LBM 3.

HEMOSTASIS
STEP 1
1. Ptechiae : is a small purplies spots on the surface the body couse by
a minor hemoraghic
2. Blood clotting : pembekuan darah
STEP 2
1.
2.
3.
4.
5.
6.
7.
8.
9.

What makes the patient easily got bruises?

What are the factor of blood clotting ?
Describe the function platelets in blood clotting?
How the mecanism of blood clotting
How ptechiae can occur?
What is the relation between ptechiae with blood clotting?
What are blood veessel function in hemostasis?
Apa saja kelainan dari hemoistasis? Apa saja terapinya?
Bagaimana hasil pemeriksaan dari pemeriksaan hasil laboratorium
dari skenario ini?

STEP 3
1. Apa definisi dari pembekuan darah?

Doctor C's Medical Guide: What You Need To Know By JOSEPH CIABATTONI, Ph.D.,
M.D.
2. What are the factor of blood clotting ?
1) Fibrinogen : merupakan prekursor fibrin
2) Protombin : protein plasma yang disintesis didalam hepar
yang akan berubah menjadi trombin
3) Tromboplastin : aktifator lipoprotein jaringan pada protombin
4) Kalsium : untuk aktifasi protombin dan pembentukan fibrin
5) Aksilator plasma globulin: suatu faktor plasma yang
mempercepat dari konversi protrombin menjadi trombin
6)
7) Aksilator konversi protombin serum
8) Globulin anti hemolitik

9) Faktor chirsmast : berikatan dengan faktor 3 dan 8 untuk

aktifasi protombin
10)
Faktor stuart power : protein plasma yang disintesis
dalam hati (memerlukan vtamin k) dan berfungsi dalam
mekanisme ektrinsik dan intrinsik
11)
Pendahulu trombo plastin plasma
12)
Hegman : untuk mengaktifasi pta
13)
Penstabil fibrin : protein yang ditemukan dalam plasma
dan trombosit yang berhubungan silang dengan filamen fibrin
14)
Fletcher
15)
Fitgeral

ocw.usu.ac.id/.../his127_slide_farmakologi_hemostasis

http://faculty.ucc.edu/biology-potter/hemostasis.htm
3. How the mecanism of blood clotting ?
Ada 3 sistem
Koagulasi ( disintesis dalam hati, tergantung vitamin k)
Penghambat koagulasi
Sistem fibrinolitik ( membentuk plasmin untuk
menghancurkan fibrin)
Ada 2

Jalur intrinsik ( bahan terdapat dalam aliran darah) perkusor in aktif,

koenzim, kofaktor
Jalur ektrinsik ( bahan dari pembuluh darah yang rusak)

Lalu bergabung yang mengakibatkan faktor 10 menjadi aktif dan

membentuk benang fibrin
Ada 3 faktor

Kerusakan pembuluh darah sendiri

Perubahan protombin menjadi trombin
Trombin sebagai enzim untuk mengubah fibrinogen menjadi benang
fibrin yang merangkai komponen sel darah

The Clotting Process (Hemostasis)

The process by which the body prevents blood loss is referred to as

coagulation.Coagulation involves the formation of a blood clot
(thrombus) that prevents further bloodloss from damaged tissues, blood
vessels or organs. This is a complicated process with a
cellular system comprised of cells called platelets that circulate in the
blood and serve to form a platelet plug over damaged vessels and a
second system based upon the actions of
multiple proteins (called clotting factors) that act in concert to produce a
fibrin clot.These two systems work in concert to form a clot; disorders
in either system can yield disorders that cause either too much or too
little clotting.Platelets serve three primary functions: 1) sticking to the
injured blood vessel (called platelet adherence), 2) attaching to other
platelets to enlarge the forming plug (called platelet aggregation), and 3)
providing support (molecules on the surface of platelets are
required for many of the reactions) for the processes of the coagulation
cascade.When a break in a blood vessel occurs, substances are exposed
that normally are not indirect contact with the blood flow. These
substances (primarily collagen and vonWillebrand factor) allow the
platelets to adhere to the broken surface. Once a plateletadheres to the
surface, it releases chemicals that attract additional platelets to the
damaged area, referred to as platelet aggregation. These two processes
are the first responses to stop bleeding. The protein based system (the
coagulation cascade) serves to stabilize the clot that has formed and
further seal up the wound.

The diagram on the previous page shows many of the reactions in the
coagulation cascade that are necessary to form a clot. As noted above,
the third role of the platelet is to support the coagulation cascade. This
support is provided, in part, by one of the components of the outside of a
platelet, called phospholipids (lipid=fat), which are required for many of
the reactions in the clotting cascade.
The goal of the cascade is to form fibrin, which will form a mesh within
the platelet aggregate to stabilize the clot. All of the factors have an
inactive and an active form.Once activated, the factor will serve to
activate the next factor in the sequence until fibrin is formed.
The coagulation cascade takes place at the site of a break in a blood
vessel that has the platelet aggregate. Tissue factor and factor VIIa (the
a denotes the active form of the factor) activate factor X, forming
factor Xa. Factor Xa is then able to activate prothrombin (also referred
to as factor II) to form thrombin (factor IIa). Thrombin converts
fibrinogen to fibrin (factors I and Ia respectively). Fibrin forms a mesh
that, in concert with the platelets, plugs the break in the vessel wall. The
fibrin mesh is further stabilized by factor XIII, which sews up the clot
(much like forming an intricate network of cross-stitched strands of
fibrin).
There are multiple other interactions detailed on the above diagram. All
of these interactions (and others) are required for coagulation to work
properly. For the purposes of understanding clotting disorders, there are
several that need to be discussed.
Factors that Accelerate Clot Formation:
Factor V and factor VIII (shown in light green) accelerate the
conversion of factor X to factor Xa by factor IXa (this is done by factor
VIII) and accelerate the conversion of prothrombin to thrombin as done
by factor Xa.

Factors that Inhibit (Slow Down) Clot Formation:

Protein C, protein S and thrombomodulin form a complex (group of
proteins) that can inactivate factor VIII and factor V. The protein C,
protein S and thrombomodulin complex is activated by thrombin.
Antithrombin (formerly called antithrombin III) serves to block the
actions of multiple clotting factors (called inhibition). Inhibition is
depicted with the red lines that end in a filled circle. The filled circle
denotes the factor that is inhibited.
Tissue factor pathway inhibitor works to inhibit the formation of factor
Xa.
All of the above interactions are required in order to maintain the
hemostatic balance(hemo=blood, stasis=state of not flowing/moving),
which prevents excessive bleeding or excessive clotting. The following
page depicts the overall process by which hemostasis (clotting) occurs at
the site of injury to a blood vessel.

http://www.med.illinois.edu/hematology/PDF
%20Files/Hemostasis.pdf
4. Describe the function platelets in blood clotting?

Trombosit mengandung dalam pembukaan darah:

Terdapat dalam membran(lapisan glikoprotein, fosfolipid)
Sitoplasma (molekul aktin dan myosin)

Role in Blood Clotting

The damaged platelets release a substance called thromboplastin. This sets in action, a series
of reactions that result in the formation of clots. These clots block the site of the injury,
avoiding excess loss of blood.

Role in Repair of Damaged Endothelium

Endothelium is the inner wall of the blood vessels. The platelets stick to the damaged portion
of the endothelium and prevent loss of blood. The platelets are not allowed to stick to healthy
endothelium by the secretion of a substance called prostacyclin.
Thrombosis is a condition during which a clot is formed in the narrowed portion
of the blood vessels. The narrowing occurs due to the deposition of substances

like the cholesterol. This also prevents secretion of prostacyclin which allows the
platelets to stick to the walls of the vessels. This results in the formation of clots
that can cause blockage of the blood vessels. These blockages in the important
vessels can also lead to death.

Clot Retraction
The clot formed is made denser and smaller by the action of platelets.

Role in Clotting
The blood contains platelets that secrete substances called the thromboplastin on being
damaged. This substance initiates reactions that result in the formation of blood clots. The
blood clots prevent excessive flow of blood
http://www.tutorvista.com/content/biology/biologyii/transportation/components-closed-circulatory-system.php
Trombosit mengandung berbagai macamkomponen yang dibutuhkan dalam
hemostasis antara: (1)yang terdapat disitoplasma seperti: molekul aktin dan
myosin, sisa-sisa reticulum endoplasmadan apparatus golgi, mitokondria dan
system enzim yang mampu membentukADP dan ATP, system enzim yang
mensintesis prostalglandin, factor stabilisasifibrin, dan factor pertumbuhan
(2)Yang terdapat pada membrannya antara lainlapisan glikoprotein dan
mengandung banyak pospolipid yang mengaktifkanberbagai tingkat dalam
proses pembekuan darah
( Guyton dan Hall, 2007; Price,S A dan Wilson, L M ,2006; Sherwood, 2001)

5. Peran dan proses pembuluh darah dalam hemostasis? Siapa yang

berperan dalam pelebaran dan penyempitan pembuluh darah

Membantu untuk menghentikan darah dengan cara vaso

kontriksi (reaksi cepat dalam perlukaan)

(Buku Ajar Fisiologi Kedokteran,Guyton & Hall,edisi 9,EGC)

Vasoconstriction of a damaged blood vessel slows the flow of blood and thus helps
to limit blood loss. This process is mediated by:

Local controls. Vasoconstrictors such as thromboxane are released at the site of the
injury.

Systemic control. Epinephrine released by the adrenal glands stimulates general

vasoconstriction.

http://www.biosbcc.net/doohan/sample/htm/Hemostasis.htm
Damage to small blood vessels and capillaries frequently occurs. When these vessels are damaged,
there are three basic mechanisms that promote hemostasis or the stoppage of bleeding.
Following damage, there is an immediate reflex that promotes vasoconstriction, thus diminishing
blood loss

http://www.mhhe.com/biosci/esp/2002_general/Esp/folder_structure/tr/m1/
s7/trm1s7_3.htm

6. What makes the patient easily got bruises? Macam-macam

perdarahan dibawah kulit?
Karena kekurangan trombosit
Easy bruising can occur when the blood vessels are weakened by diseases
(such as scurvy), medications (such as aspirin, prednisone and
prednisolone), and aging. Easy bruising can also occur because of absent
or deficient blood-clotting elements. Local leakage of blood into the skin
from the capillaries that occurs spontaneously, without injury, and results
in a flat, purplish discolored area is referred to as ecchymosis.
http://www.medicinenet.com/easy_bruising/symptoms.htm
The causes of easy bruising can be put into three main categories.
1. A problem with your platelets: from medications, illness including infections or cancer, and
von Willebrand disease.
2. A clotting problem aka coagulation disorders: coagulation factor deficiency, liver disease,
vitamin K deficiency.

3. A problem with blood vessels and surrounding tissue: physical abuse, vitamin C deficiency,
connective tissue disease.
http://www.dailystrength.org

7. How ptechiae can occur?

Karena permiabelitas nya meningkat, cairan nya banyak keluar,
trombosit menurun, sehingga darah mudah keluar

Textbook of Pediatric Emergency Medicine edited by Gary R. Fleisher,

Stephen Ludwig
8. What is the relation between ptechiae with blood clotting?
9. Pemeriksaan apa yang baik untuk mengetahui fungsi pembekuan

darah?

Fibrinogen : Pemeriksaan fibrinogen berguna untuk mengetahui adanya kelainan pembekuan darah,
mengetahui adanya resiko terjadinya pembekuan darah (peningkatan resiko terjadinya Penyaikt Jantung
Koroner (PJK) dan Stoke) dan mengetahui adanya gangguan fungsi hati
Tes Agregasi Trombosit (TAT) : TAT berguna untuk mengetahui gangguan agregasi
Hiperagregasi berarti peningkatan kecenderungan trombosit membentuk agregasi, sehingga
meningkatkan resiko Stroke dan Penyakit Jantung Koroner
Hipoagregasi berarti trombosit 'malas' membentuk bekuan, sehingga meningkatkan resiko pendarahan.
Waktu Perdarahan (BT) : sebagai pemeriksaan penyaring sebelum operasi untuk mengetahui kelainan
trombosit dan dinding pembuluh darah
Waktu Pembekuan (CT) : sebagai pemeriksaan penyaring sebelum operasi untuk mengetahui kelainan
pembekuan darah (kelainan faktor - faktor pembekuan darah)
PPT : merupakan pemeriksaan untuk mengetahui kelainan faktor pembekuan darah dan memonitor terapi
antikoagulan
Buku Saku Patofisiologi Corwin By Elizabeth J. Corwin

10.
Bagaimana hasil pemeriksaan dari pemeriksaan hasil
laboratorium dari skenario ini? Kekurangan hb, leukosit normal,
trombositnya sangat rendah, dan mengakibatkan sukar membeku
HB low, normal leukocyte and platelet deficiency which made blood
clotting disorder.
And there are some articles which can support the statement from
scenario

 Types of Bleeding Disorders

There are several bleeding disorders that can be inherited (passed down through genetics) or
acquired. Some cause bleeding spontaneously, whereas others cause bleeding following an
accident.
The most common inherited bleeding disorders are:

hemophilia A and B: caused by a deficiency or lack of certain blood

clotting proteins, called factors. This disorder causes heavy or unusual
bleeding

factor II, V, VII, X, XII deficiency: relate to blood clotting problems or

abnormal bleeding problems

von Willebrands disease: the most common inherited bleeding

disorder; caused by a deficiency of von Willebrand factor, which helps
blood platelets clump together and stick to a blood vessel wall

Certain diseases or medical conditions can also cause a deficiency of one or more blood
clotting factors. The most common causes of acquired bleeding disorders are end-stage liver
disease or vitamin K deficiency. According to the American Association of Clinical
Chemistry (AACC), this is because most blood clotting factors are produced in the liver, and
certain clotting factors are vitamin k dependent (AACC, 2011).
Identification of Bleeding Disorders| Symptoms
The main sign of a bleeding disorder is prolonged or excessive bleeding. The bleeding is
normally heavier than normal and unprovoked.
Other signs of a bleeding disorder include:

unexplained bruising

heavy menstrual bleeding

frequent nosebleeds
http://www.healthline.com/health/bleeding-disorders#Types

But for the valid result we can do this,

Laboratory Testing

These tests should be performed at a specialized coagulation laboratory and interpreted by a

pathologist or clinician with expertise in coagulation, vascular medicine or hematology.
Ideally, the tests should be done when you are not having an acute clotting event.
The most common lab tests include:

PT-INR: The prothrombin time (PT or protime) test is used to calculate

your International Normalized Ratio (INR). The information is used to
monitor your condition if you are taking warfarin (Coumadin). Your INR will
help your healthcare provider determine how fast your blood is clotting
and whether your warfarin (Coumadin) dose needs to be changed.

Activated partial thromboplastin time (aPTT): Measures the time it

takes blood to clot. This test is used to monitor your condition if you are
taking heparin.

Fibrinogen level

Complete blood count (CBC)

http://my.clevelandclinic.org/heart/disorders/vascular/hypercoagstate.aspx

Hematologi Kapita Selekta

11.

Apa saja kelainan dari hemoistasis? Apa saja terapinya?

Kapita Selekta Hematology, A.V Hoffbrand et all menyebutkan bahwa

gangguanhemostasis (perdarahan abnormal) dapat disebabkan oleh
beberapa hal dibawah ini:
1. Kelainan vaskulerKelainan vaskuler adalah sekelompok keadaan
heterogen, yang ditandai olehmudah memar dan perdarahan spontan
dari poembuluh darah kecil. Kelainan yang mendasari terletak pada
pembuluh darah itu sendiri atau dalam jaringanikat perivaskular. Pada
keadaan dseperti ini, uji penyaring standart memberhasil normal. Masa
perdarahan normal, uji hemostasis lain juga normal.Kelainan vaskular
ini terdapat dua jenis yakni herediter yang berupaTelangiektasia
hemoragik herediter, serta kelainan jaringan ikat. Jenis yanglain adalah
Defek vaskular.
2. TrombositopeniaTrombositopenia didefinisikan sebagai jumlah
trombosit kurang dari100.000/mm3. Biasanya ditandai dengan purpura
kulit spontan, perdarahanmukosa, dan perdarahan berkepanjangan
setelah trauma. Beberapa penyebabtrombositopenia antara lain:
(1)Kegagalan produksi trombosit .Ini merupakanpenyebab tersering
trombositopenia yang biasanya juga merupakan bagian darikegagalan
sumsum tulang generalisata. Penekanan megakarisit selektif
dapatdisebabkan oleh toksisitas obat atau infeksi virus. (2)Peningkatan
destruksitrombosit, Hal ini dibagi menjadi beberapa jenis yakni:
a.Trombositopeniaimun,termasuk di dalamnya ITP, karena infeksi,
purpura pascatranfusi,Trombositopenia imun karena diinduksi obat,
b.Purpura trombositopeniatrombotik c.Koagulasi intravaskular
diseminata, (3)Distribusi trombositabnormal, (4)Kehilangan akibat

dilusi, yakni berupa transfuse masif darahsimpan pada pasien dengan

perdarahan.
3. Gangguan koagulasiBisa karena herediter maupun didapat, yang
umumnya menggangu faktor-faktorkoagulasi.a.Herediter : hemofilia A dan
hemofilia Bb.Didapat : defisiensi vitamin K dan penyakit hati
4. Gangguan fungsi trombositDibagi menjadi dua jenis, yakni:
a.Didapat 1) karena obat anti trombosit seperti
aspirin,2).hiperglobulinemia,3).kelainan mieloproliferatif dan
mielodisplastik , serta 4)Uremia
b.Kelainan herediter 1) Trombastenia, 2)Sinsrom Bernard soulier, 3)
Penyakitpenyimpanan
Buku Ajar Patologi,Edisi 7.EGC
-Hemofili A

Penyakit yang diturunkan

Perdarahan karena gangguan koagulopati

Kekurangan faktor VII C

Terapi :
Tranfusi plasma

Tranfusi faktor VIII

Rekombinan Faktor VIII

Desmopresin Asetat (untuk Hemophili ringan)

Hindari aspirin

-Hemofili B

Penyakit perdarahan

Gangguan koagulasi

Kekurangan Faktor IX

Terapi :

Tranfusi Plasma

Hindari Aspirin

itsuki.files.com/2007/01/hemostasis.ppt

12.
13.

Apa hubungan demam dengan skenario!

Mekanisme penutupan luka oleh trombosit?

www.artikelbiologi.com