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ABSITE > Vascular > Flashcards

Vascular Flashcards

1
Q

MC congenital hypercoagulable disorder

A

Resistance to activated factor C (Leiden factor)

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2
Q

MC acquired hypercoagulable disorder

A

Smoking

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3
Q

Stage of Atherosclerosis

A

1st: Foam cells: Macrophages that have absorbed fat and lipids in the vessel wall
2nd: Sm muscle proliferation (wall injury)
3rd: Intimal disruption (sm muscle cell proliferation); leads to exposure of collagen in vessel wall and thrombus formation –> fibrous plaques

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4
Q

Most important risk factor for stroke

A

HTN

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5
Q

Carotids supply what % blood flow to brain

A

85%

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6
Q

T/F Normal ICA has continuous forward flow

A

True

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7
Q

First branch of ICA

A

Opthalmic artery

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8
Q

T/F Normal ECA has triphasic flow

A

True: Antegrade, retrograde, then antegrade

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9
Q

First branch of ECA

A

Superior thyroid a.

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10
Q

Communication between ICA and ECA

A

Opthalmic/internal maxillary artery

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11
Q

Most commonly diseased intracranial artery

A

MCA

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12
Q

Cerebral ischemic events most commonly from ICA embolization or thrombus

A

Embolization; or low flow state from stenotic lesion

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13
Q

Second most common source of cerebral emboli to the ICA

A

Heart

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14
Q

ACA vs. MCA vs. PCA symptoms

A

ACA: AMS, release, slowing
MCA: contralateral motor/speech, contalateral facial droop
PCA: vertigo, tinnitus, drop attachs, incoordination

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15
Q

Amaurosis fugax

A

Occlusion of the opthalmic branch of the ICA (visual changes –> shade coming down over eyes); visual changes are transient

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16
Q

What do you see on retinal examination of amurosis fugax?

A

Hollenhorst plaques

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17
Q

Carotid traumatic injury with major fixed deficit. Management if occluded vs. not occluded

A

Occluded: Do not repair (can exacerbate bleeding)

Not occluded: repair with carotid stent or open

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18
Q

Indications for carotid endarterectomy (symptomatic, asymptomatic)

A

Symptomatic: >50% stenosis
Asymptomatic: >70% stenosis

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19
Q

When is an emergent CEA indicated?

A

Fluctuating neurologic symptoms or crescnedo/evolving TIA’s

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20
Q

Which side to repair first if patient has bilateral stenosis?

A

Tightest side first

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21
Q

Which side to repair if patient has equally tight carotid stenosis bilaterally?

A

Dominant side first

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22
Q

Which of the 3 layers are removed during a CEA?

A

Intima, and part of the media

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23
Q

When to shunt during a CEA?

A

Back pressure is <50 mm Hg orif contralateral side is tight or occulded

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24
Q

If ICA is occluded, should you repair it?

A

No

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25
Q

Can you routinely divide the facial vein?

A

Yes

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26
Q

The MC cranial nerve injured during CEA

A

Vagus nerve 2/2 vascular clamping –> hoarseness (RLN comes off vagus)

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27
Q

If there is a hypoglossal nerve injury during a CEA, what are the symptoms?

A

Tongue deviates towards the side of the injury (speech and mastication difficulty)

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28
Q

If there is a glossopharyngeal injury during CEA, what are the symptoms?

A

Difficulty swallowing (during a high dissection)

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29
Q

The brachiocephalic artery is also called…

A

Innominate artery (R subclavian, R common carotid)

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30
Q

Some symptoms of ascending aortic aneurysms

A

Often asymptomatic

- Compression of vertebra (back pain), RLN (voice changes), bronchi (SOB/PNA), esophagus (dysphagia)

31
Q

Indications for ascending aortic aneurysm repair

A

Acutely symptomatic, >5.5 cm, (> 5 cm for Marfan’s), rapid increase in size (> 0.5 cm/yr)

32
Q

Another name for a descending aortic aneurysm

A

Thoracoabdominal aneurysm

33
Q

Indications for TAAA repair

A

Endovascular: >5.5cm
Open: >6.5 cm

34
Q

Endo vs. Open TAAA risks

A

Endo: 2-3%
Open: 20% (mortality, paraplegia)

*Reimplant intercostalarteries below T8 to help prevent paraplegia with open repair

35
Q

Sanford vs. DeBakey classification of aortic dissections

A

Stanford A- any ascending involvement
Stanford B- descending only

Debakey I - asc/desc
Debakey II - asc only
Debakey III - desc only

36
Q

Where do most aortic dissections start?

A

Ascending aorta; can mimic an MI

37
Q

Classic symptoms of ascending aortic dissection

A

Tearing chest pain, unequal pulses/BP in upper extremities

38
Q

Management of deep venous thrombosis resulting from upper extremity central venous lines

A

Removal of line, heparin, bridge to Coumadin for 3-6 months

39
Q

Clinical distinctions between acute arterial embolism and acute arterial thrombosis

A

Embolism: Arrhythmia, no prior claudication/rest pain; normal contra-lateral pulses; no physical findings of chronic limb ischemia

Thrombosis: No arrhythmia, history of claudication/rest pain; absent contra-lateral pulses; physical findings of chronic limb ischemia

40
Q

MCC of acute arterial embolism

A

A fib, MI with thrombus, myxoma, aorto-iliac disease

41
Q

Most common site of peripheral obstruction from emboli

A

Common femoral artery

42
Q

When do you do a fasciotomy following an embolectomy?

A

> 4-6 hours of ischemia

43
Q

Aorto-iliac emboli is treated with… (loss of both femoral pulses)

A

Bilateral femoral artery cutdowns and bilateral embolectomies

44
Q

MC site of atheroma embolism

A

Renals

45
Q

What is blue toe syndrome

A

Flaking atherosclerotic emboli off abdominal aorta or branches

46
Q

Most common source of emboli in blue toe syndrome

A

Aortoiliac disease

47
Q

Diagnosis for atheroma embolism

A

CT C/A/P to look for aneurysm, and Echo – clot or myxoma in heart

48
Q

Treatment for acute arterial thrombosis (with an without limb threat)

A

For a threatened limb – loss of sensation/motor –> give heparin and go to OR for thrombectomy

If not threatened: angiography for thrombolytics

49
Q

Thrombosis of PTFE graft

A

Thrombolytics and anti-coagulation; if limb is threatened go to OR for thrombectomy

50
Q

Which renal artery runs posterior to IVC

A

Right

51
Q

Examples of reno-vascular HTN

A

RAS: bruits, DBP > 115, HTN in children/pre-menopausal, HTN resistant to drug therapy

52
Q

Which side: atherosclrosis vs. FMD for

A

FMD: R – PTA without stent
Athero: L – gets stent

53
Q

Indications for nephrectomy with renal HTN

A

Atrophic kidney < 6 cm with persistently high renin

54
Q

MC peripheral aneurysm

A

Popliteal

55
Q

MCC popliteal aneurysm

A

Atherosclerosis

56
Q

What % popliteal aneruysm are bilateral?

A

1/2

57
Q

What % of patients have aneurysm other than popliteal?

A

50% – AAA, femoral, etc.

58
Q

Diagnosis of popliteal aneurysm

A

Ultrasound

59
Q

Surgical indications of popliteal artery aneurysm

A

Symptomatic, >2cm, mycotic

60
Q

Surgical treatment of popliteal aneurysm

A

Exclusion & bypass; 25% have a complication that requires amputation if not treated

61
Q

What is a pseudoanurysm?

A

Collection of blood in continuity with arterial system but not enclosed by all 3 layers of arterial wall

62
Q

Treatment of pseudo-aneurysm after perc intervention

A

US guided compression with thrombin injuection (surgical repair if flow remains in PSA after thrombin injection)

63
Q

If a pseudo-aneurysm occurs a suture line early after surgery

A

Needs surgical repair

64
Q

PSA that occur at suture line late after surgery (months to years) –> suggests what?

A

graft infection

65
Q

MC variant of FMD; MC treatment

A

Medial fibro-dysplasia; PTA best bypass if fails

66
Q

Stewart-Treves Syndrome

A

Lymphangioarcoma a/w breast axillary dissection and chronic lymphedema

67
Q

Lymphangioarcoma often mets to…

A

Lung

68
Q

How can you identify lymphatic channels supplying a lymphocele?

A

Isosulfan blue dye to inject

69
Q

First line treatment of lymphocele

A

Perc drainage

70
Q

Do lymphatics contain a basement membrane?

A

No

71
Q

Do deep lymphatics have valves?

A

Yes

72
Q

What causes lymphedema?

A

Obstructed lymphatics, too few in number, non-functional

73
Q

MC infection in lymphedema

A

Strep

74
Q

Congenital lymphedema is more common L or R

A

L

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