1 / 22

Overview of primary hemostasis

Overview of primary hemostasis. 진단검사의학과 안정열. I. The mechanism of blood coagulation : 혈관벽 손상시 vascular system 내에 blood 가 fluid state 로 잘 유지되도록 하는 과정 * Vasoconstriction -> PLT aggregation -> coagulation * Effectiveness of hemostatic mechanism

bryga
Download Presentation

Overview of primary hemostasis

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


  1. Overview of primary hemostasis 진단검사의학과 안정열

  2. I. The mechanismof blood coagulation :혈관벽 손상시 vascular system내에 blood가 fluid state로 잘 유지되도록 하는 과정 * Vasoconstriction -> PLT aggregation -> coagulation * Effectiveness of hemostatic mechanism - type and degree of injury - ability of vasoconstriction - PLT availability & activity - blood factor & relation to function - absence of inhibitors, circulating anticoagulants and antagonists * Fibrinolysis : the process of dissolution of the clot * Homorrhage or thrombosis

  3. II Primary hemostasis : The vascular system The platelets 1. Vascular system * a thin layer of endothelial cells : thromboresistant surface * vascular damage -> vasoconstriction -> immediate reduced blood flow * vasoactive substance (serotonin, thromboxane A2 , endothelin) 2. Platelets * 2-4um in diameter, * are produced in BM from a megakaryocyte, which produces about 2000 PLT * 70-80% circulate in blood, 20-30% pool in the spleen * life span is 7 to 10 days

  4. 1) PLT number Vs function* PLT function is more relevant than PLT numbers* ex) > 150만 : bleeding can be caused by dysfunctional PLT < 5만 : often not bleed < 1만 : spontaneous bleeding may occurs but young PLT will correct for the defects2) PLT kinetics* Adhesion : - adhere to collagen -> undergo a shape change from discs to spheres - primary aggregation and is reversible

  5. * Release : - dense granules ( ADP, ATP, ionized calcium, magnesium, epinephrin, phosphate, and serotonin) - alpha granules ( fibrin, PDGF, PAI, fibronectin, albumin, PF3, PF4, vWF, fibrinogen, ßthromboglobulin, and factor V)- secondary aggregation , is irreversible * Aggregation : PLTs cohere to other PLTs * Stabilization of the clot : - thrombus formation- release factor V and expose PF 3 to accelerate the coagulation cascade and promote activation of cloting factors -> stabilze the PLT plug with a fibrin clot

  6. III. Evaluation of bleeding in primary hemostasis1. Abnormalities of the vascular endothelium : Hereditary or Acquired vascular disorders* Ehlers-Danlos, Homocystinuria* Allergic purpura, Henoch-Schölein purpura ** Normal vessel walls provide - a surface resistant to the formation of thrombi - if disrupted, provide the initial stimuli for thrombus formation - inhibitors for PLT activity, activators for clearance of thrombus

  7. 2. Evaluation of PLT abnormalities1) Thrombocytopenia - PLTs are low in number but normal in function - immunologic, ITP - infection, viral ect - drugs (aspirin)2) Thrombocytopathia - poor PF3 activity : PLT count normal, poor in function - too little PF3, due to systemic disease (uremia, scurvy, hepatic dz) - failure or release PF3 - deficiency of plasma factor- vWF

  8. 3) Thrombocytosis - PLTs are increased in number, normal in function- acute hemorrhage, hemolysis, postsplenectomy • 4) Thrombocythemia • - PLTs increased in number, large, and bizarre forms, • bleeding time prolonged, poor clot retraction • - myeloproliferative disorders

  9. VI. Teststo evaluate a bleeding disorder of primary hemostasis (1) 출혈 시간 (Bleeding time) * 피하 혈관에 작은 절개 후 출혈이 멈출때 까지의 시간을 측정 *혈관의 수축 및 혈소판의 부착과 응집에 의한 일차성 지혈 기능 반영 *Duke법: puncture in the ear lobe 절개부위의 크기와 깊이를 일정, 정상인의 경우 1~4분7일 이내 aspirin 복용 history 없어야 *혈소판 감소증, 기능이상, vWD 및 혈관장애시 연장 *혈소판 수가 정상, 출혈시간 연장 : 혈소판 기능 장애, vWD 의심 afibrinogenemia, severe hypofibrinogenemia

  10. (2) PLT aggregation test* PLT rich plasma 에 aggregating agents를 넣으면 PLT 모양의 변화 와 aggregation 유발 => aggregometer로 percent transmittance를 측정 * Aggregation agents : ADP, EPI, Collagen, Ristocetin, Arachidonic acid * 7일 이내 aspirin 복용 history 없어야 * Interpretation : - primary curve ; aggregating agent와 PLT의 직접반응으로 PLT shape and small aggregates 생성- secondary wave; complete aggregation

  11. * ADP : Glanzmann’s thrombasthenia * Collagen : Glanzmann’s thrombasthenia, aspirin-like release disorder, storage pool disorder, uremia * Ristocetin : vWD, Bernard-Soulier syndrome

  12. (3) Capillary fragility test( = tourniquet test , vascular disorder) * Tourniquet test ; upper arm에 cuff를 놓고 diastolic 과 systolic pressure의 중간압으로 5분간 압력을 주고 풀어준 후 수 분 안에 petechiae 발생 여부를 확인 * 5개 이상, 3cm이상일 때 양성으로 판독(4) Clot retraction time* fibrin formation, from the inspection of the clot * clot retraction occurs by the interaction between PLT psuedopods and fibrin strands. * occurs within 60 minutes, and the colt occupies 50% of total volume of blood.

More Related