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发病机理:腹水的发生主要与下列三种因素有关:门脉压;血浆膨胀压;血管通透性。门脉压力的变化与门静脉的流量及其流动的阻力成正比。血浆膨胀压主要取决于血清白蛋白的含量。肝硬化失代偿期,血清白蛋白的降低常促使临床上产生腹水,并且强调血容量的显著增加先于腹水的发生。感染或内毒素血症存在时,血管通透性可能增加,而且肝静脉流出受阻可能导致肝窦通透性屏障的破坏。腹水形成的模型: 1.充盈不足学说:实际上总是不正确的。
Pathogenesis: The occurrence of ascites mainly with the following three factors: portal pressure; plasma expansion pressure; vascular permeability. The change in portal pressure is proportional to the flow of the portal vein and its resistance to flow. Plasma expansion pressure depends mainly on serum albumin content. Decompensated cirrhosis, serum albumin often prompted the clinical development of ascites, and emphasized that a significant increase in blood volume prior to the occurrence of ascites. Vascular permeability may increase in the presence of infection or endotoxemia, and obstruction of hepatic venous outflow may result in disruption of the hepatic sinus permeability barrier. Ascites formation model: 1. Inadequate theory: In fact, always incorrect.