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Met 3a > Peripheral Vascular Conditions > Flashcards

Peripheral Vascular Conditions Flashcards

1
Q

Pathogenesis of Atherosclerosis

A

Normal Artery –> Fatty streak –> Fibrofatty Plaque –> advanced/vulnerable plaque–> aneurysm + rupture/occlusion by thrombus/critical stenosis

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2
Q

Normal artery –> Fibrofatty plaque RFs

A 
At lesion prone areas
Endothelial dysfunction
Monocyte adhesion/emigration
SMC migration to intima
SMC proliferation
ECM elaboration
Lipid accumulation
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3
Q

Fibrofatty Plaque –> Advanced/vulnerable plaque

A 
Cell death/degeneration
Inflammation
Plaque growth
Remodelling of plaque and wall ECM
Organization of thrombus
Calcification
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4
Q

Advanced/vulnerable plaque –> aneurysm and rupture

A

Mural thrombosis
Embolization
Wall weakening

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5
Q

Advanced/vulnerable plaque –> occlusion by thrombus

A 
Plaque rupture 
Plaque erosion
Plaque haemorrhage
Mural thrombosis
Embolization
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6
Q

Advanced/vulnerable plaque –> critical stenosis

A

Progressive plaque growth

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7
Q

Plaques are made up of

A

Cells (SMC, macrophages and other WBC)
ECM (collagen, elastin, and PGs)
Lipids

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8
Q

Intermittent claudication

A

Pain in limb- most often noticed in calf, but may also be felt in buttocks or thighs
Brought on by exertion
Relieved at rest
Recurs on similar effort

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9
Q

Spinal ischaemia

A

Spinal cord stenosis has similar pain to intermittent claudication
Difference is that just standing doesn’t make it better, they have to sit down

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10
Q

Critical Limb ischaemia

A 
Rest pain (constant pain + opiate analgesia) +/- tissue loss
<50mmHg at ankle
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11
Q

PAD epidemiology- in population 55-74 yrs

A

25% asymptomatic PAD

5%- claudication (23% of claudicants will develop CLI over 10 years)

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12
Q

PAD epidemiology

A

Correlation of ABPI with increased risk of death
PAD has a greater mortality rate than cerebrovascular/coronary artery disease
3% death per year

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13
Q

Critical limb ischaemia facts

A

90% require reconstruction/angioplasty
25% amputation rate
50% die within 5 yrs (MI, CVA)

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14
Q

Critical limb ischaemia clinical indicators/examination findings

A

Sensation
Movement
Pain

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15
Q

Critical limb ischaemia diagnosis

A

History
Examination
Investigations

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16
Q

Critical limb ischaemia investigations

A

ABPI (confounders)
Duplex
MRA/CTA
Diagnostic angiogram

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17
Q

Critical limb ischaemia RFs

A 
Smoking
Diabetes
Hypertension
Hypercholesterolaemia
Hyperhomocysteinaemia
C reactive protein
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18
Q

Claudication timeline- in 100 claudicants-

A

50 improve
30 remain same
20 deteriorate –> 5 of these have intervention–> 1/2 amputated

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19
Q

Claudication treatment- conservative

A 
Lifestyle modification (exercise)
Stop smoking
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20
Q

Claudication treatment- medical

A

Risk factor optimisation

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21
Q

Claudication treatment- surgical

A

Endovascular- angioplasty
Open- surgical bypass
Adjuncts

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22
Q

Diabetes control- claudication

A

Reduce HbA1c by 1% –> 21% reduction in complications

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23
Q

Cholesterol control- claudication

A

Simvastatin 40mg –> 24% reduction in revascularisation

HDL protective, LDL causes atherosclerosis

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24
Q

Blood pressure control- claudication

A

HOPE study 26% reduction in events

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25
Q

Anti-platelets- claudication

A

Aspirin 75mg –> 23% reduction in events

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26
Q

Anti-oxidants and vitamins- claudication

A

Omega 3 fish oils

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27
Q

Cilostazol (pletal) - claudication

A

Phosphodiesterase inhibitor

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28
Q

Claudication- angioplasty

A

Catheter inserted into femoral artery
Balloon/stent positioned
Balloon/stent expanded

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29
Q

Angioplasty risk

A 
Failure to dilate (10-20%)
Re-stenosis
Surgical salvage (<2%)
Amputation (<0.3%)
Death (<0.2%) 
Contrast anaphylaxis
Renal dysfunction <24hrs (10%)
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30
Q

Angioplasty benefit

A

Minimally invasive
Short stay
Quick recovery

31
Q

Bypass surgery

A

Preserved for patients with CL (+/- life altering claudication)
Autologous- vein
Synthetic- PTFE/Dacron

32
Q

Dacron

A

basic tube used in bypass

33
Q

PTFE

A

tube used in bypass- synthetic

34
Q

Fem- above knee popliteal bypass: 2 yr primary patency

A

long saphenous vein- 81%
Human umbilical vein- 70%
PTFE- 69%

35
Q

Fem- above knee popliteal bypass: 5yr primary patency

A

Long saphenous vein- 73%
Human umbilical vein- 53%
PTFE- 39%

36
Q

Vein patches- risks

A 
Graft failure (variables)
MI
Infections
Limb loss
Death
37
Q

Vein patches- benefit

A

Save limb
Retain independence
Wound healing

38
Q

Non surgical treatments in CLI- Prostanoids

A

Iloporost

Better than placebo for rest pain and ulcer healing

39
Q

Non surgical treatments in CLI- lumbar sympathectomy

A

Abolishes arteriolar and capillary construction

Alters pain transmission

40
Q

Non surgical treatments in CLI- Spinal cord stimulation

A

Epidural stimulation for intractable ischaemic pain

41
Q

Non surgical treatments in CLI- gene therapy

A

Angiogenic growth factors (VEGF, PDGF)

42
Q

Non surgical treatments in CLI- Stem cell therapy

A

Endothelial progenitor cells

43
Q

Aneurysm definition

A

Localised dilatation of an artery greater than twice normal diameter

44
Q

Popliteal aneurysm

A

10% of those with a AAA have a popliteal aneurysm
50% of those with a popliteal aneurysm have an AAA
50% of popliteal aneurysms are bilateral

45
Q

Abdominal aortic aneurysm epidemiology

A 
Aortic diameter >3cm 
Growth +-10%/yr
9% prevalence in men over 65
12% incidence in hypertensive men
Mortality at rupture 90%
46
Q

AAA pathology summary

A

Intimal atherosclerosis
Mural thrombus
Destruction of elastic lamellae
Inflammatory response is due to imbalance (matrix degrading proteinases don’t equal inhibitors (MMP/plasminogen activators))
Autoimmune response, increased cytokines, chemoattractants and peptide growth factors

47
Q

Altered gene products in AAA formation (in aortic tissue/blood formation)

A 
Increased proteolysis (MMP-1, MMP-9)
Increased inflammation- (cytokines, Chlamydia Ag/Ab, Adhesion molecules)
48
Q

AAA Risk factors

A 
1-5% positive family history
Ethnicity- N Europeans > Asians/Africans
Smoking- relative risk=2 (and increased expansions)
Hypercholesterolaemia
Hypertension
NOT DIABETES
49
Q

Types of aneurysm

A

Saccular aneurysm
Fusiform aneurysm
Ruptured aneurysm

50
Q

AAA- indication for surgery

A

AAA>5.5cm diameter
Rapid AAA enlargement (<1cm/yr)
Symptomatic AAA

51
Q

AAA surgery risk

A 
Mortality (5-10%)
Myocardial infarction
Multi-organ failure
Paraplegia
Haemorrhage
Infections (wound/graft)
Fistulae
Hernia
52
Q

Endovascular AAA repair (EVAR) Pros

A

2% mortality
Decreased insult
2 day hospital stay
Can be percutaneous

53
Q

EVAR cons

A

Cost
surveillance
re-interventions
durability?

54
Q

Rupture risk in 1 year- aortic diameter <5.5cm

A

1-2%

55
Q

Rupture risk in 1 year- aortic diameter 5.5-6.5cm

A

8%

56
Q

Rupture risk in 1 year- aortic diameter 6.5-7cm

A

15-20%

57
Q

Rupture risk in 1 year- aortic diameter >7cm

A

30%

58
Q

Rupture risk in 1 year- aortic diameter 10cm

A

100%

59
Q

Most frequent misdiagnoses in patients with AAAs

A 
Miscellaneous 13%
Renal colic 23%
Diverticulitis 12%
GI bleed 13%
Acute MI 9%
Back pain 9%
Motor vehicle accident 7%
Sepsis 7%
Other GI disorders 7%
60
Q

AAA screening

A

Men
Over 65
Single trans- abdominal ultrasound

61
Q

Varicose veins epidemiology

A 
1/3 population 18-65
Probably genetic link (familial)
90,000 varicose vein procedures/year UK
Effect quality of life
Surgery improves quality of life
62
Q

Varicose vein description

A

Dilated
Tortuous
Incompetent
Refluxing

63
Q

Varicose vein clinical assessment

A

history- previous DVT, previous long bone
Examination- bleeding, skin problems
Investigation- patent deep veins, confirm root cause

64
Q

VV treatment- conservative

A

Leg elevation

Class 1 compression hosiery

65
Q

VV treatment- medical

A

topical relief

66
Q

VV treatment- surgical

A

Open ligation + stripping
Foam sclerotherapy
Endovenous solutions

67
Q

Complications of VVs

A 
Swelling
Discomfort
Itching
Varicose eczema
Haemosiderin deposition
Lipodermatosclerosis
Bleeding 
Ulceration
68
Q

VV endovenous treatment

A

Disposable catheter inserted into vein
Vein warmed and collapses
Catheter withdrawn, closing vein

69
Q

VV complications of treatment- early

A 
Bleeding
Bruising
Discomfort
Infection
DVT/PE
70
Q

VV complications of treatment- late

A

Recurrence

Parasthesia

71
Q

Endovenous technology benefits- improvement over vein stripping

A

One hour treatment time
Immediate ambulation
Can be performed in physician’s office
Much less expensive

72
Q

Aortic Dissection

A

History- cardiac type
Examination- pulses
Diagnosis- CTA

73
Q

Aortic Dissection RFs

A

Hypertension
Genetic
Connective tissue

Met 3a (7 decks)

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