Conjugated hyperbilirubenemia seen in: (A)Crigler-Najjar syndrome I & II (B)Gilbert syndrome (C)Dubin-Johnson syndrome (D)Rotor syndrome (E)Physiological jaundice

Predominantly Unconjugated Hyperbilirubinemia Excess production of bilirubin Hemolytic anaemias Resorption of blood from internal hemorrhage (e.g. alimentary tract bleeding, hematomas). Ineffective erythropoiesis syndromes (e.g. pernicious anaemia, thalassemia) Reduced hepatic uptake Drug interference with membrane carrier systems Some cases of Gilbert syndrome Impaired bilirubin conjugation Physiologic jaundice of the newborn (decreased UGT 1A1 activity decreased excretion). Breast milk jaundice (β -glucuronidases in milk) Genetic deficiency of UGT 1A1 activity (Crigler-Najjar syndrome types 1 and II) Gilberts' syndrome (mixed etiologies) Diffuse hepatocellular disease (e.g., viral or drug-induced hepatitis, cirrhosis) Predominantly Conjugated Hyperbilirubinemia Deficiency of canalicular membrane transporters Dubin Johnson's syndrome Rotor's syndrome Impaired bile flow