2nd Exam: Vascular Diseases - Part 2 Flashcards Preview

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Flashcards in 2nd Exam: Vascular Diseases - Part 2 Deck (98)
1

Leading cause of death in U.S.

CV d.

2

Earliest change in ath:

fatty streak, thickening of intima

3

wavy pink lines in normal aorta:

elastic laminae

4

all plaques are in this layer of blood vessels:

tunica intima

5

Fatty streaks are commonly distributed around these structure:

ostia of small branches

6

ath pls are more common here:

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

7

What happens after fatty streak formation?

development of fibro-fatty plaques

8

fibro-fatty plaques are made of:

dense tissue and lipid

9

Most advanced plaques:

"complicated" by ulceration, hemmorhage, thrombosis, or calcification

10

atheroma:

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

11

intima below a complicated plaque:

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

12

TF? Fatty deposits are more common in adults.

F. children, highest at 12 yo

13

Fatty fibrous plaque are commonly seen in this age range:

10-65yo, 32yo most common

14

Greatest increase risk for complicated plaques are between these years:

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

15

Intima includes:

endo and subendothelial layers

16

Adventitia is related to:

vasovorum (?)

17

Media of normal muscular artery is composed of:

sm (meaty-a)

18

Closer to the endothelium, internal or external elastic lamina:

internal

19

Pathogenesis of ath:

chronic endo injury

20

Causes of chronic endo injury:

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

21

Causes of endo dysfunction:

inc permeability, WBC adhesion

22

Response to endo injury:

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

23

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

Once macs and sm cells engulf the lipid in the intima

24

Earliest form of sclerosis:

rigid internal elastic, straight, thickened intima

25

How is an artery affected with early plaque build up?

fibers don't recoil, hardening of artery

26

Red staining in adventitia surrounding artery:

collagen (stains blue in other images)

27

Appearance of internal elastic in artery unaffected by plaque:

wavy appearance, black stained (healthy or unhealthy)

28

TF? Plaques are either circumferential or eccentric.

F. not circumferential

29

Plaques formation and location in layer of vesssl

eccentric almost always, intima

30

Composition of core of eccentric plaquez;

lipid/ cellular debris

31

Composition of fibrofatty atheroma/ eccentric plaque:

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

32

Complications that can arise from complicated plaques:

calcification, ulceration, thrombosis, hemorrhage, or rupture CUTHR

33

why do bvs grow into plaque during atheroma development?

part of inflammatory response

34

vasovasorum should be in this layer:

outer media, adventitia

35

Type of cap around lipid core of atheroma:

fibrous

36

Cause of rapid increase in plaque volume:

hemmorhage

37

Complications arising from hemmorhagic plaque:

decrease lumen diameter and blood flow

38

What splits when a plaque ruptures:

fibrous cap

39

Clefts are formed by:

cholesterol and lipids (removal of?)

40

ulceration, used to be:

a soft core of plaque

41

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

flow of blood into ulcerated plaque

42

Indication of dangerous plaque:

calcification, seriously afflicted with atherosclerosis

43

When might dentists see calcified plaque in the carotid artery?

panos

44

Calcifications almost always occur:

at bifurcations

45

Site of plaque formation is a characteristics of:

local blood flow in the area, determines location

46

Laminar flow is slower here:

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

47

Sites of stagnation and "separation" of boundary layer:

in areas of curvature, esp distal to curvature

48

Eccentric ath plaques form in these zones:

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

49

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

iron particles and strobe light

50

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

areas of curvature, branch points

51

Location of static zone at branch points:

lateral walls that are contiguous w main branch

52

How to visualize narrowing a heart vessels:

angiogram

53

3 overlapping disease that contribute to atherothrombotic disesase

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

54

stroke, what type of d.?

cerebrovascular d.

55

heart attack, what type of d.?

coronary a. disease

56

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

transient ischemic attacks, atherosclerotic dementia

57

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

cerebral infarct (stroke)

58

Cx pres. of acute blockage in coronary artery:

MI

59

Cx px of chronic blockage in coronary artery:

angina pectoris

60

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

intestinal angina

61

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

intestinal infarct

62

Cx px of chronic blockage in lower extremity:

intermittent claudication (cramping in leg induced by exercise)

63

Cx px of acute blockage in lower extremity:

limb gangren

64

Cx px of chronic blockage in aorta:

aneurysm

65

Cx px of acute blockage in aorta:

rupture, plaque embolism

66

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

F. symptoms disappear w/in 24h

67

True aneurysm:

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

68

False aneurysm:

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

69

Any blockage visible in an x-ray is:

complicated, die to calcification (check)

70

Effect on bv w calcification of atherosclerotic plaque:

enlarged and dilated

71

syphilytic aneurysm is more common in this vessel:

thoracic aorta

72

Where do most atherosclerotic aneurysms occur?

below the renal artery, abdominal aorta

73

Angiogram highlights these aspects of aortic aneurysm:

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

74

Common finding in distal iliacs and femorals:

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

75

As elastic tissues are pressurized further, what happens?

converted to fibrous scar tissue

76

Tx for abdominal aortic aneurysm:

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

77

Dissecting hematoma is aka:

dissecting aneurysm

78

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

by separating the elastic layers

79

Dissecting hematoma:

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

80

Where does dissection most often begin?

tear in intima

81

Type A Dissecting hematoma:

ascending, proximal aorta, may extend entire length

82

Type B Dissecting hematoma:

distal to origin of L subclavian a.

83

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

13

84

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

10

85

Risk factors for HD:

high cholesterol, high BP, smoking, inactivaty

86

Risk factors for HD that can't be changed:

family history, increasing age, male, race

87

Risk factors for HD that can be changed:

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

88

5 components of successful wellness-promotion programs:

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

89

Risk factors for HD that can be changed w meds:

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

90

Med to prevent trhombi formation:

anticoagulant

91

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

F. chronic

92

Greatest risk factor for stroke and heart attack:

high BP

93

Lowering BP by 5mm reduces disease rates by:

30%

94

Fraction of WNYers that don't know they have hypertension

1/2

95

Statin tx:

reduce plaque size, inc lumen size

96

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

childhood obesity, glucose intolerance (insulin resistance), hypertension

97

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

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

98

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

2 y