HEMOSTASIS

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

SPASME VASKULAR
Kerusakan pembuluh darah
Kontraksi/spasme dinding pembuluh darah
Upaya menghambat aliran darah

Lokal miogenic
spasme
nyeri
(TXA2)

refleks
saraf
kerusakan

Local humoral
factor
tromboxan A2

dinding p.d
trombosit

1. Platelet Adhesion
Platelets stick to exposed collagen underlying
damaged endothelial cells in vessel wall

PLATELET PLUG

Pembuluh darah rusak

Trombosit kontak dgn : - serat kolagen
- sel endotel
Aktivasi trombosit :
- Membengkak
- bentuk tak beraturan
- Sticky ( lengket)
- prot. kontraktil
kontraksi
Sekresi ADP >>
Tromboxan A2 ( ~ prostoglandin )
Mengaktifkan trombosit saling melekat
Membentuk sumbat longgar

2. Platelet Release Reaction

Platelets activated by adhesion
Extend projections to make contact with each other
Release thromboxane A2, serotonin & ADP activating
other platelets
Serotonin & thromboxane A2 are vasoconstrictors
decreasing blood flow through the injured vessel. ADP
causes stickiness

3. Platelet Aggregation
Activated platelets stick together and
activate new platelets to form a mass
called a platelet plug
Plug reinforced by fibrin threads formed
during clotting process

MEKANISME KOAGULASI DARAH

Terbentuknya aktivator
protrombin akibat rusaknya
pembuluh darah
Aktivator protrombin
mengkatalisisr protrombin
menjadi trombin
Trombin sebagai enzim mengubah
fibrinogen menjadi benang-

Protrombin
ekstrinsik
Ca2+
protrombin aktivator
intrinsik
Trombin
Fibrinogen

Fibrin monomer

Ca2+
Fibrin Stabilizing Factor

Prothrombinase
(Prothrombin activator)

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Blood coagulation: factors involved

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(a) Extrinsic pathway

(b) Intrinsic pathway

Tissue trauma

Blood trauma
Damaged
endothelial cells
expose collagen
fibers
Tissue
factor
(TF)

Damaged
platelets

Activated XII
Activated
platelets

Ca2+

Ca2+

+
Platelet
phospholipids
Activated X

Activated X
V

V
Ca2+

Ca2+

PROTHROMBINASE
(c) Common
pathway
Ca2+
Prothrombin
(II)

THROMBIN
Ca

Fibrinogen
(I)
Loose fibrin
threads

2+

XIII

Activated XIII

STRENGTHENED
FIBRIN THREADS

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Natural anticoagulants:
A. Endothelial surface factors
the blood which

B. Anticoagulants present in
remove THROMBIN
1. Fibrin itself

. Smoothness of endothelial wall:

o has glycocalyx which
repels clotting factors

2. Antithrombin III
-antithrombin ( globulin)
+ heparin
-removes activated factors
XII, XI, X
-removes thrombin

2. Protein C :inactivates
factors V and VIII

3. Thrombomodulin- a protein bound

o endothelium -combines with
thrombin to reduce clotting.
used

C. Anticoagulants may be

In patients:
i. Heparin
ii. Vit K antagonists
4. This combination also
activates Protein C

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Outside the body:

i. Heparin
ii. Calcium antagonists

 Normal coagulation time: 3-7

minutes (finger prick method)
Clinical implications
Coagulation disorders :
i. not enough
coagulations factors--?
(Hemophilia (factor VIII

deficiency)
Only males suffer)

transmitted by female to males.

ii. Not 17enough Vit K -

PENCEGAHAN KOAGULASI

Ekstravaskular :
1. diaduk
2. didinginkan
3. + Na sitrat, K sitrat
4. + EDTA
Intravaskular :
1. Coumarin , Warfarin
2. Heparin

TEST PEMBEKUAN DARAH

Waktu perdarahan ( Bleeding Time )
- 1- 6 menit
- tergantung : * dalamnya luka
* faktor pembekuan
darah
* trombosit
Waktu Pembekuan ( Clotting Time )
- 6 10 menit
- tgt : * kondisi gelas & ukuran tabung
* faktor pembekuan darah