靜脈血栓栓塞癥--病理生理的前沿問題-文庫吧資料
2025-01-12 09:53本頁面
【正文】 (blood /fibrin clots) extension break off travel anization PTE： Embolism— emboli revasculation damage new thrombosis anization revasculation destruction/infarction necrosis lysis Mechanism of VTE 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 內(nèi)皮細(xì)胞 A B ADP酶 D 前列環(huán)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 組織纖溶酶原活化物 纖溶酶原 纖溶酶 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 endotheliumdependent 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 heparinlike molecules
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