK
p. 169 170
MTB S2CK
p. 170
Gout/Treatment
Adverse Effects of Chronic Treatment
Hypersensitivity (rash, hemolysis, allergic interstitial
nephritis) occurs with uricosuric agents and
allopurinol
Colchicine can suppress white cell production
Toxic epidermal necrolysis or Stevens-Johnson
Stevens Johnson
syndrome may occur from allopurinol
Dont start uricosuric agents or allopurinol during
acute attacks of gout. If the patient is already on
allopurinol you can safely continue it.
MTB S2CK
p. 170
Calcium Pyrophosphate Deposition Disease

(Pseudogout)/Definition/Etiology
Calcium-containing salts depositing in

articular cartilage
Most common risk
Hemochromatosis and hyperparathyroidism
CPDD can occur:

Diabetes
Hypothyroidism
Wilson disease
MTB S2CK
p. 170

(Pseudogout)/Presentation

(Pseudogout)/Diagnostic Tests
CPDD differs from gout in that large

joints such as the knee and wrist are
affected, but not particularly the first
MCP of the foot
It differs from DJD in that DIP and PIP
arent affected
Uric acid levels normal

X-ray: calcification of cartilaginous structures
Most accurate test is arthrocentesis, which
reveals p
positively
y birefringent
g
rhomboidshaped crystals
Synovial fluid: elevated level of WBCs 2,000
to 50,000/ L - nonspecific
MTB S2CK
p. 170
MTB S2CK
Pseudogout
p. 170
Pseudogout
Source Wikimedia
Source: Boma O. Afiesimama

(Pseudogout)/Diagnostic Tests
Disease
Characteristic
History
Physical
Findings
Synovial Fluid
Analysis
DJD
Older, slow,
worse with use
DIP, PIP, hip,

and knees
< 200 WBCs,

osteophytes and
joint space
narrowing
Gout
Men, acute,
binge drinking
1st big toe
2,000 50,000
WBCs, negatively
birefringent
needles
You cannot confirm a diagnosis of

CPDD without aspiration of the joint.
MTB S2CK
p. 170
MTB S2CK
Disease
Characteristic
History
CPDD
Hemochromatosis,
Wrists and
hyperparathyroidism knees
Rheumatoid Young, female,

arthritis
morning stiffness
better with use
MTB S2CK
Physical
Findings
p. 171
Synovial Fluid
Analysis
Disease
Characteristic
History
Physical
Findings
Synovial Fluid
Analysis
2,000 50,000
WBCs, positively
birefringent
rhomboids
Septic
arthritis
High fever,
very acute
Single hot
joint
> 50,000
neutrophils,
culture of fluid
Multiple joints Anti cyclic

of hands and citrulinated
feet
peptide (anti
CCP)
p. 171
MTB S2CK
p. 171

(Pseudogout)/Treatment
Best initial therapy: NSAIDs

Severe disease not responsive to
NSAIDs give intra-articular steroids
(e g triamcinolone)
(e.g.,
Colchicine helps prevent subsequent
attacks as prophylaxis between attacks
MTB S2CK
Low Back Pain & Lumbar

Spinal Stenosis
p. 171
Low Back Pain/Etiology
Low Back Pain
Low back pain is No. 1 complaint in US

DJD on X-ray or MRI of the spine is
nearly universal in those > 50 years
totally nonspecific

If all diseases described in the following
are excluded, patient has simple low
back pain from lumbosacral strain
(idiopathic)
No imaging studies and no treatment
beyond NSAIDs
Most frequently tested issue is who

shouldnt get an imaging study
MTB S2CK
p. 171
MTB S2CK
p. 171
Compression of the Spinal Cord
Malignancy or infection compressing

spinal cord is a neurological emergency
that needs urgent identification and
treatment
Look for a history of cancer with sudden
onset of focal neurological deficits (e.g.,
sensory level)
Compression at 10th thoracic vertebra

leads to sensory loss below the
umbilicus
Point tenderness at spine with
percussion of vertebra is highly
suggestive of cord compression
Hyperreflexia is found below level of
compression
MTB S2CK
p. 171
MTB S2CK
p. 172
Disk Herniation (Sciatica)
Epidural abscess is most often from

Epidural abscess presents in same way
as cord compression from cancer, but
theress high fever and markedly
there
elevated ESR
Herniations at L4/5 and L5/S1 level

account for 95% of all disk herniations
The straight leg raise (SLR) test is pain
going into the buttock and below the knee
when the leg is raised > 60 degrees
MTB S2CK
p. 172
Although only 50% of those with a positive

SLR actually have a herniated disk;
sensitivity is 90%
A negative SLR excludes herniation with
95% sensitivity
MTB S2CK
p. 172
Nerve Root Innervation
Low Back Pain/Diagnostic Tests
Nerve root
Motor deficit
Reflex
affected (lost)
Sensory area
affected
L4
Dorsiflexion
of foot
Knee jerk
Inner calf
L5
Dorsiflexion
of toe
None
Inner
forefoot
S1
Eversion of
foot
Ankle jerk
Outer foot
MTB S2CK
p. 172
Imaging required for cord compression, epidural

abscess, ankylosing spondylitis, and cauda
equina syndrome
Best initial test for cancer with compression,
infection, and fractures is plain X-ray
Most accurate test is MRI
CT scan is used as most accurate test if theres
a contraindication to MRI (e.g., pacemaker)
Intrathecal contrast must be given to increase
accuracy (CT myelogram)
MTB S2CK
p. 172
Low Back Pain/Diagnostic Tests
Classification of Back Pain
Imaging in disk
herniation is
controversial
We recommend you
answer no MRI for
just low back pain and
a positive SLR alone
Neurological deficits =
MRI
Diagnosis
MTB S2CK
Source: Nirav Thakur, MD.
p. 172 173
Classification of Back Pain

Diagnosis
History to answer
Most Likely Diagnosis
Ankylosing
spondylitis
Disk herniation
MTB S2CK
p. 173
Under age 40, pain

worsens with rest
and improves with
activity
Pain/numbness of
medial calf or foot
History to answer
Most Likely Diagnosis
Physical Findings
Cord
Compression
History of cancer
Vertebral tenderness,
sensory level,
hyperreflexia
Epidural abscess
Fever high ESR

Fever,
Same as cord
compression
Cauda equina
Bowel and bladder

incontinence,
erectile dysfunction
Bilateral leg weakness,

saddle area anesthesia
MTB S2CK
p. 173
Low Back Pain/Treatment

Physical Findings
Chemotherapy for
Lymphoma
Decreased chest
mobility
Systemic
Glucocorticoids
Gl
ti id
Loss of knee and ankle
reflexes, positive
straight leg raise
Cord Compression
p
Radiation for
Solid Tumors
MTB S2CK
p. 174
MRSA
Vancomycin
Linezolid
Acute Neurologic
Deficits
Epidural
p
Abscess
Systemic
Glucocorticoids
MTB S2CK
MSSA
Oxacillin
Nafcillin
Cefazolin
p. 174
Cauda equina syndrome: surgical

decompression
Disk herniation (sciatica): NSAIDs with
continuation of ordinary activities
Steroid injection into epidural space achieves
rapid
id and
dd
dramatic
ti b
benefit
fit ffor th
those with
ith
sciatica
Surgery rarely needed
The most common wrong
answer for sciatica is bed rest.
MTB S2CK
p. 174
Most commonly tested point: no

imaging studies in patients without focal
neurological abnormalities or with
simple lumbosacral strain
Beta-lactam antibiotics when organism is

sensitive
Gentamicin = synergy with staph
Surgical drainage for larger collections
Thi k off epidural

Think
id l abscess
b
lik
like endocarditis
d
diti
Use vancomycin as initial empiric therapy
Switch to oxacillin if its sensitive
Drain it if the infection is large enough to
produce neurological deficits or it doesnt
respond to antibiotics alone
MTB S2CK
p. 174
Man with a history of prostate cancer comes to the emergency

department with severe back pain and leg weakness. He has
tenderness of the spine, hyperreflexia, and decreased sensation
below his umbilicus.
a. Dexamethasone
b. MRI Save neurons before seeing them
c. X-ray Low specificity
d. Radiation Not fast enough
e. Flutamide Not fast enough to save neurons
f. Ketoconazole
Not fast enough to stop androgens
g. Finasteride
Not fast enough to stop androgens
h. Leuprolide
Dangerous with peripheral blockade
i. Biopsy
Only if cause unclear
j. Orchiectomy Best long-term treatment
MTB S2CK
p. 174 175
Lumbar Spinal Stenosis/Presentation
Look for a person > 60 with back pain

while walking, radiating into buttocks and
thighs bilaterally
Pain described as worse when walking
downhill, and better when sitting, but the
pedal pulses and ankle/brachial index are
normal
Spinal stenosis can
simulate peripheral arterial disease,
but vascular studies are normal.
MTB S2CK
p. 175
MTB S2CK
p. 175
Lumbar Spinal Stenosis/Presentation
Lumbar Spinal Stenosis/Treatment
Unsteady gait and leg weakness when

walking also occur
About have diminished lower
extremity reflexes
Pain is less with activities in which
patient is leaning forward (e.g., cycling)
The only test is MRI

Weight loss and steroid injections into
the lumbar epidural space improve 25%
to 50% of cases
Surgical correction to dilate the spinal
canal is needed in 75% of patients
MTB S2CK
p. 175
MTB S2CK
p. 175
Fibromyalgia
Fibromyalgia, Carpal Tunnel

Syndrome, & Dupuytren
Contracture

Look for young woman with chronic
musculoskeletal pain and tenderness with
trigger points of focal tenderness at trapezius,
medial fat pad of knee, and lateral epicondyle
Cause is unknown
Pain occurs at many sites (neck, shoulders,
back, and hips) with:
Stiffness, numbness, and fatigue
Headaches
Sleep disorder
MTB S2CK
p. 176
Fibromyalgia/Diagnostic Tests
Fibromyalgia/Treatment
No test to confirm fibromyalgia

Based on complex of symptoms, trigger
points at predictable points
All lab tests are normal (e.g., ESR, Creactive protein
protein, rheumatoid factor (RF),
(RF)
and CPK levels)
Best initial therapy is amitriptyline

Other treatments are milnacipran and
pregabalin
Milnacipran is an inhibitor of serotonin and
norepinephrine reuptake and is approved
specifically for the management of
fibromyalgia
Trigger point injections with local anesthetic
are also sometimes used
MTB S2CK
p. 176
MTB S2CK
p. 176
Steroids are the wrong

answer for fibromyalgia.
10
Carpal Tunnel Syndrome/Definition
Peripheral neuropathy from

compression of median nerve as it
passes under the flexor retinaculum
Pressure on nerve interferes with its
sensory and motor function
Carpal Tunnel Syndrome/Etiology

Amyloidosis
p. 176
Pregnancy
Median Nerve
Compression
Rheumatoid
Arthritis
MTB S2CK
Hypothyroidism
Acromegaly
MTB S2CK
Diabetes
p. 176
Carpal Tunnel Syndrome
Carpal Tunnel Syndrome/Diagnostic Tests

Look for pain in hand affecting the palm,
thumb, index finger, and radial half of ring
finger, muscle atrophy of thenar eminence
Pain is worse at night and more frequent in
those whose work involves prolonged use of
the hands (e.g., typing)
Tinel sign:
reproduction of
pain and tingling
with tapping or
percussion of
the median
nerve
IMC 2010 DxR Development Group, Inc. All Rights Reserved.
MTB S2CK
MTB S2CK
p. 177
p. 177
Phalen sign:
reproduction of
symptoms with
flexion of wrists
to 90 degrees
Most accurate diagnostic tests are

electromyography and nerve conduction
testing
Sensory symptoms happen

before motor symptoms.
IMC 2010 DxR Development Group, Inc. All Rights Reserved.
MTB S2CK
p. 177
MTB S2CK
p. 177
11
Carpal Tunnel Syndrome/Treatment

Management
Best Initial
Wrist Splints
Immobilization to relieve pressure
NSAIDS
Avoid Manual Activity

Steroid
St
id
Injection is used if splints and NSAIDs dont
control
Surgery
Can be curative by mechanically
decompressing the tunnel such as with
cutting open the flexor retinaculum
MTB S2CK
p. 177
Dupuytren Contracture
Hyperplasia of palmar fascia leading to nodule
formation and contracture of fourth and fifth fingers
Genetic predisposition and association with
alcoholism and cirrhosis
Patients lose ability to extend fingers, which is more
often cosmetic embarrassment than functional
impairment
Triamcinolone injection
Surgical release when function is impaired
MTB S2CK
p. 177
Dupuytren Contracture
Sports Medicine &

Osteoporosis
Rotator Cuff Injury
Rotator Cuff Injury
Damage to rotator cuff of muscles,

tendons, and bursae around shoulder
leads to inability to flex or abduct the
shoulder
It presents with pain in shoulder thats
that s
worse at night when lying on affected
shoulder
There can be severe tenderness at the
insertion of the supraspinatus
MRI is the most

accurate test
Treat with
NSAIDs, rest, and
physical therapy
Steroids
Surgery
MTB S2CK
p. 177
MTB S2CK
p. 177
12
Patellofemoral Syndrome
Patellofemoral Syndrome
Cause of anterior knee pain secondary to

trauma, imbalance of quadriceps strength, or
meniscal tear
Pain in front of knee or underneath patella
Particularly bad when walking up or down
stairs
Worse just after starting to walk after having
been seated for a prolonged period
It improves after walking
Crepitus, joint locking, and instability

X-rays: normal
Most cases respond to physical therapy
and strength training with cycling
Knee
K
b
braces d
dontt help
h l
Theres nothing to fix surgically
MTB S2CK
p. 178
Plantar Fasciitis
MTB S2CK
p. 178
Plantar Fasciitis
Very severe pain in bottom of foot near

calcaneus where fascia inserts
Pain worst in the morning and improves
with walking a few steps
Point tenderness @ the fascia inserts at
the calcaneus
MTB S2CK
p. 178
Plantar Fasciitis
Osteoporosis
Treatment consists of stretching exercises,

arch supports, and NSAIDs
Steroid injection is performed if these dont
solve problem
Surgical release of plantar fascia is rarely
necessary
Look for an older person, more often a

woman, with vertebral fractures leading
to loss of height or wrist fracture
Asymptomatic, fractures are found on
routine screening with bone
densitometry, which is recommended
for all women > 65
X-ray of the foot is not useful in plantar

fasciitis. There is no correlation with the
presence of heel spurs.
MTB S2CK
p. 178
Osteoporosis gives
spontaneous fractures of
weight-bearing bones.
MTB S2CK
p. 198
13
Osteoporosis/Diagnostic Tests
Osteoporosis/Treatment
Most accurate test is bone

densitometry (DEXA) scanning
Osteopenia: bone density (T-score) is
between 1 and 2.5 standard deviations
below normal
Osteoporosis: T-score > 2.5 standard
deviations < normal
1. Vitamin D and calcium are the best

initial therapy
2. Bisphosphonates (alendronate,
risendronate, ibandronate)
3 Estrogen replacement
3.
4. Raloxifene
MTB S2CK
p. 198
MTB S2CK
1. Teriparatide is an analogue of PTH that

stimulates new bone matrix formation
2. Used as a nasal spray, calcitonin
decreases vertebral fractures risk
Bisphosphonates are
very rarely associated
with osteonecrosis of
the jaw.
MTB S2CK
p. 198
When multiple treatment options are

presented, choose vitamin D, calcium,
and bisphosphonates.
Bisphosphonates that
have prolonged contact
with the esophagus can
cause esophagitis (pill
esophagitis).
p. 198
Teriparatide has caused

osteosarcoma in rats. It
has also caused
hypercalcemia.
MTB S2CK
p. 198
Rheumatoid Arthritis/Definition/Etiology
Rheumatoid Arthritis, Systemic

Lupus Erythematosus, &
p p
p Syndrome
y
Antiphospholipid
RA is an autoimmune disorder
predominantly of joints
More common in women
MTB S2CK
p. 178
14
Rheumatoid Arthritis/Definition/Etiology
Chronic synovitis leads to overgrowth,

or pannus formation, which damages all
the structures surrounding the joint
(bone, ligaments, tendons, and
g )
cartilage)
Morning stiffness of
multiple small, inflamed
joints is key to
diagnosis.
MTB S2CK
p. 178
Morning
Stiffness > 30 min
Rheumatoid
Nodules
C1 and C2 laxity - subluxation

Baker cyst
Pericarditis and pleural disease
Carpal tunnel syndrome
PIP Hands
MCP Hands
Bilateral
Symmetrical
Rheumatoid Arthritis
Vasculitis
Episcleritis
MTB S2CK
Rheumatoid Arthritis/Presentation
Lung nodules
and effusions
p. 178
Boutonniere and
swan neck are
classic deformities of the
hands
DIP is spared in RA. DIP

involvement happens in
DJD.
MTB S2CK
MTB S2CK
p. 179
Rheumatoid Arthritis
p. 179
Source: Nirav Thakur, MD.
Rheumatoid Arthritis/Diagnostic Tests
Rheumatoid factor (RF) in 70% to 80%

RF is rather nonspecific
Anti-cyclic citrulinated peptide (antiCCP) is > 80% sensitive and > 95%
specific
MTB S2CK
p. 179
15
Elevated ESR or C-reactive protein

Anemia: normocytic
Arthrocentesis on initial presentation
excludes crystal disease or infection if
diagnosis isnt clear
Modest elevation in lymphocytes
Felty syndrome:
RA
Splenomegaly
Neutropenia
Caplan syndrome:
RA
Pneumoconiosis
Lung nodules
Sicca syndrome: dry eyes,

mouth, and other mucous
membranes
MTB S2CK
p. 179
MTB S2CK
p. 180
Rheumatoid Arthritis/Treatment
The most important issue in RA is stopping

the progression of the disease. Any patient
with erosive disease or X-ray abnormalities
needs at least methotrexate to slow disease
progression.
Disease-Modifying Antirheumatic Drugs

(DMARD)
Neither NSAIDs nor steroids stop RA
from progressing
Any patient with erosive RA needs
DMARD as part of initial therapy
The MCC of death in RA is

coronary artery disease.
MTB S2CK
p. 180
MTB S2CK
p. 180
Patient with long-standing RA is to have coronary
bypass surgery.
Which is most important prior to surgery?
Erosive disease means:

Joint space narrowing
Physical deformity of joints
X-ray
y abnormalities
a. Cervical spine X-ray

Already diagnosed to have RA
b Rheumatoid factor
b.
Doesnt change outcomes
c. Extra dose of methotrexate
Nonspecific test
d. ESR
e. Pneumococcal vaccination Has nothing to do with surgery
MTB S2CK
p. 180
MTB S2CK
p. 180
16
Methotrexate
Best initial DMARD
Adverse effects are:
Tumor Necrosis Factor (TNF)

Inhibitors (infliximab, adalimumab,
etanercept)
TNF inhibitors are first line as DMARDS
Toxicity of anti
anti-TNF
TNF drugs:
Liver toxicity
Bone marrow suppression
Pulmonary toxicity
MTB S2CK
p. 181
Reactivation of TB
Infection
MTB S2CK
p. 181
Rituximab
RA as a DMARD by removing CD20+
lymphocytes from circulation
Excellent long-term
+/- methotrexate
Hydroxychloroquine
Rare as monotherapy as a DMARD
More often used in combination with
methotrexate as a DMARD
Toxic to retina
Hydroxychloroquine
leads to retinal toxicity.
Do a dilated eye exam.
MTB S2CK
p. 181
Symptomatic Control of RA
NSAIDs are the best initial therapy for
the pain of RA
Steroids also work in a matter of hours
to control the pain of RA secondary to
inflammation
Steroids for 2 purposes
MTB S2CK
Use TNF inhibitors as a DMARD with

methotrexate after methotrexate fails
Adverse effects are mandatory for you
to know
Steroids dont prevent
the progression of RA.
NSAIDS arent working

Bridge
MTB S2CK
p. 181
p. 181
MTB S2CK
p. 181 182
17
Adverse Effects of RA Medications

Drug
Adverse effect
Anti TNF
Reactivation of tuberculosis
Hydroxychloroquine
Ocular
Sulfasalazine
Rash, hemolysis
y
Rituximab
Infection
Gold salts
Nephrotic syndrome
Methotrexate
Liver, lung, marrow
MTB S2CK
p. 182
Juvenile Rheumatoid Arthritis or

Adult Still Disease

Adult Still Disease
Definition/Etiology
Juvenile rheumatoid arthritis (JRA) is
very difficult to define and theres no
known etiology
MTB S2CK

Adult Still Disease/Presentation
Presentation
The most important feature of JRA is
the presence of high, spiking fever
(often > 104
104F)
F) in a young person that
has no clearly identified etiology, but is
associated with a rash
MTB S2CK
p. 182

Adult Still Disease
Laboratory Abnormalities
No clear diagnostic test; anemia and
leukocytosis often present
ANA is normal
Ferritin level markedly elevated
p. 182
Features of JRA rash:

Often only with fever spikes
Salmon colored
On chest and abdomen
Other features of JRA:
Splenomegaly
Pericardial effusion
Mild joint symptoms
MTB S2CK
p. 182
Systemic Lupus Erythematosus
Definition/Etiology
Autoimmune disorder
Inflammation diffusely through body
Treatment
Half of cases improve with aspirin or NSAIDs
If theres no response then use steroids
MTB S2CK
p. 183
MTB S2CK
p. 183
18
Presentation
Diagnosis of SLE is based on 4 of 11 known
manifestations of disease
Four skin-related manifestations:
1. Malar rash
2. Discoid rash
3. Photosensitivity
4. Oral ulcers
MTB S2CK
Alopecia is common in
SLE, but isnt one of
the official diagnostic
criteria.
p. 183
Presentation
Joint: arthritis is present in 90%
X-ray is normal
Serositis: inflammation of pleura and
pericardium
i di
chest
h t pain
i
Presentation
Renal: any degree of abnormality can
occur from mild proteinuria to end-stage
renal disease requiring dialysis
Most common g
glomerulonephritis
p
is
membranous
Red cell casts and hematuria occur
Neurologic: symptoms include

psychosis, seizures, or stroke from
vasculitis
MTB S2CK
p. 183
MTB S2CK
Ocular findings arent part of

formal diagnostic criteria:
Photophobia
Retinal lesions ((cotton wool
spots)
Blindness
Pneumonia, alveolar hemorrhage,

and restrictive lung disease happen
in SLE, but arent criteria for
diagnosis
g
of the disease.
MTB S2CK
p. 183
p. 183
MTB S2CK
p. 184
19
Presentation
Hematologic: hemolytic anemia is part
of diagnostic criteria, but anemia of
chronic disease is more commonly
found
Lymphopenia, leukopenia, and
thrombocytopenia are also seen
Presentation
Immunologic (laboratory)
abnormalities - criteria include positive
ANA, or any one of the following:
MTB S2CK
p. 184
MTB S2CK
p. 184
Additional findings:
Mesenteric vasculitis
Raynaud phenomenon
Antiphospholipid syndromes
MTB S2CK
Anti-double-stranded DNA
Anti-Sm
False positive test for syphilis
Positive LE cell preparation
p. 184
Diagnostic tests
ANA: found in 95% to 99% of cases
Anti-double-stranded DNA (60%) and
anti-Sm (30%):
Found
Fo nd onl
only in SLE
Extremely specific for SLE
MTB S2CK
p. 184
Diagnostic tests
Decreased complement levels:
Correlate with disease activity
Drop further with acute disease exacerbations
Anti-SSA and anti-SSB: found in 10% to 20% of

cases
Add little to diagnosis
Tests most often found in Sjgren syndrome
(65% of cases)
Dont treat
asymptomatic ANA
MTB S2CK
p. 184
34-year-old woman with history of SLE is admitted with

pneumonia and confusion. As youre wrestling with the
decision over a bolus of high-dose steroids in a person
with an infection, you need to determine if this is a flare of
lupus or simply an infection with sepsis causing
confusion.
Which of the following will help you the most?
a. Rise in anti-Sm Level doesnt change in acute disease
b. Rise in ANA Level doesnt change in acute disease
c. Decrease in complement and rise in anti-DS DNA
d. MRI of the brain MRI doesnt diagnose regardless
e. Response to steroids Not diagnostic
MTB S2CK
p. 184 185
20
Treatment
Acute lupus flare treated with high-dose
boluses of steroids
Hydroxychloroquine can control mildly
chronic disease
Lupus nephritis may need steroids either
alone or in combination with
cyclophosphamide or mycophenolate
Only way to determine the severity of lupus
nephritis is kidney biopsy
Belimumab decreases symptoms
MTB S2CK
p. 185
Treatment
Urinalysis is insufficient to determine severity
of lupus nephritis
Biopsy is the only way to diagnose simple
glomerulosclerosis or scarring of the kidney,
which will not respond to therapy
Young patients most commonly die of
infection. In older patients, accelerated
atherosclerosis makes MI the MCC of
death.
MTB S2CK
p. 185
Antiphospholipid Syndrome/Definition
Antiphospholipid Syndrome
Idiopathic disorder with IgG or IgM

antibodies made against negatively
charged phospholipids
The 2 main types are:
Presentation/Diagnostic Tests
Thromboses of both arteries and veins as
well as recurrent spontaneous abortions
Elevation of aPTT with a normal prothrombin
time (PT) and normal INR
Lupus anticoagulant
Anticardiolipin antibodies
APL = clotting + elevated aPTT and

normal PT
MTB S2CK
p. 185
MTB S2CK
p. 185
Presentation/Diagnostic Tests
False positive VDRL or RPR with a
normal FTA
Anticardiolipin antibodies - spontaneous
abortion
Lupus anticoagulant - elevated aPTT
Best initial test is mixing study
Diagnostic Tests
If the elevation in aPTT is from a clotting factor
deficiency then aPTT will come down to normal
If the APL syndrome antibody is present in
plasma then aPTT remains elevated
Most
M t specific
ifi ttestt for
f lupus
l
anticoagulant
ti
l t iis
Russell viper venom test (RVVT)
RVVT is prolonged with APL antibodies and
doesnt correct on mixing with normal plasma
MTB S2CK
p. 185 186
MTB S2CK
p. 186
21
Antiphospholipid Syndrome/Treatment
Thromboses (DVT or PE) treated with

heparin and warfarin as you would any
other form of thrombosis with an INR of
2 to 3
Lifelong vs. 6 months primary
occurrence
Recurrent thrombotic episodes are
treated lifelong
USMLE S2 CK questions have to be

unequivocally clear. If an area is
controversial, USMLE will avoid it and
ask only what is clear
clear. The exam will not
trick you.
MTB S2CK
p. 186
MTB S2CK
p. 186
Warfarin or steroids are wrong answers

for preventing spontaneous abortion.
Steroids arent effective.
Scleroderma, Polymyositis, &

Dermatomyositis
Warfarin is contraindicated in pregnancy

secondary to teratogenicity.
MTB S2CK
p. 186
Scleroderma (Systemic Sclerosis)
Limited scleroderma is also known as

CREST syndrome:
Calcinosis
Raynaud
Esophageal
E
h
ld
dysmotility
tilit
Sclerodactyly
Telangiectasia

Look for a young (20s to 40s) woman (3
times more likely than men) with fibrosis
of the skin and internal organs (e.g.,
lung kidney
lung,
kidney, and GI tract)
MTB S2CK
p. 186
MTB S2CK
p. 187
22
Scleroderma/Presentation
Raynaud Syndrome
Raynaud syndrome: increased vascular

reactivity of fingers beginning with pain and
pallor (white) or cyanosis (blue) followed by
reactive hyperemia (red)
Skin manifestations: fibrosis of hands, face,
neck,
k and
d extremities;
t
iti
telangiectasia
t l
i t i and
d
abnormalities of pigmentation occur
MTB S2CK
p. 187
Scleroderma
MTB S2CK
p. 187
Scleroderma/Presentation
Scleroderma/Diagnostic Tests
GI: esophageal dysmotility with GERD,

large-mouthed diverticuli of small and large
bowel
Renal: sudden hypertensive crisis
Lung: fibrosis leading to restrictive lung
disease and pulmonary hypertension
Cardiac: myocardial fibrosis, pericarditis,
and heart block; lung disease gives right
ventricular hypertrophy
ANA: positive in 85% to 90%, but

nonspecific
ESR: usually normal
SCL-70: most specific test (antitopoisomerase)
Anticentromere: present in half of those
with CREST syndrome
MTB S2CK
p. 187
Anticentromere antibodies are extremely

specific for CREST syndrome.
MTB S2CK
p. 187
23
Scleroderma/Treatment
Polymyositis and Dermatomyositis
Presentation
Proximal muscle weakness
They dont affect facial or ocular
muscles as occurs in myasthenia gravis
Dysphagia
Penicillamine is ineffective
Renal crisis: ACE inhibitors
Esophageal dysmotility: PPIs for GERD
Raynaud: calcium-channel blockers
Pulmonary fibrosis: cyclophosphamide
improves dyspnea and PFTs
Pulmonary hypertension is treated like
primary pulmonary hypertension with
bosentan or ambrisentan (endothelin
antagonist) or Sildenafil
MTB S2CK
p. 187
MTB S2CK
p. 188
Presentation
Dermatomyositis presents with:
Malar involvement
Shawl sign: erythema of face, neck,
shoulders,, upper
pp chest,, and back
Heliotrope rash: edema and purplish
discoloration of eyelids
Gottron papules: scaly patches over the
back of hands, particularly PIP and MCP
joints
MTB S2CK
p. 188

24
Polymyositis and Dermatomyositis/

Presentation
Dermatomyositis is associated with

cancer in 25% of cases.
Common sites are:
Ovary
y
Lung
GI
Lymphoma
MTB S2CK
p. 188
Diagnostic Tests
Best initial test is CPK and aldolase
Most accurate test is muscle biopsy
ANA is frequently positive
MRI
Electromyography
MTB S2CK
p. 188
Treatment
Steroids are usually sufficient
When patient is unresponsive or intolerant of
steroids, use:
Methotrexate
Azathioprine
IVIG
Mycophenolate
Hydroxychloroquine helps skin lesions
MTB S2CK
Sjgren Syndrome,
Vasculitis, & Seronegative
Spondyloarthropathies
p. 188 189
Sjgren Syndrome/Definition/Etiology
Sjgren Syndrome/Presentation
Idiopathic autoimmune disorder secondary to

antibodies predominantly against lacrimal
and salivary glands
90% of those affected are women
Sjgren syndrome is associated with:
Sjgren presents with dryness of

mouth and eyes
Keratoconjunctivitis sicca
Need to constantly drink water
Dysphagia
D
h i
Dental caries
RA
SLE
Primary biliary cirrhosis
Polymyositis
Hashimoto thyroiditis
MTB S2CK
p. 189
MTB S2CK
p. 189
25
Sjgren Syndrome/Presentation
Sjgren Syndrome/Diagnostic Tests
Less common manifestations are:

Vasculitis
Loss of vaginal secretions
Lung disease leads to dyspareunia.
Pancreatitis
Renal tubular acidosis (20%)
Best initial test is called a Schirmer test

Most accurate test is a lip or parotid
gland biopsy
Reveal lymphoid infiltration in salivary
glands
Lymphoma is the most dangerous

complication of Sjgren
MTB S2CK
p. 189
MTB S2CK
p. 189 190
Sjgren Syndrome/Diagnostic Tests
Sjgren Syndrome/Treatment
Best initial test on blood: SS-A and

SS-B
These are also called Ro and La and
each are present in about 65% of
patients
Best initial therapy is to water the mouth

Use frequent sips of water, sugar-free gum, and
fluoride treatments
Artificial tears to avoid corneal ulcers
Pilocarpine and cevimeline increase
acetylcholine,
t l h li
th main
the
i stimulant
ti l t to
t produce
d
saliva
Cevimeline increases rate of saliva production
No cure
Evaluate for lymphoma
SLE is associated with SS-A and SS-B in

10% to 20% of cases
Other abnormalities that are present, but
are nonspecific: ANA, RF, anemia,
leukopenia, and eosinophilia
MTB S2CK
p. 190
MTB S2CK
p. 190
Vasculitis
Polyarteritis Nodosa/Definition
Etiology unknown
Symptoms develop over weeks to
months
All vasculitides give:
Polyarteritis nodosa (PAN) is a disease

of small- and medium-sized arteries
leading to a diffuse vasculitis that
inexplicably spares the lungs
Chronic hepatitis B and C are
associated with PAN
Fever
Fe er
Malaise/fatigue
Weight loss
Arthralgia/myalgia
MTB S2CK
p. 190
MTB S2CK
p. 190
26
Common Features of PAN

Renal: glomerulonephritis without a
biopsy cant be diagnosed
Gastrointestinal: abdominal pain is

worsened by eating from vasculitis of
mesenteric vessels
UA isnt enough to confirm its PAN
Neurological: any large peripheral

nerve can be involved
Peroneal neuropathy leading to foot drop
Look for a stroke in a young person
MTB S2CK
p. 190 191
Bleeding also occurs

Nausea and vomiting are common
Skin: lower extremity ulcers are most

common; livedo reticularis, purpura,
nodules, and rarely gangrene occur
Lung is spared in PAN
MTB S2CK
p. 191
Polyarteritis Nodosa/Diagnostic Tests
Mononeuritis Multiplex
Mononeuritis multiplex is multiple
peripheral neuropathies of nerves
large enough to have a name
Most accurate test is a biopsy of a

symptomatic site
Angiography of renal, mesenteric, or
hepatic artery shows abnormal dilation or
beading.
P-ANCA is present in < 20%
Test all PAN patients for
hepatitis B and C.
MTB S2CK
p. 191
MTB S2CK
p. 191
Polyarteritis Nodosa/Treatment
Polymyalgia Rheumatica
Prednisone and cyclophosphamide

Treat hepatitis when found
Polymyalgia rheumatica (PMR) occurs in

those over age 50 with:
Pain and stiffness in shoulder and pelvic girdle
muscles
Difficulty combing hair and rising from chair
Elevated ESR
Normochromic, normocytic anemia
No Lab Findings
CPK and aldolase are normal
Steroids even at low doses great
response
MTB S2CK
p. 191
MTB S2CK
p. 191
27
Giant Cell (Temporal) Arteritis
Giant Cell (Temporal) Arteritis
The difference is the presence of:

Visual symptoms
Jaw claudication (pain in jaw when
chewing)
Scalp tenderness
Headache
Symptoms in other arteries such as
decreased arm pulses, bruits near the
clavicles, or aortic regurgitation
ESR and C-reactive protein are elevated

Most accurate test is a biopsy of affected
artery (e.g., temporal artery)
Treat with prednisone
Starting high-dose prednisone quickly is
more important than waiting for biopsy
MTB S2CK
p. 191 192
Blindness is irreversible.
MTB S2CK
p. 192
Wegener Granulomatosis
Wegener Granulomatosis/Diagnostic Tests
Presents with:
Best initial test is antineutrophil cytoplasmic

antibody (ANCA)
Most accurate test is a biopsy
Cytoplasmic antibodies are also called CANCA.
Sinusitis
Otitis media
Mastoiditis
Oral and gingival involvement
Wegener is also associated with skin, joint,

and eye lesions
Look for combination of upper and lower
respiratory tract findings in association
with renal insufficiency
MTB S2CK
p. 192
Wegener Granulomatosis/Diagnostic Tests
When asked about the best test for

Wegener, lung biopsy is better than renal
biopsy with sinus biopsy being the least
accurate
When all 3 are in the choices choose lung
biopsy
MTB S2CK
p. 192
C-ANCA = anti-proteinase-3 antibodies

P-ANCA = anti-myeloperoxidase antibodies
Wegener: C-ANCA
Churg-Strauss and
microscopic polyangiitis:
P-ANCA
MTB S2CK
p. 192
Wegener Granulomatosis/Treatment
Treat with prednisone and

cyclophosphamide
The clue to answering the most likely
diagnosis question is unresolving
diagnosis
pneumonia not better with antibiotics.
You will not first think of Wegener when
presented with the case.
MTB S2CK
p. 192
28
Churg Strauss Syndrome
Henoch Schnlein Purpura
Pulmonary-renal syndrome, ChurgStrauss also has:

Asthma
Eosinophilia
Biopsy
Bi
iis the
th mostt accurate
t test
t t
Treat with prednisone and
cyclophosphamide
Vasculitis more frequently seen in

children, Henoch-Schnlein purpura
(HSP) is characterized by involvement
of:
MTB S2CK
p. 193
HSP is most often a clinical

diagnosis; however, biopsy is the
most accurate test
Serum IgA levels are the
wrong answer. They
Th are
unreliable when testing
for Henoch-Schnlein
purpura.
MTB S2CK
p. 193
GI tract: p
pain,, bleeding
g
Skin: purpura
Joint: arthralgia
Renal: hematuria
MTB S2CK
p. 193

When the case describes
leukocytoclastic vasculitis
on biopsy, the answer is
Henoch-Schnlein
purpura.
Leukoplastic reactions
are painless, palpable
purpura of buttocks and
legs
MTB S2CK
p. 193
Source: Shreya Patel and Nishith Patel
Henoch Schnlein Purpura/Treatment
Cryoglobulinemia
Most cases resolve spontaneously

Steroids if there are severe extrarenal
mainfestations associated with renal
failure
Most commonly associated with chronic

hepatitis C
+/- endocarditis and/or Sjgren syndrome
Dont confuse cryoglobulins with cold
agglutinins
Both are IgM antibodies

Neither respond to steroids
MTB S2CK
p. 193
MTB S2CK
p. 194
29
Differences between Cryoglobulins and Cold Agglutinins

Cryoglobulins
Cold agglutinin
Associated with
Hepatitis C
EBV, Mycoplasma,
Lymphoma
Manifestations
Joint pain
Glomerulonephritis
Purpuric skin lesions
Neuropathy
Hemolysis
Interferon,
Ribavirin, and
boceprevir (or
telaprevir)
Stay warm
Rituximab,
cyclophosphamide,
cyclosporine
Treatment
MTB S2CK
p. 194
Cryoglobulinemia
Lab tests show a positive rheumatoid factor and
cold precipitable immune complexes
Steroids NOT effective
Treat the underlying cause, especially hepatitis C,
with interferon and ribavirin
Despite the rarity of the condition, the USMLE loves
cryoglobulinemia questions.
SLE
decreased C3 or
3 letters (SLE) = C3
Hep C
decreased C4 or
4 letters (Hep C) = C4
.
MTB S2CK
p. 194
Behet Syndrome
Behet Syndrome
The most common Behet questions

are:
Asian or Middle Eastern person with

painful oral and genital ulcers +/erythema
Also with:

What is pathergy?
pathergy ?
Pathergy: sterile skin
pustules from minor
trauma (e.g., needle stick)
MTB S2CK
p. 194
Ocular lesions leading to uveitis and

blindness
Arthritis
CNS lesions mimicking multiple
sclerosis
MTB S2CK
p. 194
Behet Syndrome/Treatment
Seronegative Spondyloarthropathies
Corticosteroids
To wean patients off of steroids, use:
The 3 types of seronegative

spondyloarthropathies are:
Azathioprine
Cyclophosphamide
Colchicine
C l hi i
Thalidomide
MTB S2CK
p. 195
Ankylosing spondylitis
Psoriatic arthritis
Reactive arthritis (Reiter syndrome)
MTB S2CK
p. 195
30
Men < 40 years:

Involvement of spine and large joints
Negative rheumatoid factor (hence the
name seronegative)
Enthesopathy (inflammation where
tendons and ligaments attach to bones)
Uveitis
HLA-B27
Corticosteroids arent a good treatment

for seronegative spondyloarthropathy
MTB S2CK
p. 195
D
Despite
it th
the association
i ti with
ith HLA
HLA-B27,
B27
this is never the best initial or most
accurate test for seronegative
spondyloarthropathies.
MTB S2CK
p. 195
Ankylosing Spondylitis/Diagnosis
Ankylosing Spondylitis/Diagnosis
Young man with low backache and

stiffness of his back has pain that radiates
to buttocks with flattening of the normal
lumbar curvature and decreased chest
expansion
Eventually
E
t ll th
the spine
i will
ill nott expand
d iin any
direction
Enthesopathy occurs at the Achilles tendon
Other Findings of Ankylosing

Spondylitis
Transient peripheral arthritis of knees,
hips, and shoulders (50%)
Cardiac: atrioventricular block in 3%
to 5%; aortic insufficiency
Uveitis
Bamboo spine is a late
finding with fusion of
vertebral joints.
Look for back pain

worsened by rest and
relieved by activity
MTB S2CK
p. 195
Ankylosing Spondylitis/Diagnostic Tests
MTB S2CK
p. 195
Best initial test is an X-ray of sacroiliac

(SI) joint
Most accurate test is an MRI
MRI detects abnormalities years before
the X-ray
X ray becomes abnormal
ESR is elevated in 85%
MTB S2CK
p. 196
MTB S2CK
p. 196
31
Ankylosing Spondylitis
HLA B27 is not a confirmatory diagnostic test

since 8% of general population is positive
Treatment
Exercise p
program
g
and NSAIDs are best
initial treatment
If NSAIDs are insufficient, use anti-TNF
drugs (e.g., etanercept, adalimumab, or
infliximab)
MTB S2CK
p. 196
Psoriatic Arthritis
MTB S2CK
p. 196 197
Psoriatic Arthritis
Psoriatic arthritis 80% will have

preceding psoriasis
Besides SI joint involvement,
characteristic findings are:
Sausage
Sausage digits from enthesopathy
Nail pitting
MTB S2CK
p. 197
MTB S2CK
p. 197
Psoriatic Arthritis/Diagnostic Tests
Psoriatic Arthritis/Treatment
ESR is elevated nonspecific

Best initial test is an X-ray of the joint
showing a pencil in a cup
deformity
NSAIDs are best initial therapy

Methotrexate used when question
describes severe disease or no
response to NSAIDs
Anti-TNF
Anti TNF agents are the answer when
methotrexate doesnt control disease
Steroids are a wrong choice
MTB S2CK
p. 197
MTB S2CK
p. 197
32
Reactive Arthritis (Reiter Syndrome)
Reactive Arthritis/Diagnosis
Reactive arthritis occurs secondary to:

Inflammatory bowel disease (equal
sex incidence)
Sexually transmitted infection (far
greater in men)
GI infection (Yersinia, Salmonella,
Campylobacter)
Look for triad of:

Joint pain
Ocular findings (uveitis,
conjunctivitis)
Genital
G it l abnormalities
b
liti ((urethritis,
th iti
balanitis)
Keratoderma
MTB S2CK
p. 197
MTB S2CK
Reactive Arthritis/Diagnosis
p. 198
blennorhagicum is a skin
lesion unique to reactive
arthritis that looks like
pustular psoriasis.
Reactive Arthritis/Diagnostic Tests/Treatment
No specific test for reactive arthritis

Rule out septic joint
Treat underlying cause/use NSAIDs
Sulfasalazine > NSAIDS
Antibiotics dont reverse

reactive arthritis once joint
pain has started.
Source: commons.wikimedia.org. Used with permission
MTB S2CK
p. 198
Septic Arthritis
Septic Arthritis, Gonococcal

Arthritis, & Osteomyelitis
Definition
Septic arthritis is an infection of joint space
Etiology
Septic arthritis is relatively rare in an
undamaged joint
Risk of infection is directly proportional to
degree of joint damage
MTB S2CK
p. 199
33
Septic Arthritis
Etiology of Septic Arthritis
Etiology (contd)
Osteoarthritis (DJD) provides slight risk
RA has greater risk
Greatest risk is with prosthetic joint
Bacteremia can spread into joint space,
space
which is why endocarditis and injection
drug use causes septic arthritis
MTB S2CK
p. 199
MTB S2CK
Etiology
Frequency
Staphylococcus
40%
Streptococcus
30%
Gram negative
rods
20%
p. 199
Septic Arthritis/Presentation
Septic Arthritis/Diagnostic Tests
Joint is warm, red, and immobile often

with palpable effusion
Chills and fever happen because of
bacteremia
Best initial and most accurate test is

aspiration of the joint with a needle
(arthrocentesis); X-ray, CT, and MRI arent
useful and are the wrong answers
Joint fluid shows:
Leukocytosis: more than 50,000 to 100,000
cells, predominantly neutrophils
Gram stain: positive (50%) Gram-negative
bacilli; (75%) with Staphylococcus
Synovial fluid culture: 70% to 90% sensitive
Blood cultures: 50% sensitive
MTB S2CK
p. 199
MTB S2CK
p. 199
Septic Arthritis
Other Options for Treatment of Septic Arthritis
Treatment
Ceftriaxone and vancomycin are best
initial empiric therapy
Gram negative
bacilli
Gram positive cocci

(sensitive)
Gram positive
cocci (resistant)
Quinolones
Oxacillin
Linezolid
Aztreonam
Cefazolin
Daptomycin
Cefotaxime
Piperacillin with
Tazobactam
Ceftaraline
Piperacillin
Tigecycline
Aminoglycosides
MTB S2CK
p. 199
MTB S2CK
p. 200
34
Septic Arthritis/Treatment
Septic Arthritis
Adjust antibiotics according to culture

results.
Prosthetic Joint Infection

Infected prosthetic joint gives a warm, red,
immobile, and tender joint
Must do imaging
If Staphylococcus
p y
is sensitive,,
vancomycin is associated with a worse
outcome than betalactam antibiotic
(e.g., oxacillin or cefazolin). Switch
drugs if organism is sensitive.
MTB S2CK
p. 200
MTB S2CK
p. 200
Septic Arthritis
Septic Arthritis
Prosthetic Joint Infection (contd)

MRI difficult to perform with prosthetic
joints because they are made of metal
If there is lucency around implantation
of the joint on radiologic imaging or if
joint is physically loose, infection is
likely present at implantation site
Treatment of Infected Prosthetic Joint

Remove joint, treat with antibiotics for 6
to 8 weeks, and then replace joint
MTB S2CK
p. 200
The most common

organism for recently
placed artificial joints
is Staphylococcus
epidermidis.
MTB S2CK
p. 200
Gonococcal Arthritis (Gonorrhea)
Gonococcal Arthritis/Diagnostic Tests
The difference in presentation from septic

arthritis is:
Detecting gonorrhea is much more

difficult than detecting Staphylococcus,
Streptococcus, and Gram-negative
bacilli of septic arthritis
Polyarticular involvement
Tenosynovitis (inflammation of tendon
sheaths, making finger movement painful)
Petechial rash
Gonococcal arthritis is
more frequent during
menses.
MTB S2CK
p. 200
MTB S2CK
p. 200
35
Synovial Fluid Analysis for Infectious Arthritis

Test sensitivity
Septic arthritis
Gonococcal Arthritis/Diagnostic Tests

Gonococcal arthritis
Leukocytosis
> 50,000 100,000 cells/ L
30,000 50,000 cells/ L
Gram stain
50 70% sensitive
25% sensitive
C l
Culture
90% sensitive
ii
< 50% sensitive

ii
Blood cultures
50% sensitive
< 10% sensitive
In order to reach maximum sensitivity,

multiple diffuse sites must be cultured
for gonorrhea such as:
Pharynx
What tells you to
Rectum
Rectum
culture everywhere?
Urethra
Rash
Cervix
Tenosynovitis
Polyarticular
involvement
MTB S2CK
p. 201
MTB S2CK
p. 201
Gonococcal Arthritis/Treatment
Osteomyelitis/Definition/Etiology
Ceftriaxone, cefotaxime, or ceftizoxime is the

best empiric therapy for disseminated
gonorrhea
Fluoroquinolones are not the best initial
therapy
Osteomyelitis is an infection of bone

Staphylococcus aureus is MCC
Children get osteomyelitis through
hematogenous spread, but adults get it
from a contiguous (nearby) infection
Salmonella is the most
commonly identified
organism in patients with
sickle cell disease.
If recurrent gonorrhea infection is described,

test for terminal complement deficiencya
favorite subject of USMLE Step 2 CK.
MTB S2CK
p. 201
Osteomyelitis/Diagnostic Tests
MTB S2CK
p. 201
Best initial test is an X-ray

Most accurate test is a biopsy
If X-ray is normal, the most appropriate next
step in management is MRI
CT scan isnt veryy useful
When is ESR the answer?

To follow the response to therapy
MTB S2CK
p. 202
Source: Eva M. Smietana
36
When is culturing the drainage the answer?

Never. You cannot reliably distinguish
superficial colonization from whatever
organism is inside the bone causing the
bone infection.
Bone scan is the answer
only if you want to get an
MRI and its contraindicated
(pacemaker).
MTB S2CK
p. 202
Osteomyelitis/Treatment
Osteomyelitis takes weeks to progress

Must biopsy
MSSA
Oxacillin, cefazolin, nafcillin, or
ceftriaxone
MRSA
Vancomycin or linezolid
MTB S2CK
p. 202
Gram-negative bacilli such as E. coli are

treated with fluoroquinolones (e.g.,
ciprofloxacin)
Toxicity of Quinolones
Fluoroquinolones can cause Achilles
tendon rupture
Its essential to confirm the

sensitivity of the organism prior to
treating with ciprofloxacin
They are also contraindicated in

pregnancy and children because they
interfere with bone growth
Ciprofloxacin is the only oral therapy

for osteomyelitis, but should be used
only if the organism is confirmed as a
sensitive Gram-negative bacillus.
MTB S2CK
p. 202
MTB S2CK
p. 202
37
Surgery
Preoperative Evaluation,
Postoperative Evaluation, &
Vascular Surgery
Matthew Kinney, MD
Orthopedic Resident
University of California San Diego
Preoperative Evaluation
Preoperative Evaluation
Cardiovascular
Pulmonaryy
Renal
Objective: Identify factors that increase risk of

complications in perioperative period
Age
Cardiac history
#1 predictor of perioperative complications
Diabetes status
Risk equivalent to Coronary disease
History of
Pulmonary disease
Renal disease
Stroke
MTB S2CK
p. 379
Preoperative Evaluation/Cardiac
Preoperative Evaluation/Cardiac
Must obtain detailed cardiac history
Management
If age < 35 and no history of cardiac disease
Look for indicators of previous MI or CHF

Recent MI
Defer surgery for 6 months
Follow-up stress test to ensure adequate perfusion
Evidence of CHF (JVD, edema)

Patients with EF < 35% at increased risk
ACE-Is, B-blockers, spironolactone must be
optimized
Proven to decrease overall mortality!!!
MTB S2CK
p. 379
EKG
If history of cardiac disease (MI, CHF)

EKG
Stress testing
Ensure appropriate cardiac perfusion
Echocardiography
Monitor EF
Evaluate structural damage
MTB S2CK
p. 380
Preoperative Evaluation/Pulmonary
71-year old man undergoing femoro-popliteal

bypass for severe claudication of left leg which
causes unbearable pain with exercise. Past
medical/surgical history is significant for remote
appendectomy and insulin-dependent type 2 DM.
What preoperative testing is recommended?
a.Basic Metabolic Panel (BMP) only High cardiac
risk
b.BMP + EKG
c. BMP + EKG + PFTs
Must get stress test/ECHO
d.BMP + EKG + Exercise Stress Test Cannot exercise
e.BMP + EKG + Thallium Stress Test
Must evaluate for history of lung disease (including

smoking)
PFTs required for all patients with known lung
disease
Vital capacity - most important predictor of
perioperative complications
MTB S2CK
p. 380
Must evaluate for history of lung disease (including
smoking)
PFTs required for all patients with known lung
disease
Vital capacity - most important predictor of
perioperative complications
Smokers
PFTs
Smoking cessation for 6-8 weeks preoperatively
Nicotine patch acceptable
MTB S2CK
p. 380
Preoperative Evaluation/Renal
Renal disease increases surgical risk
Intravascular fluid losses occur during surgery
Results in hypoperfusion of kidneys
Physiologic response to decreased intravascular
volume is activation of Renin-Angiotensin system
Constricts renal vasculature
Postoperative Evaluation
Fever Assessment
Complications
Renal hypoperfusion correlates with increased

mortality
Management
Aggressive IV hydration beginning 24 hours pre-op
Dialysis patients must be dialyzed 24 hours pre-op
MTB S2CK
p. 380
Post Operative Fever

WIND
Post Op Complications/Confusion
WATER WALKING
POD
1-2
3-5
Atelectasis #1
Pneumonia
CXR
-Sputum Culture
(if pneumonia
suspected)
-Incentive spirometry
-Antibiotics
Vanc. + Pip/Tazo
5-6
WEIRD
8-15
DVT
Thrombophlebitis
(IV site infection)
Doppler US
Anti-coagulation
Heparin
p
Warfarin
Replace IVs
UTI
Urinalysis
Nitrite +
Leukocyte Esterase +
Antibiotics
MTB S2CK
WOUND
Drug Reaction
Deep Abscess
D/C likely
medication
CT Scan
Drainage
of Abscess
Incision-site
Infection Cellulitis
Physical Exam
Erythema
Pus
Swelling
Abscess
Incision/Drainage
Antibiotics
p. 400
Adult Respiratory Distress Syndrome
Confused Patient
Obtain ABG, CXR, CBC
Evidence of Infection
Abnormal CBC
Evidence of Hypoxemia
Abnormal ABG
Changes on CXR?
Yes
Atelectasis vs.
Pneumonia
Incentive
spirometry
Antibiotics
MTB S2CK
No
Culture Likely Sources

Blood (Bacteremia)
Urine (UTI)
Consider PE
Spiral CT
Treat with
empiric
Antibiotics
p. 401
Etiology
Endothelial damage allows fluid to fill alveoli
Prevents O2/CO2 exchange, acts as shunt
Signs/Symptoms
HR, RR
Labored breathing (accessory muscle use)
Fever may be present
Diagnosis
ABG: pO2, pCO2
CXR: Bilateral pulmonary infiltrates
MS-4 USU Teaching File, Uniformed Services University
MTB S2CK
p. 401
Pulmonary Embolism
Treatment
Mechanical ventilation
Etiology
Maximize Positive End-Expiratory

Pressure (PEEP)
Passage of a
venous blood clot to
lungs
Origin: Deep leg
vein > 90%
Clot lodges in lung

vasculature
Prevents O2/CO2
exchange
MTB S2CK
Source: nlm.nih.gov
p. 401
Pulmonary Embolism
Risk Factors
Stasis: Immobility (post-surgical, travel, etc.),
obesity
Endothelial damage: Surgery, trauma
Hypercoagulability
yp
g
y: Oral contraceptive
p
pills (OCP), malignancy, genetic disorder
Signs/Symptoms
HR, RR, Temp
Pleuritic chest pain
MTB S2CK
62-year-old woman with no significant PMH

undergoes right total hip replacement 3 days ago.
Recovery is uncomplicated until 30 minutes ago, she
reported moderate SOB and chest pain with deep
inspiration.
Whats the next step in evaluating this patient?
a.
b.
c.
d.
e.
EKG only Insensitive for pulmonary embolism

EKG + V/Q Scan No reported contrast allergy
EKG + Spiral CT scan
EKG + D-Dimer Sensitive, but not specific
EKG + Heparin Injection Must diagnose PE first
p. 401
Pulmonary Embolism
Pulmonary Embolism
Diagnosis
ABG
pO2, pCO2
EKG
S1
Nonspecific ST-segment and T wave changes

Most common
S1-Q3-T3
Q3
MTB S2CK
T3
p. 401
Pulmonary Embolism
Pulmonary Embolism
Diagnosis
ABG
pO2, pCO2
EKG
Most common
S1-Q3-T3
Infrequent during acute PE
Can be found in massive acute PE and cor pulmonale
Spiral CT
MTB S2CK
p. 401
Pulmonary Embolism
Pulmonary Embolism
Diagnosis
ABG
Treatment
Respiratory support
Anticoagulation
pO2, pCO2
EKG
Most common
S1-Q3-T3
Infrequent during acute PE
Can be found in massive acute PE and cor pulmonale
Heparin acutely, bridge to warfarin longterm

IVC filter (if anticoagulation
contraindicated)
Spiral CT
Consider V/Q scan (if IV contrast allergy)
MTB S2CK
p. 401
MTB S2CK
Vascular
Aortic Dissection
Claudication
p. 401
69-year-old male with 50 pack-year smoking history is

brought to the ER by his wife who reports he seems
confused. He feels weak and has pain in middle of
abdomen. He is a pale, elderly male in moderate
distress. BP of 84/55, pulse 120. Palpable, pulsatile
mass in patients abdomen.
Whats the most likely diagnosis?
a.
b.
c.
d.
Ruptured peptic ulcer Would expect peritoneal signs

Hemorrhagic gastritis Would expect hematemesis
Hemorrhagic pancreatitis Would expect flank bruising
Ruptured abdominal aortic aneurysm
MTB S2CK - p. 399
Etiology
Weakening of aortic
wall secondary to
atherosclerosis
Risk Factors
Male > Female
Age
Hypertension, Hyperlipidemia
Smoking
Si
Signs/Symptoms
/S
t
Frequently asymptomatic
May report pulsatile abdominal mass
Aortic diameter
expands > 1.5x normal
Involves all layers of
vessel wall (True
Aneurysm)
90% arise from infrarenal aorta
MTB S2CK
p. 399
Source: csm.ornl.gov
MTB S2CK
p. 399

Diagnosis
CT/MRI
Provides determination
of level and
surrounding structures
Ultrasound for size

measurements
Aortic Dissection
Treatment
3.0-4.0 cm
US every 2-3 years
4.0-5.4 cm
US or CT every 6-12
months
5.5 cm,
asymptomatic
Surgical repair
Etiology
Tearing of aortic
intima forms
false lumen
Blood flows
into false
f
lumen,
extends tear
Sopurce: J. Heuser commons.wikimedia.org
MTB S2CK
p. 399
Aortic Dissection/Etiology
Aortic Dissection
Can occur in ascending or descending aorta
Risk Factors
Male > Female
Age > 40
Hypertension (#1
risk factor))
Marfans disease,
Ehlers-Danlos
syndrome
Signs/Symptoms
Sudden onset,
tearing chest pain
Radiates to the
back
Elevated BP
May be
asymmetric (R > L)
Sopurce: J. Heuser commons.wikimedia.org
Aortic Dissection/Diagnosis
Aortic Dissection
Demonstration of dissection on imaging

CXR
Widening of mediastinum
Source: NNMC
Aortic Dissection/Diagnosis
Aortic Dissection
Demonstration of dissection on imaging

CXR
Treatment
Ascending dissection = Emergent
surgery
Descending dissection = Medical
therapy
Widening of mediastinum
Transesophageal ECHO (TEE)

Acute chest pain and/or clinically unstable
MRA
Chronic chest pain and hemodynamically stable
CT angiogram
Beta-Blockers (#1)
Anti-hypertensive meds
TEE and MRI contraindicated
Claudication
Claudication/Management
Etiology
Atherosclerotic plaques prevent sufficient perfusion
to extremities (lower > upper)
Medical
Associated with smoking, DM, hyperlipidemia
Symptoms
Calf/leg pain with exercise
Relieved by rest
Diagnosis
Ankle-Brachial Index
Risk Modification
Smoking cessation (#1)
Graded exercise
Pharmacologic therapy
Cilostazol
Cil t
l
Antiplatelet agents: Aspirin, Clopidogrel
Percutaneous
Stenting, angioplasty
< 0.9 = pathologic

< 0.4 = symptomatic
Surgical
Trauma/ABC Assessment
Initial assessment rely on ABC algorithm
Airway
Shock
Trauma Assessment (ABCs)
yp of Shock
Types
Hypovolemic
Cardiogenic
Neurogenic
Septic
Anaphylactic
Breathing
Circulation
Disability (CNS)
Exposure
ABCs are a roadmap, but you must know what to do
at each step
MTB S2CK
p. 380 381
Concern for airway compromise?
AMS
Facial trauma
Apnea
A = Airway
Must assess for airway compromise
If patient can talk airway is clear
Look for traumatic obstruction, evidence of smoke
inhalation
Evaluate need for intubation
No
Yes
Assess
Breathing/
Oxygenation
Yes
Yes
Facial Trauma
Altered Mental Status
Apnea
MTB S2CK
Careful Orotracheal Intubation

Flexible bronchoscopy
p. 381
MTB S2CK
Facial Trauma?
Cricothyroidotomy
Indications
Intubate
No
Cervical Spine Injury?

No
Orotracheal Intubation
p. 381
B = Breathing
Assess breath sounds
Monitor oxygenation status with pulse oximetry
C = Circulation
Evaluate pulses (distal first, proximal if
absent)
Manage hemorrhage sites
Goal is O2 Saturation
> 90%
If O2 Sat < 90%
consider
Source:UusiAjaja, commons.wikimedia.org
MTB S2CK
a. Supplemental O2
via nasal cannula
b. O2 face mask
c. Intubation
p. 381
Direct pressure slows blood loss
Monitor blood pressure

If the patient is hypotensive, place 2 largebore IVs and begin aggressive fluid
resuscitation
Start with normal saline (only use blood
products as secondary measure)
MTB S2CK
p. 381
D = Disability (Altered Mental Status)
Assessed with Glasgow Coma Scale
Eye Response (1-4)
Verbal Response (1-5)
Motor Response (1-6)
Score < 8 requires intubation

E = Exposure
Remove all clothing on patient
Assess for hidden injuries
Thorough physical examination
52-year-old woman ejected from her car during a

high-speed motor vehicle accident . Upon arrival to
ED, she complains of severe, left-sided chest pain.
Pale, cool patient in severe distress. Heart rate 130
bpm, BP 86/44 mmHg. JVD along angle of jaw. Chest
X-ray shows anterior rib fractures on the left.
a. Hypovolemic shock Would not see JVD
b. Neurogenic shock
c. Anaphylactic shock
d. Cardiogenic shock
Warm, flush patients
e. Septic shock
MTB S2CK
p. 381
Shock
Types of Shock
Definition Inadequate perfusion/oxygenation that

impairs organ function
Signs/Symptoms
Vitals Signs
Hypovolemic
Causes: Hemorrhage (#1), Dehydration, Burns
Decreased BP
Increased HR
CNS: Confusion, altered mental status

Kidney: Decreased urine output, increased BUN/Cr
ratio
Liver: Massively elevated AST/ALT (Shock Liver)
Heart: Chest pain, shortness of breath
MTB S2CK
p. 381
MTB S2CK
p. 382
Types of Shock/Hypovolemic
Types of Shock
Signs/Symptoms
Cardiogenic
Causes: MI (#1), CHF,
arrhythmia
Signs/Symptoms
Pale, cold
Trauma
Lab Findings
Pale, cold
Symptoms associated
with MI (Chest pain,
SOB)
JVD
SVR =
CVP =
PCWP =
CO =
Treatment
Source: U.S. Navy photo by Mass Communication

Specialist 2nd Class Michael Russell, public.navy.mil
Lab Findings
CO =
SVR =
CVP =
PCWP =
Treatment
Treat cardiac problem
Do NOT give fluid!!!
Aggressive IV fluid replacement

Pressors
MTB S2CK
p. 382
MTB S2CK
Types of Shock
Types of Shock
Neurogenic
Causes: CNS damage
(cervical/thoracic spinal
cord - #1)
Signs/Symptoms:
Warm,, flush
Evidence of CNS
damage (trauma)
p. 382
Lab Findings
SVR =
CVP =
PCWP =
CO =
Treatment
Aggressive IV fluid
delivery
Pressors
Septic
Causes: Infection
E. coli and S. aureus
(most common
organisms)
Signs/Symptoms
Warm, flush
Possible nidus of
infection (UTI,
pneumonia, wound)
Source: cdc.gov
MTB S2CK
p. 382
MTB S2CK
p. 382
Types of Shock/Septic
Lab Findings
SVR =
CVP =
CO =
PCWP =
MTB S2CK
Types of Shock
Treatment
Broad-spectrum
antibiotics
Fluid and
pressors
Dopamine
Norepinephrine
p. 382
Anaphylactic
Causes: Allergy
(insects, food,
medication)
Signs/Symptoms
Warm, flush
Wheezing,
hives,
associated
evidence of
allergic reaction
MTB S2CK
Types of Shock/Anaphylactic
p. 382
Shock Algorithm
Pale/Cold
Lab Findings
CVP =
SVR =
PCWP =
CO =
Is patient pale/cold or
warm/flush?
PCWP change?
Elevated
Cardiogenic
Treat
cardiac
problem
Treatment
Epinephrine
CO change?
Decreased
Decreased
Hypovolemic
Fluid and
pressors
Elevated
Neurogenic
Fluid and
pressors
PCWP change?
Decreased
No Change
Anaphylactic
Epinephrine
MTB S2CK
Warm/Flush
Septic
Antibiotics
Fluids and
pressors
p. 382
Abdominal Trauma
Trauma
Abdominal Trauma
Thoracic Trauma
Pelvic Trauma
Penetrating
Gunshot wounds
Must do exploratory laparotomy in ALL
patients
Stab wounds
If hemodynamically stable, do a FAST
ultrasound scan
If hemodynamically unstable, perform an
exploratory laparotomy
10
Abdominal Trauma
Abdominal Trauma
Diaphragmatic Rupture
Cause
Penetrating or blunt trauma
Left > Right
Symptoms
Loops
of Bowel
Respiratory distress
Kehrs sign = Left shoulder pain
Diagnosis
CXR: Bowel loops in thorax
Absent Hemi-Diaphragm
MTB S2CK
p. 383
Source: Hariharan D, Singhal R, Kinra S, Chilton A, commons.wikimedia.org
Abdominal Trauma/Blunt
Splenic/Liver injury
Causes
Most commonly injured in blunt abdominal
trauma
Pancreatic Injury
Causes
Blunt trauma to epigastrum
Spleen #1
Liver #2
Associated with lower rib fractures

Signs/Symptoms
Hypotension (due to hemorrhage)
Kehrs sign
MTB S2CK
p. 383
Bike handlebars
Car dashboard
Signs/Symptoms
Cullens sign = Bruising around umbilicus
MTB S2CK
p. 383
Diagnosis
FAST scan (ultrasound)
To evaluate for intraabdominal bleeding
CT scan
If negative FAST
FAST, but
suspect splenic
rupture
To evaluate
retroperitoneal bleed
Fluid = Blood
Source: Herbert L. Fred, MD and Hendrik A. van Dijk, commons.wikimedia.org
MTB S2CK
p. 383
MTB S2CK
p. 383
11
Management
If hemodynamically stable
Close monitoring
Serial abdominal exams
IV fluids
33-year-old female jogging at night was struck by a

drunk driver. She complains of severe abdominal pain
that radiates to the back. Vital signs are stable. After
ER work-up, patient is admitted for evaluation. Three
days later, the following picture is taken.
If hemodynamically unstable
Exploratory laparotomy
MTB S2CK
p. 383
33-year-old female jogging at night was struck by a

drunk driver. She complains of severe abdominal pain
that radiates to the back. Vital signs are stable. After
ER work-up, patient is admitted for evaluation. Three
days later, the following picture is taken.
a.
b.
c.
d.
e.
Pancreatic pseudocyst Delayed appearance

Hemorrhagic pancreatitis
Ruptured AAA No pulsatile mass
Aortic dissection Stable BP, no chest pain
Splenic rupture Wrong side, no L shoulder pain
Source: Herbert L. Fred, MD and Hendrik A. van Dijk, commons.wikimedia.org
Thoracic Trauma
Thoracic Trauma/Pneumothorax
Pneumothorax
Etiology
Air in pleural space
pulmonary collapse
Signs/Symptoms
Chest pain
Decreased breath sounds
Hyperresonance to percussion
Tracheal deviation toward affected side
Diagnosis
CXR
Collapsed
Lung
Border
Treatment
Chest tube
Source: John Yasmer
MTB S2CK
p. 384
MTB S2CK
p. 384
12
Thoracic Trauma
Thoracic Trauma/Tension Pneumothorax
Tension Pneumothorax A MEDICAL EMERGENCY

Etiology
Resulting from laceration of cervical

trachea and mediastinal pleura
Resulting from sucking wound of valvular

type
Chest wall defect acts

as one-way valve
Air can enter pleural
space, but cannot exit
Resulting increase in
pressure can
compress vital
structures
Trachea, vena
cava
MTB S2CK
a. Laceration of cervical trachea

b. Laceration of mediastinal pleura
c. Tension pneumothorax
d. Collapsed lung
e. Shift of heart
f. Subcutaneous emphysema
g. Partial collapse of contralateral lung
Source: army.mil
p. 384
Thoracic Trauma/Tension Pneumothorax
Thoracic Trauma
Signs/Symptoms
Hemothorax
Etiology
Blood in pleural
space
Signs/Symptoms
g
y p
Chest pain
Absent breath
sounds
Dullness to
percussion
Chest pain
Hyperresonance
Decreased breath
sounds
Tracheal deviation
(away from affected
side)
Diagnosis
Source: James G. Smirniotopoulos, M.D.
CXR
Treatment
Immediate needle decompression
Chest tube placement
MTB S2CK
a. Valvular sucking wound of chest wall

b. Tension pneumothorax
c. Collapsed lung
d. Cardiac shift to intact side
e. Partial collapse of contralateral lung
p. 384
Thoracic Trauma/Hemothorax
Diagnosis
CXR
MTB S2CK
Source: army.mil
p. 384
Thoracic Trauma/Hemothorax
White-Out
Blunted costophrenic angle
CT scan
Treatment
Chest tube drainage
Thoracotomy
Posteroanterior CXR made shortly after
wounding and showing hemothorax
10 days later, after 6 thoracenteses,

three 150 cc of blood and other fluid
was removed
Source: army.mil
MTB S2CK
p. 384
13
Hemo/Pneumothorax Diagnosis
Thoracic Trauma
Symptoms
Chest Pain
Decreased/Absent Breath Sounds
Etiology
Trauma to pericardium
Broken ribs
Penetrating trauma
Response to Percussion?
Dullness
Hyperresonance
Hemothorax
Tracheal Deviation?
Chest tube drainage
Away from lung
Toward lung
Pneumothorax
Tension pneumothorax
Chest tube
Immediate needle
thoracotomy
Chest tube
Signs/Symptoms
JVD
Hypotension
Decreased heart
sounds
MTB S2CK
p. 384
Thoracic Trauma/Pericardial Tamponade
Thoracic Trauma/Pericardial Tamponade
Diagnosis
Diagnosis
EKG
EKG
Electrical Alternans
Electrical Alternans
ECHO
Diagnostic test of choice
Treatment
Pericardiocentesis
Source: army.mil
MTB S2CK
p. 384
26-year-old man suffers blow to chest with a baseball bat.

He is brought to the ED with severe right-sided chest pain
and difficulty breathing. He is tachypneic at 26
breaths/minute, with a heart rate of 130 beats/minute,
diminished breath sounds on the right, and left tracheal
deviation.
a.
b.
c.
d.
e.
Pericardiocentesis Not pericardial tamponade

Chest X-ray
Too slow. This is an emergency
Needle thoracotomy
Chest tube placement
EKG
Not indicated in this patient
MTB S2CK
p. 384
14-year-old boy hits a pothole while riding his bike and

falls directly onto the central bar. He presents to the ED
with severe groin pain and swelling. Physical examination
reveals blood at the urethral meatus and a high-riding
prostate.
What is the next appropriate step in management?
a.
a
b.
c.
d.
e.
Place a Foley Can

C ffurther
th damage
d
urethra
th
Get a retrograde urethrogram
Empiric antibiotics Must assess urethral patency
CBC and electrolytes
Discharge the patient with reassurance
MTB S2CK
p. 385
14
Abdominal Pain Differential Diagnosis

RUQ
The Abdomen Part 1

Abdominal Pain
Mesenteric Ischemia
Esophageal Pathology
Gastric Perforation
LUQ
Cholecystitis
Splenic Rupture
- Radiates to R shoulder
- Radiates to L shoulder
Cholangitis
Ischemic Bowel Disease
Perforated Ulcer Mid-Epigastrum
Pancreatitis
Aortic Dissection
- Radiates to back
RLQ
LLQ
Appendicitis
Ovarian Torsion ( )
Ectopic Pregnancy ( )
Diverticulitis (Cecal)
Diverticulitis (Sigmoid)
Sigmoid Volvulus
Ovarian Torsion ( )
Ectopic Pregnancy ( )
MTB S2CK
p. 387
Chronic Mesenteric Ischemia

66-year-old man in the ED with acute onset, severe
abdominal pain. Abdominal exam benign, without
guarding or rebound tenderness. White count
18,000/mm3 (4,500-11,000/mm3), lactic acid 4.2 mg/dL
(4.5 to 19.8 mg/dL). Only medication is coumadin.
Whats the most appropriate next step in management?
a. MRI scan off th
the abdomen
bd
T k too
Takes
t long
l
b. Exploratory Laparotomy
c. Colonoscopy
Risk of bowel perforation
d. Oral antibiotics Doesnt treat primary concern
e. EKG Symptoms not consistent with cardiac etiology
Etiology
Mesenteric artery
atherosclerosis
insufficient
blood flow to
bowel
Patients often
have other
atherosclerotic
diseases
Angina
Claudication
MTB S2CK
p. 385 386
Signs/Symptoms
Diffuse, postprandial abdominal pain
Diagnosis
CT abdomen (initial test)
Severe, crampy, associated nausea

Due to O2 requirement by gut after meals
May lead to weight loss due to fear of eating
Bloody diarrhea
Progressive disease begins with mild
ischemia, progresses to full occlusion of
blood flow
MTB S2CK
p. 386
A lack of blood flow causes ischemia to the bowel wall

and sloughing of the mucosa. Source: Niket Sonopal, MD.
Fast, non-invasive
CT angiography is most accurate

Treatment
Surgical revascularization via arterial bypass
NPO
Hydration with IV fluids
Bowel prep 24 hours preceding surgery
Nitrates may provide short-term symptom

improvement
MTB S2CK
p. 386
15
Acute Mesenteric Ischemia
Etiology
Acute occlusion of mesenteric arteries
Most commonly the superior mesenteric
Causes:
Embolism secondary to A
A-fib
fib (#1)
MTB S2CK
Source: Mikael Hggstrm from original image

created and uploaded by Dr. I-Chen Tsai,
p. 386
Etiology
Acute occlusion of mesenteric arteries
Signs/Symptoms
Sudden onset, severe
abdominal pain
Most commonly the superior mesenteric

Causes:
Embolism secondary to A
A-fib
fib (#1)
Acute thrombus formation on
atherosclerotic plaque
Pain out of
proportion to exam
Nausea,, vomiting
g
Bloody diarrhea
Results in bowel infarction
Air in bowel wall

((Pneumatosis
Intestinalis)
Edema
Ileus
CT angiography
(Most accurate)
Splenic flexure (#1) and hepatic flexure

(#2) are most common sites
MTB S2CK
Diagnosis
Labs: WBC, pH,
Lactate
Abdominal X-ray/CT
p. 386
Treatment
Emergent Laparotomy
Resection of necrotic bowel
Mesenteric artery thromboembolism. Source: Joel McFarland, Medpix 28818
MTB S2CK
p. 386
16

52-year-old woman, alcoholic, with severe chest pain
after an episode of persistent vomiting. No blood in
vomitus, only stomach contents. Exam reveals
crepitus over upper anterior chest wall.
a.
b.
c.
d.
e.
Source: haitham alfalah, commons.wikimedia.org
Ethanol level Not useful in this case

Chest X-Ray Will not show esophageal rupture
Upper Endoscopy Risk further perforation
Barium Esophagogram Not water-soluble
Gastrografin Esophagogram
MTB S2CK
p. 387
Esophageal Injuries
Mucosal Tear
Mallory Weiss Syndrome
Cause
Vomiting/Retching
Alcoholics
Symptoms
Hematemesis
Odynophagia
Location
Gastroesophageal junction
Diagnosis
Gastrografin esophagogram
No leakage
Treatment
Supportive
Cauterization if necessary
Complications Rare
MTB S2CK
Esophageal Perforation
Boerhaave Syndrome
Iatrogenic is #1 (Endoscopy)
Vomiting/Retching
Alcoholics
Retrosternal chest pain
Severe, acute onset
Radiates to L shoulder
Subcutaneous Emphysema
Distal esophagus
Left Posterolateral Aspect
Gastrografin esophagogram
Leakage
Emergent Surgery
High mortality (25%)
Acute mediastinitis
Very high mortality
57-year-old male with BMI of 37 (18.5-24.9 normal)

presents to ED with weakness. Vomiting large amounts of
blood twice in last hour and passing one bright red stool.
He has persistent pain in his mid-abdomen. Takes
omeprazole for heartburn. BP 100/60, HR 120.
What is the diagnosis?
a Gastric Perforation No
a.
N bl
bleed.
d P
Peritoneal
it
l signs.
i
b. Hemorrhagic ulcer
c. Boerhaaves syndrome No hematemesis
d. Diverticulosis No hematemesis
e. Acute mesenteric ischemia No hematochezia
p. 387 388
Gastric Perforation
Gastric Perforation
Etiology
Secondary to
peptic ulcer
disease
Risk Factors
H. Pylori
infection
NSAIDs
Burns
Trauma
Head trauma
Cancer
Ethanol
Tobacco
Increased
production of
gastric acid,
combined with
compromise of
stomach lining
results in ulcer
formation
Source: User:KGH, commons.wikimedia.org

MTB S2CK
p. 388
MTB S2CK
p. 388
17
Gastric Perforation
Gastric Perforation/Signs and Symptoms
Pathophysiology
Perforation
Hemorrhage
Ulcer completely
erodes through
visceral wall
Ulcer erodes into

gastroduodenal artery
Gastric contents are

released into abdominal
cavity
Result is damage to
peritoneal structures
Peritonitis (anterior
+ posterior ulcers)
Pancreatitis
(posterior ulcers)
MTB S2CK
More common than

gastric perforation
Seen with posterior
ulcers
Requires upper
endoscopy to
evaluate/treat bleed
p. 388
Acute onset mid-epigastric abdominal pain

May radiate to right shoulder (phrenic nerve
involvement)
Worsening over time
Peritoneal signs (if any delay in seeking

t t
treatment)
t)
Rigidity
Guarding
Rebound tenderness
MTB S2CK
Gastric Perforation
p. 389
Gastric Perforation
Management
Diagnosis
Upright
chest X-ray
1) Make Patient NPO

Prevents further extrusion of gastric contents
into peritoneal cavity
2) Place NG Tube
Free air
under
diaphragm
Suction gastric contents

Mitigates risk from newly-formed
newly formed acid
3) Medical Management
Abdominal
CT
Broad-spectrum antibiotics to combat infection

IV fluids in preparation for surgery
4) Emergent Surgery
Exploratory laparotomy
- Repair perforation
MTB S2CK
p. 389
MTB S2CK
The Abdomen Part 2

Abdominal Abscess
Inflammatory GI Conditions
Abdominal Obstruction
p. 389
16-year-old boy comes with new onset RLQ pain. He

reports vague, mid-abdominal pain for last day, but
when he awoke this morning it was much sharper and
had changed location. He displays guarding and
rebound tenderness, and palpation of LLQ hurts on
right side. WBC count of 16,000/mm3 (4,5003)
11 000/
11,000/mm
a.
b.
c.
d.
Abdominal X-ray Non-specific findings

Colonoscopy Risk of perforation
RLQ Ultrasound Non-specific findings
Laparoscopic Appendectomy
MTB S2CK
p. 389
18
Right Lower Quadrant Pain
Abdominal Abscess
Age > 60 yo?

Yes
Cause
Surgical complication (#1)
Inflammatory disease
Trauma
No
Cecal Diverticulitis
Male or Female?
Make NPO, Place NG Tube

Broad-Spectrum Abx
Female
Male
Order -HCG, Pelvic US

Appendicitis
Emergent
Laparoscopic
Appendectomy
Normal
Elevated or
Abnormal
Ovarian Torsion
Ectopic Pregnancy
Doppler US to
diagnosis
Laparoscopic
surgery
Emergent Surgery
Signs/Symptoms
Abdominal pain/distension
Non-specific symptoms
Fever/chills
GI symptoms nausea/vomiting, diarrhea
Rectal fullness
MTB S2CK
Abdominal Abscess
p. 390
Abdominal Abscess
Diagnosis
Abdominal CT
Visual evidence of abscess
Information about surrounding
structures
Source: Joel McFarland, Medpix 28716
MTB S2CK
p. 390
Abdominal Abscess
Diagnosis
Abdominal CT
Visual evidence of abscess
Information about surrounding
structures
CBC
May show elevated WBC count
Treament
Broad-Spectrum Antibiotics
Incision + Drainage
78-year-old woman with severe LLQ pain, fever, and

anorexia of one day. Shes had dark, tarry stools in the
past. The patients husband brings in a medication list,
which includes a stool softener and iron supplements.
She displays guarding and rigidity.
What is the diagnosis?
a Ectopic pregnancy Patient
a.
P ti t is
i postmenopausal
t
l
b. Acute appendicitis Rare in elderly, RLQ in location
c. Cholecystitis RUQ pain
d. Acute diverticulitis
e. Acute pancreatitis Central abd pain, radiates to back
Percutaneous (CT-guided)
versus Open
MTB S2CK
p. 390
19
Inflammatory GI Conditions
Appendicitis
Pancreatitis
Diverticulitis
Cholecystitis
Fecolith
obstructing
appendiceal
orifice
Anorexia
Fever
Periumbilical
Pain RLQ
Fecal
obstruction of
bowel wall out
pouchings
N/V
Fever
LLQ Pain
Gallstone
obstructing cystic
duct
Antibiotics (x1)
Resection (if
recurrent)
Abscess
Diagnosis
Phys. Exam
CT Scan
Alcohol
Gallstone
obstructing
pancreatic duct
N/V
Fever
Abdominal Pain
Radiates to
back
Amylase/Lipase
CT Scan (#1)
Treatment
Laparoscopic
Removal
IV Fluids
NPO
Cause
Symptoms
Complication Abscess
MTB S2CK
Pseudocyst
CT Scan
N/V
Fever
RUQ pain
Worse with
inspiration
Ultrasound
Fluid, Stones,
Thick Wall
HIDA scan (#1)
Laparoscopic
Removal
Perforation
p. 391
Bowel Obstruction
Bowel Obstruction
Pathophysiology
A mechanical or
functional obstruction of
intestines
Leads to fluid/gas
accumulation proximal
to site off obstruction
Resulting pressure
increase leads to
1. Pain
2. Decreased perfusion
(and risk of necrosis)
MTB S2CK
Causes/Risk Factors
Obstruction can be
partial or complete
Partial = GI contents
are able to pass
obstruction site
Complete = No
avenue for passage
Represents a much
more severe condition
p. 392
Signs/Symptoms
Severe, crampy
abdominal pain
Colicky in nature
Nausea/vomiting
Fever
High-pitched,
Tinkling bowel
sounds
p. 392 393
Adhesions from
previous abdominal
surgery
#1 in developed
countries
Hernia
#1 in undeveloped
countries
Volvulus = Twisting of
bowel on its mesentery
Crohns disease
MTB S2CK Only
Bowel Obstruction
MTB S2CK
55 year-old man presents to the ED with severe, intermittent

abdominal pain and nausea/vomiting. He cannot recall when
he last passed flatus, but is certain he didnt have a bowel
movement this morning. He has type 1 diabetes and had an
open appendectomy in his 30s. Temperature of 101.8. Loud,
high-pitched bowel sounds noted on auscultation. An
abdominal plain film shows a partial small bowel obstruction.
What is the best next step in management?
a. Prescribe a laxative Will not relieve obstruction (may worsen)
b. Place an NG-tube
c. Emergent exploratory laparotomy Medical management first
d. Prescribe antibiotics No evidence of bowel perforation
e. Perform a colonoscopy Will not relieve obstruction
Neoplasms
Intussusception =
Telescoping bowel
Most frequently seen
in pediatric population
Foreign bodies
Intestinal atresia =
Blind Pouch
Only seen in
neonates
p. 393
Bowel Obstruction
Diagnosis
Labs
WBC,
pH
Lactate,
Abdominal X-ray
Air-fluid levels,
dilated loops of
bowel
20
Bowel Obstruction
Bowel Obstruction
Signs/Symptoms
Severe, crampy
abdominal pain
Diagnosis
Labs
Management
1) Make Patient NPO
WBC, Lactate, pH
Colicky in nature
Prevents further increase in bowel pressure
Abdominal X-ray
Nausea/vomiting
Fever
High-pitched, Tinkling
bowel sounds
2) Place an NG Tube (w/suction)
Air-fluid levels, dilated

loops of bowel
Lowers bowel pressure proximal to obstruction
Abdominal CT w/ oral
contrast (#1)
3) Medical Management
IV Fluids
Volume is lost due to third-spacing
Clear transition zone

correlates with
obstruction
MTB S2CK
p. 392 393
4) Surgical Decompression (if indicated)

Complete obstruction (Emergent)
Lack of improvement with medical management
MTB S2CK
p. 393
Fractures Algorithm
Diagnosis
Pain
Swelling
Bony deformity
X-rays
Timing:
Acute onset
with trauma
Neurovascular
exam
Closed
(skin intact)
Closed reduction
Open
(skin puncture)
Emergency surgery
(I&D)
Management
MTB S2CK
Fracture Types
Upper
pp Extremityy Injuries
j
Back Pain
Fat Embolism
Compartment Syndrome
Knee Injuries
Symptoms:
Orthopedics
Presentation
Surgery (ORIF)
p. 393 394
Fracture Types
Fractures Types
Stress Fractures
Cause
Compression Fractures
Cause
Vertebral fracture associated with poor
bone quality
Osteoporosis
p
((classical example)
p )
Presentation Clue
Elderly patient with back pain
33% thoracic spine, 33% thoracolumbar,
33% lumbar
Overuse injury secondary to repetitive insult to bone
Presentation Clue
High-performance athlete
Common sites
1. Metatarsals
2. Tibia
Diagnosis
CT/MRI
Treatment
Rest and rehabilitation
MTB S2CK
p. 394
MTB S2CK
p. 394
21
Fractures Types/Compression Fractures
Fractures Types
Diagnosis
X-ray
CT, if
inconclusive
Pathologic Fractures
Cause
Diagnosis
Fracture in bone
weakened by disease
Metastatic cancer
Multiple myeloma
Pagets disease
Presentation Clue
Treatment
Controversial
MTB S2CK
p. 394
X-ray
Treatment
Treat fracture
ID & treat primary
disease
Patient with fracture

after minimal trauma
Source:commons.wikimedia.org
MTB S2CK
p. 394
Upper Extremity Injuries
Upper Extremity Injuries/Clavicle Fracture
Clavicle Fracture
Cause
History of fall
Blunt shoulder trauma
Presentation Clue
Pain over anterior shoulder
Clavicle step-off
Workup
X-ray
Careful distal
neurovascular
exam
Must rule out
subclavian
artery/brachial
plexus injury
Treatment
Arm sling
Source: Mark D. Travis
MTB S2CK
p. 395
Anterior Shoulder Dislocation

Cause
Fall on outstretched hand
Sports, blunt trauma
Signs/Symptoms
Severe shoulder pain, swelling
Arm is held in external rotation
MTB S2CK
p. 395
MTB S2CK
p. 395
Upper Extremity Injuries/

Anterior Shoulder Dislocation
Diagnosis
X-ray, MRI (if
necessary)
Careful distal
neurovascular exam
Must rule out
axillary artery or
nerve injury
Treatment
Reduction w/sling
immobilization
MTB S2CK
Source: Daniel Patrick Moloney
p. 395
22
Posterior Shoulder Dislocation

Cause
History of seizure or electric shock
Signs/Symptoms
g
y p
Severe shoulder pain, swelling
Arm is held in internal rotation
MTB S2CK
p. 395

Posterior Shoulder Dislocation
Diagnosis
XR, MRI (if
necessary)
Treatment
Reduction
w/sling
immobilization
MTB S2CK
p. 395
Source: Medpix 20030
19-year old with persistent wrist pain of 3 days

duration. Pain began when he braced himself from a
fall. Right wrist is notable for point tenderness and
mild swelling at base of dorsal aspect of thumb, but
no deformity. An X-ray is shown on the next slide.
Source: Medpix 6094

19-year old with persistent wrist pain of 3 days
duration. Pain began when he braced himself from a
fall. Right wrist is notable for point tenderness and
mild swelling at base of dorsal aspect of thumb, but
no deformity. An X-ray is shown below.
What is the best next step in management?
Scaphoid may be fractured
a. Reassurance
b. MRI Scan Unnecessary, worse than CT
c. Thumb Spica Cast
d. Amputation No indication
e. Open Reduction + Internal Fixation No fracture (yet)
Trigger finger
Cause
Inflammation of finger flexor pulley system
Leads to catching/locking of flexor tendon
Signs/Symptoms
Lone digit caught in flexion
Popping sensation if digit is manually extended
Moderatesevere pain
Diagnosis
Clinical Exam
Treatment
Corticosteroid injection
MTB S2CK
p. 395
23

Dupuytrens Contracture
Dupuytrens Contracture
Cause
Risk Factors
Male > Female
Age > 40
Northern European descent
Thickening of
palmar fascia,
leading to
flexion
contracture
Diagnosis
Di
i
Clinical Exam
Digits cannot
fully extend
Treatment
MTB S2CK
p. 395
Surgery
MTB S2CK
p. 395
Back Pain
A 66-year-old man comes to his PCP with bilateral
leg pain of several months duration. The pain seems
to be worst when he has to walk several blocks, and
improves when he sits down. Leaning forward (on a
bench, shopping cart, etc.) alleviates the pain. He is a
non-smoker.
What is the most appropriate next diagnostic step?
a.
b.
c.
d.
e.
Lower Extremity XR Useful for bony trauma

Doppler US of the calf Useful for DVT evaluation
Ankle-Brachial Indices Diagnoses claudication
Spine MRI
Leg MRI Useful for soft-tissue injury/stress fractures
Spinal Stenosis
Cause
Arthritic changes result in narrowing of spinal
canal
Lumbar #1, Cervical #2
Symptoms
Neck/Back Pain
Bilateral leg/buttock pain + numbness
Pseudo-claudication
Worse with walking, improves with spine
flexion
Back Pain/Spinal Stenosis
Back Pain
Diagnosis
MRI
Treatment
NSAIDs vs.
surgery
g y
Herniated Disk Disease

Cause
Intervertebral disk herniates, compressing
spinal nerve root
Often associated with lifting injury
Most frequently seen in elderly
Symptoms
Electric Pain following a dermatome

distribution
Source: nih.gov, commons.wikimedia.org
24
Back Pain/Herniated Disk Disease
Back Pain/Herniated Disk Disease

Diagnosis
Clinical Exam
(Straight Leg
Raise)
Consider
MRI if red
flags present
Treatment
NSAIDS,
Activity
Modification
Source:Mjorter, commons.wikimedia.org
Source: user:debivort, commons.wikimedia.org
Back Pain
Back Pain
Red Flags Concern for Metastasis or Abscess
Pain not relieved

by rest
Not worse with
activity
Night pain
Constant, dull pain
> 6 weeks
Fever
Neurological
deficits
Management
MRI to evaluate for mass lesion
Emergent glucocorticoids if neurological
findings
Bowel/Bladder
incontinence
Abnormal
reflexes
History of Cancer
Fat Embolism A Medical EMERGENCY

22-year-old woman was struck by a car 3 days ago while
walking her dog. The impact broke her femur, which
required immediate surgical repair. This morning the
patient is confused and has difficulty catching her breath.
ABG shows PaO2 55 mmHg, and exam reveals a
petechial rash.
a. Myocardial infarction No rash
b. Pancreatitis Expect abdominal pain
c. Rhabdomyolysis No hypoxemia
d. Fat embolism
MTB S2CK
p. 396
Etiology
Traumatic long bone
fracture (#1 = Femur)
Releases marrow fat
into circulation
Fat vesicles are too
large to pass through
capillaries
Result is vascular
occlusion
MTB S2CK
H&E stain, lungs blood vessel with fibrinoid material and an

optical empty space indicative of the presence of lipid. Source:
Boris L Kanen, Ruud JLF Loffeld, commons.wikimedia.org
p. 396
25
Fat Embolism
Fat Embolism
Signs/Symptoms Onset 0-5 days after

fracture
Respiratory Distress (V/Q mismatch)
SOB
Tachypnea
yp
Confusion (Involves brain vasculature)
Petechial Rash (Involves skin capillaries)
Chest wall, upper extremities
Diagnosis
ABG: PO2 < 60 mmHg
CBC: Decreased platelet count
Chest X-ray: Infiltrates
Urinalysis: Fat droplets in urine
T t
Treatment
t
Respiratory Support
MTB S2CK
p. 396
Goal O2 Sat > 90%

Consider intubation/mechanical ventilation if
severely hypoxic
MTB S2CK
Compartment Syndrome/Signs & Symptoms
Pathophysiology
Injury occurs, resulting in Pressure builds,
swelling
leading to severe
tissue compression
Fracture #1 (tibial,
forearm)
Nerves
Burns
Muscle
Crush injuries
Vessels
(Reperfusion syndrome) Resulting damage can
In closed compartment
(fascial sheath, cast),
theres no escape for
increasing pressure
MTB S2CK
p. 396
lead to Volkmanns
ischemic contracture,
limb loss, or death
p. 396
Early
Findings
Pain
Parathesias
Poikilothermia
Pulselessness
Severe,
worse
with
muscle
stretch
Pins and
needles
nerve
involvement
Cold, due to
decreased
blood flow
Absent distal
pulses
(ominous
finding)
Paralysis
Pallor
Pale skin from

blood flow
MTB S2CK
Inability to move
distal musculature
p. 396 397
Knee Injuries
Treatment A Medical EMERGENCY
Basic Principles
Surgical
fasciotomy
Releases
compartment
p
pressure
Late
Findings
The 6 Ps
Ligamentous/meniscal knee injuries have similar

symptoms
Knee Pain
Swelling
Instability
The key factor is time course in

which symptoms present
Pay attention to mechanism of injury!

Physical exam provides clues to etiology
Special tests for each type of knee injury
Diagnostic test of choice is always MRI

MTB S2CK
p. 397
Source: Sarte, commons.wikimedia.org
26
Knee Injuries
Mechanism of
Injury
Symptom
Onset
MCL/LCL Trauma to
Immediate
Injury
contralateral
aspect of knee
ACL Tear Twisting or
direct impact
Exam
Maneuver
Management
Medial/Lateral
Instability
Conservative
Immediate and Anterior Drawer Arthroscopic

Repair
Severe
sign
Lachman Test
Immediate but Posterior

PCL Tear Forced
Hyperextension Mild
Drawer sign
Repair vs.
Conservative
management
Meniscal Twisting Injury Delayed (12 24 Joint line

Conservative
hours)
tenderness
Tear
McMurrays
Clicking/Locking
MTB S2CK
p. 398
22-year-old hockey star is checked by an opposing

player, and his leg gets tangled as he falls. He
experiences a popping sensation in his left knee, which
immediately swells. The team physician performs a
physical exam and notes a positive anterior drawer sign
as well as medial knee instability. He recommends an
MRI to evaluate the likely ACL and MCL tears.
What other structure will likely be injured on MRI?
a.
b.
c.
d.
Lateral Collateral Ligament Different injury mechanism

Lateral Meniscus
Medial Meniscus
Posterior Cruciate Ligament
MTB S2CK
p. 398
27

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Allergy & Immunology

Allergy & Immunology

Worst form of acute allergic reaction

Synonymous with immediate hypersensitivity

Upon re-exposure, IgE binds to mast cells leading to

Results in abnormalities that essentially define

Causes of anaphylaxis = causes of any

The best initial treatment is

Source: Fashad Bagheri. MD

Angioedema is sudden swelling of

Look for recent start of ACE inhibitors

This can be from deficiency of C1 esterase inhibitor

The best initial test...

3 types of hereditary angioedema

Allergic Rhinitis/Diagnostic Tests

IgE-dependent triggering of mast cells

Common Variable Immunodeficiency (CVID)

1. Prevention & avoidance

B cells are present but decreased Igs

LOW B cells output, normal T cells

Common Variable Immunodeficiency (CVID)

Common Variable Immunodeficiency (CVID)

Recurrent sinopulmonary infections

Other manifestations are

Clue to CVID is a decrease in the

Common Variable Immunodeficiency (CVID)

Common Variable Immunodeficiency (CVID)

X linked (Bruton) Agammaglobulinemia

Severe Combined Immunodeficiency

Low B, normal T in males

LOW B AND LOW T

LOW B cells and LOW T cells. Analogous to HIV

Severe Combined Immunodeficiency

These patients present with recurrent

Hyper IgE Syndrome

Treat infections as they arise

Wiskott Aldrich Syndrome

Chronic Granulomatous Disease (CGD)

Normal T cells normal B cells decline with age

CGD is genetic disease resulting in

Normal T cells normal B cells decline with age

Chronic Granulomatous Disease (CGD)

Chronic Granulomatous Disease (CGD)

Granulomas may become obstructive in

Chronic Granulomatous Disease (CGD)

Abnormal nitroblue tetrazolium testing

Primary Immunodeficiency Disorders

The Cardiovascular System

Coronary Artery Disease (CAD)/Definition

Can be used interchangeably with:

All imply insufficient perfusion of

48-year-old woman in office with chest pain for

Risk Factors for CAD

Which of the following is most likely to benefit a

Risk factors are most important with

a. Administration of estrogen replacement at time of

Women > men eventually die of heart disease

Risk Factors for CAD

Risk Factors for CAD

Diabetes (worst risk)

Risk Factors for CAD

Family history not a risk if

Which of the following is the most dangerous to a