出血性疾病的鉴别诊断
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出血性疾病的鉴别诊断
王科富 马玫 倪建佼 指导老师：朱铁楠
2015-10-15
目录
出凝血机制 出血性疾病的诊断思路 病例分析
1 出凝血机制
PHASES OF THE Βιβλιοθήκη BaiduEMOSTATIC PROCESS
Initiation and formation of the platelet plug Propagation of the clotting process by the
Antithrombotic pathways
Antithrombin: It neutralizes most of the enzymes in the clotting cascade
Heparin: Convert antithrombin from a slow to a rapid inactivator of several coagulation factors
定
位 诊
一期止血障碍及二期止血障碍鉴别
断
临床表现
血管和血小板异常
凝血因子异常
皮肤瘀点
特征性
-
皮肤瘀斑
特征性、小片而多发
大片、质硬
深部血肿
-
特征性
关节出血
-
特征性
迟缓型出血
-
常见
表面小伤口出血
量多、较持久
量少
性别
女性多
男性多
家族史
较少见
常见
定
位 诊
如何诊断？--筛查试验
断
一期止血障碍
二期止血障碍
纤溶亢进
PLT计数 出血时间BT
APTT PT TT 纤维蛋白原Fbg
(TAFI)
2 出血性疾病的诊断思路
诊断思路
是否为出血性疾病
定位诊断 定性诊断
一期止血障碍 二期止血障碍
纤溶亢进 遗传性 获得性
凝血因子缺乏 获得性抑制物
血管异常
内源性途径 血外功小源能板性异数途常量径或
共同通路
如何诊断？--病史及查体
基本特征：性别、年龄； 出血诱因：自发 or 外伤后出血； 出血部位及表现；出血频度 既往出血史：女性（月经史） 手术或外伤史； 用药史：抗血小板药物、抗凝药、抗生素 基础疾病 家族史
coagulation cascade Termination of clotting by antithrombotic
control mechanisms Removal of the clot by fibrinolysis
FORMATION OF THE PLATELET PLUG
Platelet activation Platelet adhesion Platelet aggregation Platelet secretion
Protein C: Inactivate VIIIa and Va Protein S: Activate PC, inactivate Va and IXa Tissue factor pathway inhibitor:Inhibits factor Xa and
inactivate extrinsic pathway Prostacyclin, thromboxane, nitric oxide
Platelet aggregation
The GP IIb/IIIa complex + fibrinogen Mediate platelet spreading and clot retraction
Platelet secretion
ADP: Recruit additional platelets Serotonin: Vasoconstriction Fibronectin and thrombospondin: Reinforce and stabilize
CLOT ELIMINATION AND FIBRINOLYSIS
Tissue-type plasminogen activator (tPA) Plasminogen activator inhibitors (PAI) Alpha-2-antiplasmin Thrombin-activatable fibrinolysis inhibitor
platelet aggregates Thromboxane A2: Vasoconstriction, platelet aggregation Growth factors: Tissue repair Thiol isomerase, protein disulfide isomerase: Generation of
Platelet adhesion
GP Ib/IX/V complex + von Willebrand factor (VWF)
Significant shape changes, producing elongated pseudopods that make the platelets extremely adhesive
fibrin and platelet thrombus
CLOTTING CASCADE AND PROPAGATION OF THE CLOT
The intrinsic pathway The extrinsic pathway
Initiation
Amplification
Propagation
Platelet activation
Physiologic platelet stimuli
ADP and epinephrine are relatively weak platelet activators
Collagen and thrombin are the most potent platelet activators.
CONTROL MECHANISMS AND TERMINATION OF CLOTTING
Dilution of procoagulants in flowing blood Removal of activated factors through the
reticuloendothelial system Antithrombotic pathways
王科富 马玫 倪建佼 指导老师：朱铁楠
2015-10-15
目录
出凝血机制 出血性疾病的诊断思路 病例分析
1 出凝血机制
PHASES OF THE Βιβλιοθήκη BaiduEMOSTATIC PROCESS
Initiation and formation of the platelet plug Propagation of the clotting process by the
Antithrombotic pathways
Antithrombin: It neutralizes most of the enzymes in the clotting cascade
Heparin: Convert antithrombin from a slow to a rapid inactivator of several coagulation factors
定
位 诊
一期止血障碍及二期止血障碍鉴别
断
临床表现
血管和血小板异常
凝血因子异常
皮肤瘀点
特征性
-
皮肤瘀斑
特征性、小片而多发
大片、质硬
深部血肿
-
特征性
关节出血
-
特征性
迟缓型出血
-
常见
表面小伤口出血
量多、较持久
量少
性别
女性多
男性多
家族史
较少见
常见
定
位 诊
如何诊断？--筛查试验
断
一期止血障碍
二期止血障碍
纤溶亢进
PLT计数 出血时间BT
APTT PT TT 纤维蛋白原Fbg
(TAFI)
2 出血性疾病的诊断思路
诊断思路
是否为出血性疾病
定位诊断 定性诊断
一期止血障碍 二期止血障碍
纤溶亢进 遗传性 获得性
凝血因子缺乏 获得性抑制物
血管异常
内源性途径 血外功小源能板性异数途常量径或
共同通路
如何诊断？--病史及查体
基本特征：性别、年龄； 出血诱因：自发 or 外伤后出血； 出血部位及表现；出血频度 既往出血史：女性（月经史） 手术或外伤史； 用药史：抗血小板药物、抗凝药、抗生素 基础疾病 家族史
coagulation cascade Termination of clotting by antithrombotic
control mechanisms Removal of the clot by fibrinolysis
FORMATION OF THE PLATELET PLUG
Platelet activation Platelet adhesion Platelet aggregation Platelet secretion
Protein C: Inactivate VIIIa and Va Protein S: Activate PC, inactivate Va and IXa Tissue factor pathway inhibitor:Inhibits factor Xa and
inactivate extrinsic pathway Prostacyclin, thromboxane, nitric oxide
Platelet aggregation
The GP IIb/IIIa complex + fibrinogen Mediate platelet spreading and clot retraction
Platelet secretion
ADP: Recruit additional platelets Serotonin: Vasoconstriction Fibronectin and thrombospondin: Reinforce and stabilize
CLOT ELIMINATION AND FIBRINOLYSIS
Tissue-type plasminogen activator (tPA) Plasminogen activator inhibitors (PAI) Alpha-2-antiplasmin Thrombin-activatable fibrinolysis inhibitor
platelet aggregates Thromboxane A2: Vasoconstriction, platelet aggregation Growth factors: Tissue repair Thiol isomerase, protein disulfide isomerase: Generation of
Platelet adhesion
GP Ib/IX/V complex + von Willebrand factor (VWF)
Significant shape changes, producing elongated pseudopods that make the platelets extremely adhesive
fibrin and platelet thrombus
CLOTTING CASCADE AND PROPAGATION OF THE CLOT
The intrinsic pathway The extrinsic pathway
Initiation
Amplification
Propagation
Platelet activation
Physiologic platelet stimuli
ADP and epinephrine are relatively weak platelet activators
Collagen and thrombin are the most potent platelet activators.
CONTROL MECHANISMS AND TERMINATION OF CLOTTING
Dilution of procoagulants in flowing blood Removal of activated factors through the
reticuloendothelial system Antithrombotic pathways