Vascular Disease Flashcards

1
Q

Commonly result of atherosclerosis

Significant independent risk factor for cardiovascular / cerebrovascular morbidity/mortality

Initially asymptomatic, but typically progresses to claudication, ischemia, pain with exercise in lower extremities.

A

Peripheral Arterial Disease

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2
Q

Critical progression of PAD

A

Acute limb ischemia: pain at rest, skin ulceration, gangrene, loss of limb

Numbness, tingling

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3
Q

What may cause an acute progression of PAD

A

Arterial Thrombosis / embolism

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4
Q

Commonly the first symptom of PAD

A

Intermittent claudication
(Foot or lower leg pain with exercise, relieved by rest)

thigh or buttock pain may occur

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5
Q

How might PAD affect pulses?

A
  1. Femoral and distal pulses weak or absent

2. Aortic, iliac, femoral bruit may be present

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6
Q

Skin changes caused by PAD

A

Hair loss
Shiny atrophic skin
Pallor with dependent rubor

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7
Q

Pain, pallor, lack of pulse, paresthesias, poikilothermia, paralysis : INDICATE WHAT

A

Acute arterial occlusion

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8
Q

Highly sensitive and specific test for PAD

A

Ankle-brachial Index (ABI)

ABI <0.9 is diagnostic

ABI 1.00 + is normal

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9
Q

“Gold Standard” study

A

Angiography

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10
Q

Test used for locating stenotic sites and for accurate diagnosis of thrombosis or embolism - not used routinely, only to prepare for revascularization

A

CT or MRI

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11
Q

Test used to determine systolic pressures in peripheral arteries

A

Doppler ultrasound flow studies

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12
Q

PAD treatment

A

Aggressive risk factor modification
- tobacco use, diabetes, HTN, hyperlipidemia

Aspirin and/or clopidogrel

Beta blockers / ACE inhibitors, Statins

Exercise

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13
Q

Highest prevalence of atherosclerotic PAD in what age range

A

60-70 years

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14
Q

Primary sites of involvement for PAD

A
  1. Femoral and popliteal (80-90%)
    * *elderly and diabetic patients**
  2. Tibial and peroneal arteries (40-50%)
  3. Aortic and iliac (30%)
    * lesions often occur at branch points - due to increased turbulence*
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15
Q

T/F - Most patients with PAD are symptomatic?

A

False - fewer than 50% are symptomatic

though many have slow or impaired gait

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16
Q

What test is used to image and detect stenotic lesions, routinely?

A

Duplex utlrasonography

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17
Q

Condition that develops from superficial venous insufficiency and valvular incompetence.

A

Varicose Veins

Occurs in approx 15% of adults, esp women

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18
Q

Treatment for Varicose Veins

A
  1. Graduated elastic stockings
  2. Leg elevation / regular exercise
  3. Unna boot (compression boot dressing) for ulcers
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19
Q

Virchow’s triad for assessing risk of developing thrombophlebitis

A

Stasis, vascular injury, hypercoaguability

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20
Q

Often occurs at site of IV or PICC lines

A

Superficial thrombophlebitis

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21
Q

Associated with surgical procedures, prolonged bed rest, lower extremity trauma, oral contraceptives

A

DVT

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22
Q

Presents with dull pain, erythema, tenderness, and sometimes induration of involved vein, or no symptoms

A

DVT

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23
Q

Most common vein involved w DVT

A

Long saphenous vein

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24
Q

Percentage of patients that present DVT with no symptoms

25
Classic findings of DVT
swelling of involved area, heat and redness over the site
26
Preferred study for DVT
Duplex ultrasonography **neg duplex results in patients with high suspicion warrants further testing**
27
Most accurate method for definitive diagnosis of DVT, but associated with increased risk and rarely indicated
Venography
28
How can a D-Dimer be used?
To RULE OUT - a negative D-Dimer suggests ultrasonography may be omitted (D-dimers are elevated in a number of conditions - most hospitalized patients have elevated d-dimers)
29
Study if PE is suspected?
CT angiography is study of choice (Pulm angiography is "gold standard" but rarely performed) *V/Q scan can be used if CT contraindicated*
30
Treatment for superficial thrombophlebitis
Conservative! 1. Best rest, local heat, elevation 2. NSAIDs 3. Antibiotics **IF** evidence of infection exists
31
Preventing DVT in bed ridden patients
Elevation of foot Leg exercises Compression stockings / devices **Anticoagulants (Heparin) in high risk patients**
32
Characterized by loss of wall tension in veins, resulting in stasis of venous blood. Often associated with history of DVT, leg injury, varicose veins
Chronic Venous Insufficiency
33
Progressive edema starting at the ankle. Itching, dull pain with standing, ulceration
Chronic Veinous Insufficiency
34
Where are ulcers most commonly found in chronic veinous insufficiency?
Just above the ankle (stasis ulcer)
35
Skin changes in chronic veinous insufficiency
Skin is shiny, thin, atrophic Dark pigmentary changes and subcutaneous induration
36
Treatment of stasis dermatitis in chronic venous insufficiency
1. Wet compresses 2. Hydrocortisone cream 3. Zinc oxide 4. Antifungal cream when indicated
37
Systemic inflammatory condition of medium and large vessels. Frequently coexists with polmyalgia rheumatica.
Giant cell arteritis
38
Arteries frequently involved with giant cell arteritis?
Temporal Artery and other extra cranial branches of carotid artery
39
What can giant cell arteritis lead to if not treated aggressively?
BLINDNESS
40
Within 7 years, what can occur in 15% of patients?
Large vessel problems (e.g. thoracic aortic aneurysm)
41
Patients are typically elderly and complain of unilateral temporal headache
giant cell arteritis
42
Additional signs and symptoms of giant cell arteritis
Scalp tenderness, jaw claudication, throat pain, diplopia, elevated inflammatory markers Polymyalgia rheumatica occurs in 50% of patients: pain and stiffness of shoulder and pelvic girdle
43
Definitive diagnosis for giant cell arteritis
Temporal artery biopsy
44
Test indicating a temporal artery biopsy may be necessary
History / symptomology + SED and CRP highly elevated
45
Hematologic finding often associated with giant cell arteritis
Normochromic normocytic anemia and thrombocytosis
46
Treatment for giant cell arteritis
High-dose prednisone for 1-2 months and low-dose aspirin. **initiated immediately, not to wait to biopsy results**
47
Weakness and subsequent dilation of the vessel wall, usually caused by atherosclerotic damage to the intima
Aorta aneurysm
48
Genetic causes of aortic aneurysm
Marfan's, Ehlers-Danlos syndrome
49
Classic picture of patient with aortic aneurysm
Eldery male smoker with CAD, emphysema, and renal impairment **men are 8x more likely to have aneurysm**
50
Mortality rate for rupture of aortic aneurism (dissection)
90%
51
Substernal, back, or neck pain. Dyspnea, stridor and cough. Dysphagia. hoarseness. Superior vena cava syndrome.
Thoracic aorta aneurysm
52
Severe pain, "ripping" or "tearing" chest pain radiating to the back
Thoracic aortic dissection
53
Severe back, abdominal, flank pain. Hypotension and shock
Abdominal Aortic Aneurism Rupture
54
25% of patients with aortic aneurysms present with these diseases
Renal or lower extremity occlusive disease
55
Study of choice for abdominal aneurysms
Abdominal ultrasonography
56
Screening protocol for abdominal aneurysms
Single abdominal ultrasound for men older than 65 yrs who have ever smoked
57
Diagnosing thoracic aneurysms
May require aortography CT/MRI prefered over ultrasonography
58
Occurrence of abdominal vs thoracic aortic aneurysms
90% abdominal 10% thoracic