早期肝硬化的饮食（Diet for early cirrhosis）.docVIP

早期肝硬化的饮食（Diet for early cirrhosis） Diet for early cirrhosis Cirrhosis (hepatic) is a common chronic progressive liver disease with diffuse liver damage caused by long-term or repeated effects of one or more etiologies. In our country, most of them are cirrhosis after hepatitis, and few of them are alcoholic cirrhosis and schistosomiasis cirrhosis. On the histopathology of liver cell necrosis, extensive residual hepatocellular nodular regeneration and hyperplasia of connective tissue and fibrous septa formation, which led to the destruction of liver pseudolobule lobules and liver, deformation, harden and gradually develop into liver cirrhosis. Early because the liver compensatory function is strong without obvious symptoms, the damage to the liver function and portal hypertension as the main manifestation, and multi system involvement, often late upper gastrointestinal bleeding, hepatic encephalopathy, secondary infection, hypersplenism, ascites and malignant complications. The main pathogenesis of cirrhosis is progressive fibrosis. Collagen (type I and type III) in the interstitium of normal liver tissue is mainly distributed around the portal area and the central vein. In cirrhosis, type I and type III collagen are markedly increased and are deposited throughout the lobules. With the continuous deposition of collagen in the sinus space, the window pores of the endothelial cells were significantly reduced, which led to the gradual evolution of sinusoids into capillaries, resulting in a material exchange disorder between the blood and hepatocytes. The large amounts of collagen in cirrhosis are derived from the fat storing cell (Ito cell) located in the sinus space (Disse lumen), which is actively proliferating and can be transformed into fibroblast like cells. Initially, the hyperplastic fibrous tissue forms small cords but has not yet been connected with each other to form an interval. The hepatic lobules are called hepatic fibrosis when the hepatic lobules are reco