肝硬化疗法（Cirrhosis therapy）.docVIP

肝硬化疗法（Cirrhosis therapy） Cirrhosis therapy 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 reconstructed. If you continue to progress, fibrous septum centrilobular and portal area and other places will be connected to each other, the structure of hepatic lobule and blood circulation reconstruction and the formation of liver cirrhosis. 1. compensatory period (generally belong to Child-Pugh class a): may have the hepatitis clinical manifestation, may also conceal the onset. Can have mild fatigue, abdominal distension, slight swelling of liver and spleen, mild jaundice, liver palm, spider nevus. Imaging and biochemical examination of blood or liver cell synthesis dysfunction or portal hypertension (such as hypersplenism and esophageal and gastric varices) evidence, accordance with the diagnosis of liver cirrhosis or tissue, but no esophageal variceal bleeding, ascites and hepatic encephalopathy and other serious complications. 2. decompensated (Child-Pugh B, C general level): hepatic injury and portal hypertension syndrome. 1)