Definition

Cirrhosis is an the irreversibile alteration of hepatic tissue structure, characterised by:

• Hepatocyte necrosis and apoptosis 
• Diffuse liver fibrosis, mandatory for diagnosis
• Compensator nodular regeneration 
• Vascularization disturbances (portal hypertension)

It is a diffuse process involving the entire liver, characterized by fibrosis and conversion of normal architecture into structurally abnormal regeneration nodules of liver cells.

Etiology

Chronic alcoholism
Chronic Hepatitis B Virus
Hepatitis C Virus
Non alcoholic steatohepatitis ( NASH)
Chronic biliary obstruction
Autoimmune hepatitis
Chronic liver congestion (constrictive cardiac failure, constrictive pericarditis)
Metabolic causes (hemochromatosis, Wilson disease)
Toxic/drugs (methotrexate, amiodarone)
Primary and secondary biliary cirrhosis

Mechanism

Four important processes are involved:

Liver cell death with loss of architecture: The pathogenesis of liver cell damage varies depending on the etiologic agent.
Fibrosis: It is mainly due to the activation of hepatic stellate cells, which are transformed into highly fibrogenic cells called myofibroblasts.
Regenerating nodules: Damage and fibrosis of liver cells stimulate surviving hepatocytes to regenerate and proliferate to form regenerating nodules.
Vascular reorganization: Parenchymal damage and fibrosis disrupt the vascular architecture of the liver.

Signs and symptoms

SKIN: Jaundice, ecchymosis (thrombocytopenia or clotting factor deficiency), increased pigmentation (hemochromatosis). xanthomas (primary biliary cirrhosis);
EYES: Kayser-Fleischer rings. (corneal copper deposition seen in Wilson’s disease; scleral jaundice;
ABDOMEN: painful or painless hepatomegaly (congestive hepatomegaly), small, nodular liver (cirrhosis), palpable;

Diagnosis

• Ultrasonography;
• Laboratory tests:

AST, moderately elevated ALT. AST > ALT. Very high GGT in chronic alcoholic liver disease. Bilirubin increases as cirrhosis worsens. Albumin decreases as synthetic function decreases. Prothrombin time increases as synthetic function decreases.

Complications:

Portal hypertension
Ascites and edema
Splenomegaly (can leads to anemia, leukopenia, trombocytopenia and eventually bleeding)
Porto-systemic shunting of blood (Caput medusae, hemorrhois, esophageal varices)
Hepatic encephalopathy
Hepato-renal syndrome

Treatment

Medicines:
Antiviral medication for Hepatitis
Corticosteroids for autoimmune hepatitis
Decompensation:
Diuretics, antibiotics, laxatives. enemas, thiamine, steroids