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OD3 - Clinical Optometry Practice > DIS - Macular Diseases III: Non-Age Related - Week 2 > Flashcards

DIS - Macular Diseases III: Non-Age Related - Week 2 Flashcards

1
Q

List 7 examples of non-AMD macular diseases.

A 
Central serous chorio-retinopathy
Angioid streaks
Myopic macula degeneration
Drug toxicity
Cystoid macular oedema
Blunt trauma
Phototoxicity
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2
Q

List an example of drug toxicity causing macula disease.

A

Chloroquine/hydroxychloroquine

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3
Q

What is the histopathology od central serous chorioretinopathy (3)?

A

Subretinal fluid with RPE thinning

There may or may not be choroidal thickening

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4
Q

Is the choroid visible when doing OCT on central serous chorioretinopathy?

A

Yes, with enhanced depth imaging

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5
Q

Why does sub-retinal fluid accumulate in central serous chorioretinopathy (3)?

A

Breakdown of the RPE blood retinal barrier and RPE pumps

This promotes fluid accumulaion in the sub-retinal space over the macula

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6
Q

What detachment occurs with central serous chorioretinopathy and why?

A

Accumulation of fluid under photoreceptors
results in retinal elevation at the macula to
form a serous retinal detachment

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7
Q

Why does fluid accumulate only at the macula in central serous chorioretinopathy?

A

Poorly understood why

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8
Q

What kind of vision loss can you expect from central serous chorioretinopathy? Is it sudden or chronic? Is pain involved?

A

Sudden, painless, central vision loss

Typical VA is 6/9 to 6/36

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9
Q

What kind of visual defect would you expect with central serous chorioretinopathy?

A

Relative central/paracentral scotoma

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10
Q

How does central serous chorioretinopathy affect photostress test?

A

Prolonged

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11
Q

What happens to contrast sensitivity with central serous chorioretinopathy?

A

Loss

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12
Q

Is colour vision affected with central serous chorioretinopathy?

A

Loss of colour saturation

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13
Q

What ametropic shift is induced by central serous chorioretinopathy?

A

Hyperopic shift

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14
Q

What test is essential for management and differential diagnosis of central serous chorioretinopathy?

A

OCT

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15
Q

What kind of personalities can be a risk factor for central serous chorioretinopathy? What gender and age?

A

Young, anxious males

Type 3 AAA personalities

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16
Q

Is steroid use a risk factor for or against central serous chorioretinopathy?

A

Risk factor for

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17
Q

How does central serous chorioretinopathy appear on funduscopy? Is it easy to see?

A

Oval/round lesion at the macula - like a swelling or bubble

Hard to see

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18
Q

How wide is the lesion with central serous chorioretinopathy typically?

A

1-4DD

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19
Q

Is the foveal reflex present with central serous chorioretinopathy?

A

No

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20
Q

Is a choroidal neovascular membrane present with central serous chorioretinopathy? How does this affect treatment?

A

It is absent

-aVEGF is limited for central serous chorioretinopathy

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21
Q

List the two types of central serous chorioretinopathy. Give approximate proportion of cases for each.

A

Local serous detachment (25%)

Diffuse retinal pigment epitheliopathy (75%)

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22
Q

What distinct sign can be seen in late phase angiography with serous detachment central serous chorioretinopathy?

A

Smoke stack

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23
Q

How does serous detachment central serous chorioretinopathy appear on fundus autofluorescence?

A

A localised lesion with a prominent bright halo

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24
Q

What choroid thickness would you expect with serous detachment central serous chorioretinopathy on OCT?

A

Normal choroid thickness <300um

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25
Q

What is the prognosis of serous detachment central serous chorioretinopathy?What can happen with recurrence?

A

Usually good but can lead to diffuse retinal pigment epitheliopathy with recurrence

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26
Q

What is the treatment for serous detachment central serous chorioretinopathy (2)?

A

Usually untreated

-if needed for a longstanding case, treat with a spot laser at the leak

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27
Q

How is the location of lesions different in diffuse retinal pigment epitheliopathy compared to serous detachment central serous chorioretinopathy?

A

Diffuse retinal pigment epitheliopathy can involve para-macular locations

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28
Q

Is diffuse retinal pigment epitheliopathy typically short- or long-lived? Does it recur often?

A

Can be short-lived by recurrences often

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29
Q

What two tests are needed for diagnosis?

A

FAF or OCT

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30
Q

What can be seen on FAF with diffuse retinal pigment epitheliopathy?

A

Shows a long tail with RPE dropout

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31
Q

How does diffuse retinal pigment epitheliopathy often appear on OCT?

A

Focal RPE detachment

-pigmentary epithelial detachment

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32
Q

What choroid thickness would you expect on OCT with diffuse retinal pigment epitheliopathy?

A

Thicker than normal >300um

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33
Q

What is the treatment for diffuse retinal pigment epitheliopathy? Is it successful?

A

Spot laser - limited success but needed for local RPE detachment

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34
Q

Would you suspect the fellow eye in unilateral diffuse retinal pigment epitheliopathy?

A

It can be abnormal

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35
Q

What may chronic diffuse retinal pigment epitheliopathy lead to and why?

A

Possible that chronic choroidal thickening in CSCR leads to permanent loss and focal choroidal excavation

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36
Q

List six differential diagnoses for central serous chorioretinopathy.

A 
AMD
Optic pit related serous elevation
Retinal detachment with macular involvement
Pigmentary epithelial detachment
Choroidal tumour/inflammation
Systemic disease
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37
Q

List two examples of systemic diseases that may be a differential diagnosis for central serous chorioretinopathy.

A

Hypertension

Renal failure

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38
Q

Is it common or rare to develop a choroidal neovascular membrane with central serous chorioretinopathy? Is it more or less likely to occur with pigmentary epithelial detachment? What about if laser is used for treatment?

A

Small number develop CNVM (1-3% rare) - more likely with PED or laser

39
Q

Is it more or less likely to develop a choroidal neovascular membrane with central serous chorioretinopathy if there is also focal choroidal excavation?

A

More likely - can predispose

40
Q

Can all of VA, contrast sensitivity, and colour vision be expected to return to normal after recovery from central serous chorioretinopathy?

A

VA may, but CS and CV may not always be normal

41
Q

List three essential components of assessing central serous chorioretinopathy.

A

Dilated fundus exam
Colour fundus photography
Choroidal OCT

42
Q

What four visual parameters should be recorded when assessing central serous chorioretinopathy?

A

VA
Contrast sensitivity
Colour vision
Central VF 10-2/macula pattern

43
Q

When does vision typically improve with central serous chorioretinopathy?

44
Q

When should cases of central serous chorioretinopathy be reviewed? After what period of time should referral be made if persistent and for what?

A

Every 4 weeks

-refer if not resolved after 12 weeks for FAF and OCTa

45
Q

If a referral is made for a persistent central serous chorioretinopathy, what happens (3)?

A

OCTa and FAF
Observed by the ophthalmologist for up to 26 weeks for late recovery
-laser grid in the region of the DRPE

46
Q

If the central serous chorioretinopathy is very diffuse, what should you do (2)?

A

Refer for photodynamic therapy and anti-corticoids

47
Q

What are angioid streaks?

A

Cracks in thickened bruchs membrane

48
Q

What colour do angioid streaks have? What do they look like?

A

Orange/brown colour

-look like dark blood vessels

49
Q

What region of the retina are angioid streaks most obvious? What happens to them as you move towards the periphery?

A

Around the disc

Thins out/disappears towards the periphery

50
Q

What do you expect to see on OCT of angioid streaks?

A

Cracks/openings in bruchs membrane with in-filling of tissue

51
Q

What is the ISe like over angioid streaks?

A

Faded or lost

52
Q

What are the symptoms of angioid streaks (2)?

A

Asymptomatic

-unless CNVM

53
Q

What happens to the risk of CNVM with angioid streaks with age?

54
Q

Can angioid streaks cause haemorrhage or exudation?

55
Q

Why is OCT essential for angioid streaks?

A

To detect subretinal fluid - CNVM

56
Q

What is the management for angioid streaks (2)? What about if CNVM is present?

A

Conservative reviews
Refer for aVEGF if CNVM is present
Safety glasses for sport as the retina is fragile

57
Q

What kind of disordrrs are angioid streaks sometimes associated with?

A

Systemic collagen disorders

  • pseudoxanthoma elasticum
  • pagets disease
  • sickle cell disease
  • ehlers-danlos syndrom
58
Q

What are most ases of angioid streaks due to?

A

Idiopathic

59
Q

What is there a very high risk of with angioid streaks (2) and from what?

A

High risk of choroidal rupture and/or retinal haemorrhage from milk blunt trauma

60
Q

List three manifestations of myopic macular degeneration.

A

Diffuse thinning
Lacquer cracks
CNVM

61
Q

Why may CNVM appear with myopic macular degeneration (3)?

A

Stretched bruchs membrane may result in weaknesses that crack and produce lacquer cracks
Allows ingrowth of CNVM

62
Q

What is fuchs spot?

A

Haemorrhage and pigment proliferation with ingrowth of CNVM at the macula

63
Q

What percentage of high myopes have myopic macular degeneration?

64
Q

What ocular component does the drug quinine have affinity for?

A

Melanin in the RPE

65
Q

What poses less risk, plaquenil or quinine?

66
Q

What is the mechanism behind drug toxicity with quinine?

67
Q

What is a sign of quinine maculopathy, how does it appear, and what is it best seen with?

A

Parafoveal granularity of the RPE
-gives central zone of hyperpigmentation with a hypo-ring
-bullseye appearance
Best seen with FAF

68
Q

In what three ways does quinine maculopathy affect vision? Which is affected late?

A

Loss of sensitivity
Abnormal colour vision
VA loss
-affected late

69
Q

Is body fat a risk factor for or against quinine maculopathy?

A

Risk factor for

70
Q

Is age a risk factor for quinine maculopathy?

71
Q

What six things (including tests) should patients have done before taking quinine for monitoring maculopathy?

A 
VA (including contrast)
DFE with photos and OCT
Colour vision
Central VF 10-2
Home self-monitoring
72
Q

What is the followup schedule (3) for monitoring quinine maculopathy (patients just starting the drug)?

A

5 years
2 years
-then yearly for high risk patients according to dose, age, body fat

73
Q

What should you do if macular changes are evident when monitoring patients for quinine maculopathy?

A

Refer to their medical practitioner

74
Q

What is cystoid macular oedema and in what retinal layers (2)?

A

Leakage from retinal capillaries causing oedema and formation of cysts in the OPL/INL around the fovea

75
Q

What three conditions is cystoid macular oedema often secondary to?

A

Diabetes
BRVO
Inflammation (uveitis)

76
Q

What macular thickness do you expect on OCT of cystoid macular oedema?

A

> 350 central foveal thickness

77
Q

List and describe the two possible mechanisms f cystoid macular oedema.

A

Active
-inflammatory damage to capillary endothelial cells causing leakage
Passive
-increased venous back-pressure causing an inflammatory overlay

78
Q

What two cytokines are involved in the passive mechanism of cystoid macular oedema?

A

Increase in IL-6 and TNFalpha

79
Q

What appearance does cystoic macular oedema have on fluorescein angiography and in what phase?

A

Cysts in a radiating pattern like a flower petal

-late phase

80
Q

List 10 causes/associations of cystoid macular oedema.

A 
Diabetes
Retinal vein occlusions
Anterior uveitis
Adrenaline usage
Retinitis pigmentosa
Any intraocular surgery
-cataract, vitrectomy, scleral buckling, keratoplasty
Epiretinal membranes
Malignant choroidal melanoma
Retinal detachment
Idiopathic
81
Q

What kind of VA loss would you expect from cystoic macular oedema?

A

Mild

-6/12 to 6/19

82
Q

Does cystoid macular oedema affect contrast sensitivity?

83
Q

Is VA loss with cystoid macular oedema chronic or acute? Is VA recovered as the oedema is absorbed?

A

Chronic

VA recovered as oedema absorbed

84
Q

What can chronic cystoid macular oedema result in? Can this be reversed? What has benefit and is it small or large?

A

Permanent neuronal damage

  • no or incomplete recovery of vision
  • aVEGF medication has small benefit, NSAIDs
85
Q

List four possible sequelae of cystoid macular oedema and why they can occur if applicable.

A 
None
Lamellar retinal hole
-rupture of a cyst
Epiretinal membrane
-cellophane rinopathy
Outer retinal and RPE atrophy
-permanent visual loss in persistent leak
86
Q

What should be done as a baseline for cystoid macular oedema (4)?

A

Slit-lamp
DFE
CFP
OCT

87
Q

What is the treatment for cystoid macular oedema if central foveal thickness is >350um (4)?

A 
NSAIDs
Intravitreal steroid
aVEGF
Scatter or grid photocoagulation around the macula
-diabetes/RVO
88
Q

If blunt trauma has occurred, when should you refer for ophthalmological examination (3)?

A

If you see:

  • vitreous haemorrhage
  • commotio retinae
  • choroidal split/rupture
89
Q

What is commotio retinae (4)? What can it lead to?

A 
Glial swelling
Retinal thickening
Loss of foveal pit
nRD - appears white
-can lead to traumatic macular hole
90
Q

What does excessive exposure to light cause at the retina?

A

Excessive oxidative damage

91
Q

What does blue light tend to do to the retina?

A

Cause formation of free radicals

92
Q

What does infra-red light tend to do to the retina? How does it appear?

A

Gives heating/burning of retinal tissue

-large atrophic zone with pigmented lesion

93
Q

List three possible causes of phototoxicity.

A

Solar retinopathy
Long exposure to operating microscopes
Lasers

94
Q

What is the treatment for phototoxicity?

A

None available

OD3 - Clinical Optometry Practice (114 decks)

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