Peripheral Vascular Disease I and II Flashcards Preview

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Flashcards in Peripheral Vascular Disease I and II Deck (56):
1

peripheral artery disease (PAD)

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

2

types of PAD

claudication

rest pain

tissue loss

3

claudication

muscle pain, called intermittent claudication

typically comes on with exercise and is relieved with rest

4

rest pain

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

5

two drugs that are accepted treatment for claudication

cilostazol and pentoxifylline

cilostazol is much more effective

6

chronic changes in skeletal muscle histology

honeycomb pattern

increased adipose

increased inflammatory cells

increased angular fibers

decreased type III fibers

decreased gastroc strength - cross-sectional area

7

treatment for CAD

medication

exercise

risk factor modification and management

bypass surgery

endovascular interventions

8

emerging CAD therapies

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

stem cell therapy - bone marrow, peripheral blood

9

acute mesenteric ischemia

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

10

intestinal blood supply

celiac axis

superior mesenteric artery

inferior mesenteric artery

11

types of acute mesenteric ischemia

embolic disease

thrombolic disease

nonocclusive mesenteric ischemia

venous thrombosis

12

embolic disease

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

13

etiology of embolic disease

atrial tachyarrhythmia

MI

cardiomyopathy

heart defects

cardiac tumors

endocarditis

aortic mural thrombus

14

thrombotic disease

atherosclerosis

hypercoagulable state

15

etiology of nonocclusive mesenteric ischemia

caused by vasospasm

atherosclerosis is frequent

low flow states

hypovolemia

vasoconstrictors

vasoactive agents

aortic insufficiency

liver failure

cardiopulmonary bypass

16

venous thrombosis

superior mesenteric vein is the most common

sometimes the inferior mesenteric vein and portal vein

characterized by edema, hemorrhage, and sloughing

17

etiology of venous thrombosis

hypercoagulable state

malignancy

trauma

abdominal surgery

hepatic failure

pancreatitis

oral contraceptives

18

clinical presentation of embolic and thrombotic acute mesenteric ischemia

sudden pain out of proportion to exam

gut emptying

nausea

vomiting

diarrhea

19

clinical presentation of embolic and thrombotic chronic mesenteric ischemia

post prandial pain

weight loss

food fear

20

clincial presentation of NOMI and MVT

slower course

usually critically ill, hospitalized, intubated

abdominal pain

nausea and vomiting

bloody stool

dehydration

fluid shifts

21

diagnosis of MAD

laboratory studies

x-ray

ultrasound

CTA

MRA

contrast angiography is the gold standard

 

22

management of embolic MAD

early diagnosis

SMA embolectomy

anticoagulation

bowel resection

second look

23

management of thrombotic MAD

early diagnosis

SMA/CA bypass (venous)

anticoagulation

bowel resection

second look

24

management of NMI

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