Laboratory

Interpretation
.

.
KIDNEY
Creatinine
Creatine is synthesized in the liver. It is the chief
source of high-energy phosphocreatine for
muscle metabolism.
It loses water to become creatinine, all of which
is excreted.
Use for renal function
case
Male 60 years old came with fatigue
BUN=40/Cr=2
This is renal failure renal /prerenal?
Old man will lose muscle mass that makes low
Cr.
It might be prerenal or renal failure. You will ask
for U/A to look for sp.Gr.
Urine hCG
Normal pregnancy -secreted first by
trophoblastic cells of conceptus and later by
placenta
positive as early as 4 days after expected date of
menstruation
it is >95% reliable by the 10th to the 14th day.
Human chorionic gonadotropin (hCG) increases
to a peak between the 60th and 70th days then
decreases progressively.
Urine hCG
False-Positive Result
-Drugs, e.g., chlorpromazine, phenothiazines
-Bacterial contamination
-Protein or blood in urine
False-Negative Result
-Dilute urine
-Missed abortion
-Dead fetus syndrome
Hematuria
<3% of normal persons ( 3 RBCs/HPF )
18% of persons after very strenuous exercise.
The source of microscopic hematuria
remains obscure in ~70% of cases after
workup.
Nonglomerular Hematuria
Caused By
Trauma
Hemoglobinopathies
Polycystic disease
GU tract tumors, infections
Hematuria in Children

Caused By
-Glomerular Causes
Acute postinfectious GN
Membranoproliferative GN
IgG-IgA nephropathy (Berger disease)
Hereditary nephritis (Alport syndrome)
SLE
Renal infarction
Henoch-Schnlein purpura
-Nonglomerular Causes
Polycystic kidneys
Renal tumors
Hydronephrosis
GU tract infection, foreign body, calculi, etc.
Ketonuria
is diagnosed when ketone bodies (acetone, beta-
hydroxybutyric acid, acetoacetic acid) appear in
urine.
Use Screening for ketoacidosis, especially in
diabetes mellitus when blood is not immediately
available
case
30 year-old Female came with kussmual
breathing and underlying DM
Her BS= 500, Hco3=10,urine ketone-neg
What is her diagnosis?

DKA
Measure serum ketone or urine ketone cannot
measure beta-hydroxybutyric acid ( measure
esp.acetoacetate /acetone)
DKA +lactic acidosis have high beta-
hydroxybutyric acid
Ketonuria
Metabolic conditions (e.g., diabetes mellitus,
renal glycosuria)
Dietary conditions (e.g., starvation, high-fat
diets)
Increased metabolic requirements (e.g.,
hyperthyroidism, fever, pregnancy and lactation)
Prerenal azotemia
specific gravity >1.030 and
Urine osmolality >500 mOsm/kg)
Proteinuria

Transient(10%)
high fever
CHF
HT
Stress exposure to cold, strenuous exercise,
seizures.

Usually <2 g/d; disappears with recovery from
precipitating cause.

Proteinuria


PERSISTENT
Glomerular
Idiopathic (e.g., membranoproliferative GN, membranous
glomerulopathy)
Secondary
Infection (e.g., poststreptococcal, hepatitis B, bacterial
endocarditis, malaria)
Vascular (e.g., renal artery stenosis)
Drugs (e.g.NSAIDS, heroine, captopril, penicillamine)
Autoimmune (e.g., SLE, RA, dermatomyositis, Henoch-
Schnlein purpura, ulcerative colitis)
Neoplasia

Microalbuminuria

Microalbuminuria is defined as persistent
proteinuria that is below detection by routine
reagent strips but greater than normal.
Microalbuminuria

patients with DM: microalbuminuria
associated with longer duration of diabetes,
poorer glycemic control, higher BP, advanced
retinopathy and neuropathy, subsequent renal
failure, and increased vascular damage and risk
for cardiovascular disease.

Bence-Jones Proteinuria
UseDetection of various gammopathies
80% of tests are true positive-Myeloma (70% )

False positive
CNT (e.g., RA, SLE, scleroderma)
Chronic renal insufficiency
Lymphoma /leukemia
Metastatic carcinoma of lung, gastrointestinal, or
GU tracts
Anuria
< 100 mL of urine in 24 hours.
Caused By
Bilateral complete urinary tract obstruction
Acute cortical necrosis
Necrotizing glomerulonephritis
Certain causes of acute tubular necrosis
Oliguria
is usually defined as excretion of less than 400
mL of urine in 24 hours(in children< 15 to 20
mL/kg/24 h)
Caused By
Prerenal causes (e.g., CHF, shock)
Postrenal causes
Renal causes
Polyuria
urine volume > 2,000 mL / day.
Caused By
Osmotic diuresis( DM)
Polydipsia(DI)
Diuretic drugs
Chronic renal failure
Partial obstruction of urinary tract with impaired
urinary concentration function
acute tubular necrosis (aminoglycosides)
CARDIO
Acute rheumatic fever
occurring 10 days to 6 weeks following an
episode of group A Streptococcus infection.
Diagnostic criteria confirmation of preceding
group A Streptococcus infection by
1.Positive throat culture
2.Increased serologic titer of antistreptococcal
antibodies

Acute rheumatic fever
Symptom+2 major / 1 major + 2 minor
Minor Criteria: High ESR or CRP, prolonged P-
R interval, fever, arthralgia
Major Criteria: Carditis, arthritis, Sydenham
chorea, subcutaneous nodules, erythema
marginatum
To determine clinical activityfollow ESR,
CRP, and WBC.
Return to normal should be seen in 6 to 12
weeks in 80% to 90% of patients
it may take 6 months
Cor Pulmonale
polycythemia
Increased blood CO2
the primary lung disease (e.g., chronic
bronchitis and emphysema
Blood lipid tests
should not be performed during stress or
acute illness (2 to 3 months after illness )
after a 12- to 13-hour fast
Myocardial Infarction
Characteristics of Serum Markers for Myocardial
Damage
Early appearance: Myoglobin, CK isoforms
High specificity: cTnI, cTnT, CK-MB, CK
isoforms

Wide diagnostic window: cTnT, cTnI, LD

Risk stratification: cTnT, cTnI, CK-MB

Predicts reperfusion: Myoglobin, cTnI, cTnT, CK
isoforms

Indicates reinfarction after 24 d: CK-MB
cTn
cTn is as sensitive as CK-MB during the first 48
hours after AMI
Specificity close to 100%. High sensitivity for 6
days.
cTnT may remain increased for 14 days.
cTn
cTnI is not increased by skeletal muscle injury,
making it more highly specific for myocardial
injury.
cTnI/ cTnT may be detected in 10% to 30% of
patients with CRF
CPK-MB
Use in
Detect reinfarction or extension of MI after
72 hours.
Document reperfusion after thrombolytic
therapy.
CK-MB usually is evident at 4 to 8 hours,
peaks at 15 to 24 hours
Serum Myoglobin
is an oxygen-carrying respiratory protein found
only in skeletal and cardiac muscle.
Earliest marker for AMI.
Increased 1 to 3 hours in >85% of AMI patients
peaks 8 to 12 hours
becomes normal in about 24 to 36 hours or less;
B-type Natriuretic Peptide
hormone secreted by myocytes in the ventricles
in response to pressure overload/myocyte
stretch
use: BNP / N-terminal (NT) proBNP.
Use in
- screening and diagnosis of CHF
-Prognostic tool for classes III and IV
-Diagnosis of left ventricular dysfunction
B-type Natriuretic Peptide
cutoff values :
BNP: 80 to 100 pg/mL
NT-proBNP: 125 pg/mL for age <75

Reading <100 pg/mL rules out CHF as cause of
dyspnea.
Reading >400 pg/mL indicates 95% likelihood
of CHF
B-type Natriuretic Peptide
Increase in BNP in right heart failure is less than
in left ventricular dysfunction
BNP and NT-proBNP can be increased in renal
failure, especially if dialysis is needed
Secondary hypertension
causes <10% of cases of hypertension.

Many causes for secondary HT=?
Secondary hypertension
Endocrine diseases
Adrenal, e.g., pheochromocytoma, Cushing syndrome
Pituitary disease, e.g., acromegaly
Hyperthyroidism, hyperparathyroidism, etc.
Renal diseases
renal artery stenosis, nephrosclerosis, embolism
Parenchymal, e.g., glomerulonephritis, polycystic
kidneys
Other, e.g., toxemia of pregnancy, polycythemia, acute
porphyria
Drugs, e.g., oral contraceptives, tricyclic antidepressants,
licorice
Toxic substances, e.g., poisoning by lead or cadmium


HT+ Hypo K
Ought to think about many
diseases?
HT+ Hypo K
Primary aldosteronism
Pseudoaldosteronism (caused by excessive
ingestion of licorice)
Secondary aldosteronism, e.g., malignant
hypertension
Hypokalemia caused by diuretic
administration
Potassium loss caused by renal disease
Cushing syndrome

Infective endocarditis (IE)
2 major criteria
1 major plus 3 minor criteria
5 minor criteria
pathologic findings (vegetation or
intracardiac abscess confirmed
histologically showing active endocarditis).
Major Criteria

Typical organism in 2 blood cultures in
absence of primary focus, or persistently
positive blood cultures drawn >1 hour apart
Involvement of endocardium by
echocardiogram or valve regurgitation
Positive serology for Coxiella burnetii (IgG
>1:800)
Bacterial or fungal DNA in blood or valve
(including Bartonella sp., Tropheryma
whipplei, other new or unusual organisms)
S. aureus bacteremia, even if nosocomial or
removable source of infection is present
Positive echocardiogram (e.g., oscillating
intracardiac mass)
Typical pathogen in IE
Streptococcus viridans [~50% of
cases]
S. bovis
Staphylococcus aureus
HACEK [Haemophilus,
Actinobacillus, Cardiobacterium,
Eikenella, Kingella]
Minor Criteria

Risk factors: predisposing heart condition / IV
drug abuse
Fever >38C (100.4F)
Vascular phenomena: septic pulmonary infarcts,
major arterial emboli, Janeway lesions
Immunologic phenomena: Osler nodes, Roth spots
Microbiologic evidence: positive blood culture
other than major criteria or positive serologic
findings (Bartonella sp. or Chlamydia sp.)
Clinical: newly diagnosed clubbing or splinter
hemorrhages , microscopic hematuria
Biochemical: CRP >100 mg/L or ESR >30 mm/h
Risk Factors
Preexisting valve disease / congenital heart
diseases
Nosocomial: most are caused by enterococci and
staphylococci. Case fatality >50%:
IV lines; S. aureus in patients with central
venous catheters, parenteral lines for feeding or
chemotherapy
Hemodialysis patients: >50% are caused by S.
aureus
S. bovis in patients with colon cancer causes 20%
of cases
Enterococcus faecalis in patients: genitourinary
procedures, pelvic infections, prostate disease
Blood culture is positive in 80% to 90% of patients:
Proper blood cultures require adequate volume
of blood, at least five cultures taken during a
period of several days with temperature 101F
or higher
Beware of negative culture due to recent
antibiotic therapy.
based on 2 cultures that are positive for the
same organism.

case
Male 60 years old came with fever
His H/C- strept. Bovis
How to treat?
Treat with antibiotic
Colonoscope finds CA colon
Prosthetic Heart Valves
Early - caused by S. epidermidis, S. aureus; also
gram-negative bacteria, fungi
Late (>60 days postoperatively). Usually caused
by streptococci., S. epidermidis
Surgery is indicated if blood culture is still
positive after 5 days of appropriate antimicrobial
therapy or recurrent infection
Syphilitic Aortitis
Syphilitic aortitis is an obliterative endarteritis of
vasa vasorum of thoracic aorta that can lead to
aneurysm formation.
Aortitis is the most common expression of late
syphilis
A positive treponemal test is seen in ~90% of
cases.

Behet Syndrome
is a systemic vasculitis -a triad of recurrent
aphthous ulcers of mouth and genitalia, and
relapsing panuveitis.
No definitive laboratory tests are available.
Giant cell arteritis (GCA)
is a systemic panarteritis of the large and
medium arteries, especially the carotid arteries.
affects the extracranial > the intracranial arteries.
Biopsy of the involved segment of temporal
artery is diagnostic

The classic triad of increased ESR (50
mm/h),anemia, and increased serum ALP is
strongly suggestive of GCA
Laboratory findings reflecting specific organ
involvement (Kidney ,CNS,Heart)
Henoch-Schnlein Purpura
is a hypersensitivity systemic vasculitis of the small
vessels with IgA deposition.
abdominal symptoms are predominant
Diagnosis is made clinically
there are no pathognomonic laboratory findings.
Coagulation tests are normal.
Renal or skin biopsy supports the diagnosis; it will
show focal segmental necrotizing GN that with
IgA and C3 deposition.

Kawasaki Syndrome
(Mucocutaneous Lymph Node
Syndrome)
is a variant of childhood polyarteritis of
unknown etiology, with a high incidence of
coronary artery complications.
Diagnosis is confirmed by histologic
examination of the coronary artery (same as
polyarteritis nodosa)+Laboratory changes
due to AMI.


Takayasu syndrome
is the term for granulomatous arteritis of the
aorta.
Diagnosis is established by characteristic
arteriographic changes or histologic
examination
Thromboangiitis Obliterans
(Buerger Disease)
is the vascular inflammation and occlusion
of medium and small arteries and veins of
limbs; it is related to smoking.
Histology shows characteristic inflammatory
and proliferative lesions
Wegener Granulomatosis (WG)
is a rare autoimmune systemic necrotizing
or granulomatous vasculitis most often
affecting the respiratory tract and kidneys.
c-ANCA is highly specific (>90%) for active
WG.
GI
Diarrhea -PMN
Shigellosis,Salmonellosis,Campylobacter,
Rotavirus,Invasive Escherichia coli colitis
Ulcerative colitis
Pseudomembranous colitis

Diarrhea no cell
Cholera
Noninvasive E. coli diarrhea
Other bacterial toxins (e.g., Staphylococcus,
Clostridium perfringens)
Viral diarrheas
Parasitic infestations (e.g., G. lamblia,
Entamoeba histolytica, Dientamoeba fragilis)
Drug related

Plummer-Vinson Syndrome
an iron-deficiency anemia associated with
dysphagia, atrophic gastritis, glossitis, etc
increased risk of cancer of the esophagus
Pseudomembranous colitis
is an antibiotic-related diarrhea and colitis
caused by C. difficile.
Tissue culture assay is gold standard

Character of stool-?

Enterocolitis, Necrotizing, in
Infancy
a syndrome of acute intestinal necrosis of
unknown etiology; it is especially associated with
prematurity and exchange transfusions.
No specific laboratory tests are available.
Persistent metabolic acidosis, severe hypoNa,
and DIC are a common triad in infants.
Infarction of the Intestine
Hematemesis, hematochezia, or melena are
present in ~15% and occult blood in <50% of
cases.
Caused by
Primary (idiopathic)
Secondary (~75% of cases) to:
Emboli (SBE), nonbacterial valve vegetations, left
atrium or ventricle, atherosclerotic vascular
disease,Venous thrombosis
Ascites
blood-AF albumin gradient >1.1: portal HT
neutrophils count >250/L is presumptive of
bacterial peritonitis.
Gram stain shows few bacteria in SBP Culture
sensitivity = 50% for SBP and ~80% for
secondary peritonitis
TB acid-fast stain sensitivity = 20% to 30%
and TB culture sensitivity = 50% to 70%.






Chylous Ascites
Triglyceride is 2-8 serum level.
Due to
lymphatic obstruction (lymphoma or CA)
inflammation or obstruction of small intestine
trauma to chest or abdomen,
filariasis;
congenital lymphatic defects in pediatric
Abdominal Trauma

Criteria to diagnose penetrating abdominal
wounds by peritoneal lavage10,000 mL of
normal saline 3 to 18 hours after injury :

>10,000 RBC/L (>5,000 RBC/L for gunshot
wounds)
Bacteria, fecal or vegetable matter on Gram
stain or bile

Occult Bleeding
guaiac -detect blood losses of ~20 mL/d.
Use of fecal sample obtained by digital rectal
exam is not recommended
Stools may appear grossly normal with GI
bleeding of 100 mL/d.
Consistent melena requires 150 to 200 mL blood
in the stomach
False positive in FBC, animal blood food
RESP.
Croup or laryngotracheitis
inflammation of the upper airway below the
glottis.
Caused by
Group B Haemophilus influenzae causes >90% of
cases of epiglottitis; other bacteria include -
hemolytic streptococci and pneumococci.
Pneumonia
Prussian bluenuclear red stain strongly positive
indicates severe alveolar hemorrhage
Pap smear- intranuclear inclusions of herpes or
CMV
Giemsa,GMS of sputum - PCP
Pleural fluid
Light criteria-exudate/transudate
1.LDH in fluid > 2/3 normal serum LDH
2.Protein fluid/serum> 0.5
3.LDH fluid/serum> 0.6


4.Serum alb-fluid alb <1.2
Pleural fluid
Nonpurulent fluid with positive Gram stain,
positive blood culture, or low pH suggests that
effusion will become or behave like empyema
Streptococcus pneumoniae causes parapneumonic
effusions in 50% of cases, especially with
positive blood culture
case
Male 25 years old came with dyspnea
CXR-left pleural effusion
Pleural tapping-WBC>50,000, high neutrophils

Need ICD?
No ICD
Indication for ICD
1.PH< 7
2.SUGAR<40
3.Frank pus
4.Gram stain /Culture +
pH <7.0 and glucose <40 mg/dL indicate need
for ICD without grossly purulent fluid.
pH of 7.07.2 is a questionable indication and
should be repeated in 24 h, but ICD is favored if
pleural fluid LD >1,000 IU/L.
ICD is also indicated if there is grossly purulent
fluid or positive Gram stain or culture.
hemothorax
hematocrit (Hct) >50% of peripheral Hct
indicates a hemothorax.
Cytology establishes the diagnosis in
approximately 50% of patients.
Cytology plus biopsy is diagnostic in about 90%
of cases
Exudative effusion
Caused by
Pneumonia, malignancy, pulmonary embolism,
and gastrointestinal conditions (especially
pancreatitis and abdominal surgery) cause 90%
of all exudates
Pleural effusion
Typically left-sided: Ruptured esophagus, acute
pancreatitis, RA
Typically right-sided or bilateral: Congestive
heart failure (CHF)
Typically right-sided: Rupture of amebic liver
abscess.
Chylous
Chylous (milky) is usually due to trauma or
obstruction of duct
PF triglycerides (TG) >110 mg/dL or TG
PF:serum ratio >2 occurs only in chylous
effusion
pseudochylous effusions
Chylomicrons 50 mg/dL with cholesterol
>250 mg/dL.
Amylase

Increased PF:serum ratio >1.0
Acute pancreatitismay be normal early with
increase over time
Also perforated esophageal rupture, peptic ulcer,
necrosis of small intestine
TB pleura
Large mesothelial cells >5% are said to rule out TB
Acid-fast smears are positive in only <20% of TB
pleurisy
Sensitivity >50% in TB. Cultures from chest tubes
culture combined with histologic examination
establishes the diagnosis in 95% of cases
Adenosine deaminase >70 IU/L
Malignancy effusion

Cytology is positive in 60% of malignancies on
first tap, 80% by third tap. Is more sensitive
than needle biopsy
Combined cytology and pleural biopsy give
positive results in 90%.



Sputum exam
Optimum specimen of sputum shows >25
PMNs and 5 squamous epithelial cells/LPF
Sensitivity of sputum culture is estimated at 25%
to 50%.
Carcinoma, Bronchogenic
Cytologic examination of sputum for malignant
cells
-positive in 40% of patients on first sample
-70% with three samples
-85% with five samples.

False-positive tests are <1%.

CA lung
Classified as:
Non-small cell lung carcinoma (NSCLC) in 70% to
75% of cases
Squamous cell carcinoma (25%30%)
Adenocarcinoma (30%35%)
Large cell carcinoma (10%15%)
Small cell lung carcinoma (SCLC) in 20% to 25% of
cases
Combined pattern in 5% to 10% of cases
LE cells makes the diagnosis of SLE
CHF is typically bilateral; 20% are right-sided
and 9% are left-sided
Plasma D-dimer
is a fibrin product generated by action of
plasmin on cross-linked fibrin molecules
indicating that a clot has formed
At cutoff level of 500 g/L
Hepatobiliary
Total Serum Bilirubin

Must exceed 2.5 mg/dL to produce clinical
jaundice

Serum Bilirubin (Conjugated:total)

<20% conjugated
Constitutional (e.g., Gilbert disease, Crigler-Najjar
syndrome)
Hemolytic states
20% to 40% conjugated
Favors hepatocellular disease rather than extrahepatic
obstruction
Disorders of bilirubin metabolism (e.g., Dubin-Johnson,
Rotor syndromes)
40% to 60% conjugated: Occurs in either hepatocellular or
extrahepatic type
>50% conjugated: Favors extrahepatic obstruction rather
than hepatocellular disease
AST
Half-life of AST is 18 hours
half-life of ALT is 48 hours.
Thus, in early acute hepatitis, AST is usually
higher initially, but by 48 hours, ALT is usually
higher.
ALP

Increased ALP in liver diseases (due to
increased synthesis from proliferating bile
duct epithelium) is the best indicator of
biliary obstruction
High values (>5 normal) favor obstruction
Isolated increase of GGT is a sensitive
screening and monitoring test for alcoholism
In cirrhosis with ascites, the kidney retains
increased sodium and excessive water, causing
dilutional hyponatremia
Blood ammonia is increased in liver coma and
cirrhosis and with portacaval shunting of blood.
WBC is usually normal with active cirrhosis;
increased (<50,000/L) with massive necrosis,
hemorrhage, etc.; decreased with hypersplenism.
Hep. encephalopathy
Blood ammonia is increased in 90% of patients
but does not reflect the degree of coma. Normal
level in comatose patient suggests another cause
of coma. Not reliable for diagnosis but may be
useful to follow individual
SBP
Spontaneous bacterial peritonitisin 10% to
30% of cirrhosis cases with ascites.
70% have positive blood culture; usually single
organism, especially E. coli, pneumococcus,
Klebsiella.
250 PMNs/L is diagnostic.
AST:ALT ratio >1 associated with AST <300 U/L
will identify 90% of patients with alcoholic liver
disease; is particularly useful for differentiation
from viral hepatitis, in which increase of AST and
ALT are about the same.

Anemia in >50% of patients may be macrocytic
(folic acid or vitamin B12 deficiency), microcytic
(iron deficiency), mixed, or hemolytic.

In acute alcoholic hepatitis, GGT level is usually
higher than AST level. GGT is often abnormal in
alcoholics even with normal liver histology. Is
more useful as index of occult alcoholism
hepatitis
Hepatitis, Chronic ActiveProgressive hepatitis
>6 months duration of unknown etiology
affecting patients of all ages possibly due to an
external agent Due To
Viruses
HBV (with or without HDV)
HCV (with or without HGV)
CMV, others
hepatitis
Metabolic
Wilson disease
Alpha1-antitrypsin deficiency
Hemochromatosis
Primary biliary cirrhosis
Sclerosing cholangitis
hepatitis
Drugs (e.g., methyldopa, nitrofurantoin, isonizid,
oxyphenacetin) and chemicals
Nonalcoholic fatty liver
Alcoholic hepatitis
Autoimmune causes
Acute pancreatitis
Serum Lipase
Increases within 3 to 6 hours with peak at 24
hours and usually returns to normal over a
period of 8 to 14 days.
Is superior to amylase; increases to a greater
extent and may remain elevated for up to 14
days after amylase returns to normal.

acute pancreatitis
-In patients with signs of acute pancreatitis,
pancreatitis is highly likely (clinical specificity =
85%) when lipase 5 URL, if values change
significantly with time, and if amylase and lipase
changes are concordant.
-Lipase should always be determined whenever
amylase is determined. New methodology
improves clinical utility.

It has been suggested that a lipase:amylase ratio
>3 (and especially >5) indicates alcoholic rather
than nonalcoholic pancreatitis).

predisposing conditions of
pancreatitis
Alcohol abuse accounts ~36% of cases.
Biliary tract disease accounts 17% of cases.
Idiopathic accounts >36% of cases.
Infections (especially viral such as mumps and coxsackie,
CMV, AIDS)
Trauma and postoperative accounts >8% of cases
Drugs (e.g., steroids, thiazides) >5% of cases.
Hypertriglyceridemia (HyperlipidemiaTypes V, I, IV)
7% of cases
Hypercalcemia
Tumors (pancreas, ampulla)
Anatomic abnormalities of ampullary region causing
obstruction
Hereditary
Renal failure; renal transplantation
Prognostic laboratory findings
On admission
WBC >16,000/L
Blood glucose >200 mg/dL
Serum LD >350 U/L
Serum AST >250 units/L
Age >55 years

Within 48 hours
>10% decrease in HCT
Serum calcium <8.0 mg/dL
Decrease in Hct >10 points
Increase in BUN >5 mg/dL
Arterial pO2 <60 mmHg
Metabolic acidosis with base deficit >4 mEq/L


prognosis

Degree of amylase elevation has no
prognostic significance
CT scan, MRI, ultrasound are useful for
confirming diagnosis or identifying causes
or other conditions
CNS
CSF
CSF -WBC may be corrected for presence of
blood (e.g., traumatic tap, subarachnoid
hemorrhage) by subtracting 1 WBC for each 700
RBCs/L counted in CSF if the CBC is normal.
Neutrophilic leukocytes in CSF
are found in:
Bacteria (e.g., Nocardia, Actinomyces, Arachnia,
Brucella)
Fungal infections (Blastomyces, Coccidioides,
Candida, Aspergillus, Zygomycetes,
Cladosporium, Allescheria)
Chemical meningitis
Other conditions (e.g., SLE)
Lymphocytic cells in CSF
are found in:
Bacterial infections (e.g., Treponema pallidum,
Leptospira,, Borrelia burgdorferi [Lyme disease], M.
tuberculosis)
Fungal infections (e.g., Cryptococcus neoformans, Candida
species, Coccidioides immitis, Histoplasma capsulatum,
Blastomyces dermatitides)
Parasitic diseases (e.g., toxoplasmosis, cysticercosis)
Viral infections (e.g., mumps, lymphocytic
choriomeningitis). Atypical lymphocytes may be seen in
EBV infection and less often in CMV or HSV infection.
Parameningeal disorders (e.g., brain abscess)
Noninfectious disorders (e.g., neoplasms, sarcoidosis,
multiple sclerosis, granulomatous arteritis)
Eosinophils In CSF
be found in:
Lymphoma
Helminth infection (e.g., angiostrongyliasis,
cysticercosis)
Rarely, other infections (e.g., TB, syphilis, Rocky
Mountain spotted fever, coccidioidomycosis)
Eo>5% may indicate malfunction or infection of a
ventriculoperitoneal shunt
Multiple Sclerosis (MS)
CSF changes are found in >90% of MS patients.
Oligoclonal IgG bands or elevated IgG index
are the 2 CSF findings recognized as positive.

musculoskeletal
Serum Enzymes in Diseases of
Muscle
Creatine kinase (CK) is the test of choice. It is more
specific and sensitive than AST and LD and more
discriminating than aldolase (ALD) but AST is more
significantly associated with inflammatory myopathy and
more useful in these cases
Increased In
Polymyositis
Muscular dystrophy
Myotonic dystrophy
Some metabolic disorders
Malignant hyperthermia
Prolonged exercise; peak 24 hours after extreme exercise
(e.g., marathon); smaller increases in well-conditioned
athletes
Wilms tumors with rhabdomyomatous features (CK-MB
may also be increased
Hyperthyroidism

Normal serum M.enzyme levels
Increased urine creatine; decreased
creatine tolerance
Normal muscle biopsy findings
Causes some cases of hypokalemic
periodic paralysis
Malignant Hyperthermia
Rare autosomal dominant hypermetabolic
syndrome
causing abnormally increased release of calcium
from membrane of sarcoplasmic reticulum
triggered by various inhalational [e.g., ether] and
local anesthetic agents, muscle relaxants [e.g.,
succinylcholine, tubocurarine]
causing hyperthermia, muscle rigidity, and 70%
fatality
Combined metabolic and respiratory acidosis is
the most consistent abnormality and is diagnostic
in the presence of muscle rigidity or rising
temperature. pH is often <7.2, BE >-10, hypoxia,
and arterial pCO2 of 70 to 120 torr. Immediate
arterial blood gas analysis should be performed.
Myopathy Associated with
Alcoholism
Acute (necrotizing)
Increased serum CK, AST, and other enzymes.
Serum CK increased in 80% of patients; rises in 1
to 2 days; reaches peak in 4 to 5 days; lasts ~2
weeks.
Gross myoglobinuria
Acute renal failure
Myopathy Associated with
Alcoholism
Chronic :
Increased serum CK in 60% of patients to average of 2
ULN
Increased AST and other enzymes due to liver as well as
muscle changes
Increased urine creatine
Diminished ability to increase blood lactic acid with
ischemic exercise
Abnormalities on muscle biopsy (support the diagnosis)
Myoglobinuria

Infective Arthritis
Bacterial
In purulent arthritis, organism is recovered from joint in
90% of patients and from blood in 50% of patients. Most
often due to S. aureus (60%) and Streptococcus species.
Gram stain is positive in ~50% of patients; it is
particularly useful for establishing diagnosis promptly
and in cases in which cultures are negative.
Culture may be negative because of prior administration
of antibiotics.
In children, most common organisms are H. influenzae
type b, S. aureus, various streptococci, and gram-
negative bacilli.
In young adults, >50% of cases are due to Neisseria
gonorrhoeae; rest are due to S. aureus, streptococci, or
gram-negative bacilli.
TB arthritis
Gram stain and bacterial cultures
are negative
but acid-fast stain, culture, and
biopsy of synovia confirm the
diagnosis
Myasthenia Gravis (MG)
Acetylcholine Receptor (AChR) Binding
Antibodies is the standard assay and should
be ordered first:
Negative in 34% of patients with MG
Negative 50% of patients with ocular MG
May be negative in first 612 months

Crystalline
ArthropathyChondrocalcinosis
(Pseudogout)

Inflammatory mono- or polyarticular arthritis due
to deposition of calcium pyrophosphate dehydrate
crystals in joints
Joint fluid contains crystals identified as calcium
pyrophosphate dehydrate, inside and outside of
WBCs, and macrophages that are differentiated
from urate crystals under polarized light, which
distinguishes them from gout.
Crystals may also be identified by other means
(e.g., chemical, x-ray diffraction).
Gout
Group of disorders of purine metabolism
characterized by monosodium urate crystal
deposits in joints and soft tissues
episodes of acute inflammatory arthritis
[response to crystal deposits], and
hyperuricemia.
Most uric acid is synthesized in liver and
intestinal mucosa.
Two thirds excreted by kidney; one third
excreted by bowel.
Gout
Primary (i.e., inborn) (30% of patients)
-Idiopathic
-Increased purine biosynthesis (Lesch-Nyhan syndrome)
Secondary (70% of patients)
1.Overproduction (10% of secondary cases);
overexcreters: >750 to 1,000 mg/day of uric acid
Neoplastic and hemolytic conditions

2.Increased breakdown of adenosine
triphosphate
Glycogen storage diseases (I, III, V, VII)
Alcohol ingestion
Myocardial infarction

3.Decreased renal function (90% of secondary
cases); underexcreters: <700 mg/day of uric acid
Gout
Diagnostic Criteria:
-Presence of crystals of monosodium urate from
tophi or joint fluid viewed microscopically under
polarized light
-strongly negative birefringent needle-shaped
crystals both inside and outside PMNs or
macrophages
-differentiates it from pseudogout.
(Found in synovial fluid in 75% of patients
between attacks.)
hemato
Macrocytic anemias
Macrocytic anemias (MCV >95 fL and often >110 fL;
MCHC >30 g/dL)
Megaloblastic anemias
PA (vitamin B12 or folate deficiency)
Sprue (e.g., steatorrhea, celiac disease, intestinal resection or
fistula)
Macrocytic anemia of pregnancy
Alcoholism
Liver disease
Anemia of hypothyroidism
Carcinoma of stomach, following total gastrectomy
Drugs:
Oral contraceptives
Anticonvulsants (e.g., phenytoin, primidone, phenobarbital)
Antitumor agents (e.g., methotrexate, hydroxyurea,
cyclophosphamide)
Antimicrobials (e.g., sulfamethoxazole, sulfasalazine, trimethoprim,
zidovu-dine, pyrimethamine
Normocytic anemias
Normocytic anemias (MCV = 8094 fL; MCHC
>30 g/dL)
Following acute hemorrhage
Some hemolytic anemias
Some hemoglobinopathies
Anemias due to inadequate blood formation
case
50 years old male came with pale
BP

= 120/70, 130/80
Hct=25, MCV=80

What is the cause of anemia?


Answer
UGIH
Microcytic anemias
Microcytic anemias (MCV <80 fL; MCHC <30 g/dL)
Usually hypochromic
Iron-deficiency anemia, e.g.,
Inadequate intake
Poor absorption
Excessive iron requirements
Chronic blood loss
Pyridoxine-responsive anemia
Thalassemia
Lead poisoning
Anemia of chronic diseases
Disorders of porphyrin synthesis

summary
Kidney
Cardio
GI
Respiration
Hepatobiliary
CNS
musculoskeletal
Hemato



Ferritin
Ferritin is an acute-phase reactant and thus is increased
in many patients with:
- various acute and chronic liver diseases
- alcoholism (declines during abstinence)
- malignancies (e.g., leukemia, Hodgkin disease)
- infection and inflammation
- hyperthyroidism
Serum ferritin may not be decreased when iron
deficiency coexists with these conditions; in such cases,
bone marrow stain for iron may be the only way to
detect the iron deficiency.
Iron overload
Iron overload (e.g., hemosiderosis, idiopathic
hemochromatosis).
Can be used to monitor therapeutic removal of excess
storage iron. Transferrin saturation is more sensitive to
detect early iron overload in hemochromatosis
serum ferritin is used to confirm diagnosis and as
indication to proceed with liver biopsy.
Ratio of serum ferritin (in ng/mL) to alanine
aminotransferase (ALT) (in IU/L) >10 in iron-overloaded
thalassemic patients but averages 2 in viral hepatitis; ratio
decreases with successful iron chelation therapy.

TIBC
Iron-Binding Capacity, Total SerumTIBC (in mol/L) is obtained by
the following equation: transferrin (mg/L) 0.025.
Unsaturated iron-binding capacity = TIBC minus serum iron (g/dL).
Use in
1.Differential diagnosis of anemias
2.Should always be performed whenever serum iron is done to calculate
percent saturation (see Fig 11-2) for diagnosis of iron deficiency
3.Screening for iron overload
Increased In
-Iron deficiency
-Acute and chronic blood loss
-Acute liver damage
-Late pregnancy
Decreased In
-Hemochromatosis
-Cirrhosis of the liver
-Thalassemia
-Anemias of infection and chronic diseases (e.g., uremia, RA, some
neoplasms
SerumTransferrin
Transferrin, transports circulating Fe3 molecules.
Normally only about 1/3 of iron-binding sites are
occupied; the remainder is called unsaturated iron-binding
capacity.
Increased In
-Iron-deficiency anemia; is inversely proportional to iron
stores
-Pregnancy, estrogen therapy, hyperestrogenism
Decreased In
-Hypochromic microcytic anemia of chronic disease
-Acute inflammation
-Protein deficiency or loss (e.g., burns, chronic infections,
chronic diseases [e.g., various liver and kidney diseases,
neoplasms]), nephrosis, malnutrition)
-Genetic deficiency
Transferrin Saturation
Serum transferrin saturation is obtained by serum
iron / TIBC
normal 20% to 50%.
Use in Differential diagnosis of anemias/
Screening for hereditary hemochromatosis
Increased In
-Hemochromatosis
-Hemosiderosis
-Thalassemia
-Birth control pills (75%)
-Ingestion of iron (100%)
-Iron dextran administration causes increase for
several weeks (may be >100%)