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彌散性血管內(nèi)凝血

Chapter11中山醫(yī)學(xué)院病理生理1

DIC一、DIC原因和發(fā)病機制二、促進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)DIC2第一節(jié)概述1.血液的凝固與抗凝流動性血液運輸載體方向性內(nèi)（Ⅻ）凝血系統(tǒng)凝血外（Ⅲ）血小板：粘聚釋第一節(jié)概述1.血液的凝固與抗凝3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)纖溶亢進果栓塞溶血>120種?。焊腥尽⒛[瘤、產(chǎn)科意外凝↑／抗凝↓→栓塞4Introduction

DICischaracterizedbytheactivationofthecoagulationsystemwithresultantconsumptionofavarietyofcoagulationproteinsandplatelets,whichresultsinhemorrhagicdiathesisandischemicinjurytovarioustissues.IntroductionDICisc51.BloodCoagulation

Itispropagatedbyanenzymaticeventstermedcoagulationcascade.ContactfactorsandtheintrinsicpathwayTissuefactorandextrinsicpathway

1.BloodCoagulation62.Fibrinolysis

Itistheresultoftheactionofplasmin,aproteolyticenzymeproducedfromaninertplasmaprecursor(plasminogen)bytheactionofvarioussubstancestermedplasminogenactivators.

2.Fibrinolysis7HumoralplasminogenactivatorsTissueplasminogenactivatorsFibrinorfibrinogendegradationproductsFDP(Significantbiologicalactivity)FragmentsX,YandE(potentantithrombins)FragmentsYandD(inhibitfibrinpolymerization)Humoralplasminogenactivators8

ⅡaⅡaⅢaPCAPCTM+Ⅱ滅活PS(+)C4bC4bPS(-)

9

酶

纖溶

FDP

酶ATPC

抗

APCTM+Ⅱa

凝

PSPGI2VECTM

10第二節(jié)DIC的病因發(fā)病學(xué)一、發(fā)病原因及機理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第二節(jié)DIC的病因發(fā)病學(xué)一、發(fā)病原因及機理11EtiologyofDIC1.acuteDIC(1)septicemia(2)severetrauma(3)obstetricaccidents(4)shock2.subacuteDIC(1)malignanttumors(2)retaineddeadfetus3.chronicDIC

(1)gianthemangioma(2)systemiclupuserythematosus(SLE)EtiologyofDIC1.acuteDIC12⑵機理膠原暴露凝↑VEC釋放Ⅲ受損合成PGI2↓→TXA2↑抗凝↓表達TM↓→APC↓⑵機理132.血細胞大量受損⑴RBC受損感染：瘧疾原因：溶血G6PDase↓：蠶豆病免疫損傷：異型輸血紅細胞素（Ⅲ）機理：釋ADP→P聚集2.血細胞大量受損14⑵WBC激活或受損壞死白血病細胞→釋Ⅲ原因化療受損機理炎癥激活→合成、釋Ⅲ（內(nèi)毒素、補體、LC、P、Ag－Ab）⑵WBC激活或受損15

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、血管收縮機理PF1～11提供“反應(yīng)面”

ⅩⅡⅨa－Ca2+－ⅧaⅩa－Ca2+－ⅡaPF3PF3⑶P激活或受損163.大量致凝物質(zhì)入血腫瘤細胞

⑴Ⅲ壞死（包括產(chǎn)科意外）組織細胞

⑵帶負電顆粒物質(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3.大量致凝物質(zhì)入血17PathogenesisofDIC

1.extensivedamageofvascularendothelialcells

Intrinsicclottingcascade2.severetissueinjury

ExtrinsicclottingreactionPathogenesisofDIC1.extensiv183.excessivedestructionofthecirculatingbloodcells

Generationofprocoagulant-activesubstances

Intravascularcoagulation4.otherthromboplasticmaterialsenteringthebloodActivationofclottingsystemthroughthecontactofbloodwithanabnormalsurface3.excessivedestructionofthe19theneteffectsaresummarizedasfollows:1.lossofplasmafibrinogenasitisconsumedbytheclottingprocessandbytheactionofplasma.2.lossofotherclottingfactorsnotablyⅤ,ⅧandⅫ,astheyareusedupduringtheoperationoftheclottingcascade.3.fallintheplateletcount,astheplateletsaggregateandleavethecirculation.4.appearanceoffibrindegradationproducts,asplasminactsonitssubstrates.theneteffectsaresummarized20

二、誘因與發(fā)生機理消除致凝物質(zhì)功能血液凝血活性↑／抗凝活性↓

1.單核吞噬細胞系統(tǒng)功能內(nèi)毒素血癥、糖皮質(zhì)激素、脾消除功能↓：致凝物、Ⅱa、凝纖產(chǎn)物

二、誘因與發(fā)生機理21

2.肝功能嚴重障礙滅活活化凝血因子↓合成AT－Ⅲ、PC↓枯否細胞吞噬功能↓

3.血液的高凝狀態(tài)凝血活性↑－凝血物質(zhì)↑：懷孕、腫瘤、應(yīng)激抗纖溶：胎盤、藥抗凝活性↓抗肝素：H＋AT、PC、TM等↓

4.血流郁滯2.肝功能嚴重障礙22PredisposingfactorstoDIC1.impairmentoftheclearancemechanism.2.hypercoagulablestate.3.disorderofmicrocirculation.PredisposingfactorstoDIC1.i23第三節(jié)DIC的分期及分型高凝期

分期

消耗性低凝期繼發(fā)性纖溶亢進期急性按發(fā)病速度亞急性

分

慢性

型

代償型按代償情況失代償型過度代償型第三節(jié)DIC的分期及分型24TypesofDIC1.acuteDICMultisidebleedingdiathesisThromboticcomplicationsusuallySeverebleedingleadtoshockandsevereischemicchangeinorgans2.subacuteDICRarelybleedingTheevidenceofDICcanbedetectedbylaboratoryexaminations3.chronicDICTypesofDIC25StageofDIC1.hypercoagulablestage2.hypocoagulablestage3.secondaryfibrinolyticstageStageofDIC1.hypercoagulable26第四節(jié)臨床表現(xiàn)1.出血凝血物質(zhì)消耗性↓酶：破壞凝血因子繼發(fā)性纖溶亢進ⅡaFDP抗凝：競爭性抑制ⅢaP聚血管壁受損及溶栓第四節(jié)臨床表現(xiàn)1.出血27ConsequencesofDIC

1.disturbanceofcoagulation----bleeding(1)theconsumptionofclottingfactorsandplatelets(2)theactivationoffibrinolyticsystem(3)theproductionoffibrindegradationproducts(FDPs)ConsequencesofDIC1.disturba282.休克

出血回心血量↓微血栓阻斷通路CO↓心泵功能↓:心肌DICBP↓右心后負荷↑:肺DIC外周阻力↓:四個酶系統(tǒng)激活

↓A、B肽擴血管物質(zhì)↑FDP(通透性↑)激肽C3a、C5a

292.disturbanceofcirculation----shockMicrothromobusincapillariesandvenulesBloodreturningdecreaseCardiacmuscledamageCardiacoutputandbloodvolumereduceEffectivecirculatingbloodvolumedecreaseHypotension2.disturbanceofcirculation--30

3.栓塞微血栓器官功能BP↓供血障礙

4.溶血：微血管病性溶血性貧血

3.栓塞313.ischemictissuedamage----dysfunctionofmultipleorgansRenalinsufficiencyAcuteadrenalfailurePituitarynecrosisAdultoracuterespiratorydistresssyndrome(ARDS)Convulsionandcoma3.ischemictissuedamage----dy324.microangiopathichemolyticanemia(MHA)characteristicmorphologicabnormalityoftheredbloodcellsTwistedcells,crenatedcells,triangularcells,helmet-shapedcells,andmicrospherocytesareseenonthebloodsmear.4.microangiopathichemolytica33Pathophysiologicalbasisoflaboratorydiagnosis1.detectionofplateletcountanditsfunction2.determinationofclottingfactors3.determinationofactivityoffibrinolysis(1)thrombintimetest(TT)(2)plasmaprotamineparacoagulationtest(3Ptest)(3)euglobulinlysistime(ETL)Pathophysiologicalbasisofla34PrinciplesofmanagementofDIC1.treatmentofthecausativedisease2.clottingfactorreplacement3.anticoagulationtherapy4.othermodesoftherapyPrinciplesofmanagementofDI35TheEndgoodbyeTheEndgoodbye36($YUQMIEAvrnjfb73+*!XTOKGCyuqmiea62)%ZVRNJFBxtplhc840($YUQMIEAvrnjfb73+*!XTOKGCyuqmiea62)%ZVRNJFBxtplhc840($YUQMIEAvrnjfb73+*!XTOKGCyuqmiea62)%ZVRNJFBxtplhc840($YUQMIEAvrnjfb73+*!XTOKGCyuqmiea62)%ZVRNJFBxtplhc840($YUQMIEAvrnjfb73+*!XTOKGCyuqmiea62)%ZVRNJFBxtplhc840($YUQMIEAvrnjfb73+*!XTOKGCyuqmiea62)%ZVRNJFBxtplhc840($YUQMIEAvrnjfb73+*!XTOKGCyuqmiea62)%ZVRNJFBxtplhc840($YUQMIEAvrnjfb73+*!XTOKGCyuqmiea62-%ZVRNJFBxtplhc840($YUQMIEAvrnjfb73+*!XTOKGCyuqmiea62-%ZVRNJFBxtplhc840($YUQMIEAvrnjfb73+*!XTOKGCyuqmiea62-%ZVRNJFBxtplhc840($YUQMIEAvrnjfb73+*!XTOKGCyuqmiea62-%ZVRNJFBxtplhc840($YUQMIEAvrnjfb73+*!XTOKGCyuqmiea62-%ZVRNJFBxtplhc840($YUQMIEAvrnjfb73+*!XTOKGCyuqmiea62-%ZVRNJFBxtplhc840($YUQMIEAvrnjfb73+*!XTOKGCyuqmiea62-%ZVRNJFBxtplhc840($YUQMIEAvrnjfb73+*!XTOKGCyuqmiea62-%ZVRNJFBxtplhc840($YUQMIEAvrnjfb73+*!XTOKGCyuqmiea62-%ZVRNJFBxtplhc840($YUQMIEAvrnjfb73+*!XTPKGCyuqmiea62-%ZVRNJFBxtplhc840($YUQMIEAvrnjfb73+*!XTPKGCyuqmiea62-%ZVRNJFBxtplhc840($YUQMIEAvrnjfb73+*!XTPKGCyuqmiea62-%ZVRNJFBxtplhc840($YUQMIEAvrnjfb73+*!XTPKGCyuqmiea62-%ZVRNJFBxtplhc840($YUQMIEAvrnjfb73+*!XTPKGCyuqmiea62-%ZVRNJFBxtplhc840($YUQMIEAvrnjfb73+*!XTPKGCyuqmiea62-%ZVRNJFBxtplhc840($YUQMIEAvrnjfb73+*!XTPKGCyuqmiea62-%ZVRNJFBxtplhc840($YUQMIEAvrnjfb73+*!XTPKGCyuqmiea62-%ZVRNJFBxtplhc840($YUQMIEAvrnjfb73+*!XTPKGCyuqmiea62-%ZVRNJFBxtplhc840($YUQMIEAvrnjfb73+*!XTPKGCyuqmiea62-%ZVRNJFBxtplhc840($YUQMIEAwrnjfea62-&#WSOKGBxtplhd951)%ZUQMIEAwsokgc83+*!XTPLHDzvrmiea62-&#WSOKGBxtplhd951)%ZUQMIEAwsokgc83+*!XTPLHDzvrmiea62-&#WSOKGBxtplhd951)%ZUQMIEAwsokgc83+*!XTPLHDzvrmiea62-&#WSOKGBxtplhd951)%ZUQMIEAwsokgc83+*!XTPLHDzvrmiea62-&#WSOKGBxtplhd951)%ZUQMIEAwsokgc83+*!XTPLHDzvrniea62-&#WSOKGBxtplhd951)%ZUQMIEAwsokgc83+*!XTPLHDzvrniea62-&#WSOKGBxtplhd951)%ZUQMIEAwsokgc83+*!XTPLHDzvrniea62-&#WSOKGBxtplhd951)%ZUQMIEAwsokgc83+*!XTPLHDzvrniea62-&#WSOKGBxtplhd951)%ZUQMIEAwsokgc83+*!XTPLHDzvrniea62-&#WSOKGBxtplhd951)%ZUQMIEAwsokgc83+*!XTPLHDzvrniea62-&#WSOKGBxtplhd951)%ZUQMIEAwsokgc83+*!XTPLHDzvrniea62-&#WSOKGBxtplhd951)%ZUQMIEAzvrnjfb73+&#WSOKGCyuqmie951)%ZVRNJFBxsokgc840($YUQLHDzvrnjfb73+&#WSOKGCyuqmie951)%ZVRNJFBxsokgc840($YUQLHDzvrnjfb73+&#WSOKGCyuqmie951)%ZVRNJFBxsokgc840($YUQLHDzvrnjfb73+&#WSOKGCyuqmie951)%ZVRNJFBxsokgc840($YUQLHDzvrnjfb73+&#WSOKGCyuqmie951)%ZVRNJFBxsokgc840($YUQLHDzvrnjfb73+&#WSOKGCyuqmie951)%ZVRNJFBxsokgc840($YUQLHDzvrnjfb73+&#WSOKGCyuqmie951)%ZVRNJFBxsokgc840($YUQLHDzvrnjfb73+&#WSOKGCyuqmie951)%ZVRNJFBxsokgc840($YUQLHDzvrnjfb73+*#WSOKGCyuqmie951)%ZVRNJFBxsokgc840($YUQLHDzvrnjfb73+*#WSOKGCyuqmie951)%ZVRNJFBxsokgc840($YUQLHDzvrnjfb73+*#WSOKGCyuqmie951)%ZVRNJFBxsokgc840($YUQLHDzvrnjfb73+*#WSOKGCyuqmie951)%ZVRNJFBxsokgc840($YUQLHDzvrnjfb73+*#WSOKGCyuqmie951)%ZVRNJFBxsokgc840($YUQLHDzvrnjfb73+*#WSOKGCyuqmie951)%ZVRNJFBxsokgc840($YUQLHDzvrnjfb73+*#WSOKGCyuqmie951)%ZVRNJFBxsokgc840+*!XTPLHCyuqmiea62-&#WRNJFBxtplhd950($YUQMIEAwsojfb73+*!XTPLHCyuqmiea62-&#WRNJFBxtplhd950($YUQMIEAwsojfb73+*!XTPLHCyuqmiea62-&#WRNJFBxtplhd950($YUQMIEAwsojfb73+*!XTPLHCyuqmiea62-&#WRNJFBxtplhd950($YUQMIEAwsojfb73+*!XTPLHCyuqmiea62-&#WRNJFBxtplhd950($YUQMIEAwsojfb73+*!XTPLHCyuqmiea62-&#WRNJFBxtplhd950($YUQMIEAwsojfb73+*!XTPLHCyuqmiea62-&#WRNJFBxtplhd950($YUQMIEAwsojfb73+*!XTPLHCyuqmiea62-&#WRNJFBxtplhd950($YUQMIEAwsojfb73+*!XTPLHDyuqmiea62-&#WRNJFBxtplhd950($YUQMIEAwsojfb73+*!XTPLHDyuqmiea62-&#WRNJFBxtplhd950($YUQMIEAwsojfb73+*!XTPLHDyuqmiea62-&#WRNJFBxtplhd950($YUQMIEAwsojfb73+*!XTPLHDyuqmiea62-&#WRNJFBxtplhd950($YUQMIEAwsojfb73+-&#WSOKGCytplhd951)%ZVRNIEAwsokgc840(!XTPLHDzvrnjfa62-&#WSOKGCytplhd951)%ZVRNIEAwsokgc840(!XTPLHDzvrnjfa62-&#WSOKGCyuplhd951)%ZVRNIEAwsokgc840(!XTPLHDzvrnjfa62-&#WSOKGCyuplhd951)%ZVRNIEAwsokgc840(!XTPLHDzvrnjfa62-&#WSOKGCyuplhd951)%ZVRNIEAwsokgc840(!XTPLHDzvrnjfa62-&#WSOKGCyuplhd951)%ZVRNIEAwsokgc840(!XTPLHDzvrnjfa62-&#WSOKGCyuplhd951)%ZVRNIEAwsokgc840(!XTPLHDzvrnjfa62-&#WSOKGCyuplhd951)%ZVRNIEAwsokgc840(!XTPLHDzvrnjfa62-&#WSOKGCyuplhd951)%ZVRNIEAwsokgc840(!XTPLHDzvrnjfa62-&#WSOKGCyuplhd951)%ZVRNIEAwsokgc840(!XTPLHDzvrnjfa62-&#WSOKGCBxtplgc840($YUQMIEzvrnjfb73+*!XSOKGCyuqmiea61)%ZVRNJFBxtplgc840($YUQMIEzvrnjfb73+*!XSOKGCyuqmiea61)%ZVRNJFBxtplgc840($YUQMIEzvrnjfb73+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Chapter11中山醫(yī)學(xué)院病理生理教研室鄧宇斌彌散性血管內(nèi)凝血

Chapter11中山醫(yī)學(xué)院病理生理38

DIC一、DIC原因和發(fā)病機制二、促進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)DIC39第一節(jié)概述1.血液的凝固與抗凝流動性血液運輸載體方向性內(nèi)（Ⅻ）凝血系統(tǒng)凝血外（Ⅲ）血小板：粘聚釋第一節(jié)概述1.血液的凝固與抗凝40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)纖溶亢進果栓塞溶血>120種?。焊腥尽⒛[瘤、產(chǎn)科意外凝↑／抗凝↓→栓塞41Introduction

DICischaracterizedbytheactivationofthecoagulationsystemwithresultantconsumptionofavarietyofcoagulationproteinsandplatelets,whichresultsinhemorrhagicdiathesisandischemicinjurytovarioustissues.IntroductionDICisc421.BloodCoagulation

Itispropagatedbyanenzymaticeventstermedcoagulationcascade.ContactfactorsandtheintrinsicpathwayTissuefactorandextrinsicpathway

1.BloodCoagulation432.Fibrinolysis

Itistheresultoftheactionofplasmin,aproteolyticenzymeproducedfromaninertplasmaprecursor(plasminogen)bytheactionofvarioussubstancestermedplasminogenactivators.

2.Fibrinolysis44HumoralplasminogenactivatorsTissueplasminogenactivatorsFibrinorfibrinogendegradationproductsFDP(Significantbiologicalactivity)FragmentsX,YandE(potentantithrombins)FragmentsYandD(inhibitfibrinpolymerization)Humoralplasminogenactivators45

ⅡaⅡaⅢaPCAPCTM+Ⅱ滅活PS(+)C4bC4bPS(-)

46

酶

纖溶

FDP

酶ATPC

抗

APCTM+Ⅱa

凝

PSPGI2VECTM

47第二節(jié)DIC的病因發(fā)病學(xué)一、發(fā)病原因及機理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第二節(jié)DIC的病因發(fā)病學(xué)一、發(fā)病原因及機理48EtiologyofDIC1.acuteDIC(1)septicemia(2)severetrauma(3)obstetricaccidents(4)shock2.subacuteDIC(1)malignanttumors(2)retaineddeadfetus3.chronicDIC

(1)gianthemangioma(2)systemiclupuserythematosus(SLE)EtiologyofDIC1.acuteDIC49⑵機理膠原暴露凝↑VEC釋放Ⅲ受損合成PGI2↓→TXA2↑抗凝↓表達TM↓→APC↓⑵機理502.血細胞大量受損⑴RBC受損感染：瘧疾原因：溶血G6PDase↓：蠶豆病免疫損傷：異型輸血紅細胞素（Ⅲ）機理：釋ADP→P聚集2.血細胞大量受損51⑵WBC激活或受損壞死白血病細胞→釋Ⅲ原因化療受損機理炎癥激活→合成、釋Ⅲ（內(nèi)毒素、補體、LC、P、Ag－Ab）⑵WBC激活或受損52

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、血管收縮機理PF1～11提供“反應(yīng)面”

ⅩⅡⅨa－Ca2+－ⅧaⅩa－Ca2+－ⅡaPF3PF3⑶P激活或受損533.大量致凝物質(zhì)入血腫瘤細胞

⑴Ⅲ壞死（包括產(chǎn)科意外）組織細胞

⑵帶負電顆粒物質(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3.大量致凝物質(zhì)入血54PathogenesisofDIC

1.extensivedamageofvascularendothelialcells

Intrinsicclottingcascade2.severetissueinjury

ExtrinsicclottingreactionPathogenesisofDIC1.extensiv553.excessivedestructionofthecirculatingbloodcells

Generationofprocoagulant-activesubstances

Intravascularcoagulation4.otherthromboplasticmaterialsenteringthebloodActivationofclottingsystemthroughthecontactofbloodwithanabnormalsurface3.excessivedestructionofthe56theneteffectsaresummarizedasfollows:1.lossofplasmafibrinogenasitisconsumedbytheclottingprocessandbytheactionofplasma.2.lossofotherclottingfactorsnotablyⅤ,ⅧandⅫ,astheyareusedupduringtheoperationoftheclottingcascade.3.fallintheplateletcount,astheplateletsaggregateandleavethecirculation.4.appearanceoffibrindegradationproducts,asplasminactsonitssubstrates.theneteffectsaresummarized57

二、誘因與發(fā)生機理消除致凝物質(zhì)功能血液凝血活性↑／抗凝活性↓

1.單核吞噬細胞系統(tǒng)功能內(nèi)毒素血癥、糖皮質(zhì)激素、脾消除功能↓：致凝物、Ⅱa、凝纖產(chǎn)物

二、誘因與發(fā)生機理58

2.肝功能嚴重障礙滅活活化凝血因子↓合成AT－Ⅲ、PC↓枯否細胞吞噬功能↓

3.血液的高凝狀態(tài)凝血活性↑－凝血物質(zhì)↑：懷孕、腫瘤、應(yīng)激抗纖溶：胎盤、藥抗凝活性↓抗肝素：H＋AT、PC、TM等↓

4.血流郁滯2.肝功能嚴重障礙59PredisposingfactorstoDIC1.impairmentoftheclearancemechanism.2.hypercoagulablestate.3.disorderofmicrocirculation.PredisposingfactorstoDIC1.i60第三節(jié)DIC的分期及分型高凝期

分期

消耗性低凝期繼發(fā)性纖溶亢進期急性按發(fā)病速度亞急性

分

慢性

型

代償型按代償情況失代償型過度代償型第三節(jié)DIC的分期及分型61TypesofDIC1.acuteDICMultisidebleedingdiathesisThromboticcomplicationsusuallySeverebleedingleadtoshockandsevereischemicchangeinorgans2.subacuteDICRarelybleedingTheevidenceofDICcanbedetectedbylaboratoryexaminations3.chronicDICTypesofDIC62StageofDIC1.hypercoagulablestage2.hypocoagulablestage3.secondaryfibrinolyticstageStageofDIC1.hypercoagulable63第四節(jié)臨床表現(xiàn)1.出血凝血物質(zhì)消耗性↓酶：破壞凝血因子繼發(fā)性纖溶亢進ⅡaFDP抗凝：競爭性抑制ⅢaP聚血管壁受損及溶栓第四節(jié)臨床表現(xiàn)1.出血64ConsequencesofDIC

1.disturbanceofcoagulation----bleeding(1)theconsumptionofclottingfactorsandplatelets(2)theactivationoffibrinolyticsystem(3)theproductionoffibrindegradationproducts(FDPs)ConsequencesofDIC1.disturba652.休克

出血回心血量↓微血栓阻斷通路CO↓心泵功能↓:心肌DICBP↓右心后負荷↑:肺DIC外周阻力↓:四個酶系統(tǒng)激活

↓A、B肽擴血管物質(zhì)↑FDP(通透性↑)激肽C3a、C5a

662.disturbanceofcirculation----shockMicrothromobusincapillariesandvenulesBloodreturningdecreaseCardiacmuscledamageCardiacoutputandbloodvolumereduceEffectivecirculatingbloodvolumedecreaseHypotension2.disturbanceofcirculation--67

3.栓塞微血栓器官功能BP↓供血障礙

4.溶血：微血管病性溶血性貧血

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