Hepatology - Investigations in liver disease Flashcards
What tests best reflect synthetic liver function?
Prothrombin time (clotting factors are synthesised in the liver) and serum albumin, which are increased and reduced, respectively, with impaired function. Hypoalbuminaemia is also found in hypercatabolic states (e.g. sepsis, chronic inflammatory conditions) and where there is excessive renal (nephrotic) or intestinal (protein losing enteropathy) loss of albumin.
Prolonged prothrombin time may also occur as a result of vitamin K deficiency in biliary obstruction (low concentration of intestinal bile salts results in poor absorption of vitamin K), however, unlike in liver disease, clotting is corrected by giving vitamin K 10mg i.v. for 2-3 days.
What is bilirubin? What causes a rise in bilirubin? What is the normal range?
Bilirubin is a breakdown product of haemoglobin. An isolated rise in bilirubin with otherwise normal liver biochemistry is likely to be due to an inherited defect in bilirubin metabolism (usually Gilberts disease), haemolysis or ineffective erythropoeisis (premature death of RBCs in the bone marrow).
Hyperbilirubinaemia caused by hepatobiliary disease is almost always accompanied by other abnormalities on liver biochemistry; very high levels often occur in biliary tract obstruction.
Normal range is <17 umol/L
What are the aminotransaminases? Where else are they found?
These enzymes are present in hepatocytes and leak into the blood with liver cell damage. Very high levels may occur in acute hepatitis. Aspartate aminotransferase (AST, normal range 10-40U/L) is also present in heart and skeletal muscle and raised serum concentrations are also seen in MI and skeletal muscle damage. Alanine aminotransferase (ALT, normal range 5-40 U/L) is more specific to liver than AST.
Where is alkaline phosphatase synthesised?
Alk phos is situated in the canalicular and sinusoidal membranes of the liver. Raised serum concentrations are seen in cholestasis (bile flow impaired or completely halted) from any cause, whether intra or extrahepatic.
Circulating ALP is also derived from the placenta and bone and raised serum levels occur in pregnancy, Paget’s disease , osteomalacia, growing children and bony metastases. Measurement of ALP isoenzymes or GGT will determine if a raised level is predominantly liver or bone.
What is gamma GT?
This is a liver microsomal enzyme which may be induced by alcohol and enzyme inducing drugs - e.g. phenytoin. A raised serum concentration is a useful screening tool for alcohol abuse. In cholestasis, the GGT rises in parallel with the serum ALP because it has a similar pathway for excretion.
What pattern of LFTs suggest hepatocellular injury?
Marked elevation in ALT/ AST»_space; ALP/GGT
What pattern of LFTs suggest obstructive/ cholestatic disorders?
Elevation of bilirubin and ALP in excess of aminotransferases indicate a cholestatic disorder - e.g. PBC, PSC or extrahepatic bile duct obstruction (e.g. gall stones)
What are the contraindications to performing liver biopsy?
Contraindications include an uncooperative patient, a prolonged prothrombin time (by more than 3–5 s), platelet count <50 × 109/L, extrahepatic cholestasis and suspected haem- angioma. An US or CT guided biopsy is also performed when speci c lesions need to be biopsied. Complications include biliary peritonitis and bleeding into peritoneum or into the bile duct (haemobilia)
