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Jaundice
- 1.
- 2. Bilirubin Bilirubin is theyellow breakdown product of normal Heme catabolism taking place Reticuloendothelial system in liver and spleen
- 3. Degradation (Breakdown) ofHemoglobin is Part of Normal Catabolism in Human Body HemoglobinGlobin Heme Iron Biliverdin Bilirubin Amino acid Pool ExcretionRecycle
- 4. Degradation of Hbin RE cells leads to formation of Bilirubin Bilirubin released in blood and bound to Albumin Bilirubin taken by liver (Dissociates from Albumin) Bilirubin is conjugated and excreted in bile and then intestine In intestine, Bilirubin is converted to Urobilinogen
- 5. Types of Bilirubin •Unconjugated bilirubin: – Insoluble in water. – Indirect bilirubin travels through the bloodstream to the liver, where it is changed into a soluble form (direct or conjugated). • Conjugated bilirubin: – Soluble in water and is made by the liver from indirect bilirubin.
- 6. WHAT IS HYPERBILIRUBINEMIA? Increasedlevels of Bilirubin in the blood.
- 7. Hyperbilirubinemia Causes Jaundice •Hyperbilirubinemia is said when bilirubin in the blood exceeds 1 mg/dL. • Bilirubin accumulates in the blood, and when it reaches a certain concentration (approximately 2–2.5 mg/dL), it diffuses into the tissues, which then become yellow. That condition is called jaundice or icterus.
- 8. Jaundice is ayellowish pigmentation of the skin and conjunctiva caused by hyperbilirubinemia • Jaundice, (also known as icterus) is a yellowish pigmentation of the skin, conjunctiva and other mucous membranes caused by hyperbilirubinemia
- 9. In clinical studiesof jaundice, measurement of bile pigments is of great value • Total bilirubin in serum. • Conjugated bilirubin in serum. • Unconjugated bilirubin in serum. • Urobilinogen in urine. • Stercobilinogen in feaces.
- 10. Bile Pigments inblood Under Normal Conditions • Total bilirubin: –5.1–17.0μmol/L (0.3–1.0,mg/dL) • Conjugated" or "Direct bilirubin –1.0–5.1μmol/L (0.1–0.3mg/dl) • Unconjugated" or "Indirect bilirubin –4-12 μmol/L (0.2-.7mg/dL)
- 11. Conjugated Vs Un-ConjugatedBilirubin • Van den Bergh reaction: –The measurement of bilirubin depends on its reaction with diazosulfanilic acid to create azobilirubin. • Conjugated Bilirubin: –Water soluble reacts quickly with reagent. • Un-conjugated Bilirubin: –Insoluble in water Reacts less quickly with reagent.
- 12. URINARY EXCRETION OFBILIRUBIN • Under normal circumstances, a little amount of urobilinogen is excreted via the kidneys. • If the liver's function is impaired or when biliary drainage is blocked, some of the conjugated bilirubin leaks out of the hepatocytes and appears in the urine, turning it dark amber. • In conditions where unconjugated bilirubin is raised, urobilinogen will not appear In urine.
- 13. Types of Jaundice –Prehepatic(Hemolytic) –Intrahepatic jaundice (Hepatic) –Obstructive (Post hepatic)
- 14. Serum Bilirubin asdiagnostic parameter • Elevated levels may indicate certain diseases. –Jaundice >2 mg/dl • Hemolytic –Both, depending upon hemolysis –Mostly Uncojugated • Hepatic –Both, depending upon tissue damage • Post hepatic or obstructive –Mostly Conjugated
- 15. Prehepatic (hemolytic) jaundice •Excess hemolysis: –High serum concentrations of unconjugated bilirubin • Causes: •Autoimmune disease. •Hemolytic disease of the newborn (Rh - or ABO- incompatibility) •Mismatch Blood Transfusion. •Abnormal RBCs (Sickle cell disease) •G6PD deficiency
- 16. Hemolytic Jaundice Symptoms •Yellow or discoloration of skin and mucous membrane • Normal /Dark colored stools • Dark yellow or brown colored urine • Increased bilirubin level • Anemia • Weakness
- 17. Intrahepatic (Hepato-Cellular) jaundice •Failure in the function of hepatocytes to take up, conjugation or excrete bilirubin. • Causes: –Hepatitis (commonly viral or alcohol related) –Cirrohsis –Drugs or other toxins (Acetaminophen, alcohol, estrogens, etc) –Genetic: • Gilberts syndrome • Crigler-Najjar Syndrome –Hepatic cancer
- 18. Symptoms of HepaticJaundice • Yellow discoloration of eye ,skin and mucous membrane. • Light colored stools & dark yellow or brown colored urine. • Nausea and vomiting. • Loss of Appetite • Abdominal pain. • Fever. • Weakness.
- 19. Gilbert’s Syndrome • MildGenetic liver disorder. • Deficiency of enzyme glucuronyl transferase. • Decreased ability of the liver to conjugate bilirubin. • Characterized by mild, increases in unconjugated bilirubin.
- 20. Crigler-Najjar Syndrome • SevereGenetic disorder • Deficiency of enzyme glucuronyl transferase. • Complete absence or marked decrease in bilirubin conjugation. • Severe unconjugated hyperbilirubinemia that usually presents at birth • Type 1 is more severe and fatal.
- 21. Obstructive (Post hepatic)jaundice is Caused by an obstruction of the biliary tree –Gall Stones –Hepatitis –Pancreatic cancer –Liver Cancer –Cystic Fibrosis –Genetic (Dubin-Johnson and Rotor’s Syndromes).
- 22. Obstructive (Post hepatic)jaundice is Characterized by • Serum bilirubin is conjugated, and other biliary metabolites, such as bile acids accumulate in the plasma. • Clay white colored stools (absence of fecal bilirubin or urobilin) • Dark urine (increased conjugated bilirubin) • In a complete obstruction, urobilin is absent from the urine.
- 23. Obstructive jaundice Symptoms •Yellow discoloration of eye, skin and mucus membrane. • Dark yellow or brown colored urine and Clay white stools. • Enlarged liver / spleen. • Itching • Nausea • Fever • Weight loss • Diarrhea Upper abdominal pain
- 24. Dubin-Johnson and Rotor’sSyndromes • Genetic • Characterized by impaired biliary secretion of conjugated bilirubin. • The hyperbilirubinemia is caused by mutation in the gene encoding, the protein involved in the secretion of congugated bilirubin into the bile.
- 25. NEONATAL PHYSIOLOGIC JAUNDICE •Lack of the intestinal bacteria that facilitate the breakdown and excretion of conjugated bilirubin in the feces (this is largely why the feces of a neonate are paler than those of an adult). –Instead the conjugated bilirubin is converted back into the unconjugated form by the enzyme β-glucuronidase and a large proportion is reabsorbed through the enterohepatic circulation. • Premature Enzyme system
- 26. Toxicity of Bilirubinina new-born (Kernicterus) • Hyperbilirubinaemia in a new-born can lead to accumulation of bilirubin in certain brain regions. – Consequent irreversible damage to brain manifesting as various neurological deficits. • Seizures, abnormal reflexes and eye movements. • The neurotoxicity of neonatal hyperbilirubinemia is because of the incompletely developed blood–brain barrier.
- 27. Differentiate between Pre-hepatic, Hepatic& Post-hepatic jaundice Test Pre Hep Post Bilirubin (T) ↑ ↑ ↑ Conjugated Bilirubin ↑ ↑ ↑ Un-Conjugated Bilirubin ↑ ↑ N
- 28. Differentiate between Pre-hepatic, Hepatic& Post-hepatic jaundice Test Pre Hep Post Urobilinogen (Urine) ↑ ↓ Neg Urine Color N Dark Dark Stool Color N Light Clay Urine Bilirubin (Conj) - + +
- 29. Differentiate between Pre-hepatic, Hepatic& Post-hepatic jaundice Test Pre Hep Post ALP N ↑ ↑ ↑ ↑ AST (SGOT) N ↑ ↑ ↑ ALT (SGPT) N ↑ ↑ ↑
- 30. Bilirubin Lab Values •Normal 0.1 – 1mg/dl • Hyperbilirubinemia 1 – 2 mg/dl • Jaundice >2 mg/dl – Hemolytic • Both, depending upon hemolysis • Mostly Uncojugated – Hepatic • Conjugated • Both, depending upon tissue damage – Post hepatic or obstructive • Mostly cojugated
Editor's Notes
- #4 Heme catalyzed by heme oxygenase green pigment biliverdine is formed biliverdine is further reduced by reductase and forms bilirubin.
- #5 After 120 days rbc are taken up and degraded by RE system in spleen and liver In the intestine glucoronic acid is removed by bacteria n urobilinogen is formed some of it reabsorbed in the gut and enter into the portal circulation a portion of it participate in enterohepatic urobilinogen cycle. The remainder is transported by the blood to the kidney converted to yellow urobilin and excreted giving urine its yellow coior.
- #25 The hyperbilirubinemia is caused by mutation in the gene encoding, the protein involved in the secretion of congugated bilirubin into the bile.