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Pathobiology > Atherosclerosis > Flashcards

Atherosclerosis Flashcards

1
Q

What is arteriosclerosis vs atherosclerosis?

A

Arteriosclerosis - umbrella term meaning hardenining of arteries and loss of elasticity of vessel wall

Atherosclerosis - Arteriosclerosis caused by buildup of cholesterol plaques known as atheromas

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2
Q

When does atherosclerosis begin and when is it typically detected?

A

Begins early and has an insidious progression

Typically detected from late-stage lesions leading to overt disease such as ischemia or infarction of heart/brain, kidney, or gangrene of lower extremities

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3
Q

What types of arteries does atherosclerosis tend to affect, and at what points in the vessels?

A

Elastic and large to medium-sized muscular arteries. Lesions occur at vessel branch points and origins of exiting vessels.

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4
Q

What are the three general lesion types of atherosclerosis?

A
  1. Fatty streaks
  2. Atherosclerotic plaques (also called fibrous)
  3. Complicated plaques
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5
Q

What are the characteristic features of a fatty streak and what cell types are present?

A

Earliest stage of atherosclerotic lesion, even found in children / adolescents.

Flat or slightly elevated lesion which is made of lipid rich foam cells which does not interfere with flow. Foam cells are from intracellular inclusions in:

  1. Macrophages / monocytes
  2. Smooth muscle cells

No fibrosis / necrosis

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6
Q

What type of plaque is the “hallmark” of atherosclerosis and what are its structural sections?

A

Atherosclerotic (atheromatous / fibrous) plaque

  1. Fibrous capsule
  2. Necrotic center, containing cellular debris, cholesterol crystals, and plasma proteins
  3. Neovascularization around peripheral w/inflammatory cells at base and sides
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7
Q

What cell types are primarily present in atheromatous plaques? What produces the extracellular matrix?

A
  1. Smooth muscle cells - proliferate and produce the extracellular matrix (collagen / elastic fibers)
  2. Monocytes / macrophages
  3. T lymphocytes
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8
Q

What is the overall effect of a proliferating atherosclerotic plaque, and are lipids extracellular or intracellular?

A

Can lead to a progressive stenosis overtime, and even fully occlude a vessel, leading to ischemia.

Lipids - extracellular in the form of cholesterol crystals, AND intracellular in macrophages and smooth muscle cells (foam cells)

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9
Q

What are the two classifications of atherosclerotic plaques?

A

Stable - less likely to rupture - more fibrous ca component

Unstable - more vulnerable to rupture - more lipid corecomponent (softer, easier to break off)

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10
Q

What percentage stenosis of the arteries is considered critical, and, other than ischemia, why is this bad?

A

> 70%

Bad because turbulent blood flow distal to the stenosis caused by the plaque can induce endothelial damage, forming a complicated lesion

Further, may produce symptoms of insufficiency which cannot be compensated (angina, intermittent claudication, etc)

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11
Q

What are the five outcomes / types of complicated lesions (advanced atherosclerotic plaques)

A
  1. Calcification (dystrophic)
  2. Ulceration / focal rupture
  3. Thrombosis
  4. Hemorrhage into the plaque
  5. Aneurysmal dilatation of vessel wall
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12
Q

What happens in dystrophic calcification of the lesion?

A

The flexibility of the vessel wall is reduced

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13
Q

What happens in ulceration or focal rupture of the lesion?

A

Plaque contents may embolize

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14
Q

What happens in thrombosis of the lesion?

A

Partial or complete occlusion of the vessel, caused by clot forming on damaged endothelium

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15
Q

What happens in hemorrhage into the plaque?

A

Can cause acute expansion or rupture of the plaque (leading to ulceration or thrombosis)
-> bleeding into the intimal layer

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16
Q

What happens to cause aneurysmal dilataion of the vessel?

A

Plaque erodes into the tunica media, causing loss of elastic tissue and smooth muscle cells due to pressure from plaque, ischemic atrophy, or inflammatory damage
-> vessel ultimately balloons out

17
Q

Under what circumstances is an acute arterial occlusion likely to occur?

A

Plaque ulceration / rupture or hemorrhage into the plaque leading to rupture, causing subsequent thrombosis

This is most likely in unstable plaques

18
Q

Where is the most common site for an aneurysm?

A

Abdominal aorta

19
Q

What are the non-modifiable, major risk factors for atherosclerosis?

A
  1. Increased age
  2. Male gender (estrogen is protective)
  3. Genetics (family history of AS, genetic condition associated with AS)
20
Q

What are modifiable major risk factors for atherosclerosis?

A
  1. Hyperlipidemia
  2. Diabetes mellitus
  3. Hypertension
  4. Cigarette smoking
21
Q

What three labs are considered minor risk factors for AS?

A
  1. Increased homocysteine level
  2. Increases blood lipoprotein Lp(a) level
  3. Increased C-reactive protein level (stroke)
22
Q

What are the other minor risk factors for AS?

A

Lifestyle changes (other than cigarette smoking)

i.e. Diet, lifestyle, physical activity, obesity, presence of metabolic syndrome, etc

23
Q

Which lipoprotein particles have the greatest fraction of triglycerides, cholesterol, and proteins?

A

Triglycerides - Chylomicrons > VLDL

Cholesterol - LDL

Proteins - HDL (Remember this carries HDL to the liver from extrahepatic tissues)

24
Q

What four lipoprotein abnormalities are found in those with a high incidence of MI?

A
  1. Increased LDL levels
  2. Decreased HDL levels
  3. Increased chylomicrons remnants / IDL
  4. Increased abnormal lipoprotein (a) levels (a minor risk factor)
25
Q

How are free radicals thought to play a part in atherosclerosis pathogenesis?

A

By initiating the process of lipid peroxidation, oxidized LDL becomes chemotactic to blood monocytes and holds immune cells within the plaque. Furthermore, oxidized lipids are toxic to endothelial and smooth muscle cells, and further facilitate the development of foam cells and expansion of plaques.

26
Q

What dietary consumption is associated with higher risk for atherosclerosis?

A

Higher intake of cholesterol, saturated fats, and trans fatty acids

27
Q

What are the five major cell types of the atherosclerotic plaque?

A
  1. Monocytes / Macrophages
  2. Platelets
  3. Smooth muscle cells
  4. Endothelial cells
  5. Lymphocytes (T cells)
28
Q

What growth factors are thought to underlie the proliferation of SMCs into the intima?

A
  1. PDGF - platelet-derived growth factor
  2. FGF - fibroblast growth factor
  3. Heparin-like compounds (inhibitory growth factor)
29
Q

What experimental evidence exists for the role of smooth muscle cells in controlling their own proliferation in the atherosclerotic plaque?

A
  1. SMCs from young rats implanted into plaques of old rats did not proliferate
  2. SMCs from old rats implanted into normal intima of young rats substantially proliferated

-> growth factors must be secreted by both activated macrophages and smooth muscle cells which underlie AS

30
Q

How is the role of monocytes thought to change over the course of atherosclerotic progression?

A
  1. Early - protective effect in the activated endothelium
  2. Late - harmful effect, due to accumulation and release of toxic oxygen radicals (enhance lipid peroxidation) and cytokines to recruit more immune cells
31
Q

What is the role of T cells in atherosclerotic plaques?

A

Cross-talk with macrophages, leading to both cellular and humoral immune activation
-> promote inflammation which is associated with AS

32
Q

How might infection play a role in atherosclerosis?

A

Induces the initial endothelial damage which allows chronic inflammation to begin

33
Q

Give two procedures which can be done to actually remove plaque constituents, including lipids, residual fibrin, and plaque collagen?

A
  1. Angioplasty - mechanical opening of vessel

2. Endarterectomy - removal of intima

34
Q

What are some dietary supplements which are suggested to prevent atherosclerosis?

A

Omega-3 fatty acids, antioxidants like vitamin E, and statins

Pathobiology (20 decks)

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