LFTs Flashcards
Why check LFTs?
- Confirm a clinical suspicion of potential liver injury / disease
- To distinguish between hepatic jaundice (ie hepatocellular injury) and obstructive jaundice (cholestasis)
What blood tests assess liver function?
ALT, AST, ALP, GGT (used to distinguish between hepatic and obstructive jaundice)
Bilirubin, albumin PT (used to test liver’s synthetic function)
What is considered a large rise for ALT and ALP?
ALT - moderate rise = <10-fold, large rise = >10-fold
ALP - moderate rise = <3-fold, large rise = >3-fold
Where is ALT usually found?
Found in high concentrations WITHIN hepatocytes, and enters the blood following hepatocellular injury
Therefore it is a useful marker of hepatocellular injury
Where is ALP usually found?
Concentrated in the liver, bile duct and bone tissues
Often raised in liver pathology due to increased synthesis in response to cholestasis
Therefore it is a useful indirect marker of cholestasis
When do you review GGT?
Important to review when there is a rise in ALP
When would GGT be raised?
Can be suggestive of biliary epithelial damage and bile flow obstruction
Can also be raised in response to alcohol and drugs such as phenytoin
A markedly raised ALP + raised GGT –> highly suggestive of cholestasis
What would an isolated rise of ALP suggest?
Should raise suspicion of non-hepatobiliary pathology
Increased bone breakdown can elevate ALP (eg bone mets, vit D deficiency, bone fractures)
What if the patient is jaundiced but ALT and ALP levels are normal?
Suggests a pre-hepatic cause of jaundice eg:
Gilbert’s syndrome
Haemolysis
What is Gilbert’s syndrome?
Mild genetic liver disorder
High levels of unconjugated bilirubin due low availability of UGT in the liver. Causes a ‘backlog’ in the bloodstream
Commonly causes jaundice when patients are unwell
What are the liver’s main synthetic functions and what are the tests that measure this?
- Conjugation and elimination of bilirubin –> serum bilirubin
- Synthesis of albumin –> serum albumin
- Synthesis of clotting factors –> PT
- Gluconeogenesis –> serum blood glucose
What is the pattern of normal/dark urine and pale/normal stools in jaundiced patients?
Conjugated bilirubin turns urine dark (urobilinogen)
Fat is not absorbed if bile and pancreatic lipase cannot reach the bowel due to obstruction —> turns stool pale
Normal urine + normal stools –> pre-haptic cause (aka unconjugated hyperbilirubinaemia)
Dark urine + normal stools –> hepatic cause
Dark urine + pale stools –> obstructive cause
What are some causes of unconjugated hyperbilirubinaemia?
Haemolysis eg haemolytic anaemia
Impaired hepatic uptake eg drugs, congestive heart failure
Impaired conjugation eg Gilbert’s syndrome
Why would albumin levels fall?
(helps to bind water, cations, fatty acids and bilirubin, maintains oncotic pressure of blood)
Liver disease eg cirrhosis
Inflammation
Protein-losing enteropathies, nephrotic syndrome (causing loss of albumin)
What is the AST/ALT ratio used for?
Distinguishes between likely causes of LFT derangement
ALT>AST –> chronic liver disease
AST>ALT –> cirrhosis, acute alcoholic hepatitis