Hepatic dysfunction

Serum Albumin is a marker of Hepatic Synthetic Capacity. Albumin 1/2-life is 3 weeks, so hypoalbuminemia indicates chronic dysfunction, but won’t be apparent in acute injury. Albumin maldistribution, loss via kidneys, and degredation can also be causes of hypoalbuminemia, so can dilution from increased volume 

The liver synthesizes 11 blood coagulation proteins, most of which have short 1/2-life (ranging from 4 hours for factor VII and 4 days for fibrinogen). PT/INR are thus good markers of acutely decreased hepatic synthetic capacity. High INR indicates lack of many factors but mostly VIIa which is the most quickly cleared. INR is useful for prognosis of hepatotoxic liver injury and surgical interventions in patients with liver failure. PT/INR is also dependent on Factors I (fibrinogen), II (prothrombin), V, and X as well as VIIa, but the half-life of these components is longer 

Hepatic Dysfunction

• PT/INR: primarily reflects Factor VIIa (t1/2 4 hours), although dependent on Factors I, II, V, and X as well 
• Albumin: t 1/2 3 weeks 

Cellular injury is better reflected by AST, ALT, LDH (may reflect hepatocellular injury or extrahepatic disorders), and in some cases, glutathione-S-transferase (GST, useful in some drug-induced liver injuries). AP, 5′-Nucleotidase (5′-NP), γ-Glutamyl Transpeptidase (GGGP), and bilirubin are more useful for assessment of structural problems.