肝硬化腹水症状(Ascites symptoms of cirrhosis).docVIP

肝硬化腹水症状(Ascites symptoms of cirrhosis).doc

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肝硬化腹水症状(Ascites symptoms of cirrhosis)

肝硬化腹水症状(Ascites symptoms of cirrhosis) Ascites symptoms of cirrhosis Refers to the liver cirrhosis ascites disease led to repeated liver inflammation, fibrosis and cirrhosis formation due to a variety of pathological factors, such as portal hypertension, hypoproteinemia, sodium retention caused by clinical symptoms of abdominal cavity effusion. Ascites due to cirrhosis is not a separate disease, but the common clinical manifestation of many end-stage liver disease (decompensation). Common diseases caused by cirrhosis of the liver are: hepatitis B, C viral hepatitis, alcoholic hepatitis, autoimmune hepatitis, etc.. Once the liver disease develops to cirrhosis and ascites stage, it often indicates that cirrhosis has reached the decompensation stage. If there is no active intervention, the prognosis is poor. There are two main causes of ascites in cirrhosis. One is intra-abdominal factor, the other is systemic factor. (I) intra-abdominal factors 1, portal hypertension: more than 300mmH2O, the abdominal splanchnic vascular bed hydrostatic pressure increased, tissue fluid absorption decreased and leaked into the abdominal cavity. 2, hypoalbuminemia: albumin lower than 30g/L, the plasma colloid osmotic pressure decreased, causing blood components extravasation. 3, excessive lymphogenesis: hepatic venous obstruction, plasma from liver sinus wall penetration to sinus clearance, induced liver lymphogenesis increased (daily about 7 ~ 11L, 1 ~ 3L normal), more than the ability of thoracic duct drainage, lymph from the liver capsule and portal lymph vessels to peritoneal effusion. (two) systemic factors 1, secondary aldosteronism increased renal sodium reabsorption. 2, increased antidiuretic hormone secretion, increased reabsorption of water. 3, the effective circulation of blood volume is insufficient: the renal sympathetic nerve activity increases, prostaglandins, atrial peptides and kallikrein kallikrein activity decreased, resulting in decreased renal blood flow, excretion

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