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Flashcards in Vascular Disease Deck (58)
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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

2
Q

Critical progression of PAD

A

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

Numbness, tingling

3
Q

What may cause an acute progression of PAD

A

Arterial Thrombosis / embolism

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

5
Q

How might PAD affect pulses?

A
  1. Femoral and distal pulses weak or absent

2. Aortic, iliac, femoral bruit may be present

6
Q

Skin changes caused by PAD

A

Hair loss
Shiny atrophic skin
Pallor with dependent rubor

7
Q

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

A

Acute arterial occlusion

8
Q

Highly sensitive and specific test for PAD

A

Ankle-brachial Index (ABI)

ABI <0.9 is diagnostic

ABI 1.00 + is normal

9
Q

“Gold Standard” study

A

Angiography

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

11
Q

Test used to determine systolic pressures in peripheral arteries

A

Doppler ultrasound flow studies

12
Q

PAD treatment

A

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

Aspirin and/or clopidogrel

Beta blockers / ACE inhibitors, Statins

Exercise

13
Q

Highest prevalence of atherosclerotic PAD in what age range

A

60-70 years

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*
15
Q

T/F - Most patients with PAD are symptomatic?

A

False - fewer than 50% are symptomatic

though many have slow or impaired gait

16
Q

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

A

Duplex utlrasonography

17
Q

Condition that develops from superficial venous insufficiency and valvular incompetence.

A

Varicose Veins

Occurs in approx 15% of adults, esp women

18
Q

Treatment for Varicose Veins

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

Virchow’s triad for assessing risk of developing thrombophlebitis

A

Stasis, vascular injury, hypercoaguability

20
Q

Often occurs at site of IV or PICC lines

A

Superficial thrombophlebitis

21
Q

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

A

DVT

22
Q

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

A

DVT

23
Q

Most common vein involved w DVT

A

Long saphenous vein

24
Q

Percentage of patients that present DVT with no symptoms

A

50%

25
Q

Classic findings of DVT

A

swelling of involved area, heat and redness over the site

26
Q

Preferred study for DVT

A

Duplex ultrasonography

neg duplex results in patients with high suspicion warrants further testing

27
Q

Most accurate method for definitive diagnosis of DVT, but associated with increased risk and rarely indicated

A

Venography

28
Q

How can a D-Dimer be used?

A

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
Q

Study if PE is suspected?

A

CT angiography is study of choice

(Pulm angiography is “gold standard” but rarely performed)

V/Q scan can be used if CT contraindicated

30
Q

Treatment for superficial thrombophlebitis

A

Conservative!

  1. Best rest, local heat, elevation
  2. NSAIDs
  3. Antibiotics IF evidence of infection exists
31
Q

Preventing DVT in bed ridden patients

A

Elevation of foot

Leg exercises

Compression stockings / devices

Anticoagulants (Heparin) in high risk patients

32
Q

Characterized by loss of wall tension in veins, resulting in stasis of venous blood. Often associated with history of DVT, leg injury, varicose veins

A

Chronic Venous Insufficiency

33
Q

Progressive edema starting at the ankle. Itching, dull pain with standing, ulceration

A

Chronic Veinous Insufficiency

34
Q

Where are ulcers most commonly found in chronic veinous insufficiency?

A

Just above the ankle (stasis ulcer)

35
Q

Skin changes in chronic veinous insufficiency

A

Skin is shiny, thin, atrophic

Dark pigmentary changes and subcutaneous induration

36
Q

Treatment of stasis dermatitis in chronic venous insufficiency

A
  1. Wet compresses
  2. Hydrocortisone cream
  3. Zinc oxide
  4. Antifungal cream when indicated
37
Q

Systemic inflammatory condition of medium and large vessels. Frequently coexists with polmyalgia rheumatica.

A

Giant cell arteritis

38
Q

Arteries frequently involved with giant cell arteritis?

A

Temporal Artery

and other extra cranial branches of carotid artery

39
Q

What can giant cell arteritis lead to if not treated aggressively?

A

BLINDNESS

40
Q

Within 7 years, what can occur in 15% of patients?

A

Large vessel problems (e.g. thoracic aortic aneurysm)

41
Q

Patients are typically elderly and complain of unilateral temporal headache

A

giant cell arteritis

42
Q

Additional signs and symptoms of giant cell arteritis

A

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
Q

Definitive diagnosis for giant cell arteritis

A

Temporal artery biopsy

44
Q

Test indicating a temporal artery biopsy may be necessary

A

History / symptomology +

SED and CRP highly elevated

45
Q

Hematologic finding often associated with giant cell arteritis

A

Normochromic normocytic anemia and thrombocytosis

46
Q

Treatment for giant cell arteritis

A

High-dose prednisone for 1-2 months and low-dose aspirin.

initiated immediately, not to wait to biopsy results

47
Q

Weakness and subsequent dilation of the vessel wall, usually caused by atherosclerotic damage to the intima

A

Aorta aneurysm

48
Q

Genetic causes of aortic aneurysm

A

Marfan’s, Ehlers-Danlos syndrome

49
Q

Classic picture of patient with aortic aneurysm

A

Eldery male smoker with CAD, emphysema, and renal impairment

men are 8x more likely to have aneurysm

50
Q

Mortality rate for rupture of aortic aneurism (dissection)

A

90%

51
Q

Substernal, back, or neck pain. Dyspnea, stridor and cough. Dysphagia. hoarseness. Superior vena cava syndrome.

A

Thoracic aorta aneurysm

52
Q

Severe pain, “ripping” or “tearing” chest pain radiating to the back

A

Thoracic aortic dissection

53
Q

Severe back, abdominal, flank pain. Hypotension and shock

A

Abdominal Aortic Aneurism Rupture

54
Q

25% of patients with aortic aneurysms present with these diseases

A

Renal or lower extremity occlusive disease

55
Q

Study of choice for abdominal aneurysms

A

Abdominal ultrasonography

56
Q

Screening protocol for abdominal aneurysms

A

Single abdominal ultrasound for men older than 65 yrs who have ever smoked

57
Q

Diagnosing thoracic aneurysms

A

May require aortography

CT/MRI prefered over ultrasonography

58
Q

Occurrence of abdominal vs thoracic aortic aneurysms

A

90% abdominal

10% thoracic