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Jaundice is defined as yellow discoloration of skin, sclera and tissues caused by increased levels of circulating bilirubin. Approximately 250-350 mg of bilirubin is formed daily, mostly from the breakdown of aged RBCs (70-80%) and rest from other haem proteins in the marrow and liver. It is taken up by liver, conjugated and excreted in bile. Serum bilirubin may increase due to derangement occurring at any level:

Increased production due to excessive haemolysis, results in unconjugated hyperbilirubinaemia (>80% unconjugated serum bilirubin), jaundice is mild (bilirubin <10 mg%) and associated with absence of bilirubin in urine (acholuric jaundice).

Impaired conjugation in hepatocellular damage (usually results in increase in both fractions of bilirubin due to impaired conjugation and associated decreased canalicular excretion).

Impaired excretion due to intra- or extra-hepatic cholestasis, resulting in conjugated hyperbilirubinaemia (>50% conjugated serum bilirubin), associated with absence of urobilinogen and bile salts in urine.

Common causes of jaundice in clinical practice include acute viral hepatitis, alcoholic hepatitis, chronic hepatitis/cirrhosis, gallstones and malignancy of gallbladder/ pancreas or extra-hepatic biliary system. Chronic haemolytic anaemias are less common and usually

present in childhood or sometime in young adults.

Approach to diagnosis of jaundice includes initial differentiation between the three types of jaundice by appropriate clinical history, examination and investigations including full blood counts, liver function tests (LFTs), viral markers, ultrasound examination of liver and biliary tract and if indicated CT scan of abdomen/ERCP.

Click here for acute viral hepatitis.



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