课件：病理生理学总重点.ppt

@木鱼先生@QQ：444539762QQ交流群：127407127 @医学旅途@ @挽手帮助@ @勤奋刻苦@ @志心永驻@ @救死扶伤@ @健康是路@ 病理生理学总复习资料 THANK YOU SUCCESS * * 可编辑 * In patients with disseminated intravascular coagulation, fibrin is formed as a result of the generation of thrombin mediated by tissue factor. Tissue factor, expressed on the surface of activated mononuclear cells and endothelial cells, binds and activates factor VII. The complex of tissue factor and factor VIIa can activate factor X directly (black arrows) or indirectly (white arrows) by means of activated factor IX and factor VIII. Activated factor X, in combination with factor V, can convert prothrombin (factor II) to thrombin (factor IIa). Simultaneously, all three physiologic means of anticoagulation — antithrombin III, protein C, and tissue factor–pathway inhibitor (TFPI) — are impaired. The resulting intravascular formation of fibrin is not balanced by adequate removal of fibrin because endogenous fibrinolysis is suppressed by high plasma levels of plasminogen-activator inhibitor type 1 (PAI-1). The high levels of PAI-1 inhibit plasminogen-activator activity and consequently reduce the rate of formation of plasmin. The combination of increased formation of fibrin and inadequate removal of fibrin results in disseminated intravascular thrombosis. FDPs denotes fibrin-degradation products. 要点一：抗凝血 体液抗凝 （组织因子途径抑制物，抗凝血酶Ⅲ,蛋白C系统，纤维蛋白溶解系统FDP） 细胞抗凝（单核巨噬细胞，肝细胞） 症状： 组织因子途径抑制物 抗凝血酶Ⅲ 蛋白C系统 纤维蛋白溶解系统 1. 出血 2. 器官功能障碍 3. 休克 4. 微血管病性溶血性贫血 大量组织 损伤 血管内皮 细胞损伤 血小板 聚集 凝血因子与血小板 耗竭 纤维蛋白溶解 纤维蛋白溶酶激活 凝血因子水解 纤维蛋白 降解产物 凝血酶 血小板聚集 纤维蛋白交联 广泛微血栓 出血 血管栓塞 微血管病性溶血性贫血 缺血组织损伤 释放组织因子 - 要点二：形成机制： 要点三：分期及特点 出血机理： 1凝血因子、血小板过度消耗 2纤溶系统激活(子宫，前列腺，肺富含纤溶酶原激活物；应急，缺氧→内皮细胞释放纤溶酶原激活物↑) 3纤维蛋白降解产物(FDP)形成,对凝血酶，血小板聚集及纤维蛋白交联抑制 DIC分期及特点: 高凝期: 凝血酶增多，微血栓形成。 消耗性低凝期: 凝血因子、血小板消耗，纤溶系统激活，出血。 继发性纤溶期: 纤溶酶增多，纤维蛋白降解产物(FDP)形成。 DIC的诱发因素： 1.单核吞噬细胞系统功能减弱 2.微循环障碍 3.血液高凝状态 4.肝功能障碍 因子Ⅰ：纤维蛋白原 因子Ⅱ：凝血酶原 因子Ⅲ：组织因子（TF） 因子Ⅳ：Ca2+ 重点五：@休克@ 概念：由于大出血、创伤、烧伤、感染、过敏等各种原因引起机体有效循环血量急剧减少、织血液灌流量严重