Ocular quickfire Flashcards
Retinitis pigmentosa
a) Inheritance
b) Presentation
c) Investigations
d) Management
e) What condition is associated with retinitis pigmentosa?
f) Name another genetic eye condition
a) 60% autosomal recessive
b) Peripheral vision loss, night vision loss (rod loss), relative sparing of central vision until more advanced
- Retinal examination reveals arteriolar attentuation
- Pigmented bone spicules in the mid-periphery
c) Electroretinography to confirm rod dysfunction
d) Supportive
- If macular oedema present, consider carbonic anhydrase inhibitor (acetazolamide)
e) Usher syndrome
- Causes sensorineural deafness (in childhood if type 1 or 2 Ushers; in adulthood if type 3)
f) Malattia Leventinese (ML):
- Autosomal dominant
- Progressive vision loss as the result of drusen (small, round, yellow-white deposits)
- Loss of peripheral and night vision, onset in adolescence
Anterior uveitis
a) Presentation
b) Diagnosis
c) Management
d) Clinical severity grading
e) Anterior vs intermediate vs posterior uveitis
a) - Unilateral pain, redness and photophobia
- Miosis (as opposed to AACG which causes mydriasis in red-painful eye)
- Hypopyon (sterile, as opposed to infectious e.g. endophthalmitis post-cataract surgery)
- Characteristic sign = cells in the anterior chamber (appearance on slit-lamp is of a dark room with beam of light shining through and bits of dust floating around)
- May also have a ‘flare’ which appears like a shaft of light shining through a darkened smokey room
b) - If known systemic disease, diagnosis usually clinical
- Fluorescein angiography and OCT may be used
- If no known systemic disease, may screen using FBC, ESR, ANA, ACE, HLA testing (50% HLA-B27 positive), TB tests, urinalysis, infection workup (Lyme, syphilis)
c) - Refer within 24h
- Cycloplegic drugs (e.g. cyclopentolate) - paralyse ciliary body to reduce pain/irritation
- Steroids - topical, systemic
- Adjuncts - MTX, infliximab, etc. if severe/chronic uveitis
d) Severity grading:
- Ranging from 0 (no cells seen) to +4 (>50 cells seen)
e) Anterior: anterior chamber only
Intermediate: involvement of ciliary body and peripheral retina
Posterior: involvement of retina and choroid
Acute angle closure glaucoma (AACG)
a) Drugs that may induce it
b) Presentation
c) Treatment
a) - Anticholinergics or sympathomimetics (mydriatics), e.g. atropine, oxybutynin, amitrptylline, ephedrine, etc.
- Other drug classes implicated: antihistamines, anti-parkinsonians, antipsychotics, sulfonamides
b) Symptoms:
- Acute painful red eye with systemic upset (N&V)
- History of intermittent blurring of vision with haloes
- Classically occurs while watching TV/cinema in dimly lit room
Signs:
- Reduced VA
- Fixed mid-dilated pupil
- Increased intra-ocular pressure >21 mmHg
- Stony hard globe to palpate
- Ciliary flush (dilated scleral vessels)
c) - IV or IM acetazolamide*
- Beta-blocker eye drops (timolol) - reduce aqueous humour production
- Steroids - prednisolone
- Pilocarpine (if natural lens) or phenylephrine (if surgical lens)
- Definitive Rx: laser peripheral iridotomy
*Caution - avoid in pregnancy. Risks of hyperchloremic (normal anion gap) metabolic acidosis, hypokalaemia, hyponatraemia, renal calculi, hypotension
Anterior ischaemic optic neuropathy
a) Causes
b) Presentation
c) Diagnosis
a) - Carotid stenosis
- GCA
b) - Monocular altitudinal vision loss (horizontal loss), painless
- May be episodic (e.g. TIA, amaurosis fugax)
Diabetic retinopathy
a) Features
b) Proliferative vs non-proliferative
c) Stages and screening frequency
d) Management of focal vs widespread retinopathy
a) Haemorrhages of varying sizes, microaneurysms (MAs), hard exudates, soft exudates (cotton wool spots) intraretinal microvascular abnormalities (IRMAs), and venous looping or beading
b) Proliferative has evidence of neovascularisation
c) Stage 1 (mild NPDR)
- Have at least one microaneurysm but no other findings as above
- May have concurrent macular oedema (which should be referred to ophthalmologist) - significant if associated with retinal thickening/hard exudates
- For annual review
Stage 2 (moderate NPDR)
- Haemorrhages or microaneurysms in 1-3 retinal quadrants
and/or cotton wool spots, hard exudates, or venous beading
- For 6 monthly review
Stage 3 (severe NPDR)
- Intraretinal haemorrhages (> 20 in all 4 quadrants), venous beading in 2 or more quadrants, or an IRMA in 1 or more quadrants. This is known as the 4:2:1 rule.
- These findings must be in the absence of neovascularization, which would indicate PDR.
- Patients with severe NPDR should be monitored using both macular OCT and fluorescein angiography to detect any Diabetic macular oedema (DME) or early neovascularization
- For referral to retina specialist and review every 3 months
- Risk of progression to PDR is 50% in 1 year
Stage 4 (proliferative DR)
- Neovascularization of the disc/elsewhere or vitreous/preretinal haemorrhage
- Need urgent referral to retina specialist and review monthly until stable
- Rx: anti-VEGF intravitreal injections and panretinal photocoagulation
d) - Focal (e.g. macular oedema) anti-VEGF or focal laser therapy
- Widespread - panretinal photocoagulation
Most common causes of blindness worldwide
- how is it treated?
Chlamydia trachomatis
- Presents with keratitis/conjunctivitis
- Can progress to cause globe fibrosis and corneal opacification causing blindness
- Can be passed vertically from mother to child
- Endemic in the Middle East*
- Rx: single dose azithromycin
*compared to onchocerciasis (river blindness) which is endemic to Africa
Adie’s tonic pupil vs Argyll-Robertson pupil
- Adie’s is 80% unilateral, AR is typically bilateral
- Adie’s pupils generally dilated, AR pupils are small
- Adie’s react slowly to light and accommodation; AR accommodates but doesn’t react
- Adie’s often has sluggish DTRs
- AR may have other features of neurosyphilis
Hypertensive retinopathy: stages
(mnemonic: SAFE)
- Grade 0: No changes
- Grade 1: Silver wiring - mild arterial narrowing
- Grade 2: AV nipping - obvious arterial narrowing with focal irregularities
- Grade 3: Flame haemorrhages, exudates, cotton wool spots
- Grade 4: Edema - papilloedema (+/- macula star)
Foster-Kennedy syndrome
a) Clinical features
b) Cause
c) Pseudo-Foster-Kennedy syndrome
a) - Ipsilateral optic nerve compression and vision loss
- Contralateral papilloedema
(a compressed optic nerve will show atrophy and cannot demonstrate papilloedema)
b) Frontal lobe tumour
Olfactory groove/sphenoid wing meningioma
c) Caused by bilateral sequential anterior ischaemic optic neuropathy
Diplopia
a) Monocular vs binocular - assessment, causes
a) - Binocular diplopia - present only with both eyes open (if you cover EITHER eye, the diplopia will go away), neurological or muscular cause
- Monocular diplopia - disappears only if you cover the affected eye, generally ophthalmic cause (check with pinhole test)
Ptosis
a) vs. pseudo-ptosis
b) Causes
a) Pseudo-ptosis could be due to lid retraction in other eye or other asymmetry
b) Nerve:
- Horner’s - miosis, anhidrosis
- CN III palsy - ophthalmoplegia, mydriasis (or pupil sparing)
NMJ:
- MG - fatigable, Cogan’s lid lag sign
- LEMS
Myopathic:
- Levator palpebrae superioris dysfunction - older age, trauma, contact lens use
Transient vision loss
a) Monocular vs binocular
b) Amaurosis fugax vs hemianopia
c) Investigations
a) Monocular - Anterior circulation TIA
- usually caused by ipsilateral carotid artery disease, but can be caused by vasculitis (GCA), vasospasm, cardioembolic
- cause temporary reduction in optic nerve/retinal perfusion
- lasts seconds-minutes (if ischaemia lasts hours-days, the vision loss will not be reversible. If reversible, more likely to be another pathology e.g. optic neuritis)
Binocular - posterior circulation TIA
b) - Amaurosis fugax - curtain across vision from TOP to BOTTOM (or vice versa) as retinal blood supply is altitudinal. May also have light-induced vision loss (retinal claudication)
- Hemianopia - horizontal vision loss (as occipital cortex blood supply is contralateral)
c) - FBC, CRP and ESR in anyone >50 to rule out GCA
- Fundoscopy, etc.
- CT/MR brain. TIA clinic referral
CRAO
a) Clinical features
b) Management
a) - Sudden painless vision loss in one eye
- Cherry red macula
b) - Ocular massage to dislodge any clot
- IV acetazolamide
+/- anterior chamber paracentesis +/- thrombolysis
CRVO
a) Clinical features
b) Management
a) - Painless vision loss over hours-days
- RAPD
- Common in diabetics, other vascular RFs, thrombophilias
- Fundoscopy: disc swelling, flame/dot/blot haemorrhages*, tortuous veins
*If not in all 4 quadrants, may only be a branch occlusion
b) - Anti-VEGF injections/ laser therapy
- Treat underlying hypertension
Primary open angle glaucoma
a) Classic triad
a) - Peripheral vision loss (though often asymptomatic)
- Raised IOP
- Optic disc changes (increased cup to disc ratio)
