第十四章 凝血与抗凝血平衡紊乱课件.ppt

DIC治疗的病理生理基础 Pathophysiological Basis of DIC Treatment 1. 积极防治原发病 2. 早期发现、及时治疗 抗凝治疗 保护重要脏器功能 补充凝血物质 适当的抗纤溶治疗 本章目的要求 掌握DIC、FDP、3P试验、沃-弗综合征、席-汉综合征、微血管性溶血性贫血和裂体细胞的概念及英文。 掌握DIC的发病机制，掌握出血、器官功能障碍、休克和贫血及其机制 。 熟悉影响DIC发生发展的因素，DIC的分期、分型。 了解DIC的防治原则 病例1 病例1 * 外源性凝血系统: 15 seconds;内源性凝血系统, 1-6 min Clotting factors from livers: I, II, V, VII, IX, X, XI, XII, XIII From Platelet: III, IV(Ca2+), VIII, XIII From endothelial cells: VIII * 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 * 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, * 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. * 蛋白C 蛋白S are synthesized in the liver TM是内皮细胞膜上凝血酶的受体之一，TM与凝血酶结合之后，可降低凝血酶的凝血活性，而大大加强凝血酶激活PC的能力。 * * 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 * Common causes of DIC. 感染性疾病细菌感染败血症、内毒素血症、病毒性肝炎、流行性出血热 广泛组织损伤大面积挫伤或烧伤、挤压综合症、大手术、器官移植 产科意外胎盘早剥、羊水栓塞、宫内死胎、妊娠中毒症、流产术 恶性实质肿瘤肺、消化系及泌尿系癌、转移癌、恶性葡萄胎、绒毛膜上皮癌 急性白血病急性早幼粒白血病 其他疾病内毒素