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本文所用缩写: APTT 活化的部分凝血活酶时间 AT-Ⅲ抗凝血酶Ⅲ CLP 糜蛋白酶样蛋白质 DIC 弥散性血管内凝血 EGT 乙醇胶试验 ELP 弹性硬蛋白酶样蛋白质 ELT 优球蛋白凝块溶解试验 FDP 纤维蛋白(原)降解产物 FM 纤维蛋白单体 FPA 纤维蛋白肽A FPB 纤维蛋白肽B PF4 血小板第4因子 PT 凝血酶原时间 TCT 凝血酶凝固时间β-TG β-血小板球蛋白 TIFPB 凝血酶可增加的FPB ⅩⅢa 活化的因子ⅩⅢ(其它凝血因子亦同) ⅧR:Ag/Ⅷ:C 因子Ⅷ相关抗原/因子Ⅷ促凝活性 DIC 的病理生理各种DIC的致病因素,均可激活内源或外源凝血系统,最终使凝血酶原转变为凝血酶,后者又使纤维蛋白原转变为纤维蛋白。早期血液凝固性增高,但随着微血管内广泛血栓形成,凝血因子大量消耗,纤维蛋白溶解(下简
Abbreviations used herein: APTT activated partial thromboplastin time AT-III antithrombin III CLP chymase-like protein DIC disseminated intravascular coagulation EGT ethanol gel test ELP elastase-like protein ELT euglobulin clot lysis assay FDP Fibrinogen (prot) Degradation Product FM Fibrin Monomer FPA Fibrin Peptide A FPB Fibrotide B PF4 Platelet Factor 4 PT Prothrombin Time TCT Thrombin Coagulation Time β-TG β-Thromboglobulin TIFPB Thrombin Increased (Other coagulation factors are also the same) Ⅷ R: Ag / Ⅷ: C factor Ⅷ related antigen / factor Ⅷ procoagulant activity Pathophysiology of DIC Various pathogenic factors of DIC can activate endogenous or exogenous The source coagulation system eventually converts prothrombin to thrombin, which in turn converts fibrinogen to fibrin. Early blood coagulation increased, but with extensive microvascular thrombosis, coagulation factor consumption, fibrinolysis (Jane