第十一章弥散性血管内牵凝血（dic).pptVIP

高分子激肽原, 前激肽释放酶 are synthesized in the liver VIIIa increase the speed of the reaction from X to Xa 200,000-fold faster. IV: Ca2+ Source: Liver: fibrinogen (I), prothrombin (II), V,VII,IX,X,XI,XII,XIII Platelets: III, V,VIII,, XIII Endothelial cells: VIII, XIII Thrombin activates factor V VIII The injured tissues and endothelium very slowly release tissue plasminogen activator (t-PA；组织纤溶酶原激活物) a day or later after clot is formed and convert plasminogen to plasmin. Plasmin具有广泛的丝氨酸水解酶活性，能水解凝血终产物fibrin生成可溶性的纤维蛋白降解产物（fibrin degradation products, FDP），也能水解fibrinogen和其他多种coagulation factors、血浆蛋白与组织蛋白。 尿激酶原 is from kidney. 纤溶酶原激活物抑制物(PAIs)：from endothelium and platelets 组织因子 is a cofactor, it make VIIa 1000-fold more active; VIIIa increase the speed of the reaction from X to Xa 200,000-fold faster. 凝血酶激活:V, VIII, XII, PROTHROMBIN, DIC在临床可表现为急性全身性，也可为亚急性、慢性，主要发生在脏器局部。对机体造成严重危害的是急性全身性DIC。DIC发病率约0.2‰~0.5‰，因其早期不易诊断，且治疗复杂，急性全身性DIC死亡率高达50%~60%，是一种严重威胁患者生命的临床综合征。 抗凝血酶Ⅲ from the liver and the endothelium. The concentration of heparin is normally low so that only under special physiological conditions does it have significant antilant effects. Heparin is produced by many different cells of the body, but especially large quantities are formed by basophilic mast cells. Hepairn has no anticoagulation effect, however, it augments the antithrombin activity by a hundred to a thousand folds. 微血管病性溶血性贫血（Microangiopathic Hemolytic Anemia）:慢性DIC和有些亚急性DIC常出现hemolytic anemia的症状，外周血涂片可发现新月形、盔甲形、星形、三角形等变形红细胞，被称为裂体细胞（schistocyte）。 在DIC发病过程中，fibrin除形成microthrombus外，也有相互交织联结在微血管中形成纤维蛋白丝、纤维蛋白网，特别在DIC早期小血管中这些纤维蛋白丝网较多。当红细胞随血流快速在微血管中流动时，被纤维蛋白丝网撞击、粘挂，或红细胞嵌在VEC较大裂隙处。血流冲击使这些红细胞受到挤压、切割等机械损伤，最终红细胞变形、破裂形成schistocyte。 Schistocyte变形能力显著降低，脆性增高，在血流的冲击、碰撞下容易破裂，发生溶血。将这种因微血管发生病理变化而导致红细胞破裂引起的贫血，称为microangiopathic hemolytic anemia。外周血涂片中发现较多schistocyte（超过红细胞数2%），虽非DIC所特有，却是诊断DIC的重要参考指标。 Microangiopathic hemolytic anemias comprise thrombocytopenic thrombotic purpura, the hemolytic–uremic syndrome, chemo