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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
management of venous thrombosis
resuscitation anticoagulation laparotomy if periotneal signs ? thrombolytic therapy
26
carotid artery disease plaque anatomy
commonly occurs at bifurcations typically thickest at bulb and extends 2 cm occurs along lateral wall of the carotid artery
27
pathophysiology of stroke
embolism of overlying thrombus embolism of plaque fragment low flow through post stenotic segment
28
clinical presentation of carotid stenosis
asymptomatic transient ischemic attack (TIA) stroke
29
diagnosis of carotid stenosis
carotid duplex - imaging, velicity measurements MRA CTA contrast angiography
30
treatment of carotid artery disease
medical therapy - antiplatelet (aspirin and clopidogrel) surgical therapy - carotid enarterectome (CEA) or carotid artery stenting (CAS)
31
etiology of aortic dissection
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
type A dissections
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
type B dissections
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
pathophysiology of aortic dissection
**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
presentation of aortic dissection
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
treatment of type A aortic dissection
emergency surgery
37
treatment of type B aortic dissection
no ischemic complications - medical therapy ischemic complications - surgery rupture - surgery
38
abdominal aortic aneurysms
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
types of aortic aneurysms based on location
infrarenal juxtarenal pararenal suprarenal
40
pathophysiology of aneurysms
inflammation disruption of conective tissue architecture with loss of elastin medial thinning
41
inflammation leading to aneurysm
inflammatory cells release of cytokines activate MMPs degradation of collagen and elastin
42
matrix metalloproeinases
zinc-dependent enzymes secreted as zymogens degrade collagen, elasin, and gelatin
43
sources of MMP
vascular smooth muscle cells fibroblasts inflammatory cells endothelial cell surrounding the vaso vasorum
44
MMP-2
72kDa gelatinase A substrates - type IV collagen, gelatin, elastin elevated in small, stable aneurysms not elevated in normal aorta or occlusive disease
45
MMP-9
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
medial thinning
increased SMC apoptosis (3-fold) decreased SMC density impaired SMC proliferation
47
protective factors of abdominal aortic aneurysm
female sex black race diabetes mellitus
48
etiology of abdominal aortic aneurysm
atherosclerosis is the predominant cause
49
Marfan syndrome
fibrillin-1 defect main structural component in elastin-associated microfibrils
50
Type IV Ehlers-Danlos syndrome
type III procollagen defect
51
clinical presentation of abdominal aortic aneurysms
asymptomatic distal emboli rupture
52
How big does an aneurysm have to be to risk surgery
5.5 cm - benefits outweight risks at this point
53
diagnosis of abdominal aortic aneurysm
asymptomatic physical exam plain x-ray CT scan rupture
54
treatment of abdominal aortic aneurysms
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
indications for repair
large (\>5.5 cm) rapid expansion of \>0.5 cm/year rupture symptomatic
56
other arterial aneurysms
subclavian femoral popliteal hand

Cardiovascular (46 decks)

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