Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

OD3 Sem 2 - Clin. Optometry > 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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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]

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How do large soft drusen appear in FAF?

A

hyper-fluorescence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Does FAF generally detect early CNVM? What about CFP?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How does A2E/lipofuscin interact with the RPE?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How is drusen formed?

A

When druplets coalesce

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is reticular drusen also known as?

A

Sub-retinal Drusenoid Deposits (SDD)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

List 9 risk factors for AMD

A 
RPE disruption
Age
Smoking
Fellow Eye
Genotype
Diet
Blue eyes
Caucasian?
Female?
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Name 2 dietary nutrients/compounds that affect risk of AMD

A

Carotenoids - protection

Saturated fat - promotes progression

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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 Sem 2 - Clin. Optometry (3 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions