文档介绍：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 anization
PTE: Embolism—emboli revasculation
damage
new thrombosis
organization
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
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
降解
TM