1. Atherosclerosis Flashcards

1
Q

Define atherosclerosis.

A

A hardened plaque in the intima of an artery. It is an inflammatory process.

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2
Q

What can an atherosclerotic plaque cause?

A
  1. Heart attack.
  2. Stroke.
  3. Gangrene.
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3
Q

What are the constituents of an atheromatous plaque?

A
  1. Lipid core.
  2. Necrotic debris.
  3. Connective tissue.
  4. Fibrous cap.
  5. Lymphocytes.
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4
Q

Give 5 risk factors for atherosclerosis.

A
  1. Family history.
  2. Increasing age.
  3. Smoking.
  4. High levels of LDL’s.
  5. Obesity.
  6. Diabetes.
  7. Hypertension.
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5
Q

In which arteries would you be most likely to find atheromatous plaques?

A

In the peripheral and coronary arteries.

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6
Q

Which histological layer of the artery may be thinned by an atheromatous plaque?

A

The media.

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7
Q

What is the precursor for atherosclerosis.

A

Fatty streaks.

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8
Q

What can cause chemoattractant release?

A

A stimulus such as endothelial cell injury.

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9
Q

What are the functions of chemoattractants?

A

Chemoattractants signal to leukocytes. Leukocytes accumulate and migrate into vessel walls -> cytokine release e.g. IL-1, IL-6 -> inflammation!

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10
Q

Describe the process of leukocyte recruitment.

A
  1. Capture.
  2. Rolling.
  3. Slow rolling.
  4. Adhesion.
  5. Trans-migration.
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11
Q

Describe in 5 steps the progression of atherosclerosis.

A
  1. Fatty streaks.
  2. Intermediate lesions.
  3. Fibrous plaque.
  4. Plaque rupture.
  5. Plaque erosion.
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12
Q

Progression of atherosclerosis: what are the constituents of fatty streaks?

A

Foam cells and T-lymphocytes. Fatty streaks can develop in anyone from about 10 years old.

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13
Q

Progression of atherosclerosis: what are constituents of intermediate lesions?

A
  • Foam cells.
  • Smooth muscle cells.
  • T lymphocytes.
  • Platelet adhesion.
  • Extracellular lipid pools.
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14
Q

Progression of atherosclerosis: what are the constituents of fibrous plaques?

A
  • Fibrous cap overlies lipid core and necrotic debris.
  • Smooth muscle cells.
  • Macrophages.
  • Foam cells.
  • T lymphocytes.

Fibrous plaques can impede blood flow and are prone to rupture.

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15
Q

Progression of atherosclerosis: why might plaque rupture occur?

A

Fibrous plaques are constantly growing and receding. The fibrous cap has to be resorbed and redeposited in order to be maintained. If balance shifted in favour of inflammatory conditions, the cap becomes weak and the plaque ruptures. Thrombus formation and vessel occlusion.

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16
Q

What is the treatment for atherosclerosis?

A

Percutaneous coronary intervention (PCI).

17
Q

What is the major limitation of PCI?

A

Restenosis.

18
Q

How can restenosis be avoided following PCI?

A

Drug eluting stents: anti-proliferative and drugs that inhibit healing.

19
Q

What is the key principle behind the pathogenesis of atherosclerosis?

A

It is an inflammatory process!

20
Q

Define atherogenesis.

A

The development of an atherosclerotic plaque.