Vascular disease 1&2 Flashcards

1
Q

what is the most common classification for PAD

A

Rutherford. Stage 0-6. Asymptomatic>Degree of Claudication>Rest pain>Degree of tissue loss

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2
Q

risk of MI, stroke, death is shown by a high or low ABI?

A

Low

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3
Q

changes in skeletal muscle histology in PAD

A

decrease in muscle, increase in adipocytes and inflammatory cells. Denervation

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4
Q

What are the three biggest risk factors for vascular disease

A

smoking, diabetes, htn

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5
Q

what drug do we use for claudication

A

cilostazol

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6
Q

what are the four etiologies of mesenteric ischemia

A

embolic, thrombotic, nonocclusive, venous thrombosis

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7
Q

where does an embolism lodge and what tissue is affected

A

In SMA distal to middle colic artery. Still get flow to proximal jejunum and transverse colon

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8
Q

where do embolisms causing mesenteric ischemia originate

A

usually from heart

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9
Q

where do we see thrombi in mesenteric ischemia

A

at the origin of the SMA. Affects entire bowel

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10
Q

where does a venous thrombosis originate and what does it cause

A

superior mesenteric vein, inferior mesenteric vein, portal vein. Causes edema and hemorrage. Almost always in hypercoagulable patients

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11
Q

presentation of acute mesenteric ischemia

A

sudden things: pain, nausea, vomiting, diarrhea

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12
Q

presentation of chronic mesenteric ischemia

A

post prandial pain, weight loss, food fear

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13
Q

presentation of Nonocclusive and venous thrombosis

A

slower course. Usually hospitalized, critically ill patients

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14
Q

where does plaque tend to build up?

A

bifurcations, as in carotid artery, especially along the lateral wall

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15
Q

how does a carotid duplex evaluate stenosis

A

by the velocity of the blood

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16
Q

how can you tell the external from the internal carotid

A

the external has branches

17
Q

In what layer does blood accumulate in aortic dissection

A

the media

18
Q

what are the calssifications of Ao dissection. Who is more likely to have each class?

A

A-ascending:younger
B-descending:older (60-70)
Men, Blacks, connective tissue disorders

19
Q

what happens to each of the vascular layers in Ao dissection

A

Medial degeneration
Intimal thickening-fibrosis,calcification,FA deposits
Adventitial fibrosis-obstruction of vasa vasorum

20
Q

what are some sequela of a Type A dissection

A

Ao regurg, coronary vessel occlusion, tamponade

21
Q

sequela of type b dissection

A

ischemia of intestine, kidneys, spinal cord, lower extremities

22
Q

what is the mortality of Ao dissection

A

about 1% per hour

23
Q

what is considered an aneurysm

A

a widening of at least 50%

24
Q

what are the three central themes of AAA

A

inflammation
disruption of conn. tissue and loss of elastin
medial thinning

25
Q

where do we typically see inflammatory cells in AAA

A

in the adventitia

26
Q

What are MMPs

A

zinc-dependent zymogens which degrade collagen, elastin, gelatin.

27
Q

What two MMPs are associated with aneurysm

A

MMP-2=small, stable aneurysms

MMP-9=large, expanding aneurysms

28
Q

How does collagen/elastin compostion of Ao change as you move along it

A

More collagen and elastin higher up. But the collagen:elastin ration increases as you go down so it gets stiffer

29
Q

What are some risk factors for AAA. What is typically the cause

A

genetic, male, age, smoking. Almost always atherosclerotic degeneration

30
Q

What are the four types of AAA and where do they affect

A

Infrarenal, juxtarenal, pararenal, suprarenal

31
Q

what are some common causes of AAA

A

Atherosclerosis, mycotic, inflammatory, congenital (marfans and Ehlers-Danlos)

32
Q

what is LaPlace’s law

A

T=PxR