Unit 4 - AMD Flashcards

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1
Q

What are the 6 clinical signs of AMD?

A
  1. Drusen
  2. RPE Changes
  3. GA, absence of RPE
  4. PED
  5. CNVM
  6. Fibroglial scar
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2
Q

How many cases of AMD are genetically determined?

A

1/4

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3
Q

If you have an older sibling with AMD how much more likely are you to develop AMD?

A

3-6X

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4
Q

If you have a first degree relative with AMD how much more likely are you get AMD?

A

4X

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5
Q

If you have more than 8 hours sunlight exposure per day how much more likely are you to get dry AMD?

A

5X

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6
Q

What is the incidence of end stage AMD in the over 40 population

A

1.5%

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7
Q

What are the indications for urgent referral or wet AMD?

A

Recent onset:

  • reduced v/a,
  • Metamorphopsia,
  • Scomota or blind spot,

V/a better than 6/60

And/Or Haem Fluid on OCT Exudates

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8
Q

Once GA commences how long is the average progression to legal blindness?

A

5-9 years

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9
Q

What % of dry patients will develop wet?

A

10-15%

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10
Q

What is the differential diagnosis in dry AMD?

A
  1. Dominant drusen
  2. Stargadt’s
  3. Pathological myopia
  4. Maternally inherited deafness and diabetes
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11
Q

What are the clinical features of dominant drusen?

A
  1. Symmetrical drusen
  2. More drusen seen on FFA and FAF than obvserved
  3. Family history
  4. V/a will usually be oK but more likely to develop AMD
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12
Q

Why is the retina so prone to oxidative stress?

A
  1. High oxygen consumption
  2. Concentration of polyunsaturated fatty acids
  3. Exposure to sunlight
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13
Q

What antioxidants were used in AREDS 1?

A
  1. Vitamin C
  2. Vitamin E
  3. Betacrotene 15mg
  4. Zinc
  5. Copper
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14
Q

What changes were made in AREDS 2?

A

Removed Betacarotene and added lutein and zeaxanthin

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15
Q

What benefit was found in ARED2 compared to AREDS1?

A

20%

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16
Q

Did Omega 3 give any additional benefit?

A

No

17
Q

What problems are there with betacarotene?

A

Increased risk of lung cancer in smokers in doses > 20mg/day

18
Q

What size are small and intermediate drusen?

A

Small <63microns

Intermediate 63-125 microns

19
Q

Where are type 2/ classic CNVM

A

Penetrating RPE into retina

20
Q

What are the complications of wet AMD

A
  1. Serous retinal detachment
  2. Haem
  3. Progression of GA
  4. Subretinal fibrosis
  5. Charles Bonnet syndrome
  6. Low vision = depression, falls, fractures, loss of driving licence and lower qol
21
Q

What is retinal angiomatous proliferation?

A

Subset of wet AMD but when proliferation occurs from retinal capillaries.

Starts intra-retinally and may go sub-retinal and then into choroidal

22
Q

How do patients with RAP differ from traditional wet AMD patients?

A

Maybe be older and lesions are usually bilateral and juxtafoveal.

23
Q

Does RAP respond to anti-VEGF?

A

Partially

24
Q

What is ICPV?

A

Idiopathic choroidal polypoidal vasculopathy, a variant of wet AMD

25
Q

How are ICPV patients different from traditional wet AMD patients?

A

Usually younger and asian

26
Q

What other causes of CNVM are there? (5)

A
  1. Myopia
  2. Trauma
  3. Inflammation
  4. Angiod streaks
  5. Tumours
27
Q

What other causes of fluid leaks are there? (2)

A
  • Central serous chorioretinopathy
  • Optic disc pits
28
Q

Which inherited macula dystrophies can mimic wet AMD?

A
  • Sorsby macula degeneration
  • Adult vitelliform dystrophy