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Pathology > 2nd Exam: Vascular Diseases - Part 2 > Flashcards

2nd Exam: Vascular Diseases - Part 2 Flashcards

1
Q

Leading cause of death in U.S.

A

CV d.

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2
Q

Earliest change in ath:

A

fatty streak, thickening of intima

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3
Q

wavy pink lines in normal aorta:

A

elastic laminae

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4
Q

all plaques are in this layer of blood vessels:

A

tunica intima

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5
Q

Fatty streaks are commonly distributed around these structure:

A

ostia of small branches

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6
Q

ath pls are more common here:

A

branch points, due to turbulence and shear stress on vessel surface

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7
Q

What happens after fatty streak formation?

A

development of fibro-fatty plaques

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8
Q

fibro-fatty plaques are made of:

A

dense tissue and lipid

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9
Q

Most advanced plaques:

A

“complicated” by ulceration, hemmorhage, thrombosis, or calcification

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10
Q

atheroma:

A

Vessel wall degeneration, due to fat build up and scar formation, restricts blood, can lead to thrombus formation

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11
Q

intima below a complicated plaque:

A

increased spaces, needle like clefts, cholesterol crystals dissolved out (cholesterol clefts)

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12
Q

TF? Fatty deposits are more common in adults.

A

F. children, highest at 12 yo

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13
Q

Fatty fibrous plaque are commonly seen in this age range:

A

10-65yo, 32yo most common

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14
Q

Greatest increase risk for complicated plaques are between these years:

A

33yo-43yo and 58yo-65yo, % affected always increasing after 32yo, steeper increases bw those age ranges

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15
Q

Intima includes:

A

endo and subendothelial layers

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16
Q

Adventitia is related to:

A

vasovorum (?)

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17
Q

Media of normal muscular artery is composed of:

A

sm (meaty-a)

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18
Q

Closer to the endothelium, internal or external elastic lamina:

A

internal

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19
Q

Pathogenesis of ath:

A

chronic endo injury

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20
Q

Causes of chronic endo injury:

A

hyperlipidemia, hypertension, smoking, homocysteine, blood flow, toxins, viruses, immune reactions, shear stress

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21
Q

Causes of endo dysfunction:

A

inc permeability, WBC adhesion

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22
Q

Response to endo injury:

A

platelet aggregation at site of developing plaque, monocyte adhesion and emigration to intima, lipids accumulate in intima, sm emigration from media to intima, mac activation, macs and sm cells engulf lipid, lymphos also present

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23
Q

When can you see the fatty streak with the naked eye?

A

Once macs and sm cells engulf the lipid in the intima

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24
Q

Earliest form of sclerosis:

A

rigid internal elastic, straight, thickened intima

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25
Q

How is an artery affected with early plaque build up?

A

fibers don’t recoil, hardening of artery

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26
Q

Red staining in adventitia surrounding artery:

A

collagen (stains blue in other images)

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27
Q

Appearance of internal elastic in artery unaffected by plaque:

A

wavy appearance, black stained (healthy or unhealthy)

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28
Q

TF? Plaques are either circumferential or eccentric.

A

F. not circumferential

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29
Q

Plaques formation and location in layer of vesssl

A

eccentric almost always, intima

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30
Q

Composition of core of eccentric plaquez;

A

lipid/ cellular debris

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31
Q

Composition of fibrofatty atheroma/ eccentric plaque:

A

fibrous ct, fibroblasts, sm cells, lymphos, collagen, lipid debris, other ECM deposition, extracellular lipid

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32
Q

Complications that can arise from complicated plaques:

A

calcification, ulceration, thrombosis, hemorrhage, or rupture CUTHR

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33
Q

why do bvs grow into plaque during atheroma development?

A

part of inflammatory response

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34
Q

vasovasorum should be in this layer:

A

outer media, adventitia

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35
Q

Type of cap around lipid core of atheroma:

A

fibrous

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36
Q

Cause of rapid increase in plaque volume:

A

hemmorhage

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37
Q

Complications arising from hemmorhagic plaque:

A

decrease lumen diameter and blood flow

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38
Q

What splits when a plaque ruptures:

A

fibrous cap

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39
Q

Clefts are formed by:

A

cholesterol and lipids (removal of?)

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40
Q

ulceration, used to be:

A

a soft core of plaque

41
Q

This can cause further embolization of material, likely to form a thrombus at this site

A

flow of blood into ulcerated plaque

42
Q

Indication of dangerous plaque:

A

calcification, seriously afflicted with atherosclerosis

43
Q

When might dentists see calcified plaque in the carotid artery?

A

panos

44
Q

Calcifications almost always occur:

A

at bifurcations

45
Q

Site of plaque formation is a characteristics of:

A

local blood flow in the area, determines location

46
Q

Laminar flow is slower here:

A

boundary of vessel: stagnation point, separation zone, surface of separation

47
Q

Sites of stagnation and “separation” of boundary layer:

A

in areas of curvature, esp distal to curvature

48
Q

Eccentric ath plaques form in these zones:

A

zones of separation, outer border at beginning of curve, inner border past the curve

49
Q

How could you test to see where eccentric plaque build up will occur?

A

iron particles and strobe light

50
Q

Narrowing will happen in these sites of a vessel first with ath plaque:

A

areas of curvature, branch points

51
Q

Location of static zone at branch points:

A

lateral walls that are contiguous w main branch

52
Q

How to visualize narrowing a heart vessels:

A

angiogram

53
Q

3 overlapping disease that contribute to atherothrombotic disesase

A

coronary a. d., cerebrovascular d., peripheral arterial d.

54
Q

stroke, what type of d.?

A

cerebrovascular d.

55
Q

heart attack, what type of d.?

A

coronary a. disease

56
Q

Cx pres of chronic blockage in carotid and vertebrobasilar aa.:

A

transient ischemic attacks, atherosclerotic dementia

57
Q

Cx pres. of acute blockage in carotid and vertebrobasilar aa.:

A

cerebral infarct (stroke)

58
Q

Cx pres. of acute blockage in coronary artery:

A

MI

59
Q

Cx px of chronic blockage in coronary artery:

A

angina pectoris

60
Q

Cx px of chronic blockage in celiac and sup mes. a.:

A

intestinal angina

61
Q

Cx px of acute blockage in celiac and sup mes. a.:

A

intestinal infarct

62
Q

Cx px of chronic blockage in lower extremity:

A

intermittent claudication (cramping in leg induced by exercise)

63
Q

Cx px of acute blockage in lower extremity:

A

limb gangren

64
Q

Cx px of chronic blockage in aorta:

A

aneurysm

65
Q

Cx px of acute blockage in aorta:

A

rupture, plaque embolism

66
Q

TF? Chronic blockage in carotid and vertebrobasilar aa.: often leads to permanent brain damage.

A

F. symptoms disappear w/in 24h

67
Q

True aneurysm:

A

sacular (eccentric) or fusiform (circumferential), lumen must enlarge

68
Q

False aneurysm:

A

extravasation of blood forming hematoma, entire circ of vessel widened but not lumen, dissection can cause

69
Q

Any blockage visible in an x-ray is:

A

complicated, die to calcification (check)

70
Q

Effect on bv w calcification of atherosclerotic plaque:

A

enlarged and dilated

71
Q

syphilytic aneurysm is more common in this vessel:

A

thoracic aorta

72
Q

Where do most atherosclerotic aneurysms occur?

A

below the renal artery, abdominal aorta

73
Q

Angiogram highlights these aspects of aortic aneurysm:

A

dilated lumen, fusiform swelling of vessel distal to the site, branch point constriction

74
Q

Common finding in distal iliacs and femorals:

A

aneurysm chamber w large mural thrombus, calcification found in vessel walls and thrombus

75
Q

As elastic tissues are pressurized further, what happens?

A

converted to fibrous scar tissue

76
Q

Tx for abdominal aortic aneurysm:

A

sew endovascular stent graft into place after it is released from catheter

77
Q

Dissecting hematoma is aka:

A

dissecting aneurysm

78
Q

If blood leaves the lumen and enters the media of the aorta how can it spread?

A

by separating the elastic layers

79
Q

Dissecting hematoma:

A

blood enters media of aorta from the lumen, separates elastic layers and spreads, can also come from bleeding from vasorum in the media

80
Q

Where does dissection most often begin?

A

tear in intima

81
Q

Type A Dissecting hematoma:

A

ascending, proximal aorta, may extend entire length

82
Q

Type B Dissecting hematoma:

A

distal to origin of L subclavian a.

83
Q

HD kills __ times as many WNY men as prostate cancer.

A

13

84
Q

HD kills __ times as many WNY women as breast cancer.

A

10

85
Q

Risk factors for HD:

A

high cholesterol, high BP, smoking, inactivaty

86
Q

Risk factors for HD that can’t be changed:

A

family history, increasing age, male, race

87
Q

Risk factors for HD that can be changed:

A

Smoking, inactivity and obesity, high fat and calorie diets, alcohol

88
Q

5 components of successful wellness-promotion programs:

A

quit smoking, eat better, excercise, know numbers, take meds

89
Q

Risk factors for HD that can be changed w meds:

A

BP, chol, blocked aa., diabetes, tendency to form thrombi, chronic inflammation

90
Q

Med to prevent trhombi formation:

A

anticoagulant

91
Q

TF? Acute perio disease is assoc with risk of heart attack.

A

F. chronic

92
Q

Greatest risk factor for stroke and heart attack:

A

high BP

93
Q

Lowering BP by 5mm reduces disease rates by:

A

30%

94
Q

Fraction of WNYers that don’t know they have hypertension

A

1/2

95
Q

Statin tx:

A

reduce plaque size, inc lumen size

96
Q

Factors associated with increased rates of premature death (40s/50s):

A

childhood obesity, glucose intolerance (insulin resistance), hypertension

97
Q

Smoking prevalence in WNY is __% higher than national avg:

A

4% (U.S.:23%, NY:24%, WNY:27%)

98
Q

How long does risk of death due to smoking take to decrease to non-smoker rates after quitting?

A

2 y

Pathology (23 decks)

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