Peripheral Vascular Disease Flashcards

1
Q

Arterial stenosis is usually a result of what?

A

Atherosclerosis

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2
Q

Venous stenosis is usually a result of what?

A

Thrombosis

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3
Q

list 4 PAD risk factors

A

Diabetes (4-fold increased risk)
Smoking (2-3 X)
Lipids (2 X)
Hypertension (2X)

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4
Q

Are PAD patients at increased risk for CV death?

A

YES. 6-fold increased risk of CV death

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5
Q

What are the manifestations of PAD?

A

-Intermittent Claudication

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6
Q

describe blood flow in intermittent claudication

A

Blood flow normal at rest (no Sx), limited with exercise (Cramp, calf fatigue )

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7
Q

Describe the blood flow resulting in Ischemic rest pain/ischemic ulcers

A

Blood flow limited at rest and exercise (constant Sx)

  • Pain in the distal foot or heel, worsened by leg elevation and improved by dependency
  • Distal, painful ulcers on toes or heel
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8
Q

List some physical findings in patients with PAD

A
Decreased or absent pulses
Bruits (abdominal, femoral)
Muscle atrophy
Pallor of feet with elevation (Severe PAD)
Dependent rubor (Severe PAD)
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9
Q

What determines the severity of atrial stenosis?

A

Radius & length of the stenosis

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10
Q

What is the ABI index?

A

Ankle-Brachial Index, looks at the extent of peripheral stenosis by comparing arm BP to ankle BP.
Ankle SBP/Arm SBP = ABI
Ratio < 0.90 = PAD

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11
Q

What are the treatment GOALS for claudication?

A
  • Prevent CV events (MI, stroke, vascular death)
  • Improve limb symptoms, exercise performance and QOL
  • Heal ulcers and prevent limb loss
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12
Q

What treatment options do you have for claudication?

A

Surgery or angioplasty improves hemodynamics
Exercise training improves muscle metabolism
Drugs (cilostazol) have multiple mechanisms

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13
Q

What is an arterial aneurysm?

A

Pathological expansion of all three arterial layers

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14
Q

Normal diameter of the aorta

A

3 cm at its root;
2.5 cm mid descending thoracic aorta;
2 cm at the infra-renal aorta

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15
Q

When would you classify an expansion in the abdominal aorta as a AAA?

A
  • denoted by diameter of > 3.0 cm

- Or 50% increase in size relative to proximal normal segment

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16
Q

List the 4 mechanisms leading to aortic aneurysm formation

A

-Weakened Aortic Wall (low collagen/elastin)

17
Q

What is the 13th leading cause of death in the US?

A

Ruptured aneurysms, Annual incidence estimated 40 to 50 per 100,000 men and 7 to 12 per 100,000 women

18
Q

AAA risk factors

A

Age
Gender
Smoking
Family history

19
Q

How do AAA patients present?

A
  • 70% of patients are asymptomatic, then present with sudden death
  • 30% present with abdominal discomfort or severe pain radiating to the back, then die
20
Q

What diagnostic tests can be used to Dx AAA?

A
Plain X-ray
Ultrasound
Computerized tomography
Magnetic resonance imaging
Arteriography (May miss it because angiography views the lumen not the arterial wall)
21
Q

Prevalence of aortic dissections

A

~ 30 cases / million / yr

3-5 % sudden deaths

22
Q

What are the 2 mechanisms of aortic dissection?

A

Primary Intimal Rent/Tear

23
Q

Risk factors leading to aortic dissection

A
Hypertension (drugs e.g. cocaine)
Inherited disorders of connective tissue
Marfan syndrome
Ehlers-Danlos syndrome
Bicuspid aortic valve 
 and more...
24
Q

Presentation of pts w/ aortic dissection

A

-C/o severe, tearing pain
-Disruption of major arterial circulation leads to:
Stroke (carotid)
Syncope (vertebral)
Myocardial infarction (coronaries)
Intestinal ischemia (mesenteric vessels)
Renal failure (renal arteries)

25
Q

medical Tx of aortic dissections

A
  • Control of Pressure/Time: Beta Blockade
  • Control of Blood Pressure: Nitroprusside, ACE inhibitors, Calcium Channel Blockers
  • Control of Pain: Narcotic analgesia
26
Q

T or F: Nearly 2/3 of VTE are asymptomatic or undiagnosed

A

True

27
Q

Prevalence of VTE in patients w/ hx of MI, stroke & hip surgery

A

24% of MI patients develop VTE
60% of paralytic stroke patients develop VTE
75% of hip surgery patients develop VTE

28
Q

Stages of chronic VTE

A

Stage 1: swelling
Stage 2: Visible collateral’s
Stage 3: stasis dermatitis
Stage 4: ulcers

29
Q

Components of Virchow’s triad

A

Injury
hypercoagulability
Abnormal flow (stasis)

30
Q

Mechanisms of thrombophilia

A

Imbalance in coagulation that causes the following:

  • increases thrombin production
  • enhances platelet activation/aggregation
  • mediates endothelial activation/damage
  • and/or mediates fibrinolytic inhibition
31
Q

Thrombophilia risk factors

A
  • Severe inherited thrombophilia (homozygous protein C deficiency) is rare
  • Mild inherited thrombophilia (heterozygous Factor V Leiden) is common
  • Acquired thrombophilia is especially common in infection, inflammatory and certain drugs
32
Q

Parenteral Xa inhibitors

A

Heparin, LMWH

33
Q

Parenteral direct thrombin inhibitors

A

Argatroban, Dabigatran (can be oral as well)

34
Q

Direct oral inhibitors of Xa

A

Apixaban

35
Q

Oral anticoag targeting II, VII, IX, X

A

Warfarin