Hemostasis - Mechanism

Hemostasis - Mechanism
As soon as the blood vessel rupture exposing the components inside the
vessel wall into the blood and blood leaks outside the vessels, the hemostasis
mechanism is triggered. It can be completed within seconds (around 15
seconds) or may take several hours based on the physiological and
biochemical status of the person and the site and the degree of blood vessel
rupture.
It is a complex process that can be described into three major steps viz.
vascular spasm, platelet plug formation, coagulation, and the last step of
fibrinolysis.
Vascular Spasm
Vascular spasm, also known as vasoconstriction, is the initial response that
falls in primary hemostasis. As the endothelium cells are damaged during the
vascular rupture, endothelin-1 (a vasoconstrictor) is released which mediates
the vasoconstriction. The damaged endothelium of the vessel exposes other
chemical components like sub-endothelial collagen, ATP (adenosine
triphosphate), von Willebrand factor, and inflammatory mediators into the
circulation. All of these promote vasoconstriction.
The sub-endothelial collagens and von Willebrand factors promote platelet
accumulation and adhesion in that ruptured site. The attached platelets
rupture and release serotonin, ADP (adenosine diphosphate), and
thromboxane A2. All these components of the platelets further increase
vasoconstriction. During the rupture of the blood vessel, local pain receptors
initiate reflexes which further promote the vascular spasm.
The effect of vascular spasm is more promising in smaller vessels with minor
rupture. The effect may last for 30 minutes to several hours.
Platelet Plug Formation

The freely floating platelets in the circulation begin to clump together forming
spiked and sticky platelet clumps and attaching over the exposed vesicular
lining and collagen. Under the influence of von Willebrand factors, the platelet
plug stabilizes and further accumulates over the exposed endothelial tissue.
These attached platelets release their contents, mainly the ADP, further
attracting other platelets toward that site. These platelets bound with collagen
and endothelial lining form a temporary seal called the platelet plug.
The platelet plug temporarily seals the vessel and prevents or slows down the
rate of blood loss. This process results in primary hemostasis. Once the platelet
plug is formed, the clotting factors are activated and the secondary hemostasis
(blood coagulation process) begins.
Coagulation (Clotting)
Blood coagulation also called blood clotting, is the process of solidification of
the blood due to the formation of fibrin fiber-associated blood clots. It is the
secondary hemostasis stage and results in a stable solid blood clot. The overall
process completes three major tasks; first, the activation of clotting factors,
second the conversion of prothrombin into thrombin, and finally the
conversion of fibrinogen into fibrin fiber.
Coagulation Pathways
The coagulation process, also called coagulation cascade, is initiated through
two different pathways; the extrinsic pathway and the intrinsic pathway,
leading to a final common pathway of activating and stabilizing fibrin. The
fibrin traps the platelets and blood cells forming a stable, gelatinous, and
robust clot that ceases the hemorrhage.
The Extrinsic Pathway (Tissue Factor Pathway)
It is one of the initial cascades leading to the activation of factor X. It is a very

fast and explosive pathway that begins immediately after the exposure of
tissue factor (factor III) on circulation, and is completed within about 15
seconds of the exposure. It is induced by the tissue factor, hence the pathway
is also known as the tissue factor pathway.
Factor III (TF) contacts factor VII (FVII) in circulation and forms the TF-FVIIa
complex (activated FVII). The TF-FVIIa complex then leads to the activation of
factor X (FX) triggering the common pathway.
The Common Pathway

It is the final stage of the blood coagulation cascade which begins after the
activation of factor X. The activated factor X (FXa) combines with activated
factor V (FVa) and the Ca+2 ions on the phospholipid (PL) surface of the
platelets and forms the prothrombinase complex. This complex activates the
prothrombin (factor II) into thrombin (activated factor II (FIIa)).
Thus formed thrombin serves two primary functions; first, it activates

fibrinogen (factor I) into fibrin (activated factor I (FIa)), and second, it activates
fibrin stabilizing factor (Factor XIII (FXIII)) into activated form (activated factor
XIII (FXIIIa)). The FXIIIa then stabilizes the fibrin fiber leading to the formation
of a stable fibrin blood clot.
Fibrinolysis
It is the process of degradation of the fibrin fiber to remove the blood and
restore normal blood flow. After the formation of a blood clot healing of the
ruptured vessels begins. When the vessel is completely healed, then the fibrin
is lysed in a complex process called fibrinolysis.
Factor XII, protein catabolizing enzymes, and other co-factors activate the
plasminogen into plasmin. The activated plasmin then gradually breaks down
the fibrin degrading the stable clot.
If the process is induced via chemicals or physical stress, then the process of
degradation of the fibrin blood clot is called thrombolysis.
After fibrinolysis/thrombolysis, the blood clot is removed, and the blood
circulation continues as usual.

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Hemostasis - Mechanism

Platelet Plug Formation

It is one of the initial cascades leading to the activation of factor X. It is a very

The Common Pathway

Thus formed thrombin serves two primary functions; first, it activates

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