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Unformatted text preview: ts the large and medium-sized arteries of
almost every human in societies in which
cholesterol-rich foodstuffs are abundant.
Begins in childhood and, in the absence of
accelerating factors, develops slowly until it is
widespread in old age.
May be accelerated by a wide variety of genetic
and environmental factors.
It has been calculated that atherosclerosis is the
underlying cause of about 50% of all deaths. Risk Factors for Atherosclerosis
Weight fluctuations/ sedentary life-style
Ineffective stress management
3. Low-density serum lipoproteins breach intimal layer
Simultaneously, platelets aggregate at the site
Media smooth muscle cells, normally confined to the other
tunicas, drawn to the intima where they proliferate
4. Result: atherosclerotic plaque, primarily composed of
smooth muscle cells, lipoproteins, and inflammatory debris
5. Plaques slowly enlarge, the orifice of the artery is
decreased and perfusion is diminished
6. Can lead to hypertension, cardiac (CAD) and renal
disease, peripheral arterial disease, stroke and myocardial
infarction Pathogenesis of
It is characterized by localized fibrous thickenings of the
arterial wall associated with lipid-infiltrated plaques that
may eventually calcify.
Old plaques are prone to ulceration and rupture, triggering
the formation of thrombi that obstruct flow.
Leads to vascular insufficiency in the limbs, abnormalities
of the renal circulation, and dilations (aneurysms).
Leads to common severe and life-threatening diseases of
the heart and brain because of formation of intravascular
clots at the site of the plaques.
Possibility---high concentrations of cholesterol in the serum
in the form of low-density lipoproteins are transported into
muscle tissues of an artery where they cause irritation.
This process causes structural alterations leading to the
formation of plaque.
formation Progression of
Atherosclerosis Clinical Manifestations
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This document was uploaded on 03/25/2014.
- Spring '14