Cirrhosis Research Paper

Introduction
Cirrhosis is a progressive chronic inflammation of the liver that typically results from severe chronic hepatitis or chronic alcoholism as we know. Cirrhosis is defined histologically as a diffuse hepatic process characterized by fibrosis and the conversion of normal liver architecture into structurally abnormal nodules. In other words, The damaged hepatocytes regenerates, but the liver’s connective (scar) tissue regenerates faster. As a result, the liver becomes fatty and fibrous, depressing its normal activity. The scar tissue also obstructs blood flow throughout the hepatic portal system, causing portal hypertension. The progression of liver injury to cirrhosis may occur over weeks to years. Indeed, patients with hepatitis
It is derived from the Greek term scirrhus and refers to the orange or tawny surface of the liver seen at autopsy.
Etiology
Alcoholic liver disease once was considered to be the predominant source of cirrhosis in the United States, but hepatitis C has emerged as the nation 's leading cause of chronic hepatitis and cirrhosis.
“Many cases of cryptogenic cirrhosis appear to have resulted from nonalcoholic fatty liver disease (NAFLD). When cases of cryptogenic cirrhosis are reviewed, many patients have 1 or more of the classic risk factors for NAFLD: obesity, diabetes, and hypertriglyceridemia.[5] It is postulated that steatosis may regress in some patients as hepatic fibrosis progresses, making the histologic diagnosis of NAFLD difficult.
Up to one third of Americans have NAFLD. About 2-3% of Americans have nonalcoholic steatohepatitis (NASH), in which fat deposition in the hepatocyte is complicated by liver inflammation and fibrosis. It is estimated that 10% of patients with NASH will ultimately develop cirrhosis. NAFLD and NASH are anticipated to have a major impact on the United States ' public health infrastructure.” (Katz)
Most common causes of cirrhosis in the United States
Hepatitis C (26%)
Alcoholic liver disease
The initial event in cirrhosis is hepatic scarring or fibrosis. The scar begins as an increase in extracellular matrix components — fibrin–forming collagens, proteoglycans, fibronectin, and hyaluronic acid. Hepatocyte function is eventually impaired as matrix changes. Fat-storing cells are believed to be the source of the extracellular changes. Contraction of these cells may also contribute to disruption of the lobular structure and obstruction of the flow of blood or bile. Cellular changes producing bands of scar tissue also disrupt the lobular