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Eye disease Term 2 > Age related macular degeneration: classification, risk factors and clinical investigation > Flashcards

Age related macular degeneration: classification, risk factors and clinical investigation Flashcards

1
Q

what is the outcome of end stage AMD in wet and dry

A

complete central scotoma

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2
Q

what is visual impairment of patients with AMD associated with

A

with increased risk falls and social isolation and problems performing tasks, and recognising faces

Prevalence of depression much higher in VI older adults

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3
Q

which part of the retina is affected by AMD and which 4 structures in particular

A

outer retina is affected

AMD primarily affects:

  • Choroidal circulation
  • Bruch’s membrane
  • RPE
  • Photoreceptors
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4
Q

what is the clinical classification of AMD currently used

A

VA almost unaffected. Often asymptomatic

No apparent ageing changes:

  • No drusen
  • No AMD pigmentary abnormalities

Normal ageing changes:

  • Druplets (small drusen ≤ 63 µm)
  • No AMD pigmentary abnormalities

Early AMD:

  • Medium drusen >63 µm ≤ 125 µm
  • No AMD pigmentary abnormalities

Intermediate AMD:

  • Large drusen >125 µm and/or
  • AMD pigmentary abnormalities

And

Central visual loss gradual (GA) or rapid (nAMD)

Late AMD:
Neovascular AMD (wet AMD)
and/or
Geographic Atrophy (dry AMD)

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5
Q

which 4 retinal signs = VA almost unaffected. Often asymptomatic

A

No apparent ageing changes

Normal ageing changes

Early AMD

Intermediate AMD

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6
Q

what are the 2 signs of normal ageing changes

A

Druplets (small drusen ≤ 63 µm)

No AMD pigmentary abnormalities

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7
Q

what are the 2 signs of early AMD

A

Medium drusen >63 µm ≤ 125 µm

No AMD pigmentary abnormalities

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8
Q

what are the 2 signs of intermediate AMD

A

Large drusen >125 µm and/or

AMD pigmentary abnormalities

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9
Q

what are druplets, what size are they and when is it seen

A

small size version of hard drusen
≤ 63 µm
seen in normal ageing changes

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10
Q

what are eyes that are classified as intermediate AMD at higher risk of

A

of getting late AMD

these patients can progress to wet AMD or geographic AMD or both together

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11
Q

what 2 things can AMD pigmentary abnormalities be referred to as

A

hyperpigmention: small clumps of pigment accumulation
or
hypo pigmentation: small clumps of pigment loss

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12
Q

what is drusen

A

Localised yellow/white deposits between basement membrane of RPE and Bruch’s membrane (outer layer of the retina)

They are waste material that the RPE can’t process from e.g. the photoreceptors

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13
Q

what are the clinical features of Early / Int AMD

A
  • Hard drusen/druplets which are tiny yellow/white lesions (less than 63 um)
  • in small numbers, part of normal ageing process
  • when numerous, it is a risk factor for soft drusen and AMD
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14
Q

what is numerous hard drusen/druplets as seen in early/int AMD a risk factor for

A

soft drusen and AMD

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15
Q

which type of drusen is a hallmark sign/feature of AMD and how do they look

A

Soft drusen

larger in size
distinct or indistinct
may coalesce to form confluent drusen

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16
Q

what 2 clinical features is associated with a increased risk for progression onto advanced AMD

A
  • Larger, increased no., and more confluent drusen

- Pigmentary changes

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17
Q

what are the clinical features of intermediate AMD

A
  • focal hyper pigmentation
    seen in eyes with or without soft drusen
  • focal hypopigmentation
    seen as small patches of mottled pigment
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18
Q

what feature of AMD is seen with or without soft drusen

A

focal hyper pigmentation in intermediate AMD

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19
Q

what 3 things can focal hyperpigmenation be caused by

A

Increased melanin content of RPE
RPE cell profileration
RPE cell migration

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20
Q

what does the appearance of focal hyper pigmentation look like in flourescein angiography

A

as a dark patch, blocking the fluorescence of the choroidal circulation beneath

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21
Q

what 3 things can focal hypo pigmentation be caused by

A

Reduced melanin content of RPE cells
RPE cell atrophy
RPE layer thinning

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22
Q

what are the 5 clinical features of late AMD geographic atrophy

A

Sharply delineated, roughly round area >175µm of hypo or depigmentation, or apparent absence/atrophy of RPE

Increased visibility underlying choroidal circulation

Area of RPE death leads to photoreceptors loss and gradually the other retinal layers, causing visual loss (absolute scotoma)

Often starts in parafovea, sparing fovea until later (so first has scotoma around central vision)

Vision loss is gradual (as the retinal layers gradually die)

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23
Q

what is the clinical features of choroidal neovascularisation

A

Growth of new blood vessels from choroid to proliferate beneath RPE, or in sub retinal space (between RPE and retina)
May be seen as green/ grey lesion on fundus photograph

Fragile vessels mean sub- or intraretinal haemorrhages, hard exudates, intra-retinal fluid, sub-retinal fluid or pigment epithelial detachment common

Repeated leakage blood, serum and lipid stimulates formation of untreatable disciform scar

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24
Q

how will the growth of the new blood vessels from the choroid that proliferate beneath RPE, or in sub retinal space be seen as on a fund photograph

A

as green/grey lesions

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25
Q

what are the first symptoms of CNV wet AMD

A

recent onset distortion and deterioration of vision

therefore do an amsler test

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26
Q

what 5 things can commonly happen from the fragile vessels in wet AMD CNV

A
  • sub- or intraretinal haemorrhages
  • hard exudates
  • intra-retinal fluid
  • sub-retinal fluid
    or
  • pigment epithelial detachment
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27
Q

in wet AMD what stimulates the formation of the untreatable disciform scar and what consequence does this lead to

A

Repeated leakage of blood, serum and lipid from a neovascular membrane which stimulates scar formation

leading to a absolute central scotoma

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28
Q

what is the speed to vision loss in wet AMD and why

A

Vision loss may be rapid in AMD

due to exudates and haemorrhage, secondary cell death, and formation of scar tissue from the disciform form scar

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29
Q

what is the progression of CNV caused by

A

by hypoxia/inflammation in retina, leading to imbalance of inhibitory/stimulatory growth factors (e.g. PEDF, VEGF)

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30
Q

what does the untreated progression of CNV lead to

and what is there a high risk of with CNV

A

Untreated  1 line logMAR acuity loss in 3 months, 3 lines by 1 year

High risk in second eye in px with unilateral CNV - incidence in fellow eye of 12% by 12 months

31
Q

in end stage CNV, where does the pigment epithelial detachment occur in the retina
which 2 different outcomes can it have
what does it usually leave behind
how much if associated with CNV

A

Between basement membrane of RPE and Bruch’s Membrane

May flatten over time, but may tear (in approx 1 in 10)

Usually leaves area of atrophy or sub retinal fibrosis

> 80% associated with CNV

32
Q

what is a serous pigment epithelial detachment as seen in end stage CNV
how can it be viewed and how does it show up

A

shows elevation with accumulation of fluid beneath

seen with OCT - bright band is corresponding to RPE and fluid beneath seen as a dark region due to its low relative optical reflectivity

and dome shaped elevation seen in volk

33
Q

apart from the leakage of new blood vessels causing the disciform scar and subsequent pigment epithelial detachment in CNV, what else can cause this

A

just having drusen
as this can disrupt the blood flow hence causing detachment of the RPE

(so theres not always blood vessels if theres PED)

34
Q

what are the 2 theories/mechanisms of the pathogenesis of AMD down to

A
  • oxidative damage

- inflammation

35
Q

how is the mechanism of oxidative damage thought to be a part of the pathogenesis of AMD

A

Retina prone to oxidative damage

RPE is unable to break down products of oxidation  accumulate (the lipids, carbohydrates and proteins) in RPE and Bruch’s membrane

so the oxidative damage causes changes to the molecules in the retina and this causes it to change their structure

36
Q

how is the mechanism of inflammation thought to be part of the pathogenesis of AMD

A

Inflammatory cells e.g. macrophages found in eyes with drusen, CNV, RPE atrophy

Strong association between AMD and polymorphisms of CFH gene and other genes involves in immune response

so the waste material triggers off an inflammatory response and the long term low level of inflammation is causing damage to the retina = another mechanism for AMD

37
Q

what is the biggest risk factor for AMD

A

age - which is not modifiable

38
Q

list the 6 main risk factors of AMD

A 
age
ethnicity 
genetics
smoking
light exposure 
diet
39
Q

what is the biggest modifiable risk factor of AMD

A

smoking

40
Q

how is ethnicity a risk factor for AMD

A

Lower risk of (late) AMD in Black than White group

Prevalence similar in White and Asian groups

41
Q

why is there found to be a lower risk factor of AMD in black than white people

A

because of the melanin having a protective affect from the oxidative/light damage

42
Q

how is genetics a risk factor for AMD

A

Monozygotic twins have very high concordance for AMD, significantly greater than for dizygotic twins

First degree relatives with AMD provide up to 6–12 times higher risk than in the general population

43
Q

by how much is smoking a risk factor for AMD

A

current smokers 4x risk late AMD compared to never smokers

After 10 years ex-smokers no more likely to develop AMD than never smokers (i.e. if quit smoking for 10 years)

44
Q

which theory is the risk factor of light exposure of AMD based on
and how is this

A

based on the oxidative damage theory

Increased light exposure (esp blue light) throughout life has been associated with increased risk AMD

45
Q

what improvements in diet, which is a risk factor for AMD, s thought to reduce the chances of getting AMD

A

Possible protective effect increased antioxidant intake

Reduced progression of AMD with high intake vitamins A, C, E and zinc (AREDS study), also if vitamin A (beta carotene) is exchanged for lutein and zeaxanthin (AREDS 2)

Protective effect increased omega 3 fatty acid and oily fish intake. Not supported by AREDS2

Protective effect increased xanthophyll (lutein, zeaxanthin) intake (green leafy vegetables e.g. kale, spinach, eggs). Weak evidence from AREDS2

46
Q

why has the AREDS 2 study suggested that vitamin A should be replaced by lutein and zeaxanthin in a patients diet

A

because vitamin A is dangerous for smokers as it can cause a higher risk of cancer

47
Q

list the 5 systemic conditions which seem to predispose towards an increased risk of AMD

A 
Cardiovascular disease
Hypertension
High Body mass index (BMI)
Diabetes 
Higher plasma fibrinogen
48
Q

which gender is at a higher risk of having AMD

A

females

49
Q

when carrying out a clinical investigation of AMD, what 5 things do you want to include in your basic evaluation

A 
History and symptoms
Refraction 
Visual acuity measurement (distance and near)
Amsler chart
Fundus examination
50
Q

what 2 questions do you want to ask a older patient without AMD in your H and S

A

Family history of AMD?
History of smoking?

as these are risk factors

51
Q

what 5 questions do you want to ask a patient with AMD in your H and S and why

A

asking to check for progression

(Worsened) symptoms distorted vision, or reduced vision?

Since when? Sudden onset? (treatment implications)

Both eyes/one eye? (in patient with unilateral AMD, need to ask if they have noticed changes in good eye)

Increased difficulty with tasks e.g. reading, cooking, mobility, shopping? (refer to social services)

Taking any dietary supplements? (if not, then advise then to)

52
Q

when carrying out refraction and best corrected VA distance and near
which chart should you use
when is va not and is affected by AMD

A

Use ETDRS logMAR chart if possible

VA is relatively unaffected by early AMD, but may be substantially reduced by advanced AMD

53
Q

give 3 reasons for why measuring VA in your clinical investigation of AMD is important

A

Measure of disease progression

NICE guidelines for seeing is suitable for Lucentis treatment (VA 6/12-6/96)

Guidelines for registration (severely) sight impaired

  • if va less than 6/96 - still refer but not as urgent as cannot treat with lucentis
  • if long standing AMD - should still refer if theyre not registered as sight/severely sight impaired
54
Q

if a patient with AMD va is fine, what else may determine if a patient might benefit from a low vision assessment/advice advice on practical solutions to help with VI

A

the patient’s contrast sensitivity

can give advice on improving lighting around the house or high contrast gadgets

55
Q

what about driving standards do you need to consider when assessing a patient with AMD
and when must you inform the DVLA for group 1 and groups 2 drivers

A

Ensure spectacles enable 6/12 binocularly

Must inform DVLA if:
AMD in one eye (bus, coach, lorry drivers)
AMD in both eyes (car drivers)

must tell the DVLA of AMD if it is still good enough to drive, as can monitor it and the DVLA can get information from the optom about the patient’s level of vision

56
Q

what is the purpose of using an amsler chart on a px with AMD or suspect AMD
what may the amsler chart have the potential to do
therefore what is it more useful for
what is the instructions of the amsler chart very important for

A

To plot areas of distortion and scotomas which may indicate the presence of underlying neovascular changes

Potential to miss scotoma (‘filling in’ effect)

More useful for detecting distortions associated with the conversion to wet AMD

Instructions are very important for self-monitoring using Amsler chart

57
Q

why is monitoring a patient who already has AMD with an amsler chart useful

A

Monitoring scotomatous areas is also useful in patients with established AMD and vision loss, as it helps the practitioner to give guidance on maximising the use of residual vision, for example using an eccentric viewing strategy

58
Q

what is the best way to carry out a fundus examination when investigating AMD

A

Dilated indirect fundus examination essential e.g. Volk

Stereoscopic view needed to detect presence of sub retinal fluid (an elevated area of retina)

Fundus photography and OCT can be very useful

59
Q

list 5 further functionals tests you will want to carry out alongside your main clinical tests in investigating AMD

A
  • contrast sensitivity
  • reading speed/accuracy
  • macular photostress test
  • colour vision
  • microperimetry
60
Q

what test should be used to measure contrast sensitivity
why is it useful to carry this out
what is contrast strongly related to

A

Pelli Robson

Useful in people with established AMD (i.e. not used for diagnosis)

Strongly related to performance e.g. reading with magnifier, recognising faces, driving, mobility

Practical advice can help those with poor C.S. e.g. improve lighting in house etc

61
Q

why is reading speed/accuracy measured in AMD investigation as a functional test

A

because the patient may be able to read N5, but with difficulty and taking a long time = an implication for referring for an LV assessment

62
Q

how is the macular photostress test carried out as a functional test for investigating AMD
how is the results different in someone with AMD

A

30 secs bleach with ophthalmoscope
>60 secs to recover to within 1 line of baseline VA = abnormal

Px with AMD = their dark adaptation is impaired so takes longer to recover from bright light

63
Q

how is colour vision affected in someone with AMD and so how should it be measured in these patients

A

Primarily B/Y in early AMD, therefore Ishihara not appropriate

New computer-based tests available e.g CAD test

colour vision is not a good diagnostic test for AMD as many factors can affect colour vision with age

64
Q

which 3 imaging techniques is useful in investigating AMD

A
  • fundus photography
  • optical coherence tomography
  • flourescein angiography
65
Q

what is a advantage and disadvantage of using fundus photography is investigating AMD

A

useful for monitoring progression and for recording the presence of haemorrhage and exudates

but non-stereoscopic cameras will not provide information on retinal elevation

66
Q

how does drusen appear in an OCT image

A

White blobs

it is lumps of waste material pushing the RPE up

67
Q

how does intraretinal fluid appear in an OCT image

A

large dark ‘bubbles’ in the inner retina

due to lack of reflection of the light

68
Q

how does sub retinal fluid appear in an OCT image

A

the dark area is beneath the retina, but inner to the RPE

69
Q

how does a Choroidal Neovascular Membrane appear in an OCT image

A

an area of new vessel growth shown as a lump under the RPE (this causes sub retinal fluid)

70
Q

how does geographic atrophy appear in fluorescein angiography

A

enhanced visibility of the underlying glow from the choroidal circulation

71
Q

how does geographic atrophy appear in an OCT image

A

The OCT light goes right through, described as a window effect (as the laser is going through the RPE and illuminating the choroid behind)
when the RPE is not present to absorb/reflect the light, it is able to penetrate more deeply into the underlying choroidal vasculature

72
Q

how does geographic atrophy appear in fundus photography

A

can see the choroidal blood vessels more easily as theres no RPE to mask them

73
Q

describe how a flourescein angiography shows up in 2 types of wet AMD

A

CNV membrane may be classic or occult

Classic: well defined on FFA, becoming large and indistinct in late stage due to leakage. Caused by CNV between RPE and retina

Occult: is less well defined, and less prone to leakage out into it’s surroundings. Caused by CNV between RPE and Bruch’s
= growth of new blood vessels lower down into the retina

Eye disease Term 2 (23 decks)

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