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Jaundice – Causes, Pathophysiology, and Management
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- 2. Jaundice is aclinical symptom complex characterized by the yellowish discoloration of the skin, sclera, and body fluids, resulting from an increased concentration of bile pigments, particularly bilirubin, in the blood. It may occur due to one or more of the following mechanisms: Increased bilirubin production (e.g., hemolysis). Impaired uptake of bilirubin by hepatocytes Defective conjugation of bilirubin within the liver Impaired excretion of conjugated bilirubin into bile DEFINITION
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- 4. Pre hepatic (HemolyticJaundice) post hepatic (obstructive jaundice) hepatic(hepatocellular jaundice) ETILOGICAL CLASSIFICATION congenital hyperbilirubinemia
- 5. PRE HEPATIC JAUNDICE(HEMOLYTIC JAUNDICE) Pre-hepaticjaundice occurs due to increased bilirubin production before it reaches the liver. This is mainly caused by excessive destruction of red blood cells (hemolysis). A. Intra-Corpuscular Defects Hereditary spherocytosis Hemoglobinopathies Sickle cell anemia Homozygous beta thalassemia Sickle-thalassemia HbE-thalassemia Enzyme deficiencies G6PD deficiency Pyruvate kinase deficiency Paroxysmal nocturnal hemoglobinuria (PNH) B. Extra-Corpuscular Defects Infections: Malaria, Clostridium welchii Drugs: Methyl dopa, Quinine, Phenacetin, Sulfonamides Physical agents: Burns, Irradiation Poisons: Snake venom, Favism (fava bean sensitivity) Immunological causes: Mismatched blood transfusion, Paroxysmal cold hemoglobinuria, Lymphoma, Chronic lymphocytic leukemia (CLL), Systemic lupus erythematosus (SLE) Miscellaneous: Uremia, Cirrhosis of liver
- 6. A. Unconjugated Hyperbilirubinemia Gilbert’sSyndrome Impaired bilirubin transport Crigler-Najjar Syndrome Defective bilirubin conjugation B. Conjugated Hyperbilirubinemia Dubin-Johnson Syndrome Defect in bilirubin excretion Rotor’s Syndrome Defect in hepatic storage and reuptake CONGENITAL HYPERBILIRUBINEMIA These are inherited (genetic) disorders affecting bilirubin metabolism, causing either unconjugated or conjugated hyperbilirubinemia—without liver cell damage or obstruction.
- 7. A. Infectious Causes ViralHepatitis Weil's Disease (Leptospirosis) Septicemia Malaria, Typhoid B. Toxic Causes Anesthetic Agents: Halothane, Chloroform Anticoagulants: Phenindione Anti-TB Drugs: Rifampicin, PAS, INH, Thiacetazone Metals: Arsenic, Mercury, Gold, Bismuth Chemicals: DDT X-ray Irradiation c. cirrhosis Portal Biliary Hemochromatosis HEPATOCELLULAR (MEDICAL JAUNDICE- HEPATIC) Caused by liver cell damage, impairing bilirubin metabolism and excretion. Often due to infections or toxins.
- 8. A. Extra-Hepatic Causes Inflammatory: Gallstones Biliarystrictures Parasites Acute cholecystitis Neoplastic: Carcinoma of pancreatic head Bile duct tumors Gall bladder & Ampulla of Vater neoplasms Congenital: Biliary atresia B. Intra-Hepatic Causes Cholestatic phase of infective hepatitis Drugs: Steroids Chlorpromazine PAS Sulfonamides Chlorpropamide Tolbutamide Methyl testosterone Erythromycin Pregnancy: Intrahepatic cholestasis of pregnancy OBSTRUCTIVE JAUNDICE (POST-HEPATIC / SURGICAL JAUNDICE) Obstructive jaundice results from an interruption of bile flow distal to the liver, typically due to choledocholithiasis, malignancy, or biliary strictures."
- 9. PATHOPHYSIOLOGY I. Breakdown Phase RBCBreakdown (in RES) ↓ Hemoglobin →Heme + Globin ↓ Heme →Iron + Unconjugated Bilirubin (Indirect) II. Transport Phase Unconjugated Bilirubin + Albumin →Transport to Liver III. Conjugation Phase In Liver (Hepatocytes) ↓ Conjugation with Glucuronic Acid (via Glucuronyl Transferase) ↓ Conjugated Bilirubin (Direct, Water-Soluble) IV.Alimentary Excretion Phase Conjugated Bilirubin →Excreted via Bile →Intestine ↓ Intestinal Bacteria Convert to: →Stercobilinogen →Stercobilin (Feces – Brown Color) →Urobilinogen V. Renal Excretion Phase Urobilinogen: • Some Reabsorbed (Enterohepatic Circulation) • Some Excreted in Urine →Urobilin (Urine – Yellow Color)
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- 11. General Features (Seenin Most Types): Yellow discoloration of skin, sclera (icterus) Dark yellow urine Pale/clay-colored stools Generalized itching (especially in obstructive type) Fatigue & weakness Nausea, vomiting, anorexia Right upper abdominal discomfort CLINICAL MANIFESTATIONS
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- 16. MANAGEMENT General supportive measures Adequaterest is advised during the acute phase. Maintain proper hydration with oral or IV fluids. Provide a high-carbohydrate, low-fat diet. Supplement fat-soluble vitamins (A, D, E, K). Monitor and correct electrolyte imbalances. Avoid hepatotoxic drugs like alcohol and paracetamol. Regularly assess liver function tests and bilirubin levels. Treat symptoms with antiemetics, antipyretics, and antihistamines if needed.
- 17. Pre-hepatic Treat underlying hemolyticdisorder (e.g., autoimmune, malaria, hereditary spherocytosis). Blood transfusion (if severe anemia). Folic acid supplementation. Corticosteroids for autoimmune causes MANAGEMENT Specific Management
- 18. MANAGEMENT Specific Management Hepatic Jaundice Antiviraltherapy for HBV/HCV Corticosteroids for autoimmune hepatitis Avoid hepatotoxic drugs (e.g., alcohol, paracetamol) Nutritional support Manage complications (ascites, encephalopathy) Liver transplantation in end-stage cases
- 19. MANAGEMENT Specific Management Post-hepatic Jaundice Imaging:USG/MRCP/ERCP to localize obstruction ERCP for stone removal or stenting Surgery for tumors or strictures Antibiotics for cholangitis Vitamin K for coagulopathy due to bile flow obstruction
- 20. MEDICAL MANAGEMENT Antivirals –Used for hepatitis B and C infections Examples: Tenofovir, Entecavir, Sofosbuvir Corticosteroids – For autoimmune hepatitis and severe alcoholic hepatitis Examples: Prednisolone, Azathioprine Antibiotics – For infections like cholangitis or sepsis Examples: Ceftriaxone, Piperacillin-Tazobactam Lactulose – To manage hepatic encephalopathy by reducing ammonia levels Vitamin K – For correcting coagulopathy in obstructive jaundice Diuretics – Used in ascites associated with chronic liver disease Examples: Spironolactone, Furosemide Ursodeoxycholic acid (UDCA) – For intrahepatic cholestasis to improve bile flow IVIG – In neonatal immune hemolytic jaundice to reduce antibody-mediated hemolysis
- 21. SURGICAL MANAGEMENT ERCP (EndoscopicRetrograde Cholangiopancreatography): Used for diagnosis and treatment of biliary obstruction Helps in stone removal, stricture dilation, or stent placement Cholecystectomy: Surgical removal of gallbladder in cases of gallstone-related obstructive jaundice Biliary Stenting: Insertion of a stent to relieve bile duct obstruction due to stones or tumors Percutaneous Transhepatic Biliary Drainage (PTBD): Used when ERCP is not possible, especially in malignant obstruction Biliary Bypass Surgery: Performed in inoperable malignancies to bypass the blocked bile duct Liver Transplantation: Indicated in end-stage liver disease or acute liver failure unresponsive to medical therapy
- 22. COMPLICATIONS Hepatic encephalopathy Coagulopathy andbleeding Ascites Hepatorenal syndrome Chronic liver failure Pruritus (itching) Vitamin A, D, E, K deficiencies Kernicterus (in neonates)
- 23. “Severe neonatal hyperbilirubinaemiain European and Indian subcontinent descendent newborns: a retrospective cohort study” Background Neonatal hyperbilirubinemia is more common in populations of Asian descent. However, differences in disease severity among ethnicities are not well-documented. Objective/Aim To compare the severity of neonatal hyperbilirubinaemia between newborns of European ancestry and those from the Indian subcontinent (India, Pakistan, Bangladesh, Nepal).
- 24. “Severe neonatal hyperbilirubinaemiain European and Indian subcontinent descendent newborns: a retrospective cohort study” Method Study Design: Single-centre retrospective cohort study Duration: January 2016 to December 2021 Population: 110 newborns with unconjugated hyperbilirubinemia 27 with Indian subcontinent ancestry (study group) 83 with European ancestry (control group) Outcomes: Primary: Severe hyperbilirubinemia (TSB > 25 mg/dL, phototherapy > 6 h, or need for exchange transfusion) Secondary: TSB levels at admission and discharge Analysis: Binary logistic regression for confounder adjustment
- 25. Result TSB > 25mg/dL: Study group: 22.2% Control group: 4.8% (p = 0.006) Phototherapy > 6 h and ET: No significant difference Adjusted OR for TSB > 25 mg/dL: OR = 7.49 (95% CI: 1.23–45.50) TSB Levels: At admission: 22.0 mg/dL (study) vs. 19.6 mg/dL (control) (p = 0.013) At discharge: 13.6 mg/dL (study) vs. 11.4 mg/dL (control) (p = 0.005) Conclusion Newborns of Indian subcontinent ancestry are at greater risk for severe hyperbilirubinemia. Early treatment interventions in this group may help prevent complications.
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