Jaundice Flashcards
extravascular hemolysis or ineffective erythropoiesis: mechanism, etiology, lab findings, features
both cause consumption of RBCs and excessive production of UC bilirubin. it will overwhelm the conjugating ability of the liver. that causes high UCB in lab studies. it will eventually be conjugated, though, so we high levels of conjugated bilirubin in the bile (more source material), so there is an incr. risk for pigmented bilirubin gallstones and dark urine d/t high urine urobilinogen/urobilin (UCB is not water soluble and is therefore absent from the urine).
physiologic jaundice of the newborn: mechanism, etiology, lab findings, features
neonates have low conjugating ability- low levels of UGT (UDP-glucuronosyltransferase). this causes incr. Unconjugated bilirubin. in a new born, UCB can deposit within the brain (it is fat soluble).. can cause neuro deficits and death. tx. is phototherapy: molecule is altered to become water soluble so that it can leak out in the urine.
Gilbert syndrome: mechanism, etiology, lab findings, features
patients have an autosomal recessive low UGT activity. incr. in UCB. jaudice during stress (like severe infection); otherwise, not clinically significant
cirgler najjar syndrome: mechanism, etiology, lab findings, features
absence of UGT causes very high levels of UCB. effects the fetus and can cause kernicterus. usually fatal.
Dubin Johnson syndrome: mechanism, etiology, lab findings, features
deficiency of bilirubin canalicular transport protein. autosomal recessive.
incr. CB
liver is dark; otherwise, not clinically significant.
rotor syndrome is similar to dubin-johnson syndrome but lacks liver discoloration.
biliary tract obstruction jaundice: mechanism, etiology, lab findings, features
obstructive jaundice: usually associated with gallstones, pancreatitc carcinoma, cholangiocarcinoma, parasites, liver fluke
things in bile leak into the blood: incr. CB, decr. urine urobilinogen, and incr. alk phos; pruritis due to increased plasma bile acids, hypercholesterolemia with xanthomas.
can’t put bile into the bowel: pale stool and steatorrhea with malabsorption of fat-soluble vitamins; dark urine d/t bilirubinuria
viral hepatitis: mechanism etiology, lab findings, features
inflamation disrupts the hepatocytes and the small bile ductules: incr in both CB and UCB.
urine will be dark due to incr. urine bilirubin; urine urobilinogen is normal or decreased (urine urobilinogen is a result of conjugated bilirubin in the duodenum).
What are causes of conjugated hyperbilirubinemia?
biliary tract obstruction, biliary tract disease (primary sclerosing cholangitis or primary biliary cirrhosis), or excretion defects like dubin-johnson or rotor syndrome.
difference btw type I and type II crigler-najjar syndrome
type II is less severe and responds to phenobarbitol, which increases liver enzyme synthesis
