Unit 4 - AMD Flashcards

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?

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?

24
Q

What is ICPV?

A

Idiopathic choroidal polypoidal vasculopathy, a variant of wet AMD

25
How are ICPV patients different from traditional wet AMD patients?
Usually younger and asian
26
What other causes of CNVM are there? (5)
1. Myopia 2. Trauma 3. Inflammation 4. Angiod streaks 5. Tumours
27
What other causes of fluid leaks are there? (2)
* Central serous chorioretinopathy * Optic disc pits
28
Which inherited macula dystrophies can mimic wet AMD?
* Sorsby macula degeneration * Adult vitelliform dystrophy