Definition, Etiology, Pathophysiology and Management of Liver Cirrhosis

Abstract

Cirrhosis can be defined histologically as a diffuse process in which the normal anatomical lobules are replaced by architecturally abnormal nodules separated by fibrous tissue. Stage 3 cirrhosis encloses the advancement of swelling in the abdomen and advanced liver scarring. The etiology of cirrhosis differs based on geographically, with alcoholism, chronic hepatitis C virus infection, and nonalcoholic fatty lives disease being the consummate ubiquitous causes in western countries, whereas chronic hepatitis B is the initial cause of liver cirrhosis. The transition from chronic liver disease to cirrhosis encloses inflammation, initiation of hepatic stellate cells with following fibrogenesis, angiogenesis, and parenchymal extinction lesions caused by vascular occlusion. Only abstinence from alcohol ameliorates survival in alcoholic cirrhosis. Treatment of the underlying disease can frequently impasse or even reverse the progression of earlystage cirrhosis. The mainstay of primary prophylaxis is the use of nonselective β-adrenergic blocking agents such as propranolol or nadolol. Somatostatin and octreotide cause a reduction in portal pressure and port-collateral blood flow through inducing splanchnic vasoconstriction without causing the systemic effects consociated with vasopressin. Prophylactic antibiotic therapy should be prescribed for all patients with cirrhosis and acute variceal bleeding.