Wake Cv Atherosclerosis 1

Front 1

"athero"

Back 1

fatty or gruel

Front 2

"sclerosis"

Back 2

harden

Front 3

Atherosclerosis

Back 3

- A variable combination of changes in the INTIMA
of ARTERIES, consisting of FOCAL accumulation of LIPIDS, CELLS, FIBROUS TISSUE, complex carbohydrates, blood,
blood products and calcium, and associated medial changes with progression of disease
- is a form of arteriosclerosis
in which lipids are present. It is by far the
most common form of arteriosclerosis.

Front 4

When can atherosclerosis happen in veins?

Back 4

When a vein is grafted to an arterial point.

Front 5

What is the hallmark build up component of atherosclerosis?

Back 5

lipid

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Arteriosclerosis

Back 6

- more general term
- refers to any proliferative or degenerative stiffening of arteries

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Sites of Greatest Predilection for Development of Atherosclerosis

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1. Coronary Arteries
2. Carotids, Vertebral and basillar arteries and circle of willis
3. In the legs at the femoral and popliteal arteries
(also in the lower aorta, thoracic aorta, internal carotids)

Front 8

Key Functions of the Endothelium

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1. Permeability barrier (limit diffusion)
2. Anti-thrombogenic surface (as long as endothelium is intact)
3. Control of vascular reactivity (NO causes vasodilation)

Front 9

How does cholesterol get through the endothelium?

Back 9

Transcytosis .: higher concentrations of blood cholesterol = higher passing of cholesterol into the wall

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Intracellular Lipids

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(early event)
- Accumulation of esterified cholesterol (EC) in macrophage foam cells (first) and in some smooth muscle cell foam cells (later)
- Some increase in PL to help solublize increased cellular FC

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Extracellular Lipids

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(later event)
- Cholesterol crystals and droplets of EC, associated with necrosis of macrophage foam cells
- Little accumulation of TG

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Connective Tissue (fibrous tissue)
Produced primarily by smooth muscle cells

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Collagen
- Tensile strength
- Synthesis is stimulated by SMCs of Athero. Plaques

Elastin
- Provides elasticity to the arterial wall

Proteoglycans
- Binds LDL/VLDL in sub-endothelial space, which increases retention and facilitates oxidation, etc.

Front 13

What is the only risk factor that by itself will cause artherosclerosis?

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Hypercholesterolemia
(i.e. hypercholesterolemia is the state produced in familial hypercholesterolemia...Stormy Jones)

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Fatty Streaks

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first visible abnormal change in progression to atherosclerosis
- composed of foam cells (that contain cholesterol esters) covered by endothelium
- present in the first decage of life

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Do Fatty streaks progress faster in men or women?

Back 15

Men

Front 16

Role of
Endothelial Cells
in Atherosclerosis

Back 16

endothelial dysfunction occurs early in development of atherosclerosis, and actual desquamation (loss) of endothelial cells does NOT occur until later

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Role of
Macrophages
in Atherosclerosis

Back 17

involved early and late in process
- major intimal cell type early in dz process

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Role of
T cells
in Atherosclerosis

Back 18

early and late, but in smaller numbers than macrophages

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Role of
Smooth Muscle Cells
in Atherosclerosis

Back 19

accumulate in the intima at a later stage than macrophages, (major intimal cell type late)

- think of the smooth muscle cells as the fibroblasts of the vessel

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Role of
Mast Cells
in Atherosclerosis

Back 20

minor component later on

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Role of
Neutrophils
in Atherosclerosis

Back 21

Not usually found in atherosclerotic plaques, except following plaque rupture

Front 22

How does Plaque Rupture Occur?

Back 22

Foam cells often concentrate at the edge (shoulder) of plaques where the plaques are structurally the weakest.

Macrophage foam cells secrete many products, one of which is matrix metalloproteinases (MMPs), that breakdown collagen.

Secretion of MMPs breaks down collagen at the edge of the plaque making it susceptible to rupture.

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How Does Plaque Rupture Lead to Thrombosis and the Acute Coronary Syndrome?

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Rupture of the plaque interrupts the anti-thrombogenic endothelial cell surface

Which exposes blood platelets to underlying collagen and to macrophages that also secrete Tissue Factor.

This causes platelet aggregation which initiates thrombosis.

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What are the roles of EC, FC, PL and TG in atherosclerosis?

Back 24

Esterified cholesterol is the form of cholesterol that can accumulate within macrophages.

Free Cholesterol cannot esist in the cell without killing them (effects on plasma membrane).

Phospholipids increase to solubilize FC.

Triglycerides do not have a role in plaque... but are found in adventitia as energy source.