KULIAH HEMOSTASIS 2011

SISTEM HEMOSTASIS
= SUATU SISTEM YANG MEMPERTAHANKAN PBL DARAH DAN ISINYA DALAM KEADAAN NORMAL

TUJUAN SISTEM :
1. MENGHENTIKAN PERDARAHAN 2. MEMPERTAHANKAN SUPAYA DARAH TETAP CAIR ( BILA ADA TROMBUS ).

Gambar : Gangguan Hemostasis.

‡ GANGGUAN
-

ASIS:

ARAHAN, - ROMBOSIS

PERDARAHAN .
PROSES HEMOSTASIS ADA 3 TAHAP 1. HEMOSTASIS RIMER : BL ARAH, TROMBOSIT, ENDOTEL, AGREGASI DAN ELEPASAN FAKTOR TROMBOSIT. 3-5 MENIT BERHENTI DNG PMBTKN PLATELET PLAG ( SUMBAT TROMBOSIT). . HEMOSTASIS SEKUNDER - KOAGULASI, 3-10 MENIT TERBENTUK FIBRIN . - MEMPERKUAT SUMBAT TROMBOSIT. 3. HEMOSTASIS TERSIER FIBRINOLISIS, SBG TAHAP AKHIR, WAKTU 4 -7 AM , FIBRIN LARUT, LUKA SEMBUH.

VASKULER: * LAPISAN ENDOTEL DAN OTOT POLOS .BESAR JARINGAN . IKAT SUBENDOTEL: .BESAR TEK.(USIA MUDA > TUA 2. PROSTASIKLIN. INTRAVASKULER : TROMBOSIT. EKSTRAVASKULER: . JAR. ELASTIN DAN FIBRONEKTIN 3. KOLAGEN. ENDOTEL BERPERAN SINTESIS: . LAP.JENIS JARINGAN .MEMBRANA BASALIS. FAKTOR VON WILLEBRAND.TISSUE FACTORS. ANTI TROMBIN III DAN TROMBOMODULIN. AKTIVATOR DAN INHIBITOR : KOAGULASI DAN FIBRINOLISIS. * JAR. AKTIVATOR PLASMINOGEN.PADA PERDARAHAN ADA 3 KOMPONEN PENTING: 1. PROKOAGULAN. .

Peripheral perfusion worsens. Blood transfusion is not typically required. . (2004) American College of Surgeons' Advanced Trauma Life Support (ATLS): Hemorrhaging is broken down into 4 classes: 1. . . lass IV Hemorrhage involves loss of >40% blood volume.Manning.change in vital signs. . 3. Fluid resus. narrowing of the difference between the systolic and diastolic. JE. lass II Hemorrhage involves 15-30% blood volume. lass III Hemorrhage involves loss of 30-40% of circulating blood volume. . Mental status worsens.Peripheral vasoconstriction. 4.The patient start acting differently. blood transfusion usually necessary. The limit of the body's compensation is reached and aggressive resuscitation is required to prevent death. . . fluid resuscitation not usually necessary. .with crystalloid.Tachycardic. Heart rate increases . Blood pressure drops. . . Volume resuscitation with crystalloids (Saline solution or Lactated Ringer's). Skin pale and be cool. lass I Hemorrhage involves up to 15% of blood volume. . .

* KOMPONEN HEMOSTASIS y y y y y PEMBULUH DARAH TROMBOSIT KASKADE FAKTOR KOAGULASI INHIBITOR KOAGULASI FIBRINOLISIS .

1. ATROFI AR. TIAZID. 2. DEMAM TIFOID. ** DIDAPAT: . ENDOKARDITIS BAKTERIEL. KELAIANAN PEMBULUH DARAH : * KELAINAN STRUKTUR PBL DARAH * AKIBAT INFEKSI/ IMUN. ASPIRIN.PURPURA SIMPLEK RINGAN .AKIBAT OBAT2-AN : PINISILIN. .PURPURA SENILIS MANULA . KOLAGEN. SEPSIS. . . OKSITETRASIKLIN.AKIBAT INEKSI: DHF. OK. FIBRINOLISIS BERLEBIHAN . ** DITURUNKAN : .HEMORHAGIS TELEANGIECTASIS. ISONIACIDE. USIA SUBUR GANGGUAN FRAGILITAS PBL DARAH KULIT.

HEMOLITIK UREMIC SYNDROME: . renal failur. Terapi : plasmaparesis dan tranfusi plasma 4. kemoterapi. gangguan neurologi. ca metastase. trombositopeni.3. partial thromboplastin time. HIV. demam. * Sebab : deff. ticlopidin. aktifitas ADAMTS 13 (enzim pemecah vWF) -> agregasi trombosit. -Anemia Hemolitik.TROMBOTIC THROMBOCYTOPENIC PURPURA: -Dimulai kerusakan jaringan dan pelepasan vWF dari endotel sering pada: Kehamilan. -Prothrombin time. fibrinogen hampir normal.

ANTIGEN . ENDOTELIN 2. WEIBEL-PALADE .VASOKONSTRIKTOR : 1.VW. . TERDAPAT : . BERISI : . INTEGRIN 4. TROMBOPLASTIN .* PEMBULUH DARAH LAPISAN ENDOTEL.P-SELEKTIN 3.FAKTOR VON WILLEBRAND (VW) .

PEMBULUH DARAH RUSAK: Endotel rusak : ENDOTEL KELUARKAN ENDOTELIN UNTUK : .ENDOTELIN BERSAMA TROMBIN MENGIDUKSI ENDOTEL MENGELUARKAN SUBSTANSI ADESI: INTEGRIN DAN SELEKTIN .ENDOTELIN MENARIK LEUKOSIT DAN TROMBOSIT KE DAERAH PEMBULUH DARAH YANG RUSAK. .VASOKONTRIKSI .

NITRIC OXIDE (NO) . AKTIVATOR PLASMINOGEN . PROSTAGLANDIN (PG12) / PROSTASIKLIN . TROMBOMODULIN .VASODILATATOR : . PROTEIN C .. AT III (ANTI THROMNIN III) . ADP ± ASE .

PEMBULUH DARAH : SEL ENNDOTEL RUSAK / TERKELUPAS BILA : y ASIDOSIS y HIPOKSIA y TERPAPAR ENDOTOKSIN y TERPAPAR KOMPLEK ANTIGEN ANTIBODI SIRKULASI .

The structure of individual platelets are evident on careful examination.TROMBOSIT/ PLATELET : y UMUR 7-10 HARI y PRODUKSINYA DIATUR TROMBOPOITIN y TROMBOPOITIN DIBUAT HATI & GINJAL Platelet clumps may appear as large structures in the aspirate or the blood smear.(Peter Maslak). .

4. Rho-specific guanine nucleotide exchange factor. phosphatidylinositol-3. adenylyl cyclase. and G12/13.5-bisphosphate. . PIP3.5trisphosphate.5trisphos-phate. PIP2. protein kinase C. Gi/z. DAG indicates diacyl glycerol. PLC 2/3. RhoGEF. GPVI ligation activates the ITAM-signaling pathway. whereas stimulation of G protein±coupled receptors triggers pathways involving Gq. phospholipase C. PKC.Signaling mechanisms linking platelet receptors to integrin activation. IP3. phosphatidylinositol-4. inositol-1.4. PI-3-K /.2/3.

OBAT-OBATAN . HIPERGAMAGLOBULINEMIA.3. * KUANTITATIF : TROMBOSITOPENIA . LMH.DITURUNKAN: VON WILLEBRAND DISASE.DISTRIBUSI ABNORMAL (POOLING). KELAINAN TROMBOSIT : KUANTITATIF & KUALITATIF.IIb-IIIa) . .GANGGUAN PRODUKSI (MEGAKARIOSIT TURUN . CLL. MEGAKARIOSIT NORMAL) . .DIDAPAT : GAGAL GINJAL. SPLENOMEGALI (SEKUESTRASI) / HIPERSPLENISME . GP. * KUALITATIF: GANGGUAN FUNGSI TROMBOSIT .DISTRUKSI PERIFER BERLEBIHAN ITP. SEKUNDER : SLE. PRIMER (IDIOPATIK) . GLANZMANN THROMBOCYTOPENIA (DEFF. SINDROMA BERNARD ± SOULIER. . STORAGE POOL DISEASE.

y PADA SIKRESI ADP YANG BERLEBIH AKAN MENGAKTIFKAN MEMBRAN FOSFOLIPID (FAKTOR TROMBOSIT 3) SEHINGGA TERJADI AKTIFASI SISTIM KOAGULASI. y TROMBIN MENGHAMBAT SINTESA AMP SIKLIK PENINGKATAN ION KALSIUM HIPERAGREGASI TROMBOSIT.MUDAH MELEKAT KE KOLAGEN ENDOTEL .MUDAH MELEKAT KE TROMBOSIT LAIN (AGREGASI TROMBOSIT).* TROMBOSIT : y BILA ENDOTEL RUSAK ENDOTELIN AKAN MENARIK TROMBOSIT ADESI PADA KOLAGEN PEMBULUH DARAH.MELEPAS SUBSTASI ADP. SEROTONIN. . DLL . y TROMBOSIT AKTIF AKAN MEMBENTUK PSEUDOPODIA SEHINGGA : .

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. ITP. y Perusakan diluar lien yang meningkat.limfoma dan penyakit limfoproliferasi. obat. Imunologi : infeksi bakteri dan virus. Hipertensi portal(SH). infiltrasi sel yg mglami keganasan.TROMBOSITOPENI: y Produksi yg terganggu Aplasia. fibrosis. y Squestrasi trombosit oleh lien yang membesar. infiltrasi lien oleh sel lekemia.

cephalosporin . ACE-I y ITP .Obat kemoterapi . penisilin.Antibiotik : Sufonamis.Heparin .Tiazid.karena antibodi terhadap trombosit. .Von willebrand disease . y Gangguan trombosit fungsional .PENYAKIT DG TROMBOSITOPENI y Drug induced thrombocytopenia .

) y Defek membran trombosit : y Defek release trombosit . penyakit hati kronis . . y Defek pada penyimpanan granula .Pemakaian Aspilet dan NSAID .PENYAKIT DG TROMBOSITOPENI: (lanj. SLE.Lekemia.

PROTEIN PLASMA : y y y y y Protein koagulasi Enzim fibrinolitis Inhibitor Komplemen Kinin * PROTEIN KOAGULASI PEMBENTUKAN FIBRIN .Pembentukan faktor IX a (sistim kontak) .Pembentukan faktor Xa .Pembentukan fibrin .Pentukan trombin (faktor IIa) .

PEMBENTUKAN F IXa : y Aktifasi F XII jadi XIIa oleh : y Fosfolipid. kolagen subendotel. y F XIIa (protein serin) mengaktifkan F XI->FXIa. y F XIa bersama Ion Ca mengubah F IX-> F IXa y F IXa Mengubah F X -> F Xa .

F VII. .TF/F VIIa mengaktifkan F IX -> F IX . ion Ca ->komplek TF/fVIIa .PEMBENTUKAN F Xa: * PENGAKTIFAN F Xa MELALUI : y Jalur intrinsik y Jalur ekstrinsik .JALUR INTRINSIK: .TF/F VIIa & IXa mengatifkan F X -> F Xa.Tissue faktor.

F VII. VII.Faktor jaringan (TF). TNFa).Sitokin (IL-1. faktor trombosit 3. sel tumor mengeluarkan TF. komplemen. IX. TFPI . Ca membentuk komplek menjadi Trombin Catatan : F II. komplek imun -> merangsang endotel.TF -> TF/VIIa -> aktifan F X-> F Xa * PEMBENTUKAN TROMBIN: -F II (protrombin). Ion Ca. . F Xa. F v.* JALUR EKSTRINSIK : . . X dibuat di hepar tergantung Vit K. makrofag.

PEMBENTUKAN FIBRIN : y TROMBIN MENGUBAH F XIII -> F XIIIa y F I (fibrinogen) menjadi Fibrin monomer y Fibrin monomer diubah menjadi fibrin stabil oleh F XIIIa .

MEKANISME PEMBEKUAN DARAH .

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Gambar . Hemostasis lengkap ) .

The six major components of this hemostatic system are vascular endothelium. fibrinolytic proteins. there is no "clot" formation taking place inside the blood vessels. (7) . This highly regulated hemostatic system maintains a delicate balance between a prohemorrhagic state and a prothrombotic state. This balance is maintained by the concomitant actions of platelets. coagulation factors. and antifibrinolytic proteins. and fibrinolytic inhibitors (on one side of the "hemostatic scale")." natural anticoagulant proteins. even though a low. In the presence of an intact endothelium. platelets.The human hemostatic system can be defined as consisting of multiple independent yet integrally related cellular and protein components that function to maintain blood fluidity under normal conditions and to promote localized. and of natural anticoagulants and fibrinolytic proteins (on the other side of the scale). basal physiologic level of coagulation factor activation is occurring continuously. plasma coagulation proteins or "factors. temporary thrombus formation at sites of vascular injury.

XI. PPT.PENYAKIT PERDARAHAN: Hemofili A Hemofili B Kekurangan vit K (II. IX. IX.rusak dll). FDP > . fibrinogen turun. VII. -Trombositopeni. XI) Ganggan fungsi hati DIC : Ada tissue factor (endotoxin. protrombin.At ) y y y y .VII. V. Gangguan absorbsi dan metabolisme vit K. APTT.Al. Splenomegali -> squestrasi (Hb. X. SLE. . TT memanjang. jar. y ANTI KOAGULAN SIRKULASI (IgG): AIDS.TF aktivasi koagulasi diikuti aktifasi fibrinolitik bergantian. y PENYAKIT HATI : Sintesis: fibrinogen.

endothelial cells. .Figure 3. EC. blood-borne TF may contribute to thrombus propagation. SMC. smooth muscle cells. In addition. TF expressed by foam cells (orange) and in the necrotic core (yellow) of the plaque would be exposed to clotting factors in the blood and initiate clotting after plaque rupture. TF is constitutively expressed by adventitial cells (blue). Role of TF in thrombus formation after rupture of an atherosclerotic plaque.

. endothelial cells and platelets are activated promoting the expression of cell adhesion molecules. This vascular response promotes leukocyte rolling and tethering onto the endothelium that initiates an inflammatory event which can lead to thrombosis.Immediately after endothelial cell injury.

DDAVP has been reported to shorten the bleeding time in 50% 75% of patients with uremia. .Recombinant factor VIIa (rFVIIa) . In fact. . . Used effectively in this setting. rFVIIa appears to have a wide spectrum of clinical uses in a variety of different hemorrhagic disorders due to both platelet dysfunction and coagulopathy. predominantly endothelial cells. Is useful by causing the release of VWF from tissue stores.Treatment. .Desmospressin (DDAVP) . vasopressin analog whose pressor effects are substantially less than its antidiuretic effects .

3 µg/kg (IV.Hemostatic drugs. SC) 300 µg (Intranasal) Onset 30±60 min 60±90 min Duration 6±12 hours 6±12 hours Ca eat Tachyp hylaxis Desmopressin Acute bleeding before biopsy or emergency surgery q 12±24 hour x 4±5 doses Conjugated estrogens Drug Chronic. contraind icated in DIC and with hematuri a. Indication Dose 0. TA not available in US 30 min 2±4 hours after discontinuation or 5 g po x 1 f/b 1 gm po hourly for 8 hours 1. Renal clearance . other uses are off-label 90 (50±100) µg/kg IV bolus every 2 hours or as needed Immedia tely 2 hours Monitor for thrombos is . recurrent bleeding or before electi e surgery.5 hours Tranexamic acid (TA): 10±15 mg/kg body weight po or IV q 8 hours 30±60 min Recombinant activated factor VII Hemophilia-related inhibitors. oral bleeding or GI bleeding 0.6 mg/kg IV infusion or 50 mg po q day x 5±7 days Aminocaproic acid: 5 g IV over 1 hour *f/b 1 g/h infusion for 8 hours 7 days 2 weeks Use for < 7 days Enters the extravasc ular or GI bleeding compart ments. esp. from uremia Intractactable mennorhagia.

TERIMA KASIH .

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