红细胞及血浆输注与血栓.ppt

IIa Thrombin Anti-coagulant effects thrombomodulin IIa VIIIa Va Protein C Activated Protein C Protein S Protein C Anticoagulant Pathway 静脉注射丙种球蛋白与血栓形成 IVIG 自身抗体产生 补体活化 抑制细胞因子活性 封闭巨噬细胞Fc受体活性 应用于多种自身免疫性疾病 免疫缺陷病和炎症性疾病的治疗 严重血栓事件 心肌梗死 深静脉血栓形成 视网膜中央静脉阻塞 肺梗死 中风 血栓形成机制 85％患者的血液粘度超过正常值上限 血小板计数增高 血小板聚集活性增加 白蛋白和Fg协同导致血细胞聚集增强 制品含XIa或抗磷脂抗体，导致输注后促凝活性增强 刺激局部合成促进血管收缩的细胞因子 46个患者518次输注IVIG，6个患者发生血栓（13％），一半发生在IVIG治疗过程中，其余发生在治疗后的1－8天 输注的总量和血栓形成没有明显相关性 本身有血栓形成的危险因素，如冠心病、糖尿病、老年人、高血压病、有血栓形成史以及高胆固醇血症等，更加注意 血栓形成的诊断 侵入性 静脉栓塞的临床诊断 非侵入性 125I 腿部扫描 125I 超声波检查 SOUND 阻抗式体积描记 静脉造影术 X-Ray 侵入性 非侵入性 肺部血管造影 (参考标准) 肺部闪烁扫描 Albumin99mTC 肺灌注扫描 通气扫描 127Xe / 8lmKr Normal Lung Pulmonary Emboli 肺栓塞的临床诊断 Types of Thrombosis Arterial: platelet-based (white)thrombus Platelet-VWF interactions critical Associated with end-stage atherosclerosis Venous: Fibrin-based (red) thrombus Coagulation factors critical Venous stasis 筛选试验 血小板功能测试 凝血酶生成潜力测定 血小板功能测定 PFA-100 凝血酶生成潜力测定 all clinical states influencing thrombin are reflected by the ETP Thrombin Generation Thrombin (Factor IIa) the central enzyme of coagulation 凝血酶是血液凝固的核心酶 增加血栓风险的任何机制都增加凝血酶的产生 增加出血风险的任何机制都减少凝血酶的产生 凝血酶的增加，有利止血，但增加血栓倾向　 实时的凝血酶测量是一个很好的评估止血功能的工具　 H. C. Hemker et al., Thromb Haemost 1993 ETP: Thrombin Generation Assay 0 30 60 90 0 5 10 15 20 25 Time (min) Thrombin activity [nM] ETP - area of the thrombin generation curve Lag-phase ~ Clotting time a measure for concentrationand time of action TIA Company LOGO * Coagulation may be initiated by vascular injury, however, multiple coagulation pathways are involved in the actual formation of clot. Vasoconstriction occurs immediately following vascular injury and is followed by platelet adhesion to collagen in the vessel wall exposed by injury. Subsequently platelet aggregation results in a platelet plug which is later strengthened by fibrin. Fibrin production may begin with the conversion of factor X to factor Xa. Factor X can be activated by means of two reaction sequences. One requ