Jaundice means yellow discoloration of the skin, mucous membrane and sclera due to elevation of bilirubin level in the blood. Intensity of jaundice depends on the amount of free bilirubin circulating in the blood which can easily diffuse into the tissues. Jaundice should be distinguished from yellow coloration of the skin due to hypercarotenemia. In the latter condition sclera does not become yellow.

Regurgitant jaundice (conjugated hyperbilirubinemia)
1.  Hepatocellular jaundice.
(a)   Viral hepatitis A and B
(b)   Toxic injury to the liver-antibiotics, drugs, poisons.
(c)    Infestations: malaria, bilharzia.
(d)   Cirrhosis of the liver
(e)   Infections:  Infectious mononucleosis.
2.   Cholestatic jaundice.
(a)   Due to drug reaction to chlorpromazine, methyl testosterone, isoniazid and rifampicin.
(b)   Dubin Johnson syndrome (chronic benign conjugated hyperbilirubinemia with deposition of melanin like pigment in the liver; autosomal recessive inheritance, no mechanical obstruction of duct); Rotor syndrome (Like Dubin Johnson; no pigment in the liver).

Aemolytic jaundice
(a)   Hereditary spherocytosis.
(b)   Sickle cell anemia.
(c)   Thalassemia.
(d)   Drug induced hemolytic anemia in patients with G 6-PD deficiency.
(e)   Acute acquired hemolytic anemia.
Hepatocellular jaundice
Unconjugated bilirubin level in the blood is elevated due to impaired uptake, defective transport and diminished glucuronation of the bile by the damaged hepatic cell. Conjugated bilirubin level also rises due to the blockage of canaliculi by the thick bile and obstruction due to the inflammatory cells around the cholangioles. Altered permeability of the liver cells and rupture of the canaliculi also contribute to the elevation of the level of conjugated bilirubin.
Thus in hepatocellular jaundice, serum levels of both the conjugated and unconjugated bilirubin are elevated and bilirubin is excreted in the urine. The excretion of urobilinogen in the feces is reduced because less bile passes into the gut. A part of the urobilinogen (or stercobilinogen) is absorbed in the portal circulation but liver is unable to excrete it and therefore it is excreted mostly in the urine. As the illness becomes severe and the obstruction becomes almost complete, the bilirubin cannot be excreted into the gut. Consequently no urobilinogen is formed and absorbed from the gut. Therefore at this stage urobilinogen disappears from the urine in complete obstruction or at the peak of the disease process.

Cholestatic jaundice
Cholestatic jaundice occurs following drug reaction to chlorpromazine, methyl testosterone and isonicotinic acid hydrazide and rifampicin. The jaundice in Dubin Johnson and Rotor syndromes is also cholestatic. The defect is due to the functional disturbances in the transport of bilirubin across the liver cells.
Obstructive jaundice
Following obstruction of the bile duct, the conjugated bilirubin escapes into the circulation. This may be due to (1) rupture of the distended canaliculi into the hepatic sinusoids or lymph spaces, (2) through leaks in the canals of Hering which connect the bile canaliculi with the terminal bile ducts and (3) in the blood through the parenchymal cells. Later, hepatocellular damage may occur as a result of marked increase in the level of unconjugated bilirubin.
Complete obstruction of the extrahepatic biliary system is uncommon in children. Cholecystitis and gall bladder calculi rarely present in childhood. Partial intermittent obstruction due to cystic dilatation of a part or whole of the common bile duct may occur due to partial obstruction or neuromuscular incoordination of the ampulla of Vater.
Large cyst of the bile duct is called choledochal cyst.
Patient presents with a mass in the right upper quadrant of