Patho & Treatment - Peripheral Arterial Disease Flashcards

1
Q

What type of arteries are atheromas more likely to form in?

A

Large, high flow arteries

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2
Q

What are the main preventable risk factors driving the development of peripheral artery disease?

A

Smoking

Diabetes

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3
Q

What are the various names given to peripheral arterial disease (PAD)?

A

Peripheral artery atherosclerosis

Peripheral artery occlusive disease (PAOD)

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4
Q

What is an atheroma?

A

A collection of lipids, cholesterol, fibroblasts and S.mm cells & collagen fibres – lying under the intima & projecting into the lumen within peripheral circulation

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5
Q

What occurs within the artery when an atheroma is there?

A

Endothelial dysfunction (NO) - limited vasodilation
Vessel stenosis & tissue ischaemia
Possible thrombus formation

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6
Q

What condition are you 40-60% more likely to have if you already have PAD?

A

Cerebral artery disease, atherosclerotic disease of the coronary and cerebral circulation

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7
Q

Name the risk factors for PAD

A
  1. Dyslipidaemia
  2. Sedentary lifestyle
  3. Hypertension
  4. Age (20% of >65 year olds)
  5. Gender - males have higher risk of PAD as in the UK more men smoke than women
  6. Diabetes - the main driving force behind PAD
  7. Smoking
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8
Q

How does smoking impact the integrity of the blood vessels?

A

Smoking activates the SNS i.e. nicotine activates nicotinic receptors on the adrenal medulla causing production and release of catecholamine

  • This causes VC of arterioles - increases TPR - increasing blood pressure - increasing shearing forces and causing endothelial damage

Endothelial damage is the starting point of atheroma. The nicotine acts directly on the endothelial cells causing damage & it damages beta cells in islets of Langerhan in the pancreas

  • If enough beta cells are damaged, hyperglycaemia occurs which then causes endothelial damage through glucose attachment to lipids and protein in the endothelial wall (i.e. glycosylation). This results in the formation of advanced glycolytic end products which precipitate an inflammatory response & causing more endothelial damage
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9
Q

What is the impact of smoking on the risk of getting PAD?

A

Smokers develop PAD 10 years earlier than non-smokers
Smokers are more likely to progress to amputation
Smoking is a greater risk factor for development of PAD than it is for developing CHD

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10
Q

How does sudden blood vessel occlusion occur?

A

A thrombus sitting on top of a pre-exisiting ruptured atheroma
This will result in an AMI

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11
Q

How is glycaemic control in diabetes measured longterm?

A

The % of glycosyated haemoglobin (Hb1Ac)

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12
Q

How does type 2 diabetes potentially cause PAD?

A
  • Type 2 diabetes is associated with high levels of VAT
  • VAT occurs due to poor diet & lack of exercise
  • VAT secretes inflammatory cytokines which cause endothelial damage
  • Hyperglycaemia caused when there is insulin resistance, hyperglycaemia is worsened by beta cell dysfunction. Hyperglycaemia causes endothelial cell damage by AGEs
  • Both AGEs and cytokines cause a pro-inflammatory state
  • Lipolysis of adipocytes occurs causing the release of FFAs as an end product. Resistin helps with uptake of FFAs to be taken up by liver & converted to LDLs which cause atheroma development
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13
Q

How does type 1 diabetes potentially cause PAD?

A
  • Type 1 is driven by beta cell functioning - causing hyperglycaemia and endothelial damage
  • A lack of insulin secondary to beta cell dysfunction causes breakdown of FFAs which are taken up (without the assistance of resistin) converted to LDLs by liver which causes atheroma formation
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14
Q

How is PAD classified in terms of disease progression?

A

Non-critical limb ischaemia

Critical limb ischaemia

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15
Q

What is the main symptom of non-critical limb ischaemia?

A

intermittent claudication (i.e. pain with activity)

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16
Q

What is the main symptom of critical limb ischaemia?

A

Intermittent claudication accompanied by one of the following symptoms;

  1. Rest pain
  2. Tissue loss or ulceration
  3. Tissue necrosis/gangrene
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17
Q

Describe the different levels in the Fontaine Classification of PAD

A

I. “Subclinical” – subtle changes e.g paraesthesia/anaesthesia – cold extremities – diminished pulses & restless leg syndrome

II. Characterised by intermittent claudication (treadmill test) (depending on how far they can walk)
IIa. Intermittent Claudication > 200m
IIb. Intermittent Claudication < 200m

III. Rest pain (initially at night)

IV. Ischaemic ulcers or gangrene

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18
Q

Describe thermal imaging used to diagnose PAD?

A

identifies warm and cold areas of the leg. Warm = i.e. red areas where the blood can perfuse. Cold = purple, dark green, yellow - blood is not perfusing here and there may be an atheroma in that artery

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19
Q

Describe the ankle-brachial pressure index (ABPi)

A

Its used to diagnose PAD
Systolic pressure is taken at brachial artery and compared to systolic pressure taken at posterior tibial or the dorsalis pedis artery

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20
Q

Name all the ways PAD can be measured

A
Fontaine classifcation
Thermal imaging
Ankle brachial pressure index (ABPi)
Doppler & pulse volume recordings
Angiogram
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21
Q

Name the ABPi score for each clinical status

A

Symptom free: 1
Intermittent claudication: 0.95 - 0.5
Rest pain: 0.5 - 0.3
Gangrene and ulceration: <0.2

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22
Q

Name the symptoms of lower limb ischaemia

A
  1. Intermittent claudication - excruciating muscle pain causing a mismatch between O2 demand and actual blood flow. Is evident when patient undertakes physical activity
  2. Diminished /absent pulse - atheroma has ruptured, blood flow has been interrupted and a thrombus has formed
  3. Atrophic skin changes - poor nutrition to skin as there is inadequate arterial blood supply. Dry, flaky, shiny skin
  4. Skin colouration
  5. Elevation pallor & dependent rubor (redness) - pallor when foot is horizontal and gets worse when foot is raised.
  6. Sensory disturbances - becomes worse as the disease progresses
  7. Cold extremities
  8. Sarcopenia
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23
Q

What is the arch of pain in intermittent claudication?

Where is pain located typically in intermittent claudication?

A

Pain subsides after physical activity has ceased. When the atheroma gets larger the ischaemic threshold is reduced
Femero-popliteal (calves) is the most common artery

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24
Q

What is the outcome of intermittent claudication?

A

40% improve over 2 years
40% remain unchanged
20% will deteriorate & develop critical limb ischaemia
2-8% need amputation

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25
Q

How does sarcopenia occur in PAD?

A

Occurs due to sedentary behaviour causing disuse atrophy (due to the pain associated with intermittent claudication will cause the patient to reduce their levels of physical activity)

Loss of muscle fibres driven by age & death of anterior horn cells

Inflammatory processes (reactive oxygen species and inflammatory cytokines) drive muscle atrophy and sarcopenia

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26
Q

What are the NICE guidelines for management of non-critical limb claudication?

A
  1. Diet
  2. Smoking cessation
  3. Control hypertension
  4. Regulate HLD:LDL (statins)
  5. Regulate blood glucose & HB1AC levels
  6. Aspirin
  7. Peripheral vasodilators
  8. Supervised exercise to include walk programme
27
Q

Is weight-bearing or non-weight bearing exercises best for improving claudication in PAD?

A

Better to do weight-bearing exercises however if patients are very ischaemic then you should start them on non-weight bearing exercises

With PAD patients you should push them into ischaemic pain. In CVD patients you should never push them into pain

28
Q

Should exercise be supervised or unsupervised?

A

Supervised exercise programmes produce greater increase in distance of pain free walking (before intermittent claudication comes on)

29
Q

What is the prescription of exercise per week and what would it consist of?

A
Supervised exercise programme
2hrs / week
For 3 months
Aerobic exercise - non-weight bearing like rower, bike. Could do weight-bearing also - such as stepper/stair climber
Strength/flexibility 

and patients should do independent exercise such as walking in moderate intensity pain (4/5 on the pain scale) limits outside of their exercise plan. Walk for a minimum of 3-5 minutes. They should take a break (they should record duration & frequency of breaks) when they go into moderate intensity pain
- Repeat for 30min if possible
Increase incline - ensure they are walking for 3 minutes
Then increase speed

30
Q

What outcome measure would you use for PAD patients?

A
1. Claudication Scale - 5-point pain scale
1= no pain
2= pain/discomfort begins
3= mild pain or discomfort
4= moderate pain
5= severe pain
  1. Or Borg CR-10 Scale (not the RPE Scale)
31
Q

What physiological changes are likely to occur in a walk training programme to influence pain characteristics (freq & intensity) function?

A
  1. Improved blood supply through angiogenesis

2. Classic skeletal muscle type I training effect - improved fibre aerobic efficiency

32
Q

What causes angiogenesis to occur as a consequence to an exercise programme for PAD patients?

A

When tissues are ischaemic they release the following (which act on the arterial wall to promote the formation and development of angiogenesis)

  • Vascular endothelial growth factor (VEGF)
  • Fibroblastic growth factor (FGF)
  • Platelet derived growth factors (PDGF)
  • Tumour necrosis factor (TNF)
33
Q

Does exercise ALWAYS improve intermittent claudication?

A

Sometimes despite being on vasodilator drugs, adhering to the exercise programme and improving diet etc intermittent claudication does not improve and it interferes with QoL or worsens symptoms. If this occurs vascular surgery is performed

34
Q

What condition is more likely to occur if a patient has critical limb ischaemia (CLI)?

A

A CVD - AMI or a stroke

35
Q

Define CLI

A
Chronic ischaemia with at least one of: 
• - rest pain - often worse at night
• - ulceration 
• - gangrene
in one or both legs secondary to objectively proven occlusive disease.
36
Q

Why is rest pain worse at night?

A

Core temperature drops and due to inactivity cause a fall in metabolic demand which causes a drop in HR & BP
BP is the driving force behind perfusion compounding arterial insufficiency
They try to use gravity to help perfuse their lower limbs

37
Q

What is used to treat rest pain?

A

Opiates - morphine

Lumbar sympathectomy - identifying the autonomic nerve supplying the arteriole and severing it which removes the vasomotor control over the arteriole (reduces VC and causes arteries to VD). Very high risk procedure due to spine

Angioplasty or by-pass grafting

Amputation

Lifestyle modification

38
Q

Describe where arterial ulcers usually occur and some of the symptoms and treatments used

A
Dorsum of foot or in pre-tibial area
Irregular in shape
Very painful
Usually deep
Inflammation around the wound

Necrotic tissue is excised
Broad spectrum antibiotics are used, may need vascular reconstruction or skin grafting

39
Q

What are the NICE guidelines for management of critical limb ischaemia?

A

Continued lifestyle modifiation to prevent AMI and stroke
Angelgesia
Angioplasty (+stent)
By-pass grafting
Amputation
Cardiovascular drugs - anti-platelets (aspirin), statins to prevent thrombus formation if an atheroma ruptures

40
Q

What treatment would you give someone who has gangrene/necrosis?

A

Amputation

41
Q

What surgery is available for critical limb ischaemia?

A

Angioplasty

By-pass grafting

42
Q

At what point is surgery offered for patients with PAD?

A

When patient has critical limb ischaemia so their condition doesn’t progress to tissue death

43
Q

Describe the procedures available to remove a local atheroma in arterial insufficiency?

A

Directional or laser atherectomy
Balloon angioplasty +/- stent insertion
- Often called percutaneous transluminal angioplasty - a peripheral PCI

44
Q

Describe the procedures available to remove multiple atheromas in arterial insufficiency?

A

(same procedure used for coronary by-pass surgery)
By-pass grafting
- saphenous vein is most often used, femoral - popliteal vein is used also (both used as they are such long veins)
- the vein is inverted (turn upside down) so it can function as an artery instead of a vein

45
Q

What type of medication would patients be on?

A

Anti-platelets e.g. clopidogrel, prasugrel and ticagrelor

Statins - mandatory for atheroma-based diseases e.g. simvastatin, avrostatin, fluvastatin

Anti-hypertensives - beta-blockers i.e. olol - metaprolol, atenolol, propranolol

Anti-hyperglycaemics - sulfonyureases i.e. -ide - glimepriide, glipizide, glyburide or metformin which is a biguanide (lowers production of glucose in the liver)

46
Q

What does post-graft physiotherapy look like?

A

Mobilise patient
Aerobic and strength exercise
Education - behavioural modifications

47
Q

Name the reasons why a limb may be amputated

A

Malignancies
Trauma
Complications of diabetes mellitus
Atherosclerotic cardiovascular disease

48
Q

Name some possible co-morbidites an elderly amputee may have

A

hypertension, diabetes, peripheral neuropathy, reduced vision, peripheral vascular disease in the intact limb, deconditioned

49
Q

What are the recommended 2 components of physical activity for disabled adults?

A
  • 120-180 min a week of moderate to vigorous intensity exercise along with
  • 2 sets of strength and balance exercises X2/week
50
Q

Do amputees regularly engage in physical activity?

A

Majority do not undertake enough physical activity to be classified as sufficiently active

51
Q

When an amputee exercises what is the effect on their body (specific lung and heart measurements) ?

A

Activities are much less efficient
Cardiovascular demands are higher than in non-amputees
Lower aerobic capacity and lower VO2 peak
Metabolic costs of walking is more demanding on VO2 and HR
–The higher the amputation in the leg the greater the additional energy expenditure is

52
Q

What is the explanation for the increased metabolic costs of walking in amputees?

A

Vascular amputations often associated with a greater metabolic cost than traumatic amputations, even when the level of amputation is the same.
Elevated metabolic cost of walking may be related to the number, type, and magnitude of compensations to control balance and propulsion e.g. the hip having to control the amputated knee, hip hiking

53
Q

What are the specific benefits of aerobic training in amputees?

A

Improvement in the ventilatory response to exercise & the ventilatory threshold
Increased maximal oxygen consumption (mean of 20%)
Improved psychosocial well-being & self-efficacy
Improved insulin sensitivity & reduced risk of prediabetes or diabetes
Decrease in metabolic costs during ambulation
Decreased blood platelet adhesiveness, fibrinogen, & blood viscosity & increased fibrinolysis
Increased vagal tone & decreased adrenergic activity, resulting in improved heart rate variability

54
Q

What are the specific benefits of resistance training in amputees?

A

Reduced muscle atrophy in the amputated & intact limbs
Increased balance & stability in the intact limb
Increased hip flexor strength in the amputated limb will enable ground clearance of the prothesis during the swing-phase of the gait cycle
Increased upper body strength enables self-care activities, walking with crutches, transfers & self- propelling in a wheel-chair.

55
Q

What are the specific benefits of flexibility training in amputees?

A

(With a prosthesis) it will reduce the risk of developing hip & knee contractures

Increase gastrocnemius & soleus ROM of the intact limb to reduce the loss of dorsiflexion.

56
Q

What are the overall health benefits of physical activity in amputees?

A

Reduces;

  1. Type 2 diabetes
  2. Colon cancer
  3. Breast cancer
  4. All-cause mortality
  5. Cardiovascular disease
  6. Dementia
  7. Hip fractures
  8. Depression
57
Q

What are the aerobic FITT recommendations for individuals with lower limb amputation?

A

Frequency: 3-7 days/week
Intensity: Moderate (40-50%HHR), vigorous (60-80% HRR)
Time: 120-180 min moderate-vigorous intensity
Type: Activities using large muscle groups - treadmill, bike, rowing, swimming

58
Q

What are some considerations for aerobic training in amputees with prosthesis?

A

Avoid high impact (stump)
Lower the heart rate training zone by 10 bpm when doing arm ergometer
Avoid treadmill in early stage to avoid falls
Short bouts of 5-10min
Ensure knee locking mechanism is released so the prosthesis at the knee can bend

59
Q

What are the strength/resistance training FITT recommendations for individuals with lower limb amputation?

A

F: A minimum of 2 non-consecutive days/week (preferably 3 days/week)
I: Moderate - vigorous (60-80% of 1-RM)
8-10 exercises, 2-4 sets of 8-12 reps
T: Resistance machines, bands, free weights, partial/full bodyweight

60
Q

What are some considerations for strength/resistance training in amputees with prosthesis?

A
  • Use both open-chain and closed chain exercises (adapting open-chained in closed chain)
  • Lower-extremity regimen should include exercises for the surrounding hip muscles, especially hip abductor & hip extensor groups for pelvic stabilization
  • Shoulder stabilizers, adductors, and depressors, elbow extensors, wrist stabilizers, and hand-grasp strength are of prime importance for supporting the body for transfers and the use of walking aids
61
Q

What are the flexibility training FITT recommendations for individuals with lower limb amputation?

A

To increase ROM and decrease contractures
F: 2-3 days/week
I: Stretch to point of tightness/slight discomfort
T: Hold static stretch 10-30 sec, 2-4 reps of each exercise. Totally 60 sec
T: static, dynamic, PNF stretching

62
Q

What are the signs of ischaemia in a foot?

A
Poor quality skin and nails
No blood or oxygen
No hairs, skin dies
Toes may auto-amputate
Osteomyeslitis - bone damage - can occur and causes the patient to be unable to walk
63
Q

What occurs in wet gangrene?

A

Gas collects under the skin and foots needs to be urgently amputated

64
Q

Where does amputation usually occur?

A
Above knee - distal 1/3 of femur
Through knee
Below knee - proximal 1/3 of tibia/fibula
Symes - from distal
Forefoot - across the metatarsal bones