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SPR2015_Week3 > Blood vessels and ischeic heart disease > Flashcards

Blood vessels and ischeic heart disease Flashcards

1
Q

what is morbidity and mortality assoc with atherosclerosis

A

VIRCHOWS’
1) narrowing of vessels

2) damaged endothelial lining
3) weakened vessel walls

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2
Q

why is narrowing of vessels dangerous?

A

ischemia of tissue perfused by vessels

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3
Q

why is endothelial lining damage dangerous?

A

promotes intravascular thrombosis

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4
Q

why is weakened vessel walls

dangerous?

A

predispose to dilation/rupture

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5
Q

Virchow’s triad

A

1) abnormal blood flow = turbulence
2) hypercoagulability
3) endothelial injury

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6
Q

differentiate elastic vs muscular artery

A

elastic = accomodate/dampen pulsatile flow

muscular = regulate flow (vasconstrict/dilate)

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7
Q

ex of elastic artery

A

aorta

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8
Q

ex of muscular artery

A

renal artery

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9
Q

atherosclerosis is ____ to injury

A

response

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10
Q

____ is response to injury

A

atherosclerosis

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11
Q

why is atherosclerosis considered a normal response to injury

A

reconstituting damaged vessels

if intimal thickening increased can cause stenosis of vessels/grafts

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12
Q

examples of responses to vessel stenosis

A

1) angioplasty re-stenosis (mech)
2) transplant arteriosclerosis (immun)
3) atherosclerosis

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13
Q

subtypes of arterosclerosis

A

1) arteriolosclerosis
2) monckeberg’s
3) atherosclerosis

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14
Q

what is pathology of atherosclerosis

A

fibrofatty plaques on intima

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15
Q

define monckeberg’s medial calcific stenosis

A

calcification of MEDIA of muscular arteries

NOT AFFECT VESSEL LUMEN

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16
Q

what is disease assoc with calcification of media of muscular arteries

A

monckeberg’s medial calcific stenosis

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17
Q

where do you see arteriosclerosis

A

small arteries/arterioles

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18
Q

what is arteriolosclerosis assoc with

A

HTN

Diabetes

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19
Q

what are 3 major targets of atherosclerosis

A

1) coronary arteries –> ischemic disease
(with thrombosis –> MI)

2) cerebral arteries –> stroke, infarct, neuro
3) aorta –> AAA
4) ischemic bowel (mesenteric)

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20
Q

Pathogenesis of atherosclerosis

A

1) focal chronic endo injury
2) insudation of lipoproteins into vessel wall
3) interactions with macs and lymphs
4) incr smooth muscle prolif –> atheroma

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21
Q

what is a foam cell

A

macrophages taking up

fat globules

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22
Q

what is aneurysm

A

weakening of wall

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23
Q

where do you find aneurysms

A

1) trauma
2) local infection (mycotic aneurysm)
3) congenital defect (berry aneurysm)
4) arteriovenous aneurysm

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24
Q

what are major causes of aortic aneurysms (3)

A

1) atherosclerosis
2) cystic medial degeneration (Marfan/age)
3) syphilis

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25
Q

where do aortic aneurysms most commonly present

A

abdominal aorta, below renal

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26
Q

mechanism causing aortic aneurysm

A

1) atherosclerosis weaknes wall

2) mass effect stim tumors (compression/erosion)

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27
Q

what is most common co-occurrence with aortic dissection

A

HTN (90%)

abnormality of connective tissue

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28
Q

what is mechanism of aortic dissection

A

1) intima tear toward heart or distal

2) 2nd intimal tear, blood into lumen –> double barreled aorta

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29
Q

what is a double barreled aorta

A

2nd intimal tear when blood returns into lumen

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30
Q

symptoms of aortic dissection

A

SUDDEN EXCRUCIATING PAIN RADIATE TO BACK

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31
Q

Type A aortic dissection

Type B aortic dissection

A

Type A = ascending aorta

Type B = off great vessels

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32
Q

what are ascending aorta aortic dissections classified as?

A

type A

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33
Q

which is worse type A or B aortic dissections

A

type A because could continue into coronary arteries –> ischemia

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34
Q

define false aneurysm

A

small area in vessel wall with hematoma forming outside

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35
Q

Features of vasculitis in pathology

A

1) vessel wall inflammation
2) vessel wall damage
3) fibrinoid necrosis

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36
Q

what are underlying causes of vasculitis

A

1) localized infection (viruses)
2) radiation
3) trauma
4) arthrus rxn
5) viruses in lesion
6) SLE

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37
Q

which arteries do you see polyarteritis nodosa

A

medium to small arteries

all stages coexist

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38
Q

what vasculitis do you see in medium to small arteries

A

polyarteritis nodosa

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39
Q

what vessels do you see microscopic polyarteritis

A

arterioles
capillaries
venules

(all at same stage)

40
Q

which vessels do you see temporal arteritis (giant cell arteritis)

A

1) temporal arteries

2) ophthalmic branches –> blindness

41
Q

features of temporal arteritis

A

granulomatous inflammation

due to macrophages coalescing

42
Q

what patient population do you see temporal arteritis

A

elderly (>50)

43
Q

where do you find Wegener’s granulomatosis

A

lungs + kidneys

44
Q

features of Wegener’s granulomatosis

A

vasculitis

granulomas

45
Q

what if you don’t treat Wegener’s granulomatosis

A

> 90% die in 2 yrs

46
Q

where do you find Takayasu’s arteritis (pulseless disease)

A

aorta
aortic branches
pulmonary arteries

47
Q

why is Takayasu’s arteritis also known as pulseless disease

A

because it narrows openings of great vessels

48
Q

what are symptoms of Takayasu’s arteritis

A

coldness

numbness of fingers and legs

49
Q

what patient population do you see takayasu’s arteritis

A

young <40 y/o

more females

50
Q

where do you find Kawasaki’s disease

A

coronary arteries

51
Q

what patient population do you find Kawasaki’s disease

A

infancy

early childhood

52
Q

symptoms of kawasaki’s disease

A

fever
erythema palms and soles
rash

53
Q

where do you find Buerger’s disease

A

male cigarette smokers

also female incidence incr with smoking

54
Q

where do you find Buerger’s disease

A

thrombosis of medium vessels, tibial and radial

55
Q

complications of Buerger’s disease

A

1) gangrene

2) pain at rest (due to nerves)

56
Q

where do you find thrombophlebitis

A

clot in deep leg veins

57
Q

dangers of thrombophlebitis

A

death from PE (saddle embolus)

58
Q

predisposing factors to thrombophlebitis

A

1) immobilization/bed rest
2) cancer (hypercoag)
3) trousseau’s sign

59
Q

what is trousseau’s sign

A

clots come and go due to malignancy

60
Q

2 MAJOR dangers with ischemic heart disease

A

1) decr blood supply due to atherosclerosis of coronary arteries
2) demand ischemia caused by hypotension from infection

61
Q

when is ischemic heart disease symptomatic

A

> 75% stenosis

vasodilation not sufficient for O2

62
Q

define angina pectoris

A

intermittent chest pain from reversible myocardial ischemia

63
Q

define stable angina pectoris

A

episodic chest pain with exertion

64
Q

disease assoc with episodic chest pain with exertion

A

stable angina pectoris

65
Q

define unstable angina pectoris

A

incr freq and intensity with LESS EXERTION

can trigger irreversible myocardial ischemia

66
Q

if you have incr freq and intensity of chest pain with less exertion

A

unstable angina pectoris

67
Q

define prinzmetal’s angina

A

chest pain at rest (sleep)

68
Q

what is prinzmetal’s angina due to?

A

vasospasm

69
Q

chest pain at rest disease?

A

prinzmetal’s angina

70
Q

define myocardial infarction

A

myocardial necrosis from ischemia (many hrs, not relieved by nitro)

71
Q

myocardial infarction not relieved by ___

A

nitro

72
Q

what are most myocardial infarcts caused by

A

clots on plaques

73
Q

when does necrosis begin after MI

A

20-30 min after occlusion

74
Q

progression of myocardial infarction

A

1) necrosis begin in subendocardial (under endothelial lining)
2) migrates outward

75
Q

what is a full thickness necrosis known as

A

transmural infarction

76
Q

if MI affects right dominant circulation (more common) which vessels involved

A

Right coronary artery

supplying posterior LV

77
Q

if MI affects left dominant circulation, which vessels involved

A

Left circumflex coronary artery

supplying posterior LV

78
Q

____ occlusion produces larger infarcts

A

more proximal

79
Q

more proximal occlusion produces ____

A

larger infarcts

80
Q

what happens when main vessel 100% occluded?

A

chronic ischemia recruits additional vessels

81
Q

Gross appearance and microscopic appearance of MI at

4 hrs

A

gross = no change

microscopic = coagulation necrosis

82
Q

what time point in MI?

gross = no change

microscopic = coagulation necrosis

A

4 hrs

83
Q

Gross appearance and microscopic appearance of MI at

1 day

A

gross = pallor

micro = neutrophils

no nuclei in most myofibers

84
Q

what time point in MI?

gross = pallor

micro = neutrophils

A

1 day

85
Q

Gross appearance and microscopic appearance of MI at

1 week

A

gross = pallor

micro = macrophages

loss nuclei
hypereosinophilia
contraction bands

86
Q

what time point in MI?

gross = pallor

micro = macrophages

A

1 week

87
Q

Gross appearance and microscopic appearance of MI at

10 days

A

gross = yellow, soft, sunken

micro = granulation tissue

88
Q

what time point in MI?

gross = yellow, soft, sunken

micro = granulation tissue

A

10 days

89
Q

Gross appearance and microscopic appearance of MI at

2 months

A

gross = firm, grey scar

micro = fibrosis

90
Q

what time point in MI?

gross = firm, grey scar

micro = fibrosis

A

2 months

91
Q

complications of MI < 2 weeks after?

A

risk of rupture when mostly neutrophils and dead cells

92
Q

complications of MI?

A

ventricular aneurysms- damaged wall

mural thrombus - damage and pooling of blood

93
Q

what is sudden cardiac death most common due to?

A

marked atheroslcerosis

94
Q

mechanism of sudden cardiac death due to atherosclerosis?

A

1) plaque rupture
2) clot, vasospasm
3) fatal arrhythmia or Hypertrophy

95
Q

Stable vs Unstable plaque

A

stable angina = fixed obstruction so need more O2 delivery –> reversible ischemia

hemorrhage in clot –> may occlude remaining vessel

SPR2015_Week3 (13 decks)

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