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Duke Elder: Finals Ophthalmology (Alice) > Age-related macular degeneration > Flashcards

Age-related macular degeneration Flashcards

1
Q

What can age-related macular degeneration (AMD) cause?

A

devastating los of central vision in the ageing population

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2
Q

What is the commonest cause of blind and partial sight in the UK In the over 60s?

A

age-related macular degeneration

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3
Q

What will happen to numbers of AMD with time?

A

increase as population lives longer

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4
Q

Do patients go completely blind in AMD?

A

no - peripheral vision maintained

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5
Q

What are 4 symptoms of AMD?

A
  1. gradual loss of central vision 2. distortion usually first symptom 3. eventually severe loss of central field but maintain peripheral navigational vision 4. difficulty with reading, recognising faces
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6
Q

What is speed of onset of loss of vision like in AMD?

A

may be very slowly progressive over years, but may have sudden deterioration if associated with haemorrhage

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7
Q

What kind of chart can be used to assess for central distortion from macular disease?

A

Amsler chart (look up image)

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8
Q

What are the 2 types of AMD?

A
  1. Dry (atrophic) macular degeneration 2. West (neovascular/exudative) macular degeneration
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9
Q

What is usually the first symptom that appears in age-related macular degeneration?

A

central distortion

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10
Q

Which is the more common form of AMD?

A

Dry AMD - 90%

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11
Q

What is the classic lesion in dry AMD?

A

geographic atrophy causing severe central vision loss

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12
Q

IS there any treatment for dry AMD?

A

no - nothing can halt or reverse relentless progression of dry AMD-related vision loss

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13
Q

What is the pre-cursor lesion leading to the development of geographic atrophy in dry AMD?

A

small yellowish macular lesion called drusen

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14
Q

What are the 2 types of drusen?

A

Soft and hard

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15
Q

What are soft drusen like? (look at photos)

A

pale yellow and large with ill-defined margins

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16
Q

What are soft drusen a sign of?

A

over 55 - especially larger than 63 microns - sign of age-related maculopathy

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17
Q

What are hard drusen like? (look at photos)

A

round, yellow with well-defined boundaies

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18
Q

How common are hard drusen?

A

relatively common, not always associated with AMD

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19
Q

Which type of drusen evolves to macular degeenration?

A

soft (not hard)

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20
Q

How does wet AMD compare in severity and frequency to dry AMD?

A

wet AMD is less common but more severe

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21
Q

What proportion of all AMD is wet AMD?

A

10%

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22
Q

What proportion of all blindness from AMD is due to wet AMD?

A

90%

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23
Q

What is wet AMD characterised by (not present in dry AMD)?

A

choroidal neovascularisation (CNV), development of abnormal blood vessels beneath the retinal pigment epithelium (RPE) layer of the retina

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24
Q

How can CNV be identified?

A

Fundus fluoroscein angiograph (FFA)

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25
Q

What happens in CNV?

A

new blood vessels penetrate into the retina in the macular region and bleed, which eventually causes macular scarring which can result in profound loss of central vision (disciform scar)

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26
Q

How many people in the UK have CNV due to AMD?

A

233 000; 21 000 new cases diagnosed every year

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27
Q

What type of scar is produced in wet AMD?

A

Disciform scar

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28
Q

How long could most eyes with AMD due to CNV under fovea be legally blind after?

A

2 years after diagnosis (many within months if left untreated)

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29
Q

Look at what wet AMD CNV looks like, and the disciform scar it can develop into.

A

big yellowy grey patch that develops after neovascularisation

30
Q

What can drusen evolve from and to?

A

they can evolve from hard drusen to soft drusen

31
Q

How can hard drusen forming soft drusen lead to a certain type of AMD?

A

hard drusen increase in number, size and confluence to eventually evolve to dry or wet macular degeneration

32
Q

What is the 5-year risk of a person who is 80 years or older with soft indistinct drusen and pigmentary changes of developing macular degeneration?

A

42%

33
Q

What is the risk that you will develop retinal changes of early maculopathy if you are <60 years with a normal retina?

A

0.2%

34
Q

What is the risk of developing retinal changes of early maculopathy if you are over 80 with a normal retina?

A

22.5%

35
Q

What is the risk of developing AMD in the other eye if there is AMD in one eye?

A

39-55%

36
Q

Explain how AMD progresses.

A
  • Normal macula, hard drusen, no maculopathy –> - soft drusen with/without pigment changes = early AMD. - goes to EITHER: X geographic atrophy (dry AMD) OR X CNV and disciform scar (wet AMD)
37
Q

What are 4 strong risk factors for AMD?

A
  1. older age 2. smoking 3. positive family history 4. genetic: complement factor H (CFH) gene determined to be strongly associated with a person’s risk for developing AMD
38
Q

What are 2 further *possible* risk factors for AMD?

A
  1. sunlight 2. cardiovascular
39
Q

What are 5 aspects of treatment are there for dry AMD?

A
  1. Usually nil
  2. Low vision aids (magnifiers) to help reading
  3. Vitamins: only in patients with advanced AMD in one eye, high doses of zinc and antioxidant vitamins (vitamin C, E, beta-carotene [not smokers]) helps prevent advanced disease and deterioration of vision in the other eye
  4. Severely visually impaired (blind)/ visually impaired (partial sight) registration for assessment by authorities and benefits payments
  5. Social support
40
Q

When was the first treatment for wet AMD developed, and what was it?

A

2003 (photodynamic therapy with verteporfin)

41
Q

What 2 new treatments have been developed for wet AMD, after photodynamic therapy?

A
  1. Ranibizumab (Lucentis) 2. Bevacizumab (Avastin)
42
Q

What difference is there between ranibizumab and bevacizumab for WET AMD?

A

none but bevacizumab much cheaper

43
Q

What has been implicated as a key mediator in the pathogenesis of blood vessel growth and leakage in wet AMD?

A

VEGF-A

44
Q

Therefore, how do ranibizumab and bevacizumab treatments work?

A

Monoclonal antibody fragments (Fab) that are non-selective VEGF-A inhibitors

45
Q

How is ranibizumab for wet AMD administered?

A

multiple intravitreal injections into vitreous cavity

46
Q

What is the result of using VEGF inhibitors for AMD (ranibizumab/lucentis or bevacizumab/avastin)?

A

2-year course stabilises condition and in some cases can even restore some vision

47
Q

How much do injections of ranibizumab for wet AMD cost?

A

£1000 per injection

48
Q

How can the response of anti-VEGF injections for wet AMD be measured?

A
  • Patients require repeat examination one month after every injection
  • At each visit, visual acuity is measured preferably using the logMAR scale
  • fundal examination (fundoscopy)
  • Repeat OCT always performed
  • if any sign of new disease progression, repeat injections are arranged
49
Q

What is aflibercept (Eylea)?

A

treatment approved by NICE; soluble VEGF receptor fusion protein which binds to all forms of VEGF-A, VEGF-B

50
Q

How is aflibercept given?

A

monthly by intravitreal injection for 3 consecutive doses, followed by 1 injection every 2 months

51
Q

How are intravitreal injections given?

A

Performed either in clean room or theatre under topical anaesthetic as day case

52
Q

What are 3 key risks of anti-VEGF intravitreal injections?

A
  1. Endophthalmitis 2. Intraocular haemorrhage 3. Retinal detachment
53
Q

How do drusen cause macular degeneration?

A

kills photoreceptors in that area

54
Q

How does CNV cause wet macular degeneration?

A

Kills photoreceptors in that area due to new vessels forming and bleeding in the retina

55
Q

What is the length of the course of intravitreal VEGF injections for wet AMD?

A

2 years

56
Q

What are 2 key examinations that should be performed in suspected AMD?

A
  1. Visual acuity: Snellen chart
  2. Fundoscopy
57
Q

What visual acuity would be recorded from the patient’s view of the Snellen chart at 6m (see image)?

A

6/18: viewed from 6m, can read to line labelled 18 (i.e. individuals with normal vision can read this line at 18m)

58
Q

How could the image, found on fundoscopy, be described?

A

Haemorrhages and exudation at the centre of the macula

59
Q

What could be 3 differentials for wet AMD?

A
  1. Dry AMD
  2. Cataract: gradual loss of vision in elderly, but throughout visual field not just centre. Onset over many months and years; misty, cloudy vision but no distortion
  3. Retinal vascular disease: CRAO/CRVO cause sudden loss of vision, BRAO/BRVO - may cause sudden loss of vision
60
Q

What is another name for wet AMD due to the way it comes about?

A

Neovascular macular degeneration, due to ingrowth of new blood vessels under the retina

61
Q

What happens to the new blood vessels formed in wet AMD?

A

bleed and leak fluid causing subretinal accumulation of fluid, subretinal blood (between RPE and Bruch’s membrane), macular oedema and subsequent subretinal scarring and fibrosis

62
Q

Where are the yellow deposits that form drusen deposited in dry AMD?

A

between Bruch’s membrane and retinal pigmented epithelium

63
Q

Which 2 investigations would be most appropriate in suspected wet AMD?

A
  1. Fundus fluorescein angiogram (FFA)
  2. Ocular coherence tomography (OCT)
64
Q

What is OCT?

A

non-invasive imaging technique that uses scattering of laser light to produce a cross sectional view of retina (see healthy example in image)

65
Q

What is FFA?

A

IV injection of fluorescein allows visualisation of the retinal vasculature, and pathological new vessels under the macula.

66
Q

What are the pros and cons of FFA?

A

Gives a detailed view of retinal circulation

Time consuming and risk of anaphylactic reaction to fluorescein

67
Q

What is shown in the image?

A

FFA showing subretinal leakage of dye from neovascularisation, causing area of hyper-fluorescence at macula in wet AMD

68
Q

What are 3 aspects of treatment for wet AMD?

A
  1. Anti-VEGF injections
  2. Dietary advice: healthy diet containing anti-oxidants may help prevent, supplements including lutein and xanthine in selected cases
  3. Supportive treatment: low vision aid assessment for appropriate use of magnifiers & registration as visually impaired (partially sighted) or severely visually impaired (blind) → assessment from local authorities and benefits payments
69
Q

How can patients with wet AMD be expected to respond to anti-VEGF injections?

A

Rule of thirds: 1/3 vision improves, 1/3 vision stays the same, 1/3 vision continues to deteriorate

70
Q

What is the general regimen of anti-VEGF injections for wet-AMD?

A

Intravitreal injections given under LA, most patients require multiple given at roughly monthly intervals.

All patients require loading doses of 3 injections and on average 7 injections per year

71
Q

What is the LogMAR scale?

A

Newer way of measuring visual acuity than Snellen chart; is similar but more accurate, was initially used in research. Now especially used for children and AMD clinics (see image)

72
Q

What are 2 potential drawbacks of using the LogMAR scale rather than Snellen chart?

A
  1. No direct correlation with Snellen chart
  2. LogMAR is not intuitive as poorer vision is recorded as a higher number; 6/60 Snell = 1.00 LogMAR and 6/6 Snellen is 0.0 LogMAR

Duke Elder: Finals Ophthalmology (Alice) (20 decks)

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