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OD3 (S1&2) > DIS - Macular Diseases I: AMD - Week 1 > Flashcards

DIS - Macular Diseases I: AMD - Week 1 Flashcards

1
Q

True or false
AMD is the most prevalent macular disorder in Australia?

A

True

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2
Q

Is the prevalence of AMD projected to increase or decrease? Explain why.

A

Increase due to growing elderly population

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3
Q

Is AMD a bilateral disease? Explain.

A

Usually affects one eye, but is a bilateral disease - eventually

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4
Q

What do photoreceptors shed? What happends to these and by what?

A

Shed outer segment discs
RPE enzymes degrade and recycle them

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5
Q

What happens to light-damaged elements shed by the photoreceptors? What do they form and what do they coalesce to form?

A

Light damaged outer segment discs cannot be degraded/recycled.
They form lipofuscin vesicles
These coalesce to form BLamD

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6
Q

How can BLamD be visualised?

A

FAF

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7
Q

Where do BLamD accumulate? What happens to them eventually (forming what)?

A

They accumulate at the basement membrane of the RPE
They are shed by the RPE and form BLinD

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8
Q

What are druplets?

A

BLinD

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9
Q

What do druplets coalesce to form?

A

Drusen

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10
Q

Where does reticular drusen form? Is it more or less serious than other forms of drusen?

A

Forms at the inner surface of the RPE (interface with the photoreceptors)
More serious

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11
Q

What keeps the choriocapillaris active and what is it produced by?

A

Kept active by cytokines produced by the RPE

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12
Q

Collectively, what do BLamD, BLinD, and drusen do (2)?

A

Restrict the RPE, reducing bruch’s membrane flow

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13
Q

What is reticular drusen also known as?

A

Pseudo-drusen

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14
Q

What happens to BLinD with age? What happens to bruchs membrane alongside this? What consequence does this have?

A

It thickens
Bruchs membrane takes up cholesterol from the blood - forms plaques
Further restricts clearance and exchange of RPE

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15
Q

Consider what happens to BLinD with age. What happens to the choriocapillaris as a result and what is the consequence of this?

A

It fails to get PEDF/VEGF and atrophies

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16
Q

What promotes an immune response at bruch’s membrane? List two causes of this. Explain how these two result in either wet or dry AMD.

A

Lack of proper cytokine/metabolite exhcange:
Genotype for factor H
-increases inflammation, resulting in wet AMD
Complement suppression
-decreases inflammation, resulting in dry AMD

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17
Q

How do cholesterol plaques affect bruchs membrane’s function?

A

Cholesterol coats BLinD, which reduces BM hydraulic conductivity

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18
Q

What is cholesterol trafficking promoted by and how do genetics of this affect AMD?

A

Promoted by apo-lipoproteins
People with genetic variants in APoE get faster/worse AMD

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19
Q

What does being factor H positive promote?

A

RPE apoptosis

20
Q

List 5 factors for AMD.

A

Age
Smoking
Fellow eye with AMD
RPE disruption (RPE disorders)
Genotype for factor H/ApoE

21
Q

Can diet affect AMD risk? Consider carotenoids, antioxidants and fats (2).

A

Carotenoids and antioxidants confer protection
Saturated fats promote progression
High Omega-3 PUFA confers protection

22
Q

Can high dose antioxidants and/or minerals reduce progression early in AMD or is the eivdence poor?

A

Reduces progression by 25%

23
Q

In what colour eyes is AMD more common? Give a possible reason why.

A

More common in blue eyes
-light damage - oxidation

24
Q

What race and gender is more at risk of AMD? Is gender a risk?

A

Caucasian
Female
-not a risk factor after longevity is considered

25
Q

What proportion of AMD cases are wet and dry?

A

Wet - 15%
Dry - 85%

26
Q

List the four stages of AMD.

A

1 - druplets and drusen
2 - RPE sress, pigment irregularities
Dry - atrophic/non-exudative
Wet - exudative

27
Q

What is RPE stress best visualised by? How does it appear?

A

Fundus autofluorescence (FAF)
-appears as dropout zones

28
Q

Can atrophic areas of the RPE develop anywhere in the macula or only specific areas?

A

Anywhere

29
Q

What is dry AMD characterised by? What kind of vision loss occurs, if any?

A

Apoptosis of the RPE, giving geographic atrophy
Results in slow, very profound vision loss

30
Q

What size of geographic atrophy is clinically significant?

A

> 0.5DD

31
Q

What does the inflammaotry overlay of wet AMD promote (3)? What kind of visiion loss does this result in?

A

Choroidal neovascularisation (CNVM)
Leakage of blood/fluid from
CNVM
Serous RPE detachment

Results in acute profound vision loss

32
Q

What happens to wet AMD over time?

A

Gives a fibrous scar - disciform degeneration

33
Q

What are the four clinical classifications of AMD based on appearance?

A

Drusen size (not number)
Presence of pigmented abnormality
Fellow eye status
Other modifying factors

34
Q

Describe how drusen size is classified and note within what distance to the fovea.

A

Drusen within 2DD of the fovea:
Small - druplet <63 microns
- <1/4 BV
Intermediate - 63 - 125 microns
- <1/2 BV
Large - >125 microns
- size of a vein at the disc

35
Q

How do reticular drusen appear (2)?

A

Dark craters with a central spot

36
Q

Are reticular drusen high or low risk?

A

High risk

37
Q

What image is needed to score AMD? Is it for the eye or for the person?

A

Use colour fundus photography
Score is for the person, not the eye
Score each drusen within 2DD of the fovea

38
Q

List the scoring for AMD (criteria for each) and the maximum score (5).

A

Hyper/hypo/disrupted pigment areas >1/4DD
Large drusen >125 microns
Presence of reticular drusen
Presence of bilateral intermediate drusen
Presence of end-stage AMD in fellow eye (wet or dry)
Each criteria met is 1 score
Max score of 4 for any person (R+L)

39
Q

Descibe how to interpret risk scores for AMD.

A

0 - very low
1 - low
2 - moderate
3 - high
4+ - very high

40
Q

Describe the risk of AMD progression for each risk score.

A

0 - 0.5%
1 - 3%
2 - 12.5%
3 - 25%
4 - 50%
-progression over 5 years, 10 years is similar percentage

41
Q

How should you manage individuals with an AMD risk score of 0 or 1 (2)? Include review schedule.

A

2 year reviews with CFP/OCT
Antioxidants for 1+

42
Q

How should you manage individuals with an AMD risk score of 2 (3)? Include review schedule.

A

1 year reviews with CFP/OCT
Home monitoring
Antioxidants for 1+

43
Q

How should you manage individuals with an AMD risk score of 3 (3)? Include review schedule.

A

6 month reviews with CFP 12/12 and OCT 6/12
Home monitoring
Antioxidants for 1+

44
Q

How should you manage individuals with an AMD risk score of 4 (3)? Include review schedule.

A

3 month reviews with CFP 12/12 and OCT 3/12
Home monitoring
Antioxidants for 1+

45
Q

What are 2 options for home monitoring AMD?

A

Amsler - poor option
Tablet/smart phone

46
Q

At what risk score should antioxidant use be promoted?

A

1+

47
Q

What are patients with iAMD or advanced AMD in one eye recommended to take and why?

A

AREDS supplements to reduce risk of progression to advanced AMD (25% over 5 years)

OD3 (S1&2) (114 decks)

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