Arterial disease Flashcards

1
Q

What is peripheral vascular disease?

A

AKA Peripheral Arterial Disease includes a range of arterial syndromes caused by atherosclerotic obstruction of the lower-extremity arteries

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2
Q

What is the aetiology of peripheral vascular disease?

A

Atherosclerosis. Rarer causes are aortic coarctation (narrowing), arterial fibrodysplasia, arterial tumour, dissection, arterial emboli, thrombosis, vasospasm, arteritis, and trauma.

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3
Q

What are the risk factors for peripheral vascular disease? (x5)

A

Smoking, hyperglycaemia, hypercholesterolaemia, hypertension, genetic susceptibility.

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4
Q

What are the types of peripheral vascular disease?

A
  • ACUTE LIMB ISCHAEMIA: commonly caused by emboli or thrombus
  • CHRONIC LIMB ISCHAEMIA
  • CRITICAL LIMB ISCHAEMIA: aka. chronic limb threatening ischaemia, characterised by rest pain for at least two weeks, and gangrene or arterial ulcers.
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5
Q

What are the signs and symptoms of acute limb ischaemia?

A

6Ps: pain, pulseless, pale, peripherally cold, paralysis, paraesthesia. Hair loss and gangrene.

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6
Q

What are the signs and symptoms of chronic limb ischaemia? (x5)

A
  • Intermittent claudication
  • THEN rest pain and gangrene at extremities.
  • Both acute and chronic limb ischaemia may be pulseless, but unlike acute limb ischaemia, limbs are warm and pink with well-developed collateral arteries.
  • Muscle wasting
  • Thickened nails
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7
Q

What is Buerger’s test?

A

Legs elevated 15 degrees and continue angle of elevation until leg becomes pale (in a normal patient, the leg should not turn pale even at 90 degrees; therefore, Buerger’s angle measures severity of ischaemia). Then hand leg over side of bed. If there is reactive hyperaemia (dependent rubor; caused by arteriole dilation to remove metabolic waste from ischaemia), this is a sign of peripheral arterial disease.

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8
Q

What are the investigations for peripheral arterial disease?

A
  • ABPI (ankle-brachial pressure index): ratio of SBP in the ankle to SBP in upper arm, measured supine and with Doppler ultrasound to more easily assess SBP. If an ABI is less than 0.9, patient has PAD. Less than 0.3 indicates critical limb ischaemia
  • Exercise ABPI: used to diagnose PAD when resting ABI is normal or borderline
  • DUPLEX US: assess location and degree of stenosis
  • ANGIOGRAPHY: catheter inserted from femoral artery, radio-dense contrast agent injected, and X-ray/CT taken. Provides anatomical detail of stenoses and occlusions
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9
Q

What is a complication of limb ischaemia?

A

Compartment syndrome from ischaemic reperfusion in acute limb ischaemia: all metabolic products of ischaemia wash through the compartment post-reperfusion leading to inflammation.

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10
Q

What are arterial ulcers?

A

Insufficiency ulcers commonly located on lateral ankle due to ischaemia.

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11
Q

What is the aetiology of arterial ulcers?

A

From peripheral artery disease which leads to ischaemia.

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12
Q

What are the risk factors for arterial ulcers? (x6)

A

Diabetes, smoking, hypercholesterolaemia, hypertension, obesity, rheumatoid arthritis.

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13
Q

What is the pathophysiology of arterial ulcers? (x3)

A
  • Most ulcers develop following minor injury that is slow to heal dure to poor blood supply.
  • In severe arterial disease, spontaneous cell death may cause skin breakdown without precipitating injury.
  • Alternatively, cholesterol deposits in atherosclerosis may embolise and occlude a vessel downstream
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14
Q

What are the signs and symptoms of arterial ulcers? (x7)

A
  • Punched-out lesion, well-defined borders, usually on lateral ankle overlying bone
  • Painful especially at night and worse on elevation
  • Minimal bleeding when knocked
  • Cool, pale and bluish around ulcer
  • Loss of leg hair
  • Faint or absent pulses
  • Increased capillary refill time
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15
Q

What are the investigations for arterial ulcers? (x3)

A
  • History and examination assisted by:
  • Positive Buerger test (elevating leg with patient lying flat – patient’s foot turns pale and becomes bright red when lowered)
  • Ankle brachial pressure index: Doppler used to measure BP in ankle and arm. If there is a large discrepancy, then arterial disease is likely
  • Transcutaneous oximetry: skin oxygen content around a wound.
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16
Q

What is gangrene?

A

Death of tissue from poor vascular supply and is a sign of critical ischaemia.

17
Q

What are the risk factors of gangrene? (x11)

A

Diabetes, PAD, smoking, major trauma, alcoholism, HIV/AIDS, frostbite, COVID-19, dengue fever, influenza, necrotising fasciitis.

18
Q

What are the symptoms of gangrene? (x5)

A

Change in skin colour to red or black, numbness, pain, skin breakdown, cool to touch. Extremities are most commonly affected.

19
Q

What are the types of gangrene? (x3)

A
  • DRY: necrosis in the absence of infection. There is a line of demarcation between living and dead tissue.
  • WET: tissue death and infection, associated with discharge.
  • GAS: subset of necrotising myositis (inflammation of muscles) caused by spore-forming clostridial species.
20
Q

What is the pathophysiology of dry gangrene? Presentation?

A

Coagulative necrosis in ischaemic tissue. Most often due to PAD but can be due to acute limb ischaemia. Affected area is dry, shrunken and dark reddish-black. The line of separation usually brings about complete separation with eventual auto-amputation.

21
Q

What is the pathophysiology of wet gangrene? Presentation?

A

Characterised by thriving bacteria and sepsis which worsens prognosis. It usually develops fast, following venous blockage and bacteria growth in the static blood. There is no demarcation line like in dry gangrene, and infected fluid can communicate with circulatory fluid (leading to sepsis). Tissue swells, emits foul odour, is soft, dark and oedematous.

22
Q

What is the pathophysiology of gas gangrene?

A

Caused by bacterial exotoxin-producing clostridial species. There is rapid onset of myonecrosis, muscle swelling, gas production, and severe pain. Gas production allows infection to spread quickly and leads to sepsis.

23
Q

What is necrotising fasciitis?

A

Rapidly progressive infection of the subcutaneous tissue that may extend to the deep fascia but not into the underlying muscle. It is a type of wet gangrene.

24
Q

What is the aetiology of necrotising fasciitis? (x3 types)

A
  • Type 1: polymicrobial infection with an anaerobe such as Bacteroides or Peptostreptococcus and a facultative (meaning optional) anaerobe such as some Enterobacterales or non-group A streprococcus.
  • Type 2: monomicrobial infection with Streprococcus pyogenes (group A streptococci)
  • Fournier’s gangrene: Type 1 necrotising fasciitis of the scrotum or male perineum.
25
Q

Which type of necrotising fasciitis is most common?

A

Type 1.

26
Q

What are the risk factors for necrotising fasciitis? (x7)

A

Diabetes mellitus, peripheral vascular disease, immunocompromising conditions, chronic renal/hepatic insufficiency, chickenpox/herpes zoster, IVDU, corticosteroids.

27
Q

What is the pathophysiology of necrotising fasciitis?

A

Bacteria introduced into the skin and soft tissue from minor trauma or surgery and extends through fascia and tracks along fascial planes extending beyond the area of overlying cellulitis.

28
Q

What is cellulitis?

A

Bacterial infection in deeper layers of skin characterised by red, painful, swollen area of skin.

29
Q

What are the signs and symptoms of necrotising fasciitis? (x4)

A
  • Severe pain or anaesthesia over the site of cellulitis
  • Systemic signs from infection tracking along fascial planes: Fever, tachycardia, N&V, and hypotension (primarily due to the action of bacterial toxins).
  • Vesicles or bullae (blistering) preceded by oedema.
  • Grey discolouration of skin in some