HEMOSTASIS

Yaitu pencegahan hilangnya darah, bila pembuluh darah mengalami cedera atau pecah Melalui beberapa cara : Ada 4 langkah : 1. Spasme 2. Pembentukan platelet plug 3. Koagulasi

4. Pembentukan jaringan fibrous

1. Spasme P.darah : Reflex saraf o.k rasa nyeri / impuls dr. p.drh yang rusak P. drh pecah Spasme miogenik setempat o.k kerusakan ddg p. drh Faktor humoral setempat dr. jar. yang kena trauma & trombosit darah melepas Vasokonstriktor tromboxan A2 Makin parah kerusakan makin hebat spasmenya Aliran darah dr p. drh yg pecah <<

2. Pembentukan sumbat trombosit (platelet plug) Terjadi pd perlukaan pembuluh darah yang berukuran kecil yg terjadi tiap hari Tromb luka pbl. drh tromb.bengkak irreg. dg. tonjolan , kontraksi protein kontraktil pelepasan granula-2 dg faktor aktif trombosit lengket pd luka keluar ADP & tromboksan A2 mengaktifkan trombosit2 yang lain saling melekat sumbat tromb. + benang-2 fibrin sumbat rapat kuat Trauma permanen endotel tidak utuh platelet kontak dengan serum kolagen agregasi platelet melepaskan zat kimia (ADP) permeabilitas platelet disekitarnya menjadi lengket menempel pada agregat sebelumnya

 Proses agregasi dipacu juga oleh pembentukan TXA2, TXA2 secara : langsung : memacu terbentuknya agregasi platelet tidak langsung : merangsang agregasi platelet lebih lanjut melalui perangsangan terhadap pelepasan ADP.

3. Pembekuan darah pd pbl.darah yang rusak Trauma pbl. drh hebat terbentuk dlm waktu 15-30 Trauma pbl.drh kecil terbentuk dlm waktu 1-2 Proses : Pbl. drh rusak zat activator Tromb. & prot. drh melekat pd ddg pbl. drh. rusak 36 diisi ol. bekuan drh retraksi 20-1 jam bekuan t.u. ol tromb. Menutup luka

4. Pembentukan jaringan ikat 2 proses bekuan diinvasi oleh fibroblast membentuk jar. ikat pd seluruh bekuan penghancuran bekuan oleh aktivasi zat khusus dlm bekuan bila bekuan itu luas
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 Mekanisme Pembekuan Darah

Teori Dasar : Tergantung dr keseimbangan antara Pro koagulan & Antikoagulan

Normal : Antikoagulan > dominan drpd koagulan darah tidak membeku

Pbl.drh rusak: Prokoagulan teraktivasi > aktivasi anti koagulan bekuan

3 Langkah Pembekuan : 1. Rangkaian reaksi kimiawi yang kompleks dengan lebih dari 12 faktor pembekuan terbentuk komplek substansi teraktivasi disebut activator protrombin : sebagai respon terhadap rupturnya pembuluh darah / kerusakan darah. 2. Aktivator protrombin : mengkatalisa protrombin menjadi trombin perubahan

3. trombin sebagai enzim, mengubah fibrinogen menjadi benang-2 fibrin yang merangkai trombosit sel darah dan plasma membentuk bekuan.
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Clotting Factors

FI F II F III F IV FV

: Fibrinogen : Prothrombin : Tissue thromboplastin : Calcium : Proaccelerin ; labile factor Ac globulin (Ac-G)

F VII
F IX FX

: Stable F
: Antihaemophilic F.B : Stuart Power Factor

F VIII : Antihaemophilic F.A

F XI
F XII
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: Antihaemophilic F.C
: Hagemam F

F XIII : Fibrin stabilizing F

Contact Activation (intrinsic system)

Tissue factor (extrinsic system) Factor VII

XII

XIIa

SECONDARY HEMEOSTASIS

XI
Ca2+

XIa
Tissue factor/Ca2+

IX

IXa VIIIa,PL,Ca2+ VIII Ca2+ X Va

PL,Ca2+
Factor VIIa

Xa V
Thrombin
Fibrin Monomer

Prothrombin

Fibrinogen

XIII

Cross-linked Fibrin

TEST PT TFPI

TISSUE INJURY

HEMOSTASIS & TROMBOSIS

TF-VII Anticoagulant Pathway TF-VIIa S-Prot Factor V IXa Xa VIIIa APC X Va

APTT

IX

II

THROMBIN XI XIa Fibrinolytic Pathway

Fibrinogen FIBRIN FDPs Plasmin

C-Prot

PT & APTT Becomes active = Activates = Inhibits =

TPA
PLASMINOGEN

Povan,2004

Plasmin Inhibitor

TES HEMOSTASIS
Screening Tests Normal Value Measures Clinical Correlations

Primary Hemostasis
Platelet count
150,000300,000/ L Number of platelets per L Decreased platelet count (thrombocytopenia)bleeding usually not a problem until platelet count <50,000/mL; high risk of spontaneous bleeding including CNS with count <10,000/ L; usually due to decreased production or increased destruction

Elevated platelet count (thrombocytosis)commonly reactive to inflammation or malignancy, or in polycythemia vera; can be associated with hemorrhage or thrombosis

Bleeding time (BT)

2.510 min (template BT)

Interaction between platelets and the subendothelium

Prolonged BT caused by:

Thrombocytopenia (platelet count <50,000/ L)

Abnormal platelet function (vWD, ASA, NSAIDs

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 aPTT most 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

Cont
Thrombin clotting time (TCT)
1012 s Conversion of fibrinogen to fibrin monomer Prolonged TCT caused by: Low fibrinogen level (DIC) Abnormal fibrinogen molecule (liver disease) Presence of heparin, FDPs or a paraprotein (multiple myeloma); these interfere with the conversion

Very high fibrinogen level (acute phase reactant)

"Mixes"

Variable

Performed when one or more of If the "mix" corrects the screening test, the above screening tests is one or more factor deficiencies are prolonged; the patient's plasma present. ("abnormal") is mixed with "normal" plasma and the screening test is repeated If the "mix" does not correct the screening test, an inhibitor

TES KOAGULASI ABNORMAL

PT APTT normal
Warfarin, def. vitamin K, early liver disease, defisiensi kongenital faktor VII deficiency.

PT APTT

Overdosis warfarin, def. vitamin K, liver failure, DIC.

PT normal APTT

Unfractionated heparin (UFH), haemophilia A or B, lupus anticoagulant, rarely vWD affects APTT, factor VIII inhibitors are rare but typically prolong APTT.

PT normal APTT normal

PT and APTT normal (do not exclude a significant bleeding tendency, for example effect of low molecular weight heparin, mild factor deficiency, platelet abnormality, or very rare factor deficiency such as factor XIII)