646
UNIT 4
Maintenance of the Body
17
Hemostasis
Describe the process of hemostasis. List factors that limit
clot formation and prevent undesirable clotting.
Give examples of hemostatic disorders. Indicate the cause
of each condition.
Normally, blood flows smoothly past the intact blood vessel lin-
ing (endothelium). But if a blood vessel wall breaks, a whole
series of reactions is set in motion to accomplish
hemostasis
(he
0
mo-sta
9
sis), which stops the bleeding (
stasis
5
halting).
Without this plug-the-hole defensive reaction, we would quickly
bleed out our entire blood volume from even the smallest cuts.
Te hemostasis response is fast, localized, and carefully con-
trolled. It involves many
clotting factors
normally present in
plasma as well as several substances that are released by platelets
and injured tissue cells. During hemostasis, three steps occur in
rapid sequence
(Figure 17.13)
:
1
vascular spasm,
2
platelet
plug formation, and
3
coagulation (blood clotting). Following
hemostasis, the clot retracts. It then dissolves as it is replaced by
fibrous tissue that permanently prevents blood loss.
Step 1: Vascular Spasm
In the first step, the damaged blood vessels respond to injury
by constricting (vasoconstriction) (Figure 17.13
1
). Factors
that trigger this
vascular spasm
include direct injury to vas-
cular smooth muscle, chemicals released by endothelial cells
and platelets, and reflexes initiated by local pain receptors.
Te spasm mechanism becomes more and more efficient as
the amount of tissue damage increases, and is most effective
in the smaller blood vessels. Te spasm response is valuable
because a strongly constricted artery can significantly reduce
blood loss for 20–30 minutes, allowing time for the next two
steps, platelet plug formation and blood clotting, to occur.
Step 2: Platelet Plug Formation
In the second step, platelets play a key role in hemostasis by ag-
gregating (sticking together), forming a plug that temporarily
seals the break in the vessel wall (Figure 17.13
2
). Tey also
help orchestrate subsequent events that form a blood clot.
As a rule, platelets do not stick to each other or to the smooth
endothelial linings of blood vessels. Intact endothelial cells re-
lease nitric oxide and a prostaglandin called
prostacyclin
(or
PGI
2
). Both chemicals prevent platelet aggregation in undam-
aged tissue and restrict aggregation to the site of injury.
However, when the endothelium is damaged and the under-
lying collagen fibers are exposed, platelets adhere tenaciously to
the collagen fibers. A large plasma protein called
von Willebrand
factor
stabilizes bound platelets by forming a bridge between
collagen and platelets. Platelets swell, form spiked processes, be-
come stickier, and release chemical messengers including the
following:
Adenosine diphosphate (ADP)
—a potent aggregating agent
that causes more platelets to stick to the area and release their
contents
stamps and seeding the blood with platelets. Te plasma mem-
branes associated with each fragment quickly seal around the
cytoplasm to form the grainy, roughly disc-shaped platelets (see
±able 17.2), each with a diameter of 2–4 μm. Each microliter of
blood contains 150,000 to 400,000 tiny platelets.
Check Your Understanding
6.
Which WBCs turn into macrophages in tissues? Which other
WBC is a voracious phagocyte?
7.
Platelets are called “thrombocytes” in other animals. Which
term that you’ve just learned relates to this name? What
does this term mean?
8.
Amos has leukemia. Even though his WBC count is
abnormally high, Amos is prone to severe infections,
bleeding, and anemia. Explain.
For answers, see Appendix H.
Collagen
fibers
Platelets
Fibrin
Step
Vascular spasm
• Smooth muscle contracts,
causing vasoconstriction.
Step
Platelet plug
formation
• Injury to lining of vessel
exposes collagen Fbers;
platelets adhere.
• Platelets release chemicals
that make nearby platelets
sticky; platelet plug forms.
Step
Coagulation
• ±ibrin forms a mesh that traps
red blood cells and platelets,
forming the clot.
1
2
3
Figure 17.13
Events of hemostasis.
previous page 680 Human Anatomy and Physiology (9th ed ) 2012 read online next page 682 Human Anatomy and Physiology (9th ed ) 2012 read online Home Toggle text on/off