Ophthalmology Flashcards

1
Q

aetiology of acute angle-closure glaucoma

A

optic neuropathy due to raised IOP

RFs (impairment to aqueous outflow)
- hypermetropia (long sightedness)
- pupillary dilatation
- lens growth associated w age

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2
Q

px of acute angle-closure glaucoma

A
  • haloes around lights
  • semi-dilated non-reacting pupils
  • severe pain
  • worse with mydriasis
  • hard, red eye
  • corneal oedema -> dull or hazy cornea
  • decreased visual acuity
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3
Q

acute angle-closure glaucoma ix & mx

A

ix
- tonometry to check for elevated IOP
- gonioscopy - slit lamp lens which allows for visualisation of the angle

Mx
- urgent opthal referral

initial:
- combination eye drops (direct parasympathomimetic- pilocarpine, beta blocker- timolol, alpha-2 agonist- apraclonidine)
- IV acetazolamide

definitive mx
- laser peripheral iridotomy
(tiny holes in peripheral iris)

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4
Q

Age-related macular degeneration aetiology

A

Degeneration of the central retina (macula)

degeneration of retinal photoreceptors that results in the formation of drusen

Drusen may become confluent in late disease to form a macular scar

most common cause of blindness in the UK

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5
Q

ARMD RFs

A

advancing age (!!)
smoking
family hx
cvd rfs

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6
Q

dry macular degeneration features (ARMD)

A

a.k.a atrophic / early ARMD
90% of cases
drusen -> yellow round spots in Bruch’s membrane
Gradual reduction in visual acuity
alteration to retinal pigment epithelium (RPE)

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7
Q

wet macular degeneration features (ARMD)

A

a.k.a exudative / neovascular/ late ARMD
Choroidal neovascularisation
Leakage of serum fluid & blood
10 % of cases
worst prognosis
subacute reduction in visual acuity

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8
Q

ARMD px

A

Reduction in visual acuity, esp near field objects
Difficulties in dark adaption
Poor night vision
Daily visual fluctuations
Photopsia (flickering/ flashing) lights
Glare around objects
Charles-Bonnet syndrome - visual hallucinations

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9
Q

ARMD ix

A

Amsler grid testing -> distortion of line perception

Fundoscopy/ Slit lamp microscopy -> drusen (yellow pigment deposition in macula), pigmentary, exudative or haemorrhagic changes of retina

if neovascular ARMD: Fluorescein angiography -> to guide anti-VEGF therapy. Add indocyanine green angiography to visualise choroidal circulation changes.

Optical coherence tomography -> 3D retinal visualisations to reveal areas of disease which aren’t visible using microscopy alone

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10
Q

ARMD tx

A

Dry
- combination of zinc with anti-oxidant vitamins A,C and E

Wet
- vascular endothelial growth factor (VEGF)
— e.g. ranibizumab, bevacizumab and pegaptanib
— 4 weekly injection, start w/in first 2 months
- laser photocoagulation (complication: acute visual loss)

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11
Q

Allergic conjunctivitis tx

A

(usually seen in context of hay fever)

first-line: topical or systemic antihistamines
second-line: topical mast-cell stabilisers, e.g. Sodium cromoglicate and nedocromil

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12
Q

Anterior uveitis associations

A

HLA-B27
Ankylosing spondylitis
reactive arthritis
Ulcerative colitis
Crohn’s disease
Behcet’s disease
Sarcoidosis: bilateral disease may be seen

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13
Q

Anterior uveitis mx

A

urgent review by ophthalmology

cycloplegics (dilates the pupil which helps to relieve pain and photophobia) e.g. Atropine, cyclopentolate

steroid eye drops

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14
Q

Argyll-Robertson pupil px & aetiology

A

small, irregular pupils
no response to light but there is a response to accommodate

Causes
- diabetes mellitus
- syphilis

mnemonics
- Argyll-Robertson Pupil (ARP) is Accommodation Reflex Present (ARP) but Pupillary Reflex Absent (PRA)
- prostitutes accommodate, but don’t react

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15
Q

Blepharitis aetiology

A

Inflammation of the eyelid margins -> dry eyes -> grittiness, esp at eyelid margins (usually bilateral)

meibomian gland dysfunction (common, posterior blepharitis)
OR seborrhoeic dermatitis/staphylococcal infection (less common, anterior blepharitis)

associated w rosacea

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16
Q

Blepheritis tx

A

hot compresses BD - softening of the lid margin

‘lid hygiene’, mechanical removal of the debris
- cotton wool buds in cooled boiled water, baby shampoo, sodium bicarbonate

artificial tears for dry eyes

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17
Q

assessment & mx of blurred vision

A

visual acuity with a Snellen chart
- pinhole occluders to check if refractive error is cause

visual fields

fundoscopy

Mx
- refractive error -> optician review
- other -> opthalmology (urgent if pain or visual loss)

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18
Q

cataracts RFs

A

Ageing (!!)
Smoking
Increased alcohol
Trauma
Diabetes mellitus
Long-term corticosteroids
Radiation exposure
Myotonic dystrophy
Hypocalcaemia

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19
Q

Defect in the red reflex & Faded colour vision in which condition??

A

Cataracts

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20
Q

Cataracts Ix

A

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

Slit-lamp examination. Findings: visible cataract

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21
Q

cataract classification

A

Nuclear: change lens refractive index, common in old age

Polar: localized, commonly inherited, lie in the visual axis

Subcapsular: due to steroid use, just deep to the lens capsule, in the visual axis

Dot opacities: common in normal lenses, also seen in diabetes and myotonic dystrophy

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22
Q

Cataract mx

A

Non-surgical conservative mx initially - stronger glasses/contact lens, or use brighter lighting

Surgical - removing the cloudy lens and replacing this with an artificial one

referral for surgery should be dependent upon whether a visual impairment is present, impact on quality of life, and patient choice !!

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23
Q

cataract surgery complications

A

Posterior capsule opacification: thickening of the lens capsule

Retinal detachment

Posterior capsule rupture

Endophthalmitis: inflammation of aqueous and/or vitreous humour

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24
Q

Central retinal artery occlusion causes

A

thromboembolism (from atherosclerosis) or arteritis (e.g. temporal arteritis)

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25
Q

features of Central retinal artery occlusion

A

sudden, painless unilateral visual loss

relative afferent pupillary defect

‘cherry red’ spot on a pale retina

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26
Q

Central retinal vein occlusion (CRVO) px

A

sudden, painless reduction or loss of visual acuity, usually unilaterally

fundoscopy
- widespread hyperaemia
- severe retinal haemorrhages:’stormy sunset’

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26
Q

Central retinal vein occlusion (CRVO) mx

A

conservatively

indications for treatment in patients with CRVO include:
- macular oedema - intravitreal anti-vascular endothelial growth factor (VEGF) agents

  • retinal neovascularization - laser photocoagulation
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27
Q

corneal foreign body indications for referral to ophthalmology

A

Suspected penetrating eye injury due to high-velocity injuries (e.g. drilling, lawn moving or hammering) or sharp objects (e.g. as glass, knives, pencils or thorns)

Significant orbital or peri-ocular trauma has occurred.

A chemical injury has occurred (irrigate for 20-30 mins before referring)

Foreign bodies composed of organic material (such as seeds, soil) -higher risk of infection and complications

Foreign bodies in or near the centre of the cornea

Any red flags e.g. severe pain; irregular, dilated or non-reactive pupils; significant reduction in visual acuity.

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28
Q

Corneal ulcer aetiology

A

RFs
- contact lens use
- vitamin A deficiency: a particular problem in the developing world

causes
- bacterial keratitis
- fungal keratitis
- viral keratitis: herpes simplex, herpes zoster - may lead to a dendritic ulcer
- Acanthamoeba keratitis: associated with contact lens use

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29
Q

non-proliferative diabetic retinopathy diabetic retinopathy features depending on classification

A

Mild NPDR
- 1 or more microaneurysm

Moderate NPDR
- microaneurysms
- blot haemorrhages
- hard exudates
- cotton wool spots (‘soft exudates’ - represent areas of retinal infarction)
- venous beading/looping
- intraretinal microvascular abnormalities (IRMA) less severe than in severe NPDR

Severe NPDR
- blot haemorrhages and microaneurysms in 4 quadrants
- venous beading in at least 2 quadrants
- IRMA in at least 1 quadrant

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30
Q

proliferative diabetic retinopathy features

A

Retinal neovascularisation - may lead to vitrous haemorrhage

fibrous tissue forming anterior to retinal disc

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

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31
Q

Maculopathy (diabetic retinopathy) features

A

based on location rather than severity, anything is potentially serious

hard exudates and other ‘background’ changes on macula

check visual acuity

more common in Type II DM

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32
Q

diabetic retinopathy mx

A

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

Maculopathy
- if visual acuity affected -> intravitreal vascular endothelial growth factor (VEGF) inhibitors

Non-proliferative retinopathy
- regular observation
- if severe/very severe consider panretinal laser photocoagulation

Proliferative retinopathy
- panretinal laser photocoagulation
- intravitreal VEGF inhibitors. e.g. ranibizumab
- if severe or vitreous haemorrhage: vitreoretinal surgery

33
Q

complications of pan retinal 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
  • 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
  • macular oedema
34
Q

what medication can differentiate between episcleritis and scleritis?

A

phenylephrine drops

phenylephrine blanches the conjunctival and episcleral vessels but not the scleral vessels
if the eye redness improves after phenylephrine a diagnosis of episcleritis can be made

35
Q

Episcleritis causes & mx

A

idiopathic
inflammatory bowel disease
rheumatoid arthritis

Management
- conservative
- artificial tears may sometimes be used

36
Q

types of stye (infection of the glands of the eyelids) & mx

A
  • external (hordeolum externum): infection (usually staphylococcal) of the glands of Zeis (sebum producing) or glands of Moll (sweat glands).
  • internal (hordeolum internum): infection of the Meibomian glands. May leave a residual chalazion (Meibomian cyst)

-management includes hot compresses and analgesia. CKS only recommend topical antibiotics if there is an associated conjunctivitis

37
Q

Herpes simplex keratitis mx

A

(most commonly presents with a dendritic corneal ulcer)

immediate referral to an ophthalmologist

topical aciclovir

38
Q

Herpes zoster ophthalmicus mx

A

oral antiviral treatment for 7-10 days
- start w/in 72hrs
- iv for very severe infection or if immunocompromised

topical corticosteroids may be used to treat any secondary inflammation of the eye

ocular involvement requires urgent ophthalmology review

39
Q

Holmes-Adie pupil px

A
  • unilateral in 80% of cases
  • dilated pupil
  • once the pupil has constricted it remains small for an abnormally long time
  • slowly reactive to accommodation but very poorly (if at all) to light

Holmes-Adie syndrome
- Holmes-Adie pupil with absent ankle/knee reflexes

40
Q

Horner syndrome px

A
  • miosis (small pupil)
  • ptosis
  • enophthalmos (sunken eye)
    anhidrosis (loss of sweating one side - depends on location of lesion)
  • pupillary dilation with apraclonidine drops*

(*an alpha-adrenergic agonist causes mild pupillary constriction in the normal pupil by down-regulating the norepinephrine release at the synaptic cleft)

41
Q

Horner syndrome
- central lesion px & causes

A

Anhidrosis of the face, arm and trunk

Stroke
Syringomyelia
Multiple sclerosis
Tumour
Encephalitis

42
Q

Horner syndrome
- pre-ganglionic lesion px & causes

A

Anhidrosis of the face

Pancoast’s tumour
Thyroidectomy
Trauma
Cervical rib

43
Q

Horner syndrome
- post-ganglionic lesion px & causes

A

No anhidrosis

Carotid artery dissection
Carotid aneurysm
Cavernous sinus thrombosis
Cluster headache

44
Q

hypertensive retinopathy classification (Keith-Wagener classification)

A
  1. Arteriolar narrowing and tortuosity
    Increased light reflex - silver wiring
  2. Arteriovenous nipping
  3. Cotton-wool exudates
    Flame and blot haemorrhages
    These may collect around the fovea resulting in a ‘macular star’
  4. Papilloedema
45
Q

Infective conjunctivitis mx

A
  • normally self limiting in 1-2 wks
  • topical antibiotic therapy (Chloramphenicol: drops are given 2-3 hourly or ointment qds)
  • topical fusidic acid BD is alternative (in pregnancy)
  • advice should be given not to share towels
  • school exclusion is not necessary

contact lens users
- topical fluoresceins to identify any corneal staining
- do not wear until it resolves
- tx as above

46
Q

causes of keratitis

A

(red eye w pain, photophobia, gritty sensation, maybe hypopyon)

bacterial
- Staphylococcus aureus
- Pseudomonas aeruginosa is seen in contact lens wearers

fungal

amoebic
- acanthamoebic keratitis
- increased incidence if eye exposure to soil or contaminated water
- pain is classically out of proportion to the findings

parasitic:
- onchocercal keratitis (‘river blindness’)

viral
- herpes simplex keratitis

environmental

47
Q

keratitis mx

A

contact lens wearers w painful red eye
- same-day referral to an eye specialist for slit lamp to rule out microbial keratitis

stop using contact lens until the symptoms have fully resolved

topical antibiotics
- typically quinolones are used first-line

cycloplegic for pain relief
e.g. cyclopentolate

48
Q

Causes of mydriasis (large pupil)

A

Third nerve palsy
Holmes-Adie pupil
Traumatic iridoplegia
Phaeochromocytoma
Congenital

49
Q

Drugs which cause mydriasis

A

topical mydriatics: tropicamide, atropine

sympathomimetic drugs: amphetamines, cocaine

anticholinergic drugs: tricyclic antidepressants

50
Q

nasolacrimal duct obstruction mx

A
  • teach parents to massage the lacrimal duct
  • usually resolves in 1 yr
  • if not, opthal referral for probing
51
Q

why is hyphema dangerous?

A

Hyphema = blood in the anterior chamber of the eye

main risk to sight comes from raised intraocular pressure due to the blockage of the angle and trabecular meshwork with erythrocytes

52
Q

ocular trauma & hyphema mx

A

Strict bed rest - excessive movement can redisperse blood that had previously settled

high-risk cases are often admitted otherwise daily ophthalmic review and pressure checks initially as an outpatient.

assess for orbital compartment syndrome (e.g. secondary to retrobulbar haemorrhage) -> true ophthalmic emergency

53
Q

optic neuritis causes

A

multiple sclerosis: the commonest associated disease

diabetes

syphilis

54
Q

optic neuritis features & mx

A
  • acute unilateral decreased visual acuity - hrs or days
  • poor discrimination of colours (red desaturation)
  • pain worse on eye movement
  • RAPD
  • central scotoma

ix
MRI of the brain and orbits with gadolinium contrast

mx
high-dose steroids
recovery usually in 4-6 weeks

55
Q

Preorbital vs orbital cellulitis

A

Periorbital (preseptal) cellulitis - infection anterior to the orbital septum

Orbital cellulitis - infection of fat and muscles posterior to the orbital septum, within the orbit but not involving the globe

reduced visual acuity, proptosis, ophthalmoplegia/pain with eye movements, restricted movements, chemosis, RAPD = orbital

56
Q

causes of papiloedema

A

increased intracranial pressure
- space-occupying lesion: neoplastic, vascular
- malignant hypertension
- idiopathic intracranial hypertension
- hydrocephalus
- hypercapnia

rare other causes
- hypoparathyroidism and hypocalcaemia
- vitamin A toxicity

57
Q

vitreous detachment ix & mx

A

RF
- age
- highly myopic (near-sighted)

ix
- Weiss ring on ophthalmoscopy (the detachment of the vitreous membrane around the optic nerve to form a ring-shaped floater).
- examined by an ophthalmologist within 24hrs to rule out retinal tears or detachment.

mx
- nothing - gradually improve over a period of around 6 months
- if retinal tear/ detachment -> surgery

58
Q

orbital cellulitis ix & mx

A

CT contrast of orbit & blood culture

medical emergency -> hospital admission for IV antibiotics, urgent senior review

59
Q

orbital cellulitis causes & RFs

A
  • Most common bacterial causes – Streptococcus, Staphylococcus aureus, Haemophilus influenzae B.

Risk factors
- Childhood
- Mean age of hospitalisation 7-12 years
- Previous sinus infection
- Lack of Hib vaccination
- Recent eyelid infection/ insect bite on eyelid (periorbital cellulitis)
- Ear or facial infection

60
Q

preseptal cellulitis mx

A

All cases should be referred to secondary care for assessment

Oral antibiotics are frequently sufficient - usually co-amoxiclav

contrast CT of orbit if suspecting orbital cellulitis

61
Q

night blindness and tunnel vision?

A

Retinitis pigmentosa

fundoscopy: black bone spicule-shaped pigmentation in the peripheral retina, mottling of the retinal pigment epithelium

62
Q

Ocular manifestations of rheumatoid arthritis?

A

25% of patients having eye problems

Ocular manifestations
keratoconjunctivitis sicca (most common)
episcleritis (erythema)
scleritis (erythema and pain)
corneal ulceration
keratitis

Iatrogenic
steroid-induced cataracts
chloroquine retinopathy

63
Q

primary open-angle glaucoma mx

A
  1. offer 360° selective laser trabeculoplasty (SLT) first-line to people with an IOP of ≥ 24 mmHg

2.prostaglandin analogue (PGA) eyedrops

  1. beta-blocker eye drops
    / carbonic anhydrase inhibitor eye drops
    / sympathomimetic eye drops
  2. surgery in the form of a trabeculectomy may be considered in refractory cases
64
Q

Prostaglandin analogues
example
MoA in eye
Advese effects

A

latanoprost
Increases uveoscleral outflow
OD eye drops

Adverse effects include brown pigmentation of the iris, increased eyelash length

65
Q

Beta-blocker eye drops
example
MoA in eye
CI

A

(e.g. timolol, betaxolol)

Reduces aqueous production

Should be avoided in asthmatics and patients with heart block

66
Q

Sympathomimetics eye drops
example
MoA in eye
CI

A

(e.g. brimonidine, an alpha2-adrenoceptor agonist)

Reduces aqueous production and increases outflow

Avoid if taking MAOI or tricyclic antidepressants

Adverse effects include hyperaemia

67
Q

Carbonic anhydrase inhibitors

A

(e.g. Dorzolamide)

Reduces aqueous production

Systemic absorption may cause sulphonamide-like reactions

68
Q

Miotics (e.g. pilocarpine, a muscarinic receptor agonist)

A

Increases uveoscleral outflow

Adverse effects included a constricted pupil, headache and blurred vision

69
Q

peripheral visual field loss- nasal scotoma -> tunnel vision

decreased visual acuity

optic disc cupping

what is this?

A

primary open-angle glaucoma (POAG)

70
Q

Fundoscopy signs of primary open-angle glaucoma

A
  1. Optic disc cupping - cup-to-disc ratio >0.7 (normal = 0.4-0.7), occurs as loss of disc substance makes optic cup widen and deepen
  2. Optic disc pallor - indicating optic atrophy
  3. Bayonetting of vessels - vessels have breaks as they disappear into the deep cup and re-appear at the base
  4. Additional features - Cup notching (usually inferior where vessels enter disc), Disc haemorrhages
71
Q

Marcus-Gunn pupil?

A

a.k.a relative afferent pupillary defect

  • found by swinging light test
  • caused by a lesion anterior to the optic chiasm-> retina: detachment or optic nerve: optic neuritis e.g. multiple sclerosis

finding: the affected and normal eye appears to dilate when light is shone on the affected

72
Q

Pathway of pupillary light reflex

A

afferent: retina → optic nerve → lateral geniculate body → midbrain

efferent: Edinger-Westphal nucleus (midbrain) → oculomotor nerve

73
Q

Retinal detachment aetiology & RFs?

A

neurosensory tissue that lines the back of the eye comes away from its underlying pigment epithelium

reversible cause of visual loss, provided it is recognised and treated before the macula is affected, otherwise permanent visual loss

RFs
- diabetes mellitus
- myopia
- age
- previous cataract surgery
- eye trauma

74
Q

pt seeing flashes & floaters. what now?

A

most likely just posterior vitreous detachment

But refer urgently (<24 hours) to an ophthalmologist for assessment with a slit lamp and indirect ophthalmoscopy for pigment cells and vitreous haemorrhage

retinal detachment - also have dense shadow that starts peripherally progresses towards the central vision, central visual loss, straight lines -> curved

75
Q

Scleritis RFs

A

rheumatoid arthritis: the most commonly associated condition

systemic lupus erythematosus

sarcoidosis

granulomatosis with polyangiitis

76
Q

scleritis mx

A

same-day assessment by an ophthalmologist

oral NSAIDs first-line

oral glucocorticoids for more severe presentations

immunosuppressive drugs for resistant cases (and also to treat any underlying associated diseases)

77
Q

Squints types

A

concomitant (common)
- Due to imbalance in extraocular muscles
Convergent is more common than divergent

paralytic (rare)
- Due to paralysis of extraocular muscles

78
Q

squint ix & mx

A

important to detect as uncorrected -> amblyopia (the brain fails to fully process inputs from one eye and over time favours the other eye)

ix
- corneal light reflection test - holding a light source 30cm from face to see if the light reflects symmetrically on the pupils
- cover test - focus on object, cover one eye, observe movement of other eye

mx
- referral to secondary care
- eye patches may help prevent amblyopia

79
Q

most common causes of a sudden painless loss of vision

A
  • ischaemic/vascular a.k.a amaurosis fugax e.g. thrombosis (CRVO, CRAO), embolism, temporal arteritis, TIA, ischaemic optic neuropathy
  • vitreous haemorrhage
  • retinal detachment
  • retinal migraine
80
Q

Causes of tunnel vision

A

papilloedema
glaucoma
retinitis pigmentosa
choroidoretinitis
optic atrophy secondary to tabes dorsalis
hysteria

81
Q

Common causes of vitreous haemorrhage

A

proliferative diabetic retinopathy (over 50%)

posterior vitreous detachment

ocular trauma: the most common cause in children and young adults