《弥散性血管内凝血 DIC.ppt》由会员分享，可在线阅读，更多相关《弥散性血管内凝血 DIC.ppt（36页珍藏版）》请在taowenge.com淘文阁网|工程机械CAD图纸|机械工程制图|CAD装配图下载|SolidWorks_CaTia_CAD_UG_PROE_设计图分享下载上搜索。
1、弥散性血管内凝血 Chapter 11中山医学院病理生理教研室邓宇斌 DIC一、DIC原因和发病机制二、促进DIC发生发展的因素（诱发困素）三、DIC的分期和分型四、DIC的功能代谢变化（病理生理变化）五、DIC防治的病理生理基础第一节 概述1.血液的凝固与抗凝 流动性 血液运输载体 方向性 内（）凝血系统 凝血 外（）血小板：粘 聚 释 凝抗凝 栓塞失衡 凝抗凝 出血倾向2.DIC的概念 出血病因 微血栓 后 休克致凝 继发纤溶亢进 果 栓塞 溶血 120种病：感染、肿瘤、产科意外 Introduction DIC is characterized by the activation of
2、the coagulation system with resultant consumption of a variety of coagulation proteins and platelets,which results in hemorrhagic diathesis and ischemic injury to various tissues.1.Blood Coagulation It is propagated by an enzymatic events termed coagulation cascade.Contact factors and the intrinsic
3、pathwayTissue factor and extrinsic pathway 2.Fibrinolysis It is the result of the action of plasmin,a proteolytic enzyme produced from an inert plasma precursor(plasminogen)by the action of various substances termed plasminogen activators.Humoral plasminogen activatorsTissue plasminogen activatorsFi
4、brin or fibrinogen degradation products FDP (Significant biological activity)Fragments X,Y and E (potent antithrombins)Fragments Y and D (inhibit fibrin polymerization)a a a PC APC TM+灭 活 PS(+)C4b C4b PS(-)酶酶 纤溶纤溶 FDP 酶酶 AT PC 抗抗 APC TM+a 凝凝 PS PGI2 VEC TM第二节 DIC的病因发病学一、发病原因及机理1.VEC广泛受损 原因 感染 炎症、免疫损
5、伤（抗磷脂综合征）高低温、放射损伤 缺血缺氧 酸中毒Etiology of DIC1.acute DIC(1)septicemia (2)severe trauma (3)obstetric accidents (4)shock2.subacute DIC(1)malignant tumors(2)retained dead fetus3.chronic DIC(1)giant hemangioma(2)systemic lupus erythematosus(SLE)机理 胶原暴露 凝VEC 释放受损 合成PGI2TXA2 抗凝 表达TM APC2.血细胞大量受损RBC受损 感染：疟疾 原因
6、：溶血 G6PDase：蚕豆病 免疫损伤：异型输血 红细胞素（）机理：释 ADP P聚集WBC激活或受损 坏死 白血病细胞 释原因 化疗受损机理 炎症激活 合成、释 （内毒素、补体、LC、P、AgAb）P激活或受损 原发性：免疫损伤（抗P抗体抗磷脂抗体）继发性：DIC 粘（GPb胶原）聚（GPba fg）TXA2等 P聚、血管收缩 机理 PF111 提供“反应面”aCa2+a aCa2+a PF3 PF33.大量致凝物质入血 肿瘤细胞 坏死（包括产科意外）组织细胞 带负电颗粒物质（内毒素）a 胰蛋白酶 其它丝氨酸蛋白水解酶 a 蝰蛇毒Pathogenesis of DIC 1.extensiv
7、e damage of vascular endothelial cells Intrinsic clotting cascade 2.severe tissue injury Extrinsic clotting reaction3.excessive destruction of the circulating blood cells Generation of Generation of procoagulantprocoagulant-active-active substancessubstances IntravascularIntravascular coagulation co
8、agulation 4.other thromboplastic materials entering the blood Activation of clotting system through the Activation of clotting system through the contact of blood with an abnormal surfacecontact of blood with an abnormal surfacethe net effects are summarized as follows:1.loss of plasma fibrinogen as
9、 it is consumed by 1.loss of plasma fibrinogen as it is consumed by the clotting process and by the action of the clotting process and by the action of plasma.plasma.2.loss of other clotting factors notably 2.loss of other clotting factors notably,and and,as they are used up during the operation of,
10、as they are used up during the operation of the clotting cascade.the clotting cascade.3.fall in the platelet count,as the platelets 3.fall in the platelet count,as the platelets aggregate and leave the circulation.aggregate and leave the circulation.4.appearance of fibrin degradation products,as 4.a
11、ppearance of fibrin degradation products,as plasmin plasmin acts on its substrates.acts on its substrates.二、诱因与发生机理 消除致凝物质功能 血液凝血活性抗凝活性 1.单核吞噬细胞系统功能 内毒素血症、糖皮质激素、脾 消除功能：致凝物、a、凝纤产物 2.肝功能严重障碍 灭活活化凝血因子 合成AT、PC 枯否细胞吞噬功能 3.血液的高凝状态 凝血活性 凝血物质：怀孕、肿瘤、应激 抗纤溶：胎盘、药 抗凝活性 抗肝素：H AT、PC、TM等 4.血流郁滞Predisposing factors
12、 to DIC1.impairment of the clearance mechanism.2.hypercoagulable state.3.disorder of microcirculation.第三节 DIC的分期及分型 高凝期 分期 消耗性低凝期 继发性纤溶亢进期 急性 按发病速度 亚急性 分 慢性 型 代偿型 按代偿情况 失代偿型 过度代偿型Types of DIC 1.acute DICMultiside Multiside bleeding diathesisbleeding diathesisThrombotic Thrombotic complications usual
13、lycomplications usuallySevere bleeding lead to shock and severe Severe bleeding lead to shock and severe ischemic ischemic change in organschange in organs2.subacute DICRarely bleeding Rarely bleeding The evidence of DIC can be detected by The evidence of DIC can be detected by laboratory examinatio
14、nslaboratory examinations3.chronic DIC Stage of DIC1.hypercoagulable stage2.hypocoagulable stage3.secondary fibrinolytic stage第四节 临床表现1.出血凝血物质消耗性 酶：破坏凝血因子继发性纤溶亢进 a FDP抗凝：竞争性抑制 a P聚血管壁受损及溶栓Consequences of DIC 1.disturbance of coagulation-bleeding (1)the consumption of clotting factors and platelets (
15、2)the activation of fibrinolytic system (3)the production of fibrin degradation products(FDPs)2.休克 出血 回心血量 微血栓阻断通路 CO 心泵功能 :心肌DICBP 右心后负荷:肺DIC 外周阻力:四个酶系统激活 A、B肽 扩血管物质 FDP (通透性)激肽 C3a、C5a 2.disturbance of circulation-shockMicrothromobus in capillariesand venulesBlood returning decreaseCardiac muscle
16、damageCardiac output and blood volume reduceEffective circulating blood volume decreaseHypotension 3.栓塞 微血栓 器官 功能 BP 供血 障碍 4.溶血：微血管病性溶血性贫血 3.ischemic tissue damage-dysfunction of multiple organsRenal insufficiencyAcute adrenal failurePituitary necrosisAdult or acute respiratory distress syndrome(ARD
17、S)Convulsion and coma4.microangiopathic hemolytic anemia(MHA)characteristic morphologic abnormality of the red blood cellsTwisted cells,crenated cells,triangular cells,helmet-shaped cells,and microspherocytes are seen on the blood smear.Pathophysiological basis of laboratory diagnosis1.detection of
18、platelet count and its function2.determination of clotting factors 3.determination of activity of fibrinolysis (1)thrombin time test(TT)(2)plasma protamine paracoagulation test(3P test)(3)euglobulin lysis time(ETL)Principles of management of DIC1.treatment of the causative disease2.clotting factor replacement3.anticoagulation therapy4.other modes of therapy