Normal

Hemostasis
Tutor 2
 Hemostasis
Adalah proses kompleks yang terjadi secara spontan dan
terlokalisir yang melibatkan trombosit, faktor2 pembekuan,
dan endotel yang berfungsi untuk menghentikan perdarahan
dan mempertahankan darah tetap dalam keadaan cair di
dalam pembuluh darah.
The general sequence of events leading to hemostasis at a site of vascular
injury
a. Vasoconstriction
• occurs immediately and transient.
• It is mediated by reflex neurogenic mechanisms and
augmented by the local secretion of factors such as
endothelin, a potent endothelium-derived
vasoconstrictor.

b. Primary hemostasis: the formation of the

platelet plug.
• Disruption of the endothelium exposes subendothelial
von Willebrand factor (vWF) and collagen, which
promote platelet adherence and activation.
• Activation of platelets results shape change, as well
as the release of secretory granules.
• the secreted products recruit additional platelets,
which undergo aggregation to form a primary
hemostatic plug
• Platelet adhesion
o is mediated largely via interactions with vWF, which acts as a bridge between
the platelet surface receptor glycoprotein Ib (GpIb) and exposed collagen.
• Platelets rapidly change shape
o This change is accompanied by alterations in glycoprotein IIb/IIIa that
increase its affinity for fibrinogen (see later), and by the translocation of
negatively charged phospholipids (particularly phosphatidylserine) to the
platelet surface
• Secretion (release reaction) of granule contents occurs along with changes
in shape -> platelet activation
o triggered by a number of factors, including coagulation factor thrombin and
ADP
o Thrombin activates platelets through a special type of G-protein– coupled
receptor referred to as a protease-activated receptor (PAR),
o Activated platelets also produce the prostaglandin thromboxane A2 (TxA2), a
potent inducer of platelet aggregation.
• Platelet aggregation
o The conformational change in glycoprotein IIb/IIIa that occurs with platelet
activation allows binding of fibrinogen that forms bridges between adjacent
platelets, leading to their aggregation.
o Thrombin also converts fibrinogen into insoluble fibrin, cementing the platelets in place and
c. Secondary hemostasis: deposition of fibrin.
• Tissue factor is also exposed at the site of injury.
• Tissue factor binds and activates factor VII,
setting in motion a cascade of reactions that
culiminates in thrombin generation.
• Thrombin cleaves circulating fibrinogen into
insoluble fibrin, creating a fibrin meshwork, and
also is a potent activator of platelets, leading to
additional platelet aggregation at the site of
injury. This sequence, referred to as secondary
hemostasis

d. Clot stabilization and resorption

• At this stage, counterregulatory mechanisms
(e.g., tissue plasminogen activator, t-PA) -> limit
clotting to the site of injury (Fig. 4-4D) and
eventually lead to clot resorption and tissue
repair.