CPC 7/22 Flashcards
how is bilirubin formed and transported through the liver into the gut
1) senile RBCs are broken down in the spleen
- releasing hemosiderin (yellow)
2) hemosiderin => biliverdin (green) => bilirubin by oxygenase
3) bound to albumin to get to the liver
4) if it is unbound, it cannot be excreted by the kidney bc it cannot get into the liver
5) in the liver, it is conjugated with glucoronide by glucuronyl transferase
- now it can pass into the bile and enter small intestine
6) broken down in SI by bacterial proteases to urobilinogen
- 90% is excreted in feces, and 10% reenters via portal vein
which bilirubin result in choloric and acholoric urin
1)
four pathophysiologic mechanisms lead to hyperbilirubinemia
1) unconjugated hyperbilirubinemia
-*acholuric (No bile pigment)
- impaired liver function (no albumin means it will stay in bloodstream)
- excessive bilirubin production
- reduced uptake
- impaired conjugation
2) conjugated hyperbilirubinemia
- gets in liver but cannot get out
- ex. problems with glucuronyl transferase or problems transporting it out
- impaired excretion (bile pigment in urine, choluric)
crigler majjar syndrome
1) inherited condition typically affecting neonates that is characterized by deficiency of glucuronyl transferase
2) UCB cannot be metabolized further
gilberts disease
1) decreased activity in glucuronyl transferase
2) UGT1A1 gene mutation
dubin johnson syndrome
1) inability of CB to be transported across the hepatocyte membrane
2) cannot get to kidneys
circumstances in which urine urobilinogen is elevated
1) hemolytic anemias
2) autoimmune hemolytic anemia
3) blockage in biliary system
extrahepatic cholestasis
1) gall stones in main bile hepatic duct
1) carcinoma of bile ducts
3) obstruction of flow with retention of bile salts, impaired fat absorption and absorption of fat soluble vitamins (vitamin K)
summary
1) when excess RBC breakdown occurs, UB is elevated (acholuria), elevated urobilinogen, and kericterus
2) when bile flow is obstructed due to impaired excretion or blockages, conjugated hyperbilirubinemia
2) choluric
serum abumin
1) measures hepatocyte function
2) if decreased, blodo osmotic pressure is decreased , edema and ascites
how portal hypertension develops
1) impedance to blood flow in the portal system due to scarring in the liver, elevated venous pressure, portal hypertension
2) ascites and varices in esophagus, hemorroids, umbilical varices
3) if bleeding disorder, it can lead to death
cirrhosis forms
1) chronic alcoholic
2) biliary
- bile duct or bladder occlusion
3) postnecrotic
- infection or chemical toxins
microscopic changes in laennecs cirrhosis
1) fat mobilization from peripheral stores
2) decreased lipid breakdown
3) more synthesis of TGs
—
1) causes many effects
2) failure of liver to metabolic pharmacologic agents means prolonged effects
microscopic changes in biliary cirrhosis
1) periportal cirrhosis around portal triads with perilobular scarring
gall stones
1) calcium bilirubinate or cholesterol