FRCOPTH PART 2 > MR > Flashcards

MR Flashcards

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1
Q

What is the leading cause of blindness for the ‘over 50s’ in the Western world?

A

AMD

AMD prevalence increases with age.

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2
Q

What percentage of visually significant disease (VA ≤6/9) is found in the age group 65–75y in 1 study?

A

6%
(20% > 75)

This statistic highlights the increasing prevalence of AMD with age.

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3
Q

Name the four categories in the AREDS classification system for AMD.

A
  • Category 1: no AMD
  • Category 2: early AMD
  • Category 3: intermediate AMD
  • Category 4: advanced AMD

Each category is defined by specific clinical findings.

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4
Q

What are the clinical findings for Category 1 in the AREDS classification?

A

None or a few small drusen (<63 microns in diameter)

This category indicates no significant AMD.

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5
Q

What are the clinical findings for Category 2 in the AREDS classification?

A
  • Multiple small drusen
  • Few intermediate drusen (63–124 microns)
  • RPE abnormalities

This category indicates early AMD.

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6
Q

What are the clinical findings for Category 3 in the AREDS classification?

A
  • Extensive intermediate drusen
  • At least one large drusen (≥125 microns)
  • Geographic atrophy not involving the fovea

This category indicates intermediate AMD.

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7
Q

What are the clinical findings for Category 4 in the AREDS classification?

A
  • Geographic atrophy involving the fovea
  • Any features of neovascular AMD

This category indicates advanced AMD.

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8
Q

List some risk factors for AMD.

A
  • Smoking
  • Gender (♀ > ♂)
  • Ethnic origin (white Caucasian high risk)
  • Diet
  • CVS risk
  • Hypermetropia

These factors contribute to the likelihood of developing AMD.

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9
Q

True or false: Recent evidence finds that cataract surgery causes or worsens AMD.

A

FALSE

Recent studies do not support a link between cataract surgery and AMD progression.

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10
Q

Which genetic loci have been associated with AMD?

A
  • CFH gene on Chr 1q32
  • ARMS2/HTRA1 locus on Chr 10q26

These loci are related to the complement pathway and AMD risk.

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11
Q

What percentage of AMD cases does non-neovascular (dry) AMD account for?

A

90%

This type leads to gradual reduction in central vision.

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12
Q

What are the histological features of non-neovascular AMD?

A
  • Loss of RPE/photoreceptor layers
  • Thinning of the outer plexiform layer
  • Thickening of Bruch’s membrane
  • Atrophy of the choriocapillaris

These changes expose larger choroidal vessels to view.

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13
Q

Where are drusen located?

A

Drusen are PAS-positive amorphous deposits, lying between the RPE membrane and the inner collagenous layer of Bruch’s membrane

Symptoms usually have a gradual onset.

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14
Q

What are the characteristics of hard drusen?

A

Small (<63 microns), well-defined, of limited significance

Hard drusen are less likely to lead to complications.

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15
Q

What are the characteristics of soft drusen?

A
  • Larger
  • Pale yellow
  • Poorly defined
  • Tendency to coalesce and form confluent drusen ( ↑ risk of CNV)

Soft drusen increase the risk of CNV.

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16
Q

What are clinical features of dry AMD ?

A
  • ↓VA, metamorphopsia, scotomas; usually gradual in onset.
    • Hard drusen
    • soft drusen
  • RPE focal hyperpigmentation, RPE atrophy (‘geographic atrophy’ if well demarcated and with visibility of the underlying choroidal vessels).
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17
Q

What lifestyle changes are recommended for AMD patients?

A
  • Smoking cessation
  • ↑ intake of macular carotenoids
  • ↑ intake of omega-3 fatty acids

Foods like spinach, cabbage, broccoli, and oily fish are beneficial.

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18
Q

What vitamin supplementation has been shown to delay AMD progression in the AREDS study?

A
  • Vitamins C and E
  • α-carotene
  • Zinc

High-dose antioxidants and minerals were effective in delaying progression.

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19
Q

What is a potential risk associated with β-carotene supplementation?

A

↑ incidence of lung cancer in former smokers

This finding led to the suggestion of lutein + zeaxanthin as substitutes.

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20
Q

What does neovascular (wet) AMD lead to?

A

Rapid and severe loss of vision

Nearly 40,000 new cases occur each year in the UK, accounting for up to 90% of blind registration due to AMD.

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21
Q

What treatment advancements have been made for wet AMD in the last decade?

A

Anti-VEGF therapies

These treatments are expected to significantly reduce legal blindness attributable to wet AMD.

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22
Q

What are the two types of neovascularization in wet AMD?

A

New capillaries grow from the choriocapillaris though Bruch’s membrane and proliferate in:
* Type 1 neovascularization (sub-RPE)
* Type 2 neovascularization (subretinal space)

Type 1 is more common in AMD; type 2 is more common in younger patients E.G. myopia

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23
Q

What is retinal angiomatous proliferation (RAP)?

A

A variant of wet AMD involving the retinal circulation in 10–15% of patients - these lesions have been termed Type 3 nv

It is characterized by intraretinal vascular complexes arising from deep retinal capillaries and the choroid.

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24
Q

What is polypoidal choroidal vasculopathy (PCV)?

A

A variant of wet AMD characterized by polypoidal dilatation of the choroidal vasculature with serosanguinous PEDs

Common in Asian or African descent populations, has predilection for papillary area.

	○ Characterised by: Dilated choroidal vascular channels terminating as 'polyps' --> leading to serous and haemorhagic detachments of retina and RPE 
	○ Minimal or no cystic change of the overlying retina 
	○ Best diagnosed by ICG  EVEREST trial - increased risk of anatomical closure of polyps in PDT + ranibizumab compared with monotherapy
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25
What are common **clinical features** of wet AMD?
* ↓VA * Metamorphopsia * Scotoma * **RAP lesions** should be suspected in eyes with **parafoveal intraretinal haemorrhage, associated PED, and circinate exudate**. An adjacent retinal vessel is sometimes seen to ‘dive’ into the outer retina (‘right-angled’) ## Footnote Symptoms may be sudden in onset and associated with various signs including hemorrhage and detachment.
26
What is the role of **FFA** in diagnosing wet AMD?
Assess CNV location and classification ## Footnote It is vital for diagnosis and treatment assessment, except where contraindicated.
27
What are the **types of CNV** based on FFA and OCT findings?
* Type 1 (‘occult’) CNV * Type 2 (‘classic’) CNV * Type 3 (‘RAP’) CNV * PCV ## Footnote Each type has distinct appearances on FFA and OCT, aiding in diagnosis.
28
What is the **5-year risk** of developing advanced AMD based on risk factors?
* 0 factors: 0.5% * 1 factor: 3% * 2 factors: 12% * 3 factors: 25% * 4 factors: 50% ## Footnote Risk factors include large drusen and pigment abnormalities.
29
True or false: **Anti-VEGF therapy** is the preferred treatment for all subfoveal CNV lesions.
TRUE ## Footnote It has become the treatment of choice for wet AMD.
30
What is the **EVEREST trial** related to?
Increased risk of anatomical closure of polyps in PDT + ranibizumab compared to monotherapy ## Footnote This trial highlights treatment effectiveness in PCV.
31
What should be performed urgently for diagnosis and treatment assessment in suspected wet AMD?
FFA ## Footnote It allows for the assessment of CNV location and classification.
32
What is the **characteristic appearance** of type 2 CNV on FFA?
Early, well-demarcated, lacy hyperfluorescence with progressive leakage ## Footnote On OCT, it appears as subretinal hyperreflective material.
33
What are the **common causes of CNV**?
* AMD * Pathological myopia * Angioid streaks * Trauma * Inflammation e.g. POHS, Serpiginous choroidopathy, birdshot, VKH * Dystrophies e.g. best's * Other causes ## Footnote These include various conditions leading to choroidal neovascularization.
34
What does **VEGF-A** induce?
* Developmental angiogenesis * Pathological angiogenesis * Vascular permeability * Inflammation ## Footnote VEGF-A is a secreted protein that plays a crucial role in various vascular processes.
35
Name the **three licensed drugs** for anti-VEGF therapy.
* Pegaptanib * Ranibizumab * Aflibercept ## Footnote Bevacizumab is also commonly used off-label.
36
What is **pegaptanib**?
A pegylated aptamer that selectively inhibits VEGF-165 isoform ## Footnote It is less effective than other anti-VEGF therapies and is no longer widely used.
37
What is the mechanism of **ranibizumab**?
A humanized monoclonal antibody fragment that binds all isoforms of VEGF-A ## Footnote Bevacizumab is derived from the same humanized monoclonal antibody as ranibizumab
38
What distinguishes **aflibercept** from other anti-VEGF therapies?
* Acts as a decoy receptor * Binds VEGF-A with higher affinity than rani or beva * Binds PlGF 1 and 2 ## Footnote Aflibercept is a fusion protein that enhances its effectiveness.
39
In the **MARINA** and **ANCHOR** trials, what percentage of patients gained moderate visual improvement with ranibizumab?
~33% ## Footnote Moderate visual gain is defined as gaining ≥15 letters.
40
What did the **CATT** and **IVAN** studies reveal about **bevacizumab**?
Similar efficacy to ranibizumab, but less gain in visual acuity with OCT-guided as required retreatment ## Footnote These studies compared the effectiveness of different anti-VEGF therapies.
41
What was the mean gain in letters for patients receiving **aflibercept** in the VIEW 1 and VIEW 2 studies?
~30% gained ≥15 letters ## Footnote This indicates significant effectiveness in treating wet AMD.
42
What percentage of patients gained ≥15 letters in the **RISE** trial with ranibizumab?
44.8% ## Footnote This trial focused on patients with diabetic macular oedema.
43
What was the mean gain in letters for **aflibercept** in the VISTA and VIVID studies?
Mean gain of ten letters ## Footnote This reflects the effectiveness of aflibercept in treating diabetic macular oedema.
44
In the **CRUISE** and **BRAVO** studies, what percentage of patients gained ≥15 letters with ranibizumab?
47.5% in CRUISE and 61.1% in BRAVO ## Footnote These studies evaluated the efficacy of ranibizumab in treating retinal vein occlusion.
45
What did the **RADIANCE** study find regarding ranibizumab?
Superior to PDT with a mean gain of 10.5 and 10.6 letters ## Footnote This study assessed the effectiveness of ranibizumab in myopia-associated CNV.
46
What are the NICE guidelines for using **ranibizumab** in wet AMD?
* Best corrected VA between 6/12 and 6/96 * No permanent structural damage to the central fovea * Lesion size ≤12 disc areas * Evidence of recent disease progression ## Footnote These criteria help determine eligibility for treatment.
47
What potential side effects are associated with **intravitreal injections** of anti-VEGF therapies?
* Endophthalmitis <0.1% * Retinal detachment * Lens damage/cataract * Raised IOP * Conjunctival haemorrhage * Vitreous floaters * Intraocular inflammation * Eye pain * Visual loss ## Footnote Awareness of these risks is crucial for patient safety.
48
What is the recommended follow-up after an **intravitreal injection**?
* Test gross VA * Check for central retinal artery patency * Check IOP ## Footnote Follow-up is essential to monitor for complications and treatment efficacy.
49
Describe the appearance of **Type 2 (classic CNV) **on FFA and OCT
* FFA - early, well-demarcated, **lacy hyperfluorescence with progressive leakage**. * OCT - the neovascular tissue is associated with variable amounts of **fibrosis **and appears as **subretinal hyperreflective material (SHRM)**
50
Describe the appearance of **Type 1 (occult CNV) **on FFA and OCT
* FFA - fibrovascular PED (irregular elevation with stippled hyperfluorescence at 1–2min post-injection) or as late leakage of an undetermined source (poorly demarcated hyperfluorescence 5–10min post-injection). * On OCT, appears as irregular, broad elevation of the RPE, with separation from the underlying Bruch’s membrane
51
Describe the appearance of **Type 3 (RAP) **on FFA and OCT
* on FFA, shows a similar appearance to a small area of classic CNV, with **early hyperfluorescence and progressive leakage** (although the exact appearance may vary, depending on its stage of evolution). * On OCT, RAP lesions typically appear as **outer retinal hyperreflective foci with overlying CMO **and may be associated with **serous or fibrovascular PED.**
52
What is **PDT** ?
The laser stimulation of a photoactivated dye that results in the destruction of CNV ## Footnote This technique aims to selectively destroy the membrane while minimizing damage to adjacent structures.
53
What is the **commonest indication** for PDT?
AMD ## Footnote PDT has also been used for other CNVs, such as in myopia and inflammatory membranes.
54
What has largely replaced PDT as a single agent in the treatment of CNV?
Anti-VEGF therapies ## Footnote However, PDT is finding a new therapeutic niche in diseases such as CSC, PCV, and certain ocular tumors e.g. choroidal haemangioma.
55
What is **verteporfin** in the context of PDT?
A photoactivated dye that binds to lipoproteins and concentrates in the proliferating vascular bed of the CNV ## Footnote It is activated by laser light to catalyze the formation of free radicals.
56
What wavelength of laser light is used to activate verteporfin?
689nm ## Footnote This wavelength is directed onto the CNV to activate the dye.
57
What is the standard energy level used for tumors or AMD/polypoidal lesions in PDT?
600mW/cm2 × 83s = 50J/cm2 ## Footnote This energy level is sufficient to activate the dye without causing thermal damage. Causes local endothelial cell death and occlusion of the blood supply to the CNV
58
What are the **side effects** of PDT?
* Injection site reactions - Inflammation, leakage, hypersensitivity * Back pain (2%) * Transient visual disturbances * Significant visual loss (up to 4%) ## Footnote These side effects can occur following the procedure.
59
What are the **contraindications** for PDT?
* Liver failure * Porphyria * Allergy to any components ## Footnote These conditions may prevent a patient from safely undergoing PDT.
60
What advice should be given to patients for **48 hours post-PDT**?
Avoid direct sunlight and bright lights ## Footnote If necessary to go outside, wear protective clothing and accessories.
61
What is the **first step** on the day of the PDT procedure?
Calculate spot size (greatest linear diameter + 1,000 microns) ## Footnote This is essential for proper treatment application.
62
What should be confirmed before starting the infusion during PDT?
Consent: purpose, risks ## Footnote This ensures the patient is fully informed about the procedure.
63
What is the recommended follow-up procedure after PDT for neovascular AMD?
Review with FFA (+ ICG for polypoidal lesion) and OCT at 12 weeks ## Footnote This helps assess the effectiveness of the treatment.
64
According to NICE guidelines, what has become the first-line indication for CNV secondary to AMD?
Anti-VEGF therapies ## Footnote This shift occurred following the 2008 and 2013 NICE guidance updates.
65
How many times can PDT be repeated per year if recurrent leakage?
Up to 4x per year
66
If severe ↓VA of ≥4 lines within 1wk of treatment, can you repeat PDT?
No - unless VA returns to pre-treatment level
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