LFT interpretation Flashcards
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
jaundice: dark urine + normal stools ?
- hepatic cause
jaundice: dark urine + pale stools ?
- post hepatic cause - obstructive
causes of unconjugated hyperbilirubinaemia?
- haemolysis (e.g. haemolytic anaemia)
- impaired hepatic uptake (e.g. drugs, congestive cardiac failure)
- impaired conjugation (e.g. gilbert’s syndrome)
causes of conjugated hyperbilirubaemia?
- hepatocellular injury
- cholestasis
albumin is made where?
- in liver
- helps bind water, cations, fatty acids and bilirubin
- also plays a role in maintaining oncotic pressure of blood
albumin levels fall due to?
- liver disease -> dec production of albumin (cirrhosis)
- inflammation - triggering acute phase response temporarily decreases liver’s production of albumin
- excessive loss of albumin due to protein-losing enteropathies (disease of intestine) or nephrotic syndrome
prothrombin time
- measure of blood’s coagulation tendency, specifically assessing extrinsic pathway
- inc PT alone can indicate liver disease and dysfunction
- liver is responsible for production of clotting factors, so liver pathology can impair this process resulting in inc PT time
ALT > AST is assoc with?
- chronic liver disease
AST > ALT is assoc with?
- cirrhosis and acute alcoholic hepatitis
liver plays a significant role in gluconeogenesis. True or False?
- true
-> therefore can be indirect assessment of livers synthetic function - however last function to become impaired in context of liver failure
in context of cholestasis what LFT values are considered high?
ALP, GGT, bilirubin
(ALT norm or slightly inc)
in acute hepatocellular damage what LFT value is noted to be considerably high?
- ALT
common causes of acute hepatocellular injury?
- poisoning (paracetamol overdose)
- infection - Hep A and B
- liver ischaemia
common causes of chronic hepatocellular injury?
- alcoholic fatty liver disease
- non-alcoholic fatty liver disease
- chronic infection (Hep B or C)
- primary biliary cirrhosis
less common causes of chronic hepatocellular injury?
- alpha-1 antitrypsin deficiency
- wilson’s disease
- haemochromatosis
