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Eye Disease > AMD classification 1 and referral 2 > Flashcards

AMD classification 1 and referral 2 Flashcards

1
Q

What is the impact of AMD?

A
  1. Complete central scotoma
  2. Increased depression
  3. Increased falls, social isolation ect
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2
Q

How big is the macula?

A

Centre of the fovea spanning over to near the edge of the optic disk!
15-20 degrees visual angle

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3
Q

What is the Beckman’s grading scale for no AMD?

A
  1. No apparent aging change - nothing
  2. Normal aging changes - duplets. Smaller then 63 mircons
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4
Q

What is the classification for Beckman’s grading scale for early AMD?

A

Medium size drusen bigger then 63 microns but smaller then 125

NO pigmentation abnormalilties

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5
Q

What is the classification for Beckman’s grading scale for Intermediate AMD?

A

Bigger then 125 microns and/or amd pigmentary changes

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6
Q

What is the classification for Beckman’s grading scale for Late AMD?

A

Neovas (WET)and Georgraphic artophy (DRY)
(px will have Loss of central vision)

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7
Q

This is the only time ive been lazy, i cba to type it out, just memorise it

A
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8
Q

What is drusen?

A

This is local deposits between the RPE and bruchs membrane. They are waste material.

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9
Q

What is a psudeodrusen?

A

Between the reitina and the RPE

(on top of RPE)

drusen are below RPE

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10
Q

What are hard drusen?

A

Smaller than 63 microns. This is the smallest type of drusen.

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11
Q

Are hard drusen normal?

A

Yes in the aging population. but lots can lead to soft drusen

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12
Q

What is soft drusen?

A

Larger and they coalesce to form confluent drusen and are a hallmark for AMD. They have distinct or indiscint margins.

The larger and more confluent there is a higher risk of advanced AMD

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13
Q

What is the chance of getting foveal atrophy or choroidal neovascularisation if you have bilateral drusen?

A

3% per eye.

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14
Q

What increases the chance of advanced AMD a lot?

A

Larger drusen and pigmentary changes in both eyes increases the chances to almost 50%

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15
Q

What causes hyperpigmentation?

A
  1. Increased melanin in the RPE
  2. RPE cell proliferation (proliferation means rapid cell growth)
  3. RPE cell migration (this means when the cells are movings somewhere!)
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16
Q

What causes hyperpigmentation?

A
  1. Increased melanin in the RPE
  2. RPE cell proliferation (proliferation means rapid cell growth)
  3. RPE cell migration (this means when the cells are movings somewhere!)
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17
Q

How does hypopigmentation look on fluorescence imaging ?

A

It will be glowing patches, because there is less pigment to block it.

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18
Q

What causes hypopigmentation?

A
  1. Reduced melanin content
  2. Rpe cell atrophy
  3. Rpe layer thinning
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19
Q

What does geographic atrophy look like?

A

sharply outlined area of loss of pigmentation larger than 175 microns

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20
Q

What happens when RPE dies? (GA)

A

The photoreceptors die
The underlying chorioid will die too..

Dead areas of retina = pale areas

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21
Q

why are areas of fundus pale on the fundus with artophy?

A

Dead tissue : photocells and the choroid have died

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22
Q

Where does geographic atrophy normally start?

A

It normally starts parafovea, and then it will include the fovea eventually = central scotoma

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23
Q

Is geographic atrophy bilateral?

A

In 50% of px it is.

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24
Q

What is choroidal neovascularisation (wetAMD)?

A

This is new choroidal blood vessels growing beneath the RPE or the subretinal space.
Can be seen as a green or grey region

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25
Q

What will CNV look like on OCT?

A

Hyperreflective lump under the RPE

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26
Q

What is the prevelance of wet amd?

A

15% of px with early amd will get wet amd

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27
Q

What other findings are common with wet amd?

A
  1. Sub or intraretinal haemorrhages
  2. Hard exudates
  3. Intra-retinal fluid
  4. Sub-retinal fluid
  5. Pigment epithelial detachment is common
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28
Q

What is a disciform scar?

A

This is when there is repeated leakage of blood, serum and lipid.
It will stimulate a scar tissue to form

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29
Q

What is the vision loss like in wet AMD?

A

It is normally a rapid loss of vision

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30
Q

Why do we get vision loss in WET amd?

A
  1. Exudates
  2. Haemorrhages
  3. Secondary cell death
  4. Disciform scar
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31
Q

When we want to treat wet AMD?

A

Before the scar tissue forms!!! As the scar tissue is irreversible.

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32
Q

What causes wet AMD?

A

Inflammation and hypoxia will stimulate growth factors —> VEGF

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33
Q

What is pigment epithelial detachment?

A

Detachment between the basement of the RPE and bruchs membrane.

It can reattach but it can also tear

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34
Q

What does pigment epithelial detachment (PED) cause?

A

It will leave areas of atrophy and subretinal fibrosis

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35
Q

What is linked to PED linked too?

A

Choroidal neovas = 80%

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36
Q

What makes the other 20% chance of PED?

A

Drusen stopping fluid leaving the retina to the choroidal circulation leads to a build of fluid under the RPE

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37
Q

what will PED look like on the OCT?

A

There will a dome like elevation.
We know it is not a RD as the reflective layer of the RPE is elevated!

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38
Q

How do we know it is a PED and not a RD?

A

The reflective layer of the RPE is elevated! If the RPE layer in the oct was flat then it would a RD

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39
Q

Features of reticular pseudodrusen (RPD)?

A
  • This is yellow interlacing pattern
  • Located between the retina and the RPE.
  • This is easier seen on IR/blue light
    They will have lower Vision compared to px without RPD, esp dark adaptation
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40
Q

What does RPD causes?
(reticular pseudodrusen)

A

nothing if only a few,
loads = increased risk of developing AMD!

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41
Q

What problem is there with oxidative damage in the eye?

A
  1. The retina is prone to oxidative damage
  2. The RPE cannot break down these oxidated products, therefore they accumulate
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42
Q

why is the retina prone to oxidative damage?

A
  • lots of light intake
  • contains lots of polyunsaturated fatty acids which have double bonds which are prone to being oxidised
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43
Q

How can inflammation be linked to pathogenesis of AMD?

A
  1. inflammatory cells in those with CNV, drusen RPE atrophy
  2. link between AMD and inflammatory cell genes (CFH)
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44
Q

what are the 2 theories of pathogenesis of AMD?

A

oxidative damage
inflammation

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45
Q

What is the biggest risk factor of AMD?

A

AGE
85+ = 30% of early and 13% for late AMD

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46
Q

What other factors are there?

A
  1. Ethnicity. Less in black: Melanin the darker mandem will protect the retina from oxidative damage.
  2. Genetic : Twins both get it normally showing it is linked. Also, first degree relatives having AMD will increase the risk of AMD, by 6-12X
  3. Smoking
  4. Light exposure. Especially blue light, but research is unclear.
  5. Diet
  6. Diabetes
  7. Females
  8. Pale iris colour
  9. Hypermetropia
  10. Alcohol
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47
Q

What systemic risk factors are there?

A
  1. Cataract surgery
  2. Cardiovascular disease
  3. Hypertension
  4. BMI
  5. higher plasma fibrinogen
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48
Q

How do we do a basic evaluation?

A
  1. Refraction
  2. H and s
  3. Fundus exam
  4. Visual acuity measures
  5. Amsler chart
49
Q

What makes a good H and S?

A
  1. Smoking
  2. Family
  3. Diet
  4. Visual problems? Blurred, distortion
  5. When?
  6. Glare
  7. Both eyes or one
  8. Any difficulties with doing tasks
50
Q

How do we do best corrected va?

A

We can use the EDTR, which is good for low vision px. As there is 5 letters on the top fo the top line compared to snellen which has one.

51
Q

Why is va important?

A
  • Good to see progression
  • also see if they can take anti-VEGF
  • See if they are sight impaired or not
    Driving standards
52
Q

What VA do they need to take anti-VEGF?

A

Va has to be between 6/12 and 6/96 (will explain later why)

53
Q

When should the px inform the DVLA?

A

If driving a bus, coach or lorry they should let them know if they have it in one eye
OR
If they drive a car they should let them know when they have it in both eyes
OR
VA drops below 6/12

54
Q

What is amsler charts good for?

A

This will plot areas of scotomas and distortion.
However, they can miss scotomas. So they are better at detecting distortion

55
Q

How do we take contrast sensitivity?

A

Pelli- robson charts.

56
Q

Why do we measure contrast sensitivity?

A

It is strongly related to real life performance, such as driving and magnification
We can give some advice to px with poor contrast

57
Q

What other functional test can we carry out?

A
  1. Reading speeds
  2. Macular photostress tests
  3. Adapt dark adaptometry
  4. Colour vision
58
Q

What is the macular photo stress test?

A

This measures how well the VA will return back to normal after being dazzled by the light of the ophthalmoscope.

59
Q

What is an abnormal time for macular photo stress test and what is this indicative of?

A

Longer than 60 seconds, and this can be a sign of early AMD…..

Delayed adaptation to a bright light…

60
Q

Which colours will people with AMD struggle with?

A

Blue and yellow! (tritan defect)

61
Q

Why is Ishihara not used for AMD?

A

Ishihara will not pick up blue / yellow
We use CAD to test for this

62
Q

why would you carry out microperimetry?

A

can plot scotoma in those with dry AMD with scotoma
monitor progression throughout GA

can be useful when carrying out eccentric viewing training - lets us know which part of the retina they are able to use

63
Q

Why is fundus important when assessing amd?

A

We can see the presence of subretinal fluid, as we can see elevation.
OCT is great to see the bumps from fluid ect

64
Q

What imaging techniques are there?

A
  1. Fundus images
  2. OCT
  3. Fluorescein’s angiography ; this is gold standard in HOS. But not used in optometry clinics as there is a risk of causing a anaphylactic shock when injecting fluroscene into the eye.
  4. Fundus autofluorescence : this is when looking at the reflective lipofuscins. We can see hypo/hyper pig. It will help us see geographical atropy
65
Q

What is a anaphylactic shock?

A

a rare but severe allergic reaction that can be deadly if you don’t treat it right away- this can happen in Fluoro Angiography

66
Q

What will drusen look like on a OCT?

A

focal elevation of the reflective RPE layer. It is grey under

67
Q

What does intraretinal fluid look like?

A

dark pockets

68
Q

What does subretinal fluid look like?

A

Dark region and it is under the retina but above the RPE
It is associated to neovas and they are leaking

69
Q

What does fluorescein angiography do?

A

The fluoresce is injected into the eye
Then the eye is imaged over time using blue light

As the dye moves through the vessels, it will show leakage and choroidal neovascularisation

70
Q

What are the sub types of choroidal neovas?

A
  1. Classic
  2. Occult
71
Q

What does classic look like and where is it located?

A

It is well defined and gets larger as the angiography goes on.
It is showing Choridal Neo Vas between RPE and retina

72
Q

What does occult look like and where is it located?

A

This is not well defined
Showing CNV between RPE and bruchs

73
Q

Can you have classic and occult In the same eye?

A

YEs

74
Q

How can we evaluate geographic atrophy using angiography?

A

Window defect : we can see under the glow so we can see the choroidal vessels.

In a OCT we can see the light is shining through with the RPE layer is thin

75
Q

How can we use fundus autofluorescence to evaluate AMD?

A

You illuminate the fundus with blue light.
This blue light will illuminate the lipofuscin.

76
Q

What happens to lipofuscin as we get older?

A

The more we get. So there will be a more glow.

77
Q

In an atrophic area, would lipofuscin be detected when carrying out autofluorescence?

A

No glow, just black! As there no RPE therefore no lipofuscin.

78
Q

Why does the disc and the vessels not glow in fundus autoflurescence?

A

It is dark and not glowing as no RPE in these areas

79
Q

What is macular photocoagulation?

A

This is a laser which destroy new blood vessels. However, it will not spare healthy cells and it will no improve vision.

80
Q

Where was macular photocoagulation done on the retina?

A

Extra foveal ; cannot be on the fovea as it will causes visual acuity loss.

81
Q

Is macular photoagulation used now?

A

No

82
Q

What is photodynamic therapy?

A
  • Verteporfin (photosensitisers) injected intravenously.
  • They bind to lipoprotein & taken by new blood vessels.
  • Then lasers would activate the agent –> closure of new blood vessels
83
Q

Why is photodynamic therapy better than macular photocoagulation?

A

It does not do a lot of damage to the retina and is more targeted to the new blood vessels

84
Q

What is the problem with photodynamic therapy?

A
  1. Once the vessels were destroyed, new vessels would form around 3 months later thus repeated therapy needed
  2. Does not improve vision again, if vision is already shit
85
Q

What was the first drug to restore vision in vascular AMD?

A

Anti-VEGF drugs

86
Q

When can ranibizumab be used (anti-vegf drug) in line with the 2008 NICE guidelines?

A
  1. VA between 6/12 - 6/96
  2. No permanent structural damage to the fovea (no scar tissue)
  3. Lesion size is smaller than 12DD
  4. Evidence the disease is progressing
  5. Blood should comprise <50% of lesion area
87
Q

Why is the VA from 6/12 or worse?

A

This is the VA of the trials for the drug. There is not much clinical data on the drug with VA better then 6/12

88
Q

When should therapy stop?

A
  1. Continuous loss of VA
  2. Identifying further retina changes - this shows the treatement is not wokring
89
Q

What happens with NAMD?

A
  1. Up regulation of VEGF
  2. VEGF binds to a VEGF receptor
  3. This leads to increased vascular permeability = more leaky
  4. Proliferation and migration of endoithelial cells

This elads to new leaky blood vessels

90
Q

SO how does ranibizumab work?

A

It will bind to the VEGF which will mean it can longer bind to theVEGF receptor

91
Q

How do we treat using ranibizumab?

A
  1. We use a topical anaesthesia
  2. Inject the drug into the vitreous
  3. Ask to see how many fingers
92
Q

Why do we ask to count fingers?

A

Because when injecting things into the vitreous it can cause retinal artery perfusion. This perfusion will cause vision loss!

93
Q

How often are injections given? PRN method

A

Three monthly injections then monthly follow-up appointment to do a OCT to see any disease progression and see if they need injections

94
Q

What is treat and extend method of anti-VEGF treatment?

A

Every time they come in they get an injection but if no change the gap between the next appointment is bigger. If there is a sign the gap is smaller.

95
Q

What other anti-VEGFs are used?

A
  1. Pegaptanib : similar to the ranibizumab. But not as effective
  2. Bevacizumab : cheaper, but not licensed for intraocular use
  3. Aflibercept
  4. Brolucizumab
96
Q

What is Aflibercept (Eylea)?

A

This is a fusion protein.

It blocks VEGF-A and B and placental growth factor

97
Q

How do we give eylea?

A

Loading dose: 3/4- weekly
Maintenance dose: 8- weekly

98
Q

When was eylea approved by NICE?

A

2013!

99
Q

What is brolucizumab?

A

This is a anti-body fragment
Ad approved in 2021!!!!!!!!!!!!!!!!

100
Q

When do we refer urgently for AMD?

A
  1. Recent onset of amsler issues
  2. Recent onset of marked reduced VA
  3. Hyperopic rx shift
  4. Haemorrhage
  5. Exudates
  6. Retinal elevation
  7. Sub/intra - retinal fluid or sub-rpe fluid
    Sub-retinal neovascular membrane
101
Q

How do we refer for wet amd?

A

We need to find out the local referral pathway for wet AMD , the aim is normally to treat within 2 weeks’ time

102
Q

When do we educate the px?

A

Unilateral wet amd, they need to check for distortion in the fellow eye using the amsler chart

103
Q

What is not suitable for medical treatment?

A
  1. VA worse then 6/96 and when there is a disciform scar. However we should still refer them
  2. Geographical, early and intermediate AMD are also untreatable
104
Q

How do we educate the px when they have untreatable amd?

A
  1. Understand the disease
  2. Future prognosis
  3. Risk in the second eye
  4. Regular checks
  5. Neovas symptoms
  6. Lifestyle
  7. Provide written info
105
Q

What life style advise can we give?

A
  1. Stop smoking
  2. Wear sunglasses
  3. Diet from CoO recommends darky leafy greens, fish oils intake and a lot of fruit and veg
106
Q

What nutrients can we recommend?

A

AREDS and AREDS2 2

107
Q

Why might refraction change for px with AMD?

A

Because there eccentric viewing will change thus their correction changes.

108
Q

What should we do if they are struggling with low vision?

A
  1. Do a low vision assessment so we can give them magnifiers, telescopes ect
  2. Bilateral central scotomas may benefit from eccentric viewing training
  3. Lighting advice
  4. Refer to social services
109
Q

What does social services referral mean?

A
  1. Home visits
  2. Lighting
  3. Mobility training
  4. Advice on benefits and wellbeing emotional support
  5. Computer training
  6. Long cane training
110
Q

What can the macular society do for px?

A
  1. Councelling
  2. Research support
  3. Leaflets
  4. Eccentric viewing training
  5. Conferences
111
Q

Why might we refer if the Amd is untreatable?

A
  1. To check the other eye and see there is no neovas.
  2. For registration on SI and SSI
  3. Other diseases such as cataract
112
Q

What is AREDS?

A

Age related eye disease study

113
Q

What did AREDS show?

A

There was a 20% reduction for developing AMD in the next 5 years with zinc and antioxidants.

114
Q

What are some contraindications for takign AREDS?

A
  1. Smoking : increases risk of lung cancer taking vitamin A
  2. Vascular disease : increases chance of heart failure taking vitamin E
  3. Genitourinary complications taking Zinc
115
Q

Is there evidence that it prevents AMD in people who do not have it to start with?

A

NO

116
Q

What is AREDS 2 trial ?

A

This is adding omega 3 fatty acids, lutein+ Zeaxanthin or both, helpful? And taking beta carotene out
Answer is no

117
Q

Who may benefit from AREDS2 then?

A

Px who have shit diets

118
Q

What should we do before recommending supplements?

A

Ask the px to check with their GP if they can take it

119
Q

Are hard drusen normal?

A

Yes in the aging population. but lots can lead to soft drusen

Eye Disease (48 decks)

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