Peripheral arterial disease (PAD) Flashcards

1
Q

Why does PAD occur?

A

Due to atherosclerosis causing stenosis of arteries via a multifactorial process involving modifiable and non-modifiable risk factors

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2
Q

Pathophysiology of PAD

A

Oxygen supply/demand imbalance and ischaemia is the basic underlying pathophysiology

Stress induced physiological malfunction
First presentation
- Exercised induced angina
- Intermittent claudication

Structual and functional breakdown

  • Ischaemic cardiac failure
  • Critical limb ischaemia
  • Vascular dementia

Infarcation
Severe cases where tissues are starting to die
- Gangrene

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3
Q

Signs and symptoms of PAD

A

Symptoms:

  • Cramping pain in calf, thigh or buttock after walking for given time (claudication distance) and relieved on rest
  • Calf claudication = femoral disease
  • Buttock caludication = iliac disease
  • Ulceration, gangrene
  • Foot pain at rest - better hanging foot off bed
  • Young heavy smokers are at risk of Buerger’s disease

Signs

  • Absent femoral, popliteal or foot pulses
  • Cold, white legs
  • Atrophic skin
  • Punched out ulcers (often painful)
  • Postural/dependent colour change
  • Capillary filling time >15 seconds in severe ischaemia
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4
Q

Common presentations of PAD?

A
  1. Intermittent claudication - chief presentation (10% prevalence) - due to lactic acid formation causing pain while walking
  2. Critical leg ischaemia - rest pain, normally nocturnal (relieved by hanging leg off bed)
  3. Acute limb ischaemia - sudden cessation of blood supply blocking femoral artery in leg (leg doesn’t have. time to adapt and create collateral vessels and limb will. die if not treated) - commonest cause is thrombosis, followed by trauma.
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5
Q

Investigations for PAD?

A

Investigate the pathophysiology

  • Blood glucose - exclude DM
  • Lipids
  • Vasculitic screen
  • BP

Image the vessels

  • Colour Duplex Ultrasound* - first line - very good and non invasive (technician dependent)
  • CT/MRA - cross sectional imaging for extent and location of stenoses and quality of distal vessels if considering intervention
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6
Q

Treatment for PAD?

A
  • Risk factor modification most important (HTN, smoking cessation is vital, BP, high cholesterol)*
  • Revascularisation for ‘critical ischaemia’

Risk factor modification

  • Aim is to reduce risk of death from MI or stroke and relieve symptoms
  • Exercise to point of pain and weight reduction
  • Control HTN, DM, hyperlipidaemia
  • Antiplatelet therapy - clopidogrel advised as first line

Revascularisation
If conservative measures have failed and PAD is severely affecting the pt QOL or becoming limb-threatening, intervention is required.
- Percutaneous transluminal angioplasty = Balloon and stent - pushes the plaque against the wall of the artery and opens it up
- Surgical reconstruction = Bypass the artery (eg. femoral popliteal artery bypass)

Amputation

  • If we cannot increased blood supply or extent of damage is severe
  • < 3% of patients with intermittent claudication require amputation within 5 years (increase in diabetes).
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7
Q

6 P’s of acute limb ischaemia?

A
  • Pain
  • Pallor
  • Pulseless
  • Paralysis
  • Paraesthesia
  • Perishing cold
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