biochemical testing for liver disease Flashcards
globulins
total protein - albumin
all other plasma proteins, not all made by the liver
liver enzymes
alkaline phosphatase ALP
gamma glutamyl transferase GGT
alanine aminotransferase ALT
aspartate animotransferase AST
the amino transferases
ALT, AST
if increased, implies hepatitis
bilirubin is a breakdown product of
haem
albumin is synthesised by
the liver
low albumin implies
synthetic function of the liver inhibited
ALP and GGT imply
cholestasis
high bilirubin implies
cholestasis jaundice or increased red cell turnover
albumin may be decreased due to
failure of liver synthetic function but can also be decreased by inflammation or renal losses
high bilirubin
rises if the liver fails to excrete is, but can also be increased by haemolysis
ALT and AST are involved in
amino acid metabolism
high AST may imply
non-liver related pathology
isolates or predominant increase in AST may indicate
skeletal or cardiac macula origin
increased AST:ALT ratio seen in
alcoholic hepatitis, severe liver injury, cirrhosis secondary to chronic hepatitis C infection, non-liver disease include muscle
increased ALT and AST is seen in
viral, autoimmune, alcoholic and toxic hepatitis, and non-alcoholic fatty liver disease
liver fibrosis
assessment og the presence and degree to fibrosis can be useful in patients which chronic liver disease for prognosticating and planning specific therapies top prevent progression to cirrhosis
golda standard is liver biopsy
non-invasive tests used in place of liver biopsy for fibrosis
elastography for ultrasound or MRI
serum fibrosis markers
serum fibrosis markers
most are reported as scores derived from algorithms incorporating several markers
liver fibrosis markers examples
- hepascore
- APRI score
- FIB-4
isolated raised GGT (without raised ALP)
recent excessive alcohol ingestion
cholestasis
jaundice and pruritus
raised ALP and GGT
mild raised ALT and AST
raised bilirubin
biliary tree obstruction induces synthesis and release of
ALP and GGT
ALP can also come from
bone, placenta, and other sources
GGT can be induced by
alcohol and other drug ingestion
uncongugated bilirubin
not water soluble, so must circulate bound to plasma proteins such as albumin
bilirubin is congugated in the
liver
makes it more water soluble and it is excreted into the small intestine via bile
what happens to the congugated bilirubin
is uncongugated and converted into water soluble urobilinogen in the gut
can be reabsorbed
is ultimately excretes by the kidneys as urobilin
bilirubin if there is an abstraction to bile flow
conjugated bilirubin spills into the circulation instead of being excreted into the gut
conjugated hyper bilirubinaemia
conjugation occurs in the liver so this implies spillage of contents from the liver, ie. biliary obstruction or hepatocellular injury
- cholestatic liver disease
unconjugated hyperbilirubinaemia
implies either haemolysis, or a defect in hepatic conjugation (ie. some inborn errors of metabolism or liver failure)
- haemolytic disease
- congenital defects
- liver failure
- drugs
- physiological jaundice in neonates
cholestatic liver diseases
- extrahepatic - mass eg. head of pancreas, gallstones
- intrahepatic - primary biliary cholangitis, primary sclerosing cholangitis
- drugs
- congenital defects (failure to excrete into bile)
why are liver enzymes normal in advanced liver disease
transaminases are no longer being produced in response to damage due to liver failure to produce them
isolated high ALP indicates
malignancy of bone
cholestasis less likely if GGT is normal
