Aneurysms and Peripheral Vascular Disease Flashcards

1
Q

What is an aneurysm?

A

abnormal localized dilation (outpouching) of an artery, vein or heart

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2
Q

What is a pseudoaneurysm? What can cause it?

A

contained ruptures of the tunica intima and media and (sometimes) adventitia of an artery. Can be due to trauma, infection, or surgery.

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3
Q

What is the difference between a saccular and fusiform aneurysm?

A

A saccular aneurysm is a discrete outpouching that usually contains a thrombus. A fusiform aneurysm is a circumferential dilation of a blood vessel.

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4
Q

What is an aortic dissection?

A

a catastrophic tear of the tunica intima letting luminal blood under high pressure into the tunica media–where it tunnels a second lumen

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5
Q

What is a type A dissection?

A

involving ascending aorta (proximal lesion)- surgical emergency! More common 2/3 of cases

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6
Q

What is a type B dissection?

A

beginning beyond the subclavian artery (distal lesion affecting ONLY the descending aorta)- not a surgical emergency

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7
Q

What is ectasia?

A

generalized dilation usually associated with aging

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8
Q

What is the biggest difference between ectasia and an aneurysm?

A

NOT localized—whole things is ballooned out so you have less of a problem because no turbulent flow!

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9
Q

Are false aneurysms stable?

A

NO they are unstable and prone to bursting (losing their containment)

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10
Q

Who gets aortic aneurysms?

A

elderly white males who smoke, have HTN and have hyperlipidemia

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11
Q

Where is the most common place for aortic aneurysms?

A

abdomen (75%)

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12
Q

Describe the pathogenesis of aneurysms.

A

Increased matrix metalloproteinases (which remodel arteries) and decreased tissue inhibitors of MMPs will allow spillover inflammation from atherosclerosis to injure and weaken the tunica media

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13
Q

Is inflammation always related to aneurysms?

A

NO, genetic defects in fibrillin (Marfan syndrome) or collagen (Ehlers-Danlos syndrome) can weaken the tunica media and presdispose to aneurysms

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14
Q

What markers of inflammation can usually be found in the blood of someone who is forming an aneurysm?

A

CRP and IL-6

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15
Q

Other than genetic disorders and spillover inflammation from atherosclerosis, what can cause aneurysms?

A

infection (called “mycotic” even when not fungal, which is most of the time)
vasculitis (e.g. giant cell arteritis)

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16
Q

What is cystic medial degeneration?

A

ischemic changes in outer media leading to smooth muscle cell loss and “degenerative changes” in the aorta (fibrosis, inadequate ECM synthesis, and accumulation of amorphous proteoglycans)

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17
Q

What symptoms MAY you see in someone with aortic aneurysms?

A
back pain (if leaking)
Pulsatile mass (palpable in thin patients)
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18
Q

What is the best way to diagnose an aortic aneurysm?

A

ultrasound

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19
Q

What is the major complication of aortic aneurysms?

A

rupture

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20
Q

What is the major determinant of aneurysm rupture?

A

diameter (over 5 cm significantly increases risk of rupture)

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21
Q

How/when do you treat an aortic aneurysm? Why?

A

when >5 cm in diameter, surgically managed (with endoluminal stent graft) because 5% survival if managed, 50% mortality if rupture!

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22
Q

What is the major factor in the rate of aneurysm growth?

A

blood pressure (hypertension accelerates aneurysm growth)

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23
Q

List other complications of aortic aneurysms?

A

Mural thrombus formation (universal)
Embolism from the atheroma or thrombus
Obstruction of aortic branches
Aortoenteric fistula (aorta erodes passage into the intestine

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24
Q

True or false: aortic aneurysms are familial.

A

TRUE (if you know of a person with AAA, you probably want to screen siblings)

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25
Q

True or false: aortic dissections are very common.

A

FALSE- they are uncommon- only around 2,000 in the US every year

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26
Q

Who gets aortic dissections?

A

late middle aged black men who have hypertension (2/3 of cases) OR younger patients with Marfan syndrome OR in late pregnancy

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27
Q

Aortic dissections usually start with what change in the vessel?

A

intimal tear

28
Q

Motor vehicle accidents with deceleration can cause an intimal tear at what structure?

A

ligamentum arteriosum

29
Q

How might rupture of vasa vasorum lead to a dissection?

A

rupture of vasa vasorum may cause hemorrhage in the wall and dissection of this hemorrhage into the lumen can cause the intimal tear needed to get the dissection started

30
Q

What is the primary symptom of a type A dissection?

A

sharp, anterior tearing chest pain

31
Q

What is the primary symptom of a type B dissection?

A

sharp, tearing chest pain felt between the scapula

32
Q

What symptoms can accompany the tearing pain of a dissection?

A

arm pain or weakness (with subclavian artery compromised), altered mental status (if carotid involved), or collapse (if it ruptures)

33
Q

What are the complications of dissection?

A

1) rupture (into pericardium)
2) occlusion of aortic branches
3) aortic valve regurgitation
4) death

34
Q

How do you diagnose a dissection?

A

Transesophageal echocardiogram
Computerized tomography
OR MRI

35
Q

How do you treat a type A dissection?

A

beta-blockers and vasodilators (to treat HTN)

surgery

36
Q

What are the cases where a type B dissection would require surgery?

A

if rupture is impending
if major aortic branches are compromised
if dissection is progressing

37
Q

What is peripheral arterial disease (PAD)?

A

chronic atherosclerotic occlusive disease of large and medium arteries–primarily of the legs

38
Q

True or false: PAD is common.

A

TRUE it is in 20% of those over 70 y/o

39
Q

What is most likely the biggest factor in flow through a vessel?

A

radius of the vessel (atherosclerotic narrowing can decrease radius and reduce flow drastically)

40
Q

What is intermittent claudication?

A

ischemic pain of the periphery–usually the legs (calves) that can be brought on by exertion and relieved by rest

41
Q

What are indicators of severe PAD?

A

pain at rest and ulcers

42
Q

What are some signs of PAD?

A
diminished or lost distal pulses
bruits
pallor
skin atrophy
muscle atrophy
ulcerations
gangrene (necrosis)
43
Q

How do you make a PAD diagnosis?

A

history and physical exam

ABR

44
Q

How do you measure ankle/brachial ratio?

A

measure blood pressure in the arm and lower leg of a supine patient

45
Q

What is a diagnostic ankle/brachial ratio for PAD?

A

an ABS less than .9 requires no further diagnostic tests for diagnosis

46
Q

What is the first line of treatment for PAD?

A

exercise (walking) in order to develop collaterals

47
Q

What are the other treatment options for PAD?

A

cilostazol (vasodilates)
pentoxifylline (decrease blood viscosity)
angioplasty
surgery (bypass or amputation)

48
Q

What is an acute arterial occlusion?

A

uncommon blockage of arteries due to thromboemboli

49
Q

Where do the thromboemboli in acute arterial occlusion usually start?

A

80% from heart

  • 65% from mural thrombi after MI
  • 10% from left atrial thrombi during a-fib
  • 5% from mural thrombi from dilated cardiomyopathy
50
Q

What are the other causes of acute arterial occlusion?

A

thrombosis in situ associated with plaque ulcer/rupture, HIT, or anti-phospholipid antibody syndrome
OR
Rare paradoxical embolism through a patent foramen ovale or ASD

51
Q

What are the signs/symptoms of acute arterial occlusion?

A

5 P’s: pain, pallor, paralysis, paresthesia, pulselessness in legs (70%) or arms (8%) or brain (10%)

52
Q

How do you diagnose acute arterial occlusion?

A

physical exam

53
Q

How do you treat acute arterial occlusion?

A

Anticoagulation (heparin)
Intra-arterial thrombolytic therapy
Catheter-based thrombectomy
Surgery (thrombectomy/bypass)

54
Q

True or false: acute arterial occlusion is a surgical emergency.

A

TRUE

55
Q

What is Buerger Disease?

A

thromboangiitis obliterans–a chronic thrombosing inflammatory disease of small and medium arteries and veins of arms and legs

56
Q

Buerger disease is 100% associated with what?

A

smoking

57
Q

Buerger disease is most common in what country?

A

10-100 times more common in Asia than US

58
Q

When does Buerger disease usually start?

A

onset is typically in 20s

59
Q

What occurs in the “acute phase” of Buerger disease?

A

Segmental transmural acute inflammation with granulomas/giant cells (but NO necrosis)

60
Q

What is characteristic of acute phase Buerger disease?

A

thromboses with “microabscesses”

61
Q

What occurs in the “chronic phase” of Buerger disease?

A

nonspecific organization and recanalizaiton of thrombus with neovascularization and fibrosis

62
Q

What are the signs and symptoms of Buerger disease?

A

instep claudicaiton
cold feet
Raynaud’s phenomenon
migrating superficial nodular thrombophlebitis

63
Q

What are the complications of Buerger disease?

A

gangrene, autoamputation of finges and toes

64
Q

How do you diagnose Buerger disease?

A

history and physical exam

65
Q

What does an angiogram of Buerger disease show?

A

stenosis with corkscrew collaterals

66
Q

How do you “treat” Buerger disease?

A

cessation of smoking

amputation