Arteriosclerosis Flashcards

1
Q

what layer is artherosclerosis in?

A

arterial intima

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2
Q

what are atheromas

A

formation of focal plaques

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3
Q

what is one of the most important modifiable risk factors for atherosclerosis?

A

CIGARETTE SMOKING

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4
Q

2 risk factors increases your risk by how much?

A

4x risk

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5
Q

3 risk factors increases your risk by how much?

A

7x risk

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6
Q

as total serum cholesterol rises above _____, coronary risk rises linearly

A

160

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7
Q

genetic disorder: incr in chylomicrons, no premature AS

A

Type I: Familial lipoprotein lipase deficiency

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8
Q

genetic disorder: incr LDL, premature AS

A

IIa Familial hypercholesterolemia

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9
Q

genetic disorder: incr LDL & VLDL, premature AS

A

IIb Familial combined hypercholesterolemia

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10
Q

genetic disorder: incr IDL, premature AS

A

III Familial type III lipoproteinemia

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11
Q

genetic disorder: incr VLDL, premature AS

A

IV Familial hypertriglyceridemia

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12
Q

genetic disorder: no HDL w/ severe AS

A

V Only Familial AI/CII deficiency

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13
Q

type 5 dyslipoproteinemias and risk

A

start developing AS in their 20’s

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14
Q

what secondary disorders have high cholesterol

A
  1. nephrotic syndrome
  2. alcoholism
  3. hypothyroidism
  4. DM
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15
Q

correlation of long term elevations of CRP and atherosclerosis

A

high CRP = higher risk of atherosclerosis

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16
Q

what is the initial process driving atherosclerosis?

A

damage to endothelial cells

17
Q

what induces endothelial injury?

A

hypercholesteremia, disturbed flow

18
Q

key features of atherosclerosis (3)?

A
  1. Smooth muscle cell proliferation
  2. Accumulation of connective tissue elementscollagen, elastin, proteoglycans
  3. Lipid deposition: intra & extracellular
19
Q

what is in a fibro fatty atheroma?

A

necrotic core surrounded by foamy macrophages

20
Q

is atherosclerosis an acute or chronic inflammatory disease?

A

CHRONIC

21
Q

what are the different cells involved in atherosclerosis?

A

endothelial cell, t-lymphocyte, smooth muscle cell, platelet, macrophage

22
Q

once necrotic tissue gets into the vasculature, what is it called?

A

grumous (pro-thrombotic)

23
Q

what is the main complication of lesions?

A

rupture or ulceration–>causes instant thrombosis

24
Q

what is the most predictive in determining risk of issues assc’d with plaques?

A

VULNERABLE PLAQUE

25
Q

what is vulnerable plaque?

A

soft with lipid filling core, prone to rupture due to plaque hemorrhage or fibrous cap disruption

26
Q

role of inflammation in plaque rupture?

A

vulnerable plaque–>rupture–>thrombus–>MI

27
Q

what are methods of primary prevention

A

Statins, control BP, DM, control clotting, diet and lifestyle change

28
Q

secondary prevention?

A

Tissue plasminogen activator, angioplasty with stent

placement (coronary of carotid), carotid endarterectomy, CABG

29
Q

where do atherosclerotic lesions most often form?

A

branch points in heart vasculature, can affect major arteries throughout the body

30
Q

what is an abnormal ankle brachial pressure index (ABPI)?

A

ABPI >1.3

31
Q

what does an abnormal ABPI suggest?

A

calcification of the artery walls & incompressible vessels

32
Q

when to start worrying about potential for aortic aneurysm?

A

when thrombotic tissue >5 cm

33
Q

in minimal and moderate coronary artery disease, what happens to the size of the lumen?

A

compensatory expansion of vessel wall maintains CONSTANT lumen

34
Q

what happens to lumen on severe CAD?

A

expansion is overcome & lumen narrows

35
Q

what is the name of the hypothesis that says what happens to the size of the lumen over time with coronary remodeling?

A

glagov’s coronary remodeling hypothesis

36
Q

when the lumen is reduced by _______, the vessel can no longer dilate enough to meet demands for incr blood flow

A

70-80%