USMLE Step 2 — Lesson 1: Cardiology: Myocardial Infarction

Internal Medicine Highlights

Conrad Fischer, MD

Maimonides Medical Center

Residency Director

Cardiology

Myocardial Infarction

Differential of Chest Pain

A 52-year-old man comes to the ER with 1 hour of severe chest pain on exertion. He
is nauseated and diaphoretic with slight shortness of breath. The pain does not
change with respiration or bodily position. Exam shows normal vitals, clear lungs,
no murmurs, and no tenderness.

Changes With Respiration

• Pneumonia
• Pneumothorax
• Pulmonary embolus
• Pleuritis
• Pericarditis

All can give fever - so can MI.

Changes With Position

• Pericarditis only
• when lying back causes more pain

Changes With Palpitation

• Costochondritis only
 EKG shows 2 mm of ST segment elevation in V2-V4

Anything 1 mm in 2 electrically connected leads is sufficient for diagnosing acute MI

• II, III F: Inferior wall

• : Anterior Wall
• I,L, : Lateral wall

What would you do next?

Cardiac Enzymes

Do not answer enzyme testing next:

• Takes too long to obtain results

• Treatment should be initiated first
• Won't be positive yet
• Won’t change what to do, regardless of results (positive or negative) at this time

Cardiac Enzymes
Begins to Lasts
Elevate
CPK-MB 4-6 hr 2 days
Troponin 4-6 hr 1-2 wk
Myoglobin 1-4 hr s
LDH 12-24 hr s

LDH currently is not useful. Never answer it.

Best Answers:

Which has the best sensitivity, but poor specificity?

• Myoglobin

Which has the best specificity?

 • Troponin

CPK-MB is sensitive and specific, but not as sensitive as myoglobin or as specific as troponin.

Treatment of Acute MI in ALL Patients

DecreaseTime
Mortality
Dependa
nt
Aspirin YES (25%) YES
Nitrates ?? ?
Morphine (Analgesics) ?? ?
Thrombolytic YES (25%) YES
β -Blockers YES (10-20%) NO

Special Circumstances

• Angioplasty
o Patients with major bleeding or risk of bleeding
o Patients who can’t receive thrombolytics for any reason
o Patients failing thrombolytics and progressing to hemodynamic instability
o Equal in efficacy to thrombolytics

Special Circumstances

• ACE Inhibitor
o Patients with decreased left ventricle function or CHF
• Lidocaine
o Never as prophylaxis
o All patients who develop major vertricular arrhythmias (ventricular tachycardia
or fibrillation)

Pacemakers

• Anything slow or that could become slow

 • Third-degree AV block
• Mobitz II second degree block
• Left bundle branch block

USMLE Step 2 — Lesson 2: Cardiology: Congestive Heart

Failure
Cardiology

Congestive Heart Failure

Congestive Heart Failure/Pulmonary Edema

A 67-year-old woman comes to the ER with 1-2 hours of severe shortness of breath.
She has a history of two MIs in the past. She comes with a pizza in one hand and a
bag of Doritos in the other, and she is chewing a sausage. Her respiration rate is 34;
BP, 130/82; and PUD, 18. Jugulovenous distention is present. Chest: rales to apices.
Heart:3/6 systolic murmur at Apex 1. S3 gallop. Abd: Enlarged liver.3+ Edema of
lower extremities to mid-thigh.

What would you do next?

Do Not Answer Lab Tests

• CXR:Congestion of vasculature, enlarged heart, effusion

• Arterial blood gas: Hypoxia, respiratory alkalosis
• EKG: Sinus tachycardia
• Echocardiogram (never used in acute cases): decreased ejection fraction, mitral
regurgitation, abnormal motion of anterior and, inferior walls
• Radionuclide ventriculogram:(MUGA) – never use acute scan, most accurate
method of assessing ejection fraction

Treatment of Pulmonary Edema

• Sit the patient upright

 • Give Oxygen

Treatment of Pulmonary Edema

First Step: Preload reduction

• Diuretics – any loop diuretic intravenously

• Morphine
• Nitrates

Second Step: Only if preload reduction is ineffective

• Positive inotropes
• Dobutamine
• Amrinone

Treatment of Pulmonary Edema

Third Step: Afterload reduction

• Ace inhibitors - IV
• Nitroprusside
Congestive Heart Failure

Treatment when the patient has been stabilized

• Ace inhibitors
• Diuretics
• Digoxin
• β − Blockers (carvedilol or metoprolol)

β − Blockers

• Reduce mortality
• Increase ejection fraction
• Improve symptoms

USMLE Step 2 — Lesson 3: Infectious Diseases: Intro. to

Antibiotics
Infectious Deseases

Introduction to Antibiotics

Introduction to Antibiotics

• The organisms that cause diseases have largely not changed

• The antibiotics that go with the organisms change
• The most important aspect of infectious diseases: ascribe the antibiotics that go
with each group of organisms
• Think in terms of groups of antibiotics

Gram-positive Cocci: Staphylococcus and Streptococcus

• Penicillins:
o Oxacillin
o Cloxacillin
o Dicloxacillin
 o Nafcillin

Gram-positive Cocci: Staphylococcus and Streptococcus

With mild penicillin allergy

• First-generation cephalosporins:
o Cefazolin
o Cephalexin
o Cephradine
o Cefadroxil

Gram-positive Cocci: Staphylococcus and Streptococcus

With severe penicillin allergy

• Clindamycin
• Macrolides (erythromycin, clarithromycin, azithromycin): Used for minor, non-life-
threatening infections
• Vancomycin, Synercid, Linezolid: Used for gram-positive infections with life-
threatening allergy to penicillin and methicillin-resistant Staphylococcus

Gram-negative Bacilli

For E. coli, Proteus, Enterobacter, Klebsiella, Morganella, and Pseudomonas, ALL of

following provide >90% coverage:

• Aminoglycosides (gentamicin, tobramycin, amikacin)

• Aztreonam
• Quinolones (ciprofloxacin, levofloxacin)

Gram-negative Bacilli

For E. coli, Proteus, Enterobacter, Klebsiella, Morganella, and Pseudomonas, ALL of

following provide >90% coverage:

• Carbapenems (imipenem, meropenem)

• Extended-spectrum penicillins (piperacillin, ticarcillin, azlocillin, mezlocillin)
• Third-generation cephalosporins (especially ceftazidime)
• Fourth-generation cephalosporins (especially cefepime)

Second-generation cephalosporins (eg, cefoxitin, cefotetan,

cefuroxime)

• Good for gram-positive coverage like first-generation cephalosporins

• Good for gram-negative coverage but NOT for Pseudomonas
• Cefoxitin and cefotetan are good for anaerobes

Anaerobes

Oral anaerobes (anything above the diaphragm)

• Clindamycin
• Penicillin (any penicillin EXCEPT the Ox/Clox/Diclox/Naf group)

Abdominal anaerobes (below the diaphragm)

• Metronidazole
• Imipenem
• Second-generation cephalosporins
• Beta-lactam/ Beta-lactamase inhibitor combinations

Antivirals

Herpes simplex and varicella

• Acyclovir, valacyclovir, famciclovir

Herpes simplex, and varicella AND Cytomegalovirus

 • Ganciclovir, foscarnet, cidofovir

Antivirals

Influenza

• Oseltamivir, zanamivir
• Amantadine, rimantadine: Becoming archaeologic

Hepatitis B

• Lamivudine or interferon

Hepatitis C

• Interferon and ribavirin in combination

Antifungals

Life-threatening infections (eg, endocarditis, meningitis, fungemia)

• Amphotericin

Candida infections

• Azoles
• Fluconazole, ketoconazole, itraconazole

Onychomycosis

• Terbinafine, itraconazole

Griseofulvin is as useful as a rotary telephone

USMLE Step 2 — Lesson 4: Central Nervous System Infections

Infectious Deseases

Central Nervous System Infections

Central Nervous System Infections

A 48-year-old man comes to the ER with 1 day of fever, headache, nausea.

What could this be?

ANY of the CNS infections can present with fever, headache, and
nausea. To determine which one, the question will provide the
following clues:

Meningitis

• The patient also has photophobia and nuchal rigidity (stiff neck) on exam.

Encephalitis

• The patient is disoriented confused and lethargic with difficulty thinking.

ANY of the CNS infections can present with fever, headache, and
nausea. To determine which one, the question will provide the
following clues:

Abscess

• The patient has focal neurological deficits found on examination.

Note: There is considerable overlap between these diseases. If the question state
that he has a stiff neck AND confusion/lethargy AND focal findings, then neither you
nor anyone else could determine the precise diagnosis.

Which patients require a CT scan of the head BEFORE lumbar

puncture?
 • Focal findings
• Papilledema
• Altered mental status

If CT is required before lumbar puncture, ALWAYS answer give

treatment (ceftriaxone) before the lumbar puncture:

• Treatment is more important than the specific diagnosis

• Cell count, chemistry (protein level), gram-stain, and bacterial antigen testing can still
give the diagnosis if the antibiotics sterilize the culture

Meningitis

Diagnostic testing on lumbar puncture: Everything depends on the specific question

asked!

• MOST SPECIFIC test is CULTURE

• MOST SENSITIVE test is PROTEIN
• NEXT BEST or BEST INITIAL test on CSF is CELL COUNT. (Cell count is not as
specific as culture or as sensitive as protein level but it is the best combination of
both.)

Cultures

In general, “culture” is the answer to the

“What is the BEST - Most Accurate - Most Likely to lead to specific diagnosis” type
of question.

HOWEVER:Don’t answer, “Wait for the cultures before initiating treatment.”

Meningitis

A 48-year-old man comes to the ER with 1 day of fever, headache, and nausea. He
 has photophobia and a stiff neck. He has no focal neurological deficits or papilledema
and is fully oriented and alert. Lumbar puncture shows an elevated protein, cell count
of 3,502, and a negative gram stain. Culture is sent.

Which type of meningitis is this?

Cell Count on CSF

Any type of meningitis can cause an elevated cell count; the differential on the cell count gives
more specific information.

Neutrophils – Bacterial:

• Streptococcus pneumonia: most common

• Neisseria: look for a rash, particularly a petechial rash in the presentation
• Haemophilus: particularly in children, although greatly diminished because of
vaccination

Treatment of Bacterial Menigitis

Cell Count on CSF

Lymphocytes (look for these specific features):

• Rocky Mountain spotted fever: rash on wrists/ankles, moving centrally towards the
body
• Lyme: Facial palsy, target lesion rash (erythema migrans)
• Cryptococcus: HIV+ patients with <100 CD4 cells
• TB: Very high protein in CSF,and very low glucose, TB in lungs
• Viral: Everything negative; no particular association. Exclude the other causes

Treatment of Bacterial Meningitis

A 48-year-old man comes to the ER with 1 day of fever, headache, nausea. He has
photophobia and a stiff neck. He has no focal neurological deficits or papilledema and
 is fully oriented and alert. Lumbar puncture shows an elevated protein, cell count of
3,502, and a negative gram stain. Culture is sent. The differential shows 92%
neutrophils.

What is the best initial therapy?

Treatment of Bacterial Meningitis

What is the best intial therapy?

Ceftriaxone unless T-cell immune deficit present.

Ceftriaxone AND Ampicillin if there is steroid use, neutropenia, pregnancy lymphoma,

leukemia, HIV or if the patient is elderly or a neonate. Ampicillin covers Listeria.

Treatment of Bacterial Meningitis

A 48-year-old man comes to the ER with 1 day of fever, headache, nausea. He has
photophobia and a stiff neck. He has no focal neurological deficits or papilledema and
is fully oriented and alert. Lumbar puncture shows an elevated protein, cell count of
3,502, and a negative gram stain. Culture is sent. The differential shows 92%
neutrophils.

What is the best initial therapy?

Treatment of Bacterial Meningitis

What is the best intial therapy?

Ceftriaxone unless T-cell immune deficit present.

Ceftriaxone AND Ampicillin if there is steroid use, neutropenia, pregnancy lymphoma,

leukemia, HIV or if the patient is elderly or a neonate. Ampicillin covers Listeria.

USMLE Step 2 — Lesson 5: PPD Testing

Infectious Diseases

PPD Testing
PPD Testing

When to use the PPD? What's it for?

To screen the asymptomatic: do not use as primary method for diagnosing TB in acutely
symptomatic patients

What is considered a positive PPD?

• >10 mm induration, not erythema in most patients; >5 mm in HIV+ patients and close
contacts
• Always get CXR after a positive PPD
• Treatment for a positive PPD means INH alone

Treat all PPD+ patients if the risk of developing TB is greater than risk of hepatitis from the
isoniazid:

• ANY recent (past 2 years) converter

• ANYONE with severe immune deficiency (eg, HIV, steroid use, leukemia, diabetes,
lymphoma)
• ANYONE <35 years old

What is the effect of BCG on these recommendations?

BCG has NO effect on these recommendations.

Which of the following patients should receive isoniazid

prophylactic therapy?

• A 19-year-old, HIV- woman entering college with 8 mm of induration and a negative

test last year.

Which of the following patients should receive isoniazid

prophylactic therapy?

• A 32-year-old, HIV- physician from India who received BCG as a child and has never
been tested before. She has 12 mm of induration at health screening before starting
an internship in the US.

Which of the following patients should receive isoniazid

prophylactic therapy?

• A 47-year-old HIV+ man who had never been tested before and has 7 mm of
induration.
• A 95-year-old, HIV-, female nursing home resident who was PPD- last year and has
11 mm of induration this year.

Which of the following patients should receive isoniazid

prophylactic therapy?

• A 3,725-year-old Egyptian mummy who was PPD- last year and is PPD+ this year.

Which of the following patients should receive isoniazid

prophylactic therapy?

The 19-year-old woman: NO

The 32-year-old physician: YES
The 47-year-old-HIV+ man: YES
The 95-year-old nursing home resident: YES

The 3725-year-old Eqyptian mummy:

YES, YES, YES!

USMLE Step 2 — Lesson 6: HIV

Infectious Diseases

HIV
HIV

A 37-year-old man comes to your office after having been recently diagnosed with
HIV. He has no symptoms. His physical examination is normal. His CD4 count is
575, and his viral load is 1,000.

Which medications are appropriate for this patient?

None for this patient: CD4>500, viral load <20,000

Antiretroviral Medications and their most common adverse

effects

Nucleoside reverse transcriptase inhibitors

• Zidovudine (anemia)
• Didanosine (pancreas, neuropathy)
• Stavudine (pancreas, neuropathy)
• Zalcitabine (pancreas, neuropathy)
• Lamivudine

Protease inhibitors: hyperlipidemia, hyperglycemia

• Nelfinavir
• Ritonavir
• Indinavir
• Saquinavir
• Amprenavir

When to start therapy?

CD4 < 500 or viral load > 20,000

What to start?

Any two reverse transcriptase inhibitors AND any protease inhibitor

A 37-year-old man comes to your office after having been recently diagnosed with
HIV. He has no symptoms. His physical examination is normal. His CD4 count is
575, and his viral load is 1,000.

NONE for this patient: CD4 >500, viral load <20,000

A 37-year-old man comes to your office after having been recently diagnosed with
HIV. He has no symptoms. His physical examination is normal. His CD4 count is
275, and his viral load is 1,000.

What medications are appropriate?

Any two nucleosides AND a protease inhibitor

A 37-year-old man comes to your office after having been recently diagnosed with
HIV. He has no symptoms. His physical examination is normal. His CD4 count is
575, and his viral load is 71,000.

What medications are appropriate for this patient?

Any two nucleosides AND a protease inhibitor

A 37-year-old man comes to your office after having been recently diagnosed with
HIV. He has no symptoms. His physical examination is normal. His CD4 count is
175, and his viral load is 31,000

Any two nucleosides AND a protease inhibitor AND . . .

Pneumocystis Prophylaxis: when the CD4 <200

Trimethoprim/Sulfamethoxazole(first choice) Dapsone Atovaquone

A 37-year-old man comes to your office after having been recently diagnosed with
HIV. He has no symptoms. His physical examination is normal. His CD4 count is 45,
and his viral load is 31,000.

Any two nucleosides AND a protease inhibitor +

 trimethoprim/sulfamethoxazole AND . . . Mycobacterium avium complex
prophylaxis: when the CD4 <50

Azithromycin (once a week)

A 37-year-old man comes to your office after having been recently diagnosed with
HIV. He has no symptoms. His physical examination is normal. His CD4 count is 5,
and his viral load is 371,000
.
Any two nucleosides AND a protease inhibitor AND
trimethoprim/sulfamethoxazole AND azithromycin AND…

NOTHING!!

USMLE Step 2 — Lesson 7: Hematology: Microcytic Anemia

Hematology

Microcytic Anemia

Microcytic Anemia

A 32-year- old woman presents with several weeks of fatigue. She complains of
nothing else. Initial CBC reveals an hematocrit of 28%.

Symptoms of anemia are largely based on severity not etiology. Iron deficiency
with hematocrit of 28% will give the same symptoms and the anemia of chronic
disease, folate deficiency, thalassemia, etc, with hematocrits of 28%.

A 32-year-old woman presents with several weeks of fatigue. She complains of

nothing else. Initial CBC reveals hematocrit of 28%. The other portions of the CBC
are normal, and the MCV is 70 (normal 80-100).

What is the most likely diagnosis?

After determining that the patient has anemia, the next most useful step is to
determine the cell size. This is the next easiest clue as to the etiology of the
 anemia.

Low MCV

• Iron deficiency
• Anemia of chronic disease (can also be normocytic)
• Sideroblastic
• Thalassemia

High MCV

• Vitamin B12 deficiency

• Folate deficiency
• Alcohol
• Drug toxicity

Normal MCV

• Hemolysis

A 32-year-old woman presents with several weeks of fatigue. She complains of

nothing else. Initial CBC reveals an hematocrit of 28%; other portions of the CBC are
normal, and MCV is 70 (normal 80-100).

What is the next best step in the management of this microcytic patient? (ie:
What is the best initial diagnostic test?)

What is the next best step in the management of this microcytic

patient?

Iron Studies

• Iron deficiency: low ferritin, high iron binding capacity

• Chronic disease: high ferritin, low iron binding capacity
• Sideroblastic: high serum iron
 • Thalassemia: normal iron studies

After the iron studies, how would you address other questions
about the specifics of the various low MCV anemias? (“What is
the most accurate diagnostic test?”)

Iron Deficiency

• High red cell distribution of width (RDW)

• What is the most specific test? Bone marrow for stainable iron.

Sideroblastic anemia
What is the most specific test? Prussian blue stain for ringed sideroblasts
Thalassemia
What is the most specific test? Hemoglobin electrophoresis

What is the best therapy for this patient?

Iron Deficiency

• Iron replacement
• Ferrous sulfate tablets

Chronic Disease

• Correct the underlying disease

What is the best therapy for this patient?

Sideroblastic anemia

• Pyridoxine

Thalassemia trait
 • No therapy

USMLE Step 2 — Lesson 8: Hematology: Macrocytic Anemia

Hematology

Macrocytic Anemia

A 32-year-old woman presents with several weeks of fatigue. Initial CBC reveals an
hematocrit of 28%.

Symptoms of anemia are largely based on the severity not the etiology. Iron
deficiency with hematocrit of 28% will give the same symptoms and the anemia
of chronic disease, folate deficiency, thalassemia, etc, with an hematocrit of
28%.

A 32-year-old woman comes to the office with several weeks of fatigue. In addition,
she complains of a sensation of pins and needles in her hands and feet. She drinks
almost a quart of vodka per day. Initial CBC reveals an hematocrit of 28%. The MCV
is 120 (normal 80-100).

What is the next best step in the management of this macrocytic patient?

Macrocytic anemia is largely due to either vitamin or folate deficiency, although

several drug toxicities (eg, severe alcoholism, zidovudine or methotrexate use) can do
it as well. You do NOT need neurological symptoms to have anemia from
deficiency. However the presence of neurological symptoms means it cannot be folate
deficiency alone. Alcohol can give neurological symptoms as well.

Which neurological problems can occur with B12 deficiency?

• Motor, sensory, psychiatric, ataxia, position, vibratory, cognitive, autonomic, sexual

 • ANY neurological symptom can occur with deficiency

Which is the most common neurological symptom with B12 deficiency?

• Peripheral neuropathy

B12 Deficiency

What is the best intial test?

Presence of hypersegmented neutrophils and a low B12 level (NOT a Schilling test).

Folate Deficiency

What is the best initial test?

Presence of hypersegmented neutrophils and a low folate level.

Alcohol or other drug toxicity

What is the best initial test?

Absence of hypersegmented neutrophils and to exclude the B 12 and folate deficiency
and look for the drug in the history.

What are the specific tests you would do to determine the

specific etiology of the B12?

• Elevated methylmalonic acid and elevated LDH are characteristic of deficiency.

• Antibodies to intrinsic factor and an elevated gastrin level are characteristic of
pernicious anemia
• Schilling’s test is the least often used but most specific way to determine precisely
how a patient is malabsorbing . Do NOT answer Schilling’s test if the case gives
you the elevated LDH, antibodies to intrinsic factor and elevated gastrin level.
What is the best therapy?

• B12 deficiency: Replace the B12

• Folate deficiency: Replace the folate
• Drug/Alcohol toxicity: Stop the drug/alcohol

USMLE Step 2 — Lesson 9: Hematology: Hemolysis

Hematology

Hemolysis

Hemolysis

A 42-year-old man is admitted to the hospital because of weakness, fatigue, and dark
urine. On examination he appears jaundiced with scleral icterus. Initial CBC shows an
hematocrit of 28% with a normal MCV. His indirect bilirubin, LDH level and
reticulocyte count are all elevated.

What is the cause of his anemia?

All forms of hemolysis present with elevated LDH levels, reticulocyte count, and
indirect bilirubin. The dark urine can be either from hemoglobin filtered into the urine
in intravascular hemolysis or from the bilirubin alone. Sometimes the MCV can be
slightly elevated because reticulocytes are slightly larger.

Which clues in the history will tell you which type of hemolytic
anemia it is?

• Autoimmune:Lupus, lymphoma, leukemia, rheumatoid arthritis, viral infections,

penicillin or quinidine use
• Glucose 6 phosphate dehydrogenase deficiency (G6PD): Very sudden onset,
current infection, oxidant stress from drugs (eg, dapsone, primaquine, or sulfa) or fava
bean ingestion
Which clues in the history will tell you which type of hemolytic
anemia it is?

• Paroxysmal nocturnal hemoglobinuria (PNH): Dark morning urine, major venous

thrombosis such as the portal vein
• Hemolytic uremic syndrome (HUS): Renal failure and thrombocytopenia

Which clues in the history will tell you which type of hemolytic
anemia it is?

• Thrombotic thrombocytopenic purpura (TTP): Renal failure and thrombocytopenia

and neurological symptoms and fever
• Hereditary spherocytosis: Splenomegaly

Which diagnostic testing is useful to distinguish between these?

All EXCEPT the hereditary spherocytosis can also give:

• low haptoglobin level

• hemoglobinuria
• Hemosiderinuria

Hereditary spherocytosis will not give these because it is extravascular hemolysis.

Extravascular means it occurs in the spleen.

Which of the following tests is the “most specific”, “most

accurate”, and “most likely to lead to a definite diagnosis” in
each of these forms of anemia?

• Autoimmune: Coombs test

• G6PD: G6PD level
• PNH: Sugar-water and Ham’s test
• HUS: Finding renal failure and thrombocytopenia with hemolysis; no specific test
 • TTP:Finding renal failure, thrombocytopenia, and neurological symptoms and fever
with hemolysis; no specific test
• Hereditary spherocytosis:Spherocytes on the smear AND an osmotic fragility test

Which of the following is the best intitial therapy and most

definitive therapy?

• Autoimmune:: Initially, steroids; with life-threatening hemolysis, IV immunoglobulin;

recurrent, splenectomy
• G6PD:Avoid the oxidant stress
• PNH:Steroids
• HUS:Initially, spontaneous resolution; with life-threatening disease, plasmapheresis
• TTP:Plasmapheresis
• Hereditary spherocytosis:Splenectomy

USMLE Step 2 — Lesson 10: Nephrology: Acute Renal Failure

Nephrology

Acute Renal Failure

An 87-year-old woman with a history of gout and osteoarthritis is found on the floor of
her apt. by her family. It is not clear how long she has been on the floor. She uses
NSAIDs for joint pain. In the ER she is found to be confused. Her temperature is 102
F, pulse is 117, and systolic BP blood is 92; rales are heard on lung examination. She
has a head CT with contrast to evaluate her confusion and receives penicillin and
gentamicin for her pneumonia. She has no urine output since admission. On hospital
day 2 her BUN and creatinine begin to rise.

How many causes of renal failure can you identify in this

patient?

The first step in evaluating a patient with acute renal failure is to determine whether
 there is a problem inside the kidney (tubules, glomeruli, vascular) or with the
perfusion of the kidney (prerenal) or drainage out of the kidney (postrenal).

The fever, tachycardia, relatively low BP, and the fact that she was found on the
floor are all sufficient suggestions of pre-renal azotemia.

The best initial tests to determine whether it is pre-renal

azotemia is as follows:

Pre-renal Acute Tubular

Necrosis
BUN/Creatini > 20:1 10.1
ne
Ratio
Urine Sodium Low < 20 High > 40
Urine High > Low < 350
Osmolality 500

To exclude post-renal azotemia (obstruction to drainage OUT of

the kidney) the following are useful:

• Physical examination to detect enlarged bladder

• Ultrasound to look for bladder size and hydronephrosis
• Urinary catheter placement

Do NOT assume that the decreased urine output described is from the renal failure. The renal
failure could simply be from decreased urine output and obstruction.

Intra-renal Damage (ATN)

Damage to the kidney could affect tubules, glomeruli, or vasculature. It is NOT very
useful to think of the diseases as cortical or medullary. Glomerular diseases, eg,
lupus, Goodpasture, Alport syndrome, Berger disease, or even post-streptococcal
disease, are unlikely to occur this acutely and without other history of systemic
disease. The same is true of vascular diseases, eg, polyarteritis nodosa, Wegener
granulomatosis, TTP, HUS, or Henoch Schonlein purpura.
Intra-renal Damage (ATN)

Acute renal failure such as this is most often from tubular diseases, which are most
often from various toxins combined with possible ischemia from hypoperfusion.

How many different toxins can you identify in this case?

An 87-year old woman with a history of gout and osteoarthritis is found on the floor
of her apartment by her family. It is not clear how long she has been on the floor. She
uses NSAIDs for joint pain. In the ER she is found to be confused. Her temperature is
102 F, pulse is 117, and systolic BP blood is 92; rales are seen on lung examination.
She has a heat CT with contrast to evaluate her confusion and receives penicillin
and gentamicin for her pheumonia. She has no urine output since admission. On
hospital day 2 her BUN and creatinine began to rise.

You could simply say that the tubular diseases are from toxins. However, since
the answers to questions concerning initial and best tests and treatments are
different, they must be subdivided so they can be addressed individually.

Direct Toxins

Gentamicin acts directly as a toxin to the kidney's tubule. Other drugs include
amphotericin, cisplatin, NSAIDs, and cyclosporine. Contrast agents also act in the
same way.

Best test: Exclude other causes of renal failure. There is no test to determine the
specific etiology of any toxin-mediated organ toxicity. Biopsy will NOT determine the
specific agent.

Direct Toxins:

Best therapy: Stop the offending agent. There is no specific therapy to reverse ANY
toxin-mediated organ damage beyond this. Dialysis does NOT reverse the damage; it
supports the patient while waiting for the kidneys to come back to life on their own.
Allergic Interstitial Nephritis:

Penicillin causes damage to the kidney, as it causes an allergic reaction against the
kidney tubule. Other drugs include sulfa drugs, allopurinol, phenytoin, rifampin and
NSAIDs.

Keys to recognizing this as the cause of the renal failure are fever and rash,
although these do not have to be present.

Allergic Interstitial Nephritis:

Best initial test: Measure blood and urinary eosinophils. IgE levels are not
sufficiently sensitive. Renal biopsy is the most accurate test but should seldom, if
ever, be used.

Best initial therapy: Stop the medications. Very severe cases can be treated with
steroids.

Crystals:

Uric acid crystals from the gout as well as from oxalate crystals from ethylene glycol
ingestion can also damage the tubules. Look for gout or ethylene glycol ingestion in
the history.

Best initial test: Urinalysis to look for crystals.

Therapy: Either allopurinol for gout or ethanol infusion for the ethylene glycol
ingestion.

Pigments:

Myoglobin from rhabdomyolysis and hemoglobin from hemolysis are directly toxic to
the tubule. The fact that this patient was found lying on the floor of her apartment is
suggestive of rhabdomyolysis. Clues to pigments as the cause of the renal failure are
hemolysis or muscle breakdown, as dark urine, on history.

Pigments:
 Best initial tests: EKG to exclude signs of life-threatening hyperkalemia and
urinalysis to show dipstick positive for blood with no RBCs on the microscopic
examination.

Most accurate and specific tests: Myoglobin in urine and elevated CPK level in
blood for rhabdomyolysis.

Best initial therapy: Hydration and alkalinization of the urine with bicarbonate.

USMLE Step 2 — Lesson 11: Nephrology: Hyponatremia

Nephrology

Hyponatremia

A 59-year-old man with a history of lung cancer 1 cm from his carina is admitted to the
hospital because of mild confusion, which has developed over the past several days.
His sodium level is 119 (normal 135-145)

What is the etiology of his hyponatremia?

The first step in evaluating hyponatremia is to determine the

volume status of the patient.

• Hypervolemic (presence of rales, edema, jugulovenous distention):

o Congestive heart failure
o Nephrotic syndrome
o Cirrhosis

The first step in evaluating hyponatremia is to determine the

volume status of the patient.

• Hypovolemic (orthostasis, dry mucous membranes, decreased skin turgor):

o GI fluid loss
o Urinary loss, diuretics
o Skin losses, sweating, fever, burns
 • The above also require replacement with free water to drive sodium down

The first step in evaluating hyponatremia is to determine the

volume status of the patient.

Normal volume:

• Addison’s disease does not require free water to drive the sodium down.
• Psychogenic polydipsia
• Pseudohyponatremia
• Syndrome of inappropriate antidiuretic hormone (SIADH)
• Hypothyroidism

A 59-year-old man with a history of lung cancer 1 cm from his carina is admitted to the
hospital because of mild confusion, which has developed over the past several days.
His sodium level is 119 (normal 135-145). Physical examination reveals normal
skin turgor and no orthostasis, edema, or rales.

What is the best initial test?

If a normal person’s sodium were suddenly driven below normal, the body’s response
would be to immediately shut off all ADH secretion, allowing the maximal amount of
free water to be released. The normal response would be to maximally dilute the
urine. The normal response to hyponatremia would be to have a urine osmolality at
the lowest possible amount. The range of urine osmolarity is 50-1200 mOsm/kg. The
normal response would be urine osmolarity around 50 mOsm/kg and urine osmolality
less than serum osmolarity. Urine sodium should also be low.

The best initial test is the

urine osmolality

A 59-year-old man with a history of lung cancer 1 cm from his carina is admitted to the
 hospital because of mild confusion, which has developed over the past several days.
His sodium level is 119 (normal 135-145). Physical examination reveals normal skin
turgor and no orthostasis, edema, or rales. His serum osmolality is 250 mOsm/kg
(normal 280-300), urine osmolality is 425 mOsm/kg and urine sodium is 42
mEq/L.

What is the best therapy for this patient?

• The urine osmolality in this patient is higher than the serum osmolality. Combined with
a high urine sodium level this is confirmatory of SIADH. We do not use ADH levels.
• Therapy for SIADH is divided as follows:

Mild, asymptomatic hyponatremia: Fluid restriction to 1/L/day

• Moderate hyponatremia with mild or moderate neurological symptoms: Saline infusion

and loop diuretic
• Severe hyponatremia with severe symptoms: 3% hypertonic saline sometimes
combined with diuretic

What are the complications of changing sodium levels too

rapidly?

(>1-2 mEq/L/hr)

• Too rapid a RISE => central pontine myelonolysis

• Too rapid a DROP => cerebral edema

The patient described above has his sodium corrected by normal saline infusion and
a diuretic. His neurological symptoms resolve.

What is the next best step in his management?

 This patient’s underlying problem probably can’t be corrected; lung cancer at the
carina typically can’t be resected. Hence, as soon as the saline and diuretic therapy is
stopped the hyponatremia will recur. He will probably not be thrilled with maintaining
lifelong fluid restriction.
What is the management of chronic SIADH?

Demeclocycline to block the effect of the ADH at the level of the kidney tubule
on a chronic basis.

USMLE Step 2 — Lesson 12: Nephrology: Hyperkalemia

Nephrology

Hyperkalemia

A 27-year-old man presents to the ER at your hospital after having just taken the
physical exam to join the NY City Fire Department. As part of this exam he must do
50 push-ups followed by suddenly lifting a 175-lb bag of sand. He then has to run up
and down 3 flights of stairs and across a balance beam followed by 50 more push-
ups. He comes to see you because of severe muscle pain, muscle tenderness, and
dark urine developing over the next several hours.

What is the most important first step in his management?

The patient seems to have rhabdomyolysis on the basis of severe, sudden exertion.
Several tests are needed: CPK level, urinalysis looking for blood on dipstick, urine
microscopic exam, potassium level, and possibly urine myoglobin level. However, you
must choose the MOST URGENT test. No matter how high the CPK level is,
hyperkalemia is more immediately life-threatening. Even if the potassium level is
elevated, it is more important to know whether there are EKG abnormalities from the
hyperkalemia, which mean he will suddenly die of an arrhythmia.

The EKG shows peaked T-waves

What is the NEXT best step in management?

Calcium chloride or calcium gluconate is given intravenously

What is the NEXT best step in management?

Half normal saline infusion and bicarbonate as well as an

ampule of 50% dextrose is given with insulin.

The original potassium level (on entry, before therapy) comes back at 7.9 mEq/L. His
CPK level is markedly elevated at 48,000 and the urinalysis is dipstick positive for
blood, but no RBCs are seen on microscopic exam.
What is the NEXT best step in management?

The fluid and bicarbonate infusion is continued.

• Kayexalate is given orally to remove potassium from body.

• Repeat potassium level 2 hours later is 6.8 mEq/L. A further level 2 hours after that is
5.8 mEq/L.

USMLE Step 2 — Lesson 13: Emergency Medicine: Overdose

Emergency Medicine

Overdose

A 25-year-old medical student gets very depressed while preparing for USMLE Step
2. After finishing studying at midnight she takes a bottle of pills at 12:15 am in an
attempt to commit suicide. She removes the label from the bottle so no one can
determine what she took. After 12:15 she finds that her last practice test score was
87% and she will easily pass. She walks across the street to the ER at 12:30 am to
seek treatment.

What is the best initial step in the management of this patient?

Ipecac is given immediately

Gastric emptying with ipecac has limited utility because it must be given within the
 first hour of management. Do NOT give ipecac with ingestions of caustic substances
since they will burn the GI tract and mouth on their way out.

Do NOT answer “toxicology screen.” This takes too long to come back to be useful
and it will not change management. No matter what pills she took, the initial answer in
the first hour of management is to empty the stomach.
Why NOT the gastric lavage?

Gastric lavage with an oropharyngeal hose is not very useful, and most awake
patients do not need this and will not tolerate it. Use gastric lavage in patients with an
acute overdose who have an altered mental status in the first hour after a pill
ingestion. You cannot give ipecac to these patients because they will aspirate.

• Perform endotracheal intubation with gastric lavage to protect the airway when
the patient has altered mental status.

Do NOT lavage patients with caustic, acid or alkali ingestion.

After the ipecac, what is the NEXT best step in

management?

Activated charcoal

Charcoal is useful in almost all overdoses and is not dangerous in anybody. In

addition, charcoal will even remove drug from the body that has already been
absorbed into the blood stream.

A 25-year-old medical student gets very depressed while preparing for USMLE Step
2. After finishing studying at midnight she takes a bottle of pills at 12:15 am in an
attempt to commit suicide. She removes the label from the bottle so no one can
determine what she took. At 12:30 am she finds that her last practice test score was
87% and she will easily pass. She walks across the street to the ER at 1:00 am to
seek treatment.
 The patient is confused, disoriented, lethargic, sleepy, and
obtunded and is not thinking so well.

What is the best initial step in the management of this patient?

• Naloxone
• Thiamine
• Dextrose

Although you will want to intubate the patient to perform gastric lavage,
you must FIRST give the naloxone, thiamine, and dextrose. If the
patient took an opiate or is hypoglycemic she will awaken immediately.
You will NOT have to do lavage then because the problem will have
been solved.

She awakens after being given the naloxone, dextrose and thiamine.
What is the NEXT best step in management?

Activated charcoal for the same reasons as described above.

After this management, then toxicology and specific drug levels are used to determine
the specific etiology of the overdose.