1. Cirrhosis of liver

2. Great minds discuss ideas;
Average minds discuss events;
Small minds discuss people
Genius silently acts.

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

22. Learn from the
mistakes of others.
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enough to make them
all yourself…!