Editing Jaundice (section)

==== Hepatic pathophysiology ====
Hepatic jaundice (hepatocellular jaundice) is due to significant disruption of liver function, leading to hepatic cell death and necrosis and impaired bilirubin transport across [[hepatocyte]]s. Bilirubin transport across hepatocytes may be impaired at any point between hepatocellular uptake of unconjugated bilirubin and hepatocellular transport of conjugated bilirubin into the gallbladder. In addition, subsequent cellular [[oedema|edema]] due to inflammation causes mechanical obstruction of the intrahepatic biliary tract. Most commonly, interferences in all three major steps of bilirubin metabolism—uptake, conjugation, and excretion—usually occur in hepatocellular jaundice. Thus, an abnormal rise in both unconjugated and conjugated bilirubin (formerly called '''cholemia''') will be present. Because excretion (the rate-limiting step) is usually impaired to the greatest extent, conjugated hyperbilirubinemia predominates.<ref>{{cite book|title=Medicine: Prep Manual for Undergraduates|vauthors=Mathew KG|date=2008|publisher=Elsevier India|isbn=978-81-312-1154-0|edition=3rd|pages=296–297}}</ref>

The unconjugated bilirubin still enters the liver cells and becomes conjugated in the usual way. This conjugated bilirubin is then returned to the blood, probably by rupture of the congested bile canaliculi and direct emptying of the bile into the [[lymph]] exiting the liver. Thus, most of the bilirubin in the plasma becomes the conjugated type rather than the unconjugated type, and this conjugated bilirubin, which did not go to the intestine to become [[urobilinogen]], gives the urine a dark color.<ref>{{cite book|title=Textbook of Medical Physiology|vauthors=Hall JE, Guyton AC|date=2011|publisher=Saunders/Elsevier|isbn=978-1-4160-4574-8|page=841}}</ref>{{what|date=May 2022}}
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