Hemostasis is a complex
process which changes blood from a fluid to a solid state. Intact blood vessels
are central to moderating blood's tendency to clot. The endothelial cells
of intact vessels prevent thrombus formation by secreting tissue plasminogen
activator (t-PA) and by inactivating thrombin and adenosine diphosphate (ADP).
Injury to vessels overwhelms these protective mechanisms and hemostasis ensues.
Hemostasis proceeds in two phases: primary and secondary hemostasis.
- Primary hemostasis
is characterized by vascular contraction, platelet adhesion
and formation of a soft aggregate plug. It
begins immediately after endothelial disruption. Injury causes temporary
local contraction of vascular smooth muscle. Vasoconstriction slows blood
platelet adhesion and activation.
- Adhesion occurs
when von Willebrand factor(vWf) produced by endothelial cells near the injury attaches to the
exposed subendothelial collagen. Next, glycoproteins on the platelet surface adhere
to the "sticky"
von Willebrand factor(vWf).
Platelets collect across the injured surface. These platelets are then
"activated" by contact with collagen. Collagen-activated platelets
form pseudopods which stretch out to cover the injured surface and bridge
exposed collagen fibers. The collagen-activated platelet membranes expose receptors
which bind circulating fibrinogen to their surfaces. Fibrinogen has
platelet binding sites. An aggregation of platelets and fibrinogen build
up to form a soft plug. Platelet aggregation occurs about 20 seconds
short lived. The immediate post injury vascular constriction abates
quickly. If flow is allowed to increase, the soft plug could be
sheared from the injured surface, possibly creating emboli.
- Secondary hemostasis
is responsible for stabilizing the soft clot and maintaining vasoconstriction.
Vasoconstriction is maintained by platelet secretion of serotonin, prostaglandin
and thromboxane. The soft plug is solidified through a complex interaction
between platelet membrane, enzymes, and coagulation factors.
- Coagulation factors
are produced by the liver and circulate in an inactive form until the
coagulation cascade is initiated. The cascade occurs in steps. The completion
of each step activates another coagulation factor in a chain reaction
which leads to the conversion of fibrinogen to fibrin.
spasm, platelet plug formation, and clot formation all help to stop excessive
blood loss after tissue injury.