Liver Function Tests Flashcards
what are transaminases
intracellular enzymes in the liver
how are transaminases relseased
released from liver in context of hepatocellular injury
types of transaminases
catalyse gamma-amino group transfers alanine aminotransferase (ALT) aspartate aminotransferase (AST)
examples of catalyse gamma-amino group transfers
aspartate
alanine -> ketoglutarate
describe ALT
more sensitive than AST
short half life circa 47 hours
where is ALT located
cytosol in the liver
where is AST located
cytosol and mitochondria in;
liver, heart, pancreas, skeletal muscle, brain, lungs, RBCs, WBCs
describe when aminotranferases would be raised
become deranged in aetiologies - increase in hepatocellular pathologies
levels may/may not reflect the extent of damage
levels of aminotransferases in obstructive jaundice
less than 500 U/L
what are alkaline phosphatase
enzymes that catalyse the hydrolysis of a number of organic phosphate esters
how are alkaline phosphatases raised
long half life and so therefore often lag to rise and slow precipitation in resolution of pathology
where are alkaline phosphatase found
biliary (epithelial cells of ducts) cholestasis enhances synthesis and release of ALP bone placenta intestine kidney
what are gamma glutamyl transpeptidases (GGT)
enzyme involved in gluthionine metabolsim, transfer of amino acids across cellular membranes and leukotriene metabolism
where are GGTs located
cell membranes of; liver kidneys bile duct pancreas gallbladder spleen heart brain seminal vesicle
what does raised GGT indicate
diagnostic marker for liver or cholestatic diseases
determines whether elevated ALP is of bone or liver origin
what may cause GGT to rise
consumption of alcohol
liver diseases
describe unconjugated bilirubin
transported to liver bound to albumin
describe conjugated bilirubin
bilirubin becomes water soluble and so is excreted in urine and faeces
what clotting factors does the liver synthesise
factor; I (fibrinogen) II (prothrombin) V VII IX X XII XIII
what does prothrombin measure
the conversion time from PT to thrombin and thus reflects a vital component of the liver
why would prothrombin be elevated
reduced synthetic functionality drugs (warfarin) bilie malabsorption causing relative Vitmain K deficiency consumptive coagulopathies congenital coagulopathy
patterns of hepatocellular injury
ALT/AST > ALP
increase bilirubin
patterns of cholestasis
ALP > ALT/AST
increased bilirubin
patterns of prolonged jaundice/vitamin K, malabsorption and hepatocellular dysfunction
increased prothrombin time
increased INR
what enzyme is difficult to use in isolation
albumin
