Cirrhosis

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

• Venkatesh Murthy Shashidhar
• Senior Lecturer in Pathology
• Fiji School of Medicine

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Jaundice

• Yellow discoloration of skin sclera due to
  presence of bilirubin.
• gt 40umol/l, (3mg/dl)
• Many patients with liver disease are not
  jaundiced.
• Liver disease is not the only cause of Jaundice.
• Bile salt accumulation pruritus obstruction.

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Jaundice

• Post Hepatic (Obstructive) Stone, tumor
• Conjugated/Direct Bil, High colored urine,
• Pre Hepatic (Acholuric) - Hemolytic
• Unconjugated/Indirect Bil, pale urine
• Hepatocellular Jaundice - Viral
• Liver damage - unconjugated
• Swelling, canalicular obstruction - Conjugated

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Cirrhosis

• Dr. VM Shashidhar
• Senior Lecturer in Pathology
• Fiji School of Medicine

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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.

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Definition

• Diffuse disorder of liver characterised by
• Complete loss of normal architecture,
• Replaced by extensive fibrosis with,
• Regenerating parenchymal nodules.

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Normal Liver
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Normal Liver Histology
CV
PT
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Alcoholic Fatty Liver
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Cirrhosis
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Cirrhosis
Fibrosis Regenerating Nodule
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Etiology of Cirrhosis

• Alcoholic liver disease 60-70
• Viral hepatitis 10
• Biliary disease 5-10
• Primary hemochromatosis 5
• Cryptogenic cirrhosis 10-15
• Wilsons, ?1AT def rare

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Pathogenesis

• Hepatocyte injury leading to necrosis.
• (Alcoholic, infections including virus, drugs,
  genetic etc.).
• Chronic inflammation - (hepatitis).
• Bridging fibrosis - (Ito cells, TNF,TGF,IL).
• Regeneration of remaining hepatocytes.
• Proliferate as round nodules.
• Loss of sinusoids, vascular arrangement rendering
  regenerating hepatocytes ineffective.

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Cirrhosis Features

• Hepatocyte injury fibrosis
• Parenchymal regeneration but non functional.
• Vascular disruption Porta systemic shunts (blood
  bypasses hepatocyte) Liver failure
• Portal hypertension
• Encephalopathy

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Pathogenesis of Hepatic Encephalopathy
BRAIN LIVER Toxic N2 metabolites From
Intestines
Porta systemic shunts
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Micronodular cirrhosis
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Micronodular cirrhosis
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Macronodular Cirrhosis
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Stone in Bile Duct
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Alcoholic Fatty Liver
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Hemochromatosis
Prussian blue stain for Iron
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Bile Lakes in Biliary Cirrhosis
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P.B.C. Demonstration of antimitochondrial
antibodies in rat kidney
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Nutmeg Liver-Cardiac Sclerosis
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Clinical Features

• Hepatocellular failure.
• Malnutrition, low albumin clotting factors,
  bleeding.
• Hepatic encephalopathy.
• Portal hypertension.
• Ascites, Porta systemic shunts, varices,
  splenomegaly.

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CirrhosisClinical Features
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Porta-systemic anastomosis Prominent abdominal
veins.
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MRI Cirrhosis
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Complications

• Congestive splenomegaly.
• Bleeding varices.
• Hepatocellular failure.
• Hepatic encephalitis / hepatic coma.
• Hepatocellular carcinoma.

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Hepatocellular Carcinoma
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Conclusions

• Common end result of diffuse liver damage.
  (common causes Viral hepatitis Alcohol)
• Characterised by complete loss of architecture.
• Replaced by fibrosis regenerating parenchymal
  nodules.
• Hepatocellular insufficiency portal
  hypertension.