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    Hemostaza

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    Mischa Vlăsceanu
    1. Defects of primary hemostasis (platelet defects) cause bleeding immediately after trauma in superficial sites, while defects of secondary hemostasis (plasma protein defects) cause delayed bleeding in deep sites. 2. Physical findings in primary hemostasis defects include petechiae and ecchymoses, while secondary hemostasis defects cause hematomas and hemarthroses. 3. Defects of primary hemostasis usually have an autosomal dominant family history, while defects of secondary hemostasis often have an autosomal or X-linked recessive family history.

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    Hemostaza

    Uploaded by

    Mischa Vlăsceanu
    82 views7 pages
    1. Defects of primary hemostasis (platelet defects) cause bleeding immediately after trauma in superficial sites, while defects of secondary hemostasis (plasma protein defects) cause delayed bleeding in deep sites. 2. Physical findings in primary hemostasis defects include petechiae and ecchymoses, while secondary hemostasis defects cause hematomas and hemarthroses. 3. Defects of primary hemostasis usually have an autosomal dominant family history, while defects of secondary hemostasis often have an autosomal or X-linked recessive family history.

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    Hemostaza

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    1. Defects of primary hemostasis (platelet defects) cause bleeding immediately after trauma in superficial sites, while defects of secondary hemostasis (plasma protein defects) cause delayed bleeding in deep sites. 2. Physical findings in primary hemostasis defects include petechiae and ecchymoses, while secondary hemostasis defects cause hematomas and hemarthroses. 3. Defects of primary hemostasis usually have an autosomal dominant family history, while defects of secondary hemostasis often have an autosomal or X-linked recessive family history.

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    82 views7 pages

    Hemostaza

    Uploaded by

    Mischa Vlăsceanu
    1. Defects of primary hemostasis (platelet defects) cause bleeding immediately after trauma in superficial sites, while defects of secondary hemostasis (plasma protein defects) cause delayed bleeding in deep sites. 2. Physical findings in primary hemostasis defects include petechiae and ecchymoses, while secondary hemostasis defects cause hematomas and hemarthroses. 3. Defects of primary hemostasis usually have an autosomal dominant family history, while defects of secondary hemostasis often have an autosomal or X-linked recessive family history.

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    of 7

    Differences in the Clinical Manifestations of Disorders of Primary and Secondary Hemostasis

    Manifestations Defects of Primary Hemostasis


    (Platelet Defects)
    Defects of Secondary Hemostasis (Plasma Protein
    Defects)
    Onset of bleeding after trauma Immediate Delayed (hours or days)
    Sites of bleeding Superficial skin, mucous membranes, nose, gastrointestinal
    and genitourinary tracts
    Deep (joints, muscle, retroperitoneum)
    Physical findings Petechiae, ecchymoses Hematomas, hemarthroses
    Family history Autosomal dominant Autosomal or X-linked recessive
    Response to therapy Immediate; local measures effective Requires sustained systemic therapy








    EXPLORAREA HEMOSTAZEI PRIMARE
    TESTELE DE SCREENING :
    Timpul de sangerare - TS
    Numararea placutelor sanguine






    Primary Hemostatic (Platelet) Disorders
    1. Defects of platelet adhesion
    - von Willebrand's disease
    - Bernard-Soulier syndrome (absence or dysfunction of GpIb/IX)
    2. Defects of platelet aggregation
    - Glanzmann's thrombasthenia (absence or dysfunction of GpIIb/IIIa)
    3. Defects of platelet release
    Decreased cyclooxygenase activity
    - Drug-induced (aspirin, nonsteroidal anti-inflammatory agents)
    - Congenital
    Granule storage pool defects
    - Congenital
    - Acquired
    Uremia
    Platelet coating (e.g., penicillin or paraproteins)
    4. Defect of platelet coagulant activity
    - Scott's syndrome








    Evaluation of Platelet Function
    Bleeding time
    Modified Ivy method
    Skin incision (time to stop bleeding)
    Global screen of platelet role in hemostasis
    von Willebrand factor assays
    vWF Ag (immunoassay of total vWF protein)
    vWF R:Cof (bioassay of vWF that measures ability of patient plasma to support agglutination of normal platelets in the presence of ristocetin)
    Factor VIII (coagulation assay of factor VIII bound and carried by plasma vWF)
    Platelet aggregometry
    Measures platelet aggregation in response to a panel of agonists, usually ADP, collagen, arachidonic acid, and epinephrine
    Membrane glycoproteins
    Presence of glycoproteins Ib-IX and IIb-IIIa can be measured using monoclonal antibodies and flow cytometry
    Platelet granule content
    Dense granules (electron microscopy or uptake and retention of radiolabeled serotonin)
    Alpha granules (electron microscopy and/or immunoassays for platelet-associated proteins - vWF, fibrinogen, platelet factor four



    EXPLORAREA HEMOSTAZEI SECUNDARE (COAGULAREA)
    TESTE DE SCREENING :
    TCG TC (aPTT)
    TIMPUL DE PROTROMBINA (QUICK) = PT
    TIMPUL DE TROMBINA
    FIBRINOGENEMIA

    Relationship between Secondary Hemostatic Disorders and Coagulation Test Abnormalities
    Prolonged partial thromboplastin time (PTT)
    No clinical bleeding (factors XII, HMWK, PK)
    Mild or rare bleeding (factor XI)
    Frequent, severe bleeding (factors VIII and IX)
    Prolonged prothrombin time (PT)
    Factor VII deficiency
    Vitamin K deficiency - early
    Warfarin anticoagulant ingestion
    Prolonged PTT and PT
    Factor II, V, or X deficiency
    Vitamin K deficiency - late
    Warfarin anticoagulant ingestion
    Prolonged thrombin time (TT)
    Mild or rare bleeding, afibrinogenemia
    Frequent, severe bleeding, dysfibrinogenemia
    Heparin-like inhibitors or heparin administration
    Prolonged PT and/or PTT not corrected with normal plasma
    Specific or nonspecific inhibitor syndromes
    Clot solubility in 5 M urea
    Factor XIII deficiency
    Inhibitors or defective cross-linking
    Rapid clot lysis
    a2 plasmin inhibitor



    Dg. diferential : deficit de FPC / deficit de VK
    TESTUL KOLLER
    DEFICIT FPC DEFICIT DE VK
    APTT / PT APTT / PT

    Administrare de VK (i.m.)
    8 12 ore
    APTT / PT (nu se corecteaza) APTT / PT = N (se corecteaza)
    TEST KOLLER (-) TEST KOLLER (+)


    EXPLORAREA FIBRINOLIZEI
    TLCS
    TLCE
    D-DIMER


    SEMNIFICATIA D-DIMERULUI

    SINDROM FIBRINOLITIC SINDROM FIBRINOLITIC
    PRIMAR SECUNDAR

    APTT = N APTT
    PT = N PT
    TT = N TT
    Fibrinogenemie (disproportionat) Fibrinogenemie
    Tr-citopenie Tr-citopenie
    TLCS, TLCE TLCS, TLCE
    PDF +++ PDF +++
    D-Dimer = N D-Dimer

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