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My Own Deck > Macula > Flashcards

Macula Flashcards

1
Q

What makes up the macula?

A

Fovea 1.5mm
Foveola 0.35mm
FAZ
Umbo

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2
Q

Which is the thinnest part of the macula?

A

Foveola

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3
Q

Where is the macula located?

A

B/w superior and inferior temporap arcades

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4
Q

Where is the reflex observed in the macula?

A

Umbo

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5
Q

Which aspect is important for high resolution in the macula?

A

Fovea

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6
Q

Which part of the macula holds no blood vessels?

A

FAZ

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7
Q

What part of the macula help reduce the degradation of the image?

A

Foveola, the laterally displaced RGC

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8
Q

How do we assess the macula function?

A
  1. VAs
  2. Amsler chart
  3. Retinal imaging and fundoscopy
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9
Q

What test would indicate that the reason behind reduced vision is pathologological and not a refractive error?

A

Pinhole test

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10
Q

How is an amsler chart used?

A

Monocular and at 30cm
Wearing the correct reading add for dist
Not use varis
Ask- “look at the central fixation dot and if there is any distortion or scotoma

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11
Q

Whats the best way to view subtle changes of the macula?

A

OCT

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12
Q

What is the most common cause of irreversible visual impairment in the UK?

A

ARMD

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13
Q

What is the prevalence of AMD?

A

AMD prevalence increases with age

30% of > 75 yrs effected by AMD
4.8% >65 yrs diagnosed with Advanced AMD
Rises by 12.2% >80 yrs

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14
Q

What are the risks factors?

A
  1. Age
  2. Ethnicity— Caucasian
  3. Genetics— 1st degree 3x risk
  4. Gender— Females
  5. Smoking— 2x
  6. Obesity
  7. Systemic HT
  8. High fat diet
  9. CVD history
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15
Q

What 2 types of disease processes are there in AMD?

A

Geographic atrophy

Wet

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16
Q

How prevalent of all AMD is geographic atrophy compared to wet?

A

Geographic 90%

Wet 10%

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17
Q

Where is the earliest change of AMD?

A

Level of Bruchs membrane

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18
Q

What is the role of Bruce’s membrane?

A

Regulating transportation of toxic metabolic waste from retina to choroidal blood vessels.

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19
Q

What happens to Bruchs membrane with age?

A

BM thickens
Reduces permeability
Inhibits toxin removal
Waste products i.e. lipofusin accumulate

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20
Q

What are the sxs of Dry AMD in each stage?

A

Early- Asymptomatic
Progression- Gradual deterioration in Central vision
Advanced- Difficulty with fine detail resolution
Severe cases- Aware of central scotoma

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21
Q

What are the sxs of wet AMD?

A 
Painless
Sudden onset 
Blurred 
Distorted Central vision (metamorphosis)
Unilateral
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22
Q

What are the signs of AMD?

A

Drusen (hard, soft and calcified)

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23
Q

If Unilateral, how likely is a px to develop wet in the fellow eye?

A

37% will develop in a year

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24
Q

What is the 1st visible sign of AMD?

A

Drusen

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25
Q

What is drusen and how do they effect vision?

A

Waste products made up of lipids and collagen. They disrupt the orientation and organisation of RPE resulting in depigmentation and hyperpigmentation.

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26
Q

At which age are drusen common in?

A

50 yrs +

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27
Q

When does drusen indicative of AMD?

A

Size and number

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28
Q

What are the black arrows indicating

A

Soft drusen

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29
Q

What is this image showing

A

Calcified drusen

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30
Q

When is hard drusen a low risk of visual impairment?

A

When its without other signs

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31
Q

At what stage of AMD is geographic atrophy present?

A

End stage

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32
Q

What happens to the retinal tissue when there is geographic atrophy?

A

Reduce thickness and exposes underlying blood vessels of choroid and choriocappilaries

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33
Q

What is the hallmark or wet AMD?

A

Choroidal neovascularisation

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34
Q

What 2 things are the arrows pointing too and can they be referred as?

A

Top arrow hyperpigmentation
Bottom arrow hypopigmentation

Referred as ‘pigment clumping’

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35
Q

Whats the prevelance for dry to become wet in AMD?

A

10-15%

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36
Q

What are risk factors for CNV and why?

A

Degeneration of RPE
Confluent soft and geographic
These are angiogenic stimulus which is ischaemia

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37
Q

Where does new blood vessel arise from?

A

Endothelial cells from choroidal capillaries

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38
Q

What is the subretinal neovas membrane referring to?

A

A fibrovascular membrane supporting the structure of the new blood vessel

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39
Q

What are the signs of subtle fibrobascular membrane?

A

Grey, green, yellow colour
Difficult to identify
Obscured by RPE, BM, SRL
May not have leakage

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40
Q

If there is no haemm but a fibrovascular membrane is spotted, what action is taken?

A

Urgent referral whether its suspected or confirmed. Haemm is inevitable

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41
Q

What is being shown here and when is it seen?

A

Disciform scar, seen on the end stages of wet AMD

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42
Q

What other signs could be seen with a desciform scar?

A

Retinal and subret haemm haemm and oedema. This gives the surface and irregular and elevated during ophthalmoscopy

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43
Q

In cases of dry AMD, when is referral not needed?

A

When the px is Asymptomatic…

…although counselling is needed about the implications to potential vision loss. 12/12 recall

44
Q

When is referral needed for dry AMD pxs?

A
  1. Unsure of retinal signs despite dilation
  2. Symptomatic dry AMD
  3. Dry related vision loss
45
Q

What key aspects of dry AMD would the px need counseling of?

A
  1. No licensed tx
  2. Slow progression
  3. Continue to deteriorate vision
  4. No impact in early stages
  5. Possibly develop wet
  6. Make aware of wet sxs: sudden reduction in VA
  7. Self monitor- Amsler chart
  8. Compare vision
  9. Information on modifiable risk factors
46
Q

What 2 pigments are present in the macula that aids in protecting against free radicals?

A

Lutein and zeaxanthin

47
Q

Where can Lutein and zeaxanthin be found?

A

In leafy greens I.e. spinach and kale

The body cannot produce these

48
Q

Why does the retina have a high amount of free radicals?

A

Its due to it high metabolic activity

49
Q

Aside from Lutein and zeaxanthin, what other antioxidants can help protect the macula?

A

Vitamin c
Vitamin e
Cartenoids

50
Q

What actions are taken for those with advanced dry AMD?

A

Refer to the GP

Theyay benefit from LVAs

51
Q

What merits an Urgent referral in AMD?

A

Exudative/ wet AMD…

…especially if sudden onset reduced vision. Even if signs are not clear

52
Q

Where are wet AMD pxs sent and how?

A

Macula clinic via Fast track

53
Q

Once wet pxs are referred, how long till they are seen by ophthalmologists?

A

2/52

54
Q

If a fast track is unavailable locally what other options are there?

A

On call at local HES Same day

OR Refer A+E

55
Q

What is the primary tx for wet AMD?

A

Intravitreal injections (Antivegf tx)

56
Q

Which type of VEGF is responsible for mediating the process of new blood vessels?

A

VEGF A

57
Q

What are the common anti VEGF treatments called?

A

Ranizumab- Lucentis
Aflibercept- Elyea
Bevacizumab- Avastin

58
Q

What are the non- AMD forms?

A 
Cystoid macula oedema 
Central serous retinopathy 
Epiretinal membrane 
Macula hole
Myopic degeneration 
Hereditary macula dystrophy
59
Q

Where is CMO usually located?

A

Sensory retinal layers AKA intraretinal layers

60
Q

Where is the fluid from CMO originate from?

A

Intravascular peri foveal ret capillaries which are dilated

61
Q

What is the sign of early stages CMO?

A

Reduced/Abolished reflex

62
Q

What is the common cause of CMO?

A

Cataracts expansion AKA Irvine-Gass syndrome

63
Q

What are the less common cause of CMO?

A

Intraocular inflammation (post uveitis >ant uveitis)
Diabetic retinopathy
C/BRVO

64
Q

What are the sxs of advanced CMO?

A

Sudden
Painless
Blurred V
Distorted Central vision

65
Q

How is CMO treated?

A

Resolve usually without any treatment, may need to treat underlying condition

66
Q

Wht ate the pharmaceutical options for treatment of CMO?

A
  1. CAI- increase fluid outflow into choroid
  2. Corticosteroids- reduce inflammation
  3. Laser photocoagulation- stimulate repair of BRB
67
Q

What are the optometric management?

A

Depends on the cause:
Cataract- refer routinely
Vascular- Call HES for advice
Uveitis suspicion- Emergency referral same day

68
Q

Which other condition shares the same symptoms as CMO?

A

CSR Central serous retinopathy

69
Q

Where does the fluid originate from in CSR?

A

Fluid from choroid, break down of Outer BRB

70
Q

What is CSR prevelance?

A

Males
Age 20-50 yrs
Unilateral
30% recurrent

71
Q

How would CSR be managed?

A

If sxs- discuss with local HES

Treatment unlikely as resolves spontaneously

72
Q

How is epiretinal membrane formed?

A

Disruption from tractional forces in PVD causing ILM cells to proliferate and form epirtinal membrane

73
Q

What are other causes of epiretinal membrane?

A

Most ERMs idiopathic

Retinovascular/intraocular inflamm

74
Q

What can bunched up or concertinaed ERMs lead to?

A

Macula hole

75
Q

What surgery would be appropriate for a ERM?

A

Virectomy and membrane peel

76
Q

What is visible sign of ERM?

A

Reflective shimmer around the macula

77
Q

Wha is cellophane maculopathy?

A

Early stage sign in ERM that doesn’t effect VA

78
Q

How is ERM differentiated from macula pathology?

A

Slow progressing 12/12 to develop

79
Q

If VA is effected in ERM, What action is taken?

A

Routine referral via GP

…if not effected than a a normal routine recall of 12/12

80
Q

What causes a macula hole?

A

Vitreo ret traction which warps the fovea retinal structures. As adhesions are strong here this can cause retinal breaks

81
Q

Where is the break in retina limited to?

A

Sensory layers, RPE is still intact

82
Q

Which test would be used to determine the effected break?

A

Wazke-allen test- 0.5 disc diam width beam centered on the macula
A break in the beam would suggest the shape of the break

83
Q

Who are more prone to macula holes?

A

Females

Myopes

84
Q

What are the early stages of a macula hole?

A

Small diam lesion
Little to see
Visible sign- reduced/absent fovea depression + red/yellow spot ring a fovea
Mild reduced VA, Blurred Vision and distortion
Sudden onset, unilateral , painless

85
Q

When is a macula hole unlikely to resolve spontaneously?

A

Intermediate/ end stages

If left untx may leave a permanent Central vision loss

86
Q

What is dependent on the successful of the tx?

A

The time elapsed since inset

87
Q

Why isnt there a treatment need for a macula hole compared to an RRD?

A

Slower progressing that RRD

88
Q

What is the referral route for the different stages of the macula hole?

A

Ealry/interm- referral via GP (1/12)
End- routine referred

Cannot rule out diff dx- refer suspected macula hole via fast track AMD

89
Q

How likely is it to effect the following eye?

A

By 15%

90
Q

Wha is the ophthalmological management?

A

Relieving VRT via virectomy

91
Q

What is the alternative to virectomy and what does it do?

A

Intravitreous injection of ocriplasmim- helps dissolve proteins in adhesions

92
Q

Why is myopic degeneration considered a non AMD form?

A

Retina and choroid are thinned which makes them susceptible to atrophy.

93
Q

Wha are the signs of myopic degeneration?

A
  1. PPA
  2. Chorioretinal atrophy around ONH
  3. Thinned retina
  4. Optoc disc tilt
  5. Possibly breaks on BM
  6. Excessive axial elongation
  7. Washed out red/yellow colour
  8. Hyperpigmentation
  9. Exposed choroidal blood vessels
  10. Possible similarities to end stage dry AMD
94
Q

What are the sxs of myopic degeneration?

A

No sxs!
Gradual atrophy- resultant loss of LR function
Similar to dry AMD-
Gradual, painless, bilateral, asymmetric

95
Q

What are the rare symptoms of myopic degeneration?

A 
CNV
Sudden
Unilateral
Blurred 
Distorted
96
Q

When is myopic degeneration considered for referral?

A

Suspicion/sign CNV development

VA drop…. refe routinely via GP

97
Q

What are the hereditary macula dystrophies?

A

Stargardts disease-
Pattern dystrophy
Cone dystrophy

98
Q

What are the typical sign of cone dystrophy?

A

Late stage- bulls eye and symmetrical in BE

99
Q

What is indicative of a progressing cone dystrophy?

A

Onset adulthood

Reduced VA and colour vision

100
Q

Which disease falls under a vitelliform dystrophy and what are the typical signs?

A

Best disease
Signs- egg yolk lesion at macula
Lipofuscin build up at macula

101
Q

How would hereditary macula dystrophy be managed?

A

Caution!
Reduced VA- Refer via GP
No tx

102
Q

How can hereditary macula dystrophys be confirmed?

A

ERG and LVA assessment needed

103
Q

What is this called and what is it a result of?

A

Petaloid

This is fluid like cysts accumulated resulting in laterally displaced ganglion cell layer

104
Q

What 2 aspects are being shown here?

A

Top arrow PED

Bottom arrow Serous detachment

105
Q

What is causing the distortion of the retinal layers?

A

ERM

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