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1. What is blood clotting?

Blood coagulation, or clotting, is the transformation of blood from a liquid into a
solid gel. Formation of a clot on top of the platelet plug strengthens and supports the
plug, reinforcing the seal over a break in a vessel. Furthermore, as blood in the vicinity
of the vessel defect solidifies, it can no longer flow. Clotting is the bodys most powerful
hemostatic mechanism. It is required to stop bleeding from all but the most minute
Source : Sherwood, Lauren. 2010 . Human Physiology From Cell to Sitem 7th . USA : Brooks/Cole
2. How the mechanism of blood clotting ( hemostasis ) ?

Hemostasis is the arrest of bleeding from a broken blood vesselthat is, the
stopping of hemorrhage (hemo means blood; stasis means standing). For bleeding
to take place from a vessel, there must be a break in the vessel wall and the pressure
inside the vessel must be greater than the pressure outside it to force blood out through
the defect

Hemostasis involves three major steps: (1) vascular spasm, (2) formation of a
platelet plug, and (3) blood coagulation (clotting). Platelets play a pivotal role in
hemostasis. They obviously play a major part in forming a platelet plug, but they also
contribute significantly to the other two steps.

Vascular spasm reduces blood ow through an injured vessel.

A cut or torn blood vessel immediately constricts. The underlying mechanism is

unclear but is thought to be an intrinsic response triggered by a paracrine released
locally from the inner lining (endothelium) of the injured vessel. This constriction, or
vascular spasm, slows blood flow through the defect and thus minimizes blood loss.
Also, as the opposing endothelial surfaces of the vessel are pressed together by this
initial vascular spasm, they become sticky and adhere to each other, further sealing off
the damaged vessel. These physical measures alone cannot completely prevent further
blood loss, but they minimize blood flow through the break in the vessel until the other
hemostatic measures can actually plug up the hole.

Platelets aggregate to form a plug at a vessel tear or cut.

Platelets normally do not stick to the smooth endothelial surface of blood

vessels, but when this lining is disrupted because of vessel injury, platelets adhere to
and are activated by the exposed collagen, which is a fibrous protein in the underlying
connective tissue. When platelets passing by in the blood are exposed to collagen, they
become tethered to the collagen by means of specific membrane proteins, such as
integrin, a cell adhesion molecule that binds with the collagen. This adhesion prevents
these platelets from being swept forward in the circulation. This layer of stuck platelets
forms the foundation of a hemostatic platelet plug at the site of the defect. Collagen
activates the bound platelets. Activated platelets quickly reorganize their actin
cytoskeletal elements to develop spiky processes, which help them adhere to the
collagen and to other platelets. Activated platelets also release several important
chemicals from their storage granules. Among these chemicals is adenosine diphosphate
(ADP), which activates other nearby circulating platelets and causes their surfaces to
become sticky so that they adhere to the fi rst layer of aggregated platelets. These
newly aggregated platelets release more ADP, which causes more platelets to pile on,
and so on; thus, a plug of platelets is rapidly built up at the defect site, in a positive-
feedback fashion. This aggregating process is reinforced by the ADPstimulated
formation of a paracrine similar to prostaglandins, thromboxane A2, from a component
of the platelet plasma membrane. Thromboxane A2 directly promotes platelet
aggregation and further enhances it indirectly by triggering the release of even more
ADP from the platelet granules. Thus formation of a platelet plug involves the three
successive, closely integrated events of adhesion, activation, and aggregation.
Given the self-perpetuating nature of platelet aggregation, why does the platelet
plug not continue to develop and expand over the surface of the adjacent normal vessel
lining? A key reason is that ADP and other chemicals released by the activated platelets
stimulate the release of prostacyclin and nitric oxide from the adjacent normal
endothelium. Both these chemicals profoundly inhibit platelet aggregation. Thus, the
platelet plug is limited to the defect and does not spread to the nearby undamaged
vascular tissue

Clot formation results from a triggered chain reaction involving plasma clotting
CLOT FORMATION The ultimate step in clot formation is the conversion of
fibrinogen, a large, soluble plasma protein produced by the liver and normally always
present in the plasma, into fibrin, an insoluble, threadlike molecule. This conversion into
f brin is catalyzed by the enzyme thrombin at the site of the injury. Fibrin molecules
adhere to the damaged vessel surface, forming a loose, netlike meshwork that traps
blood cells, including aggregating platelets. The resulting mass, or clot, typically appears
red because of the abundance of trapped RBCs, but the foundation of the clot is formed
of fi brin derived from the plasma. Except for platelets, which play an important role in
ultimately bringing about the conversion of fibrinogen to fibrin, clotting can take place
in the absence of all other blood cells. The original fibrin web is rather weak, because
the fi brin strands are only loosely interlaced. However, chemical linkages rapidly form
between adjacent strands to strengthen and stabilize the clot meshwork. This cross-
linkage process is catalyzed by a clotting factor known as factor XIII (fibrin-stabilizing
factor), which normally is present in the plasma in inactive form
THE CLOTTING CASCADE Yet another activated plasma clotting factor, factor X,
converts prothrombin to thrombin; factor X itself is normally present in the blood in
inactive form and must be converted into its active form by still another activated
factor, and so on. Altogether, 12 plasma clotting factors participate in essential steps
that lead to the final conversion of fibrinogen into a stabilized fibrin mesh.
INTRINSIC AND EXTRINSIC PATHWAYS The clotting cascade may be triggered by the intrinsic
pathway or the extrinsic pathway:

Fibrinolytic plasmin dissolves clots.

A clot is not meant to be a permanent solution to vessel injury. It is a transient device to stop
bleeding until the vessel can be repaire
Source : Sherwood, Lauren. 2010 . Human Physiology From Cell to Sitem 7th . USA : Brooks/Cole
3. What are the factors that blood difficult clotting?
The answer :
These factors are designated by roman numerals in the order in which the factors were
discovered, not the order in which they participate in the clotting process.

Factor Number Name

I Fibrinogen
II Prothombin
III Tissue factor
IV Calcium ion
V Proaccelerin (labile
VII Proconvertin (stabile
VIII Hemophilia A factor
IX Hemophilia B factor
X Stuart prower factor
XI Hemophilia C factor
XII Hageman factor
XIII Fibrin Stabilizing Factor
Fitzgerald High molecular weight
Fletcher Prekallekrein

Most of these clotting factors are plasma proteins synthesized by the liver. Normally,
they are always present in the plasma in an inactive form, such as fibrinogen and prothrombin.
Sorces :

Setiati, Siti, dkk. 2015. Internal Medicine. Jakarta : Interna Publishing

Source : Sherwood, Lauren. 2010 . Human Physiology From Cell to Sitem 7th . USA :

4. How long blood can clotting ?

Lee white method : 4 8 minute

5. Explain the relevantion of history of bleeding with kind of bleeding disorder ?

a. Von Willebrand disease
Definition : Heredititary bleeding disorder caused by a deficiency of Von Willebrand factor.
Tipically is an autosomal dominan inheritance
Classification :
There is 3 main variant of von willebrand disease
Quantitative disorder of FVW
Tipe 1 (partial deficiency)
This type of abnormalities are mild, and be come most cases (80% from von
willebrand patient). Followed by decrease from VIII factor
Tipe 3 (Kuantitatif disorder)
This tipe is the severest form. This tipe is rare.
Qualitative disorder of FVW
Tipe 2 (Kualitatif disorder)

Sources :

Hoffbrand, A. V. 2013. Kapita Selekta Hematology . Jakarta : EGC

Setiati, Siti, dkk. 2015. Internal Medicine. Jakarta : Interna Publishing

b. Hemophilia
X link-resesive
There is two classification of hemophilia, that is Hemophilia A and
Hemophilia B
Hemophilia A caused by F. VIII deficiency
Hemophilia B caused by F. IX deficiency
Hemophilia A is 85%, while hemophilia B is 15% of hemophilia cases.
Hemophilia is foun in men, and women mostly carier

The degree of hemophilia disease :

Severe : F. VIII/F. IX activity < 1 %

Moderate : F. VIII/F. IX activity 1-5 %
Mild : F. VIII/F. IX activity 5-30 %

6. What is disorder from the scenario ?