الفهرس 
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Abstract
Cirrhosis is the end result of hepatocellular injury that leads to both fibrosis and regenerative nodules which disturb the whole normal architecture of the liver. Cirrhosis and chronic liver failure are considered leading causes of morbidity and mortality, with the most of preventable cases are due to viral hepatitis, excessive alcohol consumption or nonalcoholic fatty liver disease.
Cirrhosis is often an indolent disease; most patients remain asymptomatic until the incident of decompensation present, characterized by hepatic encephalopathy, variceal bleeding, ascites or spontaneous bacterial peritonitis from portal hypertension. In the majority of patients, approximately 80 to 90 percent of the liver parenchyma must be damaged already before liver failure is manifested clinically.
Portal hypertension is a clinical syndrome affected by intrinsic liver disease, obstruction, or change in the structure resulting in increased portal blood flow or high hepatic resistance. All this leads to a pathological increase in portal venous pressure and formation of portosystemic collaterals that divert portal blood flow to systemic circulation, bypassing the liver. The high portal pressure causes an increase in the pressure gradient between hepatic vein and portal vein.
Clinical portal hypertension isn’t found in all patients with increased portal venous pressure, as portal hypertension complications are detected only when the portal pressure gradient is raised above the threshold value of about 10 mm Hg. This value