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MSc IOVS > Age-Related Macular Degeneration (AMD) Lectures > Flashcards

Age-Related Macular Degeneration (AMD) Lectures Flashcards

1
Q

What is the main cause of severe visual loss worldwide? How many people are affected globally?

A

AMD, 20-25 million (8 million severe), 2nd to cataract in visual loss

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2
Q

Which studies looked at AMD prevalence globally?

A

Beaver Dam, Blue Mountain, Rotterdam

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3
Q

What symptoms are seen in AMD?

A

Blurred distorted vision, wavy lines/odd shapes, central vision loss

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4
Q

How is AMD diagnosed?

A

VA testing, Amsler grid test, fundoscopy, FFA

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5
Q

What are the characteristic clinical findings seen in AMD?

A 
Drusen
Retinal pigment epithelium (RPE) changes
Visual loss (later stages)
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6
Q

What are the two main types of AMD?

A

Dry (Geographic Atrophy)

Wet (Neovascular)

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7
Q

What fundoscopy signs are visible in geographic atrophy?

A

Pale hypopigmented macula

Choroidal vessels visible (RPE loss)

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8
Q

What types of geographic atrophy are there?

A

Normal: Small drusen, normal pigment
At-risk: Reticular drusen, RPE pigment change, thick BM, CC loss
Atrophic: RPE/photoreceptors death, inflamed CC, Muller cells, astrocytes

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9
Q

What is the pathogenesis of neovascular AMD?

A

Angiogenesis due to VEGF buildup forms weak, leaky retinal vessels which damage the retina and form scar tissue

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10
Q

What else does VEGF cause besides angiogenesis?

A

Capillary leakage
Macrophage and granulocyte chemotaxis
VEGF receptor 1 binds to PIGF, VEGF-B, VEGF-A

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11
Q

Which type of late AMD is most common?

A

Dry (90% of cases)

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12
Q

Which type of late AMD is treatable? What is the treatment?

A

Wet (neovascular AMD): Anti-VEGF agents

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13
Q

What conditions are included under the umbrella term “Neovascular AMD”?

A

Choroidal Neovascularisation (CNV)
Pigment Epithelial Detachment (PED)
Retinal Angiomatous Proliferation (RAP)
Polypoidal Choroidal Vasculopathy (PCV)

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14
Q

Which imaging modality highlights vessel leakage in neovascular AMD?

A

Infrared angiography

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15
Q

What layers of the retina are affected by early AMD?

A

Retinal pigment epithelium (RPE)
Bruch’s membrane: extracellular matrix
Choriocapillaris: fenestrating capillaries

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16
Q

What are the risk factors for developing AMD?

A 
Age (biggest)
Genetics (1st degree relative with AMD triples risk)
Smoking (doubles risk)
Ethnicity (Caucasians higher risk)
Obesity, high fat diet
Hypertension
High sunlight exposure
Other: Aspirin use, cataract surgery
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17
Q

What is a single nucleotide polymorphism (SNP)?

A

Genome variations present in more than 1% of the population

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18
Q

What is a haplotype?

A

Polymorphism sets that tend to be inherited together

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19
Q

What is a diplotype?

A

2 haplotypes on alleles of homologous chromosomes

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20
Q

What are the 3 main gene variants linked to AMD development?

A

Y402H variant of CFH gene (Chromosome 1)

HTRA1, ARMS2 genes (Chromosome 10)

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21
Q

Which gene variant on chromosome 1 is linked to an increased risk of developing dry AMD?

A

Y402H variant of CFH gene (4x risk)

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22
Q

Which gene variants on chromosome 10 are linked to an increased risk of developing wet AMD?

A

HTRA1, ARMS2 genes (8x risk)

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23
Q

Which research paper identified 34 genetic loci associated with increased AMD risk?

A

Fritsche et al. 2016 (Nature Genetics)

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24
Q

What factors influence AMD staging?

A

Drusen presence and size
Presence of retinal pigmentary abnormalities
Presence of geographic atrophy or neovascularisation

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25
Q

How are drusen formed?

A

Incomplete photoreceptor breakdown leading to extracellular debris (lipofuscin) buildup in Bruch’s membrane, detaches RPE from choroid which causes oxidative stress and drusen formation

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26
Q

Where are drusen found?

A

Between the RPE and Bruch’s membrane

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27
Q

Which drusen are not associated with AMD?

A

Small ‘hard’ drusen (<63μm), linked to normal ageing

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28
Q

Which drusen are associated with early AMD?

A

Medium drusen (63-125μm)

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29
Q

Which drusen are associated with intermediate AMD?

A

Large ‘soft’ drusen (>125μm)

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30
Q

What imaging techniques are used to detect drusen?

A 
Fluorescein angiography (FA): Drusen appears hyperfluorescent
Optical Coherence Tomography (OCT)
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31
Q

What is the complement cascade?

A

A component of the innate immune system which destroys pathogens and clears away immune complexes

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32
Q

What are the 3 main pathways of the complement cascade?

A

Classical
Lectin
Alternative

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33
Q

What is the ultimate goal of these 3 pathways?

A

Forming C3 convertase to cleave C3 into C3b

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34
Q

How do the Classical and Lectin pathways produce C3 convertase?

A

C4b cleaves C2 into C2a + C2b

C4b and C2b combine, forming Classical/MBL pathway C3 convertase

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35
Q

How does the Classical pathway form C4b?

A

C1q activated by binding to IgG + IgM
C1q activates C1r which activates C1s
C1s cleaves C4 into C4a and C4b

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36
Q

How does the Lectin pathway form C4b?

A

Mannose-binding Lectin (MBL) binds to carbohydrates on microbial surfaces
MASP2 is activated and cleaves C4 into C4a and C4b

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37
Q

What is the difference between the Alternative complement pathway and the other 2 pathways?

A

Alternative pathway is always active, not dependent on microbes being present

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38
Q

How does the Alternative pathway form C3 convertase?

A

C3 is hydrolysed into C3(H2O)
Factor B cleaves C3(H2O) into C3(H2O)B
Factor D cleaves Factor B, forming C3(H2O)Bb
C3 converts to C3b, forming C3 convertase: C3bBb

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39
Q

How is the Alternative pathway regulated?

A

It is regulated through a cascade loop:
C3 convertase + C3b form C5 convertase
C5 convertase binds to C5 to form C5a + C5b
C5b recruits C6 and C7 to form C5b67
C5b67 inserts C8 into membrane, C9 makes pores in it
A membrane attack complex (MAC) has formed

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40
Q

Which protein also regulates the Alternative pathway besides the cascade loop?

A

Complement Factor H (bloodborne)

Inactivates C3b via Complement Factor I

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41
Q

Where else does the mechanism of AMD occur in the body?

A

Kidneys (type 2 glomerulonephritis)

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42
Q

What substance recruits Complement Factor H from the blood into Bruch’s membrane?

A

Heparan sulphate

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43
Q

Which polymorphism prevents Complement Factor H binding onto Bruch’s membrane?

A

Y402H

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44
Q

Which protein can pass through the blood-retinal barrier (BRB) in place of Complement Factor H?

A

Factor H-like protein 1 (FHL-1), potential future AMD therapy

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45
Q

What medium is used to create OCT images?

A

Near infrared light

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46
Q

How is the OCT image produced?

A

Reference and sampling beams reflect off tissue into the detector
Echo time delay and light intensity is measured after the beams are combined by an interferometer

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47
Q

What parameters are observed in OCT imaging?

A 
Axial resolution
Transverse resolution
Measurement time
Detection sensitivity
Image penetration depth by tissue
Image contrast
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48
Q

What is the most superficial retinal layer?

A

Internal limiting membrane

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49
Q

What is the deepest retinal layer?

A

Choroid sclera junction (Choroidal stroma)

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50
Q

Which retinal layers are found between the internal and external limiting membranes? (Superficial to deep)

A 
Retinal nerve fibre layer
Ganglion cell layer
Inner plexiform layer
Inner nuclear layer
Outer plexiform layer
Henle fibre layer
Outer nuclear layer
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51
Q

Which retinal layers are found between the external limiting membrane and the choroid sclera junction? (Superficial to deep)

A 
Photoreceptors
Retinal Pigment Epithelium (RPE)
Bruch's membrane
Choriocapillaris
Inner choroid layer (Sattler’s)
Outer choroid layer (Haller’s)
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52
Q

Which photoreceptor inner segment layer contains mitochondria?

A

Ellipsoid

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53
Q

Which photoreceptor inner segment layer contains ribosomes (protein synthesis organelles)?

A

Myoid

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54
Q

Which imaging type highlights the posterior border of the choroid layers

A

Enhanced depth imaging (EDI)

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55
Q

What are the key steps in OCT analysis?

A

Identifying normal, abnormal and artefacts in the image
Observing all line scans
Qualitative retinal image (good/bad?)
Quantitative measures (retinal thickness/volume)

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56
Q

What OCT signs are seen in early phase AMD?

A

Hyperfluorescence between the RPE and Bruce’s membrane surrounded by a margin of hypofluorescence

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57
Q

What OCT signs are seen in occult phase AMD?

A

Irregular RPE elevation

Stippled fluorescence with diffuse leakage visible

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58
Q

Who first identified retinal angiomatous proliferation (RAP) as a form of neovascular AMD?

A

Yannuzzi

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59
Q

What are the 3 main types of retinal angiomatous proliferation (RAP)?

A

RPE
Choroidal
Intraretinal

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60
Q

What are the 3 stages of retinal angiomatous proliferation?

A 
Intraretinal neovascularisation (IRN)
Subretinal neovascularisation (SRN)
Choroidal neovascularisation (CRN)
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61
Q

What form of neovascular AMD involves orange-reddish choroidal lesions invading the subretinal space?

A

Idiopathic polypoidal choroidal vasculopathy (IPCV)

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62
Q

What are the features of polyps in IPCV?

A

Orange-reddish
Nodular
Hypofluorescent halo
Branching vascular network

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63
Q

Besides polyps what other features are seen in IPCV?

A

RPE and retinal detachment
Haemorrhages (invading vitreous)
Exudates

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64
Q

Besides OCT what imaging modality is used to detect IPCV?

A

Indocyanine green angiography (ICGA)

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65
Q

Which 3 or more OCT findings are diagnostic for IPCV?

A

Multiple RPE detachments
Sharp RPED notch/peak
Hypofluorescent lumen (polyps)
Hyperfluorescent intraretinal exudates

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66
Q

Which neovascular AMD signs may be left untreated depending on severity?

A 
Pigment epithelial detachment (PED)
Intraretinal fluid (IR) up to 200μm
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67
Q

Which cause of subretinal fluid has a worse prognosis: neovascularisation or vitreous degeneration?

A

Vitreous degeneration due to retinal detachment

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68
Q

What lesions are a result of inflammation due to microglial cell activation?

A

Subretinal hyperreflective exudative (SHE) lesions

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69
Q

What signs indicate a retinal pseudocyst?

A

Thinner overlying retina
Squared off lesion
Surrounding atrophy

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70
Q

What signs indicate retinal tubulation?

A 
Retinal rosettes (photoreceptor degeneration)
Atrophic change (late stage)
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71
Q

How are OCT-A images produced?

A

Laser light reflected off moving red blood cells in retinal vessels creating multiples images which are then combined

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72
Q

What types of OCT-A artefact are there?

A

Vessel thickness (overestimated)
Projection
Thresholding
Fringe washout (microsaccade)

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73
Q

What vasculopathy is identified better by OCT-A than FA?

A

DR microaneurysms

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74
Q

What are some OCT-A segmentation errors?

A

Superficial vessels interfering with deep vessel images
Vessel leakage not visible
Image size smaller than that of FA

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75
Q

OCT-A is good at identifying what retinal vascular features?

A

Chorioretinal anastamoses
Small areas of PED
CNV
CSR

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76
Q

What is the pathogenesis of fibrosis in neovascular AMD?

A

Inflammatory mediator release following CNV

Fibroblast aggregation

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77
Q

What are the consequences of fibrosis in neovascular AMD?

A

Photoreceptor, RPE and choroidal vessel destruction

Visual acuity drop (especially if external limiting membrane intact)

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78
Q

What are the main challenges in neovascular AMD fibrosis management?

A

Existing therapy resistance
Quantifying subretinal fibrosis
Identifying types of fibrosis
Timing of therapy

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79
Q

How does AMD impact peoples’ daily lives?

A 
Difficulty in driving, reading and recognising faces
Increased falling and injury risk
Greater need for supportive care
Lower quality of life
Exacerbation of existing co-morbidities
Increased risk of depression
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80
Q

What is the estimated cost of AMD detection and treatment for 2010-2020?

A

£16.4 billion

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81
Q

What is the percentage risk of an AMD patient developing AMD in the contralateral eye over 2 years?

A

28.9%

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82
Q

What forms of diet supplementation could aid AMD treatment?

A

High dietary carotenoid and omega-3 levels

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83
Q

What is the name of the main diet-related AMD study?

A

AREDS (Bird et al)

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84
Q

What AMD categories are highlighted by the AREDS1 study?

A

1: No AMD, >20/32 VA in both eyes
2: Many small/1+ intermediate drusen or pigment changes in 1/both eyes, >20/32 VA in both eyes
3: Many intermediate/1+ large drusen, GA outside fovea
4: Advanced AMD in 1 eye

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85
Q

Which dietary supplements were included in the AREDS1 study?

A

Vitamin C, E
Beta-carotene
Zinc
Copper

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86
Q

What were the results of the AREDS1 study?

A

Antioxidants and zinc reduced AMD risk by 25% in AMD category 3/4 participants

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87
Q

What cautions were associated with the AREDS1 study?

A

Beta-carotene: Lung cancer risk (smokers)
Zinc: Alzheimer’s, genitourinary hospital admission risk
Vitamin E: Heart failure risk (HOPE study)

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88
Q

Which additional dietary supplements were added to AREDS1 for AREDS2?

A

Lutein
Zeaxanthin
Omega-3 (DHA and EPA)

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89
Q

What were the results of the AREDS2 study?

A

Lutein/zeaxanthin: 26% more AMD risk reduction
Zinc: Higher doses higher benefit
Omega-3: No effect on AMD risk

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90
Q

What dietary recommendations followed the AREDS studies?

A

Dark green leafy vegetables
“Colour on the plate”
Eggs, fish

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91
Q

What factors affect the simplified AREDS risk score?

A

Drusen >125μm in 1 eye
Drusen 63-125μm in both eyes
Pigment changes

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92
Q

What are the two most common forms of CNV in neovascular AMD?

A

Occult (>85%)

Classic (12%)

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93
Q

What are the symptoms of neovascular AMD?

A

Blurred, distorted vision
Decreased central vision
Increased glare sensitivity
Reduced night vision

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94
Q

Which type of CNV responds to anti-VEGF and photodynamic therapy?

A

IPCV

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95
Q

Which type of CNV responds well to therapy but can be aggressive?

A

Classic

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96
Q

Which type of CNV responds to therapy but requires many injections?

A

RAP

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97
Q

Which type of CNV progresses slowly?

A

Occult

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98
Q

What are the main types of RPE detachment?

A

Drusenoid
Serous
Haemorrhagic
Fibrovascular (Occult)

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99
Q

Which retinal layer is affected by drusenoid PED?

A

Outer nuclear layer

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100
Q

What OCT findings indicate serous PED?

A

Optically empty, smooth-domed elevation

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101
Q

What OCT findings indicate vascularised PED?

A

Irregular hyperreflective elevation

Serous PED may also be present

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102
Q

Which types of RPE detachment are treated with anti-VEGF?

A

Fibrovascular

Haemorrhagic (with PDT)

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103
Q

What studies introduced PDT and what were the conditions for treatment?

A

2001 TAP study, 2003 NICE study

Classic CNV, >6/60 VA

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104
Q

What is the name of the drug used in PDT?

A

Verteporfin

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105
Q

Which study introduced anti-VEGF and what was the drug name?

A

2008 NICE study

Ranibizumab (Lucentis)

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106
Q

How is anti-VEGF better than PDT in treating AMD?

A

PDT only slows deterioration

Anti-VEGF stabilises/improves vision

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107
Q

Which cells proliferate to form new vessels due to VEGF-A?

A

Endothelial cells

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108
Q

Who first discovered angiogenic growth factors?

A

Judah Folkman (1970’s)

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109
Q

When was VEGF then its isomers (e.g. VEGF-A) identified?

A

VEGF (and VPF): 1980’s

VEGF-A and other isomers: 1990’s

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110
Q

Who pioneered intravitreal anti-VEGF injections?

A

Rosenfeld

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111
Q

Where is VEGF found in the eye and what is its normal function?

A

RPE

Embryonic, skeletal and reproductive angiogenesis

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112
Q

What factors stimulate VEGF accumulation?

A

Growth factors, hormones, cytokines

Hypoxia

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113
Q

What are the pathological effects of VEGF?

A

Endothelial cell proliferation
Inappropriate angiogenesis
Vascular leakage and oedema

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114
Q

What is the role of placental growth factor (PlGF)?

A

Enhances angiogenesis

Binds to VEGF-R1 so VEGF-A binds to VEGF-R2

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115
Q

Which VEGF receptor has the greatest effect in neovascular AMD?

A

VEGF-R2 (binds VEGF-A, C, D)

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116
Q

What are the 3 main anti-VEGF drugs?

A

Lucentis (Ranibizumab)
Avastin (Bevacizumab)
Eylea (Aflibercept)

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117
Q

Which studies provided evidence for Lucentis (Ranibizumab) use?

A

ANCHOR (Monthly vs PDT)
MARINA (Monthly vs sham)
PIER (3-monthly vs sham)
PrONTO/SUSTAIN (PRN)

118
Q

What indicated “stable” vision according to the ANCHOR and MARINA studies?

A

Losing <15 letters from baseline

119
Q

What were the results of the MARINA study?

A

20.3-21.4 letters gained over sham after 2 years

120
Q

What were the results of the PIER study?

A

19.1-2 letters improvement over sham after 2 years

121
Q

What was the extended PIER study called?

A

HORIZON

122
Q

What were the results of the ANCHOR study?

A

17.9-20.5 letters gained over PDT after 2 years
VFQ-25: 15-point mean difference
15-42.1% >6/12 VA after 2 years

123
Q

What were the results of the EXCITE study?

A
  1. 3 letters improvement from monthly Lucentis (1 year)

- 105μm retinal thickness (1 year)

124
Q

What was the patient criteria for the PrONTO/SUSTAIN studies?

A

> 5 letters vision loss + fluid

>100μm central retinal thickness

125
Q

Which study investigated 3-monthly vs monthly Lucentis use?

A

EXCITE

126
Q

Which studies involved 3 loading doses followed by monthly review?

A

PrONTO
SUSTAIN
Mont-BLANC

127
Q

What was the retreatment criteria in the PrONTO study?

A

New Classic CNV/haemorrhage

Persistent fluid following last injection (2nd year: any more fluid)

128
Q

Why was the SUSTAIN study less successful than the PrONTO study?

A

Too rigid retreatment criteria
Too many Occult CNV cases (40%)
0.3mg rather than 0.5mg dose

129
Q

Which treatment interval yielded the best results? Which studies did these involve?

A

Monthly: 8 letters gained

ANCHOR, MARINA, EXCITE

130
Q

Which treatment interval yielded the worst results? Which studies did these involve?

A

3-monthly: 2.2 letters gained

PIER, EXCITE, SAILOR

131
Q

What were the results of the HARBOR study?

A

10.1 and 8.2 letters gained for Lucentis monthly and PRN respectively after 12 months

132
Q

Which studies were combined to outline long term PRN Lucentis use?

A

PIER, HORIZON, SEVEN-UP

133
Q

What are the 3 types of treatment responses seen in the Lucentis studies?

A

Gained/maintained
Gained/not maintained
No gain

134
Q

Which dosing approaches are examples of individualised dosing?

A

PRN

Treat and Extend

135
Q

What is the Treat and Extend approach?

A

Treat at all visits
Inactive disease: longer treatment intervals and vice versa
Individualising patient care

136
Q

What is the maximum interval between treatments in the Treat and Extend approach?

A

12 weeks

137
Q

What are the potential benefits of the Treat and Extend approach?

A

Greater capacity through longer review intervals

Large vision drops unlikely

138
Q

What are the potential drawbacks of the Treat and Extend approach?

A

Inactive disease being treated
Costs
Injection risks

139
Q

Which studies have provided evidence for the Treat and Extend approach?

A

Prospective: LUCAS, Toalster, Abedi
Retrospective: Gupta, Oubraham, Engelbert
Ongoing: TREND, T-REX, RANGE

140
Q

What was the LUCAS T&E study retreatment criteria?

A

Fluid on OCT
Haemorrhage or dye leakage
Increased lesion size on FA

141
Q

What was the aim of the Fight Retinal Blindness (FRB) project?

A

Verifying that wet AMD treatment evidence in clinical trials applied in real world settings (Australia/New Zealand)

142
Q

Which study examined the Treat and Extend approach over 2 years?

A

Arnold et al.

143
Q

What drug treats wet AMD as well as colorectal cancer?

A

Bevacizumab (Avastin)

144
Q

Which study compared Lucentis vs Avastin monthly/PRN over 2 years?

A

CATT

145
Q

What are the benefits of using Avastin instead of Lucentis for wet AMD treatment?

A

Higher rate of SAE
Longer half-life (20 days)
Cheaper

146
Q

What are the drawbacks of using Avastin instead of Lucentis for wet AMD treatment?

A

Not licensed

No standard dose: Contamination risks (inflammation, raised IOP)

147
Q

What is the first fully human intravitreal fusion protein?

A

Eylea (Aflibercept)

148
Q

Which are the main studies providing evidence for Eylea (Aflibercept) use?

A

VIEW1/2

149
Q

When did NICE permit the use of Eylea (Aflibercept) in treating wet AMD?

A

July 2013

150
Q

Which study evaluated Eylea (Aflibercept) use in treating wet AMD over 7 years?

A

Gillies et al.

151
Q

What are the risks associated with intravitreal injections?

A 
Endophthalmitis
Retinal detachment
Lens damage
Atrophy
Stroke
MI
152
Q

Which ethnic group is more prone to developing PCV in wet AMD?

A

East Asians

153
Q

What combination therapy is ideal in treating PCV in wet AMD?

A

Anti-VEGF agents and PDT

154
Q

Which study provided evidence for combination therapy in treating PCV in wet AMD?

A

EVEREST

155
Q

What potential X-ray based treatment may be used in treating wet AMD?

A

Stereotactic radiotherapy (Oraya IRay)

156
Q

Which study provided evidence for stereotactic radiotherapy use in treating wet AMD?

A

INTREPID

157
Q

What were the results of the INTREPID study in treating wet AMD?

A

33% less injections needed after 1 year

Treatment response not dependent on dosage

158
Q

According to the Royal College of Ophthalmologists guidelines, where in a hospital can doctors carry out intravitreal injections?

A

Theatre

Dedicated outpatient rooms

159
Q

What are the minimum requirements to perform an intravitreal injection?

A

Surgical scrub

Sterile mask and gloves

160
Q

What topical anaesthesia can be given before administering intravitreal injections?

A

Oxybuprocaine

Tetracaine

161
Q

What substance is used for disinfection before administering intravitreal injections?

A

5-10% povidone iodine

162
Q

Which scleral injection site is ideal for intravitreal injections and what angle should the needle be inserted at?

A

3.5-4.0mm from the limbus

Perpendicular to the sclera

163
Q

What is the maximum appropriate volume for an intravitreal injection

A

0.1ml

164
Q

Which method should be used for wide-bore injections?

A

Stepped entry

165
Q

What is the preparation policy for bilateral intravitreal injections?

A

Each eye prepared separately

Different set of instruments per eye

166
Q

What are discharged patients no longer prescribed following intravitreal injections?

A

1-2 topical antibacterial drops after injection then QDS for 3+ days

167
Q

Why are patients no longer given topical antibacterial drops after intravitreal injections?

A

Increased microbial resistance (63.6%)

168
Q

What are the contraindications for intravitreal injections?

A

Conjunctivitis
Severe blepharitis
Allergies

169
Q

What are the complications associated with an intravitreal injection volume of >0.05ml

A

Raised IOP risk
Glaucoma
Sudden no perception of light (NPL)

170
Q

What are the complications associated with ocular injections?

A 
Endophthalmitis (very rare, 0.048% risk)
Intraocular inflammation/haemorrhage
Trauma, retinal detachment
Raised IOP
Hypotony
171
Q

What is the human visible spectrum?

A

400-700nm (555nm peak)

172
Q

How does the crystalline lens optical density change with age? Which light does it absorb more with age?

A

Rises with age, more blue light is absorbed

173
Q

What is macular pigment? Where is it found? What is it made up of?

A

Yellow oily substance
Central 6 degrees of retina in fibres of Henle
Lutein and zeaxanthin

174
Q

What does macular pigment do?

A

Absorbs harmful blue light toxic to retina

Antioxidant, anti-inflammatory (protective in AMD)

175
Q

What factors affect macular pigment levels?

A

AMD, diet, smoking, obesity, high BP, iris colour (more if darker)

176
Q

What naturally occurring carotenoid has more lutein than zeaxanthin?

A

Xanthophyl

177
Q

How can macular pigment levels be increased?

A

Consuming green leafy vegetables

Lutein/zeaxanthin supplementation

178
Q

Which method is used to measure macular pigment levels?

A

Heterochromatic flicker photometry

179
Q

How does heterochromatic flicker photometry work in macular pigment testing?

A

2 superimposed lights (blue 450nm, green 540nm) set with 15Hz flicker, subjects identify point of minimum flicker in central and peripheral fixation

180
Q

How is the luminence ration calculated in macular pigment testing?

A

Blue light luminence divided by green light luminence

181
Q

What is the critical flicker fusion frequency in macular pigment testing?

A

Flicker too quick for the human eye to detect

182
Q

Which formula is used in the age-estimate technique for macular pigment testing?

A

Periphery luminence ratio = 4 + age x 0.02

183
Q

Which study produced the equations used in macular pigment calculations?

A

Van der Veen et al. (2009)

184
Q

Which study investigated the effect of lutein supplementation on macular pigment and VA? What were the results?

A

CLEAR study
68% increase in MP
VA increase over 1 year

185
Q

Which type of photoreceptor is lost first in early AMD?

A

Rods

186
Q

What do RPE cells surrounding photoreceptors do?

A

Facilitate daily renewal, dispose of outer segment discs across Bruch’s membrane into choroid

187
Q

How does Bruch’s membrane influence photoreceptors?

A

It regenerates rhodopsin which make up rods

188
Q

What is dark adaptation?

A

The process by which eyes become more sensitive to light in reduced illumination

189
Q

In which conditions is dark adaptation abnormal?

A

AMD, vitamin A deficiency, diabetes, alcoholism, Crohn’s, Stargardt disease

190
Q

How is dark adaptation measured?

A

Target presented at central 8 degrees of vision after bright flash of light dazzles eyes, takes longer for older eyes to adjust

191
Q

Which study compared dark adaptation between normal and AMD-affected eyes?

A

RapidDA study

192
Q

What are the aims of AMD imaging?

A

Monitor disease progression and response to treatment

193
Q

What does fundus fluorescein angiography highlight?

A

Vascular leakage

194
Q

What are the stages of fundus fluorescein angiography?

A

Red-free, choroidal (8-10s): Backgrounnd flush, patchy/lobe,

Arterial (10-12s), capillary (10-13s), venous (12-14s): early, mid, late

195
Q

What does indocyanine green angiography highlight? What is contraindicated?

A

Delineates vasculature beyond RPE

Iodine, shellfish

196
Q

What are the phases of indocyanine green angiography?

A

Early-mid (5-10 mins): Choroid vessels

Late (10-30 mins): Choriocapillaris

197
Q

What does optical coherence tomography highlight?

A

Retinal structures, CNV activity (thickening/fibrosis)

198
Q

What wide-field imaging device is commonly used? What is the field of view?

A

Optos

200 degrees

199
Q

Which region of the retina yields the highest VEGF production? According to which paper?

A

Mid-periphery

Shimizu

200
Q

Which were the first wide-field imaging devices introduced?

A

Pomerantzeff (1984)
Panoret (2000’s)
Staurenghi lens
Optos, RetCam (contact), Spectralis (non-contact)

201
Q

What is autofluorescence?

A

Spontaneous light emission from cells following exposure to different wavelenghts of light

202
Q

What can be seen using autofluorescence?

A

Vessel anatomy, leaks, RPE function, cortical vitreous/retina/choroid

203
Q

What types of autofluorescence are there?

A

Near infrared, fundus and cSLO

204
Q

Which ocular structures are secondary fluorophores?

A

Sclera, hyaluronic acid, inner retina flavins, choroid, macular pigments

205
Q

What pathologies can increase AF levels?

A

Photoreceptor outer segment change, RPE loss

206
Q

What pathologies can reduced AF levels?

A

Photoreceptor death, RPE atrophy (GA)

207
Q

Which study assessed near-infrarer cSLO imaging to examine RPE and choroidal melanin? What were the limitations?

A

Delori et al.

Focused on posterior pole, not useful centrally

208
Q

Which 8 FAF patters identified by the FAM study group evaluated advanced AMD progression?

A

1: Normal
2: Minimal change
3: Focal increase
4: Patchy
5: Linear
6: Lace-like
7: Reticular
8: Speckled

209
Q

How does autofluorescence differentiate drusen types?

A

Mildly raised AF suggests AMD drusen, hyper-AF suggests other drusen

210
Q

Which study examined GA progression in relation to abnormal AF levels?

A

Holt et al. (2007)

211
Q

What can AF highlight peripherally?

A

Photoreceptor loss, serpiginous choroiditis, DR PRP

212
Q

What retina feature are seen in retinitis pigmentosa?

A

Bone spicules, narrow vessels, optic nerve pallor, CMO

213
Q

What did the OTELLO study examine?

A

Peripheral AMD changes via Optomap FAF images: better visualisation

214
Q

What were the results of the Bird et al (2001) OCT study?

A

OCT as sensitive as FA for oedema (acetazolamide response)

215
Q

What types of OCT have there been from 1997 to 2011?

A

Time domain, spectral domain then swept source

216
Q

What are the benefits of swept source OCT imaging?

A

Twice as fast as spectral domain, uniform sensitivity, more visibility, less light scatter

217
Q

What does OCT measure in terms of the choroid? How does this change with AMD?

A

Choroidal thickness

Gets thinner with AMD

218
Q

What features can be identified using Topcon En-Face?

A

Epiretinal membranes, DMO

219
Q

How do classic CNV lesions appear?

A

Subfoveal, all between RPE and Bruch’s membrane (FFA)

220
Q

How do occult CNV lesions appear?

A

Stippled lacy membrane, irregular dye leak (FFA)

221
Q

How does fibrovascular PED appear on OCT?

A

Blister, RPE rip: Hyperreflective, hyporeflection due to blockage

222
Q

What can Fourier domain OCT highlight?

A

Sub/intraretinal fibrosis

223
Q

How does polypoidal choroidopathy (IPCV) appear on indocyanine green angiography?

A

PED, exudates, subhyaloid blood, choroid polyps, RD

224
Q

How do retinal angiomatous proliferation (RAP) lesions appear on OCT, FFA and ICG?

A

OCT: Superficial haemorrage, IR fluid, PED, CMO
FFA: Early IR leak, occult
ICG: Visible mid-late, anterior to RPE

225
Q

How does geographic atrophy appear on AF?

A

RPE atrophy, high edge? Progression risk

226
Q

What lesions can be seen with OCT and FFA +/- ICG?

A

CNV, IPCV, RAP lesions

227
Q

What lesions can be seen with OCT and AF?

A

Drusen, GA

228
Q

What was the resolution of the first OCT image? How deep did it penetrate tissue?

A

17μm, 1.5mm

229
Q

What is the order of colours from low to high reflectivity on OCT?

A

Black, blue, green, yellow, red, white

230
Q

Which retinal layers are found from the internal to the external limiting membrane?

A 
Nerve fibre layer
Ganglion cell layer
Inner plexiform layer
Inner nuclear layer
Outer plexiform layer
Fibres of Henle layer
Outer nuclear layer
231
Q

Which retinal layers are found below the external limiting membrane?

A 
Ellipsoid zone
Retinal pigment epithelium
Bruch's membrane
Choriocapillaris
Choroid (Sattler's, Haller's layers)
232
Q

What are the main components of photoreceptors?

A

Synaptic body, nuclear segment, fibre, myoid zone, ellipsoid zone, outer segment

233
Q

What does Stratus OCT highlight? Which is the deepest layer it can image?

A

Sub-retinal fluid

Stops at RPE

234
Q

What does Cirrus/Topcon OCT highlight? Which is the deepest layer it can image?

A

Sub-retinal fluid, CNV

Stops at RPE

235
Q

What does Spectralis OCT highlight? Which is the deepest layer it can image?

A

Sub-retinal fluid, CNV, PED

Stops at Bruch’s membrane

236
Q

Changes in which retinal layer most closely suggest wet AMD?

A

Retinal pigment epithelium

237
Q

What RPE changes may occur?

A

Thickening, thinning, detachment

238
Q

What types of RPE detachment are there?

A

Drusenoid
Serous (fluid)
Haemorrhagic
Fibrovascular (occult)

239
Q

How does drusenoid PED appear on OCT?

A

RPE elevation, outer nuclear alteration

240
Q

How does serous PED appear on OCT?

A

Optically empty RPE elevation, smooth-domed +/- CNV

241
Q

How does fibrovascular PED appear on OCT?

A

Irregular RPE elevation, hyper-reflective +/- serous

242
Q

How does haemorrhagic PED appear on OCT?

A

1+ dome-like RPE elevations, hyperreflective top

243
Q

How is drusenoid PED treated?

A

Dry AMD advice

244
Q

What CNV type is being treated in fibrovascular PED? How?

A

Occult membranes, CNV

Anti-VEGF

245
Q

What CNV type is being treated in haemorrhagic PED? How?

A

IPCV

Anti-VEGF, PDT

246
Q

What changes can occur in the neurosensory retina?

A

Fluid, thickening

Intra-retinal cysts

247
Q

What disease causes fluid build-up in the ellipsoid layer?

A

Adult vitelliform dystrophy (juvenile: Best’s disease)

248
Q

How can lipofuscin deposits produce false positives?

A

Optically empty, mask choroid, mistaken for fluid

249
Q

What is schisis?

A

Mechanical stretching of the retina due to myopia

250
Q

What is central serous retinopathy?

A

Idiopathic sub-retinal fluid between ellipsoid and RPE layers

251
Q

Which structures surround photoreceptors in a wall-like appearance?

A

Outer retinal tubulations

252
Q

What are the aim of AMD retreatment?

A

Ideally curing CNV effects, mitigating damage caused by it, stabilising vision

253
Q

In AMD retreatment which two strategies are used?

A

PRN

Treat and extend

254
Q

What questions are asked before AMD retreatment?

A

Is the disease due to CNV active? Worse, stable or improving? Is the diagnosis correct?

255
Q

When would AMD treatment be continued (PRN) or interval kept the same (T&E)?

A

Persistent lesion activity

No contraindications

256
Q

When would AMD treatment stop (PRN) or the interval extend (T&E)?

A

Inactive disease

Adverse events

257
Q

In AMD retreatment, how is the disease defined as inactive?

A

No reappearance of CNV indicators post-treatment (OCT), no deterioration in VA, no leak on FFA (if done)

258
Q

What adverse events can occur with AMD treatment?

A

Uveitis, RD, endophthalmitis, periocular infection, thrombo-emboli

259
Q

What should be considered before discontinuing AMD treatment?

A

Drug hypersensitivity
<15 letters BCVA in 2 visits, >30 letters drop
Lesion shape worse despite treatment

260
Q

What should be considered before discharging AMD patients?

A

Treatment discontinuation, no other issues, low reactivation risk (poor central vision, scar)

261
Q

How is disease activity judged in AMD retreatment?

A

VA, OCT: retinal oedema, haemorrhages, exudation

262
Q

When would you consider treating in AMD retreatment?

A

Vision drop, SR/IR fluid, fresh haemorrhage, worse symptoms,

263
Q

When would you consider not treating in AMD retreatment?

A

Severe vision drop, dry macula, stable vision, adverse event

264
Q

When was the certificate of visual impairment (formerly BD8) introduced in England and Wales?

A

England: September 2005, Wales: April 2007

265
Q

What is the purpose of the certificate of visual impairment?

A

Provides a reliable route for those with sight loss to be brought to the attention of social care

266
Q

How many UK individuals are visually impaired? How many have certificates of visual impairment? Which age group has the most registrants?

A

2 million
Approximately 300000
>75 year old’s

267
Q

What is main cause of visual impairment for (a.) >65’s, (b.) working age, (c.) children?

A

(a. ) AMD
(b. ) DR/DMO
(c. ) Optic neuropathy

268
Q

What is the definition of sight impaired?

A

Substantial, permanently handicapped by defective vision due to congenital illness or injury

269
Q

What are the criteria for sight impaired registration?

A

VA 6/24-6/60 (0.6-1.0 logMAR), large field restriction, media opacity/aphakia or
VA <6/18 (0.5 logMAR), gross field defect and constriction

270
Q

What is the definition of severely sight impaired?

A

So blind as to be unable to perform any work for which eyesight is essential

271
Q

What are the criteria for severely sight impaired registration?

A

VA <3/60 or VA <1/18 (1.30 logMAR) with restricted visual field

272
Q

How are low vision assessments carried out? Which organisation approves these? Which eye specialist provides the visual impairment letter? Who signs it?

A

Eye clinic appointments
Royal National Institute of Blind People (RNIB)
Optometrists
Consultant ophthalmologist

273
Q

What is considered in visual impairment needs assessments?

A 
Domestic tasks
Safe transport
Accommodation
Communication
Finances, jobs
Leisure
274
Q

Who carries out mobility assessments for the visually impaired?

A

Rehabilitation officer

275
Q

What is included in visually impaired quality of life assessments?

A

Physical, psychological, functional, social, economic well-being
Personality, religion, social support, health, education level

276
Q

What visually impaired quality of life questionnaires are there?

A

Low Vision Quality of Life
Adaptation to Age-Related Vision Loss (AVL-12)
Keele Participation Restriction Questionnaire (KAP)

277
Q

What benefits are there in registering for CVI?

A

Needs assessment, assistance, concessions, sight tests, early detection

278
Q

What direct and indirect costs are linked to impaired vision?

A

Direct: Productivity, care, medical support
Indirect: Falls, exacerbations, depresssion

279
Q

Which quality of life assessments were used in the Manchester conventional vs enhanced low vision rehab RCT?

A

Generic: SF-36
Vision-specific: VCM1 Psychological: NAS
Self-rated activity restriction: MLVQ

280
Q

Besides QoL assessments, what outcome measures were used in the Manchester conventional vs enhanced low vision rehab RCT?

A

LVR device use

AMD/VI knowledge at start and 1 year later

281
Q

What were the results of the Manchester conventional vs enhanced low vision rehab RCT?

A

Home visits ineffective for QoL, LVR high benefit

282
Q

What are the goals in low vision patient rehabilitation?

A

Restoration
Optimal function levels
Maximise residual vision for independence, LVA: Reading, magnifying, illuminating

283
Q

What other impairments is low vision linked to?

A

Daily activity dependence, low physical activity, isolation, depression

284
Q

Why are logMAR charts preferred to Snellen for low vision assessment?

A

Standardised, logarithmic letter size progression

285
Q

How is the magnification required for visually impaired children calculated?

A

Actual near visual acuity divided by required near visual acuity

286
Q

Which study investigated the reliability of VA measures?

A

Intersession Repeatability of VA Scores in AMD (Patel et al, 2008)

287
Q

What clinical contrast sensitivity tests are there?

A

Arden Grating Vistech/FACT
Cambridge
Bailey-Lovie/Regan Pelli-Robson

288
Q

Which electronic vision enhancement systems are there for the visually impaired?

A 
Contrast, reduced glare, tints, task lighting
Software: Supernova, Jaws (DSS)
Audio description
Eccentric viewing
Steady Eye Strategy
289
Q

How does Charles Bonnet syndrome commonly present? How is it managed?

A

Visual hallucinations in those with vision loss

Treat cause, reassurance, changing environment

290
Q

What can cause homonymous hemianopia? How does it present?

A

Stroke, brain tumour, trauma

Navigation issues, tripping, bumping into obstacles

291
Q

Which triaging method uses a ‘custom and practice’ appoach for low vision assessment?

A

Telephone review

MSc IOVS (4 decks)

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