EXAM #1: ARTERIOSCLEROSIS Flashcards

1
Q

What is the definition of arteriosclerosis?

A

“Hard arteries” due to thickening of the blood vessel wall

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2
Q

What are the three sub-categories of arteriosclerosis?

A

1) Atherosclerosis
2) Arteriolosclerosis
3) Monckeberg medial calcific sclerosis

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3
Q

What is the definition of Atherosclerosis?

A

INTIMAL plaque that obstructs blood flow

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4
Q

Describe the composition of an atherosclerotic plaque.

A
  • Necrotic lipid core (cholesterol)
  • Fibromuscular cap

*Often undergoes dystrophic calcification

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5
Q

What vessels are most commonly involved in atherosclerosis?

A

Large and medium sized arteries i.e.

1) Abdominal aorta
2) Coronary artery
3) Popliteal artery
4) Internal carotid artery

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6
Q

What are the modifiable risk factors in atherosclerosis?

A

1) HTN
2) Hypercholesterolemia (LDL)
3) Smoking
4) DM
- Inactivity
- Stress
- Obesity

Note that these risk factors are synergistic/ additive

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7
Q

What are the nonmodifiable risk factors in atherosclerosis?

A

1) Age
2) Gender
- Males
- Post-menopausal women (estrogen is protective)
3) Genetics

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8
Q

What total serum cholesterol increases the risk of atherosclerosis?

A

160 mg/dL

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9
Q

Which familial dyslipoproteinemias are associated with premature atherosclerosis?

A

1) Familial hypercholesterolemia (increased LDL)
2) Familial combined hypercholesterolemia (Increased LDL and VLDL)
3) Familial Type III Lipoproteinemia (IDL)
4) Familial hypertriglyceridemia (VLDL and TAG)
5) Familial AI/CII (no HDL)

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10
Q

Which of the familial dyslipoproteinemia is associated with the most severe premature atherosclerosis?

A

Familial AI/CII i.e. lack of HDL

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11
Q

What is the impact of smoking on the etiology of atherosclerosis?

A

Smoking= 200% risk

Smoking cessation= 1/2 of the prior risk

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12
Q

What are the two “unusual” risk factors associated with atherosclerosis?

A

1) Homocystine

2) Chlamydia pneumonia

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13
Q

Outline the pathogenesis of atherosclerosis.

A

1) Endothelial injury:
- Damage to endothelium allows LIPIDS to lead into INTIMA
2) Macrophage response
- Lipids are oxidized and consumed by macrophages–>foam cells
3) INFLAMMATION and healing
- Leads to deposition of ECM and proliferation of smooth muscle

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14
Q

What cellular adhesion molecule is over-expressed in response to endothelial injury in the pathogenesis of atherosclerosis?

A

Vascular cell adhesion molecule-1 (VCAM-1)

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15
Q

What receptor on macrophages allows them to take up lipids to form foam cells?

A

Scavenger receptors

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16
Q

What recruits macrophages to sites of intimal injury from accumulated lipids?

A

Monocyte chemo-attractant protein 1 (MCP-1)

17
Q

What is the significance of foam cells in the intima?

A

1) Cause smooth muscle cell emigration from the media to the intima
2) Further secretion of cytokines for inflammatory response

Causes further macrophage activation

18
Q

What factor is highly implicated in the proliferation of smooth muscle cells in the pathogeneis of athersclerosis ?

A

PDGF

19
Q

What are the two morphologic stages of atherosclerosis?

A

1) Fatty streaks
2) Proliferative lesion
2) Atherosclerotic plaque, or “atheroma”

20
Q

What is a fatty streak?

A

Flat yellow lesions of the intima consisting of foam cells/ lipid laden macrophages

21
Q

What process do atherosclerotic plaques undergo?

A

Dystrophic calcification i.e. “hardening” of the artery

22
Q

Where do atherosclerotic plaques begin to develop? Why?

A

Adjacent to bifurcations b/c of the changes in blood flow in these regions

Shear stress= endothelial injury

23
Q

What are the major complications of atherosclerotic lesions?

A

1) Calcification
2) Hemorrhage
3) Rupture or ulceration
4) Thrombosis

24
Q

Why is rupture of an atherosclerotic plaque dangerous?

A

Substances exposed by the rupture induces thrombogenesis

25
Q

What are the implications of the strength of the fibromuscular cap of an atherosclerotic plaque?

A

Thickness is directly correlated with stability

The thicker the cap, the less likely it is to rupture and thrombose

26
Q

What is the primary prevention for atherosclerosis?

A

Prevention with:

1) Statins
2) Anti-hypertensives
3) Aspirin to prevent clotting

Lifestyle modification is key to prevention

27
Q

What is secondary prevention in atherosclerosis?

A

Treatment once an atherosclerotic plaque has ruptured i.e:

1) TPa
2) Angioplasty
3) CABG

28
Q

What is the primary cause of an abdominal aortic aneurysm?

A

Atherosclerosis

29
Q

Why does atherosclerosis predipose one to an abdominal aortic aneurysm?

A
  • Atherosclerosis in the media increases the diffusion barrier to the media
  • Hypoxia from limited diffusion leads to atropthy and weakness of the vessel wall
  • Ballooning of the vessel occurs
30
Q

What is the ABPI?

A

Ankle Brachial Pressure Index

*Comparison of ankle BP to arm BP

31
Q

What ABPI is considered abnormal?

A

Less than 0.9

*The lower the number, the worse the PVD

32
Q

What is the major complication of peripheral atherosclerosis? What patient population is this most common in?

A

Gangrene

*DM

33
Q

What happens when there is a MI or ischemic CVA?

A

Atherosclerotic plaque rupture and thrombosis that:

  • Occludes coronary artery (MI)
  • Occludes the cerebral artery (CVA)
34
Q

What degree of stenosis must occur for there to be complications?

A

70%

35
Q

What is the Glagov coronary remodeling hypothesis?

A
  • As the vessel lumen narrows, it will initially expand to compensate
  • Eventually the vessel will not be able to expand further

This point, where the vessel can no longer expand is when severe disease results