Hepatobiliary Testing Flashcards
AST (Aspartate Aminotransferase)
aka SGOT
Reference Range: 5 – 40 IU/L
AST is an intracellular enzyme; cellular damage causes enzyme to leak into plasma
Found in liver cells, cardiac muscle, skeletal muscle, renal cells, brain cells, pancreas, WBCs & RBCs
AST Clinical use
Primarily for the evaluation of hepatocellular injury/necrosis
Previously used for detection of cardiac ischemia or myocardial infarction
AST Increased levels implications
Liver disease
Heart disease
Skeletal muscle disease/injury
Acute hemolytic anemia
Acute pancreatitis
Acute cholangitis
AST Decreased levels implications
Acute renal disease
Chronic renal dialysis
ALT (Alanine Aminotransferase)
Reference Range: 5 – 53 IU/L
Intracellular enzyme that is more specific than AST for liver
Clinical Uses for ALT
Diagnose and monitor hepatocellular injury or necrosis
Aid in diagnosis of jaundiced patient
Viral hepatitis
Alcoholic hepatitis
Mild ALT increase implications
Myositis
Pancreatitis
Myocardial infarction
Infectious mononucleosis
Moderate ALT increase implications
Moderate Increase
Cirrhosis
Cholestasis
Hepatic tumor
Obstructive jaundice
Severe burns
Muscle trauma
Severe ALT increase implications
Severe Increase
Hepatitis, hepatic necrosis/ ischemia
LDH (Lactic Dehydrogenase)
Reference Range: 90 – 190 IU/L
Intracellular enzyme in many body tissues
Total LDH elevation is relatively nonspecific; LDH isoenzymes offers more specificity
LDH 1 – myocardium, RBCs, brain, kidney
LDH 2 – myocardium, RBCs, brain, lung
LDH 3 – brain, kidney, lungs
LDH 4 – liver, skeletal muscle, brain, kidney
LDH 5 – liver, skeletal muscle, kidney
Clinical Uses for LDH
Important diagnostic tool for hepatic dysfunction
Hemolysis and transfusion reactions
Specific injury patterns
LDH 1:2 “Flip” – cardiac necrosis
LDH 4 & 5 ⇑ - hepatitis, cirrhosis
LDH 5 ⇑ - hepatocellular disease/injury or skeletal muscle disease/injury
LDH 2, 3, 4, 5 ⇑ - lung and liver abnormality
All fractions ⇑ - multi-organ dysfunction or failure
ALP (Alkaline Phosphatase)
Reference Range: 42 – 128 U/L
Enzyme originating mainly in the bone, liver and placenta
Clinical use for ALP
Detection of bone diseases
Detection of liver diseases
Obstructive biliary diseases/conditions
Metastatic liver cancer
More specific ALP isoenzymes can help differentiate between liver & bone disease
Implications of Increased levels of ALP
Cirrhosis
Biliary obstruction
Liver cancer
Normal pregnancy
Growing children
Bone mets
Intestinal ischemia
Hyperthyroidism
Hyperparathyroidism
Implications of Decreased levels of ALP
Malnutrition
Hypothyroidism
Pernicious anemia
Magnesium deficiency
Celiac sprue
GGT (Gamma-Glutamyltransferas)
Reference Range: <45 yrs = 5-27 U/L ; >45 yrs = 8-38 U/L
Highest concentrations in liver & biliary tract
Clinical Uses of GGT
Sensitive indicator of hepatocellular disease or biliary obstruction
Elevations parallel ALP ⇑ but more sensitive
Indicate heavy & chronic alcohol use – elevations in chronic drinkers 75% of the time
Implications of Increased levels of GGT
Liver disease
Pancreatic disease
Many cancers
ETOH
Phenytoin, barbituates
DM
Obestity
Common patterns in liver disease
Billirubin source and excretion
Breakdown of RBCs in RES releases Hgb + globin portion from the RBCs; heme is converted to biliverdin → bilirubin
Bilirubin initially is unconjugated (indirect)
Unconjugated bilirubin conjugates with glucuronide in the liver to form a conjugated (direct) form of bilirubin
Direct bilirubin is excreted from liver cells to hepatic ducts → common bile duct → bowel
Bilirubin testing organization
Differentiation between direct & indirect to determine etiology of defect
Protect sample from light (>1 hr exposure can decrease bilirubin levels
Clinical uses of bilirubin
Hepatocellular/Biliary tract disease/dysfunction
Evaluation of jaundice in adult patients
Evaluation of jaundice in newborns
Interference of testing methods with hemolysis and lipemic specimens
Implications of increased indirect bilirubin
(pre-hepatic)
Erythroblastosis fetalis
Transfusion reaction
Sickle cell, pernicious, & hemolytic anemia
Large volume blood transfusion
Hepatitis, cirrhosis
Neonatal hyperbilirubinemia
Crigler-Najjar syndrome, Gilbert syndrome
Implications of increased direct bilirubin
⇑ Levels of Direct (posthepatic)
Extrahepatic duct obstruction
Extensive metastatic liver cancer
Congenital defects in enzyme quantity
Implications of increased levels of both indirect and direct bilirubin
⇑ Levels with both Direct & Indirect (hepatic)
Hepatocellular disease
Hepatotoxins
Hepatoma
Markers of Hepatic Synthesis
The liver is largely responsible for coagulation factor and protein synthesis
Albumin – decreased levels indicate a chronic condition & are useful for monitoring progression of disease
Prothrombin time (PT) – in pts with chronic & severe hepatocellular injury, the PT is markedly prolonged (PTT is usually prolonged as well)
Ammonia source hepatic implication
Ammonia is a breakdown product of protein catabolism which is converted to urea in liver & excreted by kidneys
In severe hepatocellular dysfunction it cannot be catabolized into urea
Clinical uses of Ammonia
Specimen should be drawn in a green top tube and placed on ice immediately
Monitoring of severe liver disease and diagnosis or follow-up of hepatic encephalopathy
Implications of increased Ammonia
*Hepatic encephalopathy
*Hepatocellular disease
Portal hypertension
GI bleeding
Obstruction with mild liver disease
