Liver Function TestsALT and ASTALT and AST are both a marker of
hepatocyte damage and circulating hepatocyte enzymes -
hepatocellular patternAspartate transaminase (AST) (normal: 0-31
U/L)Lesser amounts also found in skeletal muscle, brain, myocardium
kidneyLevels rise slowly after damage and clear quickly after
damage ceases half life 12-24hAlanine transaminase (ALT) (normal:
0-31 U/L)Most LIVER specificRises slowly after damage and clears
gradually after damage ceases half life of 40-60h Acronym for
conditions causing hepatitis ABCDEFGHIAutoimmune (via genetic
predisposition or acute liver infection)Hep BHep C(viral
hepatitis)DrugsEthanolFatty liver disease (NASH/NAFLD)Growth
tumoursHaemodynamic factors heart failureInfiltrative
haemachromatosis, wilsons disease (copper deposition)Conditions and
AST, ALT ratiosAlcoholic related hepatic injury(only about 10% of
problem drinkers have elevated AST)AST > ALT generally in 2:1
ratio toASTedAlso mild macrocytosis (MCV >100fl) in 30-60%
Non-alcoholic steatohepatitis (NASH) aka non alcoholic fatty
liver disease (NAFLD)ALT > ASTElevations within 3x UNL
Hepatitis Hep ABCDE, drug induced hepatitis, industrial chemical
(toxic) hepatitisALT > ASTElevations of both > 10x UNL (upper
normal limit)
Acetaminophen toxicityMassive AST and ALT riseBoth >20x
UNLALP aka APAlkaline phosphatase (normal: 0-125 U/L) indicative
for damage to the biliary treeAnywhere along the tree left and
right hepatic duct, common hepatic duct, cystic duct,
CBDcholestatic picture chole means bile and static means stasisAlso
found in bone, placenta and gut i.e rapidly dividing or
metabolically active tissue. Increase in ALP may indicate damage OR
accelerated cellular division in these areasGGTGamma glutamyl
transferase (normal: 0-45 U/L)If also raised with ALP, tells you
that any present ALP is coming from the biliary treeif GGT negative
then try to find another cause for the raised ALPAlso found in the
kidneyConditions and ALP, GGTPBC - Primary biliary cirrhosis
(autoimmune)Pathology slow progressive destruction of small bile
ducts of the liver build up of bile in the liver (cholestasis)
tissue damage (scarring fibrosis cirrhosis)Look for deranged LFTs
GGT, ALP. Also antibodies ANA, AMAPSC primary sclerosing
cholangitisCholelithiasis cholestasisAcute cholecystitis can lead
to abscess and fistulaCholedocholithiasis stone in the CBDAscending
cholangitis infection inside the biliary tree airising from
microbes migrating upwards from the duodenumMeasuring Liver
function PT via coagulation factors (makes all factors except
factor VIII-vWF), albumin, bilirubinProthrombin time PTReflective
of whether the liver is still functioningLiver okay = still making
I, II V, IX, X, XIITakes a while before PT is altered 80% of liver
cells are already deadAlbuminmost ubiquitous protein produced by
the liver and provides most of the oncotic pressure of the
bloodBilirubinDegradation product of heme with 90% arising from
haemoglobin and a smaller % from myoglobinProduction 4mg/kg/day and
usually matched by excretion levels remain low and stableHigh
bilirubin can displace drugs that have a high propensity for
albumin increase of free drug concentration
