Cirrhosis

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Cirrhosis

  1. 1. Cirrhosis of liver
  2. 2. Great minds discuss ideas; Average minds discuss events; Small minds discuss people Genius silently acts.
  3. 3. Cirrhosis: End stage complication of liver disease “Diffuse disorder of liver characterised by; Complete loss of architecture, Replaced by extensive fibrosis with, Regenerating parenchymal nodules.
  4. 4. Introduction  Cirrhosis is common end result of many chronic liver disorders.  Starts as hepatocellular necrosis & inflammation  Proceeds to bridging fibrous septa.  Regeneration of remaining hepatocytes form nodules.  Loss of normal architecture & function.
  5. 5. Normal Liver
  6. 6. Normal Liver Histology CV PT
  7. 7. Cirrhosis
  8. 8. Cirrhosis Fibrosis Regenerating Nodule
  9. 9. Etiology of Cirrhosis  Alcoholic liver disease 60-70%  Viral hepatitis 10%  Biliary disease 5-10%  Primary hemochromatosis 5%  Cryptogenic cirrhosis 10-15%  Wilson’s, α1AT def rare
  10. 10. Pathogenesis:  Diffuse liver injury leading to necrosis.  (Alcohol, virus, drugs, toxins, genetic etc.)  Chronic inflammation & healing (hepatitis).  Bridging fibrosis – loss of architecture.  Regeneration  nodules.  Obstruction to blood flow & shunts.  Portal hypertension spleen, varices  Liver failure – Debilitation, Jaundice, Ascites, edema, bleeding, hepatic encephalopathy  Hormone imbalance – spider nevi, testes atrophy etc..
  11. 11. Pathogenesis of clinical features: Jaundice Impaired conjugation or obstruction. Dark urine Conjugated hyperbilirubinemia (vs. acholuric) Pale stools Biliary obstruction Oedema Low albumin – low oncotic pressure. Steatorrhoea Bile obstruction. Pruritis Bile obstruction  Bile salt in blood. Ascites Portal hypert, low alb, hyper aldosterone Bleeding Coag. factor synthesis Haematemesis Oesophageal varices. (hemorrhoids) Encephalopathy Toxic nitrogen products – gut bacteria. Foetar hepaticus Musty odor (mercaptans by gut bacteria)
  12. 12. Clinical Features  Hepatocellular failure  Malnutrition, low albumin & clotting factors, bleeding.  Hepatic encephalopathy.  Portal hypertension.  Ascites, Porta systemic shunts, varices, splenomegaly.
  13. 13. Clinical Features  Ascites  Accumulation of free fluid in peritoneal cavity  Hypoalbuminemia  Portal hypertension  Decreased effective intravascular volume  hyperaldosteronism
  14. 14. Clinical Features  Bleeding tendencies  Decreased synthesis of prothrombin complex  Thrombocytopenia  Epistaxis, bleeding gums, ecchymosis,  Upper GI bleed  Lower GI bleed
  15. 15. Clinical Features  Hepatic encephalopathy  Portosystemic shunting of portal blood  Precipitating factors  Protein over load  Upper GI bleed  Constipation  Drugs  Diuretics / large volume peritoneocentesis  alkalosis
  16. 16. Clinical Features  Portal hypertension  Splenomegaly  Hypersplenism  Porto-systemic anastomosis  Caput medusae  Esophageal varices  Hemorrhoids  Hepato-pulmonary syndrome
  17. 17. Cirrhosis Clinical Features
  18. 18. Porta-systemic anastomosis: Prominent abdominal veins.
  19. 19. Complications  Congestive splenomegaly.  Bleeding varices.  Hepatocellular failure.  Hepatic encephalitis / hepatic coma.  Hepatocellular carcinoma.
  20. 20. Hepatocellular Carcinoma
  21. 21. Learn from the mistakes of others. You can't live long enough to make them all yourself…!

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