病理学局循障碍2013秋五年制3-2.pptVIP

下肢深静脉血栓栓子嵌在肺动脉的分支上（骑跨性栓塞） 肺动脉瓣 肺动脉分支栓塞 系统性栓塞(systemic embolism) 80%－85%是心肌梗塞后发生的附壁血栓脱落所致 栓塞的部位 下肢占70%－75%，内脏10%，脑10%，上肢5% * Schematic illustration of some of the pro- and anticoagulant activities of endothelial cells. Not shown are the pro- and antifibrinolytic properties. vWF, von Willebrand factor; PGI2, prostacyclin; NO, nitric oxide; t-PA, tissue plasminogen activator. Thrombin receptor is referred to as protease activated receptor (PAR; see text). * Virchow triad in thrombosis. Endothelial integrity is the single most important factor. Note that injury to endothelial cells can affect local blood flow and/or coagulability; abnormal blood flow (stasis or turbulence) can, in turn, cause endothelial injury. The elements of the triad may act independently or may combine to cause thrombus formation. * Diagrammatic representation of the normal hemostatic process. A, After vascular injury, local neurohumoral factors induce a transient vasoconstriction. * Diagrammatic representation of the normal hemostatic process. B, Platelets adhere to exposed extracellular matrix (ECM) via von Willebrand factor (vWF) and are activated, undergoing a shape change and granule release; released adenosine diphosphate (ADP) and thromboxane A2 (TxA2) lead to further platelet aggregation to form the primary hemostatic plug. * Diagrammatic representation of the normal hemostatic process. C, Local activation of the coagulation cascade (involving tissue factor and platelet phospholipids) results in fibrin polymerization, cementing the platelets into a definitive secondary hemostatic plug. * Diagrammatic representation of the normal hemostatic process. D, Counter-regulatory mechanisms, such as release of tissue type plasminogen activator (t-PA) (fibrinolytic) and thrombomodulin (interfering with the coagulation cascade), limit the hemostatic process to the site of injury. * Mural thrombi. Laminated thrombus in a dilated abdominal aortic aneurysm. * Mural thrombi. A, Thrombus in t