静脉血栓栓塞症--病理生理的前沿问题PPT.pptVIP

静脉血栓栓塞症--病理生理的前沿问题 中国医学科学院 中国协和医科大学 北京协和医院呼吸科 陆慰萱 约80%DVT无临床表现 致死性PTE生前确诊不足50％ Update conception VTE DVT PTE Leg ischemia Post-thrombotic syndrome Recurrent thromboemlism shock recurrence Non-resolution mortality Pulmonary hypertension Deep venous thrombosis（DVT）——marker of PTE Mechanism of VTE DVT：Thrombosis—thrombus lysis (blood /fibrin clots) extension break off travel organization PTE： Embolism—emboli revasculation damage new thrombosis organization revasculation destruction/infarction necrosis lysis Triad of etiologic factors of DVT In 1856 Rudolf Virchow : venous stasis vein wall injury procoagulants in the blood Update Virchow’s triad factors subtle vein wall injuries: microscopic endothelial tears; exposure of subendothelial tissue abnormal viscosity and fluidity of blood anticoagulants deficiencies, decreased fibrinolytic activity and abnormal activity of platelet C 内皮细胞 A B ADP酶 D 前列环素 一氧化氮 抑制血小板 聚集 ADP 腺苷酸 蛋白 C 凝血酶 活化 蛋白 C 蛋白 S 组织纤溶酶原活化物 纤溶酶原 纤溶酶 肝素 抗凝血酶III The vascular endothelium’s role in maintaining d fluidity in the absence of significant insult is subserved everal molecules that are either on the surface of endoal calls or released by them. Included are prostacyclin and endothelium-dependent relaxing factor(EFRF), OR NITRIC OXIDE (NO), witch inhibit platelet adhesin (A). Along with ADPase,PGL2 and EDRF(NO)also inhibit platelet activation and aggregation (B). Thrombomodulin and heparin-like molecules inhibit coagulation(C), and tissue-type plasminogen activator(t-PA)activateds fibrinolysis(D). 血浆 抑制血小板 活化和聚集 降解因子Va 和 VIIIa 抑制凝血酶 活性 纤维蛋白