Editing Jaundice (section)

=== Abnormalities in heme metabolism and excretion ===
One way to understand jaundice pathophysiology is to organize it into disorders that cause increased bilirubin production (abnormal heme metabolism) or decreased bilirubin excretion (abnormal heme excretion).{{citation needed|date=August 2020}}

==== Prehepatic pathophysiology ====
Prehepatic jaundice results from a pathological increase in bilirubin production: an increased rate of erythrocyte hemolysis causes increased bilirubin production, leading to increased deposition of bilirubin in mucosal tissues and the appearance of a yellow hue.{{citation needed|date=August 2020}}

==== 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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==== Posthepatic pathophysiology ====
Posthepatic jaundice, also called obstructive jaundice, is due to the blockage of bile excretion from the biliary tract, which leads to increased conjugated bilirubin and bile salts there. In complete obstruction of the bile duct, conjugated bilirubin cannot access the intestinal tract, disrupting further bilirubin conversion to urobilinogen and, therefore, no [[stercobilin]] or [[urobilin]] is produced. In obstructive jaundice, excess conjugated bilirubin is filtered into the urine without urobilinogen. Conjugated bilirubin in urine (bilirubinuria) gives urine an abnormally dark brown color. Thus, the presence of pale stool (stercobilin absent from feces) and dark urine (conjugated bilirubin present in urine) suggests an obstructive cause of jaundice. Because these associated signs are also positive in many hepatic jaundice conditions, they cannot be a reliable clinical feature to distinguish obstructive versus hepatocellular jaundice causes.<ref>{{cite journal|vauthors=Beckingham IJ, Ryder SD|date=January 2001|title=ABC of diseases of liver, pancreas, and biliary system. Investigation of liver and biliary disease|journal=BMJ|volume=322|issue=7277|pages=33–36|doi=10.1136/bmj.322.7277.33|pmc=1119305|pmid=11141153}}</ref>