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SPR2015_Week3 > Clinical pathophys of endothelium > Flashcards

Clinical pathophys of endothelium Flashcards

1
Q

normal endothelium is (3 things)

A

1) anti-inflamm
2) anti-thrombotic
3) vasodilatory

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2
Q

what is endothelium

A

single cellular layer lining blood/lymph vessles, heart, and other cavities

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3
Q

what does internal elastic lamina separate

A

intima and media

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4
Q

what does external elastic lamina separate

A

media and adventitia

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5
Q

tunica intima made of

A

endothleium + thin layer connective tissue

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6
Q

tunica media made of

A

vascular smooth muscle + connective tissue

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7
Q

tunica adventitia made of

A

loose connective tissue

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8
Q

distinguish large arteries, smaller arteries, and arterioles

A

large arteries = more elastin

smaller arteries = more collagen

arterioles = more smooth muscle

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9
Q

activated endothelium

A

1) permeable to macrophages and monocytes
2) incr inflammatory cytokins
3) incr leukocyte adhesion molecules
4) incr vasodilatory molec
5) incr antithrombotic molec

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10
Q

activated smooth muscle

A

1) incr inflammatory cytokines
2) incr ECM syntheiss
3) incr migration and proliferation into subintima

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11
Q

where is nitric oxide synthase expressed

A

on luminal side of endothelium

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12
Q

where does NO diffuse to?

A

smooth muscle in media

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13
Q

fxns of NO synthase

A

1) responds to multiple stimuli
2) make NO from arginine
3) cGMP-mediated vasodilation

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14
Q

what generates inflammatory state?

A

decr NO due to oxid stress

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15
Q

what are inflammatory molecules

in endothelium

A

1) selectins
2) cell adhesion molec
3) cytokines

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16
Q

what is process of forming atherosclerotic plaque

A

1) monocytes enter intima
2) macrophage engulf foam cells
3) smooth muscle activ/migr, apoptosis, fibrosis, ongoing inflamm

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17
Q

stages of atherosclerotic plaque

A

1) fatty streak
2) plaque progression
3) plaque disruption if lose endothelial cap

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18
Q

fibrous cap in atherosclerotic

A

Foam cells

MMP = degrade fibrous cap over atherosclerotic plaque

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19
Q

compare vulnerable vs. stable plaque

A

vulnerable plaque

1) less fibr tissue
2) less calcified
3) more lipid content
4) more inflamm
5) more apoptosis

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20
Q

much of thrombosis is regulated by _____ on ____

A

regulated by molec expressed

on surface of or secreted by endothelium

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21
Q

examples of molec expressed on or secreted by endothelium

A

1) hep sulfate/thrombin
2) NO/platelet activ
3) prostacyclin

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22
Q

risk factors for coronary atherosclerotic plaque formation

A

requires 3 risk factor

1) HTN
2) hyperlipidemia
3) smoking
4) diabetes
5) age

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23
Q

CAD can cause

A

1) MI
2) unstable angina
3) myocardial infarction

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24
Q

Renal artery disease can cause

A

1) atheroembolic renal disease

2) renal artery stenosis

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25
Q

peripheral artery disease can cause

A

1) limb claudication

2) limb ischemia

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26
Q

mechanism of ischemia

stroke

A

atheroembolism from carotid bifurcation lesion

thromboembolism from LAtrial appendage with a-fib

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27
Q

mechanism of ischemia

myocardial infarction

A

thromboembolism

28
Q

mechanism of ischemia

angina

A

ruptured plaque, in situ thrombosis

29
Q

mechanism of ischemia

claudication

A

trauma

in situ thrombosis

30
Q

mechanism of ischemia

acute limb ischemia

A

stable obstructive plaque

31
Q

mechanism of ischemia

pulmonary embolism

A

vasospasm

32
Q

mechanism of ischemia

raynaud’s phenomenon

A

vasospasm

33
Q

for stroke, what is unique about the source lesion?

A

source lesion doesn’t need to be obstructive ( embolizes to brain

34
Q

with stroke

what is common artery?

A

ophthalmic artery (1st branch off carotid artery)

35
Q

what are common effects of CAD?

A

1) myocardial infarction

2) chronic stable angina

36
Q

what is mechanism behind MI in CAD?

A

1) rupture plaque
2) in-situ thrombosis (don’t have to be obstructive before rupture)

normal stress test

37
Q

what is mechanism behind angina in CAD?

A

stable, obstructive (>70% reduction diameter) lesion

abnormal stress test

38
Q

how to treat non-occlusive plaque rupture and thrombosis?

A

1) some flow but intermittent occlusion/embol
2) STABILIZE WITH ANTICOAG/VASODILATOR

present with NSTEMI

39
Q

how to treat occlusive plaque rupture?

A

1) no flow down artery
2) emergency and RECANALIZE

administer thrombolytics or coronary angiogram/plasty/stent

40
Q

which has positive serum biomarkers + ST depression +/- T wave inversion

A

NSTEMI

41
Q

which has occlusive thrombus + ST elevation + biomarkers

A

STEMI

42
Q

WHAT ARE clinical manifestation of peripheral artery disease?

A

claudication

acute limb ischemia

43
Q

what does claudication and acute limb ischemia mean?

A

peripheral artery disease

44
Q

what does MI and chronic stable angina indicate?

A

coronary artery disease

45
Q

mechanism behind claudication in peripheral artery disease

A

1) obstructive (>70% diam reduction), STABLE PLAQUE

46
Q

mechanism behind acute limb ischemia in peripheral artery disease

A

1) obstruct blood flow before develop collaterals

2) ~ atheroemboli (AAA) or thromboemboli (A-fib)

47
Q

what is acute limb ischemia rarely due to?

A

rarely in-situ thrombosis

48
Q

compare stable vs unstable/vulnerable plaques

A

stable plaque
1) less biol active

2) cause angina and claudication (exertional ischemia) if obstructive (>70% diam reduction)
3) less likely to cause thrombotic/embolic

vulnerable
2) more likely cause MI/stroke

49
Q

what are common manifestation of venous thromboembolic disease?

A

1) DVT

2) PE

50
Q

what do DVT and PE indicate underlying?

A

venous thrombosis different than arterial thrombosis

51
Q

a

A

a

52
Q

a

A

a

53
Q

compare venous and arterial thrombosis

major component of clot

A

venous = fibrin rich

arterial = platelet rich

54
Q

compare venous and arterial thrombosis

occur from …

A

venous = RBC

arterial = plaque rupture

55
Q

compare venous and arterial thrombosis

found in areas of ?

A

venous = areas of stasis

arterial = areas of high flow

56
Q

compare venous and arterial thrombosis

predisposing factors?

A

venous = genetic, environmental

arterial = atherosclerosis, trauma, anti-phospholipid antibody

57
Q

compare venous and arterial thrombosis

treatment?

A

venous = anticoagulation

arterial = antiplatelet

58
Q

WHAT IS PRIMARY RAYNAUD’S

A
  • vasospasm in digital arteries of fingers or toes
  • brought on with cold
  • managed with lifestyle or vasodilators
59
Q

WHAT IS SECONDARY RAYNAUD’S

A
  • PT HAS SCLERODERMA, LEUKEMIA OR LYMPHOMA
60
Q

Pain at rest that won’t improve with meds
STEMI

–> due to?

A

fibrous cap of atherosclerotic plaque rupture

50% occlusive –> now 100% obstrucitve to blood flow

61
Q

NSTEMI

due to?

A

ruptured plaque has thrombus not completely obstructive ~90%

62
Q

ST depression on exercise treadmill

chest pain with exertion relieved at rest (angina) due to?

A

atherosclerotic plaque 70% + obstructive

myocardium receives adequate flow at rest but not with exercise

63
Q

how to treat angina (pain with exertion)

A

1) control BP
2) long acting nitrates to dilate
3) revascularized

64
Q

angina + right calf discomfort with exertion relieved with rest (claudication)

–> patho in right superficial femoral?

A

atherosclerotic plaque 70% obstructive

blood flow limited with exercise not at rest

65
Q

Hx Afib

sudden pain in right foot –> cool and no pulse

–> patho in right popliteal artery

A

due to thromboembolism

thrombus from left atrial appendage d/t a-fib and lack of anticoag

migrated to right popl artery; acute so no time for collaterals

66
Q

sudden loss of vision in right eye

50% right internal carotid artery stenosis

A

atheroembolism

plaque migrate from right internal carotid to right ophthlamic artery

only manifests as right eye loss b/c did not involve other cerebral arteries

SPR2015_Week3 (13 decks)

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