CHAPTER 9
Circulatory System
169
SYNOPSIS 9-3
Pathological and Clinical Terms for the Circulatory System
Vasculitis
: Infl ammation and damage to blood vessels often resulting in ischemia of the tissue served by the affected vessels;
may be related to infection, medications, and various autoimmune disorders.
Angina
: Chest pain associated with ischemia of the myocardium, most often due to severe atherosclerosis of the coronary
arteries; the pain of angina, often described as pressure, is typically substernal but may radiate to the arms or neck.
Myocardial infarction
: Necrosis of cardiac muscle due to interruption of its blood supply, most often due to coronary
artery atherosclerosis.
Atherosclerosis
: The most clinically signiF cant form of arteriosclerosis (“hardening of the arteries”), characterized by the
accumulation of lipid within the intima of arteries producing plaques that cause narrowing, or “stenosis,” of the artery.
Arteriosclerosis
: A general term referring to any hardening (loss of elasticity) of arteries, especially small arteries. High
blood pressure is the most common cause. Atherosclerosis is one form of arteriosclerosis.
Thrombus
: A blood clot formed within an artery or vein as a result of endothelial injury, abnormal blood fl
ow, or an
increased tendency to form clots (hypercoagulability); rupture of an atherosclerotic plaque in a coronary artery promotes
the formation of a thrombus.
CLINICAL CORRELATIONS
Figure 9-12A.
Coronary Artery Atherosclerosis.
H&E,
3
21
Coronary artery atherosclerosis
, also known as
CAD
, is
characterized by the presence of atherosclerotic changes
within the walls of the coronary arteries (see ±ig. 3-3C).
These changes include accumulation of lipid, formation of
atherosclerotic plaques, and thickening of arterial tunica
intima. Eventually, normal blood fl ow to the heart muscle is
impaired or obstructed. Rupture of an atherosclerotic plaque
promotes the formation of a blood clot, or
thrombus
, which
may occlude the lumen of the coronary artery. Angina (car-
diac chest pain), even MI (heart muscle death) (see ±ig. 9-4C),
can develop when blood fl ow is reduced below a certain level.
CAD is a progressive disease process that generally begins in
childhood and manifests clinically in mid-to-late adulthood.
Lifestyle changes to lower blood cholesterol and control
hypertension and diabetes are important in preventing the
disease and reducing the severe consequences.
Figure 9-12B.
Polyarteritis Nodosa (Vasculitis), Small Artery
in Intestine.
H&E,
3
71
Polyarteritis nodosa
is a multisystem
necrotizing vasculitis
of
small and medium-sized muscular arteries in which involve-
ment of renal and visceral arteries is characteristic. Classic
polyarteritis nodosa spares the pulmonary arteries. The cause
of the disease is not clear, but it is associated with hepatitis B
virus infection in 20% to 30% of cases. Symptoms may be
nonspeciF c, making it difF
cult to diagnose. ±ever, weight loss,
and
malaise
are present in more than 50% of cases. Patients
may present with fever, headache, weakness, abdominal pain,
and
myalgias
. Histologically, affected arteries are characterized
by segmental transmural infl ammation. Internal and external
elastic laminae are disrupted, which may lead to aneurysms
and bleeding. Polymorphonuclear leukocytes and mononu-
clear leukocytes are visible in the cellular inF ltrate. Steroids
are the major drugs used to control disease progression.
Fibrous
thickening of the
tunica intima
Central lipid core
(with cholesterol
clefts)
Tunica media
Tunica adventitia
Narrow lumen
Internal elastic
lamina
A
Inflammatory
Inflammatory
leukocytes
leukocytes
Diminished
lumen
of the
small artery
Inflammatory
leukocytes
Fibrous
thickening of the
tunica intima
Disrupted
internal elastic
lamina
B
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