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  • Factor 5: Vit K-Dep: 2, 7, 9, 10

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    1. Platelets play a key role in primary hemostasis through secretion of coagulation factors like fibrinogen and von Willebrand factor, and receptor-mediated adhesion and aggregation. 2. The platelet surface provides a procoagulant site for the assembly of coagulation complexes during secondary hemostasis. 3. Coagulation factors of the intrinsic and extrinsic pathways activate each other in a cascade culminating in thrombin generation and fibrin formation to form a clot. Natural anticoagulants then regulate coagulation to prevent excessive clotting.

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    응고 인자 정리본.pdf

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    1. Platelets play a key role in primary hemostasis through secretion of coagulation factors like fibrinogen and von Willebrand factor, and receptor-mediated adhesion and aggregation. 2. The platelet surface provides a procoagulant site for the assembly of coagulation complexes during secondary hemostasis. 3. Coagulation factors of the intrinsic and extrinsic pathways activate each other in a cascade culminating in thrombin generation and fibrin formation to form a clot. Natural anticoagulants then regulate coagulation to prevent excessive clotting.

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    9 views1 page

    Factor 5: Vit K-Dep: 2, 7, 9, 10

    Uploaded by

    C C
    1. Platelets play a key role in primary hemostasis through secretion of coagulation factors like fibrinogen and von Willebrand factor, and receptor-mediated adhesion and aggregation. 2. The platelet surface provides a procoagulant site for the assembly of coagulation complexes during secondary hemostasis. 3. Coagulation factors of the intrinsic and extrinsic pathways activate each other in a cascade culminating in thrombin generation and fibrin formation to form a clot. Natural anticoagulants then regulate coagulation to prevent excessive clotting.

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    of 1

    Primary hemostatic plug 역할

    α-granule Fibrinogen Aggregation (cross-linking), Afibrinogenemia Secretion


    GP 2b/3a (Rc 결핍 : Glanzmann's thrombasthenia) Aggregation
    Clot retraction
    vWF GP 1b/9/10 (Rc 결핍 : Bernard-Soulier)
    Adhesion
    Component
    vWF disease
    Factor 5
    - Secreton defect(경증) 시 민감x)

    Dense granule Ca+ Acquired platelet secretion defect (aspirin) : COX 차단


    (PFA-100 : Closure time 확인

    Secretion
    ADP Weak activator, Recruitment of more plt
    P2Y1, P2Y12 (Ticlopidine, clopidogrel Rx)
    Secretion
    Plt secretion defect (Storage pool d/s)
    Platelet

    Strong Collagen GP 1a/2a/6, subendo Adhesion


    Thrombin (Coagulation에서 thrombomodulin과 결합, PC활성화)
    Activator

    Weak Thromboxane A2 Secreted, Recruitment of more plt,


    Prostagladin H2 Plt secretion defect (Storage pool d/s)
    Secretion
    Acquired platelet secretion defect (aspirin)

    Epi

    Inhibitors CD39 (ADPase)


    NO
    PGI2

    Secondary hemostatic plug


    Activation 시 Plt mbr 안 --> 밖 translocation
    Phosphatidyl serine Providing surface for pro-coagulant complex
    응고장소 (Plt 표면) 제공
    Scott's s/d (defective translocation)

    12 결핍되도 no problemo

    Vit K-dep : 2, 7, 9, 10
    11
    Intrinsic

    8 vWF 결핍 -> F8 stabilisation defect

    Tenase (9a-8a-Ca) 10 활성화


    (혈우병 : 감소 -> 출혈)
    Coagulation factor

    항상 발현 중 : fibroblast, smooth mm.


    Tissue Factor (3) Inducible : endo (혈관 손상), monocyte, microparticle Coagulation initiator
    Extrinsic
    7 10, 9 활성화

    10
    5 5a의 R506Q 경우 APC 저항성 생김 (F5 Leiden)
    Common

    Prothrombinase (10a-5a-Ca)
    Prothrombin (2)
    Fibrinogen (1)
    Fibrin 형성 후 cross-linkage를 통해 clot을 견고하게.
    13
    Ptn C 활성화된 APC + PS -> F5a, 8a 비활성화
    Ptn C def : thromobophilia
    Natural Anticoagulant

    Ptn S APC와 결합 -> F5a, 8a 비활성화


    Ptn C system

    Thrombomodulin Thrombin와 결합 -> APC (활성화된 PC) Anti-coagulation


    (항응고)
    Blood thining.
    Antithrombin Thrombin과 F10 억제; activated by heparin

    Tissue Factor Pathway Inh (TFPI) Extrinsinc과 F10 억제

    tPA, uPA Inactive한 plasminogen이 plasmin으로 활성화


    Plasminogen activator 간질환, 전립선암에서 증가 -> 출혈
    Fibrin clot 제거
    Plasmin Fibrin clot 용해 -> FDP + D-dimer (섬유소 용해)
    Fibrolytic factors

    α2-antiplasmin Free plasmin과 결합해, 과도한 fibrinolysis를 차단

    PAI-1 > 2 Plasminogen activator (tPA > uPA)와 결합해 작용억제


    Inactivator

    TAFI Fibrin 구조를 바꿔 plasmin이 작용 못 함

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