542
UNIT FOUR
Prevention of Coagulation
In a healthy cardiovascular system, the endothelium of the
blood vessels partly prevents spontaneous blood clot for-
mation. This smooth lining lowers the risk of platelets and
clotting factors accumulating. Endothelial cells also produce
a prostaglandin (see chapter 13, p. 491) called
prostacyclin
(PGI
2
), which inhibits the adherence of platelets to the inner
surface of healthy blood vessel walls.
When a clot is forming, fibrin threads latch onto or
adsorb
thrombin, thus helping prevent the spread of the clot-
ting reaction. A plasma alpha globulin,
antithrombin,
inac-
tivates additional thrombin by binding to it and blocking its
action on F brinogen. In addition, basophils and mast cells in
the connective tissue surrounding capillaries secrete the anti-
coagulant
heparin.
This substance interferes with formation
of prothrombin activator, prevents the action of thrombin on
F
brinogen, and promotes removal of thrombin by antithrom-
bin and F
brin adsorption. Heparin and another compound,
coumadin (warfarin), are used to prevent abnormal clotting.
Thrombocytopenia
(throm
bo-si
to-pe
ne-ah) occurs when the
platelet count drops below 100,000 platelets per microliter of blood.
Symptoms include bleeding easily; capillary hemorrhages through-
out the body; and small, bruiselike spots on the skin called petechiae.
Thrombocytopenia is a common side eF
ect of cancer chemotherapy
and radiation treatments and can be a complication of pregnancy,
leukemia, bone marrow transplantation, infectious disease, cardiac
surgery, or anemia. Conventional treatment is transfusion of plate-
lets. Treatment with thrombopoietin (TPO) stimulates formation and
maturation of megakaryocytes and thereby boosts platelet levels.
travels and then blocks a vessel that supplies a vital organ,
such as the lungs (pulmonary embolism), affects the portion
of the organ that the blocked blood vessel supplies.
Drugs based on “clot-busting” biochemicals can be lifesavers.
Tissue
plasminogen activator
(tPA) may restore blocked coronary or cerebral
circulation if given within an hour of a heart attack or within three
hours of a stroke.
Abnormal clot formations are often associated with con-
ditions that change the endothelial linings of vessels. ±or
example, in
atherosclerosis
(ath
er-o
skle-ro
sis), accumu-
lations of fatty deposits change arterial linings, sometimes
initiating inappropriate clotting. This is the most common
cause of thrombosis in medium-sized arteries
(f g. 14.20)
.
Clinical Application 14.3 discusses deep vein thrombosis.
Coagulation may also occur in blood fl
owing too slowly.
The concentration of clot-promoting substances may increase
to a critical level instead of being carried away by more rap-
idly moving blood, and a clot may form. This imbalance is
the usual cause of thrombosis in veins.
PRACTICE
40
Distinguish between extrinsic and intrinsic clotting mechanisms.
41
What is the major event in blood clot formation?
42
What factors initiate the formation of ±
brin?
43
What prevents the formation of massive clots throughout the
cardiovascular system?
44
Distinguish between a thrombus and an embolus.
45
How might atherosclerosis promote the formation of blood clots?
Lumen
Lumen
Artery wall
Plaque
Artery wall
(a)
(b)
FIGURE 14.20
Artery cross sections. (
a
) Light micrograph of a normal artery (50
×
). (
b
) The inner wall of an artery changed as a result of
atherosclerosis (100
×
).
previous page 572 David Shier Hole's Human Anatomy and Physiology 2010 read online next page 574 David Shier Hole's Human Anatomy and Physiology 2010 read online Home Toggle text on/off