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Cardiovascular > Peripheral Vascular Disease I and II > Flashcards

Peripheral Vascular Disease I and II Flashcards

1
Q

peripheral artery disease (PAD)

A

when blood flow to the extremities is blocked, usually due to atherosclerosis of the vessels

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2
Q

types of PAD

A

claudication

rest pain

tissue loss

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3
Q

claudication

A

muscle pain, called intermittent claudication

typically comes on with exercise and is relieved with rest

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4
Q

rest pain

A

as atherosclerosis progresses and blockage becomes more severe, pain may occur in the feet even when at rest

rest pain occurs because the arteries of the leg can no longer deliver adequate blood flwo to the feet, even at rest

generally worsens when the legs are elevated, such as wehn lying in bed at night

relieve may occur only when the feet are dangled

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5
Q

two drugs that are accepted treatment for claudication

A

cilostazol and pentoxifylline

cilostazol is much more effective

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6
Q

chronic changes in skeletal muscle histology

A

honeycomb pattern

increased adipose

increased inflammatory cells

increased angular fibers

decreased type III fibers

decreased gastroc strength - cross-sectional area

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7
Q

treatment for CAD

A

medication

exercise

risk factor modification and management

bypass surgery

endovascular interventions

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8
Q

emerging CAD therapies

A

gene therapy - VDGF165, VEGF121, hepatocyte growth factor (HGF), fibroblast growth factor 1 (FGF-1)

stem cell therapy - bone marrow, peripheral blood

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9
Q

acute mesenteric ischemia

A

caused by decreased intestinal blood flow that can be caused by a number of mechanisms

results in ischemia and subsequent reperfusion damage that may progress to the development of mucosal injury, tissue necrosis, and metabolic acidosis

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10
Q

intestinal blood supply

A

celiac axis

superior mesenteric artery

inferior mesenteric artery

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11
Q

types of acute mesenteric ischemia

A

embolic disease

thrombolic disease

nonocclusive mesenteric ischemia

venous thrombosis

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12
Q

embolic disease

A

embolus tends to lodge in SMA distal to middle colic artery

this preserves the proximal jejunum and transverse colon

doesn’t go into the celiac because of the angle of the vessels

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13
Q

etiology of embolic disease

A

atrial tachyarrhythmia

MI

cardiomyopathy

heart defects

cardiac tumors

endocarditis

aortic mural thrombus

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14
Q

thrombotic disease

A

atherosclerosis

hypercoagulable state

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15
Q

etiology of nonocclusive mesenteric ischemia

A

caused by vasospasm

atherosclerosis is frequent

low flow states

hypovolemia

vasoconstrictors

vasoactive agents

aortic insufficiency

liver failure

cardiopulmonary bypass

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16
Q

venous thrombosis

A

superior mesenteric vein is the most common

sometimes the inferior mesenteric vein and portal vein

characterized by edema, hemorrhage, and sloughing

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17
Q

etiology of venous thrombosis

A

hypercoagulable state

malignancy

trauma

abdominal surgery

hepatic failure

pancreatitis

oral contraceptives

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18
Q

clinical presentation of embolic and thrombotic acute mesenteric ischemia

A

sudden pain out of proportion to exam

gut emptying

nausea

vomiting

diarrhea

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19
Q

clinical presentation of embolic and thrombotic chronic mesenteric ischemia

A

post prandial pain

weight loss

food fear

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20
Q

clincial presentation of NOMI and MVT

A

slower course

usually critically ill, hospitalized, intubated

abdominal pain

nausea and vomiting

bloody stool

dehydration

fluid shifts

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21
Q

diagnosis of MAD

A

laboratory studies

x-ray

ultrasound

CTA

MRA

contrast angiography is the gold standard

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22
Q

management of embolic MAD

A

early diagnosis

SMA embolectomy

anticoagulation

bowel resection

second look

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23
Q

management of thrombotic MAD

A

early diagnosis

SMA/CA bypass (venous)

anticoagulation

bowel resection

second look

24
Q

management of NMI

A

correct underlying problem

systemic vasodilator infusion

catheter directed vasodilator infusion

25
Q

management of venous thrombosis

A

resuscitation

anticoagulation

laparotomy if periotneal signs

? thrombolytic therapy

26
Q

carotid artery disease plaque anatomy

A

commonly occurs at bifurcations

typically thickest at bulb and extends 2 cm

occurs along lateral wall of the carotid artery

27
Q

pathophysiology of stroke

A

embolism of overlying thrombus

embolism of plaque fragment

low flow through post stenotic segment

28
Q

clinical presentation of carotid stenosis

A

asymptomatic

transient ischemic attack (TIA)

stroke

29
Q

diagnosis of carotid stenosis

A

carotid duplex - imaging, velicity measurements

MRA

CTA

contrast angiography

30
Q

treatment of carotid artery disease

A

medical therapy - antiplatelet (aspirin and clopidogrel)

surgical therapy - carotid enarterectome (CEA) or carotid artery stenting (CAS)

31
Q

etiology of aortic dissection

A

dissection of blood between and along the laminar planes of the media, with formation of a blood-filled channel within the aortic wall

the inciting incident is usually related to severe hypertension

32
Q

type A dissections

A

very life-treatening and usually require emergent surgical treatment

dissection may affect aortic valve, causing sudden valvular incompetence and death

rupture into the pericardium and sudden death is not unusual

50-60 years of age

33
Q

type B dissections

A

begin and remain distal to the left subclavian artery

less life-treatening as the heart is not involved

branches of the arota may be occluded, causing symptoms such as paraplegia, renal failure, valvular hypertension, bowel gangrene, or leg ischemia

if not life-threatening, management involves medical rather than surgical treatment

60-70 years of age

34
Q

pathophysiology of aortic dissection

A

Hyptertension

medial degeneration - deterioration of medial collagen and elastin, loss of vascular smooth muscle cells

intimal thickening - fibrosis, calcifications, fatty acid deposition

adventitial fibrosis - obstruct small intramural vasa vasorum

inherited connective tissue disorders

association with cocaine use

circadian pattern

35
Q

presentation of aortic dissection

A

severe excruciating pain in the anterior chest and back

malperfusion syndrome:

stroek

intestinal ischemia

lower extremity ischemia

paralysis

cardiac tamponade/coronary ostia compromise

hypotension/shock

36
Q

treatment of type A aortic dissection

A

emergency surgery

37
Q

treatment of type B aortic dissection

A

no ischemic complications - medical therapy

ischemic complications - surgery

rupture - surgery

38
Q

abdominal aortic aneurysms

A

enlargement of the arterial diameter, usually 1.5 times the adjacent normal arterial diameter or more

shapes are either fusiform or saccular

95% are below the renal arteries

rupture of aortic aneurysms is usually posterior and to the left

39
Q

types of aortic aneurysms based on location

A

infrarenal

juxtarenal

pararenal

suprarenal

40
Q

pathophysiology of aneurysms

A

inflammation

disruption of conective tissue architecture with loss of elastin

medial thinning

41
Q

inflammation leading to aneurysm

A

inflammatory cells

release of cytokines

activate MMPs

degradation of collagen and elastin

42
Q

matrix metalloproeinases

A

zinc-dependent enzymes

secreted as zymogens

degrade collagen, elasin, and gelatin

43
Q

sources of MMP

A

vascular smooth muscle cells

fibroblasts

inflammatory cells

endothelial cell surrounding the vaso vasorum

44
Q

MMP-2

A

72kDa gelatinase A

substrates - type IV collagen, gelatin, elastin

elevated in small, stable aneurysms

not elevated in normal aorta or occlusive disease

45
Q

MMP-9

A

92kDa gelatinase B

main substrate is elastin

elevated in large, rapidly expanding aneurysms

tissue and circulating levels of MMP-9 correlate with aneurysm size

46
Q

medial thinning

A

increased SMC apoptosis (3-fold)

decreased SMC density

impaired SMC proliferation

47
Q

protective factors of abdominal aortic aneurysm

A

female sex

black race

diabetes mellitus

48
Q

etiology of abdominal aortic aneurysm

A

atherosclerosis is the predominant cause

49
Q

Marfan syndrome

A

fibrillin-1 defect

main structural component in elastin-associated microfibrils

50
Q

Type IV Ehlers-Danlos syndrome

A

type III procollagen defect

51
Q

clinical presentation of abdominal aortic aneurysms

A

asymptomatic

distal emboli

rupture

52
Q

How big does an aneurysm have to be to risk surgery

A

5.5 cm - benefits outweight risks at this point

53
Q

diagnosis of abdominal aortic aneurysm

A

asymptomatic

physical exam

plain x-ray

CT scan

rupture

54
Q

treatment of abdominal aortic aneurysms

A

open repair

endovascular repair

size is not a limitation

proximal “landing zone” at least 15mm

proximal neck angulation <60 degrees

delivered by bilateral transfemoral route

limited by tortuous, calcified, small iliacs

concomitant aneurysms limit use

55
Q

indications for repair

A

large (>5.5 cm)

rapid expansion of >0.5 cm/year

rupture

symptomatic

56
Q

other arterial aneurysms

A

subclavian

femoral

popliteal

hand

Cardiovascular (46 decks)

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