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opthamology > age-related macular degeneration > Flashcards

age-related macular degeneration Flashcards

1
Q

risk factors for AMD

A

race - caucasian

age - increases with age

medical history - HTN, CVS disease, dyslipidaemia, diabetes mellitus

personal history - smoking

FH - complement factor H, gene variant Y402H

ocular characteristics

  • light iris
  • hyperopia
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2
Q

what is complement factor H

A

does the inflammatory part esp for the macular degeneration part

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3
Q

what is macula

A

5.5 mm in diameter with the fovea at its centre

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4
Q

what is the fovea

A

metabollically active - cone cells

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5
Q

what is RPE

A

provide nutrition and to metabolise the end products of the visual cycle

act as a choroid and retina barrier

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6
Q

Retinal pigmented cells rol

A
  • outer blood retinal barrier - pumps put metabolic waste products
  • facilitates photoreceptor turnover
  • absorbs stray light
  • storage, met and transport of Vit A in visual cycle
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7
Q

drusen?

A

• Undigested cellular debris from degeneration
of RPE cells as part of normal ageing process
accumulates as ‘drusen’
– Yellow/white material that builds up between the
RPE and Bruch’s membrane

yellow deposits

hallmark of dry ARMD

non degradable products from photoreceptors accumulate in the RPE - loads become toxic

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8
Q

RPE alterations are

A

hyperplasia - pigment clumping

atrophy

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9
Q

what is hard drusen

A

well defined

less than half a retinal vein width in diameter

little increased risk of visual loss

subretinal

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10
Q

what is soft drusen

A

bigger

less distinct

get bigger and coalesce into RPE - ‘‘drusenoid RPE detachment’

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11
Q

‘drusenoid RPE detachment” ?

A

soft drusen lift the RPE away from the Bruch’s membrane

  • hypoxic state
  • inflammation
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12
Q

what are the advanced stages of dry AMD

A
  • confluent drusen
  • central and paracentral degeneration of the macula
  • atrophy og choriocapillaris, RPE and photoreceptors
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13
Q

end stage of dry AMD

A

geographic atrophy (GA) is a term used to describe advanced map-like area of atrophy (punched out) extending to foveal centre

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14
Q

differentiate between dry and wet

A

dry - atrophic

wet - neovasculairsation due to VEGF leaking ECF and blood whichc causes destructive scarring and visual loss

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15
Q

symptoms of AMD

A
  • a reduction in visual acuity, particularly for near field objects
  • difficulties in dark adaptation with an overall deterioration in vision at night
  • fluctuations in visual disturbance which may vary significantly from day to day
  • they may also suffer from photopsia, (a perception of flickering or flashing lights), and glare around objects

early - asymptomatic

  • loss of visual acuity
  • loss of contrast sensitivity - driving
  • abnormal dark adaptation
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16
Q

progression of dry AMD

A
  • gradual insidious vision loss over months/years
  • mild occasional metamorphosia - change
  • central/paracentral scotomas - gaps
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17
Q

classification of AMD

A

Early AMD

  • non-exudative
  • few medium sized drusen
  • pigmentary abnormalities
  • alterations to the RPE

intermediate AMD

  • large druse/numerous
  • geographical atrophy - does not extend to macular centre

late AMD - neovascularisation, exudative

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18
Q

Pathogenesis of AMD

A

VEGF A- abnormal vessels to grow and leak

19
Q

pathophysiology of AMD

A

drusen

inflammation

monocytes/macrophages

RPE oxidative stress

inflammation increase in VEGF-A

inappropriate vessel growth

exudation and haemorrhage

disciform scar formation

20
Q

disciform scar?

A

seen in wet AMD
its when scar tissue replaces the retinal tissue
represents the portion of the macula that has been permanently damaged

will cause a blind spot (scotoma) in the field of vision

21
Q

classification of wet AMD

A

based in location in relation to fovea

  • subfoveal
  • juxtafoveal
  • extrafoveal
22
Q

what Ix we do to look for new vessels in eye

A

fundus fluorescein angiogram classification

23
Q

risk factors to develop wet AMD in the second eye

A
  • more than five drusen
  • large (soft or confluent drusen)
  • pigment clumping in the RPE
  • systemic HTN
24
Q

symptoms of wet AMD

A
  • decrease in visual acuity
  • decreased contrast sensitivity
  • metamorphosia
  • central scotoma
25
Q

what is charles Bonnet syndrome

A

visual hallucinations - common in with wet AMD visual loss

26
Q

Diagnosis of AMD

A
  • patient history
  • best corrected visual acuity
  • amsler grid - look for distortion
  • fundoscopy
  • optical coherence tomography - subretinal spaces
  • fluorescein angiogrpahy
27
Q

test for AMD and other macular diseases

A

amsler grid

28
Q

fundoscopy findings for dry AMD

A
  • drusen
  • hypo/hyperpigmentation of the RPE
  • atrophy at the macula
29
Q

fundoscopy findings for wet AMD

A
  • exudate
  • blood
  • elevation of retina due to fluid
  • cystic oedema of the sensory retina overlying the CNV
  • advanced bug haem and exudation and fibrosis
30
Q

treatment for dry AMD

A

stop smoking
diet advice
occular nutritional supplememtns - zinc and antioxidant vitamins

31
Q

treatment for wet AMD

A

Photodynamic theraphy with verteperfin

Anti-VEGF therapy

  • bevacizumab
  • ranibizumab
32
Q

what is AMD

A

degeneration of retinal photoreceptors that results in the formation of drusen which can be seen on fundoscopy and retinal photography.

degeneration of the central retina bilateral

33
Q

what is dry AMD

A

characterised by drusen - yellow round spots in Bruch’s membrane

34
Q

what is wet AMD

A

characterised by choroidal neovascularisation.

Leakage of serous fluid and blood can subsequently result in a rapid loss of vision.

Carries worst prognosis

35
Q

signs of AMD

A
  • distortion of line perception may be noted on Amsler grid testing
  • fundoscopy reveals the presence of drusen, yellow areas of pigment deposition in the macular area, which may become confluent in late disease to form a macular scar.
  • in wet ARMD well demarcated red patches may be seen which represent intra-retinal or sub-retinal fluid leakage or haemorrhage.
36
Q

Ix for AMD

A
  • slit-lamp microscopy is the initial investigation of choice, to identify any pigmentary, exudative or haemorrhagic changes affecting the retina which may identify the presence of ARMD. This is usually accompanied by colour fundus photography to provide a baseline against which changes can be identified over time.
  • fluorescein angiography is utilised if neovascular ARMD is suspected, as this can guide intervention with anti-VEGF therapy. This may be complemented with indocyanine green angiography to visualise any changes in the choroidal circulation.
  • ocular coherence tomography is used to visualise the retina in three dimensions, because it can reveal areas of disease which aren’t visible using microscopy alone.
37
Q

treatment for AMRD

A

the AREDS trial examined the treatment of dry ARMD in 3640 subjects. It showed that a combination of zinc with anti-oxidant vitamins A,C and E reduced progression of the disease by around one third. Patients with more extensive drusen seemed to benefit most from the intervention. Treatment is therefore recommended in patients with at least moderate category dry ARMD.
Vascular endothelial growth factor, (VEGF) is a potent mitogen and drives increased vascular permeability in patients with wet ARMD. A number of trials have shown that use of anti-VEGF agents can limit progression of wet ARMD and stabilise or reverse visual loss. Evidence suggests that they should be instituted within the first two months of diagnosis of wet ARMD if possible. Examples of anti-VEGF agents include ranibizumab, bevacizumab and pegaptanib,. The agents are usually administered by 4 weekly injection.
Laser photocoagulation does slow progression of ARMD where there is new vessel formation, although there is a risk of acute visual loss after treatment, which may be increased in patients with sub-foveal ARMD. For this reason anti-VEGF therapies are usually preferred.

38
Q

contradictions for antioxidant dietary supplements

A

Beta-carotene has been found to increase the risk of lung cancer and hence antioxidant dietary supplements are not recommended for smoker

39
Q

major risk factors of dry AMD

A

large hard and soft drusen in the macula

plus extensive pigment irregularities or de-pigmentation

40
Q

what is the role of macula

A

specialised acuity of vision
high-resolution
central vision

41
Q

what is the bruchs membrane

A

separates the RPE from choroid

42
Q

pathophysiology of ARMD

A

when RPE secretions cant get into the bruchs membrane they start accumulating

RPE and photoreceptors cell layer ischaemia and atrophy

43
Q

patients typically present with

A

subacute onset of visual loss with:

  • a reduction in visual acuity, particularly for near field objects
  • difficulties in dark adaptation with an overall deterioration in vision at night
  • fluctuations in visual disturbance which may vary significantly from day to day
  • they may also suffer from photopsia, (a perception of flickering or flashing lights), and glare around objects

opthamology (16 decks)

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