Peripheral Vascular Disease Flashcards

1
Q

What is the prevalence of peripheral artery disease in the adult population? What about for those over 70 or diabetic or smoker?

A

Adult population: 10-12 %

Old/diabetic/smokers: 20%

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2
Q

PAD patients have a 6 fold increase of CV death. Out of the following risk factors, which has a greatest risk increasing PAD?

Diabetes

Smoking

Lipids

Hypertension

A

Diabetes (4-fold increased risk)

Smoking (2-3 X)

Lipids (2 X)

Hypertension (2X)

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3
Q

Your patient is a 68 year old with a typical case of PAD. What would you expect the patient to have in each of the following? 1) Past Medical History 2) Risk factors 3) Physical exam

A

PMH: Developing symptoms of calf cramping on walking 1 block, relieved by rest

Risk factors: 50 pack years smoking, LDL 135, & diabetes

Physical exam: Bruit Left leg: absent femoral and pedal pulses Right leg: normal femoral and pedal pulses

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4
Q

Ok so the signs of PAD are bruits, absent pulses, muscle atrophy, leg ischemia (ulcers, gangrene, pallor of feet with elevation, rubor). But what are the symptoms they will complain of?

A
  • Intermittent claudication (cramping, fatigue with exercise) or Ischemic pain/ ulcers/ gangrene at BOTH rest and exercise
  • Pain in distal foot worsened with elevation
  • Distal, painful ulcers on toes or heel
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5
Q

What is the ankle-brachial index (ABI)?

A

Its a ratio of the blood pressures at the ankle and arm

*Should be equal

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6
Q

If a patient has an ABI of 0.6 what condition would he have? 0.9?

A

< 0.9 = PAD

0.9 - 1.00 = atherosclerosis

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7
Q

What different factors would change arterial hemodynamics (determine blood flow in an artery with occlusive disease)?

Which would have the greatest impact?

A
  • Perfusion pressure
  • blood viscosity
  • Arterial stenosis (plaque build up)
  • radius *Greatest impact
  • length

-Flow velocity (hemodynamic severity ^ with higher velocities)

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8
Q

In peripheral arterial disease you have a stenosis that causes turbulent flow and impaired endothelial function. What effect does this have downstream?

A
  • Inability to increase flow with exercise
  • mismatched O2 supply/ demand
  • Reduced ABI
  • Inefficient oxidation
  • High oxidant stress
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9
Q

What are your approaches for therapy for someone with claudication?

A
  • Prevent CV events from coronary or carotid plaque rupture (MI, stroke, vascular death)
  • Improve limb symptoms, exercise performance and quality of life
  • Heal ulcers and prevent limb loss from gangrene
  • Treatments:
    • Surgery or angioplasty improves hemodynamics
    • Exercise training improves muscle metabolism
    • Drugs (cilostazol) have multiple mechanisms
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10
Q
  1. What layers of the vessel have pathology in an aneurysm?
  2. What’s the normal width or the aorta, and 3. how would you classify an aortic aneurysm?
A
  1. Pathological expansion of all three arterial layers
  2. The normal aorta in an adult:
  • 3 cm at its root;
  • 2.5 cm mid descending thoracic aorta;
  • 2 cm at the infra-renal aorta
  1. AAA denoted by diameter of > 3.0 cm
    * Or 50% increase in size relative to proximal normal segment
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11
Q

What are four mechanisms by which aneurysms can form?

A
  1. Weakened aortic wall (decr. elastin/ collagen)
  2. Inflammation
  3. Proteolytic enzymes (mmp’s)
  4. Biomechanical stresses (turbulent flow, thrombus)
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12
Q

At what maximum aneurysm diameter is there a 5 year rupture rate of 25%?

a. < 4 cm
b. 4.0-4.9
c. 5.0-5.9
d. 6.0-6.9
e. >7.0

A

a. < 4 cm 2%
b. 4.0-4.9 3-12%

c. 5.0-5.9 25%

d. 6.0-6.9 35%
e. >7.0 75%

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13
Q

T/F: the majority of aneurism cases are asymptomatic and then present with sudden death?

A

TRUE

  • 70% of patients are asymptomatic, then present with sudden death
  • 30% present with abdominal discomfort or severe pain radiating to the back, then die
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14
Q

How are aneurysms usually found?

Then how are they diagnosed?

A
  • Aneurysms are rarely detected by PE, and usually found through incidently while imaging for something else.
  • Diagnosis:
    • Plain X-ray
    • Ultrasound
    • Computerized tomography
    • Magnetic resonance imaging
    • Arteriography
      • May miss it because angiography views the lumen not the arterial wall
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15
Q

Why is there a propensity for abdominal aortic aneurysms?

A
  • Fewer elastic lamellae than the thoracic aorta, making it less able to accommodate decreases in elastin levels.
  • Decreased vasa vasorum (perfusion) causes:
  • increased vessel rigidity,
  • decreased compliance,
  • decreased ability to accommodate pulsatile flow.

-Pattern of blood flow: this section withstands the greatest level of oscillating blood flow and reflected pressure waves

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16
Q

With an aortic dissection, blood penetrates in between which two layers?

Where in the aorta are dissections most common?

A

=Separates the intimal/ adventitial layer by primary intimal tear or rupture of vaso vasorum

60% of aortic dissections originate in the ascending aorta 2 cm above the coronary sinus,

10% in the aortic arch

30% in the descending aorta just distal to the left subclavian artery

17
Q

The two important factors for an aortic dissection are an inherent structural weakness in the arterial wall and an initiating event. What are risk factors for an aortic dissection?

A
  • Hypertension (drugs e.g. cocaine)
  • Inherited disorders of connective tissue
    • Marfan syndrome
  • Bicuspid aortic valve
  • Coarctation
  • Pregnancy
  • Trauma
18
Q

What clues in the patient will help you to think of an aortic dissection?

A
  • Severe, tearing pain! (only symptom in 70%)
  • Disruption of major arterial circulation leads to:

– Stroke (carotid)

– Syncope (vertebral)

– Myocardial infarction (coronaries)

– Intestinal ischemia (mesenteric vessels)

– Renal failure (renal arteries)

19
Q

Explain the medication and surgical treatment for an aortic dissection

A

Medical Rx

  • Control of Pressure/Time (Beta B)
  • Control of Blood Pressure (Nitroprusside, ACEI, CCB)
  • Control of Pain (Narcotic analgesia)

Surgical

  • Type A (aorta) if acute or chronic regurg.
  • Type B (distal) if rupture, ischemia, Marfans
20
Q
  • 25 year old female medical student
  • Flies coach to Europe
  • 24 hours after arrival has tender, swollen right calf, pain on standing

What’s wrong, and what is the treatment?

A

=DVT

-Started on LMWH heparin in hospital, then 6 months warfarin

21
Q

Describe each components of Virchow’s triad contributing to thrombosis

A
  1. Stasis (immobility, Right HF): decrease return
  2. Endothelial damage (diabetes, catheter)
  3. Thrombophilia (infection, estrogen drugs, inherited disorders)
    • increases thrombin production
    • enhances platelet activation/aggregation
    • mediates endothelial activation/damage
    • and/or mediates fibrinolytic inhibition
22
Q

LO: Describe the major sites of action in the clotting cascade of warfarin and heparins

A

Warfarin (oral):

  • Inhibits activation of Factors II VII, IX, X

Heparin (IV):

  • Factor Xa inhibitors
  • Antithrombin III activation
23
Q

What are four stages of Venous Thrombo Emboli progression?

A