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HEMOSTASISAda 4 fase : 1. Spasme Pembuluh darah / Vasokonstriksi 2. Pembentukan Sumbat trombosit 3. Koagulasi Darah 4. Pertumbuhan Jaringan ikat

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3SPASME VASKULARKerusakan pembuluh darah

Kontraksi/spasme dinding pembuluh darahUpaya menghambat aliran darah

Lokal miogenic refleks Local humoralspasme saraf factor

nyeri kerusakan tromboxan A2 (TXA2) dinding p.d trombosit41. Platelet AdhesionPlatelets stick to exposed collagen underlying damaged endothelial cells in vessel wall

5PLATELET PLUGPembuluh darah rusakTrombosit kontak dgn : - serat kolagen - sel endotelAktivasi trombosit :Membengkak - bentuk tak beraturanSticky ( lengket) - prot. kontraktil kontraksiSekresi ADP >>Tromboxan A2 ( ~ prostoglandin )Mengaktifkan trombosit saling melekatMembentuk sumbat longgar62. Platelet Release ReactionPlatelets activated by adhesionExtend projections to make contact with each other Release thromboxane A2, serotonin & ADP activating other plateletsSerotonin & thromboxane A2 are vasoconstrictors decreasing blood flow through the injured vessel. ADP causes stickiness

73. Platelet AggregationActivated platelets stick together and activate new platelets to form a mass called a platelet plugPlug reinforced by fibrin threads formed during clotting process

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9MEKANISME KOAGULASI DARAHTerbentuknya aktivator protrombin akibat rusaknya pembuluh darah

Aktivator protrombin mengkatalisisr protrombin menjadi trombin

Trombin sebagai enzim mengubah fibrinogen menjadi benang-benang fibrin.10 Protrombin ekstrinsik Ca2+ protrombin aktivator intrinsik Trombin

Fibrinogen Fibrin monomer Ca2+ Fibrin Stabilizing Factor

Benang Fibrin11

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Prothrombinase(Prothrombin activator)1313Blood coagulation: factors involved

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Tissue traumaTissuefactor(TF)Blood traumaDamagedendothelial cellsexpose collagenfibers(a) Extrinsic pathway(b) Intrinsic pathwayActivated XIICa2+DamagedplateletsCa2+PlateletphospholipidsActivated XActivatedplateletsActivated XPROTHROMBINASECa2+VCa2+Prothrombin(II)Ca2+THROMBINCa2+Loose fibrinthreadsSTRENGTHENEDFIBRIN THREADSActivated XIIIFibrinogen(I)XIII(c) Common pathwayV123++1515Natural anticoagulants:

A. Endothelial surface factors B. Anticoagulants present in the blood which remove THROMBIN

C. Anticoagulants may be used

1. Smoothness of endothelial wall: so has glycocalyx which repels clotting factors

2. Protein C :inactivates factors V and VIII3. Thrombomodulin- a protein bound to endothelium -combines with thrombin to reduce clotting.

4. This combination also activates Protein CIn patients:i. Heparinii. Vit K antagonists

Outside the body:HeparinCalcium antagonists1. Fibrin itself

2. Antithrombin III -antithrombin ( globulin) + heparin-removes activated factors XII, XI, X-removes thrombin1616Normal coagulation time: 3-7 minutes (finger prick method)

Clinical implications

Coagulation disorders :

i. not enough coagulations factors--? (Hemophilia (factor VIII deficiency) transmitted by female to males. Only males suffer)

ii. Not enough Vit K -

1717PENCEGAHAN KOAGULASIEkstravaskular : 1. diaduk 2. didinginkan 3. + Na sitrat, K sitrat 4. + EDTA

Intravaskular : 1. Coumarin , Warfarin 2. Heparin18TEST PEMBEKUAN DARAHWaktu perdarahan ( Bleeding Time ) - 1- 6 menit - tergantung : * dalamnya luka * faktor pembekuan darah * trombositWaktu Pembekuan ( Clotting Time ) - 6 10 menit - tgt : * kondisi gelas & ukuran tabung * faktor pembekuan darah

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