581
CHAPTER FIFTEEN
Cardiovascular System
as the tibial, peroneal, popliteal, or
femoral veins, the consequences can
be serious, particularly if the blood in
the affected vessel clots and blocks
normal circulation. This condition,
called
thrombophlebitis,
introduces
a risk that a blood clot in a vein will
detach, move with the venous blood,
pass through the heart, and lodge in
the pulmonary arterial system in a
lung. Such an obstruction is called a
pulmonary embolism.
Varicose veins
are abnormal and
irregular dilations in superF
cial veins,
particularly in the legs. This condition
is usually associated with prolonged,
increased back pressure in the
ected vessels due to gravity, such
as when a person stands. Crossing
the legs or sitting in a chair so that its
edge presses against the area behind
the knee can obstruct venous blood
²
ow and aggravate varicose veins.
Increased venous back pressure
stretches and widens the veins. The
valves in these vessels do not change
size, so they soon lose their abili-
ties to block the backward flow of
blood, and blood accumulates in the
enlarged regions.
Increased venous pressure is also
accompanied by rising pressure in
the venules and capillaries that sup-
ply the veins. Consequently, tissues
in a±
ected regions typically become
edematous and painful.
Genetics, pregnancy, obesity,
and standing for long periods raise
the risk of developing varicose veins.
Elevating the legs above the level
of the heart or putting on support
hosiery before arising in the morning
can relieve discomfort. Intravenous
injection of a substance that destroys
veins (a sclerosing agent) or surgical
removal of the a±
ected veins may be
necessary.
I
n the arterial disease
atherosclerosis
(ath
er-
o-skle
˘-ro
sis), deposits of fatty materials,
particularly cholesterol, form within the
intima and inner lining of the arterial walls. Such
deposits, called
plaque,
protrude into the lumens
of the vessels and interfere with blood ²
ow (F
g.
15³). ³urthermore, plaque often forms a surface
texture that can initiate formation of a blood
clot, increasing the risk of developing thrombi
or emboli that cause blood deF
ciency (
ischemia
)
or tissue death (
necrosis
) downstream from the
obstruction.
The walls of a±
ected arteries may degener-
ate, losing their elasticity and becoming hard-
ened or
sclerotic.
In this stage of the disease,
called
arteriosclerosis,
a sclerotic vessel may rup-
ture under the force of blood pressure.
Risk factors for developing atherosclero-
sis include a fatty diet, elevated blood pressure,
tobacco smoking, obesity, and lack of physical
exercise (see chapter 18, pp. 703–704). Genetic
factors may also increase the risk of developing
atherosclerosis.
If atherosclerosis so weakens the wall of
an artery that blood pressure dilates a region of
it, a pulsating sac called an
aneurysm
may form.
Aneurysms tend to grow. If the resulting sac
develops by a longitudinal splitting of the middle
layer of the arterial wall, it is called a
dissecting
aneurysm.
An aneurysm may cause symptoms by
pressing on nearby organs, or it may rupture, pro-
ducing great blood loss.
Aneurysms may also result from trauma,
high blood pressure, infections, inherited dis-
orders such as Marfan syndrome, or congenital
defects in blood vessels. Common sites of aneu-
rysms include the thoracic and abdominal aorta
and an arterial circle at the base of the brain (cir-
cle of Willis).
Phlebitis,
or inflammation of a vein, is rela-
tively common. It may occur in association with
an injury or infection or after surgery, or it may
develop for no apparent reason.
If in²
ammation is restricted to a superF
cial
vein, such as the greater or lesser saphenous
veins, blood flow may be rechanneled through
other vessels. But if it occurs in a deep vein, such
15.2
CLINICAL APPLICATION
Blood Vessel Disorders
Lumen
(a)
Lumen
Plaque
(b)
Lumen
Plaque
(c)
FIGURE 15F
Development of atherosclerosis.
(
a
) Normal arteriole (100×). (
b, c
) Accumulation of plaque
on the inner wall of the arteriole (
b
and
c
100×).
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