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

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
where do we typically see inflammatory cells in AAA
in the adventitia
26
What are MMPs
zinc-dependent zymogens which degrade collagen, elastin, gelatin.
27
What two MMPs are associated with aneurysm
MMP-2=small, stable aneurysms | MMP-9=large, expanding aneurysms
28
How does collagen/elastin compostion of Ao change as you move along it
More collagen and elastin higher up. But the collagen:elastin ration increases as you go down so it gets stiffer
29
What are some risk factors for AAA. What is typically the cause
genetic, male, age, smoking. Almost always atherosclerotic degeneration
30
What are the four types of AAA and where do they affect
Infrarenal, juxtarenal, pararenal, suprarenal
31
what are some common causes of AAA
Atherosclerosis, mycotic, inflammatory, congenital (marfans and Ehlers-Danlos)
32
what is LaPlace's law
T=PxR