Paediatric Ophthalmology Lectures Flashcards

1
Q

Which key questions form a paediatric ophthalmology history?

A
Presenting complaint
Age of onset, duration
Uni/bilateral? Constant/intermittent?
Discharge (watery/pus)
Pain/photophobia/vision loss
Affected contacts
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2
Q

What birth history questions should be asked in paediatric ophthalmology?

A

Trauma?
Prematurity? (ROP)
C-section?

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3
Q

How can photographs taken by parents aid a paediatric ophthalmology history?

A

Documenting changes in squint

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4
Q

What are the main causes of ophthalmia neonatorum?

A

Chlamydia trachomatis
N. gonorrhoeae
S. aureus, Strep pneumoniae, Haemophilus, Pseudomonas
Herpes simplex virus

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5
Q

How does gonococcal neonatal conjunctivitis present? (Note: Same for other bacteria but 2-5 days instead)

A

1-3d of birth:

Severe purulent discharge, lid oedema, chemosis, keratitis

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6
Q

How does chlamydial neonatal conjunctivitis present?

A

4-28d of birth:

Mucopurulent discharge, papillae, pre-septal cellulitis

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7
Q

How do you investigate and treat ophthalmia neonatorum?

A

MC&S: Prewet swab or conjunctival scrapings
Gonococcal: Cefotaxime IM
Chlamydial: Erythromycin
Other: Chloramphenicol (gram +ve) or tobramycin (gram -ve)

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8
Q

What are the signs and symptoms of conjunctivitis?

A
Irritation (pain if cornea involvement)
Conjunctival hyperaemia (max in fornix)
Associated discharge
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9
Q

What are the signs of bacterial conjunctivitis?

A

Bilateral mucopurulent discharge, papillary reaction, ‘glued eyes’, no itching

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10
Q

How is bacterial conjunctivitis treated?

A

Topical Abx: Chloramphenicol

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11
Q

How is viral conjunctivitis treated?

A

Infection control, spread prevention

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12
Q

What are the signs and symptoms of allergic conjunctivitis?

A

Itchy, watery discharge, lid oedema, chemosis, mild papillary hypertrophy,

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13
Q

How is allergic conjunctivitis treated?

A

Limit allergen exposure

Flare-ups: Cold compress, artificial tears, topical NSAID’s, corticosteroids, antihistamines, mast cell stabilisers

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14
Q

What are the features of vernal keratoconjunctivitis?

A

80% atopic history, 5-15 years onset

Itchy, thick mucous discharge, cobblestone papillae, shield ulcers, keratitis

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15
Q

How is vernal keratoconjunctivitis treated?

A

Steroids, subtarsal injection

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16
Q

How does microbial keratitis present?

A

Painful red eye, mucopurulent discharge, photophobia, blurred vision
Epithelial defect, infiltrate, hypopyon

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17
Q

How is microbial keratitis treated?

A

Controls ulcer swab

Topical Abx: Ofloxacin

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18
Q

How are corneal abrasions treated?

A

Fluorescein drops to visualise

Topical anaesthesia, chloramphenicol, oral analgesia, pad

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19
Q

What is blepharitis?

A

Meibomian gland (produces lipid layer of tears) infection in the lid margin, chalazia may be present

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20
Q

How is blepharitis treated?

A

Cold compress, lid hygiene

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21
Q

What is the difference between a chalazion and a stye/hordeolum?

A

Chalazia: Usually non-painful lumps from clogged oil gland deep in eyelid
Styes: Painful lumps near lid margin due to infection

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22
Q

How does herpetic eye disease present and how is it treated?

A
Epithelial defect (dendritic ulcers seen via fluorescein drops)
3% aciclovir 5x daily, weekly review
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23
Q

What is assessed when investigating a corneal foreign body?

A

Mechanism and depth of injury, intraocular pressure check

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24
Q

What test is used to assess full thickness corneal laceration?

A

Seidel’s test via fluorescein drops

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25
Q

How do you treat corneal foreign body?

A

Remove if trained

Chloramphenicol

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26
Q

What is hyphaema?

A

Blood in the anterior chamber

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27
Q

What types of ocular chemical injuries can occur?

A

Acid, alkali, thermal, UV

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28
Q

How are ocular chemical injuries investigated?

A
Intraocular pressure check, visual acuity, slit-lamp examination
Lid eversion (foreign bodies?)
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29
Q

How are ocular chemical injuries treated?

A

Irrigation (check pH), Abx, cycloplegia, vitamin C

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30
Q

How does juvenile idiopathic arthritis present in the eye?

A
Anterior uveitis (no symptoms/floaters/less VA)
Keratic precipitates, cataract, glaucoma, vitritis, CMO, IOP change, posterior synechiae
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31
Q

What could a hazy cornea indicate in juvenile idiopathic arthritis?

A

Pankeratopathy, CMO

Vitreous cells in cornea

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32
Q

How is juvenile idiopathic arthritis treated?

A

Steroids, cycloplegia, methotrexate, anti-TNF agents

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33
Q

What is the main cause of endophthalmitis?

A

Recent eye surgery

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34
Q

How does endophthalmitis present?

A

Painful red eye, rapid visual loss, hypopyon, vitritis, hazy cornea

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35
Q

What pathology causes watering eyes and how is it treated?

A

Nasolacrimal duct blockage

Massage/compress (persistent: syringing/probing)

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36
Q

How does pre-septal cellulitis present and what causes it?

A

Painful swollen lid, fever, malaise

Staph, strep

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37
Q

How does orbital cellulitis present?

A

Sinusitis, facial cellulitis, dacryocystitis, dental abscess

Swollen painful lids, proptosis, less eye movements, optic nerve dysfunction

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38
Q

What are the complications of orbital cellulitis?

A

Meningitis, cavernous sinus thrombosis, orbital/cerebral abscesses

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39
Q

What are the differentials of leucocoria?

A

Retinoblastoma, cataract, toxocariasis, Coat’s disease, ROP, RD

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40
Q

What is pathogenesis of retinoblastoma?

A

13q14 deletion: 90% sporadic uni/bilateral primitive photoreceptor cell tumour

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41
Q

How is retinoblastoma treated?

A

External-beam radiation, plaque radiotherapy, cryotherapy, chemotherapy, enucleation

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42
Q

What features are seen in optic disk swelling?

A

Ill-defined disk margins, tortuous retinal vessels, cotton wool spots, haemorrhages
No symptoms or nausea /photophobia

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43
Q

How is optic disk swelling investigated?

A

OCT (drusen?), AF

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44
Q

What can ptosis and congenital cataracts cause?

A

Amblyopia

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45
Q

How are congenital cataracts treated?

A

Atropine, patching

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46
Q

In which embryological week does the retina become completely vascularised?

A

Week 36

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47
Q

What causes retinopathy of prematurity?

A

Angiogenesis following retinal ischaemia due to incomplete vascularisation

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48
Q

What were the main paediatric amblyopia trials?

A

ATS (PEDIG), ROTAS, MOTAS

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49
Q

What did ATOM stand for in the ATOM trial?

A

Atropine for the Treatment Of childhood Myopia

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50
Q

Which were the main ROP trials?

A

CRYO-ROP, ET-ROP, LIGHT-ROP, STOP-ROP, BEAT-ROP, PHOTO-ROP, HOPE-ROP, ROP1

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51
Q

What were the main paediatric cataract studies?

A

IATS, IOLu2

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52
Q

What were the results of the IOLu2 study?

A

Uni/bilateral IOL implant effects on cataract negligible

Glaucoma risk when cohort >4 y/o

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53
Q

What were the main paediatric exotropia studies?

A

CITS, Newcastle Control Score

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54
Q

What did ATS stand for and how many studies have been published?

A

Amblyopia Treatment Studies

17 (#18 being reviewed)

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55
Q

How did ATS classify amblyopia according to BCVA?

A

Mild to moderate: >20/80 in amblyopic eye

Severe: 20/100-20/400 in amblyopic eye

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56
Q

What is occlusion therapy to treat amblyopia?

A

Patching of the non-amblyopic eye to stimulate the amblyopic eye

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57
Q

What is penalisation therapy to treat amblyopia?

A

Atropine drops to blur vision in non-amblyopic eye to stimulate the amblyopic eye

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58
Q

What did the “Prescribed patching regimens for severe amblyopia” study reveal?

A

6-hour daily patching increased VA as much as full-time patching

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59
Q

What were the daily patching recommendations following the severe amblyopia study?

A

Mild: 2 hours daily
Moderate: 4 hours daily
Severe: 6 hours daily

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60
Q

What were the treatment criteria for the “Atropine vs patching for moderate amblyopia” study?

A

Patching group: >6-hours daily

Atropine group: 1 drop daily

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61
Q

What were the results of the “Atropine vs patching for moderate amblyopia” study?

A

Mean VA improvement of 3 lines (20/60 to 20/30)

Daily vs weekend atropine: Similar results after 17 weeks

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62
Q

When is the critical period for amblyopia treatment?

A

First 7 years of life

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63
Q

What amblyopia treatment may improve vision in those aged 7-12?

A

2-6 hours daily patching

Near activities, atropine

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64
Q

What amblyopia treatment may improve vision in those aged 13-17?

A

2-6 hours daily patching

Near activities

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65
Q

How effective are 2 hours daily patching and near activities to treat amblyopia in those aged 3-7?

A

Not at all according to the respective trial

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66
Q

What was the inclusion criteria for the refractive correction anisometropic amblyopia study?

A

No prior treatment
VA 20/40-20/250
Occlusion + spectacles

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67
Q

When is the glasses adaptation period?

A

16-18 weeks

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68
Q

What were the results of the refractive correction anisometropic amblyopia study?

A

77% >2 lines VA gain
60% >3 lines VA gain
Glasses alone work not occlusion therapy

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69
Q

What conclusions could be drawn from the amblyopia studies?

A

Moderate amblyopia: Occlusion vs atropine, 2 hrs vs 6 hrs daily patching, weekend vs daily patching all equally effective
Severe amblyopia: Part-time vs full-time patching equally effective

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70
Q

What studies examined amblyopia occlusion treatment compliance rates? How so? What were the results?

A

MOTAS, ROTAS
Occlusion dose monitor
<50% compliance rate, parents respond to child’s discomfort

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71
Q

What is the global incidence of RD in >6D myopia?

A

3%

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72
Q

What did ATOM1 investigate?

A

Effect of 1 daily 1% atropine drop in 1 eye over 2 years to treat myopia

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73
Q

What were the results of the ATOM1 study?

A

77% reduction in myopic progression

Increased myopia progression following treatment cessation

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74
Q

What did ATOM2 investigate?

A

Effect of 0.5% vs 0.1% vs 0.01% atropine over 12 months to treat myopia

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75
Q

What were the results of the ATOM2 study?

A

All doses: Similar effects

  1. 5%: Increased post-cessation myopia progression
  2. 01%: Less pupil dilation and accommodation loss
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76
Q

What was done in the 5-year ATOM2 extension trial?

A

Those with post-cessation myopia progression were restarted on atropine

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77
Q

What were the results of the 5-year ATOM2 extension trial?

A

Myopia progression and axial elongation change lowest in 0.01% atropine group

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78
Q

What does CRYO-ROP stand for? What were the results of this study?

A

Cryotherapy for ROP
Introduced threshold ROP in staging
50% had visual loss and RD despite treatment

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79
Q

What does ET-ROP stand for? What were the results of this study?

A

Early treatment for ROP
Introduced pre-threshold ROP
Poor visual and structural outcomes reduced by 5.5% and 6.6% respectively

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80
Q

What do HOPE-ROP and STOP-ROP stand for? What were the results of these studies?

A

High O2 percentage in ROP
Supplementary O2 therapy in ROP
Inconclusive results

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81
Q

What does LIGHT-ROP stand for? What were the results of this study?

A

Ambient light in ROP

No effect on ROP progression

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82
Q

What did the PHOTO-ROP study investigate?

A

Digital fundus imaging vs indirect ophthalmoscopy in ROP screening

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83
Q

What were the results of the PHOTO-ROP study?

A

Digital fundus imaging sensitivity, specificity, accuracy depends on image quality
Immediate review <24 hours recommended

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84
Q

What did the BEAT-ROP study investigate?

A

Bevacizumab vs laser to treat stage 3+ ROP

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85
Q

What were the results of the BEAT-ROP study?

A

ROP recurrence: 4% with Avastin, 22% with laser

Zone I/II ds benefit with Avastin

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86
Q

Which was the lowest effective Avastin dose in treating ROP?

A

0.031mg

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87
Q

What is the inheritance pattern of metabolic disorders affecting the eye?

A

Generally autosomal recessive

X-linked recessive: Fabry’s disease, ornithine transcarbamylase deficiency

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88
Q

Which lysosomal storage disorders affect the eye?

A
Fabry’s disease
Cystinosis
Mucopolysaccharidoses
Neuronal ceroid lipofuscinosis
Neumann-Pick disease
Gaucher’s type 3
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89
Q

Which metabolic disorders have unique eye findings?

A

Fabry’s disease
Mucopolysaccharidoses
Cystinosis

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90
Q

Which metabolic disorders have unique eye findings?

A

Fabry’s disease
Mucopolysaccharidoses
Cystinosis

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91
Q

In which metabolic disorders are the eyes affected late in the disease course?

A
Mucopolysaccharidoses
Propionic acidaemia
LCHAD deficiency
Refsum's
Homocystinuria
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92
Q

In which metabolic disorders are the eyes affected late in the disease course?

A

Propionic acidaemia

LCHAD deficiency

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93
Q

Which metabolic disorders have no effect on vision?

A

Fabry’s disease

Wilson’s disease

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94
Q

Which metabolic disorders present with vision loss?

A

Batten’s disease

Gyrate atrophy

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95
Q

Which metabolic disorders affect eye movement?

A

Gauchers type 3

Niemann-Pick type C

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96
Q

Which metabolic disorder presents with transient vision loss?

A

Ornithine transcarbamylase deficiency

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97
Q

What causes Fabry’s disease?

A

α-galactosidase A deficiency

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98
Q

What are the systemic signs of Fabry’s disease?

A

Acroparesthesia
Angiokeratoma corporis diffusum
Neuropathy, renal failure
Hypertrophic cardiomyopathy, stroke

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99
Q

What are the ocular manifestations of Fabry’s disease?

A

Corneal verticillata
Conjunctival + retinal vessel tortuosity
Retinal vascular occlusion, cataracts

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100
Q

What term is used to describe corneal verticillata? What causes them? Do they affect vision?

A

Vortex keratopathy (‘whorls’)
Fabry’s disease, amiodarone
No effect on vision

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101
Q

What fundoscopy signs are seen in Fabry’s disease? What causes these?

A

Venous dilation, arterial narrowing, AV-nicking

Cytoplasmic inclusions in endothelial cells and pericytes

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102
Q

What is the pathogenesis of corneal verticillata? How are they visualised? How are amiodarone deposits different?

A

Corneal epithelial basal layer intracellular inclusions
Slit-lamp, confocal scanning laser microscopy
Amiodarone deposits more reflective, different size

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103
Q

What conjunctival signs are seen in Fabry’s disease?

A

Venous dilation/tortuosity
Sludged blood, microaneurysms
Chronic chemosis
Lymphangiectasia

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104
Q

How do cataracts appear in Fabry’s disease?

A

Bilateral wedge shape

Along suture lines from posterior pole (Spoke-like)

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105
Q

What ocular symptoms occur following strokes in Fabry’s disease?

A

Homonymous hemianopia (37%)

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106
Q

How is Fabry’s disease treated?

A

ERT: Fabrazyme, replagal

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107
Q

What causes cystinosis? What is the pathophysiology?

A

CTNS gene mutation (cystinosin)

Cystine buildup in kidneys, bone marrow, pancreas, muscles, brain and eye

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108
Q

How does cystinosis present systemically? Which syndrome is it linked to?

A

Renal failure, anaemia, short stature

Fanconi’s syndrome

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109
Q

How does cystinosis present in the eye?

A

Crystals: Cornea, conjunctiva, retina (later erosions and NV)
Photophobia

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110
Q

How is cystinosis treated?

A

Topical cysteamine (0.44%)

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111
Q

What are the main types of mucopolysaccharidoses?

A

I: Hurler, Hurler-Scheie, Scheie
II: Hunter, IV: Morquio
VI: Maroteaux-Lamy

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112
Q

Which bodily systems do MPS affect?

A

Skeletal
Cardiovascular
Neurological
Eyes

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113
Q

Which MPS types involve corneal clouding, photophobia and exposure keratopathy? How are these treated?

A
I, IV, VI, VII
Corneal transplantation (PK, DALK)
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114
Q

What anterior segment changes occur in MPS?

A

Thicker peripheral cornea
Variable central cornea thickness
Altered corneal hysteresis
Thicker iris, narrower angle

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115
Q

What optic nerve changes occur in MPS?

A
Thicker sclera, greater optic nerve diameter, risk of high ICP damage
Optic atrophy (severe visual loss)
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116
Q

How does glaucoma present in MPS?

A

Raised IOP, optic disc GAG deposition, corneal opacity, poor dilation, visual fields affected

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117
Q

Retinopathy occurs in which types of MPS? How does it present?

A

I, II, III
Nyctalopia, peripheral field loss
II: Choroidal folds, maculopathy, RD

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118
Q

Which genes are affected in neuronal ceroid lipofuscinosis?

A

CLN1-10
CLN10: Congenital, 11p15, Cathepsin D
CLN1: Infantile, 1p32, Palmitoyl thioesterase
CLN3: Batten’s, 16p12

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119
Q

What is gyrate atrophy? What causes it?

A

Amino acid metabolism disorder

Ornithine aminotransferase deficiency

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120
Q

How does gyrate atrophy present?

A

Progressive vision loss, myopia

Cataracts, chorio-retinal degeneration

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121
Q

What lifestyle factor can slow gyrate atrophy progression?

A

Arginine restricted diet

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122
Q

What causes propionic and methylmalonic acidaemias?

A

Branched chain amino acid catabolism defects

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123
Q

How do propionic/methylmalonic acidaemias present?

A

Vomiting, drowsiness, acidosis, hyperammonaemia, late severe visual loss (optic neuropathy)

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124
Q

How are propionic/methylmalonic acidaemias treated?

A

Dietary protein restriction

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125
Q

Which protein is inadequately metabolised in homocystinuria? Where is this condition more prevalent?

A

Methionine

Ireland (1 in 52000)

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126
Q

How does homocystinuria present systemically?

A

Development delay, seizures, PE, DVT

Tall, long limbs, fair, blue iris

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127
Q

How does homocystinuria present in the eyes?

A

90%: Ectopia lentis

Myopia, cataract, RD, RAO, glaucoma, anaesthesia risky

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128
Q

What is galactosaemia? What causes it?

A

Carbohydrate metabolism disorder

Galactokinase deficiency

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129
Q

How does galactosaemia present? How can it be stabilised?

A

Jaundice, poor feeding, oil-droplet cataract (progress to lamellar)
Hepatosplenomegaly
Dietary control

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130
Q

Which sterol metabolism disorders affect the eye?

A

Cerebrotendinous xanthomatosis

Smith-Lemli-Opitz syndrome

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131
Q

What causes cerebrotendinous xanthomatosis? How does it present?

A

Sterol 27-hydroxylase gene mutation (CYP27A1)
Diarrhoea, ataxia, seizures
Cataracts, optic neuropathy
Tendon xanthomas, atherosclerosis

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132
Q

How is cerebrotendinous xanthomatosis treated?

A

Chenodeoxycholic acid, statins

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133
Q

What causes Smith-Lemli-Opitz syndrome? How does it present?

A

Raised 7-dehydrocholesterol
Microcephaly, polydactyly, genital/heart/gut malformations
Cataract, ptosis, strabismus, optic atrophy

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134
Q

Which process involves LCHAD?

A

Mitochondrial fatty acid beta-oxidation

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135
Q

How does LCHAD deficiency present?

A

Hypoglycaemia, hypotonia, seizures, cholestatic liver
Chorioretinal breakdown, myopia
Visual loss, photophobia, nyctalopia

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136
Q

What types of Niemann-Pick disease are there? What causes them?

A

A, B: Sphingomyelinase deficiency

C, D: Brain sphingolipid buildup

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137
Q

Which epidemiological group is most affected by Niemann-Pick disease types A and B?

A

Ashkenazi Jewish population

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138
Q

How do Niemann-Pick disease types A and B present?

A

A: Neurological degeneration
B: Hepatosplenomegaly
Cherry red spot, pre-orbital fullness, macular granular deposits

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139
Q

How does Niemann-Pick disease type C present?

A

NPC 1 or 2 gene mutation
Liver disease, splenomegaly, seizures, ataxia, dystonia
Vertical supranuclear gaze palsy

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140
Q

How is Niemann-Pick disease type C treated?

A

Miglustat

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141
Q

What causes Gaucher’s disease type 3?

A

Glucocerebrosidase gene mutation

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142
Q

How does Gaucher’s disease type 3 present? How is it treated?

A

Oculomotor apraxia (defective horizontal saccades), intermittent strabismus, vertical gaze palsies
Failure to thrive, hepatosplenomegaly
ERT: Recombinant glucocerebrosidase

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143
Q

What is ornithine transcarbamylase deficiency?

How does it present?

A

Urea cycle disorder
Bilateral vision loss, encephalopathy, headaches
Sluggish pupils, nystagmus, flat VEP’s

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144
Q

What are the UK risk factors for Retinopathy of Prematurity?

A

<32 weeks gestational age, <1501g birth weight, supplemental O2, M>F, Caucasians, mechanical ventilation

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145
Q

Which aggressive form of ROP progresses rapidly?

A

AP-ROP

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146
Q

What are the UK risk factors for Retinopathy of Prematurity?

A

<32 weeks gestational age

<1501g birth weight

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147
Q

What percentage of premature babies are affected by ROP?

A

20%

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148
Q

How is ROP detected?

A

Clinical examination

No signs/symptoms

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149
Q

What retinal development occurs at 16 weeks gestation?

A

Blood vessels grow out from the optic nerve

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150
Q

Which cells form retinal blood vessels? In which gestational weeks do they grow then form vessels?

A

Spindle cells
Grow: 16 weeks
Form vessels: 29 weeks

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151
Q

What environmental factors affect the immature retina?

A

Systemic O2 levels

VEGF levels

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152
Q

Which cells form retinal blood vessels? In which gestational weeks do they form then develop?

A

Spindle cells
Grow at 16 weeks
Form vessels at 29 weeks

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153
Q

What term is used for the state of the retina in early foetal development?

A

Physiological hypoxic state

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154
Q

What promotes early foetal vasculogenesis

A

Increased retinal thickeness thus increased local metabolic demand

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155
Q

What is the pathophysiology of ROP?

A

Premature neonate exposed to higher O2 levels, incomplete retinal vessel development, scarring, RD/blindness

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156
Q

What is the pathophysiology of ROP?

A

Premature neonate exposed to higher O2 levels, incomplete retinal vessel development, scarring, RD/blindness

157
Q

What factors cause abnormal retinal vessel development?

A

Low IGF-1 (O2)
High VEGF (O2)
Genetics
Poor early weight gain

158
Q

How does supplemental O2 affect ROP progression?

A

Retinal vasoconstriction
Vascular closure, endothelial loss
Proliferating endothelial nodules (popcorn) canalise through ILM

159
Q

Which genes are linked to ROP?

A
FEVR similar phenotype
Norrie disease (NDP) gene
160
Q

How is ROP classified?

A

Location (Zones 1-3), extent (clock hours), severity (0-5), plus disease, AP-ROP

161
Q

How are zones 1-3 defined in ROP?

A

1: 2x optic disc diameter
2: Circumferential from nasal aura
3: Remainder of temporal region

162
Q

How is stage 0 defined in ROP?

A

Immature retina

163
Q

How is stage 1 defined in ROP?

A

Demarcation line of vascularisation

164
Q

How is stage 2 defined in ROP?

A

Fibrovascular ridge (late: popcorn)

165
Q

When does a double demarcation line form?

A

Stage 2/3 ROP regressing: Retinal vascularisation passes the ridge then recurs

166
Q

When does a double demarcation line form?

A

Stage 2/3 ROP regresses: Retinal vascularisation passes the ridge then recurs

167
Q

How are stages 4a and 4b defined in ROP?

A

Partial retinal detachment (4a: Fovea-sparing, 4b: Non-sparing)

168
Q

How is stage 5 defined in ROP?

A

Complete retinal detachment (funnel-shaped), retrolental fibroplasia

169
Q

What is seen in Plus disease in ROP?

A

Posterior retinal vessel abnormal dilatation and tortuosity, iris rigidity

170
Q

How is Pre-Plus disease defined in ROP?

A

Insufficiently severe Plus disease in 2+ quadrants

171
Q

What causes Plus disease in ROP?

A

Periphery shunting through ridge tissue

172
Q

What vascular sign of aggressive ROP normally disappears after birth?

A

Tunica vasculosa lentis

Capillary network over posterior/lateral lens

173
Q

What stage of ROP warrants immediate treatment?

A

Stage 3 with 2+ quadrants of Plus disease

174
Q

What is seen in AP-ROP? What can it cause?

A

No demarcation line, zone 1, can lead to RD

175
Q

What are the stages of prematurity in ROP screening? When must patients first be seen for each?

A

<32 weeks PMA: Term
27-32 weeks: 30-31 weeks PMA
<27 weeks (extreme): 32-35 weeks PMA

176
Q

How is ROP treated?

A

Mild ROP: Resolves itself
Laser, anti-VEGF
RD surgery

177
Q

How is ROP treated?

A

Mild ROP: Resolves itself

Laser, anti-VEGF

178
Q

What are the post laser sequelae for ROP?

A

Myopia, strabismus, amblyopia, glaucoma, retinal vessel dragging

179
Q

What forms of RD surgery are done for ROP?

A

Vitrectomy (oil/gas or scleral buckle)

Endoscopic VR surgery

180
Q

When can imaging be useful in paediatric ophthalmology?

A

Documenting, diagnosis, telemedicine, education, research, teaching, screening, EUA alternative

181
Q

What are the imaging challenges in paediatric ophthalmology?

A

Cooperation, attention, fatigue, positioning, photophobia, disabilities

182
Q

How are imaging challenges in paediatric ophthalmology overcome?

A

Quick, mobile devices, adjustable light intensity, good communication, parental support, prioritise, positioning. EUA

183
Q

When is external photography useful in paediatric ophthalmology?

A

Strabismus surgery outcome, disease progression, treatment analysis

184
Q

When is external photography useful in paediatric ophthalmology?

A

Recording surgical outcomes (strabismus)

Disease progression, treatment analysis

185
Q

What are the benefits of external photography in paediatric ophthalmology?

A

Readily available, easy, fast, cheap, non-contact, no cooperation needed, familiar, low light intensity

186
Q

What are the drawbacks of external photography in paediatric ophthalmology?

A

Flash causes shadow rings, limited, low magnification

187
Q

When is slit lamp photography used in paediatric ophthalmology?

A

Magnified, detailed or slit beam anterior segment images (cystinosis, MPS)

188
Q

What are the benefits of slit lamp photography in paediatric ophthalmology?

A

Video: Movement tolerated, recorded (Siedel’s test)
Flash: Brief, moderate light intensity, sharp, less movement artefact

189
Q

What are the drawbacks of slit lamp photography in paediatric ophthalmology?

A

Video: Intense light
Flash: Expensive, training, good cooperation needed

190
Q

How is corneal tomography done in paediatric ophthalmology? Which principle is used?

A

Placido-based systems (Pentacam)

Scheimpflug

191
Q

What does Pentacam measure?

A

Corneal thickness (pachymetry)

192
Q

When is Pentacam useful in paediatric ophthalmology?

A

Keratoconus, corneal/lens thickness, anterior chamber depth, some refractive surgeries

193
Q

What are the benefits and drawbacks of Pentacam use?

A

Pros: Fast, easy, non-contact, low light intensity
Cons: Cooperation needed

194
Q

What system is used for handheld digital fundus cameras?

A

RetCam

195
Q

How are digital fundus images captured?

A

White light ring on fundus, reflected light captured on charge coupled device

196
Q

What types of handheld digital fundus imaging are there?

A
Direct contact (video)
Anterior segment (goniophotography)
197
Q

What ocular structure does goniophotography highlight?

A

Iridocorneal angle

198
Q

When is digital fundus imaging used?

A

Documenting examination findings

Telemedicine

199
Q

What are the benefits and drawbacks of digital fundus imaging?

A

Pros: Both A/P segments seen, awake
Cons: Expensive, difficult to use, slow, cooperation needed

200
Q

How are anterior segment OCT images formed? What domains may be used?

A

Interferometry

Time domain, Fourier/spectral domain (swept source)

201
Q

When is anterior segment OCT used in paediatric ophthalmology?

A

Corneal issues, placing IOL’s/glaucoma draining tubes, corneal thickness, anterior chamber angle check

202
Q

What are the benefits and drawbacks of anterior segment OCT in paediatric ophthalmology?

A

Pros: Non-contact, fast, easy, light tolerated, flexible, eye tracking functions
Cons: Cooperation needed, expensive

203
Q

What are the forms of posterior segment imaging?

A

OCT, OPTOS/SLO, FFA, B-scan, RetCam

204
Q

What does OPTOS allow in terms of imaging?

A

Ultra-wide fundus imaging: 200 degrees field of view

205
Q

When is OPTOS used in paediatric ophthalmology?

A

Complex posterior uveitis, peripheral retinal disease

206
Q

What are the benefits and drawbacks of OPTOS in paediatric ophthalmology?

A

Pros: Non-contact, fast, undilated, high resolution
Cons: Cooperation needed, noise, not true colour

207
Q

How is fundus fluorescein angiography carried out?

A

Rapid fundus images following IV sodium fluorescein using fundus camera or SLO

208
Q

When is fundus fluorescien angiography useful in paediatric ophthalmology?

A

Assessing retina/choroid vasculature (Coat’s disease, CNV, uveitis)

209
Q

What risks are associated with fundus fluorescein angiography?

A

Anaphylaxis, injection risks

210
Q

Where is light focused in emmetropic eyes?

A

Directly onto the retina

211
Q

Where is light focused in hypermetropic eyes?

A

Behind the retina

212
Q

Where is light focused in myopic eyes?

A

In front of the retina

213
Q

Which spherical lenses correct myopia?

A

Concave (minus) lenses

214
Q

Which spherical lenses correct hypermetropia?

A

Convex (plus) lenses

215
Q

What is astigmatism?

A

Deviation from spherical curvature, rays do not meet at common focus, distorted vision, cylindrical lenses needed

216
Q

What occurs in accommodation?

A

Crystalline lens flat when distant focus, thickens for near objects

217
Q

What is presbyopia?

A

Accommodation loss with age

218
Q

What is aphakia?

A

Absence of the eye’s crystalline lens

219
Q

What % of neonates and 6-8y/o’s have spherical refraction of 2 and 1 respectively?

A

22%

35%

220
Q

What refraction type do most neonates have?

A

Hypermetropic (<3.00), decreases with age, 17mm

221
Q

How is a child’s prescription checked objectively?

A

Trial frame worn, room lights dimmed, distance fixation target (Thompson), retinoscopy determines lens power

222
Q

How is a child’s prescription checked subjectively? Which minimum age does it work best with?

A

Offer +/- lenses (push the +): Cross cyl to check astigmatic axis and power, 7+ y/o

223
Q

When is cycloplegic refraction needed?

A

For those whom it is difficult to obtain accurate subjective measurements from

224
Q

What agent is used for cycloplegic refraction?

A

Cyclopentolate 1%

225
Q

What are the benefits and drawbacks of cycloplegic refraction?

A

Pros: No accommodation,
easy cooperation
Cons: Invasive, acidic irritation, blurred vision for hours

226
Q

What are the benefits of refractive correction?

A

Preventing amblyopia/strabismus

Providing clear, binocular vision

227
Q

When is refractive correction prescribed for children of any age?

A

Extreme refractive errors
Strabismus/amblyopia
Anisometropia

228
Q

How is insignificant refractive error managed above and below 2 years old?

A

<2y/o: Monitor only

>2y/o: Monitor if refractive error not decreasing

229
Q

How is significant refractive error defined in those >2 years old?

A

> +3.00D hypermetropia (>+2.00 if no binocular issues), +2.50D astigmatism

230
Q

What can cause paediatric aphakia?

A

Congenital cataract, trauma, lens subluxation (Marfan’s, ectopia lentis)

231
Q

What is the corneal radius and axial length of eyes on average at birth?

A

Corneal radius: 6.9mm

Axial length: 17mm (21mm at 6/12 months)

232
Q

What prescription are aphakic paediatric spectacles?

A

+25DS to +15DS in 1st year of life

233
Q

What are the benefits and drawbacks of aphakic paediatric spectacles?

A

Pros: No infection risk, well-tolerated
Cons: Challenging if unilateral, expensive, easily break, poor cosmesis

234
Q

What are the benefits and drawbacks of paediatric contact lenses?

A

Pros: Light, easy upon insertion better unilaterally, good cosmesis
Cons: Infection/abrasion risk, difficulty inserting, easily taken out

235
Q

Which paediatric aphakic lenses are currently in use?

A

Silicone hydrogel lenses (Ultravision)

236
Q

What are benefits and drawbacks of silicone hydrogel paediatric contact lenses?

A

Pros: Flexible, stable, less corneal hypoxia risk
Cons: Red/sticky eyes, handling, lens loss, de-centering, compliance

237
Q

What is the aftercare involved with paediatric contact lenses?

A

Addressing issues, compliance, lens fit/centration, over-refraction, gross corneal examination (Burton or slit-lamp)

238
Q

What refractive correction is prescribed for aphakic infants?

A

Until mobile/toddling: +2.00D overcorrection (CL’s/glasses)
Toddlers: +1.00D overcorrection
Preschool: Distance correction with CL’s/bifocals, add +3.00D for near work

239
Q

How many individuals worldwide suffer from childhood blindness? How many in the UK aged under 18?

A

1.4 million globally

UK visual loss <18y/o: 28000

240
Q

What is included with Low Vision Assessment Clinic appointment letters?

A

Parent/guardian questionnaire covering education, school, support, QTVI hours, font size, etc.

241
Q

What is involved in Low Vision Assessment histories?

A

Who supports child, health concerns, mobility/orientation, TV/reading/playing issues, interaction with others

242
Q

What low vision aids are available in schools?

A

Larger font, sit at front of class, sloping boards, contrast/lighting, magnifiers (Fresnel)

243
Q

What does QTVI stand for?

A

Qualified Teacher of the Visualy Impaired

244
Q

How is distance visual acuity assessed?

A

Monocular (worse eye first) then binocularly start at easier distance
Appropriate test: LogMAR/Snellen/Lea symbols

245
Q

How is near visual acuity assessed?

A

Binocular: Symbols/words/sentences with M or N notation

246
Q

Why is assessing only visual acuity insufficient? What visual factors should also be considered?

A

Determining effect on daily tasks difficult

Contrast sensitivity, colour vision, visual fields

247
Q

How are contrast sensitivity and colour vision tested in children?

A

Contrast: Hiding Heidi
Colour: Panel 16 Quantitative Colour Vision test (adult: D15)

248
Q

Which conditions can reduce contrast sensitivity?

A

Visual pathway issues, cataract, glaucoma, optic atrophy, macular/retinal dystrophies, amblyopia

249
Q

Which techniques are used for visual field tests? Which strategies are used for central and peripheral scotomas

A

Goldmann techniques
Central: Optimal reading
Peripheral: Enhancement

250
Q

Which near vision/reading and distance magnifiers are available?

A

Near: Bar/Brightfield, handheld, stand, illuminated
Distance: Binoculars

251
Q

What does P-EVES stand for in terms of low vision aids?

A

Portable Electronic Vision Enhancement

252
Q

How is strabismus defined? What impairment may it highlight?

A

Misalignment of the eyes, visual axes are not simultaneously directed at the object in one or all directions
Loss of binocular vision

253
Q

What are the Worth’s classification grades of binocular vision?

A

I: Simultaneous macular perception, II: Fusion, III: Stereopsis

254
Q

What are the horizontal forms of ocular deviation?

A

Esotropia (inward), exotropia (outward)

255
Q

What are the vertical forms of ocular deviation?

A

Hypertropia (upward), hypotropia (downward)

256
Q

What affects the extent of misalignment in comitant squints?

A

Accommodation

257
Q

What factors determine squint classification?

A

Deviation direction, duration, comitancy, refraction, accommodative effort, fixation distance, strabismus surgery, visual status

258
Q

What ocular consequences can squints cause?

A

Diplopia, suppression, amblyopia, psycho-social issues (e.g. bullying)

259
Q

What occurs in suppression due to squint?

A

Brain ignores image from deviating eye, common in <7y/o’s

260
Q

How is amblyopia defined?

A

Reduced visual acuity in the absence of physical eye abnormalities

261
Q

How is amblyopia treated?

A

Patching good eye, atropine, near objects

262
Q

What is the difference between a ‘tropia’ and a ‘phoria’?

A

A ‘tropia’ occurs when both eyes are uncovered, a ‘phoria’ occurs for covered eye(s)

263
Q

What is nystagmus?

A

Involuntary movement of the eyes

264
Q

What types of nystagmus are there?

A

Manifest (always)
Latent (covered)
Manifest-latent

265
Q

How should manifest-latent nystagmus be treated?

A

Atropine

266
Q

When does infantile esotropia occur? At which angle and refraction?

A

<6 months old
Moderate angle
Normal refraction

267
Q

What is cross fixation?

A

Fixation between eyes switches when object moves between L and R visual fields

268
Q

How are cover tests carried out?

A

Cover fixing eye, other eye visual axis straightens

269
Q

If there is a right hypertropia what tropia is usually seen in the left eye?

A

Hypotropia?

270
Q

What is Dissociated Vertical Deviation? Which tropia is most common in this?

A

When only one eye moves during a cover test in vertical squints
95% hypertropia

271
Q

What are the two types of accommodative esotropia?

A

Refractive

Non-refractive

272
Q

When do children develop the ability to accommodate?

A

> 1 years old

273
Q

Which other tropia is refractive accommodative esotropia linked with? How is it treated?

A

Hypermetropia

Spectacles (bifocals if convergence excess)

274
Q

What eye movement issue is seen in non-refractive accommodative esotropia?

A

Convergence excess (high AC/A ratio)

275
Q

When does exotropia usually present? What refraction and angle is seen?

A

Adulthood
Normal refraction
Large angle

276
Q

What affects intermittent exotropia?

A

Distance, concentration, bright light (loss of fusion)

277
Q

How are macular stress tests carried out?

A

Shine bright light in patient’s eye then test visual acuity

278
Q

When does sensory exotropia occur?

A

Drops in visual acuity (e.g. cataract)

279
Q

In paralytic strabismus, what ocular issues do CN III, IV and VI palsies cause?

A

III: Ptosis, mydriasis, exotropia, hypotropia
IV: Hypertropia
VI: Esotropia

280
Q

What is another term for incomitant esotropia?

A

Brown’s syndrome

281
Q

What can cause incomitant esotropia?

A

CN VI palsy, Duanes syndrome, medial orbital floor fracture, myasthenia gravis, myositis, thyroid myopathy

282
Q

What is Duane’s syndrome

A

Abnormal extraocular muscle co-contraction

283
Q

How is incomitant esotropia managed?

A

Examination, refraction, ocular deviation stability, surgery (medial recti), 2-3 botox injections

284
Q

Which are the key laws of eye movement?

A

Sherrington’s (reciprocal innervation)

Hering’s (equal innervation)

285
Q

What tests are carried out during strabismus surgery?

A

Forced duction/resistance test under local or general anaesthesia for passive eye movement

286
Q

What is the manoeuvre which tests CN VI function? How is it carried out?

A

Doll’s head manoeuvre

Move head to one side, eye should remain fixed

287
Q

How is hypermetropic esotropia treated?

A

Spectacles, variable patching

288
Q

What are the terms used for pathological and non-pathological DNA variants?

A

Pathological: Mutation

Non-pathological: Polymorphism

289
Q

How are DNA variants scaled?

A

Benign, uncertain, pathogenic

290
Q

What types of DNA changes are there?

A

Substitutions (SNP’s)
Insertions/deletions
Splice site changes
Structural/chromosomal

291
Q

Which inheritance types involve a single gene or multiple components?

A

Mendelian

Multifactorial

292
Q

What are the 3 main types of Mendelian inheritance?

A

Autosomal
X-linked
Mitochondrial

293
Q

Which tables are used to calculate inheritance patterns?

A

Punnett squares

294
Q

What are the types of autosomal inheritance? How many alleles can lead to disease and what are the inheritance chances for each?

A

Dominant: 1 allele needed, 50% chance
Recessive: Both alleles needed, 25% chance

295
Q

In X-linked inheritance which sex displays the disease phenotype?

A

Males

296
Q

X-linked recessive case: Affected dad, unaffected mum. What are the son/daughter phenotypes?

A

Unaffected sons

Carrier daughters

297
Q

X-linked recessive case: Unaffected dad, carrier mum. What are the son/daughter phenotypes?

A

50% affected sons

50% carrier daughters

298
Q

Mitchondrial inheritance is from which parent? Which sex does it affect?

A

Always from mother

Both sexes affected

299
Q

What is penetrance?

A

The extent to which those with the disease genotype express the phenotype

300
Q

What is consanguinity? What risk to offspring is there? What inheritance pattern is it linked with?

A

Parents being related as second cousins or closer, genetic mutation risk, autosomal recessive

301
Q

Which inheritance pattern is suggested by 1 parent affected, 50% offspring affected?

A

Autosomal dominant

302
Q

Which inheritance pattern is suggested by unaffected parents, rarely affected offspring?

A

Autosomal recessive

303
Q

Which inheritance pattern is suggested by severely affected males, no male-to-male transmission?

A

X-linked recessive

304
Q

Which inheritance pattern is suggested by no male-to-male transmission, affected mothers producing affected/carrier offspring?

A

Mitochondrial

305
Q

What are the typical inheritance patterns of simplex or sporadic cases?

A

Usually autosomal recessive, dominant if less family history or de novo, males: X-linked?

306
Q

What % of childhood visual impairment is accounted for by inherited eye disease?

A

33%

307
Q

What types of inherited eye disease are seen?

A

Structural globe (6%), anterior segment (11%), retinal (14%), albinism (4%)

308
Q

Which 3 inherited structural globe abnormalities are seen in the eye?

A

Anophthalmia
Microphthalmia
Coloboma

309
Q

What horizontal corneal diameter indicates microphthalmia? How is it investigated?

A

<1cm

Ultrasound

310
Q

What is a coloboma? What causes it?

A

Absence of an ocular tissue in the eye

Optic fissure non-closure in week 6 of development

311
Q

What is investigated in a MAC (micro/anophthalmia/coloboma) assessment?

A

Corneal diameter
USS, CT/MRI
Cryptophthalmia (fused eyelids)

312
Q

What are 6 anterior segment developmental abnormalities?

A
Posterior embryotoxon
Axenfield-Rieger syndrome
Peter’s anomaly
Aniridia
Paediatric glaucoma
Congenital cataracts
313
Q

What abnormalities often occur alongside iris malformation?

A

Dental, navel abnormalities

314
Q

What causes posterior embryotoxon?

A

Descemet’s membrane ends anteriorly (10-15%)

315
Q

What makes up Axenfeld-Rieger syndrome?

A

Axenfeld anomaly: Anterior iris strands

Rieger anomaly: Iris hypoplasia

316
Q

What is Peter’s anomaly?

A

Central corneal opacity, irido/lenticulocorneal adhesions

317
Q

What are the features of aniridia?

A

Iris/fovea hypoplasia, nystagmus, peripheral corneal opacity

318
Q

Which tumour is linked to aniridia? How is it investigated?

A

Wilm’s tumour

Abdominal ultrasound

319
Q

What causes paediatric glaucoma?

A

Primary: Trabeculodysgenesis
Secondary: Post-cataract surgery

320
Q

What features are seen in paediatric glaucoma?

A

Lacrimation, blepharospasm, photophobia

Corneal opacities

321
Q

What % of congenital cataracts are bilateral and isolated?

A

66% bilateral, 55% isolated

322
Q

What commonly causes unilateral congenital cataracts?

A

Hyperplastic primary vitreous

323
Q

When are congenital cataracts referred?

A

Infection, biochemical or metabolic disorders

324
Q

What cause of congenital cataracts warrants genetic testing?

A

Cancer (70% diagnosis if bilateral)

325
Q

What congenital cataracts occur in the lens of the eye?

A

Nuclear (yellow/brown), lamellar/zonular

external to lens nucleus

326
Q

What type of cataract occurs in the posterior lens? What can it cause? How is it treated?

A

Polar cataract
Amblyopia risk
Vitreo-retinal surgery

327
Q

What causes oil-droplet cataracts?

A

Galactosaemia

328
Q

How do cortical cataracts appear?

A

White wedge opacities extending spoke-like from lens periphery to centre

329
Q

Which structures do inherited retinal diseases often affect? What are the two main types?

A

Rods, cones, RPE
Stationary (dysfunction)
Progressive (dystrophy)

330
Q

How do stationary and progressive inherited retinal disorders differ in onset, fundus and extraocular appearance?

A

Stationary: Congenital, normal fundus, rarely extraocular
Progressive: Variable age, abnormal fundus, some extraocular

331
Q

What is affected in stationary cone>rod disorders? What condition does it cause?

A

Colour vision

Achromatopsia

332
Q

What are the main progressive inherited retinal disorders?

A

Stargardt disease (AR)
Retinitis pigmentosa
Leber’s congenital amaurosis, SECORD, Best disease, gyrate atrophy

333
Q

How does Stargardt disease present?

A

Bullseye appearance around macula, hyper-AF flecks, VA drop

334
Q

How does Stargardt disease present?

A

Bullseye appearance around macula, hyperAF flecks, decreased VA

335
Q

What is retinitis pigmentosa? How does it present?

A

Rod-cone dystrophy, peripheral RPE dysfunction

Early life nyctalopia

336
Q

In which inherited retinal disorders are both rods and cones affected? How do they present?

A

LCA, SECORD, Best disease, gyrate atrophy

Severe VA drop, nystagmus, initial normal fundus

337
Q

What is albinism?

A

Non-degenerative disorder of melanin production/transport

338
Q

How does albinism present in the eye?

A

Nystagmus, VA drop, iris/retina hypopigmentation, foveal hypoplasia

339
Q

In which day of gestation does eye development begin? By which week are the main structures formed?

A

Day 22

Week 5

340
Q

By which week of gestation are precursors of retinal cells present and final ocular structures formed?

A

Week 8

341
Q

Which ocular structures are formed in month 4 of gestation?

A

Retinal vessels
Iris, ciliary body
Canal of Schlemm

342
Q

From months 5-8 of gestation what ocular developments occur?

A

5: Eyelids separate
6: Nasolacrimal duct forms
7: Optic nerve myelination
8: Anterior chamber forms

343
Q

Which years are described as the critical period of vision maturation?

A

5-7 years old

344
Q

Which years are described as the critical period of vision maturation?

A

5-7 years

345
Q

By which age can pupils react to light?

A

From birth

346
Q

By what age can pupils react to light?

A

From birth

347
Q

By 6 months old how developed is light sensitivity compared to adult levels? By which age is it fully developed?

A

2/3rd of adult levels

12-14 years old

348
Q

By which age ranges is central vision good enough to (a.) react to faces, (b.) distinguish objects, (c.) shapes, (d.) drawn images?

A

(a. ) 4-6 months old
(b. ) 2-3 months old
(c. ) 7-10 months old
(d. ) 2-3 years old

349
Q

When does colour perception begin and then fully develop? Which colours are recognised first?

A

2-6 months old
4-5 years old
Red, blue then green

350
Q

How much narrower is field of view at pre-school age than adulthood? By which age is at adult levels?

A

10%

School age

351
Q

How much larger are blind spots at school age than adulthood from 1m away?

A

2-3cm larger

352
Q

Which is the last visual function to develop? What does it allow perception of?

A

Binocular vision

Allows 3D perception

353
Q

At which ages are (a.) 2D, (b.) depth through touch, (c.) direction, (d.) distance, (e.) stereopsis perceived?

A

(a. ) 2 months old
(b. ) 3 months old
(c. ) 4 months old (grasp reflex)
(d. ) 6 months old (crawling)
(e. ) 2-7 years old

354
Q

What are the 3 requirements for stereopsis (ability to see in 3D)?

A

Simultaneous perception
Sensory fusion
Motor fusion

355
Q

What stereopsis tests are there?

A

Wirt (Titmus)
Lang Stereo Test
Frisby
TNO

356
Q

How might a child’s 3D vision not develop?

A

Squint before 6 months old, eyes cannot straight

357
Q

When is the critical age range to test children’s vision?

A

Birth-7.5 years old

358
Q

How would you test visual acuity in babies/infants?

A

Preferential looking
Fixing and following (<1 month)
Objection to occlusion (>3 months)
Picking up fine objects (>6 months)

359
Q

How is fixing and following tested?

A

Bright light/toy, 33-50cm away, neither or 1 eye occluded

360
Q

What are the main preferential looking tests used to test visual acuity in babies/infants?

A

Keeler
Teller (1974)
Cardiff (Woodhouse, 1994)

361
Q

What is observed in fixing and following?

A

Position, persistence, steadiness, speed

362
Q

Which preferential looking tests involves black and white stripes on (a.) circular, (b.) square grating patterns?

A

(a. ) Keeler acuity cards

(b. ) Teller acuity cards

363
Q

Which preferential looking test involves vanishing optotypes on grey cards tested from 50cm or 1m away?

A

Cardiff acuity cards

364
Q

What are the benefits of preferential looking tests and Cardiff cards?

A

Detects gross amblyopia

Monitor treatment progress for e.g. cataracts, strabismus

365
Q

What are the limitations of preferential looking tests and Cardiff cards?

A

Overestimates vision, interest/fatigue/looking speed vary, guessing (repeating helps), observer bias

366
Q

How do you test fine stimulus response in babies?

A

Hundreds and thousands test

367
Q

What is the Kay picture test (1983)?

A

Visual acuity test for those aged 2-3, 3-4 objects per page at each acuity level from 6m away

368
Q

How would you test visual acuity in children >2 years old?

A

Kay picture test

Cardiff acuity cards

369
Q

How would you test visual acuity in children >3/4 years old?

A

Kay picture test
Sheridan-Gardiner test
LogMAR
Keeler logMAR

370
Q

Which visual acuity test is aimed at amblyopic children?

A

Keeler logMAR

371
Q

Which visual acuity test for those aged 2-5 involves matching single optotypes from 3m or 6m away?

A

HOVT or Sheridan-Gardiner test

372
Q

Which variant of the Sheridan-Gardiner test uses multiple optotypes?

A

Sonksen-Silver logMAR test

373
Q

How would you test visual acuity in children >5 years old?

A

Snellen chart

375
Q

What are the test age ranges for (a.) fixing and following, (b.) preferential looking, (c.) Cardiff cards?

A

(a. ) 2-3 months old
(b. ) 2 months-1 year old
(c. ) 1-2.5 years old

376
Q

What are the test age ranges for (a.) Crowded Kays, (b.) Keeler LogMAR (crowded), (c.) LogMAR/Snellen’s?

A

(a. ) 2.5-3.5/4 years old
(b. ) 4-5/6 years old
(c. ) >5-6 years old

377
Q

What shoud be considered in suspected non-accidental head injuries?

A

Not necessarily abuse?
Medicolegal issues
Child protection

378
Q

What are the most common abuse-related eye injuries?

A

Subluxation of the lens

Orbital fractures

379
Q

How might abuse-related eye injuries present?

A

Bruising (e.g. near ears), behaviour change (encephalopathy?), emesis, squint

380
Q

How might brainstem injury present?

A

Sun-setting: Eyelids retract, down-facing pupils, superior sclera visible

381
Q

What types of retinal haemorrhages are there?

A

Pre-retinal (under fovea), flame (retinal nerve fibre layer), dot and blot (deep retinal)

382
Q

Non-accidental head injury and birth are the only causes of what?

A

Multiple retinal haemorrhages without disease or severe trauma

383
Q

What can cause retinal haemorrhages?

A

High ICP
Post-partum hypoxia
Newborn haemolytic disease (vitamin K deficiency)
Coagulation disorders

384
Q

Which studies suggested retinal haemorrhages are insufficient to diagnose non-accidental head injuries?

A

Geddes III

CONI study

385
Q

What ocular features suggest brain injury or optic nerve damage?

A

Unreactive pupils, RAPD

386
Q

How are paediatric head injuries assessed in ophthalmology?

A

Pre: MRI (haemorrhages or fractures)

RetCam, direct ophthalmoscopy after eye drops instilled

387
Q

How does Shaken Baby Syndrome present?

A

Hypoxia
Low venous pressure
Vitreous shearing, traction, retinal haemorrhages (flame)

388
Q

Which courts address suspected non-accidental head injury cases?

A

City County Court

389
Q

What occurs in suspected non-accidental head injury court proceedings? How long do these last?

A

Single joint expert witness (or treating clinician) assesses trier of fact
26-week track