This document discusses atherosclerosis, defined as a disease of arteries characterized by atheromatous plaques composed of lipid cores and fibrous caps. Risk factors include age, gender, genetics, hyperlipidemia, hypertension, smoking, diabetes, obesity, and inactivity. The response-to-injury hypothesis views it as a chronic inflammatory response to endothelial injury, involving modified lipoproteins, macrophages, and T-cells interacting with artery walls. Plaques can rupture, causing thrombosis. Unstable plaques with large lipid cores and thin fibrous caps are more vulnerable to rupture. Advanced lesions can rupture, bleed, aneurysm, or form fatty streaks composed of foam cells.

1. Atherosclerosis
Latha Karuniathi
Farith
Maariah Qibtiah

2. Definition
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Atherosclerosis: disease primarily of elastic arteries and
large/medium sized muscular arteries. It is characterized
by the presence of intimal lesions called atheromas (or
atheromatous or atherosclerotic plaques).
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Atheromatous plaques are raised lesions composed of
soft grumous lipid cores (mainly cholesterol and cholesterol
esters, with necrotic debris) covered by fibrous caps
Atherosclerotic plaques can mechanically obstruct vascular
lumina and are prone to rupture, resulting in catastrophic
vessel thrombosis.
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3. Risk factors
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Age
Male gender
Family history
Genetic abnormalities
Hyperlipidemia
Hypertension
Cigarette smoking
Diabetes
Obesity
Physical inactivity
Hardened unsaturated fat intake

4. Pathogenesis
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Response-to-injury hypothesis, the model views
atherosclerosis as a chronic inflammatory response
of the arterial wall to endothelial injury.
Lesion progression involves interaction of modified
lipoproteins (oxidized lipoprotein), monocyte-derived
macrophages, T lymphocytes, and the cellular
constituents of the arterial wall.

5. Response-to-injury hypothesis
1. Cell injury
2. Accumulation of lipoproteins (mainly oxidized LDL
and cholesterol crystals) in the vessel wall
3. Platelet adhesion
4. Monocyte adhesion to the endothelium, migration
into the intima, and differentiation into macrophages
and foam cells
5. Lipid accumulation within macrophages (foam
cells), which release inflammatory cytokines

6. Response-to-injury hypothesis
6. Smooth muscle cell recruitment due to factors
released from activated platelets, macrophages, and
vascular wall cells
7. Smooth muscle cell proliferation and ECM
production
- Smooth Muscle Proliferation and Matrix
Synthesis
8. Formation of fatty streak
9. Formation of lipid plaque/atheroma/atheromatous
plaque

9. Types of Atherosclerotic Plaque
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Stable plaque and Unstable plaque
Compared to stable atherosclerotic plaques,
unstable plaques that are vulnerable to rupture
contain a larger necrotic lipid core rich in
inflammatory cells and a thinner fibrous cap. LpPLA2 is secreted by inflammatory cells in the lesion
or carried on LDL particles. Lp-PLA2 cleaves oxPC
on the outer surface of oxLDL to generate lysoPC
and oxFA. These two bioactive lipid products
promote necrotic core expansion and thinning of the
fibrous cap. oxFA, oxidized fatty acid.

11. Pathological Changes
The advanced lesion of ATH is the most vulnerable to the
following pathologic changes that have clinical significance:
- Focal rupture, ulceration or lesion of the luminal surface
of atheromatous plaques may result in exposure of highly
thrombogenic substances that induce thrombus formation
or discharge debris into bloodstream, producing
microemboli
- Hemorrhage into a plaque initiated by rupture of either
the overlying fibrous cap or the thin walled capillaries that
vascularize the plaque.
- Aneurysmal dilation may result from ath induced
pressure or ischemic atrophy of the underlying media with
loss of elastic tissue causing weakness and potential
rupture
- Fatty streak composed of lipid laden foam cells

13. Aorta : fatty streaks

14. Aorta : mild, moderate, severe atherosclerosis

15. Thank You