静脉血栓栓塞症病理生理的前沿问题.pptVIP

静脉血栓栓塞症--病理生理的前沿问题 约80%DVT无临床表现致死性PTE生前确诊不足50％ Update conception VTEDVTPTELeg ischemiaPost-thrombotic syndromeRecurrent thromboemlismshockrecurrenceNon-resolutionmortalityPulmonaryhypertension 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 revasculationdestruction/infarctionnecrosislysis Mechanism of VTE Triad of etiologic factors of DVTIn 1856 Rudolf Virchow : venous stasis vein wall injury procoagulants in the blood Update Virchow’s triad factorssubtle vein wall injuries: microscopic endothelial tears; exposure of subendothelial tissue abnormal viscosity and fluidity of bloodanticoagulants deficiencies, decreased fibrinolytic activity and abnormal activity of platelet C内皮细胞ABADP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IIIThe 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 orreleased 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降解TM 凝 血 与 纤 溶 途 径凝血纤溶内源性FIXaF VIII外源性F VII组织因子凝血酶纤溶酶原纤溶酶原激活物(PA)纤溶酶原激活抑制物(PAI)纤溶酶a2-抗纤溶酶纤维蛋白降解产