LFTs Flashcards
what is bilirubin derived from and what is the source of this
haem from Hb
what does haem convert to
biliverdin (then converted to unconjugated and conjugated bilirubin)
what is excreted in the bile (to the intestine)
bilirubin glucuronide
what is bilirubin glucuronide converted to by what
bilirubin in the intestine by B glucuronidase
what is bilirubin converted to in the intestine
urobilinogen
what happens to the urobilinogen
some is reabsorbed back into the circulation other is metabolised further to urobilinogen stercobin
what happens to some of the reabsorbed urobilinogen
some is excreted back into the bile, the rest in the urine
what is total bilirubin
conjugated and unconjugated bilirubin
what is direct bilirubin
conjugated only
what is indirect bilirubin
unconjugated. calculated by the total- direct.
what does raised ALT (alanine transaminase) show
hepatocellular damage (more specific than AST).
where is ALT found
hepatocytes and small amount in the muscle
what does raised AST (aspartate transamine) show
hepatocellular damage (less specific than ALT)
where is AST found
hepatocytes, muscle and erythrocytes
what does raised ALP (alkaline phosphatase) show
cholestasis
where is ALP found
biliary canalicular membrane of hepatocytes and biliary epithelium. also placenta, bone and intestine
what does GGT co localise with
ALP
what can cause a rise in GGT
drug induced, including alcohol
what is albumin
the main plasma protein produced by the liver
is albumin a good indicator of function
no as the liver has good synthetic function and the half life is only 20 days so would have to have a prolonged duration of injury. also negative acute phase reactant so decreases in inflammation
what is the best measure of function
prothrombin time
what is prothrombin time dependent on
vitamin K dependent coagulation factors.
why is PT a good indicator
eg VII half life is 6 hours so if it is decreased and prolonged PT shows liver injury quickly
what are the LFTs in cholestasis
ALP»_space; ALT. bilirubin may or may not be elevated
what are the LFTs in hepatocellular damage
ALT»_space; ALP. bilirubin may or may not be elevated
what can cholestatic causes of liver disease be split into
intra and extra hepatic
examples of extra hepatic biliary obstruction
gallstones, carcinoma of head of pancreas, cholangiocarcinoma, stricture of the bile duct
examples of intra hepatic biliary obstruction
cirrhosis, primary biliary cirrhosis, malignant liver disease, sepsis, drugs, primary sclerosing cholangitis
causes of hepatocellular damage
infectious hepatitis (hep A,B,C,E,EBV; bacterial and protozoa); drugs/toxins (alcohol, paracetemol, statins, antibiotics); metabolic (fatty liver disease, haemachromatosis); autoimmune hep and ischaemia/infarction
what test do you need to do if you suspect haemachromatosis
ferritin- do alongside CRP as ferritin is an acute phase reactant
what liver autoantibody is tested if suspecting primary biliary cirrhosis
AMA (anti mitochondrial antibody)
what liver autoantibody is tested if suspecting primary sclerosing cholangitis
ANCA
what liver autoantibody is tested if suspecting chronic active hepatitis
anti smooth muscle antibody
what liver autoantibody is tested if suspecting autoimmune hep
ANF and anti kidney microsomal antibody
what test should be done if suspect Wilsons
serum copper/caeroloplasmin - both raised.
what is Wilsons
inherited defect in copper metabolism
evaluating consequences of liver disease- total protein and globulins
globulins can be high in inflame liver disease also high in inflam conditions, myeloma
evaluating consequences of liver disease- platelets
low which shows portal hypertension
evaluating consequences of liver disease- glucose
prone to hypoglycaemia because impaired function of liver- glycogenolysis and gluconeogenesis
evaluating consequences of liver disease- lipids
increase cholesterol in cholestatic liver disease, increased triglycerides in fatty liver
evaluating consequences of liver disease- urea
may be low in chronic liver disease
where is the main site of urea production
LIVER
evaluating consequences of liver disease- ammonia
may be high in liver disease and decompensated cirrhosis due to shunting of portal blood
what are the principal signs of obstructive jaundice
pale stool, dark urine
why is the stool pale (obstructive)
stercobilin not formed as bilirubin cant reach GIT
why is the urine dark (obstructive)
as conjugated bilirubin is excreted in the urine
urobilinogen would be negative on a urine dipstick why (obstructive jaund)
because it is only formed in the GIT so in obstructive jaundice it is not reaching GIT
if bilirubin is not present in the urine what form will it be in
unconjugated form
how is unconjugated bilirubin transported
bound to albumin but not covalently bound
what can cause an isolated increase in serum bilirubin
defect in conjugation of bilirubin, or haemolysis
what is the most common cause of hyperbilirubinaemia
Gilberts
what is Gilberts syndrome
deficiency of UDP glucuronyl transferase which is needed for the conjugation of bilirubin thus leading to an unconjugated hyperbilirubinaemia. the same deficiency is seen in Criggler-Najjar syndrome which presents in infants and young children but it is more severe here
what does the LFT show in acute hep
very high ALT and bilirubin
which product of haem breakdown enters the enterohepatic circulation
urobilinogen
