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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. Pembentukan platelet 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  150,000 –300,000/ 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) 

2.5 –10 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 

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SECONDARY HEMOSTASIS

Prothrombin time

(PT) and

International

Normalized Ratio

(INR) 

11–13 s, depending on

reagent; INR 1.0

Extrinsic system and common

pathway—factors VII, X,V,

prothrombin, and fibrinogen 

Prolonged PT —most commonly caused by:

Use of warfarin (inhibits vitamin K–dependent

factors II, VII, IX, and X) 

Liver disease with decreased factor synthesis 

Antibiotics, some cephalosporins,

(moxalactam, cefamandole, cefotaxime,

cefoperazone) that inhibit vitamin K–dependent

factors 

Activated partial

thromboplastin

time (aPTT) 

22–34 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 

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Con’t 

Thrombinclotting time(TCT) 

10–12 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); theseinterfere with the conversion 

Very high fibrinogen level (acute phase

reactant) 

"Mixes"  Variable  Performed when one or more of

the above screening tests is

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

"normal" plasma and the

screening test is repeated 

If the "mix" corrects the 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 affects APTT, 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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