why check LFTs?
- confirm clinical suspicion of potential liver injury or disease
- to distinguish between hepatocellular injury (hepatic jaundice) and cholestasis (post-hepatic or obstructive jaundice)
what is involved in assessing liver function?
- ALT (alanine transaminase)
- AST (aspartate aminotransferase)
- ALP (alkaline phosphatase)
- GGT (gamma-glutamyltransferase)
- bilirubin
- albumin
- prothrombin time (PT)
ALT, AST, ALP, and GGT are used to distinguish between what?
- hepatocellular damage and cholestasis
bilirubin, albumin, and PT are used to assess what?
- liver’s synthetic function
ALT is found in high conc within hepatocytes and enters blood following?
- hepatocellular injury
ALP is particularly concentrated in the liver, bile duct and bone tissues. It is raised in response to what?
- cholestasis
- and also other liver pathology
a > 10-fold inc in ALT and < 3-fold inc in ALP suggests a predominantly?
- hepatocellular injury
-> if ALT raised markedly higher THINK hepatocellular pattern of injury
< 10-fold inc in ALT and > 3-fold inc in ALP suggests?
- cholestasis
-> possible to have mixed pic involving hepatocellular injury and cholestasis
-> if ALP raised markedly higher THINK cholestasis
in presence of a raised of ALP, a raised GGT may indicate?
- biliary epithelial damage and bile flow obstruction
-> very high ALP and raised GGT is highly suggestive of cholestasis
when else can GGT be raised?
- in response to alcohol and drugs e.g. phenytoin
isolated rise of ALP should raise suspicion of ?
- non-hepatobiliary pathology
- ALP also found in bone - so anything leads to inc bone breakdown can inc ALP
- bony mets or primary bone tumours e.g. sarcoma
- Vit D deficiency
- recent bone fractures
- renal osteodystrophy
patient is jaundiced but ALT and ALP levels are normal?
- isolated rise in bilirubin -> pre-hepatic cause of jaundice
- Gilbert’s syndrome - most common cause
- Haemolysis: check blood film, FBC, reticulocyte count, haptoglobin, and LDH levels to confirm
what is Gilbert’s syndrome?
- slightly higher than normal bilirubin build up in blood
- as gene involved in bilirubin transportation into bile does not work, bilirubin builds up in blood stream -> jaundice
what are triggers of jaundice episodes in gilbert syndrome?
- being dehydrated
- fasting
- drinking too much alcohol
- being ill
- heavy physical exertion
- not getting enough sleep
- menstruation
- having surgery
-> is largerly asx
who is affected by gilberts syndrome?
- affects more men than women
- usually dx in person’s late teens or early 20s
diagnosis of Gilberts syndrome
- LFT
liver’s main synthetic functions?
- conjugation and elimination of bilirubin
- synthesis of albumin
- synthesis of clotting factors
- gluconeogenesis
investigations to assess synthetic liver function?
- serum bilirubin
- serum albumin
- prothrombin time
- serum blood glucose
bilirubin is a breakdown product of what?
- haemoglobin
- unconjugated bilirubin is taken up by liver and then conjugated
when is hyperbilirubinemia usually visible as jaundice?
- > 60ummol/l
unconjugated bilirubin is now water soluble and thus does not affect?
- colour of patient’s urine
conjugated bilirubin can pass into urine as what?
- urobilinogen -> causing urine to become darker
if bile and pancreatic lipases are unable to reach bowel due to blockage (in obstructive post-hepatic pathology), fat is not able to be absorbed resulting in?
- pale, bulky and more difficult to flush stools
jaundice: normal urine + normal stools ?
- pre-hepatic cause
