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OD3 S2 > D: Macular Disease 1 - Week 1 > Flashcards

D: Macular Disease 1 - Week 1 Flashcards

1
Q

What 2 main processes are involved in AMD development?

A

RPE changes
Bruchs membrane/choriocapillaris changes

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2
Q

Explain how lipofuscin accumulates in RPE cells

A

Pr OS phagocytosis by RPE cells (for the visual cycle) results in O2 free-radical formation, which damages RPE cells over time. These damaged components of the RPE cells cannot be degraded (e.g. by RPE autophagy) and are called “lipofuscin”

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3
Q

How does lipofuscin formation in RPE cells differ from formation in most other cells in the body?

A

RPE: forms as a result of Pr OS phagocytosis
Other cells: form as a result of own internal autophagy

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4
Q

How can we visualise RPE lipofuscin? What is the major lipofuscin component contributing to this?

A

Lipofuscin is the major source of FAF (Fundus Auto-Fluorescence). This fluorescence mainly comes from A2E.

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5
Q

What does Hyper- and Hypo- fluorescence in FAF imaging represent?

A

Hyperfluorescence = Excess lipofuscin
Hypofluorescence = RPE cells are dead (no lipofuscin) = Geographic atrophy (well demarcated region of loss)

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6
Q

How do small and intermediate drusen appear in FAF?

A

Small drusen - may remain undetected.
Intermediate drusen - central hypo- fluorescence with annulus of hyper-fluorescence [likely b/c of central RPE atrophy surrounded by abnormal RPE]

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7
Q

How do large soft drusen appear in FAF?

A

hyper-fluorescence

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8
Q

Does FAF generally detect early CNVM? What about CFP?

A

For both: No, not early. Later on yes.

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9
Q

How does A2E/lipofuscin interact with the RPE?

A

Interferes with RPE cell function, leading to apoptosis and subsequent GA (geographic atrophy)

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10
Q

What does the accumulation of lipofuscin ultimately result in?

A

Lipofuscin vesicles which coalesce to give BlamD (basal laminar deposits) which are shed by the RPE to form BLinD (Basal linear deposits) or sub-retinal drusenoid deposits (Druplets)

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11
Q

How is drusen formed?

A

When druplets coalesce

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12
Q

What are the two types of drusen and which one is more serious?

A

Reticular drusen (located above RPE) - more serious
(classic) drusen (located below RPE).

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13
Q

What is reticular drusen also known as?

A

Sub-retinal Drusenoid Deposits (SDD)

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14
Q

What happens to the bruchs membrane with age? (2) How does this affect bm interaction with the RPE?

A

Gets thicker and more complex
Takes up more cholesterol (develops chol. plaques)

Results in reduced exchange of RPE cells with the choriocapillaris. Which reduces VEGF exchange.

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15
Q

What is factor H (CFH)?

A

CFH = Complement Factor H. It is the major soluble inhibitor of complement, preventing complement activation and thus reducing positive feedback/inflammation

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16
Q

How does the presence of factor H affect the process of AMD development? (2)

A

Factor H +ve: promotes RPE apoptosis and leads to Dry AMD
Factor H -ve: increased inflammation from complement and leads to Wet AMD.

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17
Q

List 9 risk factors for AMD

A

RPE disruption
Age
Smoking
Fellow Eye
Genotype
Diet
Blue eyes
Caucasian?
Female?

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18
Q

What genotypes are risk factors for AMD?

A

Increased incidence of AMD in patients with a family history
CFH mutation (Y402H + other variants)
Apo-E variants

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19
Q

Name 2 dietary nutrients/compounds that affect risk of AMD

A

Carotenoids - protection
Saturated fat - promotes progression

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20
Q

What are the clinical stages of AMD? What percentage of AMD cases are dry/wet?

A
  1. Druplets and drusen
  2. RPE stress: pigment irregularities (hyper/hypo-fluorescent)
    3a. Dry atrophic (85% of cases)
    3b. Wet exudative (15% of cases)
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21
Q

What does the inflammatory overlay in wet AMD promote? (3) What is the end histopathological result expected over time?

A

CNVM
Leakage of blood/fluid from CNVM
Serous RPE detachment

Over time results in a fibrovascular scar ‘disciform degeneration’ (RHS)

22
Q

With what 4 criteria can we classify AMD based on appearance?

A

Drusen size (large or small)
Presence of pigment abnormality (hypo/hyper/disrupted)
Fellow eye status
Other modifying factors

23
Q

From what distance within the fovea are drusen judged as for AMD?

A

2 disc diopters

24
Q

What are the sizes of small (druplet), intermediate, and large drusen?

A

Small - <63 microns (<1/4 BV)
Intermediate - 63-125 microns (1/2 BV)
Large - > 125 microns (size of vein @ disc)

25
Q

What stage of AMD are the following deposits classified as?
Druplets
Intermediate Drusen
Large Drusen
Reticular Drusen

A

Druplets - normal ageing
Intermediate - early AMD
Large - intermediate AMD

Reticular - high risk modifying factor

26
Q

How do you score with AREDS?

A
  1. Take CFP (colour fundus photo)
  2. Score drusen and pigment within 2DD of foveola (vascular arcades) as:
    - hyper/hypo or disrupted (>1/4DD) = +1
    - Large drusen > 125 microns = +1

Modifiers incl.
- Reticular drusen = +1
- Bilateral intermediate drusen = +1
- End stage AMD in fellow eye (wet or dry) = +1

Max score = 4 for any person

27
Q

How do you manage an AMD patient with AREDS = 0-1? [low risk] (2)

A

2 yearly reviews: CFP/OCT
Anti-oxidant (AO) for AREDS = 1

28
Q

How do you manage an AMD patient with AREDS = 2 [medium risk] (2)

A

1 yearly reviews: CFP/OCT
Home monitor + Anti-oxidant (AO)

29
Q

How do you manage an AMD patient with AREDS = 3 [high risk] (2)

A

6 monthly reviews: CFP 1 yr, OCT 6 mth
Home monitor + Anti-oxidant (AO)

30
Q

How do you manage an AMD patient with AREDS = 4 [very high risk] (2)

A

3 montly reviews: CFP 1 yr, OCT 3 mth
Home monitor + Anti-oxidant (AO)

31
Q

For how long in the progression of AMD should you monitor (with OCT and function) until referring?

A

Until ‘nascent’/newly developing GA or ‘pre-wet’ AMD. Refer when functional loss or OCT change established.

32
Q

How can a patient monitor AMD weekly at home? (2)

A

Amsler
Tablet or smart phone

33
Q

When do anti-oxidants stop being protective against AMD? Do we still use them?

A

Not protective once score >2. We still use them though.

34
Q

List 6 components of an AMD workup (6)

A

Visual function: VA - LC/HC/LLLC; VF-mac
DFE: look for foveal/mac swelling, CNVM
CFP: colour fundus photo
OCT: to identify cases for referral

FAF-SLO
OCTA for CNVM

NB: LLLC = Low luminance low contrast

35
Q

On what OCT results do we refer AMD cases? (2)

A

Foveal thickness > 300 microns
Central retinal thickness > 350 microns

36
Q

List the 5 OCT signs of CNVM

A

ISe disruption (indicates advanced disease)
Sub-retinal fluid (dark bands)
Cystic formation within inner retinal layers (dark bubbles)
PED (clear internal cf drusen)
Increase in foveal thickness >100 microns b/w eyes (or >350 microns)

37
Q

List the order of development of nascant GA in OCT in 6 steps. How long does this take?

A

Stages 1-5 develop over 12-15 months.

ISe disruption
Drusen regression (12th month)
Subsidence of OPL and INL
Hypo-reflective wedge (15th/18th month)
Increased signal below BM
Complete loss of OS/RPE

38
Q

What is the normal loss in acuity for a LLLC chart compared to HC (i.e. in healthy patient)?

A

2-3 lines

39
Q

List 4 tests that provide a functional assessment of unilateral vision loss in macula disease

A

Visual acuity (pH, LL, LC, SF filter)
RAPD (retina 1+; ON > 2+)
Colour vision
Amsler grid

40
Q

Why is the amsler grid not useful in 50% of macula disease patients?

A

Due to cortical filling

41
Q

Other than assessing unilateral vision loss, how else can we functionally assess macula disease? (25)

A

Mac perimetry (HFA 10-2)
Ipad/iphone + home monitor
Dark adaptation (photostress)
Maddox rod (watzke sign: better than amsler)
mfERG (implicit time delayed with retinal disease)

42
Q

Why do we use 10-2 instead of FDT 24-2 for assessing the macula?

A

10-2 has the points/spots closer together. Better accuracy.

43
Q

What interventions can we use for AMD patients (medium + risk, score >1)? (2)

A

Diet (anti-oxidants)
nanosecond laser

44
Q

According to AREDS 2, how does anti-oxidant intake affect AMD? (2)

A

reduces risk for developing wet AMD by 26%
reduces risk for disease progression by 18%

45
Q

When do we use nanosecond laser on AMD patient? What does it do?

A

when score >/= 3.
Gives drusen regression, but progression of AMD to dry? especially if reticula drusen (so it stops wet but not dry)

46
Q

What 2 interventions are/were used for advanced AMD?

A

Photodynamic therapy (PDT. Not used anymore)
aVEGF - intravitreal injections (e.g. avastin, lucentis, eyelea) = best option to retain current vision.

47
Q

Are there any interventions for advanced dry AMD?

A

NO. Low vision aids.

48
Q

What is RAP?

A

Retinal angiomatous proliferation. Is when the neovascularisation occurs in the inner retina instead of it’s typical location under the RPE

49
Q

In what percentage of AMD CNVM does it occur as RAP?

A

20%

50
Q

Does RAP show cystic formation early with OCT?

A

yes.

51
Q

What size of geographic atrophy is clinically significant?

A

> 0.50DD

OD3 S2 (3 decks)

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