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Term 2 eye disease lectures > Lecture 12: AMD > Flashcards

Lecture 12: AMD Flashcards

1
Q

What is the prevelance of AMD?

A

50% over 65’s have features of early or late AMD-Eureye study

approx 1/2 of all CVI in England are due to AMD

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2
Q

What is the impact of AMD?

A

-end stage is complete central scotoma
-VI with increased risk of falls, social isolation
- problems performing tasks
- recognising faces
-high prevalence of depression

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3
Q

How big is the macula?

A

15–20 degrees
foveola, fovea, parafovea, perifovea

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4
Q

What is the clinical classification of AMD?

A

Early AMD
Low risk:Medium drusen (>63 µm ≤ 125 µm) or pigment abnormalities.

Medium risk: large drusen (≥125 µm), or reticular drusen, or medium drusen with pigmentary abnormalities.

High risk: large drusen with pigmentary abnormalities, or reticular drusen with pigmentary abnormalities, or vitelliform lesion without significant visual loss, or atrophy <175 micrometres and not involving the fovea

Late AMD
Intermediate: RPE degeneration and dysfunction, serous PED without CNV

Wet active: Classic CNV, Occult CNV, Mixed, retinal angiomatous proliferation (RAP), polypoidal choroidal vasculopathy (PCV).

Dry: GA (minus nAMD), VA<6/18 with dense/confluent drusen or advanced pigmentary lesions and/or atrophy, or vitelliform lesion.

Wet inactive: Fibrous scar or RPE tear

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5
Q

What is drusen?

A

Localised deposits between basement membrane of RPE and Bruch’s membrane.

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6
Q

What are the types of drusen?

What are the risk factors for progression to advanced AMD?

A

Hard drusen/druplets: tiny yellow/white lesions (<63µm).

Soft drusen
- larger in size
-distinct or indistinct
- may coalesce to form confluent drusen
- hallmark of AMD

-larger and confluent drusen
-increase in number of drusen
-pigmentary changes

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7
Q

What types of pigmentary changes can you get?
What are they caused by?

A

Focal hyperpigmentation

Caused by:
Increased melanin content of RPE
RPE cell profileration
RPE cell migration.

Focal hypopigmentation seen as small patches of mottled pigment

Caused by:
Reduced melanin content of RPE cells
RPE cell atrophy
RPE layer thinning.

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8
Q

What is a clinical feature of Late dry AMD?

A

Geographic atrophy:
-sharply delineated
- roughly round area >175µm of hypo or depigmentation or apparent absence of RPE.
-Increased visibility choroidal circulation.
-Often starts in parafovea, sparing fovea until later.

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9
Q

What clinical feature to do with the choroid can you get in late AMD?
What are the symptoms?

What other pathology can you get with it?

A

-Growth of new blood vessels from choroid to proliferate beneath RPE, or in subretinal space.
-May be seen as green/ grey lesion.
-Easier to detect on stereoscopic viewing or via OCT

recent onset distortion and deterioration of vision.

Fragile vessels mean sub- or intraretinal hemorrhages, 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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10
Q

Why is vision loss rapid in neovascular AMD?

A

due to exudates and haemorrhage, secondary cell death, and formation of disciform scar.

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11
Q

What causes the progression of choroidal neovascularisation?

What is the risk in the other eye?

A

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

High risk in second eye in px with unilateral CNV.

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12
Q

What type of detachment can you get in Late AMD?

A

serous pigment epithelium detachment
-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 subretinal fibrosis.
->80% associated with CNV.

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13
Q

What is reticular pseudodrusen?
Where is it located?
What is the prevalence?

A

Yellow, interlacing pattern in the outer macula and beyond.

Located between retina and RPE (instead of between RPE and Bruch’s membrane like other drusen)

Prevalence increases with increasing AMD severity, but also found in ‘normal’ eyes.
Have poorer vision than eyes without RPD, especially dark adaptation.
Eyes with reticular pseudodrusen have a 4-8 fold greater risk of 5-year progression to late AMD than eyes with drusen alone.

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14
Q

What is the pathogenesis of AMD?

A

Inflammation
-Inflammatory cells found in eyes with drusen, CNV, RPE atrophy.
-Strong association between AMD and polymorphisms of CFH gene and other genes involves in immune response.

Oxidative Damage
-Retina prone to oxidative damage
-RPE is unable to break down products of oxidation: accumulate in RPE and Bruch’s membrane.

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15
Q

What are the risk factors for AMD?

A

Age
ethnicity (lower risk of late AMD in black people)
genetics (1st degree relative 6-12x higher risk)
smoking (4x more risk)
light exposure
diet (need omega-3, antioxidant vitamins and minerals, macular carotenoids like lutein and zeaxanthin, low glycaemic index diet)

systemic RF:
-prev cataract surgery
-cardiovascular disease
-hypertension
-BMI
-Higher plasma fibrinogen

other:
-DM
-Female
-Higher alcohol intake
-hypermetropia
-pale iris colour

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16
Q

What must you ask in the History and Symptoms to investigate AMD?

A

Family history of AMD?
History of smoking?
Taking any dietary supplements? Diet?
Visual symptoms – distortion? blurred vision? Problems at near or distance? Is it worse under low light levels?
Since when? Sudden onset?
Both eyes/one eye?
Increased difficulty with tasks e.g. reading, cooking, mobility, shopping?

17
Q

What chart should you use to investigate vision?

Why is it important to measure VA?

A

ETDRS logMAR chart

-Measure of disease progression.
-NICE guidelines for Lucentis (VA 6/12-6/96).
-Guidelines for registration (severely) sight impaired

18
Q

What are the DVLA rules about AMD?

A

-ensure spectacles enable 6/12 binocularly.

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

19
Q

What is the purpose of Amsler?
How sensitive is the Amsler test?

A

-To plot areas of distortion and scotomas
-Can indicate neovascular changes
-helps practitioner give guidance for eccentric viewing

-many patients will not notice blind spots in their vision, because the brain is adept at filling in missing information from the visual scene.

-In one study 2/3 of people with a scotoma less than 6 degrees in diameter could not identify it using an Amsler chart.

-It may be better at detecting subtle distortion changes, which are associated with conversion to wet AMD.

20
Q

What instructions should you give to someone using the Amsler chart

If we want a simpler approach, what can we use?

A
  1. Do any of the lines in the grid appear wavy, blurred or distorted?
  2. Do all the boxes in the grid look square and the same size?
  3. Are there any “holes” (missing areas) or dark areas in the grid?
  4. Can you see all corners and sides of the grid (while keeping your eye on the central dot)?
    (30cm)

looking ar blinds or a window frame every day

21
Q

What functional tests an you do to investigate AMD?

A

-Contrast sensitivity e.g. Pelli Robson
-Strongly related to real world performance

-Reading speed / accuracy
-Macular photostress test
-AdaptDx dark adaptometry
-Microperimetry (plot scotoma, useful for eccentric training)
-Colour vision (mainly B/Y defects so CAD more useful than Ishihra)

22
Q

What types of imaging techniques can be useful in AMD?

A

Fundus Photography – useful for monitoring progression, no information on retinal elevation.

Optical Coherence Tomography – Very useful for diagnosis and monitoring of AMD when correctly interpreted.

Fluorescein Angiography – gold standard for identifying wet AMD in hospital eye clinic.

Fundus autofluorescence – useful for evaluating geographic atrophy (usually in hospitals) (area of atrophy is seen as dark)

23
Q

What are the two types of CNV on fluorescein angiography?

A

-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. Caused by CNV between RPE and Bruch’s.

24
Q

What was the first recognised treatment for neovascular AMD?

How does it work?

A

Macular photocoagulation

-Destruction of new blood vessels with thermal laser.
-Slows visual loss by destroying new vessels, but does not restore vision.
-Causes scotoma in lasered region (retina destroyed in lasered area too).
-Retreatment often required.
Only suitable for about 1/20 px with nAMD (had to be classic and extrafoveal)

25
Q

How does photodynamic therapy (PDT) work?

Why is it better then photocoagulation?

A

-Photosensitiser (verteporfin) injected intravenously
-Binds to low density lipoproteins in the blood
-Low density lipoproteins (and verteporfin) taken up by active endothelial cells in growing blood vessels.
-Photosensitiser activated with low power laser (15 mins after start of infusion).
-New blood vessels closed off (often CNV recurs within approx 3 months: repeated treatment necessary).

more targeted destruction of vessels so less collateral damage to retina

26
Q

What drugs can be used in AMD treatment?
What is Ranibizumab?

What are the guidelines for using lucentis?
What is the criteria for discontinuation?

A

anti-VEGF drugs

Lucentis
-anti-VEGF antibody, binds to & inhibits all forms VEGF-A
-impedes choroidal neovascular growth

VA 6/12-6/96
No permanent structural damage to fovea
Lesion size < 12 disc areas
Evidence of disease progression.
Blood < 50% lesion area

persistent deterioration VA
identification of anatomical changes in retina indicating inadequate response to therapy

27
Q

Whar is the mechanism of anti-VEGF therapy for neovascular AMD?

A

-vascular endothelial growth factor molecules bind to VEGF receptors.
-This starts a cascade of chemical reactions, which leads to angiogenesis (the development of new vessels).
-Anti VEGF therapy attempts to disrupt this cycle, treating neovascular AMD.

-Ranibizumab is an antibody which binds to all forms of the angiogenic Vascular Endothelial Growth Factor A.
-When the Ranibizumab molecule is bound to VEGF, VEGF is no longer able to bind to, and activate, its receptor, hence the chemical cascade initiating CNV is inhibited

28
Q

How is Ranibizumab administered?

A

-anaesthetise the eye using anaesthetic drops, -inject the drug into the vitreous chamber.
-After injection, check that central retinal artery CRA is still perfused by asking to count fingers.

-three monthly loading injections on first diagnosis, followed by monthly follow up with injections as required.
-treat and extend: retreats follow a regular pattern with expanding gaps

-First diagnosis is always based on fluorescein angiography.
- At monthly follow ups, a combination of OCT, VA and fundus examination is used

29
Q

What other drugs can be used in anti-VEGF treatment?

A

Pegaptanib (Macugen)
-First anti-VEGF drug licensed for intraocular use (2004)
-Binds to VEGF-165 and inhibits its activity.
-NICE does not recommend for treatment of wet AMD (less effective than Ranibizumab)

Bevacizumab (Avastin)
-Monoclonal anti-VEGF antibody
-Developed for intravenous use in cancer treatment
-Not licensed for intraocular use, therefore not recommended by NICE

Aflibercept (Eylea)
-Not an antibody, but a fusion protein
-3 x 4-weekly loading dose. 8-weekly maintenance dosing.
2013: NICE approved for use in same patients eligible for Ranibizumab. Effectiveness very similar.

Brolucizumab
-Brolucizumab is a single-chain antibody fragment
-Approved by NICE in 2021 as an alternative option for treating nAMD.

30
Q

What is the referral and management for neovascular AMD?

A

URGENT REFERRAL IF:
-Recent onset markedly distorted, blurred, or absent lines on Amsler grid
-Recent onset marked reduction in VA
-Hyperopic shift in Rx

And/ or retinal signs include any one of the following:
-Haemorrhage (sub-RPE, sub-retinal, intra-retinal)
-Exudates (requires urgent referral as it is a sign of leakage from new vessels)
-Visible retinal elevation
-Sub-retinal, intra-retinal or sub-RPE fluid
-Sub-retinal neovascular membrane

31
Q

What type of AMD is not suitable for treatment?

A

-Longstanding wet AMD with scar tissue formation, and nAMD with VA worse than 6/96 is not suitable for medical treatment
-best to refer all newly diagnosed wet AMD for ophthalmological opinion.- non-urgent referral

Geographic atrophy
early AMD
intermediate AMD

32
Q

How can you manage untreatable AMD?

A
  1. Education
    -Disease awareness
    -Future prognosis
    -Risk of development of AMD in second eye
    -Need for check ups with Optom / Ophthalmologist
    -Symptoms of neovascular AMD (monitoring of fellow eye)
    -Risk factors (see Lifestyle Advice)
    -Provide written information.
  2. Lifestyle Advice
    -Stop smoking (biggest modifiable risk factor)
    -Wear sunglasses
    -Diet:
    Eat balanced diet containing lots of coloured fruit and vegetables.
    Increased dark leafy veg intake
    Increased oily fish intake (x2 per week)
  3. Nutritional supplements
    -AREDS and AREDS2
33
Q

How can you manage the low vision in AMD?

A

-refraction
-LV assessment: eccnetric training, LVA, lighting advice

-referral to social services: home visit, advice on daily living skills, discussion on lighting, demonstration on non-optical aids, mobility training, emotional support

-referral to the voluntary sector (Macular society, RNIB)

-referral to HES (assessment of fellow eye, registration as SI/SSI)

34
Q

What are the disadvantages of AREDS1?

A

-Increased risk lung cancer in smokers taking beta-carotene.
I-ncreased risk heart failure in people with vascular disease taking vit E.
-Increased genitourinary complications in people taking zinc
-slight increased risk of mortality
-No evidence that it prevents AMD in people who don’t have it to start with.

CHECK WITH GP BEFORE STARTING SUPPLEMENTS

35
Q

What are the fundus features of early/intermediate AMD?

What is the functional status?

What is the optometric action?

A

-soft drusen
-focal hyperpigmentation

-slight distortion on Amsler corresponding to drusen
-gradual reduction in VA

-Monitor, advise on lifestyle changes (e.g. stopping smoking and nutritional supplements)
-provide Amsler grid for self-assessment.

36
Q

What are the fundus features of wet AMD (suitable for treatment)?

What is the functional status?

What is the optometric action?

A

Haemorrhage
Exudates
Visible retinal elevation
Sub-retinal fluid or pigment epithelial detachment
Sub-retinal neovascular membrane may be seen as greenish grey lesion

-Presence of markedly distorted, blurred, or absent lines on Amsler grid
-Recent onset marked reduction in VA (6/12 to 6/96)
-Hyperopic shift in Rx

REFER URGENTLY

37
Q

What are the fundus features of advanced AMD (not suitable for treatment)?

What is the functional status?

What is the optometric action?

A

Geographic atrophy
Disciform scar
Extensive exudates, haemorrhage, fibrosis, macular elevation

Central scotoma on Amsler chart
VA reduced to below 6/96

Refer non-urgently to assess fellow eye, and consider LVA assessment and training, visual impairment counselling and registration.
Refer urgently if in any doubt Re. treatment suitability.

Term 2 eye disease lectures (18 decks)

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