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1、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 血液運輸載體 方向性 內(nèi)（） 凝血系統(tǒng) 凝血 外（） 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?。焊腥尽⒛[瘤、產(chǎn)科意外 Introduction DIC is characterized by the activation of the coagulation
2、system with resultant consumption of a variety of coagulation proteins and platelets, which results in hemorrhagic diathesis and ischemic injury to various tissues. 1.Blood Coagulation It is propagated by an enzymatic events termed coagulation cascade. 2.Fibrinolysis It is the result of the action o
3、f plasmin, a proteolytic enzyme produced from an inert plasma precursor (plasminogen) by the action of various substances termed plasminogen activators. Humoral plasminogen activatorsTissue plasminogen activatorsFibrin or fibrinogen degradation products (Significant biological activity)Fragments X,
4、Y and E (potent antithrombins)Fragments Y and D ( inhibit fibrin polymerization) a a a PC APC TM+ 滅 活 PS(+) C4b C4b PS(-) FDP AT PC APC TM+a PS PGI VEC TM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 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Etiology of DIC1.acute DIC(1)septicemia (2)severe trauma (3)obstetric accid
5、ents (4)shock2.subacute DIC(1)malignant tumors(2)retained dead fetus3.chronic DIC (1)giant hemangioma(2)systemic lupus erythematosus (SLE)機(jī)理 膠原暴露 凝VEC 釋放受損 合成PGI2TXA2 抗凝 表達(dá)TM APC2.血細(xì)胞大量受損RBC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（） 機(jī)理： 釋 ADP P聚集WBC激活或受損 壞死 白血病細(xì)胞 釋原因 化療受損機(jī)理 炎癥激活 合成 、釋 （內(nèi)毒素、補(bǔ)體、LC、P、
6、AgAb） P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（GPb膠原） 聚（GPba fg） TXA2等 P聚、血管收縮 機(jī)理 PF111 提供“反應(yīng)面” aCa2+a aCa2+a PF3 PF33.大量致凝物質(zhì)入血 腫瘤細(xì)胞 壞死（包括產(chǎn)科意外） 組織細(xì)胞 帶負(fù)電顆粒物質(zhì)（內(nèi)毒素）a 胰蛋白酶 其它絲氨酸蛋白水解酶 a 蝰蛇毒Pathogenesis of DIC 1.extensive damage of vascular endothelial cells 2.severe tissue injury 3.excessive destruction of t
7、he circulating blood cells 4.other thromboplastic materials entering the bloodthe net effects are summarized as follows:1.loss of plasma fibrinogen as it is consumed by the clotting process and by the action of plasma.2.loss of other clotting factors notably , and , as they are used up during the op
8、eration of the clotting cascade.3.fall in the platelet count, as the platelets aggregate and leave the circulation.4.appearance of fibrin degradation products, as plasmin acts on its substrates. 二、誘因與發(fā)生機(jī)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(xì)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、a 、凝纖產(chǎn)物 2.肝功能嚴(yán)重障礙 滅活活化凝血因子 合成AT、PC 枯否細(xì)
9、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Predisposing factors to DIC1.impairment of the clearance mechanism.2.hypercoagulable state.3.disorder of microcirculation.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(jìn)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Types of DIC 1.acute DIC2.suba
10、cute DIC3.chronic DIC Stage of DIC1.hypercoagulable stage2.hypocoagulable stage3.secondary fibrinolytic stage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(jìn) a FDP抗凝：競爭性抑制 a P聚血管壁受損及溶栓Consequences of DIC 1.disturbance of coagulation-bleeding (1)the consumption of clotting factors and platelets (2)the activation
11、of fibrinolytic system (3)the production of fibrin degradation products (FDPs)2.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(fù)荷 : 肺DIC 外周阻力: 四個酶系統(tǒng)激活 A、B肽 擴(kuò)血管物質(zhì) FDP (通透性) 激肽 C3a、C5a 2.disturbance of circulation-shockMicrothromobus in capillariesand venulesBlood returning decreaseCardiac muscle damageCardia
12、c output and blood volume reduceEffective circulating blood volume decreaseHypotension 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.ischemic tissue damage-dysfunction of multiple organsRenal insufficiencyAcute adrenal failurePituitary necrosisAdult or acute respiratory distress syndrome (ARDS)Convulsio
13、n and coma4.microangiopathic hemolytic anemia (MHA)characteristic morphologic abnormality of the red blood cellsTwisted cells, crenated cells, triangular cells, helmet-shaped cells, and microspherocytes are seen on the blood smear.Pathophysiological basis of laboratory diagnosis1.detection of platel
14、et count and its function2.determination of clotting factors 3.determination of activity of fibrinolysis (1)thrombin time test (TT) (2)plasma protamine paracoagulation test (3P test) (3)euglobulin lysis time (ETL) Principles of management of DIC1.treatment of the causative disease2.clotting factor replacement3.anticoagulation therapy4.other modes of therapy
彌散性血管內(nèi)凝血 Cha
