Half-life 20 days \(\to\) often normal in hyperacute liver failure
Part of Child-Pugh score in cirrhosis
Also lowered by inflammation (acute phase reactant), starvation, kwashiorkor, nephrotic syndrome
Prothrombin time
Time taken for clotting to occur after addition of tissue factor
Normal = 12-15 seconds (INR 0.8-1.2)
Liver generates all clotting factors except for factor VIII, VWF, calcium and tissue factor
But liver also generates antithrombotic protein C and S
Both impaired with synthetic failure
Therefore acute liver failure \(\to \ \uparrow\)PT that is disproportionate to in vivo coagulopathy (i.e. overestimates bleeding risk)
PT can also be elevated by vitamin K deficiency, anticoagulants (esp. warfarin), nephrotic syndrome, consumption (e.g. DIC)
Glucose
Primary metabolic fuel in human body
Normal = 5-10mmol/L
Normally, liver stores glucose as glycogen + can perform gluconeogenesis \(\to\) mobilize glucose \(\to\) "glucostat" function
Acute liver failure \(\to\) hypoglycaemia
In chronic liver failure, failure of insulin clearance \(\to\) chronic hyperinsulinaemia \(\to\) insulin resistance \(\to\) hyperglycaemia
Confounded by nutrition, diabetes mellitus, medications (e.g. exogenous insulin)
Ammonia
Product of amino acid and purine catabolism
Normal = <35\(\mu\)M
Normally, 100% of circulating ammonia \(\to\) liver \(\to\) urea cycle \(\to\) urea, which is 75% renally excreted and 25% excreted in stool (where some undergoes enterohepatic recirculation)
Failure of urea cycle due to metabolic liver failure \(\to\) ammonia accumulation
Causative agent in hepatic encephalopathy and cerebral oedema
Bilirubin
Product of haem catabolism; exclusively cleared by biliary route
Normal = <5\(\mu\)M
Normally unconjugated bilirubin \(\xrightarrow{\text{in liver}}\) conjugated bilirubin \(\to\) eliminated in bile