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Flashcards in Jaundice and Ascites Deck (46)
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-Yellow pigmentation of skin, sclerae and mucus membranes resulting from elevated serum bilirubin levels
-Typically levels above 3 mg/dL will lead to jaundice, icterus

-A sign of various illnesses, including liver disease and hematologic disorders


The liver has a large reserve capacity of enzymes and thus ______

liver function tests may remain relatively normal until liver dysfunction is severe!!


Liver function tests measure

-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 and Prothrombin time 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)

*If pt has hypoalbuminemia and normal Prothrombin time – Consider malnutrition, renal or GI losses


Prothrombin time is dependent on

coagulation factors II, V, VII and X
(2, 5, 7, 10)

-Norm = 10.5 to 13 seconds
-Responds rapidly to altered hepatic function
*However, these are dependent upon Vitamin K and a coexistent vitamin k deficiency must be ruled out.


Screening for hepatobiliary disease

Tests of biliary obstruction and cholestasis
Tests of hepatocellular damage

-Important to realize lack of specificity of these tests
-Primary use lies in overall pattern of tests as well as magnitude of abnormality


Serum Bilirubin reflects

balance between production, conjugation, and excretion into bile by the liver

-Unconjugated (indirect) and Conjugated (direct)
-Normal = 0.2 – 1 mg/dL
-Conjugated (direct) represents up to 30% of total


Serum Alkaline phosphatase
is a group of isoenzymes derived from

Liver, bone, intestine and placenta


Elevation of Serum Alkaline phosphatase occurs in a variety of conditions:

-Cholestasis, partial or complete bile duct obstruction
-Bone regeneration
-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 are

Intracellular amino-transferring enzymes in hepatocytes

-After injury or death – these are released into the circulation
-These aminotransferases are sensitive (not specific) for liver damage
-Quantity of enzyme level correlates with the severity of hepatic necrosis



-Found 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)



-Found 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 3 times that of 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
-Can be helpful in determining reason for elevation of Alkaline Phosphatase level in serum (see next slide)


If GGT is low or normal, then elevation of Alk Phose is likely due to

bone disease rather than liver injury or insult

-A low level or normal GGT level also makes it less likely that the person has consumed alcohol or has liver disease


Most bilirubin (80%) is derived from

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


Bilirubin is detected in biologic fluids by the van den Bergh reaction:

Direct-reacting fraction -> Conjugated bilirubin

Indirect-reacting fraction -> Unconjugated bilirubin

Total minus direct= indirect


Causes of Unconjugated Hyperbilirubinemia

-Impaired hepatic uptake
-Decreased conjugation of bilirubin
**Not usually associated with significant hepatic disease


Pre-Hepatic Etiology of Unconjugated Hyperbilirubinemia

1. Any condition that results in excessive bilirubin production
(Hemolysis, Hematomas, Pulmonary emboli-->all things that break down RBCs and make bilirubin)
-Genetic disorders: Glucose-6-phosphate dehydrogenase deficiency, Sickle cell anemia, Spherocytosis

-Infectious diseases (Malaria)


Jaundice resulting from hemolysis is usually

(pre hepatic)


-Serum bilirubin levels rarely exceed 5 mg/dL in the absence of coexisting hepatic diseases


Hemolysis can be investigated by examining: (pre hepatic)

-Peripheral blood smear (and bone marrow smear)
-Measuring reticulocyte count, haptoglobin, lactate dehydrogenase (LDH), erythrocyte fragility and Coomb’s test


Unconjugated hyperbilirubinemia from Hepatic etiology:

-anything causing hepatic injury can cause hepatic jaundice
-Hepatitis (Any causes: Infectious, toxic metabolites, drugs, auto-immune disorders, and liver tumors)
-Gilbert syndrome
-Crigler-Najjar syndrome
-Niemann-Pick disease type C


Impaired Hepatic Uptake can cause jaundice and occurs after

administering certain drugs

-Such as Rifampin
-Those involved in treating Gilbert syndrome


Impaired conjugation can be due to

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


Two primary causes of neonatal jaundice

**Immature hepatic metabolic pathways are unable to conjugate bilirubin as efficiently and quickly as in adults
-Bilirubin production is increase


Increased bilirubin production in neonates leads to

unconjugated hyperbilirubinemia between 2nd and 5th day of life

-Lasts until the 8th day in normal births or 14th day in premies
-Usually harmless and doesn’t require any type of therapy


Severe pathologic unconjugated hyperbilirubinemia in neonatal jaundice is usually caused by

hemolysis (due to blood group incompatibility) and defective conjugation

*This is a serious condition which requires immediate attention
-Can lead to severe hyperbilirubinemia which is a risk for permanent neurologic damage (Kernicterus)
**Phototherapy is the treatment of choice (If there is no response to phototherapy – seek another cause of the jaundice)


Conjugated Hyperbilirubinemia is associated with

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

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


Impaired hepatic excretion (Intrahepatic cholestasis) during Conjugated Hyperbilirubinemia can be caused by

-many things
-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