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(Haima=darah, stasis=berhenti)
Yaitu Proses penghentian perdarahan secara spontan dari pembuluh
darah yang mengalami kerusakan.
HEMOSTASIS
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HEMOSTASIS :
is the process which retains the blood within the vascular system.
Hemostatic process is designed to repair the break and arrest
hemorrhage.

The most immediate response to bleeding are from:
1. Vascular
By Vasoconstriction mechanism, which decreases the blood flow
through the injured blood vessel
2. Platelets
Platelets clump together and adhere to the injured vessel in this
area in order to form a plug, and further inhibit bleeding
3. The Coagulation factors
By forming a fibrin meshwork or clot to stop the bleeding
completely
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Hemostasis diperankan oleh 3 faktor:
1. Faktor VASKULER
2. Faktor TROMBOSIT
3. Faktor PEMBEKUAN
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Hemostasis diperankan oleh 3 faktor:
1. Faktor VASKULER
2. Faktor TROMBOSIT
3. Faktor PEMBEKUAN
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Hemostasis diperankan oleh 3 faktor:
1. Faktor VASKULER
2. Faktor TROMBOSIT
3. Faktor PEMBEKUAN
Mekanisme Hemostasis
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Hemostasis or haemostasis (from the Ancient Greek: haimstasis "styptic
(drug)") is a process which causes bleeding to stop, meaning to keep
blood within a damaged blood vessel (the opposite of hemostasis is
hemorrhage)

Hemostatis adalah proses dimana darah dalam sistem sirkulasi tergantung
interaksi dari 5 faktor, yaitu :
1. dinding pembuluh darah,
2. trombosit,
3. faktor koagulasi,
4. sistem fibrinolisis, dan
5. inhibitor.

Hemostasis bertujuan untuk menjaga agar darah tetap cair di dalam
pembuluh, mencegah kehilangan darah karena luka, memperbaiki aliran
darah selama proses penyembuhan luka. Hemostasis juga bertujuan
untuk menghentikan dan mengontrol perdarahan dari pembuluh darah
yang terluka
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Vasoconstriction of a damaged blood vessel
slows the flow of blood and thus helps to limit
blood loss. This process is mediated by:
1. Local controls. Vasoconstrictors such as
thromboxane are released at the site of the injury.
2. Systemic control. Epinephrine released by the
adrenal glands stimulates general vasoconstriction.

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Formation of a Platelet Plug.
When a blood vessel is damaged, the blood is exposed to
collagen fibers in the basement membrane of the vessel .
Platelets stick to collagen and become activated. Activated
platelets release chemicals such as ADP, and thromboxane,
that cause the aggregation of more platelets to the site of
injury. Platelet aggregation results in the formation of a
platelet plug which acts to stem the flow of blood from the
broken vessel.
It is essential that platelets become activated only at the site
of a broken vessel. Otherwise activated platelets would form
plugs and induce clots in inapropriate places. Healthy
vessels secrete an enzyme called prostacyclin that functions
to inhibit platelet activation and aggregation.
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Clotting of Blood
The blood contains about a dozen clotting factors. These factors are
proteins that exist in the blood in an inactive state, but can be called into
action when tissues or blood vessels are damaged. The activation of
clotting factors occurs in a sequential manner. The first factor in the
sequence activates the second factor, which activates the third factor and
so on. This series of reactions is called the clotting cascade.
Blood clotting is the transformation of liquid blood into a semisolid gel.
Clots are made from fibers (polymers) of a protein called fibrin. Fibrin
monomers come from an inactive precursor called fibrinogen. The body
of the fibrinogen molecule has caps on its ends that mask fibrin-to-fibrin
binding sites. If the caps are removed then fibrin monomers polymerize
to form fibrin polymers. This process requires thrombin, the enzyme that
converts fibrinogen to fibrin. This process also requires calcium, which
acts as a kind of glue to hold the fibrin monomers to each other to form
the polymeric fiber. The fibrin fibers form a loose meshwork that is
stabilized by clotting factor XIII. The stabilized meshwork of fibrin fibers
traps erythrocytes, thus forming a clot that stops the flow of blood.
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FASE TROMBOSIT
JUMLAH : 150.000. - 400.000/mm
UMUR : + 10 HARI
DIAMETER : 2 - 3
1 MEGAKARIOSIT : 3.000 - 4.000 TROMBOSIT
DIPENGARUHI : TROMBOPOIETIN (GINJAL) 7 - 8 x
TIDAK BERINTI
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1. ZONA PERIVER
EXTERIOR COAT
UNIT MEMBRANE
SUB MEMBRANE

FUNGSI:
MERUPAKAN TEMPAT ADHESI & AGREGASI
MENGANDUNG RESEPTOR UNTUK KOLAGEN, ADP, THROMBIN
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FILAMEN SUB MEMBRANE
MIKROTUBULI
MIKRO FILAMEN
SUMBER PROTEIN KONTRAKTIL

FUNGSI :
MEMBERI BENTUK TROMBOSIT
PSEUDOPODI (KONTRAKSI WAKTU AGREGASI)
2. ZONA SOL-GEL
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TERSEBAR BEBAS DALAM SITOPLASMA
FUNGSI :
RESPIRASI
EKSKRESI
PRODUKSI
MENYIMPAN / MELEPASKAN ENERGI
MENGATUR RESPON KIMIA TERHADAP STIMULUS
3. ZONA ORGANEL
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3 MACAM GRANULA
1. LISOSOM ENZIM HIDROLITIK
2. GRANULA PADAT a. ATP
b. ADP
c. Ca
++

d. SEROTONIN
e. EPINEPHRINE
f. NOR-EPINEPHRINE
3. GRANULA ALFA a. -TROMBOGLOBULIN
b. PLATELET FAKTOR 4 P4
c. PLATELET DERIVED GROWTH FACTOR PDGF
d. GLIKO PEPTIDA MERANGSANG REPLIKASI
OTOT HALUS DAN FIBROBLAS
e. PROTEIN ~ PLASMA : - F.V
- F. VIII
- FIBRINOGEN
- FIBRONECTIN
f. TROMBOSPONDIN - TSP

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vascular
HEMOSTATIC

PLUG = SUMBATAN
PASE1 : - SUMBATAN AGREGASI
- REVERSIBEL
PASE 2 : - AGGREGASI SEKUNDER
- IRREVERSIBEL


UNTUK AGREGASI DIPERLUKAN:
1. ION KALSIUM
2. FIBRINOGEN
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ADHESI
PERLEKATAN TROMBOSIT PADA PERMUKAAN ASING TERUTAMA SERAT KALOGEN
PERMUKAAN ASING 1. KOLLAGEN
2. MIKROFIBRIL
3. JARINGAN IKAT SUBENDOTEL.
VIII : v WF (FACTOR VIII VON WILLEBRANDS)
1. TROMBIN
2. ADP
3. KOLLAGEN
4. ADRENALIN
5. ADESI - AGREGASI
MEMBRAN TROMBOSIT
TROMBOSIT
FOSFOLIPID
ASAM ARA
KHIDONAT
PROSTA GLANDIN
G2 ( PGG2)
TROMBOKSAN A2
TX A2
REAKSI PELEPASAN AGREGASI
FOSF LIPASE A2
SIKLO
OKSIGENASE
TROMBOKSAN
SINTETASE
5-HT
ADP
TSP
-TG
PF 4
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ADHESI Perlekatan Trombosit pada permukaan Asing
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KELAINAN FAKTOR
TROMBOSIT
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I. KELAINAN JUMLAH
A. TROMBOSITOSIS
B. TROMBOSITEMIA
C. TROMBOSITOPENIA
II. KELAINAN FUNGSI
A. KELAINAN ADESI
B. KELAINAN PELEPASAN
C. KELAINAN AGREGASI
KELAIANAN TROMBOSIT
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A. TROMBOSITOSIS :
Thrombocytosis is the presence of high platelet counts
in the blood, and can be either reactive or primary (also
termed essential and caused by a myeloproliferative
disease). Although often symptomless (particularly
when it is a secondary reaction), it can predispose to
thrombosis in some patients.

Peningkatan jumlah trombosit sementara
- FISIOLOGI : - GERAK BADAN
- PATOLOGIS : - TRAUMA
- KEGANASAN
- PERADANGAN
RANGSANGAN HILANG --------> N
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B. TROMBOSITEMIA :

Thrombocythemia is a myeloproliferative blood
disorder. It is characterized by the production
of too many platelets in the bone marrow. Too
many platelets make normal clotting of blood
difficult.

What causes thrombocythemia?
There is no known cause for thrombocythemia.
- TROMBOSITOSIS YANG MENETAP
- FUNGSI : ABNORMAL
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C. THROMBOCYTOPENIA :
Thrombocytopenia is any disorder in which there are not
enough platelets .

Causes
Thrombocytopenia is often divided into three major
causes of low platelets:

1. Low production of platelets in the bone marrow
2. Increased breakdown of platelets in the bloodstream (called
intravascular)
3. Increased breakdown of platelets in the spleen or liver (called
extravascular)
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TROMBOSITOPENIA
STEM CELL POOL
HYPOPLASIA
IMMATURE
MEGAKARYOEXT
E
POOL
MATURE
DISORDERED
REGULATION
THROMBOPOI
TIC
STIMULI
INEFFECTIVE
THROMBOPOISIS
PLATELET
PRODUCTION
CIRCULATING
PLATELET POOL
SPLENIC
PLATELET
POOL
NORMAL :
70%
30%
10 - 40%
60 - 90%
ABNORMAL POOLING
OR DISTRIBUTION
PLATELET
UTILIZATION
ACCELERATED
DESTRUCTION
ABNORMA
L :
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IDIOPHATIC THROMBOCYTOPENIC PURPURA
AKUT
- ANAK - ANAK : 2 - 6 TAHUN
- =
- LAMANYA: 2 - 6 MINGGU
- REMISI : 80 %
- TROMBOSIT : <20.000/mm
3
KRONIK
PUBERTAS - 50 TAHUN.
>
BEBERAPA BULAN BEBERAPA TAHUN
(-) FLUKTUASI
30.000 - 80.000/mm
3
( I T P )
- UMUR TROMBOSIT :
- 50.000/ mm
3 :

- < 10.000/ mm
3 :

- AUTOANTIBODI :
MELEWATI PLASENTA

2 - 3 HARI (C
r
51)
1 - 2 HARI
< 2 JAM
Ig G
CONGENITAL ITP
PADA ITP AKUT PADA MUSIM DINGIN INFEKSI SALURAN NAPAS ITP
LABORATORIUM : TROMBOSIT
- < 50.000/ mm
3
PERDARAHAN

AN. DEFISIENSI FE

-

DITEMUKAN : MEGATROMBOSIT (GIANT TROMBOSIT)
- WAKTU PERDARAHAN >> RETRAKSI BEKUAN JELEK
- RUMPEL LEEDE TES : (+)
- SS. TL MEGAKARIOSIT ; GRANULA <<
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KELAINAN FUNGSI
TROMBOSIT
1. KELAINAN ADHESI TERHADAP KOLAGEN
- EHLERS-DANLOS SYNDROME (KELAINAN VASKULER)
2. KELAINAN ADHESI TERHADAP SUBENDOTEL
- SINDROMA BERNARD SOULIER (KELAINAN TROMBOSIT )
- SINDROMA VON WILLBRAND (KELAINAN PLASMA )
3. KELAINAN PELEPASAN
- SINDROMA HERMANSKY - PUDIAK
- SINDROMAWISKOTT - ALDRICH DEFISIENSI STORAGE
POOL
- SINDROMA CHEDIAK - HIGASHI
DEFISIENSI CYCLO - OXYGENASE (GANGGUAN MEKANIK
PELEPASAN)
PENYAKIT GLIKOGEN TIPE I (GANGGUAN METABOLISME
NUCLEOTIDE)
4. KELAINAN AGREGASI ADP (KELAINAN TROMBOSIT)
- THROMBASTHENIA GLANZMANN
- AFIBRINOGEMIA