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1、彌散性血管內(nèi)凝血Chapter11中山醫(yī)學(xué)院病理生理教研室鄧宇斌DIC一、DIC原因和發(fā)病機(jī)制二、促進(jìn)DIC發(fā)生發(fā)展的因素（誘發(fā)困素）三、DIC的分期和分型四、DIC的功能代謝變化（病理生理變化）五、DIC防治的病理生理基礎(chǔ)第一節(jié)概述1.血液的凝固與抗凝流動性血液運(yùn)輸載體方向性內(nèi)（Ⅻ）凝血系統(tǒng)凝血外（Ⅲ）血小板：粘聚釋凝↑／抗凝↓→栓塞失衡凝↓／抗凝↑→出血傾向2.DIC的概念出血病因微血栓后休克致凝繼發(fā)纖溶亢進(jìn)果栓塞溶血>120種?。焊腥?、腫瘤、產(chǎn)科意外IntroductionDICischaracterizedbytheactivationofth
2、ecoagulationsystemwithresultantconsumptionofavarietyofcoagulationproteinsandplatelets,whichresultsinhemorrhagicdiathesisandischemicinjurytovarioustissues.1.BloodCoagulationItispropagatedbyanenzymaticeventstermedcoagulationcascade.ContactfactorsandtheintrinsicpathwayTissuefactora
3、ndextrinsicpathway2.FibrinolysisItistheresultoftheactionofplasmin,aproteolyticenzymeproducedfromaninertplasmaprecursor(plasminogen)bytheactionofvarioussubstancestermedplasminogenactivators.HumoralplasminogenactivatorsTissueplasminogenactivatorsFibrinorfibrinogendegradationproduc
4、tsFDP(Significantbiologicalactivity)FragmentsX,YandE(potentantithrombins)FragmentsYandD(inhibitfibrinpolymerization)ⅡaⅡaⅢaPCAPCTM+Ⅱ滅活PS(+)C4bC4bPS(-)酶纖溶FDP酶ATPC抗APCTM+Ⅱa凝PSPGI2VECTM第二節(jié)DIC的病因發(fā)病學(xué)一、發(fā)病原因及機(jī)理1.VEC廣泛受損⑴原因感染炎癥、免疫損傷（抗磷脂綜合征）高低溫、放射損傷缺血缺氧酸中毒EtiologyofDIC1.acuteDIC(1)septice
5、mia(2)severetrauma(3)obstetricaccidents(4)shock2.subacuteDIC(1)malignanttumors(2)retaineddeadfetus3.chronicDIC(1)gianthemangioma(2)systemiclupuserythematosus(SLE)⑵機(jī)理膠原暴露凝↑VEC釋放Ⅲ受損合成PGI2↓→TXA2↑抗凝↓表達(dá)TM↓→APC↓2.血細(xì)胞大量受損⑴RBC受損感染：瘧疾原因：溶血G6PDase↓：蠶豆病免疫損傷：異型輸血紅細(xì)胞素（Ⅲ）機(jī)理：釋ADP→P聚集⑵WBC激活或受損壞
6、死白血病細(xì)胞→釋Ⅲ原因化療受損機(jī)理炎癥激活→合成、釋Ⅲ（內(nèi)毒素、補(bǔ)體、LC、P、Ag－Ab）⑶P激活或受損原發(fā)性：免疫損傷（抗P抗體抗磷脂抗體）繼發(fā)性：DIC粘（GPⅠb－膠原）聚（GPⅡb／Ⅲa－fg）TXA2等P聚、血管收縮機(jī)理PF1～11提供“反應(yīng)面”ⅩⅡⅨa－Ca2+－ⅧaⅩa－Ca2+－ⅡaPF3PF33.大量致凝物質(zhì)入血腫瘤細(xì)胞⑴Ⅲ壞死（包括產(chǎn)科意外）組織細(xì)胞⑵帶負(fù)電顆粒物質(zhì)（內(nèi)毒素）→Ⅻa胰蛋白酶⑶其它絲氨酸蛋白水解酶→Ⅱa蝰蛇毒PathogenesisofDIC1.extensivedamageofvascularendothelial
7、cellsIntrinsicclottingcascade2.severetissueinjuryExtrinsicclottingreaction3.excessivedestructionofthecirculatingbloodcellsGenerationofprocoagulant-activesubstancesIntravascularcoagulation4.otherthromboplasticmaterialsenteringthebloodActivationofclottingsystemthroughthecontactofb
8、loodwithanabnormalsurfacetheneteffectsaresummar
