2. Hemostasis - Trombosit

8/11/2019 2. Hemostasis - Trombosit

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Haima=darah, stasis=berhenti) Yaitu Proses penghentian perdarahan secara spontan dari pembuluhdarah yang mengalami kerusakan.

HEMOSTASIS
http://www.infofisioterapi.com/wp-content/uploads/2011/10/Proses-Pembekuan-Darah.jpg


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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 arresthemorrhage .

The most immediate response to bleeding are from:

1. VascularBy Vasoconstriction mechanism, which decreases the blood flowthrough the injured blood vessel

2. PlateletsPlatelets clump together and adhere to the injured vessel in thisarea in order to form a plug, and further inhibit bleeding

3. The Coagulation factors By forming a fibrin meshwork or clot to stop the bleedingcompletely


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Hemostasis diperankan oleh 3 faktor:1. Faktor VASKULER

2. Faktor TROMBOSIT3. Faktor PEMBEKUAN


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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 keepblood within a damaged blood vessel (the opposite of hemostasis ishemorrhage )

Hemostatis adalah proses dimana darah dalam sistem sirkulasi tergantunginteraksi 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 dalampembuluh, mencegah kehilangan darah karena luka, memperbaiki alirandarah selama proses penyembuhan luka. Hemostasis juga bertujuanuntuk menghentikan dan mengontrol perdarahan dari pembuluh darah

yang terluka 8
http://en.wikipedia.org/wiki/Ancient_Greekhttp://en.wikipedia.org/wiki/Antihemorrhagichttp://en.wikipedia.org/wiki/Bleedinghttp://en.wikipedia.org/wiki/Bleedinghttp://en.wikipedia.org/wiki/Antihemorrhagichttp://en.wikipedia.org/wiki/Ancient_Greek


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Formation of a Platelet Plug. When a blood vessel is damaged, the blood is exposed tocollagen fibers in the basement membrane of the vessel .

Platelets stick to collagen and become activated. Activatedplatelets release chemicals such as ADP, and thromboxane,that cause the aggregation of more platelets to the site ofinjury. Platelet aggregation results in the formation of a

platelet plug which acts to stem the flow of blood from thebroken vessel.

It is essential that platelets become activated only at the siteof a broken vessel. Otherwise activated platelets would form

plugs and induce clots in inapropriate places. Healthy vessels secrete an enzyme called prostacyclin that functionsto inhibit platelet activation and aggregation.

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Clotting of Blood The blood contains about a dozen clotting factors. These factors areproteins that exist in the blood in an inactive state, but can be called intoaction when tissues or blood vessels are damaged. The activation ofclotting factors occurs in a sequential manner. The first factor in thesequence activates the second factor, which activates the third factor andso 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 bodyof the fibrinogen molecule has caps on its ends that mask fibrin-to-fibrinbinding sites. If the caps are removed then fibrin monomers polymerizeto form fibrin polymers. This process requires thrombin , the enzyme that

converts fibrinogen to fibrin. This process also requires calcium , whichacts as a kind of glue to hold the fibrin monomers to each other to formthe polymeric fiber. The fibrin fibers form a loose meshwork that isstabilized by clotting factor XIII . The stabilized meshwork of fibrin fiberstraps erythrocytes, thus forming a clot that stops the flow of blood. 11


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FASE TROMBOSITJUMLAH : 150.000. - 400.000/mmUMUR : + 10 HARIDIAMETER : 2 - 3 1 MEGAKARIOSIT : 3.000 - 4.000 TROMBOSITDIPENGARUHI : TROMBOPOIETIN (GINJAL) 7 - 8 xTIDAK BERINTI


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1. ZONA PERIVER

EXTERIOR COATUNIT 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

EKSKRESIPRODUKSI

MENYIMPAN / MELEPASKAN ENERGI

MENGATUR RESPON KIMIA TERHADAP STIMULUS

3. ZONA ORGANEL


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3 MACAM GRANULA1. LISOSOM ENZIM HIDROLITIK

2. GRANULA PADAT a. ATP

b. ADPc. Ca ++

d. SEROTONIN

e. EPINEPHRINE

f. NOR-EPINEPHRINE

3. GRANULA ALFA a. -TROMBOGLOBULIN

b. PLATELET FAKTOR 4 P 4c. 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 KALSIUM2. FIBRINOGEN


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ADHESI Perlekatan Trombosit pada permukaan Asing


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KELAINAN FAKTORTROMBOSIT


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I. KELAINAN JUMLAHA. TROMBOSITOSIS

B. TROMBOSITEMIA

C. TROMBOSITOPENIAII. KELAINAN FUNGSI

A. KELAINAN ADESI

B. KELAINAN PELEPASANC. KELAINAN AGREGASI

KELAIANAN TROMBOSIT


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A. TROMBOSITOSIS :Thrombocytosis is the presence of high platelet countsin the blood , and can be either reactive or primary (alsotermed essential and caused by a myeloproliferativedisease ). Although often symptomless (particularlywhen it is a secondary reaction), it can predispose tothrombosis in some patients.

Peningkatan jumlah trombosit sementara- FISIOLOGI : - GERAK BADAN- PATOLOGIS : - TRAUMA

- KEGANASAN- PERADANGAN

RANGSANGAN HILANG --------> N
http://en.wikipedia.org/wiki/Platelethttp://en.wikipedia.org/wiki/Bloodhttp://en.wikipedia.org/wiki/Myeloproliferative_diseasehttp://en.wikipedia.org/wiki/Myeloproliferative_diseasehttp://en.wikipedia.org/wiki/Thrombosishttp://en.wikipedia.org/wiki/Thrombosishttp://en.wikipedia.org/wiki/Myeloproliferative_diseasehttp://en.wikipedia.org/wiki/Myeloproliferative_diseasehttp://en.wikipedia.org/wiki/Myeloproliferative_diseasehttp://en.wikipedia.org/wiki/Bloodhttp://en.wikipedia.org/wiki/Platelet


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B. TROMBOSITEMIA :

Thrombocythemia is a myeloproliferative blooddisorder. It is characterized by the productionof too many platelets in the bone marrow. Toomany platelets make normal clotting of blooddifficult.

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 .

CausesThrombocytopenia is often divided into three majorcauses of low platelets:

1. Low production of platelets in the bone marrow2. Increased breakdown of platelets in the bloodstream (called

intravascular)3. Increased breakdown of platelets in the spleen or liver (called

extravascular)

TROMBOSITOPENIA


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TROMBOSITOPENIASTEM CELL POOL

HYPOPLASIA

IMMATURE

MEGAKARYOEXTE

POOLMATURE

DISORDEREDREGULATION

THROMBOPOITIC

STIMULIINEFFECTIVE

THROMBOPOISIS PLATELETPRODUCTION

CIRCULATING

PLATELET POOL

SPLENICPLATELETPOOL

NORMAL :

70%

30%

10 - 40%

60 - 90%

ABNORMAL POOLINGOR DISTRIBUTION

PLATELETUTILIZATION

ACCELERATED

DESTRUCTION

ABNORMAL :

IDIOPHATIC THROMBOCYTOPENIC PURPURA


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IDIOPHATIC THROMBOCYTOPENIC PURPURA

AKUT

- ANAK - ANAK : 2 - 6 TAHUN

- = - LAMANYA: 2 - 6 MINGGU- REMISI : 80 %- TROMBOSIT : BEBERAPA BULAN BEBERAPA TAHUN(-) FLUKTUASI30.000 - 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 JAMIg GCONGENITAL 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 FUNGSITROMBOSIT1. 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

Documents

2. Hemostasis - Trombosit