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OD3 (S1&2) > LV - Low Vision Conditions - Week 9 > Flashcards

LV - Low Vision Conditions - Week 9 Flashcards

1
Q

Can pigment change without drusen be considered AMD? Is there a significant risk of progression to late AMD?

A

No
-no significant risk of progression

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2
Q

Define the following classifications of AMD
Normal ageing changes
Early AMD
Intermediate AMD
Late AMD

A

Normal ageing changes - only druplets and no AMD pigmentary changes
Early AMD - medium drusen and no AMD pigmentary abnormalities
Intermediate AMD - large drusen and/or any AMD pigmentary abnormalities
Late AMD - neovascular AMD and/or geographic atrophy
-within 2DD of the fovea in either eye

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3
Q

What kind of advice can be given to all AMD patients (2)?

A

Stop smoking if they do so
Self-monitor with amsler

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4
Q

What is the treatment for atrophic AMD?

A

None available

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5
Q

What is the treatment for neovascular AMD (3)? Note the costs and whether or not they are TGA approved for AMD.

A

Anti-angiogenesis therapies
-lucentis (ranibizzumab) - more expensive
-avastin (not TGA approved for AMD) - less expensive
Eyelea (aflibercept) - same cost as lucentis but better half-life

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6
Q

Describe the effectiveness of lucentis for AMD treatment. Compare it to avastin and eyelea.

A

After 24 months of monthly lucentis injections, visual acuity stabilises or improves in 90% of patients
-reduces retinal thickness
-promotes resoprtion of fluid
Studies have found similar effectiveness with avastin
Eyelea injected every 2 months was found to be similar to avastin and lucentis as well

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7
Q

What do studies suggest of the effectiveness of vitamin and mineral supplements? For which severities of AMD are of particular note?

A

AREDS supplements were found to reduce the risk of moderate visual loss among some patients with AMD

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8
Q

List the components of AREDS supplements (5). Compare it to AREDSII.

A

Beta-carotene
Vitamin C
Vitamin E
Zinc oxide
Cupric oxide
AREDSII removed beta-carotene, zince lowered
Role of lutein, zeaxanthin, and long chain polyunsaturated fatty acids

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9
Q

List some foods rich in lutein and xeaxanthin antioxidants.

A

Spinach
Silver beet
Corn
Capsicum
Peas
pumpkin
Brussels sprouts
Broccoli

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10
Q

List some fish rich in omega-3.

A

Salmon
Mackerel
Anchovies
Trout

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11
Q

List some foods rich in vitamin E.

A

Nuts
Whole grains

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12
Q

List some foods rich in zinc.

A

Oysters
Seafood
Nuts
Legumes

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13
Q

List some foods rich in selenium.

A

Nuts, especially brazil nuts

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14
Q

What is the incidence of fellow eye involvement during the first two years of AMD? What about five years after that?

A

28-36%
6-12% for the five years after

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15
Q

Is useful peripheral vision maintained indefinitely with AMD?

A

Yes, never will go black blind

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16
Q

What level of visual acuity loss can be expected with exudative and non-exudative AMD and what effect does antiVEGF treatment have?

A

Non-exudative - to about 6/120
Exudative - can be worse than 6/120
AntiVEGF can hold vision at the level it was when treatment started

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17
Q

What kind VF defects do you expect to see in those with AMD (2)?

A

Central or paracentral scotoma with normal periphery

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18
Q

What would symptom would you expect of AMD patients related to near work?

A

Difficulty reading

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19
Q

What would symptom would you expect of AMD patients related to distance work (3)?

A

Loss of detail in distance
Difficulty recognising faces
Television difficulties

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20
Q

What is colour vision like with AMD?

A

Decreased

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21
Q

Do AMD patients tend to struggle with mobility?

A

Generally no, mobility is fair even in advanced cases

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22
Q

What visual hallucination is common with AMD and what is generally required for this to occur? Note percentage of cases among AMD patients.

A

Charles bonnet syndrome
-requires low bilateral visual acuity
-10 to 25% of patients with macular degeneration report it

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23
Q

How do individuals with AMD tend to view things and why?

A

Eccentrically view because of the central scotoma
-some people automatically develop this technique, others do not, while some dont adopt the best eccentric viewing position

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24
Q

List distance low vision management options for AMD patients. List 3 for glare.

A

Distance
-magnification
-telescopes
-decreased viewing distance (closer, larger screen)
Glare
-UV shields
-tinted lenses
-hat with brim

25
Q

What is the management for charles bonnet syndrome?

A

Advice and reassurance

26
Q

Can eccentric viewing be trained? Explain.

A

Yes, but benefits are controversial
Good for enhancing awareness of scotoma

27
Q

What often precedes progression to late AMD and what form?

A

Spontaneous drusen regression
-geographic atrophy

28
Q

Briefly describe retinitis pigmentosa.

A

Rod-cone dystrophies that represent an inherited group of disorders characterised by progressive visual field loss and night blindness

29
Q

What mode of inheritence do majority of retinitis pigmentosa forms have?

A

Autosomal recessive

30
Q

What occurs in retinitis pigmentosa?

A

Progressive atrophy of rods and cones

31
Q

Which modes of inheritence of retinitis pigmentosa have the worst prognosis (2)?

A

X-linked and autosomal recessive

32
Q

What causes the bony spicule appearance in retinitis pigmentosa?

A

Migration of pigment into neural retina

33
Q

How do arterioles appear in retinitis pigmentosa? What about the ONH?

A

Attenuated
ONH has waxy pallor

34
Q

What can be expected of dark adaptation on first presentation in patients with retinitis pigmentosa?

A

They present with defective dark adaptation

35
Q

What are the first posterior signs of retinitis pigmentosa you expect to see (3)?

A

Arteriolar narrowing
Fine dust-like intra-retinal pigmentation
Loss of pigment from RPE

36
Q

What are mid-stage posterior signs of retinitis pigmentosa you expect to see (1) and where first?

A

More pigmentary changes
with a perivascular bone-spicule configuration seen initially in the midperiphery

37
Q

What eventually occurs with retinitis pigmentosa?

A

Pigment spreads both posteriorly and anteriorly

38
Q

Describe what happens to visual fields as retinitis pigmentosa progresses.

A

Contraction of the visual field ultimately leaving a tiny island of central vision

39
Q

When does the optic nerve begin to take on a waxt pallor with retinitis pigmentosa? Is VA typically good? Explain.

A

When visual fields are significantly affected, is around the time the optic nerve head looks waxy
VA is generally good until this later stage

40
Q

What typically occurs after visual fields are significantly contracted with retinitis pigmentosa? Why does this occur and what can be said of the arterioles and ONH appearance?

A

Unmasking of larger choroidal blood vessels give the fundus a tessellated appearance
Severe aerteriolar attenuation
Marked optic disc pallor

41
Q

List 6 associated ocular findings that may be present alongside retinitis pigmentosa.

A

Maculopathy
-atrophic or cystoid macular oedema
Cataract
-posterior subcapsular
Myopia
Optic disc drusen
Open agle glaucoma
Keratoconus

42
Q

What do you expect to see on electroretinogram of retinitis pigmentosa? What about early stages?

A

Abnormal, even early stages

43
Q

What is dark adaptation like in retinitis pigmentosa? What happens to the threshold and what can be said of the rod-cone break?

A

Delayed
Elevation of dark adaptation threshold
Absence of rod-cone break

44
Q

Describe the range of vision that individuals with retinitis pigmentosa may have.

A

6/6 to NLP

45
Q

Describe what vision is usually like with retinitis pigmentosa (prognosis).

A

Typically good until late stages
-unless associated conditions like cataract or maculopathy

46
Q

What kind of decline do you expect to see on visual fields of retinitis pigmentosa? Where does decline begin and which region is more often abnormal?

A

Exponential
-approx 5% per year
Begins in the mid-periphery
Often superior visual field abnormal

47
Q

Is visual field loss symmetrical between the eyes in retinitis pigmentosa?

A

Yes

48
Q

List two common syndromes associated with retinitis pigmentosa. Note what each is characterised by.

A

Ushers syndrome
-characterised by congenital profound deafness
Laurence-moon-biedl syndrome
-characterised by RP, intellectual impairment, polydactyly, obesity, hypogenitalism

49
Q

What is the treatment for retinitis pigmentosa?

A

None at present
-future treatments are likely to come from genetic therapy or retinal transplants

50
Q

Describe the prognosis for retinitis pigmentosa for each of the following modes of inheritence
X-linked
Autosomal recessive
Autosomal dominant

A

X-linked - blindness may occur by fifth decade
Autosomal recessive - blindness may occur by sixth or seventh decade
Autosomal dominant - blindness may occur by eighth decade

51
Q

Do patients with retinitis pigmentosa often have difficulty with mobility symptoms?

A

Yes, particularly at night

52
Q

Do patients with retinitis pigmentosa often struggle with glare?

A

Yes

53
Q

Does retinitis pigmentosa affect colour vision?

A

Yes, in the late stages it decreases

54
Q

What effect does having peripheral constrictions have on the benefits of magnification as a low vision aid for patients with retinitis pigmentosa?

A

Limits the benefit, better to use hand magnifier away from the eye where the field area is larger

55
Q

What can be done to aid mobility in individuals with retinitis pigmentosa (5)?

A

Reverse telescopes or concave lenses for scanning
Scanning strategies
Guide dogs
Canes
Wide angle torches for low light levels

56
Q

Does cataract affect colour vision?

A

Yes, faded

57
Q

Give some examples of low vision aids for individuals with cataracts (3).

A

Magnification
Telescopes and magnifiers
Focal illumination for near tasks

58
Q

List four conditions in children that may contribute to them having low vision. What is one thing to keep in mind with children and low vision?

A

Albinism
Retinopathy of prematurity
Stargardts
Congenital nystagmus
Children have accommodation - allows even children with 6/120 vision to manage with little magnification assistance

OD3 (S1&2) (114 decks)

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