Interpreting liver chemistries Flashcards
Liver chemistry abnormalities indicating hepatocellular damage
AST and ALT
Liver chemistry abnormalities indicating cholestasis, impaired conjugation or biliary obstruction
bilirubin
liver chemistry abnormalities indicating cholestasis, infiltrative disease, or biliary obstruction
alkaline phosphatase
liver chemistry abnormalities indicating synthetic dysfunction
albumin, prothrombin time
What does PT (prothrombin time) assess?
extrinsic clotting pathway
prolonged PT
significant hepatocellular dysfunction, vitamin K deficiency
role of AST/ALT aminotransferases
catalyze transfer of amino acid groups to form hepatic metabolites
organs expressing AST
liver, heart, muscle, blood
organs expressing ALT
liver only
AST:ALT ratio > 2
suggests alcoholic liver disease.
preferential alcohol-induced injury to mitochondria enriched in AST
Causes of severe ( > 15x normal) AST and ALT elevations
acute viral hepatitis, meds/toxins, ischemic hepatitis, autoimmune hepatitis, Wilson’s disease, acute Budd-Chiari syndrome, thrombosis
alkaline phosphatase role
hydrolase –> removes phosphate groups from nucleotides, proteins and alkaloids
causes of alk phos elevation
cholestatic/infiltrative diseases of liver, obstruction of biliary system, bone disease, pregnancy, chronic renal failure
What lab is used to differentiate hepatobiliary vs nonhepatobiliary etiology for rise in alk phos?
5’ nucleotidase and
GGT: not present in bone. elevated in alcohol consumption and almost all types of liver disease
infiltrating liver diseases –> high alk phos
sarcoidosis, tuberculosis, fungal infection, amyloid, lymphoma, metastasis, HCC
process of bilirubin conjugation
unconjugated bilirubin in the sinusoids –> uptake to hepatocytes via oatp –> conjugation –> ATP pump of conjugated bilirubin into bile canaliculus
mechanism of hemolytic jaundice
high levels of unconjugated bilirubin in the blood –> overwhelmed oatp –> unconjugated bilirubin cannot be completely taken up by hepatocytes –> rise in indirect bilirubin levels
mechanism of biliary obstruction jaundice
conjugated bilirubin cannot exit canaliculus/duct –> shunt to blood –> rise in serum direct bilirubin levels
Gilbert’s disease
stress-related hyperbilirubinemia (rise in indirect bilirubin)
Crigler-Najjar syndrome
Autosomal recessive
Type 1 = absence of UDP-GT –> severe jaundice, neuro impairment
Dubin-Johnson syndrome
defective secretion of conjugated bilirubin (mutated MRP2 in ATP binding region) –> elevated conjugated bilirubin
benign
mechanism of bilirubin elevation in cirrhosis
increased fibrosis –> decreased unconjugated bilirubin into the hepatocytes –> rise in indirect bilirubin
increased hemolysis in severe liver disease
