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Flashcards in jaundice and ascites Deck (43):

case w. jaundice ddx

Liver cirrhosis
Liver neoplasm
Primary biliary cirrhosis


what labs to get

CMP: some liver tests: ALT, AST, total bilirubin (may want fractionated also) , alk phos, albumin
hepatitis Abs
CBC: anemia (hemolysis), thrombocytopenia
white count? not always indicates just infection


will see jaundice when levels are

-above 3 mg/dL will lead to jaundice, icterus



-characterizes underlying liver disease
-Do not necessarily directly measure liver function
-measurements of serum levels of compounds that are:
Synthesized, metabolized, or excreted by the liver
-The liver has a large reserve capacity and thus liver function tests may remain relatively normal until liver dysfunction is severe


LFTs specifics

Aspartate aminotransferase (AST); Aka - Serum glutamic oxaloacetic transaminase (SGOT)
Alanine aminotransferase (ALT); Aka - Serum glutamic pyruvic transaminase (SGPT)
Serum albumin
Prothrombin time
Serum bilirubin
Serum alkaline phosphatase
Gamma-Glutamyl transferase (GGT)


Serum Albumin

Reflect hepatic capacity for protein synthesis
-Albumin levels fall with prolonged liver dysfunction or in acute liver impairment (Norm: 3.5-5.5 mg/dL)


Prothrombin time

dependent on coagulation factors II, V, VII and X
-Norm = 10.5 to 13 seconds
-Responds rapidly to altered hepatic function
*these are dependent upon Vitamin K and a coexistent vitamin k deficiency must be ruled out*


In light of hypoalbuminemia and normal Prothrombin time – Consider ??

malnutrition, renal or GI losses


screening for hepatobiliary disease

alk phos, ALT, AST
Tests of biliary obstruction and cholestasis and hepatocellular damage
-lack of specificity of these tests; look at overall pattern of tests as well as magnitude of abnormality


Serum Bilirubin

reflects balance btw production, conjugation, and excretion into bile by the liver
Normal = 0.2 – 1 mg/dL
-Conjugated (direct) represents up to 30% of total
-Evaluated in conjunction with other LFTs
-Once insult is resolved – bilirubin takes some time to return to normal levels


Serum Alkaline phosphatase

Group of isoenzymes derived from: Liver, bone, intestine and placenta
Elevation occurs in:
-Cholestasis, partial or complete bile duct obstruction
-Bone regeneration, pregnancy
-Neoplastic, infiltrative, and granulomatous liver diseases

An isolated elevated alkaline phosphatase may be the only clue to pathology


Aspartate (AST/SGOT) and Alanine (ALT/SGPT) aminotransferases

IC amino-transferring enzymes in hepatocytes
After injury or death- released into the circulation
-sensitive (not specific) for liver damage
-Quantity of enzyme level correlates with the severity of hepatic necrosis



-primarily in hepatocytes
More specific than AST for liver disease
In most hepatocellular disorders, ALT is higher than AST
Except in alcoholic liver disease (where its reversed)



-primarily in liver and cardiac muscle; but also in skeletal muscle, kidneys, brain, lungs pancreas, leukocytes, erythrocytes
Will be higher than ALT in alcoholic liver disease
(Usually 2 or 3x ALT)



Increased in any cause of acute damage to the liver or bile ducts
-Not very specific and thus not really part of work-up for acute liver dysfunction/injury
-helpful in determining reason for alk phos elevation in serum
-If GGT is low or normal than elevation of Alk Phos is likely due to bone disease rather than liver injury or insult
-A low level or normal level also makes it less likely that the person has consumed alcohol or has liver disease


jaundice: Most bilirubin (80%) is derived from the breakdown of ??

senescent red blood cells (RBCs)
-remainder derives from ineffective erythropoiesis and catabolism of myoglobin and hepatic hemoproteins
-Normal rate of production is about 4 mg/kg body weight daily


Differentiated by the phase of hepatic bilirubin metabolism

uptake, conjugation, excretion
also ategorized as:


Bilirubin is detected in biologic fluids by the

van den Bergh reaction
D=C, I=U
(total minus direct)


Unconjugated hyperbilirubinemia

Primary mechanisms:
Overproduction, Impaired hepatic uptake, Decreased conjugation of bilirubin
*Not usually associated with significant hepatic disease


Pre-Hepatic Etiology (UC bili):
Any condition that results in ??

excessive bilirubin production:
Hemolysis, Hematomas, PE
Genetic disorders, G6PD deficiency, SCD anemia
Spherocytosis, Infectious diseases (Malaria)


Pre-Hepatic Etiology: mild or severe?

Jaundice resulting from hemolysis is usually mild
-Serum bilirubin levels rarely exceed 5 mg/dL in the absence of coexisting hepatic diseases


Pre-Hepatic Etiology: Hemolysis can be investigated by examining ??

-Peripheral blood smear (and bone marrow smear)
-Measuring reticulocyte count, haptoglobin, lactate dehydrogenase (LDH), erythrocyte fragility and Coomb’s test (done by specialist, not PC)


Unconjugated hyperbilirubinemia: Hepatic Etiology
Every condition resulting in hepatic injury can cause ??

hepatic jaundice:
-Hepatitis: Infectious, toxic metabolites, drugs, auto-immune disorders, and liver tumors
-Gilbert syndrome, Crigler-Najjar syndrome, Niemann-Pick disease type C


UC hyperbili: Impaired Hepatic Uptake

Causes jaundice that occurs after administering certain drugs: Rifampin, Those involved in treating Gilbert syndrome


UC hyperbili: Impaired Conjugation: can be due to ??

-Crigler-Najjar syndrome
-Acquired defects of UDP glucoronyl transferase (UGT) induced by drugs such as chloramphenicol


Neonatal jaundice: Two primary causes??

*Immature hepatic metabolic pathways are unable to conjugate bilirubin as efficiently and quickly as in adults*
Bilirubin production is increase, leads to UC bili btw day 2-5, last until day 8 (normal), day 14 in premies, typ. harmless and doesn't need tx

put on bililytes? if more severe, electrophoresis


neonatal jaundice: Severe pathologic UC bili: usually caused by ??

hemolysis (due to blood group incompatibility) and defective conjugation
-serious condition which requires immediate attention
Can lead to severe hyperbili; risk for permanent neurologic damage (Kernicterus)
tx of choice: Phototherapy
-If there is no response to phototherapy – seek another cause of the jaundice


Conjugated Hyperbilirubinemia: associated with ??
two primary mechs??

impaired formation or excretion of all components of bile (cholestasis)

-defect in the excretion of bilirubin from hepatocytes into bile (intrahepatic cholestasis)
-mechanical obstruction to the flow of bile through the bile ducts


C bili: Impaired hepatic excretion (Intrahepatic cholestasis)
Caused by many conditions

-Drugs – can impair canalicular transport
-Destruction of intrahepatic bile ducts (Primary biliary cirrhosis)


Primary biliary cirrhosis

Chronic, progressive liver disease, Occurs primarily in women
-Destroys small lobular bile ducts
-Leads to progressive cholestasis -> portal inflammation -> fibrosis -> cirrhosis


drugs that can induce cholestasis (impaired hepatic excretion, C bill)

-Nitrofurantoin, oral contraceptives, anabolic steroids
-Erythromycin, cimetidine, chlorpromazine
-Prochlorperazine, imipramine, sulindac, and Penicillins

ALSO Post-operative Jaundice:
Occurs 1-10 days after surgery, 15% incidence after heart surgery


Post-hepatic (Obstructive jaundice, C bili): Due to partial or complete ??

most common causes??
other causes??

obstruction of intrahepatic or extrahepatic bile ducts

-*Gallstones in the common bile duct, Pancreatic head tumors*
-others: Biliary atresia, ductal carcinoma, strictures of the common bile duct, Pancreatitis, pancreatic pseudocysts, or liver flukes (parasites)


clinical approach to jaundice

good hx (esp. social, travel) and PE
lab tests: Comprehensive metabolic panel [electrolytes, liver enzymes (including direct and indirect-bilirubin)], lipase, complete blood count
imaging: US, CT, MRI, MRCP, ERCP
MRCP: looking at GB, pancreas, biliary duct system, purely diagnostic
ERCP: endoscopy, can go in and remove stone if see it



most common cause??

Accumulation of excess fluid in the peritoneal cavity
-Liver cirrhosis
-high albumin (greater than 1.1 g/dL): cirrhosis, chronic hep congestion, RVHF, Budd-Chiari, constrictive pericarditis, massive liver metastasis, mycetoma, mixed ascites
-low albumin (less than 1.1 g/dL): peritoneal carcinomatosis, peritoneal TB, pancreatic/biliary disease, nephrotic syndrome


The ?? has replaced the exudative-transudative classification of ascites
an elevated gradient signifies ??

serum ascites-albumin gradient
-An elevated serum ascites-albumin gradient (more than 1.1 g/dL) signifies the presence of portal HTN

-typically ascites is transudative


Ascites becomes clinically detectable with fluid accumulation of greater than ??
most sensitive sign of ascites??
imaging for smaller volumes??

500 mL
-Shifting dullness to percussion
-Ultrasound is able to detect smaller volumes (250 mL)


ascites overflow theory:

Overflow of fluid into the peritoneum resulting from portal HTN and splanchnic vasodilation: Excess renal sodium, Water retention


ascites underflow theory:

Decreased effective circulating BV from systemic arterial vasodilation leading to activation of neurohumoral systems: Sodium and water retention


Intervention is typically done when ??
procedure of choice??

symptomatic: I.e. dyspnea, abdominal pain, etc
Paracentesis: Usually done under ultrasound, Can drain as much as 5-8 liters of fluid


ascites flow chart

hyponatremia-->Na+ and H2O restriction
normal Na+-->Na+ restriction

recurrent ascites-->diuretic: spironolactone and furosemide


ascites flow chart: if refractory ascites despite max diuretic dose OR e-lyte abnormality/renal dysfunction at submax dose

-large-volume paracentesis w. colloid expansion (IV albumin)
-shunt placement: TIPS/sx shunt

if these fail, consider liver transplant


P of SOAP: workups of jaundice

Complete blood count
Comprehensive metabolic panel
Direct and indirect bilirubin
Hepatitis panel
Prothrombin time
RUQ ultrasound ??
CT scan of abdomen ??


how would you tx??

-abx: cephalosporin, usyn, augmentin
-remove stone: cholecystectomy w. intraoperative cholangiagram (look to see if stone), ERCP