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Surgery > vascular > Flashcards

vascular Flashcards

1
Q

mc cause of arterial stenosis and occlusion

A

atherosclerosis

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2
Q

mc sites of atherosclerotic plaques

A

coronary arteries, carotid bifurcation, proximal iliac arteries, and adductor canal region of distal superficial femoral arteries

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3
Q

difference between true and false aneurysms

A

true-includes dilation of all 3 layers of arterial wall;

false (pseudo)- not all 3 and secondary to trauma, infection, or disruption of an arterial bypass anastomosis

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4
Q

mc site of aneurysms

A

infrarenal aorta, iliac arteries, and popliteal arteries

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5
Q

most life threatening occurrence of an aneurysm

A

rupture

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6
Q

best screening test for aneurysm

A

US

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7
Q

imaging for AAA

A

confirmed by US then CT; +/- angiography

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8
Q

adv of retroperitoneal incision compared to midline abdominal incision for open surgery for AAA

A

ease of access to perirenal and suprarenal aorta as well as dec postop pulmonary dysfunction

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9
Q

operative approach for AAA

A

normal infrarenal aorta and distal arteries are dissected and isolated. After heparinization, the aorta is clamped and the aneurysm incised. A prosthetic graft is sewn in place and covered with the residual aneurysm sac

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10
Q

adv of endovascular repair of AAA

A

dec periop mortality, dec blod loss, shortened hospital stay, and more rapid return to normal activty

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11
Q

disadv of endovascular repair of AAA

A

need for reg f/u requiring annual abdominal us or ct, inc rate of secondary interventions to correct problems w fixation of aortic graft, leakage of blood into aortic aneurysm safe, and risk of renal dysfunction secondary to contrast agents

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12
Q

classic triad of AAA

A

back pain, hypotension, pulsatile abd mass

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13
Q

permissive hypotension

A

w rupture AAA, restrict volume resuscitation so systolic bp stays between 70-80 w monitoring of mental status and organ perfusion; it minimizes ongoing blood loss through aortic defect

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14
Q

immediate complications of aortic aneurysm repair

A

MI, renal failure, colonic ischemia, distal emboli, hemorrhage

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15
Q

long term complications of aortic aneurysm repair

A

aortic graft infx, aortoenteric fistula, and graft thrombosis

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16
Q

pt who experiences diarrhea postop after aortic aneurysm repair should undergo what and why

A

sigmoidoscopy to eval sigmoid and rectum; can be colonic ischemia from disruption of pelvic arterial collateral flow, ligation of IMA, or period hypotension

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17
Q

sudden upper GI bleeding (“herald bleed”) after AAA replacement w prosthetic grafts

A

aortoenteric fistula; best imaging is upper endoscopy

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18
Q

endoleak I after repair of aortic or iliac aneurysm

A

leak at either the proximal or distal attachment site. This is associated with a high rate of expansion and rupture, and should be repaired with either placement of an additional stent graft or replacement of the endovascular graft with an open repair

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19
Q

endoleak II after repair of aortic or iliac aneurysm

A

persistent flow into and out of the aneurysm sac from lumbar or inferior mesenteric arteries. Generally, type II endoleaks are not treated unless there is expansion of the aneurysm sac or symptoms.

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20
Q

endoleak III after repair of aortic or iliac aneurysm

A

occur from a modular disconnection between components of the stent graft or a tear in the fabric of the graft. They should be repaired when identified

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21
Q

endoleak IV after repair of aortic or iliac aneurysm

A

due to diffusion of blood and serum through the graft and generally will resolve once anticoagulation is reversed at the conclusion of the surgical procedure.

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22
Q

PAD is dictated by what

A

number and severity of occlusions, degree of collateralization, and pt’s tolerance to limitations in walking distance

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23
Q

between the ages of 45-65 what two arteries are more likely to become stenosed or occluded in PAD

A

aorta and iliac

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24
Q

PAD below the inguinal ligament is known as

A

femoropopliteal occlusive disease- usually asymp except w extensive exercise

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25
Q

mc site of PAD

A

distal superficial femoral artery (SFA) within the adductor (hunter’s) canal

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26
Q

PAD below popliteal trifurcation known as

A

tibial occlusive ds- common in pt w diabetes, end stage renal failure, and adv age

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27
Q

leading cause of development of symptoms of PAD

A

enlargement of an atherosclerotic plaque

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28
Q

after what % of stenosis can the artery no longer adapt its diameter leading to the dev of stenosis

A

40%

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29
Q

ischemia of the lower extremity can cause

A

intermittent claudication, ischemic rest pain, skin ulceration, and gangrene

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30
Q

claudication related to PAD and not meeting the metabolic demands to muscles during exercise result in

A

conversion to anaerobic metabolism and painful local metabolic acidosis

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31
Q

Leriche syndrome

A

impotence, lower ext claud, and muscle wasting of buttocks due to aortoiliac occlusion

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32
Q

occlusion of SFA causes claudication where

A

calf

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33
Q

what does ischemic rest pain indicate

A

more advanced peripheral ischemia

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34
Q

what is rest pain caused by and what is a temporary relief

A

caused by nerve ischemia of tissues that are most sensitive to hypoxia; relief by dangling legs over side of bed or walking

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35
Q

arterial ulceration location and presentation

A

toes/heel/dorsum of foot; painful; ischemic ulcers may have punched out appearance and a pale or necrotic base

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36
Q

location of venous ulcers

A

medial or lateral malleolus (“gaiter zone”)

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37
Q

dry vs wet gangrene

A

dry is mummification of digits of foot without assoc purulent drainage or cellulitis; wet is assoc w ongoing infx, malodorous w copious purulent drainage

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38
Q

s/sx of PAD on PE

A

loss of hair on distal aspect of leg, muscle atrophy, color changes in leg, and ulcers or gangrene; Buerger’s sign

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39
Q

Buerger’s sign

A

assoc w PAD; dependent rubor; foot dangled, pooling of oxygenated blood in the maximally dilated arteriolar bed distal to an arterial occlusion causes the foot to appear red; when elevated, hydrostatic pressure dec, pooled blood drains and foot becomes white

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40
Q

what should pts w extremity ischemia be examined w

A

continuous wave doppler us

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41
Q

normally a triphasic waveform is seen on Doppler, what is seen for proximal stenosis

A

biphasic waveform and as progresses will become wider and monophasic

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42
Q

ankle-brachial index (ABI)

A

comparison of the systolic blood pressure at the level of the ankle divided by the brachial arterial pressure; this ratio provides an assessment of the degree of lower extremity arterial occlusive disease, with the brachial arterial pressure used as a control

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43
Q

results of ABI

A

> 0.9 normal,

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44
Q

dx imaging for pt w severe lifestyle limiting claudication, rest pain or gangrene

A

MRA or CTA; contrast arteriography

45
Q

leading cause of death for patients with PAD

A

MI

46
Q

medical tx PAD

A

diet modification, exercise, tobacco cessation, antiplatelet therapy, heart rate, and myocardial contractility control w beta blocker, and tx of htn, dyslipidemia, and DM

47
Q

what has been used to tx short segment stenosis of peripheral arteries

A

percutaneous transluminal angioplasty (PTA)- balloon inflated for dilation

48
Q

atherectomy

A

removal of plaque by using rotational or orbital blades or laser energy

49
Q

what meds are used after endovascular intervention for SFA stenosis/occlusions to prevent acute thrombosis

A

clopidogrel, along w aspirin, should be used for at least 1 month, followed by aspirin alone indefinitely

50
Q

standard operative tx for carotid bifurcation atherosclerosis

A

endarterectomy- excision of diseased arterial wall, including the endothelium, the occluding plaque, and portion of the media (limited use for PAD)

51
Q

principal operative tx for PAD

A

bypass procedures

52
Q

extra anatomic bypasses

A

axillary artery to femoral artery bypass grafts and femoral artery to femoral artery bypass grafts

53
Q

tx pt with ischemic rest pain and occluded superficial femoral arteries w proximal profunda femoral artery stenosis

A

opening the stenoses by profundaplasty combined with femoral endarterectomy can increase lower leg perfusion through collaterals and relieve most symptoms. However, if the ischemia has progressed to tissue loss or gangrene, it is unlikely that profundaplasty alone can adequately increase arterial inflow into the leg to heal the ulcerative lesions. In this case, arterial bypass must be performed.

54
Q

tx infrainguinal occlusive ds

A

bypass to popliteal artery above the knee (better results than below); use saphenous vein

55
Q

for limb threatening ds such as rest pain, tissue loss, or gangrene what is best tx option

A

bypass

56
Q

s/sx chronic intestinal ischemia

A

postprandial abd pain (1hr) and wl

57
Q

dx intestinal ischemia

A

pe, duplex us, cta and mesenteric angiography

58
Q

tx intestinal ischemia

A

mesenteric revascularization; prox mesenteric artery balloon angioplasty and stenting; endarterectomy or bypass w synthetic grafts

59
Q

six P’s of limb threatening acute arterial occlusion

A

pallor, pain, paresthesia, paralysis, pulselessness, poikilothermia

60
Q

causes of acute mesenteric ischemia

A

arterial occlusion (embolus or thrombosis), mesenteric venous occlusion, or nonocclusive mesenteric ischemia

61
Q

where do most emboli to the SMA lodge

A

just distal to origin of middle colic artery, approx 5-10cm from origin of SMA

62
Q

dx mesenteric ischemia

A

labs, CT w IV contrast- shows thrombus within mesenteric veins as well as thickened bowel wall

63
Q

tx of acute mesenteric venous thrombosis

A

anti coat (heparin); prompt surgery w venous thrombectomy only for an acute abdomen

64
Q

causes of arterial cerebrovascular insufficiency

A

occlusive, ulcerative, or aneurysmal ds of the carotid or vertebral arteries

65
Q

most devastating complication of cerebrovascular insufficiency

A

stroke

66
Q

what are strokes caused by

A

infarction or hemorrhage within the cerebral hemispheres; 1/3 by embolism from atherosclerotic plaques in the carotid arteries of the neck

67
Q

cerebral ischemia and infarction occur after perfusion reaches

A

ischemia

68
Q

mc cause of cerebral infarction

A

atheroembolism

69
Q

amaurosis fugax

A

fleeting blindness; transient monocular blindness that is caused by emboli to opthalmic artery (cerebral vasc)

70
Q

curtain of blindness being pulled down from superior to inferior and involving the eye ipsilateral to carotid lesion

A

amaurosis fugax

71
Q

repetitive changes in mentation, vision, or sensorimotor function that completely rev within 24hr

A

TIA- cerebral artery distribution, pts often have contralateral arm, leg, and facial weakness

72
Q

cerebrovascular accident

A

cerebral infarction; permanent neurologic deficit or stroke; region of nonviable cerebral tissue; MRI diffuse weighted imaging

73
Q

mc involved area causing neurologic deficit with cerebral vasc

A

middle cerebral artery (parietal lobe); main outflow vessel of carotid artery

74
Q

what does hypo perfusion of the middle cerebral artery cause

A

contralateral hemiparesis or hemiplegia and occasionally paralysis of the contralateral lower part of the face

75
Q

dominant hemisphere involved with cerebral vasc

A

difficulty with speech (aphasia)

76
Q

mc finding in a patient with carotid stenosis

A

cervical bruit (high freq systolic murmur) heard at angle of jaw; pt complain of buzzing or heartbeat in ear

77
Q

dx carotid artery stenosis

A

doppler us, duplex scan; definitive dx of extra cranial carotid arterial system is arteriography

78
Q

medical tx for cerebrovasc ds

A

control rf (htn, smoking, dm, hyperlipoproteinemia); anticoag (warfarin); anti platelet drugs (aspiring, clopidogrel)

79
Q

all pt with carotid stenosis whether asymp or symp must be on

A

antiplatelet (aspirin or clopidogrel) therapy, statins, and beta blockers

80
Q

risk factors for DVT

A

virchow’s triad: stasis, venous endothelial injury, and hyper coagulable states

81
Q

what happens once valves are damaged from DVT

A

ambulatory venous pressure becomes much higher and results in stasis and venous dissension, which may injure the venous endothelium and allow protein to leak into sub cut tissue causing inflammation in the interstitium

82
Q

lipodermatosclerosis

A

end process of damaged valves of DVT; scarring of the sub cut tissue in the limb

83
Q

s/sx DVT

A

asym; pain secondary to inflammation and edema; for many the first symptom is pulmonary embolism

84
Q

which venous system is more commonly the cause of DVT

A

left iliac venous system because of the potential for compression of left iliac vein by aortic bifurcation and crossing of the right iliac artery

85
Q

pe findings of DVT

A

unilateral extremity swelling or pain; calf pain precipitated by dorsal flexion of the foot (Homan’s sign)

86
Q

dx DVT

A

duplex us; doppler us; d dimer

87
Q

primary therapy of DVT

A

anticoag initially with heparin, then long term w warfarin (coumadin); INR 2-3; +/- thrombolytics

88
Q

contraindications to anticoag therapy for DVT

A

bleeding diathesis, gi ulceration, recent stroke, cerebral avms, recent surgery, hematologic disorders, bone marrow suppression

89
Q

pulmonary embolism

A

result from migration of venous clots to pulmonary arteries

90
Q

s/sx pulmonary embolism

A

pleuritic chest pain, dyspnea, tachypnea, tacycardia, cough, hemoptysis

91
Q

what is seen on ekg for PE

A

right sided heart strain

92
Q

dx PE

A

ct of chest, ventilation-perfusion lung scan or pulmonary angiogram; wedge shaped or lobar defect

93
Q

tx PE

A

anticoag; if unstable then inotropic support; if stable but compromised then thrombolytic therapy; vena caval filters

94
Q

mc cause of primary varicose veins

A

dev of incompetence of the venous valve at junction of the saphenous vein w femoral vein in inguinal region

95
Q

s/sx superficial (primary) varicose veins

A

heaviness and fatigue after prolonged standing, night cramps, and occasionally ankle edema, superficial thrombophlebitis or hemorrhage from superficial veins

96
Q

dx superficial veins (primary)

A

pe; duplex us

97
Q

tx options for superficial veins (primary)

A

stripping the saphenous vein; saphenous ligation; endogenous closure w radio frequency ablation (RFA); branch vein excision by micro incision (stab phlebotomy)

98
Q

chronic venous insufficiency is a direct result of

A

local venous hypertension

99
Q

s/sx chronic venous insufficiency

A

swollen legs, hyperpigmentation, venous ulceration in “gaiter” zone of ankleorange-brown skin discoloration at ankle w hemosiderin deposition, lower extremity edema, superficial varicosities and/or ulceration

100
Q

dx chronic venous insufficiency

A

venous duplex us, MRI/MRV or CT venogram

101
Q

where do chronic venous insufficiency ulcers usually occur

A

medial and lateral malleoli of ankle; result of venous htn and usually postthrombotic

102
Q

tx chronic venous insufficiency

A

gradient compression stocking; if ulcers medicated tightly wrapped compressions; split thickness skin grafting for wound healing

103
Q

A 68-year-old man comes to the office because he noted a pulsatile bulge in his abdomen for the past 2 years, and it is becoming more prominent. He has a remote history of Ml, and his only risk factors are one pack per day of smoking and hypertension, controlled with a diuretic. His physical exam is normal except for a pulsatile, nontender mass above his umbilicus, which measures 7 cm. What is the best initial test for this patient?

A

ct scan w contrast of the abdomen and pelvis

104
Q

A 70-year-old woman responds to an advertisement for cardiovascular screening, which includes an ABI, an EKG, an ultrasound for AAA, and a carotid duplex ultrasound. She is told that she has a stenosis in her left carotid artery of 50% to 70%, and no significant stenosis in the right carotid bulb What should your recommendation to her be?

A

repeat carotid duplex us

Carotid stenosis Is often found by screening studies but must be confirmed by another diagnostic test before treatment. Of the options available, only repeat duplex ultrasound is a low risk diagnostic test. When a screening study is abnormal, confirmation of the findings with a repeat full-length study Is often the best approach to confirm the findings. An angiogram carries a risk of stroke and has little additional information that cannot be obtained with an MR angiogram or CTA. The decision for treatment in an asymptomatic patient should be preceded by risk factor modification with low dose antiplatelet therapy, statins, and ß-blockers. Carotid stent is not approved in asymptomatic patients and CEA should not be performed in asymptomatic women until their stenosis becomes >80%.

105
Q

A 50-year-old type 1 diabetic woman has developed an ulcer that penetrates into the fat on the plantar aspect of the left foot, under the ball of her big toe. She has foot swelling so pulses are not palpable, but she has good capillary refill in the toes. The ulcer is not painful and Is not clinically Infected. What is the next best step for this problem?

A

measure ankle brachial index and toe pressures

This patient has a mal perforans ulcer, which is a neuropathic ulcer on the ball of the foot due to changes in the motor, sensory, and autonomic nerves In the extremity. The absence of ulcer pain, in itself, tells you that she has a severe peripheral neuropathy. She Is at risk for a major amputation unless she has adequate blood supply to heal, good local wound care with offloading of the ulcer, and then good footwear once the ulcer is healed. The presence of blood supply Is critical to preventing amputation, and physical exam Is not accurate for assessing perfusion, so she needs noninvasive testing, Including an ABI, toe pressures, and assessment of tissue perfusion around the ulcer. If she has a significant pressure deficit In the foot, then an angioplasty or bypass is needed to provide enough blood supply to heal the ulcer. Amputation and IV antibiotics will not be effective If there Is Inadequate blood supply.

106
Q

A 55-year-old man has degenerative hip disease and must undergo a total hip replacement. His BMI is 36.3. He is otherwise healthy and has never had an episode of deep venous thrombosis. The most appropriate DVT prophylaxis for him is: e.

A

This patient represents a high risk for DVT post-op due to his risk factor of obesity and the procedure that he is undergoing, total hip arthroplasty. Orthopedic procedures carry one of the highest risks of DVT due to the relationship between the procedure and the deep veins and the post-op immobilization often required. Of the options presented, only low molecular weight heparin (LMWH) has been demonstrated to prevent DVT in high-risk patients. Support hose are used primarily in low risk patients. Sequential compression is useful for all patients pre- and post-op, but is not as successful in preventing DVT In high-risk procedures. A venacaval filter does not prevent DVT—it merely protects the patient from DVT progressing to pulmonary embolism. Aspirin is more effective for prevention of arterial thrombosis and has minimal effect on preventing DVT.

107
Q

A 35-year-old woman comes to the office because of an ulcer on the skin of her left ankle. She developed pigmentation In her left medial ankle several years ago and then developed a superficial, painless ulcer in the center of the pigmented area 2 months ago. She had been in excellent health prior to that. She works as a schoolteacher and is on her feet most of the day. She has been unable to heal it with local wound care and comes to see you for treatment. Which of the following diagnostic tests would be most useful?

A. Ankle brachial index

B. Wound culture

C. Labs tests for autoimmune disease

D. Venous duplex ultrasound

E. Ulcer biopsy

A

Based on the location and description, as well as the age of the patient and absence of significant other medical problems, this patient has chronic venous insufficiency, the pigmentation represents lipodermatosclerosis, and the venous ulcer is likely due to reflux In the superficial, perforator, and deep venous systems. An ABI is unlikely to be helpful in a woman at her age, with the ulcer in its current location. Wound cultures are helpful occasionally in management of venous ulcers, but not to diagnose them, and the location and age make both serum autoimmune disease tests and biopsies unlikely to make the diagnosis.

108
Q

A 25-year-old man comes to the office because of right arm weakness. He is an elite swimmer, who Is otherwise healthy, but is now unable to compete due to arm weakness. On exam his left arm is stronger than his right and he has a reduced right radial pulse with shoulder elevation. The best approach to his problem is:

A. physical therapy

B. change in type of physical activity

C. angiogram and arterial repair

D. MRI followed by first rib resection

E. MR venogram, followed by thrombolysis

A

This patient has signs and symptoms of neurogenic TOS, which is commonly associated with physical activity and repetitive sports. Since he already exercises regularly, physical therapy (PT) is unlikely to help. He is an elite swimmer and is unlikely to give up his lifestyle unless there are no other options. Even though his pulse Is diminished, this is a common finding in many patients and the primary problem is thoracic outlet compression, not Intrinsic arterial disease. MRI can help determine the location of compression and other pathology, such as cervical rib. Following MRI, a first rib resection, with cervical rib removal if present, is a treatment that is likely to return him to normal function. His symptoms are primarily neurogenic, and not venous, which would be arm swelling, arm pain, and prominent veins. Therefore, venography and thrombolysis are unlikely to be needed.

Surgery (21 decks)

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