Disease of the Peripheral Arteries, Aorta, and Vasculitis Flashcards

1
Q

What is intermittent claudication?

A
  • Cramping, tightness, fatigue
  • Involves buttock, hip, thigh, calf, foot
  • Exercised-induced
  • Distance to claudication is unchanged
  • Does not occur with standing
  • Relieved by rest (Usually within 5 minutes)
  • Only ~ 1/3 of the PAD patients experience classic IC
    • remaining have either atypical symptoms or are asymptomatic
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2
Q

Why is peripheral artery disease (PAD) so difficult to treat?

A

PAD patients are not getting proper care

  • Among hypercholesterolemic patients:
    • 68% of CAD patients were on lipid lowering therapy
    • 46% of PAD patients on lipid lowering therapy (p=0.08)
    • 94% of CAD patients were told to follow a low fat/cholesterol diet
    • 83% of PAD patients told the same (p=0.01)
  • Exercise:
    • 71% of CAD patients exercised
    • 50% of PAD patients exercised (p<0.01)
    • 74% of CAD patients were told to exercise by their physician
    • 46% of PAD patients were told to exercise (p<0.01)
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3
Q

What is done on physical examination for PAD?

A
  • Auscultate the abdomen, femoral arteries, for the presence of bruits
  • Palpate for the presence of an abdominal aortic aneurysm
  • Palpate the femoral, popliteal, posterior tibial, and dorsalis pedis pulses
  • Inspect the feet for ulcers, fissures, calluses, tinea, tendinous xanthomas, and evaluate overall skin care

There can be a congenital absence of ankle pulses

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4
Q

How are pulses graded?

A
  • normal: 2
  • diminished: 1
  • absent: 0
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5
Q

What can be inspected in a patient with PAD?

A
  1. Hair loss
  2. Muscle atrophy
  3. Thickened and brittle toenails
  4. Smooth and shiny skin
  5. Subcutaneous fat atrophy
  6. Skin fissures
  7. Ulceration
  8. Gangrene
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6
Q

What is the difference betwen pallor and dependent rubor in PAD patients?

A
  1. Pallor
    • Supine position or elevation
  2. Dependent rubor
    • Filling of dilated skin capillaries with deoxygenated blood
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7
Q

What are some noninvasive evaluations for PAD?

A
  1. Ankle-Brachial Index
  2. Ankle-Toe Index
  3. Exercise treadmill testing
  4. Segmental limb pressures
  5. Pulse volume recordings
  6. Arterial Duplex ultrasonography
  7. Doppler Ultrasonography
  8. CT Angio
  9. MRI
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8
Q

What is ABI?

A

ABI = Ankle systolic pressure/ Brachial artery systolic pressure

  • Systolic blood pressures are measured in each arm and then at each Dorsalis Pedis and Posterior Tibialis
  • ABI for each leg is calculated by dividing the higher of either the PT or DP by the higher of the two brachial
  • If normal, repeat on treadmill
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9
Q

How can you determine the severity of PAD using ABI?

A
  • ABI values:
    • Noncompressible vessels: > 1.30
    • Normal: 0.90–1.30
    • Mild: 0.70–0.89
    • Moderate: 0.40–0.69
    • Severe: < 0.40
  • ABI<0.9 is up to 95% sensitive and specific for detecting angiographic arterial disease
  • ABI does not define the disease location
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10
Q

What radiographic tool is used to aid in PAD diagnosis?

A

Ultrasonography

  • Vessel anatomic characteristics
  • Functional significance of stenosis
  • Color flow Doppler:
    • Twofold increase in PSV→ ≥ 50% stenosis
    • Threefold increase in PSV→ ≥ 75% stenosis
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11
Q

What are the treatment goals for patients with PAD?

A
  • Smoking cessation
  • Lipid control
    • LDL-C, ≤ 100 mg/dL (Ideally <70)
    • BP control
      • Blood Pressure <140/90)
      • Use ACE inhibitors
      • B-blockers acceptable
  • Diabetes control
    • HbA1C ≤ 7.0%
  • Antiplatelet therapy
    • ASA, clopidogrel
  • Achieving ideal body weight
  • Exercise
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12
Q

How is cigarette smoking involved in PAD?

A
  • Two to fivefold increased risk of PAD
  • Approximately 84%-90% of patients with claudication are current or ex-smokers
  • Smoking increases the risk of PAD >> CAD
  • Diagnosis of PVD is made 10 years earlier among smokers
  • Amount and duration of tobacco use correlate directly with the development of PAD
  • Patients that continue to smoke experience
    • More common progression to CLI and limb loss
    • Decreased the LE arterial bypass patency rates
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13
Q

How is diabetes mellitus involved in PAD?

A
  • Two to fourfold increased risk of PAD
  • Different anatomic characteristics:
    • Extensive disease
    • Greater propensity for vascular calcification
    • Infrapopliteal disease more common
  • Among patients with PAD diabetics more likely to have an amputation
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14
Q

What is the importance of the reudction in HbA1C?

A

UK prospective diabetes study (UKPDS):

  • Risk reduction per 1% reduction in HgA1c:
    • Risk for amputation: 37%
    • Death from PAD: 43%
    • Myocardial infarction: 14%
    • Stroke: 12%
    • Heart failure: 16%
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15
Q

When are pentoxifylline and cilostazol used for PAD?

A

only in emergencies

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16
Q

What is the contraindication for cilostazol?

A

heart failure

17
Q

Exercise: Just Do It! (Nike)

Why is it beneficial?

A
  • Supervised exercise walking programs improve symptoms of claudication
    • Sessions of 30 min in duration
    • At least 3 times a week
    • At least 6 months
  • Possible mechanisms:
    • Formation of collateral vessels
    • Improvement of endothelium-depended vasodilators
    • Improvement of muscle metabolism
    • Improved walking efficiency
18
Q

What two antiplatelet drugs are beneficial in PAD treatment?

What drug is ineffective?

A
  • Aspirin, typically in daily doses of 75 to 325 mg, is recommended (Level of Evidence: B)
  • Clopidogrel (75 mg per day) is recommended as a safe and effective alternative antiplatelet therapy to aspirin (Level of Evidence: B)
  • Warfarin has no benefits and can be potentially harmful ⇒ ↑ risk of major bleeding
19
Q

Indications for Revascularization for Intermittent Claudication:

A
  • Lifestyle-limiting symptoms
  • Continued disability despite appropriate non-surgical management
  • Technically feasible revascularization options exist
  • Expectation of favorable risk/benefit ratio
  • Revascularization options:
    • Percutaneous
    • Surgical
    • Combined
20
Q

What patients are at risk for acute aortic dissection (AoD)?

A

Consider acute aortic dissection in patients with:

  1. Chest, back or abdominal pain
  2. Syncope
  3. Symptoms consistent with perfusion deficit
    • CNS, mesenteric, myocardial, or limb ischemia
21
Q

What is seen on physical exam in a patient with AoD?

A
  • Vital signs at baseline
  • Cardiac exam- Murmurs , heaves, and pulses
  • Pulmonary exam- Rales
  • Neuro exam: Focal deficits
22
Q

What is the differential diagnosis for AoD?

What do you look for on CxR, ECG, echocardiogram and CT chest?

A
  • Differential diagnoses:
    1. Acute myocardial infarction
    2. Aortic dissection
    3. Aortic aneurysm
    4. Pulmonary embolism
  • Chest X Ray: Heart size and contour
  • ECG: Identify ischemia, pericardial effusion,
  • Echocardiogram: Look at the heart valves, cardiac function, aortic disease
  • CT Chest: Look for pulmonary embolism or aortic dissection
23
Q

What are the high risk features associated with AoD?

A
24
Q

What is done in a patient with two or more high risk features?

A

immediate surgical consultation and arrange for expedited aortic imaging

25
Q

What do you do to stabilize a high risk AoD patient prior to surgery?

A

Reduce the wall stress on the aorta

  1. IV metoprolol to lower blood pressure and heart rate (60 beats/min)
  2. DO NOT LOWER HEART RATE IF SEVERE AORTIC INSUFFICIENCY IS PRESENT
  3. Calcium channel blockers (e.g. diltiazem) can be used if patients cannot tolerate beta blocker
  4. Once heart rate is controlled and Blood Pressure is >120 mmHg, then IV ACE inhibitors or vasodilators can be given
  5. DO NOT GIVE VASODILATORS (HYDRALAZINE) BEFORE BETA BLOCKER! (REFLEX TACHYCARDIA INCREASES WALL STRESS)