Flashcards in Jaundice and Ascites Deck (46)
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1
Jaundice/Icterus
-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
-Hyperbilirubinemia
-A sign of various illnesses, including liver disease and hematologic disorders
2
The liver has a large reserve capacity of enzymes and thus ______
liver function tests may remain relatively normal until liver dysfunction is severe!!
3
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)
4
Serum Albumin and Prothrombin time reflect
hepatic capacity for protein synthesis
5
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
6
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.
7
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
8
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
9
Serum Alkaline phosphatase
is a group of isoenzymes derived from
Liver, bone, intestine and placenta
10
Elevation of Serum Alkaline phosphatase occurs in a variety of conditions:
-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
11
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
12
ALT
-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)
13
AST
-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
14
GGT
-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)
15
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
16
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
17
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
18
Causes of Unconjugated Hyperbilirubinemia
-Overproduction
-Impaired hepatic uptake
-Decreased conjugation of bilirubin
**Not usually associated with significant hepatic disease
19
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)
20
Jaundice resulting from hemolysis is usually
(pre hepatic)
mild
-Serum bilirubin levels rarely exceed 5 mg/dL in the absence of coexisting hepatic diseases
21
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
22
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
23
Impaired Hepatic Uptake can cause jaundice and occurs after
administering certain drugs
-Such as Rifampin
-Those involved in treating Gilbert syndrome
24
Impaired conjugation can be due to
-Crigler-Najjar syndrome
-Acquired defects of UDP glucoronyl transferase induced by drugs such as chloramphenicol
25
Two primary causes of neonatal jaundice
**Immature hepatic metabolic pathways are unable to conjugate bilirubin as efficiently and quickly as in adults
OR
-Bilirubin production is increase
26
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
27
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)
28
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
29
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)
30
