faal henoestasis

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    HEMOSTASIS

    Yaitu pencegahan hilangnya darah, bila pembuluh darah

    mengalami cedera atau pecah

    Melalui beberapa cara :

    Ada 4 langkah :

    1. Spasme

    2. Pembentukanplatelet plug

    3. Koagulasi4. Pembentukan jaringan fibrous

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    1. Spasme P.darah :

    Reflex saraf o.k rasa nyeri / impuls dr.

    p.drh yang rusak

    P. drh pecah Spasme miogenik setempat o.kkerusakan ddg p. drh

    Faktor humoral setempat dr. jar. yang

    kena trauma & trombosit darah

    melepas

    Vasokonstriktor tromboxan A2Makin parah kerusakan makin hebat spasmenya

    Aliran darah dr p. drh yg pecah

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    2. Pembentukan sumbat trombosit (platelet plug)Terjadi pd perlukaan pembuluh darah yang berukuran kecil yg

    terjadi tiap hariTromb luka pbl. drh tromb.bengkak irreg. dg. tonjolan, kontraksi protein kontraktil pelepasan granula-2 dgfaktor aktif trombosit lengket pd luka keluar ADP &tromboksan A2 mengaktifkan trombosit2 yang lainsaling melekat sumbat tromb. + benang-2 fibrin

    sumbat rapat kuat Trauma permanen endotel tidak utuh platelet kontak

    dengan serum kolagen agregasi platelet melepaskanzat kimia (ADP) permeabilitas platelet disekitarnyamenjadi lengket menempel pada agregat sebelumnya

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    Proses agregasi dipacu juga olehpembentukan TXA2, TXA2 secara :

    langsung : memacu terbentuknya agregasiplatelet

    tidak langsung : merangsang agregasi

    platelet lebih lanjut melalui perangsanganterhadap pelepasan ADP.

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    Mekanisme Pembekuan Darah

    Teori Dasar : Tergantung dr keseimbangan antara Prokoagulan & Antikoagulan

    Normal : Antikoagulan > dominan drpd koagulandarah tidak membeku

    Pbl.drh rusak: Prokoagulan teraktivasi > aktivasi antikoagulan bekuan

    3 Langkah Pembekuan :

    1. Rangkaian reaksi kimiawi yang kompleks dengan lebihdari 12 faktor pembekuan terbentuk kompleksubstansi teraktivasi disebut activator protrombin :sebagai respon terhadap rupturnya pembuluh darah /kerusakan darah.

    2. Aktivator protrombin : mengkatalisa perubahanprotrombin menjadi trombin

    3. trombin sebagai enzim, mengubah fibrinogen menjadibenang-2 fibrin yang merangkai trombosit sel darah danplasma membentuk bekuan.

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    Clotting Factors

    F I : Fibrinogen

    F II : Prothrombin

    F III : Tissue thromboplastin

    F IV : Calcium

    F V : Proaccelerin ; labile factor

    Ac globulin (Ac-G)F VII : Stable F

    F VIII : Antihaemophilic F.A

    F IX : Antihaemophilic F.B

    F X : Stuart Power FactorF XI : Antihaemophilic F.C

    F XII : Hagemam F

    F XIII : Fibrin stabilizing F

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    XII XIIa

    XI XIa

    IX

    VIIIa,PL,Ca2+

    IXa

    Fibrin Monomer

    Thrombin

    Fibrinogen

    Prothrombin

    VVa

    XaX

    Factor VII

    Ca2+

    Tissue factor/Ca2+

    Factor VIIa

    Tissue factor (extrinsic system)

    Cross-linked FibrinXIII

    VIII

    Contact Activation (intrinsic system)

    Ca2+

    PL,Ca2+

    SECONDARY HEMEOSTASIS

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    XIaXI

    FDPs

    TISSUE

    INJURY

    TF-VII

    TF-VIIa

    IXaIX

    Anticoagulant

    PathwayS-Prot

    Factor V

    VIIIa

    XaX Va

    APC

    C-ProtII THROMBIN

    Fibrinogen

    Fibrinolytic

    Pathway

    FIBRIN Plasmin

    TPA

    PLASMINOGEN

    Plasmin Inhibitor

    TFPI

    PT

    APTT

    PT &

    APTT

    TESTHEMOSTASIS & TROMBOSIS

    Becomes active =

    Activates =Inhibits =

    9Povan,2004

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    TES HEMOSTASISScreening Tests Normal Value Measures Clinical Correlations

    Primary Hemostasis

    Platelet count 150,000300,000/ L Number of platelets per L Decreased platelet count (thrombocytopenia)bleedingusually not a problem until platelet count

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    SECONDARY HEMOSTASIS

    Prothrombin time

    (PT) and

    International

    Normalized Ratio

    (INR)

    1113 s, depending on

    reagent; INR 1.0

    Extrinsic system and common

    pathwayfactors VII, X,V,

    prothrombin, and fibrinogen

    Prolonged PTmost commonly caused by:

    Use of warfarin (inhibits vitamin Kdependent

    factors II, VII, IX, and X)

    Liver disease with decreased factor synthesis

    Antibiotics, some cephalosporins,

    (moxalactam, cefamandole, cefotaxime,

    cefoperazone) that inhibit vitamin Kdependent

    factors

    Activated partial

    thromboplastin

    time (aPTT)

    2234 s Intrinsic system and common

    pathway including factors XII,

    XI, IX, VIII, X, V, prothrombin,

    and fibrinogen

    Prolongation of aPTTmost commonly caused

    by:

    Depends on type of

    thromboplastin used;

    "activated" with Kaolin

    Heparin therapy

    Factor deficiencies; factor levels have to be

    >30% of normal to cause prolongation

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    Cont

    Thrombinclotting time(TCT)

    1012 s Conversion of fibrinogen to

    fibrin monomerProlonged TCTcaused by:

    Low fibrinogen level (DIC)

    Abnormal fibrinogen molecule (liver

    disease)

    Presence of heparin, FDPs or a

    paraprotein (multiple myeloma); theseinterfere with the conversion

    Very high fibrinogen level (acute phase

    reactant)

    "Mixes" Variable Performed when one or more ofthe above screening tests is

    prolonged; the patient's plasma("abnormal") is mixed with

    "normal" plasma and the

    screening test is repeated

    If the "mix" correctsthe screening test,

    one or more factor deficiencies are

    present.

    If the "mix" does not correct the

    screening test,an inhibitor

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    TES KOAGULASI

    ABNORMAL

    PT APTT normal

    Warfarin, def. vitamin K, early liver disease, defisiensikongenital faktor VII deficiency.

    PT APTT

    Overdosis warfarin, def. vitamin K, liver failure, DIC.PT normal APTT

    Unfractionated heparin(UFH), haemophilia A or B, lupusanticoagulant, rarely vWD affectsAPTT,factor VIIIinhibitors are rare but typically prolong APTT.

    PT normal APTT normal

    PT and APTT normal (do not exclude a significant bleedingtendency, for example effect of low molecular weightheparin, mild factor deficiency, platelet abnormality, or veryrare factor deficiency such as factor XIII)

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