Age related macular degeneration Flashcards

1
Q

What can AMD cause?

A

gradual loss of central visual field
= most commonest cause of blind and partial sight registration in the western world
Do NOT go completely blind, and maintain independence as peripheral vision is maintained

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2
Q

Which age group is most affected by AMD?

A

typically >60s with incidence increasing sharply after 80
- with increasing ageing population prevalence is going to increase
AMD in one eye means there is a 50% chance of the other eye becoming affected

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3
Q

What is normally the first symptom?

A

distorted vision, eventually leading to severe loss of central visual field with difficulty reading and recognising faces

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4
Q

When can the deterioration be sudden?

A

If associated with haemorrhage - this is Wet AMD

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5
Q

What are the risk factors for AMD?

A

increasing age
smoking
family history
possibly sunlight and cardiovascular disease (hypertension, hypercholesterolaemia, obesity)

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6
Q

What is the pathogenesis of AMD?

A

accumulation of drusen within the macula, they start off hard and then progress to soft

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7
Q

What are hard drusen like?

A

round, yellow and well-defined - they are common and not necessarily associated with AMD

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8
Q

What are soft drusen like?

A

pale yellow, large and ill-defined

They evolve and increase in size, number and confluence to eventually become dry or wet AMD

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9
Q

What do the drusens do in dry AMD?

A

Atrophic macular degeneration
- most common type
soft drusen lifts up the pigment epithelium of the retina, causing atrophy of the photoreceptors
- geographic atrophy causing severe central vision loss

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10
Q

What do the drusens do in wet AMD?

A

neovascular/exudative

abnormal growth of blood vessels from choroid into region of soft drusen (retina) causing bleeding

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11
Q

What is the treatment for dry AMD?

A

usually no treatment so progression cannot be halted or prevented

  • low vision aids can be used to help reading
  • vitamins are used in advanced stages (high dose zinc and antioxidants)
  • social support and blind/partial sight registration is important
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12
Q

What is wet AMD characterised by?

A

choroidal neovascularisation - development of abnormal blood vessels beneath the retinal pigment epithelial layer of the retina

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13
Q

How can choroidal neovascularisation be identified?

A

identified on fundus fluorescein angiography - growth of new vessels can penetrate into the macular region of the retina and bleed - bleeding of vessels will eventually cause macular scarring

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14
Q

What is the consequence of the scarring in CNV?

A

the disciform scars can result in a profound loss of central vision

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15
Q

How is wet AMD treated?

A

non-selective VEGF-A inhibitors - ranibizumab / bevacizumab

- VEGF-A is a key mediator in the pathogenesis of blood vessel growth and leakage

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16
Q

How are anti-VEGF-A commonly given?

A

intravitreal injections in the eye - associated risk of endopthalmitis, intraocular haemorrhage and retinal detachment

17
Q

How quickly do people with AMD due to CNV go blind?

A

most with CNV under the fovea would be legally blind within 2 years of diagnosis - many within months if left untreated

18
Q

How is response to anti-VEGF treatment monitored?

A

monthly optical coherence tomography (non-invasive) scans and fundus fluorescein angiogram if appropriate

19
Q

What is aflibercept?

A

soluble VEGF receptor fusion protein which binds to all forms of VEGF-A, VEGF-B
Given monthly by intravitreal injection for 3 consecutive doses followed by 1 injection every 2 months