Age related macular degeneration: optometric management and medical treatment Flashcards

1
Q

what leads to the increase in VEGF being produced in AMD

A

hypoxia increases VEGF being produced and then the vessels become more leaky

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2
Q

what was the first medical treatment for AMD

A

Macular laser photocoagulation for nAMD

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3
Q

for which type of AMD were all these drugs only treatable for and what type of AMD was it not treatable for and therefore what type of treatment was available for them

A

all medical treatments were only treatable for nAMD

not for early or dry AMD which required more lifestyle changes

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4
Q

what did research find that the anti-VEGF treatment Ranibizumab (Lucentis) for nAMD could do

A

could actually restore vision in those people with vision loss due to wet AMD

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5
Q

how does Macular Photocoagulation work in treating nAMD
what can this cause as a consequence
what was required
in how many and what type of AMD patients was this only suitable for

A

Destruction of new blood vessels with thermal laser (seals off the new blood vessels)
Slows visual loss by destroying new vessels, but does not restore vision

Causes scotoma in lasered region (retina destroyed in lasered area too due to the very high intensity)

Retreatment is often required (~60% of px in 3 years)

Only suitable for about 1/20 px with nAMD as had to be classic and extrafoveal

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6
Q

how does Photodynamic Therapy (PDT) work in treating nAMD

A

Photosensitiser (verteporfin) injected intravenously (into the blood supply)

Binds to low density lipoproteins in the blood

Low density lipoproteins taken up by active endothelial cells in growing blood vessels, such as those which occur in neovascular AMD

Therefore, verteporfin is taken up by and accumulates in the CNV membrane

A low powered laser is directed onto the area of CNV to activate the photosensitiser. This takes place 15 minutes after the start of the infusion

When the photosensitiser, verteporfin, is activated, the new blood vessels are closed off

therefore this damages the new blood vessels and stop them from growing and does not blast off the retina as the laser is just used to activate the drug thats accumulated in the new blood vessels, so is a better treatment as does not cause a scotoma

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7
Q

what is the difference between treating nAMD with Macular Photocoagulation and Photodynamic Therapy (PDT)

A

Photodynamic Therapy (PDT) = More targeted destruction of vessels – less collateral damage to retina than photocoagulation

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8
Q

how effective was treatment using Photodynamic Therapy (PDT) compared to someone with nAMD receiving no treatment at all

A

both treated and untreated groups lose vision over 2 years, but greater VA loss in untreated group

e.g. the mean visual loss was just over 20 letters with the placebo group and 10 letters with the group who received PDT treatment

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9
Q

what is a disadvantage of Photodynamic Therapy (PDT)

A

often results in the development of geographic atrophy over repeated retreatments due to reduced choroidal perfusion

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10
Q

what was the NICE guidelines for Photodynamic Therapy (PDT) use (give 2 conditions)

and what did this mean about the amount of nAMD px’s that were suitable for this treatment

A

NICE recommends PDT for people with wet AMD who have:

  • a confirmed diagnosis of classic subfoveal (under fovea) choroidal neovascularisation (CNV), with no sign of occult CNV
  • VA 6/60 or better

[i.e. still not suitable for all px]
Only about 1 third of wet AMD patients suitable for treatment

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11
Q

why is anti-VEGF drugs the new treatment of choice

A

as were first treatment to restore vision, suitable for most forms of nAMD

(so not restricted to classic or subfoveal like in PDT and was the first treatment that could restore vision rather than just slow down)

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12
Q

which anti-VEGF therapy is the treatment of choice

A

Ranibizumab (‘Lucentis’)

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13
Q

what is Ranibizumab (‘Lucentis’) and how does it work

A

is anti-VEGF antibody, binds to and inhibits all forms VEGF-A, thereby impeding choroidal neovascular growth beneath the retina

i.e. sticks to the VEGF molecule and inhibits them

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14
Q

what is the NICE guidelines and RCO guidelines for Ranibizumab as treatment of choice for nAMD when all of the 5 following criteria apply

A

VA 6/12-6/96 (as no evidence it improves vision in px with 6/12)

No permanent structural damage to fovea (as won’t get better)

Lesion size less than 12 disc areas

Evidence of disease progression

Blood of less than 50% in the lesion area

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15
Q

what is the NICE and RCO guidelines for stopping treatment/discontinuation of Ranibizumab

A

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

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16
Q

describe the mechanism of how VEGF occurs in wet AMD

A

Vascular endothelial growth factor (VEGF) molecules bind to it’s receptor

This starts a cascade of chemical reactions, which leads to proliferation of vascular endothelial cells, and increased permeability and migration of vessels, all of which results in angiogenesis (the development of new vessels)
It also makes blood vessels more leaky = why we see blood build up in someone who has wet AMD

Anti VEGF therapy attempts to disrupt this cycle, thereby providing a way of treating all types of neovascular AMD

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17
Q

describe the mechanism of how Anti VEGF therapy attempts to disrupt this cycle of how VEGF occurs in wet AMD

A

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

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18
Q

what are the 4 steps of carrying out the treatment of nAMD using

A

Topical anaesthesia
Injection into vitreous
Check retinal artery perfusion (count fingers)
Antibiotic drops (to avoid infection)

19
Q

after injecting the Ranibizumab into the patient’s eye, what must you do/check and why

A

Check retinal artery perfusion by asking px to count fingers

As it is possible that as the pressure goes up when injecting the drug that it can block the flow of blood going through the central retinal artery, so must check that px is losing vision

20
Q

what is the course of Ranibizumab treatment

what is also carried out during these treatments and why

A

three monthly loading injections on first diagnosis, followed by monthly follow up appointments pro re nata (as required)
At monthly follow ups, a combination of OCT, VA and fundus examination is used which will indicate if need to give further injections

21
Q

when will Ranibizumab injections only be given to a patient

A

First diagnosis is always based on fluorescein angiography

Injections will only be given if theres signs of progression, diagnosed by FA

22
Q

what outcome/improvement did Ranibizumab injections treatment show after 2 treatments

A

all of the fluid has now been reabsorbed
the macula is thinner (as swelling and elevation has gone down)
va has gone from 6/18 with injection 1 to 6/9 on injection 2
= immediate affect

23
Q

name 3 other anti-VEGF drugs used other than Ranibizumab (‘Lucentis’) for nAMD treatment

A

Pegaptanib (Macugen)
Bevacizumab (Avastin)
Aflibercept (Eylea; VEGF Trap Eye)

24
Q

what is the anti-VEGF drug Bevacizumab (Avastin)

A

Monoclonal anti-VEGF antibody

Developed for intravenous use in cancer treatment

Not licensed for intraocular use, but its effectiveness in the treatment of neovascular AMD has been established in randomised controlled trials, and it is used off-label as a treatment
It is not used by the NHS, but it is cheaper, so some private treatments may use it instead

25
Q

how does the anti-VEGF drug Aflibercept (Eylea; VEGF Trap Eye) work
what is the course of treatment

A

Not an antibody, but a fusion protein made of two parts of VEGF-receptor molecule

In this way it binds to and inhibits/blocks VEGF-A and B and Placental Growth Factor

3x 4-weekly loading dose
8-weekly maintenance dosing (potential advantage over monthly follow-ups required for Ranibizumab)

26
Q

what advantage does anti-VEGF drug Aflibercept (Eylea; VEGF Trap Eye) have over Ranibizumab and what do some hospitals do

A

after the first 3 month dose, they only need a follow up every 2 months instead of every 1 months with Ranibizumab = cheaper for hospitals

Used by some hospitals on patients unresponsive to Ranibizumab

27
Q

what is the speed of referral for nAMD i.e. with suspect newly developed neovascular AMD

A

Urgent referral

28
Q

what 8 following signs need to be true of a suspect newly developed neovascular AMD in order to warrant rapid access pathways for a urgent referral

A
  • Recent onset markedly distorted, blurred, or absent lines on Amsler grid
  • Recent onset marked reduction in VA
  • Hyperopic shift in Rx (retina smaller, eyes swollen)

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 (which may be seen as a green/grey lesion)

if there is a recent onset reduction in VA (whilst treatment will only be given to those in the range 6/12-6/96, newly developed CNV should still be referred urgently if the VA is outside of this range), or if a hyperopic shift in Rx has occurred

29
Q

what 3 things should you do for when referring and managing a px with nAMD

A

Find out your LOCAL REFERRAL PATHWAY for wet AMD – many areas have special referral paths to rapid access clinics straight to the local macular specialist - so don’t always have to go via GP

EDUCATE patients with unilateral nAMD of symptoms of wet AMD (check for distortions and sudden onset visual loss), and encourage them to monitor fellow eye daily using Amsler chart, window frame, or similar.

Advise on LIFESTYLE CHANGES, e.g. stopping smoking, changing diet to green leafy vegetables and potential vitamin supplementation (AREDS formula) may also be appropriate

30
Q

which 2 types of patients with end stage AMD is not suitable for treatment and what should you still do

A

Not treatable:
Longstanding wet AMD with scar tissue formation, and nAMD with VA worse than 6/96

Geographic atrophy

However best to refer all newly diagnosed wet AMD for ophthalmological opinion and let them diagnose px as not treatable

31
Q

list 8 things as optometrists we should do to help patients with of untreatable end stage nAMD and GA

A
Check fellow eye
Education
Lifestyle Advice
Nutritional Supplements
Refraction
Low vision assessment
Referral to Social Services, ROVIs etc
Referral to Voluntary Sector
32
Q

why would you want to check the fellow eye of a px with untreatable end stage nAMD and GA and how

A

For signs of incipient neovascular AMD, which may be amenable to treatment
To make sure of no new met AMD in other eye
Or for people with GA, check their GA just to double make sure theres no new wet AMD

Thorough fundus check, Amsler chart

33
Q

list 7 ways of how you will educate a px with untreatable end stage nAMD and GA

A
  • Disease awareness
  • Future prognosis
  • Risk of development of AMD in second eye (12% chance every year)
  • Need for check ups with Optom / Ophthalmologist for any other pathology
  • Symptoms of neovascular AMD (monitoring of fellow eye)
  • Risk factors (see Lifestyle Advice)
  • Provide written information - for px to remember all this
34
Q

what 3 pieces of lifestyle Advice will you give to a px with untreatable end stage nAMD and GA

A

Stop smoking (biggest modifiable risk factor)

Wear sunglasses

Diet: College of Optometrists recommend…

  • Eat balanced diet containing lots of coloured fruit and vegetables.
  • Increased dark leafy veg intake likely to be protective.
  • Increased oily fish intake likely to be beneficial in AMD.
35
Q

which Nutritional Supplements is advised to be taken by a px with untreatable end stage nAMD and GA

A

AREDS and AREDS 2 formulae only ones with proven effect at preventing AMD progression

36
Q

give 3 reasons why it is useful to carry out a thorough refraction when managing a px with untreatable end stage nAMD and GA

A

Improves VA in 11% of low vision patients

Amblyopic eye may become better eye - this px who used to have a balance lens will now need full rx

Refraction may change as eccentric viewing develops

37
Q

list all the reasons why you will want to manage a px with untreatable end stage nAMD and GA with a low vision assessment (by referring or manage ourselves)

A

Help for reading

Patients with bilateral central scotoma, may benefit from eccentric viewing and steady eye strategy training

Help for distance vision includes:

  • Prescription of telescopes
  • Practical advice may also be given, such as getting a larger TV
  • When going to the cinema, theatre, sports events, try to get a seat nearer to the front
  • Use audio description facilities on TV

Lighting advice
- Light falls in an inverse square fashion
“Halve the distance, quadruple the light”
- Over the shoulder minimises glare
- Type of bulb unimportant

38
Q

when a px with untreatable end stage nAMD and GA is referred to Social Services, ROVIs etc, list all the 8 types of help they should get from them

A
  • Home visit
  • Advice on performing daily living skills
  • Discussion (provision?) of lighting
  • Demonstration (supply?) of non-optical aids
  • Mobility training if required
    including symbol cane, long cane, training
  • Advice on benefits/welfare rights
  • Advice on computer training
  • Emotional support (remember prevalence of depressive symptoms in people with advanced AMD ~30-40%)

Anyone can refer px to social services, so doesnt have to be via the GP, px can refer themselves or we can write a letter

39
Q

when a px with untreatable end stage nAMD and GA is referred to the Voluntary Sector, which 2 main voluntary sectors are there and list all types of help they should/can get from them

A

The macular society:

  • Information distribution
  • “Sideview”
  • Information leaflets
  • Conferences
  • Counselling/emotional support
  • Active web forum
  • Local groups
  • Research support
  • Eccentric viewing training

RNIB:

  • support
  • information
  • courses
  • resource centres
  • books
  • campaigning

and local societies

40
Q

when managing a px with untreatable end stage nAMD and GA, for what 3 reasons will you still want to refer them to the ophthalmologist

A
  • Assessment of fellow eye - if px wants second opinion
  • Registration as sight impaired / severely sight impaired
  • Other diseases e.g. cataract
41
Q

what is the 5 main things you will do to manage are those with bilateral early AMD – that is, just drusen and or pigmentary changes
and what 2 things do you want to look out for

A
As theres no medical treatment for early AMD: 
Education
Self monitoring
Lifestyle changes
Nutritional supplements
Patient support groups

Look out for:

  • Risk factors for progression present? e.g. lots of large soft and confluent drusen, focal pigmentary changes
  • Monitor these patients carefully - review this px yearly if theres no other concerns
42
Q

what did the AREDS 1 trial results reveal

A

Significant reduction in OR (~20% risk reduction) for development of advanced AMD in 5 years with zinc + antioxidants.

Effect increased if people with early AMD excluded - i.e. showed no sign of benefitting

And no evidence for those who don’t have AMD as they weren’t included in the trial

Therefore those who should be treated with AREDS 1 are - those with middle/intermediate stage AMD and ones who got advanced AMD in one eye and not the other

43
Q

what are the 4 risks/disadvantages to the AREDS 1 supplement

A

Increased risk lung cancer in smokers taking beta-carotene/vit A

Increased risk heart failure in people with vascular disease taking vit E

Increased genitourinary complications in people taking zinc?

No evidence that it prevents AMD in people who don’t have it to start with

So recommend px to discuss with GP before starting the supplements