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Fiser ABSITE Review + Decker + TrueLearn > Chapter 27 - Vascular I > Flashcards

Chapter 27 - Vascular I Flashcards

1
Q

What is the most common congenital hypercoagulable disorder?

A

Resistance activated protein C Leiden factor

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2
Q

What is most common acquired hypercoagulability disorder?

A

Smoking

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3
Q

What are the three stages of atherosclerosis?

A

1) Foam cells - macrophages that have absorbed fat and lipids in the vessel wall
2) Smooth muscle cell proliferation - caused by growth factors released from macrophages; results in wall injury
3) Intimal disruption from smooth muscle cell proliferation - leads to exposure of collagen in the vessel wall and eventual thrombus formation - fibrous plaques then form in these areas with underlying atheromas

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4
Q

What are the risk factors for atherosclerosis?

A

Smoking
hypertension
cholesterolemia

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5
Q

Atherosclerosis is a disease of what part of the blood vessel?

A

Disease of intima

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6
Q

Hypertension is a disease of what part of the blood Vessel?

A

Disease of the media

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7
Q

Stroke is the _____ cause of death in United States

A

Third

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8
Q

What is the most important risk factor for stroke in asymptomatic patients?

A

Hypertension

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9
Q

Where is the most common site for stenosis in the carotid arteries?

A

Bifurcation

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10
Q

The normal internal carotid artery has what type of flow?

A

Continuous forward flow

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11
Q

The normal external carotid artery has what type of flow?

A

Triphasic flow

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12
Q

Where is the communication between the internal carotid artery and the external carotid artery?

A

Ophthalmic artery (first branch of ICA) and internal maxillary artery off ECA

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13
Q

What is the most commonly diseased Intracranial artery?

A

Middle cerebral artery

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14
Q

What is the most common etiology of cerebral ischemic events?

A

Arterial embolization from the ICA

-Heart is the second most common source of emboli

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15
Q

Anterior cerebral artery events cause what?

A

Mental status changes, release, slowing

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16
Q

Middle cerebral artery events cause what?

A

Contralateral motor and speech loss; contralateral facial droop

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17
Q

What is amaurosis fugax?

A

Occlusion of the atomic branch of the ICA visual changes, shade coming down over eyes; visual changes are transient
-Can see Hollenhorst plaques on ophthalmologic exam

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18
Q

What do you do with carotid traumatic injury with major fixed deficit?

A

If occluded do not repair-can exacerbate injury with bleeding
If not occluded-repair

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19
Q

When do you consider a carotid endarterectomy?

A

Any pt with symptoms + >70% stenosis.
Asymptomatic pts w/ 70 to 80% stenosis controversial.
Any pt w/ >80 to 90% stenosis should have CEA if technically possible.

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20
Q

The patient has a recent completed stroke, when do you perform CEA?

A

4 to 6 weeks

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21
Q

When can an emergent CEA be of benefit?

A

When there are fluctuating neurologic symptoms or crescendo/evolving TIAs

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22
Q

When do you shunt during a CEA?

A

When the stump pressure is less than 50

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23
Q

What is the most common cranial nerve injury with a carotid endarterectomy?

A

Vagus nerve secondary to vascular clamping during endarterectomy. Patients get hoarseness

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24
Q

What happens with a hypoglossal nerve injury during CEA?

A

Tongue deviation to the side of the injury – speech and mastication difficulty

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25
Q

What happens with a glossopharyngeal nerve injury during a CEA?

A

Unlikely. Could occur with a really high carotid lesion. Causes difficulty swallowing.

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26
Q

What happens if you damage the Ansa cervicalis during a CEA?

A

Innervates strap muscles; no serious deficits

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27
Q

What happens if you damage the mandibular branch of the facial nerve during a CEA?

A

Affects corner of mouth (smile)

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28
Q

What do you do if there’s an acute event immediately after a CEA?

A

Go back to the OR to check for flap or thrombosis

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29
Q

How do you detect a pseudoaneurysm after a CEA and what do you do about it?

A

Pulsatile, bleeding mass after CEA. Draped and prepped before intubation, intubate, then repair

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30
Q

What percentage of patients have hypertension following a CEA and why?

A

20%. Caused by injury to carotid body. Treat with nipride to avoid bleeding.

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31
Q

What is the restenosis rate after a CEA?

A

15%

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32
Q

What are the symptoms of Vertebral artery disease and what is the treatment?

A

Diplopia, dysarthria, vertigo, tinnitus, drop attacks, incoordination, binocular vision loss.
-PTA, vertebral artery transposition to subclavian, transsubclavian endarterectomy, osteophyte resection, unroofing of transverse process foramina, resection of musculotendinous bands

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33
Q

How do carotid body tumors present?

A

Painless neck mass, usually at the bifurcation, made up of neural crest cells
-treat with resection

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34
Q

How do you get a thoracic aortic transection and what you do about it?

A

Deceleration injury

Address other life threatening injuries first

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35
Q

What are ascending aortic aneurysms usually caused by?

A

Usually caused by connective tissue disorder; cystic medial necrosis most common abnormality-Marfan syndrome

  • Often asymptomatic and picked up on routine CXR
  • Can get compression of vertebral, whore’s whisper, dyspnea, trouble swallowing
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36
Q

Transverse aortic arch aneurysms

A

From atherosclerosis. Repair symptomatic, greater than 5.5 cm, with Marfan’s greater than 5 cm

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37
Q

Descending aortic aneurysms etiology? Management?

A

From atherosclerosis. Repair if greater than 5.5 cm. Reimplant intercostal vessels below t8 to help prevent paraplegia

38
Q

Classifications of dissections?

A 
Stanford:
A) Any ascending aortic involvement
B) Descending aortic involvement only
DeBakey:
I) Ascending and descending
II) Ascending only
III) Descending only
39
Q

Where do most dissections start in the aorta?

A

Ascending aorta

40
Q

What are symptoms of an aortic dissection?

A

Can mimic MI, Searing chest pain, unequal pulses or BP in upper extremities. 95% have severe hypertension

41
Q

What are the risk factors for aortic dissection?

A

Hypertension
Marfan’s
Previous aortic coarctation repair atherosclerosis
syphilis

42
Q

And what layer of the aorta does a dissection occur?

A

Media

43
Q

Why does aortic insufficiency occur with aortic dissection?

A

Occurs in 70% with acute disease. Caused by annular dilatation or when aortic valve cusp is sheared off. Can also have occlusion of the coronaries and major aortic branches.
Death from aortic insufficiency or tamponade.

44
Q

What aortic dissections need operations?

A

All ascending aortic dissections
Descending aortic dissections with visceral, renal, or leg ischemia; persistent pain; large-size
Need to follow with lifetime serial CT scans; 30% will eventually get aneurysm formation requiring surgery

45
Q

What are the most common postop complications for thoracic aorta surgery?

A

MI, renal failure, paraplegia due to occlusion of the intercostal arteries and artery of adamkiewicz during repair

46
Q

How big is the normal aorta?

A

2 to 3 cm

47
Q

What causes abdominal aortic aneurysms?

A

Most commonly due to atherosclerosis. Form from degeneration of the medial layer. Risk factors include hypertension, male gender, smoking, elderly age

48
Q

What is the leading cause of death in AAA patients without an operation?

A

Rupture

49
Q

What is the five-year rupture risk of a 5 cm AAA? What is the five-year rupture risk of an 8 cm AAA?

A

15 to 20%. 100%.

50
Q

What is seen on the CT of a ruptured AAA?

A

Fluid in retroperitoneal space, extraluminal contrast

51
Q

Where are AAA’s most likely to rupture?

A

Left posterior lateral wall, 2 to 4 cm below renals
Most likely rupture in presence of diastolic hypertension or COPD
50% mortality with rupture

52
Q

When do you need to re-implant the IMA?

A 
When back pressures less than 40 MM HG
Previous colonic surgery
Stenosis at SMA
Float to left colon appears inadequate
Ligate bleeding lumbar arteries
Maintain flow to at least one internal iliac artery
53
Q

What major vein injury is common with AAA repair

A

Retroaortic renal vein with proximal cross-clamp

54
Q

What is the mortality of an elective AAA repair?

A

5%

55
Q

What is the number one cause of acute death after AAA surgery?

A

MI

56
Q

What is the number one cause of late death after surgery for a AAA?

A

Renal failure

57
Q

What is the rate of AAA repair graft infection?

A

1%

58
Q

What is the risk of pseudoaneurysm after AAA graft placement?

A

1%

59
Q

What is the most common late complication after aortic graft placement?

A

Atherosclerotic conclusion

60
Q

What can cause ischemic colitis after a AAA repair?

A

The inferior mesenteric artery is often sacrificed

61
Q

What is a type endoleak?

A

Proximal or distal attachment zone
Stent migration
Treats with proximal or distal extension cuff

62
Q

What is a type II endoleak?

A

Retrograde endoleak
patent lumbar, IMA, intercostals, accessory renal etc.
Treat w percutaneous coil embolization

63
Q

What is a type III endoleak?

A

Midgraft component disconnection
Fabric tear
Treat with secondary Endograft

64
Q

What is a type IV endoleak?

A

Graft wall porosity or suture holes

Treat with secondary stenting or observe

65
Q

What is a type V endoleak?

A

High intrasac pressure without leak shown

Secondary repair or open repair

66
Q

What is an inflammatory aneurysm?

A

Occurs in 10% of patients
Adhesions to the third and fourth portions of the duodenum
Ureteral entrapment in 25%
Not secondary to infection
Weight loss, increased ESR, thickened rim above calcifications on CT scan

67
Q

Mycotic aneurysms etiology? Symptoms? Imaging findings? Management?

A

Salmonella number one cause, staphylococcus number two
Pain, fevers, positive blood cultures and 50%
Periaortic fluid, gas, retroperitoneal soft tissue edema, lymphadenopathy
Need extra Anatomic bypass and resection of infrarenal abdominal aorta to clear infection

68
Q

Aortic graft infections etiology? Imaging findings? Management?

A

Staphylococcus number one, E. coli number two
See fluid, gas, thickening around graft
Resect graft and bypass through non-contaminated field
Blood cultures negative in many patients
More common with graphs going to groin

69
Q

Aortoenteric fistula timing? Symptoms? Location?

A

Usually occurs more than six months after surgery
Herald bleed with hematemesis, then blood per rectum
In third or fourth portion of duodenum near proximal suture line

70
Q

What is affected in the anterior leg compartment?

A

Deep peroneal nerve-dorsiflexion, sensation between first and second toes
Anterior tibial artery

71
Q

What is affected in the lateral leg compartment?

A

Superficial peroneal nerve-Eversion, lateral foot sensation

72
Q

What is affected in the deep posterior leg compartment?

A

Tibial nerve-plantarflexion, posterior tibial artery, peroneal artery

73
Q

What is affected in the superficial posterior leg compartment?

A

Sural nerve

74
Q

What are the signs of PVD?

A

Power, hair loss, dependent rubor, abnormal nail growth, slow capillary refill
Most commonly due to atherosclerosis

75
Q

What is the number one prevention agent for atherosclerosis?

A

Statin drugs

76
Q

Gluteal claudication pain is due to blockage of what artery?

A

Aorto iliac disease

77
Q

Midthigh claudication is due to disease in what artery?

A

External iliac

78
Q

Calf claudication is due to disease of what arteries?

A

Common femoral artery or proximal superficial femoral artery

79
Q

Foot claudication is due to disease of what artery?

A

Distal superficial femoral artery or popliteal disease

80
Q

What can mimic claudication?

A

Lumbar stenosis

81
Q

What can mimic rest pain?

A

Diabetic neuropathy

82
Q

What is Lerich syndrome?

A

No femoral pulses
Gluteal or thigh claudication
Erectile dysfunction
Lesion at aortic bifurcation or above

83
Q

Where is the most common atherosclerotic occlusion in the lower extremities?

A

Hunters canal-distal superficial femoral artery exits here. Sartorius muscle covers hunters canal

84
Q

What is postnatal angiogenesis?

A

Budding from pre-existing vessels; AngioGenin involved

85
Q

At what ABI do you get rest pain?

A

Less than .5

86
Q

At what ABI do you get ulcers?

A

Less than .4. Ulcers usually start in toes

87
Q

Why are ABI’s inaccurate in patients with diabetes?

A

Incompressible vessels

88
Q

What are the surgical indications for PVD?

A

Rest pain, ulceration or gangrene, lifestyle limitation, atheromatous embolization

89
Q

When does PTSD have decreased patency?

A

When the graft crosses the knee

90
Q

Aorto iliac occlusive disease?

A

Treat with AF two
In high-risk patients perform bilateral axillary femoral bypasses or an axillary femoral bypass with a femoral to femoral crossover To stay out of the abdomen

91
Q

What do you do with isolated iliac lesions?

A

Angioplasty with stent is first choice; if that fails perform aorto bifemoral repair or femoral to femoral crossover

92
Q

What is the patency of femoropopliteal grafts?

A

75% for five years. Improved patency rate in patients with surgery for claudication as opposed to limb salvage

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