Liver Jaundice PDF

# LIVER ## JAUNDICE - Yellow discoloration of the skin (earliest sign is scleral icterus - yellow discoloration of the sclera). - Due to increased serum bilirubin, usually greater than 2.5 mg/dL. - Arises with disturbances in bilirubin metabolism. ### Normal bilirubin metabolism: 1. RBCs are cons...

# LIVER ## JAUNDICE - Yellow discoloration of the skin (earliest sign is scleral icterus - yellow discoloration of the sclera). - Due to increased serum bilirubin, usually greater than 2.5 mg/dL. - Arises with disturbances in bilirubin metabolism. ### Normal bilirubin metabolism: 1. RBCs are consumed by macrophages of the reticuloendothelial system. 2. Protoporphyrin (from heme) is converted to unconjugated bilirubin (UCB). 3. Albumin carries UCB to the liver. 4. Uridine glucuronyl transferase (UGT) in hepatocytes conjugates bilirubin. 5. Conjugated bilirubin (CB) is transferred to bile canaliculi to form bile, which is stored in the gallbladder. 6. Bile is released into the small bowel to aid in digestion. 7. Intestinal flora convert CB to urobilinogen, which is oxidized to stercobilin (makes stool brown) and urobilin (partially reabsorbed into blood and filtered by kidney, making urine yellow). # Table 11.1: Causes of Jaundice | Disease | Etiology | Laboratory Findings | Clinical Features | |---|---|---|---| | Extravascular hemolysis or Ineffective erythropoiesis | High levels of UCB overwhelm the conjugating ability of the liver. | ↑ UCB | Dark urine due to ↑ urine urobilinogen (UCB is not water soluble and, thus, is absent from urine) Increased risk for pigmented bilirubin gallstones | | Physiologic jaundice of the newborn | Newborn liver has transiently low UGT activity. | ↑ UCB | UCB is fat soluble and can deposit in the basal ganglia (kernicterus) leading to neurological deficits and death. Treatment is phototherapy (makes UCB water soluble). | | Gilbert syndrome | Mildly low UGT activity; autosomal recessive | ↑ UCB | Jaundice during stress (e.g., severe infection); otherwise, not clinically significant | | Crigler-Najjar syndrome | Absence of UGT | ↑ UCB | Kernicterus; usually fatal | | Dubin-Johnson syndrome | Deficiency of bilirubin canalicular transport protein; autosomal recessive | ↑ CB | Liver is dark; otherwise, not clinically significant Rotor syndrome is similar to Dubin-Johnson syndrome, but lacks liver discoloration. | | Biliary tract obstruction (obstructive jaundice) | Associated with gallstones, pancreatic carcinoma, cholangiocarcinoma, parasites, and liver fluke (Clonorchis sinensis) | ↑ CB, ↓ urine urobilinogen, and ↑ alkaline phosphatase | Dark urine (due to bilirubinuria) and pale stool Pruritus due to ↑ plasma bile acids Hypercholesterolemia with xanthomas Steatorrhea with malabsorption of fat-soluble vitamins | | Viral hepatitis | Inflammation disrupts hepatocytes and small bile ductules. | ↑ in both CB and UCB | Dark urine due to ↑ urine bilirubin; urine urobilinogen is normal or decreased. |