Cirrhosis is the end stage of many chronic liver diseases where the liver architecture is completely disrupted by extensive fibrosis and the formation of regenerating nodules. It results from chronic liver injury and inflammation that causes hepatocyte necrosis initially and progresses to bridging fibrosis that destroys the liver structure. Common causes include alcohol, viral hepatitis, and primary biliary cirrhosis. Cirrhosis leads to liver failure and complications of portal hypertension like ascites, variceal bleeding, and hepatic encephalopathy.

1. Cirrhosis of liver

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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. 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. Normal Liver

6. Normal Liver Histology
CV
PT

8. Cirrhosis

9. Cirrhosis
Fibrosis
Regenerating Nodule

10. 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

11. 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..

12. 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)

13. Clinical Features
 Hepatocellular failure
 Malnutrition, low albumin & clotting factors,
bleeding.
 Hepatic encephalopathy.
 Portal hypertension.
 Ascites, Porta systemic shunts, varices,
splenomegaly.

14. Clinical Features
 Ascites
 Accumulation of free fluid in peritoneal cavity
 Hypoalbuminemia
 Portal hypertension
 Decreased effective intravascular volume
 hyperaldosteronism

15. Clinical Features
 Bleeding tendencies
 Decreased synthesis of prothrombin complex
 Thrombocytopenia
 Epistaxis, bleeding gums, ecchymosis,
 Upper GI bleed
 Lower GI bleed

16. Clinical Features
 Hepatic encephalopathy
 Portosystemic shunting of portal blood
 Precipitating factors
 Protein over load
 Upper GI bleed
 Constipation
 Drugs
 Diuretics / large volume peritoneocentesis
 alkalosis

17. Clinical Features
 Portal hypertension
 Splenomegaly
 Hypersplenism
 Porto-systemic anastomosis
 Caput medusae
 Esophageal varices
 Hemorrhoids
 Hepato-pulmonary syndrome

18. Cirrhosis
Clinical
Features

19. Porta-systemic anastomosis:
Prominent abdominal veins.

20. Complications
 Congestive splenomegaly.
 Bleeding varices.
 Hepatocellular failure.
 Hepatic encephalitis / hepatic coma.
 Hepatocellular carcinoma.

21. Hepatocellular Carcinoma

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