24. Visual disturbance/impairment Flashcards

1
Q

differentials for sudden vision loss

A

ischaemic/vascular
- retinal vein occlusion
- retinal artery occlusion: TIA/stroke/giant cell arteritis
- anterior ischaemic optic neuropathy: TIA/stroke/giant cell arteritis

  • vitreous haemorrhage
  • retinal detachment
  • acute angle closure glaucoma
  • optic neuritis
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2
Q

differential for gradual vision loss?

A

Refractive error
Cataracts
Macular degeneration
Chronic (open angle) glaucoma
Diabetic retinopathy
Hypertensice retinopathy

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3
Q

differentials for diplopia

A

eye muscle problem:
- myasthenia gravis
- graves
- strabismus

neurological:
- head injury
- stroke
- migraine
- tumour
- wernikes

Nerve problem (eg 3rd CN, 4th CN or 6th CN)
- diabetes
- congenital
- raised ICP
- MS
- guilian barre

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4
Q

examination vision loss

A

Inspection: is it RED (acute angle closure)

Optic nerve: acuity, visual fields, attention, accommodation, pupils, colour vision
- Pupil unreactive/not responding/ well to light/RAPD suggests optic nerve dysfunction therefore could be due to anterior optic neuropathy (GCA or TIA), optic neuritis etc

Eye movements: H test, any double vision? any pain on movement? (any CN palsys?)

To complete…
Opthalmoscopy
HbA1c, BP
Referral for slit lamp examination

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5
Q

what should you be able to label on fundoscopy

A

optic disc
optic cup

macula
fovea

retinal vein
retinal artery (thinner than veins)

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6
Q

history taking vision loss/disturbance

A

PC: onset? sudden? is the vision loss in one portion of your vision? eg the sides or the middle etc. floaters/flashes?

HoPC: PAIN?? - suggests acute angle closure glaucoma. pain on eye movement? (optic neuritis), do colours look the same? (loss of red in optic neurtis)

Associated symptoms: headache especially near temples?(GCA) weakness?

SHx:
eye trauma e.g. boxing, ask about occupation and hobbies

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7
Q

what is amaurosis fugax? causes

A

Amaurosis fugax describes a temporary loss of vision caused by a temporary interruption to the blood supply - like a curtain coming down…

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8
Q

causes of amaurosis fugax?

A

ischaemic/vascualr causes of sudden vision loss eg

Retinal vein occlusion
Retinal artery occlusion: TIA/stroke/GCA
Anterior ischaemic optic neuropathy: TIA/stroke/GCA
Giant-cell arteritis

As this may represent a TIA, 300mg aspirin is given

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9
Q

central retinal vein occlusion

presentation
causes
examination
fundoscopy
management

A

presentation: sudden, painless, reduction or loss in visual acuity, unilateral

causes:
Risk factors
increasing age
hypertension
cardiovascular disease
glaucoma
polycythaemia

examination: reduced visual acuity

fundoscopy:
“stormy sunset” multiple haemorrhages

management:
majority conservative
if macualr oedema, consider VGEF

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10
Q

central retinal artery occlusion

presentation
examination
fundoscopy
management

A

presentation:
sudden, painless, unilateral vision loss

examiantion: RAPD

causes:
TIA/stroke/GCA

fundoscopy
‘cherry red’ spot on a pale retina

management:
think of it as TIA/stroke/GCA
–> any underlying conditions should be identified and treated (e.g. intravenous steroids for temporal arteritis)

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11
Q

Anterior ischaemic optic neuropathy

presentation
causes
examination
fundoscopy
management

A

presentation: loss of vision

causes: TIA/stroke/GCA

examination: RAPD

fundoscopy: swollen pale disc and blurred margins

management:
think of it as TIA/stroke/GCA
–> any underlying conditions should be identified and treated (e.g. intravenous steroids for temporal arteritis)

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12
Q

vessel occluded in AION

A

posterior ciliary artery

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13
Q

cherry red spot

A

central retinal artery

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14
Q

blood supply optic nerve

A

central retinal artery

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15
Q

“stormy sunset” multiple haemorrhages

A

central retinal vein occlusion

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16
Q

Giant cell arteritis causing visual symptoms

presentation
examination
fundoscopy
management

A

PC: decreased visual acuity, temporal headache

examination: reduced visual acuity, tenderness over temple

fundoscopy: Retinal splinter haemorrhages or disc oedema. AION swollen pale disc and blurred margins.

management:
medical emergency due to risk of
- stroke
- blindness (a strple affecting the retinal vessels, optic nerve) - 90% AION (Anterior Ischemic Optic Neuropathy)

phone rheum on-call

Should have confirmatory test: USS halo sign or temporal artery biopsy

Initial
1. High dose oral glucocorticoids eg oral methylprednisolone

With visual loss:
1. IV methylprednisolone
+ Urgent ophthalmology review
+ Bone protection for steroids

refractory/relapsing : tocilizumab

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17
Q

vitreous haemorrhage

presentation
causes
examination
fundoscopy
management

A

presentation: painless vision loss, dark spots obscuring vision with a red hue

causes:
- DIABETES, bleeding disorders, anticoagulants

examination: decreased visual acuity, visual field defect if severe haemorrhage

dilated fundoscopy: may show haemorrhage in the vitreous cavity

if new onset rf urgently (<24hrs) for slit-lamp examination,
other stuff may be used eg:
ultrasound: useful to rule out retinal tear/detachment and if haemorrhage obscures the retina
fluorescein angiography: to identify neovascularization
orbital CT: used if open globe injury

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18
Q

retinal detachment

presentation
causes
examination
fundoscopy
management

A

PC: vision loss, curtain or shaddow progressing to the centre from the periphery, floaters or flashes,

risk factors
diabetes mellitus
myopia
age
previous surgery for cataracts
eye trauma e.g. boxing

examination

fundoscopy
the red reflex is lost and retinal folds may appear as pale, opaque or wrinkled forms
if the break is small, however, it may appear normal.

It is a reversible cause of visual loss, provided it is recognised and treated before the macula is affected.

rf urgently

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19
Q

plan pt with new onset flashes and floaters

A

Arrange immediate referral to an ophthalmologist with retinal surgery expertise to be seen on the same day, if there are signs of sight-threatening disease, such as:
- Visual field loss or changes in visual acuity.
- Fundoscopic signs of retinal detachment or vitreous haemorrhage.

any patients with new onset flashes and floaters WITHOUT VISUAL/FUNDOSCOPY CHANGES should be referred urgently (<24 hours) to an ophthalmologist for assessment with a slit lamp and indirect ophthalmoscopy for:

pigment cells

vitreous haemorrhage

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20
Q

posterior vitreous detachment

presentation
causes
examination
fundoscopy
management

A

presentation: no vision loss, floaters, flashes, blurred vision, cobwebs

causes:
ageing
myopia

fundoscopy: weiss ring

Investigations:
All patients with suspected vitreous detachment should be examined by an ophthalmologist within 24hours to rule out retinal tears or detachment.

Management:
Posterior vitreous detachment alone does not cause any permanent loss of vision. Symptoms gradually improve over a period of around 6 months and therefore no treatment is necessary.
If there is an associated retinal tear or detachment the patient will require surgery to fix this.

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21
Q

optic neuritis

presentation
causes
examination
fundoscopy
management

A

PC: unilateral decrease in visual acuity over hours or days
poor discrimination of colours, ‘red desaturation’
pain worse on eye movement
central scotoma

causes:
multiple sclerosis: the commonest associated disease
diabetes
syphilis

examiantion: relative afferent pupillary defect

Mangement
MRI of the brain and orbits with gadolinium contrast is diagnostic in most cases

high-dose steroids
recovery usually takes 4-6 weeks

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22
Q

most common cause of blindness in the UK

A

Age-related macular degeneration

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23
Q

what is age related macualr degenertaion

A

Degeneration of the central retina (macula) is the key feature with changes usually bilateral.

ARMD is characterised by degeneration of retinal photoreceptors that results in the formation of drusen which can be seen on fundoscopy and retinal photography. It is more common with advancing age and is more common in females.

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24
Q

fundoscopy how is wet AMD different to dry? pathophysiology

A

In wet AMD, new vessels develop from the choroid layer and grow into the retina (neovascularisation). These vessels can leak fluid or blood, causing oedema and faster vision loss. A key chemical that stimulates the development of new vessels is vascular endothelial growth factor (VEGF). This is the target of medications to treat wet AMD.

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25
Q

which is more common wet or dry AMD?

A

dry = 90%

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26
Q

risk factors macualr degeneration

A

Older age
Smoking
Family history
Cardiovascular disease (e.g., hypertension)
Obesity
Poor diet (low in vitamins and high in fat)

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27
Q

dry and wet AMD

compare presentation

A

Presentation:
both:
- vision loss- reduction in visual acuity particualrly for close objects
- difficulties in dark adaptation
- fluctuations in visual disturbance
- visual hallucinations may also occur resulting in Charles-Bonnet syndrome
- photopsia, (a perception of flickering or flashing lights), and glare around objects

gradual in dry ARMD
subacute in wet ARMD
Wet AMD presents more acutely than dry AMD. Vision loss can develop within days and progress to complete vision loss within 2-3 years. It often progresses to bilateral disease.

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28
Q

differentiating AMD and glaucoma presentation

A

Glaucoma is associated with peripheral vision loss and halos around lights. AMD is associated with central vision loss and a wavy appearance to straight lines. This helps you tell them apart in exams

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29
Q

examination and fundoscopy ARMD

A

Reduced visual acuity using a Snellen chart
Scotoma (an enlarged central area of vision loss)
Amsler grid test can be used to assess for the distortion of straight lines seen in AMD
Drusen may be seen during fundoscopy

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30
Q

what invetsigation is useful for wet
ARMD

A

Fluorescein angiography involves giving a fluorescein contrast and photographing the retina to assess the blood supply, showing oedema and neovascularisation in wet AMD.

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31
Q

management wet ARMD

A

Anti-VEGF medications

laser photocoagulation but is more risky

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32
Q

management dry ARMD

A

Management involves monitoring and reducing the risk of progression by:
Avoiding smoking
Controlling blood pressure
Vitamin supplementation has some evidence in slowing progression

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33
Q

what are cataracts

A

A cataract is a common eye condition where the lens of the eye gradually opacifies i.e. becomes cloudy. This cloudiness makes it more difficult for light to reach the back of the eye (retina), thus causing reduced/blurred vision

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34
Q

causes of cataracts

A

Normal ageing process: most common cause

Other possible causes
Smoking
Increased alcohol consumption
Trauma
Diabetes mellitus
Long-term corticosteroids
Radiation exposure
Myotonic dystrophy
Metabolic disorders: HYPOCALCAEMIA

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35
Q

presentation cataracts

A

Reduced vision
Faded colour vision: making it more difficult to distinguish different colours
Glare: lights appear brighter than usual
Halos around lights

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36
Q

o/e cataracts

A

A Defect in the red reflex: the red reflex is essentially the reddish-orange reflection seen through an ophthalmoscope when a light is shone on the retina. Cataracts will prevent light from getting to the retina, hence you see a defect in the red reflex.

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37
Q

invetsigations catracts

A

Ophthalmoscopy: done after pupil dilation. Findings: normal fundus and optic nerve

Slit-lamp examination. Findings: visible cataract

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38
Q

management cataracts

A

conservative: stronger glassess, use brighter lights

surgical
This involves removing the cloudy lens and replacing this with an artificial one. NICE suggests that referral for surgery should be dependent upon whether a visual impairment is present, impact on quality of life, and patient choice

39
Q

complications post-cataracts surgery

A

Posterior capsule opacification: thickening of the lens capsule
Retinal detachment
Posterior capsule rupture
Endophthalmitis: inflammation of aqueous and/or vitreous humour

40
Q

define glaucoma

A

Glaucoma refers to the optic nerve damage caused by a rise in intraocular pressure.

41
Q

risk factors for open-angle glaucoma

A

Increasing age
Family history
Black ethnic origin
Myopia (nearsightedness)

42
Q

presentation open angle glaucoma

A

Glaucoma affects the peripheral vision first, resulting in a gradual onset of peripheral vision loss (tunnel vision). It can also cause:
Fluctuating pain
Headaches
Blurred vision
Halos around lights, particularly at night

43
Q

gold standard way to measure intraocualr pressure

A

Goldmann applanation tonometry

It involves a device mounted on a slip lamp that makes contact with the cornea and applies various pressures.

44
Q

investgations open angle glacuoma

A

Goldmann applanation tonometry for the intraocular pressure
Slit lamp assessment for the cup-disk ratio and optic nerve health
Visual field assessment for peripheral vision loss
Gonioscopy to assess the angle between the iris and cornea
Central corneal thickness assessment

45
Q

when is treatment indicated for open angle closure glaucoma

A

intraocular pressure of 24 mmHg or above.

46
Q

management open angle closure glaucoma

A
  1. 360° selective laser trabeculoplasty (lazer hole to improve drainage of aqueous humour…delays need for eye drops)
  2. Prostaglandin analogue eyedrops (e.g., latanoprost) are the first-line medical treatment. They increase uveoscleral outflow. Notable side effects are eyelash growth, eyelid pigmentation and iris pigmentation (browning).

the next line of treatments includes:
beta-blocker eye drops
carbonic anhydrase inhibitor eye drops
sympathomimetic eye drops
surgery in the form of a trabeculectomy may be considered in refractory cases.

47
Q

adverse effects of miotics such as pilocarpine

A

constricted pupil, headache and blurred vision

48
Q

adverse effects of prostaglandin analogues eg latanoprost

A

brown pigmentation of the iris, increased eyelash length

49
Q

who shouldn’t get beta blocker eye drops (e.g. timolol, betaxolol)

A

Should be avoided in asthmatics and patients with heart block

50
Q

most common cause of blindness in adults adults aged 35-65 years-old?

A

diabetic retinopathy

51
Q

types ofclassification of dianetic retinopathy

A

non-proliferative diabetic retinopathy (NPDR)

proliferative retinopathy (PDR)

Maculopathy.

52
Q

characteristics of non-proliferative diabetic retinopathy - fundoscopy

A

microaneurysms
blot haemorrhages
hard exudates
cotton wool spots
venous bleeding
Intraretinal microvascular abnormalities (precursor to neovascularisation)

53
Q

characteristics of proliferative diabetic retinopathy - fundoscopy

A

retinal neovascularisation - may lead to vitrous haemorrhage
fibrous tissue forming anterior to retinal disc

54
Q

what type of diabetic retinopathy is more common in type 1 DM

A

PROLIFERATIVE

more common in Type I DM, 50% blind in 5 years

55
Q

characteristics of maculopathy in diabetic retinopathy

A

hard exudates and other ‘background’ changes on macula

check visual acuity

56
Q

management diabetic retinopathy for all patients

A

All patients:
optimise glycaemic control, blood pressure and hyperlipidemia
regular review by ophthalmology

57
Q

managemet maculopathy diabetic retinopathy

A

if there is a change in visual acuity then intravitreal vascular endothelial growth factor (VEGF) inhibitors

58
Q

management non-prolifertaive diabetic retinopathy

A

non-prolifertive:
regular observation
if severe/very severe consider panretinal laser photocoagulation

59
Q

management prolifertaive dianetoc retinopathy

A

prolifertaive:
panretinal laser photocoagulation
+/- intravitreal VEGF inhibitors

60
Q

complications panretinal laser photocoagulation

A

following treatment around 50% of patients develop a noticeable reduction in their visual fields due to the scarring of peripheral retinal tissue
other complications include a decrease in night vision (rods are predominantly responsible for vision in low light conditions, the majority of rod cells are located in the peripheral retina), a generalised decrease in visual acuity and macular oedema

61
Q

example of intravitreal VGEF inhibitor

A

ranibizumab

62
Q

stages of hypertensive retinopathy

A

SAC papilloedema

Stages:
1. S = silver wiring (increased light reflex) and arteriolar narrowing
2. A = arteriovenous nipping
3. C = cotton wool exudates and flame and blot haemorrhages
4. Papilloedema

63
Q

Contralateral hemiparesis and sensory loss, upper extremity > lower, Contralateral homonymous hemianopia, Aphasia

A

Middle cerebral artery

64
Q

Contralateral homonymous hemianopia with macular sparing, Visual agnosia

A

Posterior cerebral artery

65
Q

contralateral hemiparesis/hemisensory loss of face arma dn leg, higher cog dysfunction such as aphasia, homonymous hemianopia

A

total anteroir ciruclation infact, if only 2 = partial

66
Q

Bitemporal hemianopia

A

Midline lesion at chiasm

upper quadrant defect > lower quadrant defect = inferior chiasmal compression, commonly a pituitary tumour

lower quadrant defect > upper quadrant defect = superior chiasmal compression, commonly a craniopharyngioma

67
Q

Right nasal hemianopia

A

Lesion involving right perichaismal area

68
Q

Left homonymous hemianopia

A

Lesion or pressure on right optic tract (posterior to chiasm, before optic radiations)

Lesion or pressure across all right optic radiations

69
Q

Left homonymous hemianopia with macular sparing

A

Lesion in right occipital lobe (both banks of calcarine fissure) posterior cerebral artery

70
Q

Left superior homonymous quadrantanopia

A

PITS = parietal inferior, temporal superior therefore;
Temporal as superior

Right sided tract

Lesion to the right inferior optic radiations in the temporal lobe (meyer’s loop)

71
Q

Right inferior homonymous quadrantanopia

A

PITS = parietal inferior, temporal superior therefore;
Parietal as inferior

Right visual field so left optic tract

Lesion to the left superior optic radiations in the parietal lobe

72
Q

How do patients with pituitary adenoma present?

A

Patients will present with the consequences of hormone excess (e.g. Cushing’s due to ACTH, or acromegaly due to GH) or depletion.

Compression of the optic chiasm will cause a bitemporal hemianopia due to the crossing nasal fibers.

73
Q

Most common paediatric supratentorial tumour? how does it present?

A

Craniopharyngioma

hormonal disturbance, symptoms of hydrocephalus or bitemporal hemianopia.

74
Q

features of third nerve palsy

A

eye is deviated ‘down and out’
ptosis

if surgical:
pupil may be dilated (sometimes called a ‘surgical’ third nerve palsy)
painful

75
Q

causes of third nerve palsy

A

consider surgical :
eg posterior communicating artery aneurysm

other serious:
- false localizing sign* due to uncal herniation through tentorium if raised ICP
- Weber’s syndrome stroke

other:
diabetes mellitus
vasculitis e.g. temporal arteritis, SLE

76
Q

features of fourth nereve palsy

A

Trochlear nerve
LR6SO4

Defective downward gaze –> vertical diplopia
Nasal upshoot is how it looks!!!!
head tilted to the other side

77
Q

causes of 4th nerve palsy

A
  • CONGENITAL (esp if head tilted)
    Vasculopathy (htn, diabetes)
    Tumour
    Congenital (esp if head tilt)
    Trauma
78
Q

features of 6th nerve palsy

A

defective lateral gaze

appear cross-eyed

79
Q

causes of 6th nerve palsy

A

think RAISED ICP eg IIH

Vasculopathic
Tumour

80
Q

types of strabismus

A

Manifest strabismus = there all the time
Latent = underlying - picked up with cover test - may be symptomatic
Intermittent exotropia = strabismus when looking far

Esotropia - inwards towards nose
Exotropia - outwards
Hypertropia - upwards
Hypotropia - downwards

81
Q

causes strabismus

A

non-paralytic squint (excess tone in one muscle compared to other)
- Hereditary
- Refractive error - most common is long sighted - associated with esophoria -need glasses

Paralytic squint
- disease of the III, IV and VI cranial nerves

82
Q

pseudostrabismus cuases

A

Broad epicanthus as not much sleral showing medially
Narrow or wide interpupillary distance
Facial asymmetry
Unilateral ptosis

83
Q

examination ?diplopia ?strabismus

A

Cover/uncover : shows manifest strabismus (when other eye is covered, the squint corrects itself)

Alternate cover test : shows latent strabismus (squint present when covers so when uncovered it moves in opposite direction)

Fundoscopy (or red reflex) to rule out retinoblastoma, cataracts and other retinal pathology

Visual acuity

84
Q

differentiating features non-paryltic vs paryltic squint

A

non-paralytic
- usually congenital
- no diplopia
- full movement in both eyes if tested separately
- extraocular muscles and nerves are grossly normal

85
Q

what is amblyopia

A

Defective visual acuity which persists after correction of the refractive error and removal of any pathology

the brain will cope with this misalignment by reducing the signal from the less dominant eye. This results in one eye they use to see (the dominant eye) and one eye they ignore (the “lazy eye”). If this is not treated, this “lazy eye” becomes progressively more disconnected from the brain and over time the problem becomes worse. This is called amblyopia.

86
Q

management of ambylopia

A
  1. Wear appropriate glasses for 16-18 weeks
  2. Occlusion of better seeing eye (patching/atropine)
87
Q

management of strabismus

A

Aim:
- To restore comfortable binocular single vision (BSV)
- To achieve good alignment
- To eliminate diplopia

Conservative:
Optical - glasses/contact lenses
Prisms
Orthoptic exercise

Surgery:
Resection of muscles to shorten

Botulinum toxin
Injecting into muscle to temporarily paralyse muscle

88
Q

why should you always check red reflex in children especially with strabismus

A

RETINOBLASTOMA

absence of red-reflex, replaced by a white pupil (leukocoria) - the most common presenting symptom

89
Q

pathophysiology retinoblastoma

A

autosomal dominant
caused by a loss of function of the retinoblastoma tumour suppressor gene on chromosome 13
around 10% of cases are hereditary

90
Q

presentation retinoblastoma

A

absence of red-reflex, replaced by a white pupil (leukocoria) - the most common presenting symptom
strabismus
visual problems

91
Q

management of retinoblastoma

A

classically enucleation

other options now available: external beam radiation therapy, chemotherapy and photocoagulation

92
Q

how to interpret snellen chart?

A

6/6 is normal eg 20/20 in america
1st number is what pt can see
2nd number is average number

6 metres from snellen chart

therefore
9/6 is rly good
2/6 is bad

93
Q

how to use a snellen chart

A

pt stood at 6 metres the whole time. cover one eye and test separetly

interpret it off the chart

which metre they land on is first number