Nancy Test 1 Atherosclerosis Flashcards

1
Q

Steps to vascular injury

A

Uninjured cells migrate to injured intima OR are derived from precursors

SMCs proliferate and synthesize ECM (collagen)

Intimal thickening occurs

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2
Q

What is effected in arteriolosclerosis

A

small arteries and arterioles

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3
Q

What causes arteriolosclerosis

A

hypertension and diabetes

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4
Q

What are the types of arteriolosclerosis? What are they seen in

A

Hyaline- mild chronic htn

Hyperplastic- “onionskin” malignant/accelerated htn

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5
Q

What do you see in Monckeberg arteriosclerosis

A

ring like calcifications on x-ray (ulnar and radial a)

calcium deposits in media of muscular arteries

This is not clinically significant

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6
Q

What has intimal lesions that are found in elastic and muscular arteries

A

Atherosclerosis

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7
Q

What are the nonmodifiable risk factors of atherosclerosis

A

Age- greater with age

Gender- men and postmenopausal women(estrogen protects before this)

Genetics

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8
Q

Marker for atherosclerosis

A

C reactive protein

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9
Q

Modifiable risk factors for atherosclerosis

A

Hyperlipidemia
Hypertension
Smoking
Diabetes

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10
Q

Steps of atherosclerosis

A

1) injury
2) lipoproteins move into vessel wall (LDL)
3) monocytes stick and turn into macrophages and foam cells
4) platelests stick and release factors
5) SMCs produce ECM

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11
Q

What is the earliest lesion in atherosclerosis and what is it made of

A

Fatty streak is made of lipid filled foamy macrophages

Seen in children

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12
Q

atherosclerotic plaques consist of

A

intimal thickening

fibrous cap

flow disturbances

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13
Q

Where is atherosclerosis most likely to occur

A

lower abdominal aorta

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14
Q

What is in the center of a plaque

A

debris, cholesterol crystals, calcium, foam cells (lipid core)

calcification causes hardening

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15
Q

What options occur in acute plaque change

A

Rupture/fissue

Erosion/ulceration

Hemorrhage

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16
Q

When a plaque is disrupted, what happens

A

thrombi form on the disruption (vasoconstriciton can cause this to occlude further)

17
Q

What is >75% occlusion considered

A

Critical stenosis (O2 demand is greater than supply

18
Q

Where is different below the renal arteries

A

no vasa vasorum

19
Q

What makes a plaque vulnerable

A

Fibrous cap is thinner

lipid core is large

20
Q

What is the difference between 75% fixed obstruction and 90%

A

75% only shows angina during exercise

90% shows angina at rest

21
Q

When do most MI’s occur

A

In the morning due to heightened stimulation

22
Q

What is considered angina

A

15 sec to 15 min attack

comes and goes with recurrent attacks

23
Q

Who cannot feel angina

A

diabetics and heart transplants

24
Q

What is stable angina

A

Not dangerous

caused by fixed obstruciton (inc HR triggers)

25
Q

Treat stable angina?

A

rest

nitroglycerin

26
Q

What causes unstable angina

A

disruption of atherosclerotic plaque with superimposed partially occluding thrombus

27
Q

How is unstable angina characterized

A

increasing frequency of attacks

less effort causes attacks

warns of impending MI

28
Q

What causes prinzmetal angina

A

coronary artery spasms

29
Q

What characterizes prinzmetal angina

A

episodic attacks with no relation to activity, HR, or BP

30
Q

How do you treat prinzmetal angina

A

Nitroglycerin

Ca channel blockers