Liver Function Tests
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Direct answer
Liver function tests are a panel of blood tests organised by what each group reflects: hepatocellular injury (ALT and AST), cholestasis (alkaline phosphatase and GGT), synthetic function (albumin and prothrombin time/INR) and excretory function (bilirubin, with or without bile acids). No single test measures overall liver function; the diagnostic value lies in recognising patterns — hepatocellular, cholestatic or mixed — alongside the clinical setting.
What you must remember
- ALT (SGPT) is the most liver-specific transaminase; AST (SGOT) also rises in muscle injury, myocardial infarction and haemolysis. ALT above AST suggests viral hepatitis, while an AST/ALT ratio above two favours alcoholic liver disease.
- Alkaline phosphatase rises in cholestasis but also in bone disease, pregnancy and the adolescent growth spurt; a parallel rise in GGT (or 5'-nucleotidase) confirms the hepatic origin of a raised ALP.
- Albumin, with a half-life of about twenty days, reflects chronic synthetic capacity; a low albumin suggests chronic liver disease, malnutrition or protein loss.
- Prothrombin time depends on clotting factors with much shorter half-lives (factor VII about four to six hours); a prolonged INR that fails to correct with vitamin K indicates failing hepatic synthesis and is a marker of severity.
- Fractionated bilirubin directs the diagnosis — predominant unconjugated bilirubin suggests haemolysis or conjugation defects, predominant conjugated bilirubin suggests hepatocellular or obstructive disease.
- Supporting tests for specific diagnoses: alpha-fetoprotein for hepatocellular carcinoma surveillance, caeruloplasmin for Wilson disease, ferritin and transferrin saturation for haemochromatosis, autoantibodies for autoimmune hepatitis, and viral serology.
- The Child-Pugh score (bilirubin, albumin, INR, ascites, encephalopathy) grades the severity and prognosis of cirrhosis.
Common confusion
A raised alkaline phosphatase is often misread as liver disease in a patient with bone pathology. GGT resolves the doubt: it rises with hepatic but not bone ALP, though it is itself inducible by alcohol and anticonvulsants. A second trap is assuming normal LFTs exclude liver disease — a well-compensated cirrhosis, and even early hepatocellular carcinoma, can coexist with near-normal values.
Exam-focused takeaway
For theory, classify the tests into the four functional groups, give one example and one limitation for each, then interpret a given pattern. Viva questions ask which marker best reflects acute injury (ALT), chronicity (albumin) and prognosis or synthetic failure (INR). MCQs test the factor with the shortest half-life, the AST/ALT ratio in alcoholic hepatitis, the GGT role in separating bone from liver ALP, and the components of the Child-Pugh score.
Frequently asked questions
Which LFT best indicates acute hepatocellular damage?
ALT, because it is predominantly hepatic in distribution; very high levels accompany acute viral hepatitis and paracetamol injury.
Why is prothrombin time prolonged in liver disease?
Reduced synthesis of vitamin K-dependent clotting factors; failure to correct after vitamin K administration points to parenchymal failure rather than cholestasis.
What does a raised GGT signify?
Hepatic origin of a raised alkaline phosphatase, cholestatic disease, or enzyme induction by alcohol or drugs; it is sensitive but not specific.
Why can LFTs be normal in cirrhosis?
The liver has a large functional reserve, so compensated cirrhosis may show normal or near-normal enzymes until decompensation occurs.
Which tests assess synthetic function?
Serum albumin and prothrombin time/INR, reflecting long-term and short-term synthetic capacity respectively.