liver function tests LFTs Flashcards
what is ALT/AST
serum transaminases
ie alanine aminotransferases
aspartate aminotransferases
ALP
alkaline phosphatases
GGT
gamma glutamyl transpepridase
what are the indices of intrinsic synthetic function
albumin
prothrombin time (INR)
bilirubin
transaminases
they catalyse y-amino group transfers
ie ALT/AST > ketoglutarate
ALT characteristics
more sensitive than AST
predominantly cytosol located
predominantly liver
short half-life circa 47 hours
AST characteristics
in cytosol and mitochondria
present in liver, heart, pancreas, skeletal muscle, brain , lungs RBCs WBCs
has a half life of about 17 hours
aminotransferases
-marked increase in hepatocellular pathologies
-usually less than 500U/L in obstructive jaundice
»except acute phase of biliary obstruction with passage of stone into the CBD - this process may coincide with ALT values >1-2000 U/L
alkaline phosphatases
these are enzymes that catalyse the hydrolysis of a number of organisms phosphate esters
- have a half life of about one week therefore often lag to rise and slow precipitation in resolution of pathology
what is the origin of alkaline phosphatases
biliary - cholestasis enhances synthesis and release of ALP bone placenta intestine kidney
what is GGT
an enzyme involved in gluthionine metabolism, transfer of amino acids across cellular membranes and leukotriene metabolism
- not found in the bone
- used as a diagnostic marker for liver or cholestatic diseases
- useful in determining whether elevated ALP is of bone or of liver origin
- GGT is inducible
- levels of GGT can be increased with consumption of alcohol
what is bilirubin involved in
the breakdown of the product of Heme
what is the difference between conjugated and unconjugated hyperbilirubinaemia
conjugated bilirubin = water soluble and secreted into bile
unconjugated bilirubin = waste product of haemoglobin breakdown that is taken up by the liver
what is prothrombin time
measure the conversion time from PT > thrombin and thus reflects a vital component of the liver
-an elevated PT may reflect reduced synthetic functionality
**the liver is responsible for synthesis of most clotting factors ie factor I = fibrinogen
factor II = prothrombin
factors V VII IX X XII and XIII
what is a normal reference range
!!!!
what areas should be converted in history taking
- use exposure to any chemical medication
- accompanying symptoms ( ie pruritus, jaundice, arthralgia, weight loss, exanthema, fever, anorexia )
- parenteral exposures ie IV medications/blood transfusions/intranasal drugs/tattoos/sexual history
- travel history inclusion of timings and exposure risks ie contact
- alcohol exposure
- occupational exposures
- temporal variation
in relation to medication in history taking - what should be covered
timings ! has anything changed? are they on : antibiotics antidepressants HMG Co A inhibitors statins sulphonamides sulphonylureas NSAIDS anti-epileptics anti-TBs
over the counter medications?
When the ration of of ALT/AST > ALP BiliN/ increases - what does this signify
hepatocullular injury
when ALPs are greater then ALT/AST Bili - what does this signify
cholestasis
when there is an increase in PT/INR what could the cause be
prolonged jaundice/ vit K malabsorption
hepatocellular dysfunction