第四节-血栓与止血检测.ppt

第四节第四节 血栓与止血血栓与止血检测检测 血血栓栓与与止止血血检检测测（二）血小板的作用（二）血小板的作用1.形成血小板血栓形成血小板血栓(白色血栓白色血栓)，机械性修复受，机械性修复受损血管。损血管。2.血管受损血管受损GPb经经vWf粘附粘附3.释放血小板第三因子（释放血小板第三因子（PF3）直接参与凝血反）直接参与凝血反应。应。4.活化血小板在前激肽释放酶及高分子量激肽活化血小板在前激肽释放酶及高分子量激肽原存原存在的条件下，直接激活在的条件下，直接激活F及及F。5.ADP(来自红细胞来自红细胞)、凝血酶、胶原、凝血酶、胶原血小板血小板GPb/a结合结合Fg血血栓栓与与止止血血检检测测（三）凝血因子的作用（三）凝血因子的作用1.外源性凝血途径外源性凝血途径2.内源性凝血途径内源性凝血途径3.凝血共用途径凝血共用途径注意注意12个凝血因子除个凝血因子除F、F、和、和部分部分F外，主要产生于肝脏。外，主要产生于肝脏。F、F、F、F是维生素是维生素K依赖因子依赖因子血友病（甲、乙、丙）三种分别缺少血友病（甲、乙、丙）三种分别缺少F、F、F，均影响内源性凝血途径。，均影响内源性凝血途径。Intrinsic XII,XI,IX,VIII(APTT)Extrinsic-VII(PT)ProthrombinThrombinFibrinogenFibrinCommon Path(TT)FXFXaXIIIXIIIa aXIIIXIIIThrombinFibrinFibrin(strong)(strong)FibrinogenFibrinogenFibrinFibrin(weak)(weak)IXIXXIXIXIXIa aIXIXa aXaV Va aXIIXIIa aProthrombinProthrombinTF-VIIa(Prothrombinase)(Prothrombinase)PLPLPLPL(Tenase)(Tenase)VIIIVIIIa aPLPLXIntrinsic PathwayHKHKa aExtrinsic PathwayTF PathwayProtein C,Protein S,Antithrombin III血血栓栓与与止止血血检检测测（四）抗凝血系统的作用（四）抗凝血系统的作用1.细胞抗凝作用细胞抗凝作用2.体液抗凝作用体液抗凝作用抗凝血酶抗凝血酶（AT-）肝素介导下肝素介导下灭活凝血酶、灭活凝血酶、Fa、Fa、Fa、Fa灭活灭活TF/aa、FaTFPI蛋白蛋白C和蛋白和蛋白S灭活灭活Fa、Fa激活纤溶系统激活纤溶系统血血栓栓与与止止血血检检测测（五）纤维蛋白溶解（纤溶）系统的作用（五）纤维蛋白溶解（纤溶）系统的作用组织型组织型纤溶纤溶酶原激活物酶原激活物（t-PA）尿激酶型尿激酶型纤纤溶酶原激活物溶酶原激活物(u-PA)激活激活纤溶酶原纤溶酶原（PLG）纤溶酶纤溶酶（PL）抗纤抗纤溶酶溶酶纤溶酶抑纤溶酶抑制物制物降解降解降解降解纤维蛋纤维蛋白原白原纤维纤维蛋白蛋白凝血凝血因子因子降解为碎片降解为碎片X、Y、D、E等等抗血小板聚集及抗凝血作用抗血小板聚集及抗凝血作用NORMAL HEMOSTASIS GENERAL COMPONENTSVASCULAR WALLPLATELETSCOAGULATION CASCADEHemostasis:BV InjuryPlateletActivationPlt-FusionBloodVesselConstrictionCoagulationActivationStableHemostaticPlugThrombin,FibrinReducedBloodflowTissueFactorPrimaryhemostaticplugNeuralAdhesion GpIIb/IIIaPlatelet Activation Pathways(1)GpIIb/IIIaGpIIb/IIIaAggregationADPAdrenalinePlateletGpIbExposed CollagenEndotheliumvWFCOLLAGENGpIIb/IIIaGpIIb/IIIaAggregationGpIIb/IIIaGpIIb/IIIaAggregationAdhesionAdhesionADPAdrenalineTHROMBINPlatelet Activation Pathways(2)Platelet AggregationFibrinogenTXATXA2 2Fibrinogen Binding SiteFibrinogen Binding SiteADPThrombinThrombinPlateletI-FibrinogenI-FibrinogenII-ProthrombinII-ProthrombinIII-ThromboplastinIII-ThromboplastinIV-CalciumIV-CalciumV-Labile f.V-Labile f.VI-Suture VI-Suture deficiencydeficiencyVII-Stable f.VII-Stable f.VIII-AHF-AVIII-AHF-AIX-AHF-BIX-AHF-BX-Stuart-Prower f.X-Stuart-Prower f.XI-AHF-CXI-AHF-CXII-Hageman f.XII-Hageman f.XIII-Fibrin XIII-Fibrin Stabilizing f.Stabilizing f.COAGULATION CASCADECoagulation FactorsIntrinsic XII,XI,IX,VIII(APTT)Extrinsic-VII(PT)ProthrombinThrombinFibrinogenFibrinCommon Path(TT)FXFXaXIIIXIIIa aXIIIXIIIThrombinFibrinFibrin(strong)(strong)FibrinogenFibrinogenFibrinFibrin(weak)(weak)IXIXXIXIXIXIa aIXIXa aXaV Va aXIIXIIa aProthrombinProthrombinTF-VIIa(Prothrombinase)(Prothrombinase)PLPLPLPL(Tenase)(Tenase)VIIIVIIIa aPLPLXIntrinsic PathwayHKHKa aExtrinsic PathwayTF PathwayProtein C,Protein S,Antithrombin IIINormal HemostasisFirst step in hemostasis is formation of a platelet aggregateAt the molecular level interaction of coagulation factors takes place on the surface of activated plateletsThe Tissue FactorFVIIa complex is the physiological activator of normal hemostasisAntithrombin III and HeparinAntithrombin III and HeparinProteins C and SProteins C and STFPITFPIControl of coagulationFibrinolysis血血栓栓与与止止血血检检测测二、血管壁检查二、血管壁检查（一）毛细血管抵抗力试验（一）毛细血管抵抗力试验（CRT，又称束臂试验），又称束臂试验）方方法法5cm直径圆圈内新出血点的数目：直径圆圈内新出血点的数目：男性男性5个；女性及儿童个；女性及儿童10个。个。参考值参考值血血栓栓与与止止血血检检测测临床意义临床意义新出血点的数目超过正常为阳性，见于新出血点的数目超过正常为阳性，见于：血管壁结构和（或）功能缺陷，如遗传性出血性血管壁结构和（或）功能缺陷，如遗传性出血性毛细血管扩张症、过敏性紫晚单纯性紫疫及其他毛细血管扩张症、过敏性紫晚单纯性紫疫及其他血管性紫癫血管性紫癫；血小板的量和（或）质异常，如原发性和继发性血小板的量和（或）质异常，如原发性和继发性血小板减少症血小板减少症、血小板增多症、先天性（遗传性）血小板增多症、先天性（遗传性）和获得性血小板功能缺陷症；和获得性血小板功能缺陷症；血管性血友病（血管性血友病（vonWillebranddisease，VWD）等。）等。血血栓栓与与止止血血检检测测（二）出血时间测定（二）出血时间测定参考值参考值IvyIvy法：法：2 26min6min，超过，超过 7min 7min为异常；为异常；出血时间测定器法：出血时间测定器法：6 69 9土土 2 2lminlmin，超过超过 gmingmin为异常，目前推荐用此法作为为异常，目前推荐用此法作为 BT BT的检测方法。的检测方法。血血栓栓与与止止血血检检测测临床意义临床意义BTBT延长见于：延长见于：血小板明显减少，如原发性或继发性血小血小板明显减少，如原发性或继发性血小 板减少性紫痴；板减少性紫痴；血小板功能异常，如血小板无力症和巨大血小板功能异常，如血小板无力症和巨大 血小板综合征；血小板综合征；严重缺乏血浆某些凝血因子，如严重缺乏血浆某些凝血因子，如 VWD VWD、DICDIC；血管异常，如遗传性出血性毛细血管扩张症；血管异常，如遗传性出血性毛细血管扩张症；药物干扰，如服用乙酸水杨酸、双嘧达莫药物干扰，如服用乙酸水杨酸、双嘧达莫 （潘生丁）等。（潘生丁）等。血血栓栓与与止止血血检检测测三、血小板检测三、血小板检测（一）血小板计数（一）血小板计数（PC或或plt）参考值参考值（100100300300）109/L109/L临床意义临床意义1。血小板减少：。血小板减少：PC低于低于10010109 9/L/L称为血小称为血小 板减少。常见于：板减少。常见于：血小板生成障碍血小板生成障碍血小板破坏或消耗过多血小板破坏或消耗过多血小板分布异常血小板分布异常血血栓栓与与止止血血检检测测2。血小板减少：。血小板减少：PC高于高于40010109 9/L/L称为血小称为血小 板增多。常见于：板增多。常见于：原发性增多原发性增多反应性增多反应性增多（二）血小板相关免疫球蛋白测定（二）血小板相关免疫球蛋白测定（PAIg）血小板相关免疫球蛋白测定包括：血小板相关免血小板相关免疫球蛋白测定包括：血小板相关免疫球蛋白疫球蛋白G（PAlgG）、）、PAIgM和和PAIgA测定。测定。参考值参考值PAlgG 0PAlgG 078.8ng78.8ng10107 7血小板；血小板；PAlgM 0PAlgM 07.0ng7.0ng10107 7血小板；血小板；PAIgA 0PAIgA 02.0ng2.0ng107107血小板。血小板。血血栓栓与与止止血血检检测测临床意义临床意义1.PAIg1.PAIg增高增高 见于见于ITPITP、同种免疫性血小板减少性输血后紫癫、同种免疫性血小板减少性输血后紫癫、药物免疫性血小板减少性紫癫恶性淋巴瘤、药物免疫性血小板减少性紫癫恶性淋巴瘤、慢性活动性肝炎、慢性活动性肝炎、SLESLE、慢性淋巴细胞性白血病、慢性淋巴细胞性白血病、多发性骨髓瘤、多发性骨髓瘤、EvanEvan综合征、良性单株丙球蛋白综合征、良性单株丙球蛋白血症等。血症等。9090以上以上ITPITP患者的患者的PAIgGPAIgG增高，若同时测定增高，若同时测定:PAIgMPAIgM、PAIgAPAIgA和血小板补体和血小板补体3 3（PAC3PAC3），则阳性率），则阳性率可高达可高达 100 100。2 2观察病情观察病情经治疗后经治疗后ITPITP患者的患者的PAIgPAIg水平下降；水平下降；复发后，则又可升高。复发后，则又可升高。血血栓栓与与止止血血检检测测四、凝血和抗凝的检测四、凝血和抗凝的检测（一）凝血时间测定（一）凝血时间测定（CT）参考值参考值 普通试管法为普通试管法为6 612min12min 硅管法为硅管法为1.5 1.5 32min32min临床意义临床意义lCTCT延长见于延长见于因子因子、II、明显减少，如明显减少，如A A、B B型血友病、型血友病、因子因子缺乏症；缺乏症；血血栓栓与与止止血血检检测测凝血酶原重度减少，如严重的肝损伤等；凝血酶原重度减少，如严重的肝损伤等；纤维蛋白原严重减少，如纤维蛋白原缺乏症、严重纤维蛋白原严重减少，如纤维蛋白原缺乏症、严重 肝损伤等；肝损伤等；应用肝素、口服抗凝药时；应用肝素、口服抗凝药时；纤溶亢进使纤维蛋白原降解增加时；纤溶亢进使纤维蛋白原降解增加时；循环抗凝物质增加，如类肝素物质增多等。循环抗凝物质增加，如类肝素物质增多等。2CTCT缩短见于高凝状态缩短见于高凝状态血血栓栓与与止止血血检检测测（二）活化部分凝血活酶时间（二）活化部分凝血活酶时间（APTT或或KPTT）原原理理参考值参考值该该测定是在受检血浆中加入测定是在受检血浆中加入APTT试剂（接触因试剂（接触因子激活剂和部分磷脂）和钙离子后，观察其凝固时间。子激活剂和部分磷脂）和钙离子后，观察其凝固时间。本试验是反映本试验是反映内源性内源性凝血系统各凝血因子总的凝凝血系统各凝血因子总的凝血状况的筛选试验。血状况的筛选试验。手手工工法法：32433243秒秒，较较正正常常对对照照值值延延长长1010秒秒 以上为异常。以上为异常。血血栓栓与与止止血血检检测测临床意义临床意义 同凝血时间（同凝血时间（CTCT）但较普通试管法）但较普通试管法CTCT为敏感，为敏感，它是目前推荐应用的内源凝血系统的筛选试验。它是目前推荐应用的内源凝血系统的筛选试验。此外，此外，APTTAPTT又是监测又是监测肝素肝素的首选指标。的首选指标。（三）血浆纤维蛋白原测定（三）血浆纤维蛋白原测定参考值参考值g/Lg/L血血栓栓与与止止血血检检测测1.增高增高见于糖尿病、急性心肌梗塞、急性感染、见于糖尿病、急性心肌梗塞、急性感染、结缔组织病、急性肾炎、烧伤、多发性结缔组织病、急性肾炎、烧伤、多发性骨髓瘤、休克、大手术、妊高症、恶性骨髓瘤、休克、大手术、妊高症、恶性肿瘤、血栓前状态肿瘤、血栓前状态.减低减低见于见于DIC、原发性纤溶症、重症肝炎和肝、原发性纤溶症、重症肝炎和肝硬化硬化（四）血浆凝血酶原测定（四）血浆凝血酶原测定原原理理该该测定是在受检血浆中加入钙离子和组织因子后，测定是在受检血浆中加入钙离子和组织因子后，观察其凝固时间。观察其凝固时间。本试验是反映本试验是反映外源性外源性凝血系统各凝血因子总的凝凝血系统各凝血因子总的凝血状况的筛选试验。血状况的筛选试验。临床意义临床意义血血栓栓与与止止血血检检测测参考值参考值11131113秒，较正常对照值延长秒，较正常对照值延长3 3秒以上为异常。秒以上为异常。临床意义临床意义1.PT延长见于延长见于先天性凝血因子先天性凝血因子、缺乏缺乏后天性凝血因子缺乏：严重肝病、维生素后天性凝血因子缺乏：严重肝病、维生素k缺乏、缺乏、纤溶亢进、纤溶亢进、DIC、口服抗凝剂、异常凝血酶原增加。、口服抗凝剂、异常凝血酶原增加。.PT缩短见于缩短见于高凝状态如高凝状态如DIC早期、心肌梗塞、早期、心肌梗塞、脑血栓形成、脑血栓形成、DVT、多发性骨髓瘤。、多发性骨髓瘤。血血栓栓与与止止血血检检测测（一）优球蛋白溶解时间（一）优球蛋白溶解时间参考值参考值加钙法为加钙法为129.841.1min;129.841.1min;加酶法为加酶法为157.559.1min157.559.1min临床意义临床意义1.1.纤维蛋白凝块在纤维蛋白凝块在70min70min内完全溶解内完全溶解，表明纤溶活性，表明纤溶活性 增强，见于原发性先纤溶和继发性纤溶，如手术、增强，见于原发性先纤溶和继发性纤溶，如手术、应激状态、创伤、休克、变态反应、胎盘早剥、羊应激状态、创伤、休克、变态反应、胎盘早剥、羊 水栓塞、急性白血病等水栓塞、急性白血病等2.2.纤维蛋白凝块完全溶解时间延长纤维蛋白凝块完全溶解时间延长，表明纤溶活性减，表明纤溶活性减 低，见于血栓前状态、血栓性疾病和应用抗低，见于血栓前状态、血栓性疾病和应用抗 纤溶药纤溶药 等。等。五、纤溶系统的检测五、纤溶系统的检测血血栓栓与与止止血血检检测测（二）血浆硫酸鱼精蛋白副凝试验（二）血浆硫酸鱼精蛋白副凝试验参考值参考值阴性阴性 临床意义临床意义1 1 阳性阳性 见于见于DICDIC的早、中、期，但在恶性肿瘤不、的早、中、期，但在恶性肿瘤不、上消化道出血、外科大手术后、败血症、上消化道出血、外科大手术后、败血症、肾小球疾病、人工流产、分娩等也可出现肾小球疾病、人工流产、分娩等也可出现 假阳性。假阳性。2 2 阴性阴性 见于正常人、晚期见于正常人、晚期DICDIC和原发性纤溶症，也和原发性纤溶症，也 有假阳性。有假阳性。血血栓栓与与止止血血检检测测（三）血浆纤维蛋白（原）降解产物测定（三）血浆纤维蛋白（原）降解产物测定参考值参考值小于小于5mg/L5mg/L临床意义临床意义增高见于增高见于:原发性纤溶症、原发性纤溶症、DICDIC、恶性肿瘤、急性早、恶性肿瘤、急性早 幼粒细胞白血病、肺梗塞、幼粒细胞白血病、肺梗塞、DVTDVT、肝脏疾、肝脏疾 病等。病等。血血栓栓与与止止血血检检测测（四）血浆（四）血浆D-二聚体检测二聚体检测参考值参考值胶乳凝集法胶乳凝集法为为阴性；阴性；ELISAELISA法法为为小于小于200ug/L200ug/L 临床意义临床意义继发性纤溶症（如继发性纤溶症（如DICDIC）为阳性或增高；而原发性纤）为阳性或增高；而原发性纤溶症为阴性或不升高，此是两者鉴别的重要指标。溶症为阴性或不升高，此是两者鉴别的重要指标。但是本试验在血栓形成和临床出血时也可出现阳性。但是本试验在血栓形成和临床出血时也可出现阳性。血血栓栓与与止止血血检检测测（五）血浆凝血酶时间（五）血浆凝血酶时间参考值参考值161618s18s，受检，受检TTTT值延长超过正常对值延长超过正常对照照3s3s以上为延长以上为延长临床意义临床意义延长见于延长见于:低（无）纤维蛋白原血症和异常纤维蛋低（无）纤维蛋白原血症和异常纤维蛋 白原血症；血中白原血症；血中FDPFDP增高（如增高（如DICDIC）；血）；血 中有肝素或类肝素物质存在（如肝素治中有肝素或类肝素物质存在（如肝素治 疗中、疗中、SLESLE和肝脏疾病等。）和肝脏疾病等。）血血栓栓与与止止血血检检测测（六）血浆纤溶酶原活性测定（六）血浆纤溶酶原活性测定参考值参考值75%75%140%140%临床意义临床意义1 1增高增高 表示纤溶活性减低，见于血栓前状态和表示纤溶活性减低，见于血栓前状态和 血栓性疾病血栓性疾病2 2减低减低 表示纤溶活性增高，见于原发性纤溶和表示纤溶活性增高，见于原发性纤溶和 继发性纤溶和先天性继发性纤溶和先天性PLGPLG缺乏症缺乏症Tests of HemostasisScreening testsBT(Bleeding Time)-Platelet&BV function BT(Bleeding Time)-Platelet&BV function CRT(Capillary Resistance Test)CRT(Capillary Resistance Test)PC(Platelet Count)PC(Platelet Count)CRT(Clot Retraction Test)CRT(Clot Retraction Test)CT(Clotting Time)CT(Clotting Time)PT(Prothrombin Time)ExtrinsicPT(Prothrombin Time)ExtrinsicAPTT InstrinsicAPTT InstrinsicTT(Thrombin Time)Both pathsTT(Thrombin Time)Both pathsAPTTPF3-like materialPF3-like materialcalciumcalciumheat/agitateheat/agitateend product-clotend product-clotAbnormal:Abnormal:hemophilias,heparin,hemophilias,heparin,depletion states,depletion states,severe hepatic dzsevere hepatic dzEXIIXICa+Ca+Ca+IVIIIIXVIXVIIICa+Prothrombin Time(PT)calciumcalciumplateletsplateletstissue phospholipidtissue phospholipidheatheatclotclotAbnormal:factor Abnormal:factor depletion,coumadin,depletion,coumadin,severe liver disease,severe liver disease,(heparin)(heparin)EXIIXICa+Ca+Ca+IVIIIIXVIXVIIICa+Thrombin Time(TT)EXIIXICa+Ca+Ca+IVIIIIXVIXVIIICa+citrated plasmaadd thrombin,heatend product-clotAbnl:low fibrinogen(200 mg%),hep activated AT-3,FSP,abnl type fibrinogenHemostasis and ThrombosisVic Vernenkar,D.O.St.Barnabas HospitalDept.of SurgeryNormal HemostasisA well regulated processMaintains blood in a fluid,clot free state in normal vessels Induces the rapid formation of a localized hemostatic plug at the site of vascular injuryThrombosisPathological stateInappropriate activation of the normal hemostatic process within the non-interrupted vascular system.Thrombus(blood clots)formationBlocks blood flow to vital areas Normal sequence of Hemostasis(4 steps)(4 steps)1.Arteriolar vasoconstriction(transient)Reflex neurogenic mechanismsReflex neurogenic mechanismsBleeding would resume after vasoconstriction Bleeding would resume after vasoconstriction if it werent for the activation of platelets or if it werent for the activation of platelets or coagulation systemscoagulation systems2.Exposure of subendothelial ECM when there is endothelial injuryECM,especially collagen,is highly ECM,especially collagen,is highly thrombogenicthrombogenicPlatelets adhere and become activatedPlatelets adhere and become activatedChange in shapeChange in shapeRelease of secretory productsRelease of secretory productsAggregationAggregation of platelets forms of platelets forms hemostatic plughemostatic plugThis is This is primary hemostasisprimary hemostasisFirst two steps of normal hemostasisNormal hemostasis continuedNormal hemostasis continued3.Tissue factor released at the site of injury(by endothelial cells)Works with secreted platelet factorsActivates coagulation cascadeA series of proteins where A series of proteins where thrombinthrombin is is activatedactivatedInduces further platelet recruitment and Induces further platelet recruitment and granule releasegranule releaseEnds in fibrin depositionCalled secondary hemostasisNormal hemostasis continuedNormal hemostasis continued4.Formation of permanent plugPrevents further hemorrhagePolymerized fibrin and platelet aggregationCounter regulatory mechanisms(t-PA)limit the plug to the site of the injurySteps 3 and 4The Main Players in HemostasisEndothelial cellsPlateletsCoagulation cascadeEndothelial CellsProduce vWF(vonWillebrand factor)A product of normal endothelium A product of normal endothelium found in the plasmafound in the plasmaessential for platelet binding to collagen and essential for platelet binding to collagen and other surfacesother surfacesSecrete Tissue factorinduced by cytokines(TNF,IL-1)induced by cytokines(TNF,IL-1)activates the activates the extrinsic clotting pathwayextrinsic clotting pathwayEndothelial Cells have Prothrombotic EffectVia vWF and tissue factor factors that depress fibrinolysis factors needed for the clot are not destroyed before clot formsCollagenishighlyCollagenishighlythrombogenicthrombogenicFor wound healingFor inflammationFor hemostasisEndothelial cells have Anti-thrombotic properties,tooAntiplatelet effectsIntact cells are barrier to Intact cells are barrier to subendothelial ECMsubendothelial ECMPGI-2 and NO prevent PGI-2 and NO prevent platelets from adheringplatelets from adheringFibrinolytic propertiesTissue type Tissue type plasminogen plasminogen activatoractivator(t-PA)(t-PA)promotes activity to clear promotes activity to clear fibrin deposits from fibrin deposits from endothelial surfacesendothelial surfacesAnticoagulant propertiesMembrane Membrane associated associated moleculesmoleculesHeparin like Heparin like molecules and molecules and thrombomodulithrombomodulin nInactivate thrombin Inactivate thrombin and several and several coagulation factorscoagulation factorsFactors that favor or inhibit thrombosisSOooo.Endothelial cells modulate the balance of hemostasisEndothelial injury is the dominant influence that leads to thrombosisPlateletsExpress glycoprotein receptors on membranes.Gp Ib,IIb/IIIaHave three types of granulesAlpha granulesFibrinogen,fibronectin,factor V and Fibrinogen,fibronectin,factor V and VIII,PDGF,TGFVIII,PDGF,TGFb bDense bodies or delta granulesATP/ADP,ionized calcium,histamine,ATP/ADP,ionized calcium,histamine,serotonin,epinephrineserotonin,epinephrineLysosomal granulesPlateletsHyalomereandgranulomereHyalomereandgranulomerePlatelets continuedPlatelets continuedUpon encountering the ECM,platelets undergo three general reactions:1.Adhesion and shape change mediated by vWF and glycoprotein Ib2.Secretion(release reaction)calcium required in coagulation cascadecalcium required in coagulation cascadeADP as mediator of platelet aggregationADP as mediator of platelet aggregationSurface expression of phospholipid Surface expression of phospholipid complexcomplexBinding site for calcium ions and coagulation Binding site for calcium ions and coagulation factorsfactorsPlatelets continuedPlatelets continued3.AggregationADP and ADP and TXATXA2 2(vasoconstrictor thromboxane vasoconstrictor thromboxane A A2 2)are the stimuli for the formation of the)are the stimuli for the formation of the primary hemostatic plugprimary hemostatic plugAspirin inhibits synthesis of TXAAspirin inhibits synthesis of TXA2 2Fused mass of plateletsFused mass of plateletsCreated by coagulation cascade that produces Created by coagulation cascade that produces thrombinthrombin Thrombin also convertsThrombin also converts fibrinogenfibrinogen to to fibrinfibrin cementing platelets in placecementing platelets in placeThrombocytopeniaSpontaneous bleeding,prolonged bleeding timeLowered platelet countUremia,too much aspirin and rare genetic Uremia,too much aspirin and rare genetic disordersdisordersVarious marrow failure or injuryVarious marrow failure or injuryAplastic anemia,leukemiaAplastic anemia,leukemiaSometimes immunologically mediatedSometimes immunologically mediatedDestruction of platelets by prosthetic heart Destruction of platelets by prosthetic heart valvesvalvesBleeding into CNS a concernCommon hematologic manifestation of AIDSCoagulation CascadeA series of conversions