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弥散性血管内凝血

Chapter11中山医学院病理生理教研室邓宇斌弥散性血管内凝血

Chapter11中山医学院病理生理1

DIC一、DIC原因和发病机制二、促进DIC发生发展的因素（诱发困素）三、DIC的分期和分型四、DIC的功能代谢变化（病理生理变化）五、DIC防治的病理生理基础DIC2第一节概述1.血液的凝固与抗凝流动性血液运输载体方向性内（Ⅻ）凝血系统凝血外（Ⅲ）血小板：粘聚释第一节概述1.血液的凝固与抗凝3凝↑／抗凝↓

→栓塞失衡凝↓／抗凝↑

→出血倾向2.DIC的概念出血病因微血栓后休克致凝继发纤溶亢进果栓塞溶血>120种病：感染、肿瘤、产科意外凝↑／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灭活PS(+)C4bC4bPS(-)

9

酶

纤溶

FDP

酶ATPC

抗

APCTM+Ⅱa

凝

PSPGI2VECTM

10第二节DIC的病因发病学一、发病原因及机理1.VEC广泛受损

⑴原因感染炎症、免疫损伤（抗磷脂综合征）高低温、放射损伤缺血缺氧酸中毒第二节DIC的病因发病学一、发病原因及机理11EtiologyofDIC1.acuteDIC(1)septicemia(2)severetrauma(3)obstetricaccidents(4)shock2.subacuteDIC(1)malignanttumors(2)retaineddeadfetus3.chronicDIC

(1)gianthemangioma(2)systemiclupuserythematosus(SLE)EtiologyofDIC1.acuteDIC12⑵机理胶原暴露凝↑VEC释放Ⅲ受损合成PGI2↓→TXA2↑抗凝↓表达TM↓→APC↓⑵机理132.血细胞大量受损⑴RBC受损感染：疟疾原因：溶血G6PDase↓：蚕豆病免疫损伤：异型输血红细胞素（Ⅲ）机理：释ADP→P聚集2.血细胞大量受损14⑵WBC激活或受损坏死白血病细胞→释Ⅲ原因化疗受损机理炎症激活→合成、释Ⅲ（内毒素、补体、LC、P、Ag－Ab）⑵WBC激活或受损15

⑶P激活或受损原发性：免疫损伤（抗P抗体抗磷脂抗体）继发性：DIC粘（GPⅠb－胶原）聚（GPⅡb／Ⅲa－fg）TXA2等P聚、血管收缩机理PF1～11提供“反应面”

ⅩⅡⅨa－Ca2+－ⅧaⅩa－Ca2+－ⅡaPF3PF3⑶P激活或受损163.大量致凝物质入血肿瘤细胞

⑴Ⅲ坏死（包括产科意外）组织细胞

⑵带负电颗粒物质（内毒素）→Ⅻa胰蛋白酶

⑶其它丝氨酸蛋白水解酶→Ⅱa蝰蛇毒3.大量致凝物质入血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、诱因与发生机理消除致凝物质功能血液凝血活性↑／抗凝活性↓

1.单核吞噬细胞系统功能内毒素血症、糖皮质激素、脾消除功能↓：致凝物、Ⅱa、凝纤产物

二、诱因与发生机理21

2.肝功能严重障碍灭活活化凝血因子↓合成AT－Ⅲ、PC↓枯否细胞吞噬功能↓

3.血液的高凝状态凝血活性↑－凝血物质↑：怀孕、肿瘤、应激抗纤溶：胎盘、药抗凝活性↓抗肝素：H＋AT、PC、TM等↓

4.血流郁滞2.肝功能严重障碍22PredisposingfactorstoDIC1.impairmentoftheclearancemechanism.2.hypercoagulablestate.3.disorderofmicrocirculation.PredisposingfactorstoDIC1.i23第三节DIC的分期及分型高凝期

分期

消耗性低凝期继发性纤溶亢进期急性按发病速度亚急性

分

慢性

型

代偿型按代偿情况失代偿型过度代偿型第三节DIC的分期及分型24TypesofDIC1.acuteDICMultisidebleedingdiathesisThromboticcomplicationsusuallySeverebleedingleadtoshockandsevereischemicchangeinorgans2.subacuteDICRarelybleedingTheevidenceofDICcanbedetectedbylaboratoryexaminations3.chronicDICTypesofDIC25StageofDIC1.hypercoagulablestage2.hypocoagulablestage3.secondaryfibrinolyticstageStageofDIC1.hypercoagulable26第四节临床表现1.出血凝血物质消耗性↓酶：破坏凝血因子继发性纤溶亢进ⅡaFDP抗凝：竞争性抑制ⅢaP聚血管壁受损及溶栓第四节临床表现1.出血27ConsequencesofDIC

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

出血回心血量↓微血栓阻断通路CO↓心泵功能↓:心肌DICBP↓右心后负荷↑:肺DIC外周阻力↓:四个酶系统激活

↓A、B肽扩血管物质↑FDP(通透性↑)激肽C3a、C5a

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

3.栓塞微血栓器官功能BP↓供血障碍

4.溶血：微血管病性溶血性贫血

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+*!XSOKGCyuqmiea61)%ZVRNJFBxtplgc840($YUQMIEzvrnjfb73+*!XSOKGCyuqmiea61)%ZVRNJFBxtplgc840($YUQMIEzvrnjfb73+*!XSOKGCyuqmiea61)%ZVRNJFBxtplgc840($YUQMIEzvrnjfb73+*!XSOKGCyuqmiea61)%ZVRNJFBxtplgc840($YUQMIEzvrnjfb73+*!XSOKGCyuqmiea62)%ZVRNJFBxtplgc840($YUQMIEzvrnjfb73+*!XSOKGCyuqmiea62)%ZVRNJFBxtplgc840($YUQMIEzvrnjfb73+*!XSOKGCyuqmiea62)%ZVUQMIEAwsokgc73+*!XTPLHDzvqmiea62-&#WSOJFBxtplhd951)$YUQMIEAwsokgc73+*!XTPLHDzvqmiea62-&#WSOJFBxtplhd951)$YUQMIEAwsokgc73+*!XTPLHDzvqmiea62-&#WSOJFBxtplhd951)%YUQMIEAwsokgc73+*!XTPLHDzvqmiea62-&#WSOJFBxtplhd951)%YUQMIEAwsokgc73+*!XTPLHDzvqmiea62-&#WSOJFBxtplhd951)%YUQMIEAwsokgc73+*!XTPLHDzvqmiea62-&#WSOJFBxtplhd951)%YUQMIEAwsokgc73+*!XTPLHDzvqmiea62-&#WSOJFBxtplhd951)%YUQMIEAwsokgc73+*!XTPLHDzvqmiea62-&#WSOJFBxtplhd951)%YUQMIEDzvrnjfb73-&#WSOKGCyuqmhd951)%ZVRNJFAwsokgc840($YUPLHDzvrnjfb73-&#WSOKGCyuqmhd951)%ZVRNJFAwsokgc840($YUPLHDzvrnjfb73-&#WSOKGCyuqm($YUQMIEAvrnjfb73+*!XTOKGCyuqm37弥散性血管内凝血

Chapter11中山医学院病理生理教研室邓宇斌弥散性血管内凝血

Chapter11中山医学院病理生理38

DIC一、DIC原因和发病机制二、促进DIC发生发展的因素（诱发困素）三、DIC的分期和分型四、DIC的功能代谢变化（病理生理变化）五、DIC防治的病理生理基础DIC39第一节概述1.血液的凝固与抗凝流动性血液运输载体方向性内（Ⅻ）凝血系统凝血外（Ⅲ）血小板：粘聚释第一节概述1.血液的凝固与抗凝40凝↑／抗凝↓

→栓塞失衡凝↓／抗凝↑

→出血倾向2.DIC的概念出血病因微血栓后休克致凝继发纤溶亢进果栓塞溶血>120种病：感染、肿瘤、产科意外凝↑／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灭活PS(+)C4bC4bPS(-)

46

酶

纤溶

FDP

酶ATPC

抗

APCTM+Ⅱa

凝

PSPGI2VECTM

47第二节DIC的病因发病学一、发病原因及机理1.VEC广泛受损

⑴原因感染炎症、免疫损伤（抗磷脂综合征）高低温、放射损伤缺血缺氧酸中毒第二节DIC的病因发病学一、发病原因及机理48EtiologyofDIC1.acuteDIC(1)septicemia(2)severetrauma(3)obstetricaccidents(4)shock2.subacuteDIC(1)malignanttumors(2)retaineddeadfetus3.chronicDIC

(1)gianthemangioma(2)systemiclupuserythematosus(SLE)EtiologyofDIC1.acuteDIC49⑵机理胶原暴露凝↑VEC释放Ⅲ受损合成PGI2↓→TXA2↑抗凝↓表达TM↓→APC↓⑵机理502.血细胞大量受损⑴RBC受损感染：疟疾原因：溶血G6PDase↓：蚕豆病免疫损伤：异型输血红细胞素（Ⅲ）机理：释ADP→P聚集2.血细胞大量受损51⑵WBC激活或受损坏死白血病细胞→释Ⅲ原因化疗受损机理炎症激活→合成、释Ⅲ（内毒素、补体、LC、P、Ag－Ab）⑵WBC激活或受损52

⑶P激活或受损原发性：免疫损伤（抗P抗体抗磷脂抗体）继发性：DIC粘（GPⅠb－胶原）聚（GPⅡb／Ⅲa－fg）TXA2等P聚、血管收缩机理PF1～11提供“反应面”

ⅩⅡⅨa－Ca2+－ⅧaⅩa－Ca2+－ⅡaPF3PF3⑶P激活或受损533.大量致凝物质入血肿瘤细胞

⑴Ⅲ坏死（包括产科意外）组织细胞

⑵带负电颗粒物质（内毒素）→Ⅻa胰蛋白酶

⑶其它丝氨酸蛋白水解酶→Ⅱa蝰蛇毒3.大量致凝物质入血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、诱因与发生机理消除致凝物质功能血液凝血活性↑／抗凝活性↓

1.单核吞噬细胞系统功能内毒素血症、糖皮质激素、脾消除功能↓：致凝物、Ⅱa、凝纤产物

二、诱因与发生机理58

2.肝功能严重障碍灭活活化凝血因子↓合成AT－Ⅲ、PC↓枯否细胞吞噬功能↓

3.血液的高凝状态凝血活性↑－凝血物质↑：怀孕、肿瘤、应激抗纤溶：胎盘、药抗凝活性↓抗肝素：H＋AT、PC、TM等↓

4.血流郁滞2.肝功能严重障碍59PredisposingfactorstoDIC1.impairmentoftheclearancemechanism.2.hypercoagulablestate.3.disorderofmicrocirculation.PredisposingfactorstoDIC1.i60第三节DIC的分期及分型高凝期

分期

消耗性低凝期继发性纤溶亢进期急性按发病速度亚急性

分

慢性

型

代偿型按代偿情况失代偿型过度代偿型第三节DIC的分期及分型61TypesofDIC1.acuteDICMultisidebleedingdiathesisThromboticcomplicationsusuallySeverebleedingleadtoshockandsevereischemicchangeinorgans2.subacuteDICRarelybleedingTheevidenceofDICcanbedetectedbylaboratoryexaminations3.chronicDICTypesofDIC62StageofDIC1.hypercoagulablestage2.hypocoagulablestage3.secondaryfibrinolyticstageStageofDIC1.hypercoagulable63第四节临床表现1.出血凝血物质消耗性↓酶：破坏凝血因子继发性纤溶亢进ⅡaFDP抗凝：竞争性抑制ⅢaP聚血管壁受损及溶栓第四节临床表现1.出血64ConsequencesofDIC

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

出血回心血量↓微血栓阻断通路CO↓心泵功能↓:心肌DICBP↓右心后负荷↑:肺DIC外周阻力↓:四个酶系统激活

↓A、B肽扩血管物质↑FDP(通透性↑)激肽C3a、C5a

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

3.栓塞微血栓器官功能BP↓供血障碍

4.溶血：微血管病性溶血性贫血

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