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Phase 4 > Ophthalmology > Flashcards

Ophthalmology Flashcards

1
Q

describe periorbital cellulitis

A

anatomical landmark: orbital septum
> pre-septal: periorbital cellulitis
> post-septal: orbital cellulitis

risk factors
- younger age
- local skin trauma
- lid or lacrimal infections e.g. stye, infection chalazion, dacryocystitis
- sinusitis
- dental infections

clinical features
- swollen, erythematous lid
- pain
- white eye
- ocular and orbital examination normal

management
- adults: oral co-amoxiclav

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2
Q

describe orbital cellulitis

A

infection around the eyeball involving the tissues behind the orbital septum

clinical features
- pain worse on eye movement
- reduced vision
- diplopia
- pyrexia
- reduced VA
- proptosis
- RAPD
- reduced colour vision
- restriction of EOM
- lid swelling / injection / chemosis

imaging: CT head, orbit and sinuses with contrast

causative organisms: staph aureus, strep pyogenes

management
- emergency admission under ophthalmology + ENT

  • intravenous antibiotics e.g. cefotaxime + flucloxacillin
  • surgical drainage if periosteal/orbital abscess

complications; loss of vision, meningitis, cavernous sinus thrombosis

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3
Q

explain the visual pathway

A

photoreceptor cells (rods and cones) send signals to retinal ganglion cells, which converge to form the optic nerve

signal is transmitted through optic nerve to optic chiasm, where nerve fibres decussate

> LEFT visual field goes to RIGHT visual cortex

> RIGHT visual field goes to LEFT visual cortex

each optic tract travels via respective cerebral hemisphere to the lateral geniculate nucleus (thalamus)

then onto optic radiations (PITS)

> upper optic radiation
> aka parietal optic radiation
> corresponds to INFERIOR visual field

> lower optic radiation (Meyer’s loop)
> aka temporal optic radiation
> corresponds to SUPERIOR visual field

finally reaches visual cortex in occipital lobe

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4
Q

describe the assessment of visual function

A

central vision - visual acuity
> Snellen chart
> tested at 6m
> recorded as fraction
> numerator: distance in metres from patient to chart
> denominator is distance at which normal eye could see
> normal vision is 6/6

peripheral vision - visual field
> confrontational fields - dynamic visual field testing
> Goldman chart: moving light source
> Humphrey visual field testing: static visual field testing

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5
Q

describe visual field defects

A

ipsilateral monocular blindness: optic nerve

Bitemporal hemianopia
lesion of optic chiasm

> upper quadrant defect = inferior chiasmal compression - pituitary tumour

> lower quadrant defect = superior chiasmal compression - craniopharyngioma

Left homonymous hemianopia means visual field defect to the left, i.e. Lesion of right optic tract

homonymous quadrantanopias: PITS (Parietal-Inferior, Temporal-Superior)

superior: inferior optic radiations (temporal lobe)

inferior: superior optic radiations (parietal lobe)

Contralateral homonymous hemianopia with macular sparing - lesion of occipital cortex

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6
Q

list causes of sudden / subacute loss of vision

A

retina
- central retinal artery occlusion
- central retinal vein occlusion
- retinal detachment

optic nerve
- anterior ischaemic optic neuropathy
- optic neuritis

macula
- wet age-related macular degeneration

vitreous
- vitreous haemorrhage

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7
Q

describe normal fundus anatomy

A
  • fundal reflex present
  • optic disc (3 Cs): optic nerve
    > contour: clear well-defined borders
    > colour: orange-pink doughnut with pale centre
    > cup: pale centre of orange-pink doughnut
  • retina (4 quadrants) & retinal vessels
    > superior temporal
    > superior nasal
    > inferior temporal
    > inferior nasal
  • macula
    > lateral to the optic disc and is yellow in colour
    > fovea is in the centre of macula, darker in colour, same diameter as optic disc
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8
Q

describe central retinal artery occlusion (CRAO)

A

causes: atherosclerosis, GCA

features
- sudden painless loss of vision
- reduced visual acuity
- RAPD

fundoscopy
- pale retina
- discontinuity in arteries
- papilloedema
- cherry red spot

  • Branch retinal artery occlusion (BRAO) affects less of the retina

management
- ocular massage

  • increase blood oxygen content and dilate retinal arteries
    > sublingual isosorbide dinitrate or oral pentoxifylline
    > inhalation of a carbogen or hyperbaric oxygen
  • reduce intraocular pressure
    > IV acetazolamide or mannitol
    > anterior chamber paracentesis
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9
Q

describe arteritic anterior ischaemic optic neuropathy (AION)

A

Anterior ischaemic optic neuropathy refers to ischaemia of the optic nerve leading to visible papilloedema

> if optic nerve ischaemia is present without visible papilloedema this is posterior ischaemic optic neuropathy

2 types of AION:
- arteritic: temporal/giant cell arteritis
- non-arteritic

symptoms of AAION
- sudden onset painless visual loss
- headache
- jaw claudication
- scalp tenderness
- diplopia

signs
- profoundly reduced visual acuity
- dyschromatopsia (reduced colour vision)
- RAPD
- scalp and temporal artery tenderness
- pulseless temporal artery

fundoscopy: pale swollen optic disc

investigations
- bloods: FBC, U&Es, lipids, glucose, CRP, ESR

risk factors: polymyalgia rheumatica

management:
- pulsed IV methylprednisolone 1g/day with PPI cover

  • temporal artery biopsy
    > mononuclear cell infiltration or granulomatous inflammation with multinucleate giant cells
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10
Q

describe vitreous haemorrhage

A

causes
- proliferative diabetic retinopathy
- PVD/retinal detachment
- subarachnoid haemorrhage (Terson’s syndrome)
- trauma

symptoms
- sudden painless visual loss or haze
- red hue in vision
- floaters/shadows/dark spots in vision
- decreased VA, visual field defect if severe

investigations:
> fundoscopy: haemorrhage in vitreous cavity
> slit-lamp exam: RBCs in anterior vitreous
> ultrasound (B-scan): rule out retinal tear/detachment
> orbital CT: if open globe injury

management
- conservative: watch and wait
- vitrectomy
- laser (panretinal photocoagulation) or intravitreal therapy, if required

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11
Q

describe age-related macular degeneration (ARMD)

A

dry age-related macular degeneration aka non-neovascular or atrophic, 90% of cases

  • management: conservative
    > smoking cessation
    > diet / zinc with antioxidant vitamins C, E + beta carotene supplementation

> support: low visual aids clinic, sight impairment registration

> monitor for conversion to wet ARMD: regular Amsler chart testing

wet age-related macular degeneration, aka choroidal neovascularisation, or exudative, 10% of cases
> presents more acutely

  • management
    > anti-VEGF injections: ranibizumab, bevacizumab
  • laser photocoagulation
    > if end-stage, observe
  • risk factors: dry ARMD or wet ARMD in other eye, age, female, smoker, family history, hypertension, CVD, hyperlipidaemia
  • fundoscopy
    > drusen: yellow or “amber” retinal deposits
    > atrophy of retinal pigment epithelium, geographical atrophy
    > degeneration of photoreceptors
  • investigations
    > optical coherence tomography (OCT)
    > fluorescein angiography
    > slit lamp examination
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12
Q

describe central retinal vein occlusion (CRVO)

A

categories: ischaemic, non-ischaemic

symptoms
- sudden painless unilateral blurred vision or loss of vision

signs
- reduced visual acuity
- RAPD
- visual field defect

DDX: branch retinal vein occlusion, where less of fundus is affected

risk factors: age, hypertension, CVD, glaucoma, polycythaemia

fundoscopy: blood and thunder appearance
> dilated tortuous retinal veins
> flame and blot haemorrhages
> retinal oedema
> cotton wool spots
> hard exudates

branch retinal vein occlusion: retinal haemorrhages confined to one area of retina

management
- if macular oedema:
> anti-VEGF infections to prevent neovascularisation
> dexamethasone intravitreal implant
> laser photocoagulation

  • if no macular oedema: observe and review
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13
Q

Describe retinal detachment

A

when the neurosensory layer of the retina detaches from the retinal pigment epithelium due to retinal tear

symptoms
- sudden peripheral visual loss / blurred vision
- shadow across vision “curtain coming down”
> starts peripherally and progresses towards central vision
- flashes / floaters
- straight lines appear curved
- central visual loss

signs
- reduced vision
- visual field defect
- RAPD
- tobacco dust (Shaffer’s sign) - on slit lamp
- detached retina
- retinal tear
- vitreous haemorrhage

risk factors: myopia, diabetes, age, previous cataract surgery, trauma

management
- vitrectomy
- scleral buckle
- pneumatic retinopexy

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14
Q

describe optic neuritis

A

causes: multiple sclerosis, syphilis, diabetes

symptoms
- acute/subacute unilateral loss/blurring of vision
- pain worse on eye movements
- reduced VA
- RAPD
- reduced colour vision (red desaturation)
- central scotoma
- 1/3 cases: optic disc swelling + haemorrhages

investigations: MRI brain + orbits with gadolinium contrast

management
- recovery within weeks
> can result in optic atrophy
- high dose steroids: pulsed IV methylprednisolone

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15
Q

list causes of acute red eye

A

inflammation/infection
- conjunctivitis
- keratitis
- episcleritis/scleritis
- iritis/uveitis
- endophthalmitis
- orbital cellulitis

acute angle closure glaucoma

trauma
- subconjunctival haemorrhage
- corneal abrasion
- corneal foreign body
- globe rupture
- penetrating injury
- retrobulbar haematoma
- chemical injury

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16
Q

describe conjunctivitis

A

symptoms
- irritable, red, bloodshot eye
- itchy or gritty sensation
- discharge
> purulent discharge - bacterial
> clear discharge - viral (often preceded by URTI)

  • allergic has seasonal variation and more characterised by itch

management
- usually resolves within 1-2 weeks

  • bacterial: topical chloramphenicol or fusidic acid
    > avoid rubbing eyes and sharing towels/bedding
  • viral: cold compresses + lubricants
  • allergic: cold compress + lubricants + anti-histamine
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17
Q

describe bacterial keratitis

A

keratitis or corneal ulcer refers to sight-threatening infection and inflammation of the cornea

symptoms
- reduced visual acuity
- pain
- red eye
- irritation
- foreign body sensation
- photophobia
- purulent discharge

risk factors: contact lens wearers, corneal trauma, ocular surface disease, immunosuppression

bacterial - round appearance of abscess (hypopyon)

often caused by Pseudomonas aeruginosa in contact lens wearers

investigations
- corneal scrapes and conjunctival swaps
- send contact lenses, cases and solutions for culture and sensitivity

management
- frequent topical antibiotics e.g. fluoroquinolone
- close review
- period of no contact lens use

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18
Q

describe herpes simplex keratitis

A

aka viral keratitis

symptoms
- painful photophobic eye
- discomfort, grittiness
- red eye
- reduced visual acuity
- epiphora (watering of the eye)
- previous history of cold sore on lip

signs
> dendritic appearance of ulcer
> can be seen with fluorescein dye

investigations - conjunctival and corneal swabs for viral PCR

management
- topical antiviral e.g. ganciclovir, aciclovir
- epithelial debridement
- stop wearing contact lens

risk factors - steroids

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19
Q

describe episcleritis

A

symptoms
- localised or diffuse redness (often a patch of redness in the lateral sclera)
- no pain or mild pain
- dilated episcleral vessels

no photophobia, discharge and normal visual acuity

associated with RA and IBD

> phenylephrine used to differentiate between episcleritis and scleritis
> if blanching, episcleritis, if not, scleritis

management of episcleritis
- self-limiting and resolves within 1-2 weeks
- oral NSAIDs / topical NSAIDs / topical steroids

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20
Q

describe anterior uveitis

A

aka iritis, iridocyclitis (if iris and ciliary body) - inflammation of the uveal tract, comprising iris, ciliary body and choroid

symptoms
- painful, red, photophobic eye
- reduced vision
- tearing
- systemic: malaise, fever, weight loss
> joint pain, back pain

signs
- small fixed oval pupil
- irregular edges of pupil
- ciliary injection/flush
- cloudy cornea and hazy view of iris
- cells in anterior chamber
- hypopyon

  • slit lamp examination
    > circumferential redness (ciliary flush)
    > inflammatory cells in anterior chamber
    > foggy appearance of anterior chamber (flare)
    > adhesions between lens and pupil which distort shape (posterior synechiae)

management
- topical steroids (tapering course)
- dilating (cycloplegic/mydriatic) drops e.g. atropine, cyclopentolate: short courses to alleviate photophobia
- treat underlying cause

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21
Q

describe endophthalmitis

A

overwhelming infection of internal structures of eye that can result in permanent blindness and loss of eye

categories:
> endogenous: seeding from infection elsewhere
> exogenous: post-procedure
» recent intraocular surgery or intravitreal injections

symptoms
- severe pain
- rapidly progressive visual loss
- photophobia
- floaters
- diffuse conjunctival injection
- RAPD
- corneal haze with limited view of pupil and iris
- hypopyon

management
- intravitreal tap + intravitreal antibiotics
- admission for daily review
- vitrectomy if poor vision

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22
Q

describe pathophysiology, signs and symptoms of acute angle closure glaucoma (AACG)

A

iris bulges forward and seals off trabecular meshwork from anterior chamber, preventing aqueous humour from draining leading to increased IOP

symptoms
- severe painful red eye
- blurred vision
- halos around lights
- associated headache, nausea +/- vomiting
- conjunctival injection
- corneal oedema leads to hazy cornea
- semi-dilated unreactive pupil
- decreased visual acuity
- hard eyeball on gentle palpation

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23
Q

state normal eye pressure

A

8-21 mmHg

raised IOP is asymptomatic until around 40 mmHg

measurement via applanation tonometry

ophthalmic poke - not fluctuant, hard like a rock

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24
Q

describe subconjunctival haemorrhage

A

occur when a small blood vessel within conjunctiva ruptures

causes
- heavy lifting/straining e.g. intense coughing fit
- trauma
- hypertension
- bleeding disorders
- anticoagulants e.g. DOACs, warfarin

features
- dense, opaque red patch under conjunctiva
- painless and does not affect vision

management
- harmless and self-resolve around 2 weeks
- lubricating eye drops can help if irritation

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25
Q

describe a corneal abrasion

A

causes
- damaged contact lenses (may be associated with Pseudomonas infection)
- fingernails
- foreign bodies
- tree branches
- makeup brushes
- entropion (inward turning eyelid)

investigation: fluorescein staining with cobalt blue filter on slit lamp

management
- rule out other ocular injury
> high index of suspicion for mechanism e.g. high speed injury

  • frequent chloramphenicol ointment
  • OTC analgesia
  • if large, lubrication (carbomer gel) nightly for 1 month to reduce risk of recurrent corneal erosion syndrome (RCES)
  • chemical abrasions e.g. acid require immediate extensive irrigation
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26
Q

describe penetrating eye injuries and intraocular foreign bodies

A

penetrating eye injury: full thickness laceration of the globe

clinical presentation
- severe pain, blurred or double vision
- light sensitivity
- foreign body sensation

investigations - CT scan orbit

management
- eye shield placement
- analgesia and anti-emetics
- systemic prophylactic antibiotics
- check tetanus status

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27
Q

describe penetrating eye injury / globe rupture

A

signs
- object through full thickness of cornea
- Seidel’s +ve defect
- peaked/irregular pupil +/- uveal prolapse

often high-velocity injury e.g. industrial accent

investigations - CT orbits with fine cuts

management
- avoid pressure on globe
- eye shield
- parenteral analgesia and anti-emetics
- IV antibiotics
- tetanus status

  • emergency exploration + primary repair in theatre
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28
Q

describe retrobulbar haemorrhage

A

aka orbital compartment syndrome

often history of trauma

features
- proptosis
- redness
- resistance to retropulsion
- tense eyelid, difficult to open
- diminished visual acuity
- RAPD
- reduced colour vision

investigations - CT orbit

management
- immediate decompression via lateral canthotomy and cantholysis

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29
Q

describe chemical injury

A

worse in alkaline injuries compared to acidic injuries

signs
- involvement of eyelids
- conjunctival injection / blanching
- limbal ischaemia
- corneal opacification
- epithelial defect

management
- pH check - litmus paper
- topical proxymethacaine
- irrigation 3-5L
- sweep fornices when able

  • when pH neutral, examination at slit lamp if possible
  • chloramphenicol
  • topical steroid
  • consider oral ascorbic acid or oral tetracycline
30
Q

describe cataracts and their risk factors

A

clouding of the lens
> proteins accumulate inside lens leading to obstruction of light

risk factors
- age
- smoking
- diabetes - sorbital accumulation
- steroid use
- hypocalcaemia
- uveitis
- trauma
- surgery
- congenital cataracts: rubella, CMV

3 main types

  • nuclear cataracts
    > Most common type
    > caused by sclerosis of lens nucleus, associated with ageing
    symptoms
    > myopia (short-sightedness)
    > colours appearing dull
  • posterior subcapsular cataract
    > caused by opacifications in the posterior aspect of the lens capsule
    > affect younger patients and people taking steroids
    > progress more rapidly
    > glare looking at lights (esp night)
  • cortical cataracts
    > caused by opacification of lens cortex which look like the spokes of a wheel
    > vision often unaffected
  • congenital cataract
    > amblyogenic (lazy eye)
    > idiopathic/inherited
  • traumatic cataract
    > blunt / penetrating trauma
    > zonular injury
31
Q

describe symptoms and examination findings in cataracts

A

symptoms
- slow reduction in visual acuity
- progressive blurring of the vision
- colours becoming more faded, brown or yellow
- starbursts can appear around lights, especially at night

examination
- loss of fundal reflex
- clouded lens

32
Q

describe management of cataracts

A

conservative

surgical - clear lens extraction
- to treat angle closure glaucoma
- to improve visualisation of retina to manage co-pathology e.g. diabetic retinopathy

selection of most appropriate intraocular lens implant is via biometry
> measures corneal curvature and length of eye

complications
- intraoperative - posterior capsular rupture

  • post-operative
    > endophthalmitis
    > uveitis
    > cystoid macular oedema
    > retinal detachment
    > posterior capsular opacification
33
Q

describe non-arteritic anterior ischaemic optic neuropathy

A

symptoms:
- acute painless loss of vision in one eye (blurring/cloudiness)
- patients often become aware upon waking in the morning

signs:
- reduced visual acuity (less profound than temporal arteritis)
- dyschromatopsia (reduced colour vision)
- RAPD
- visual fields: altitudinal field defect (usually inferior hemisphere)

fundoscopy
- pale swollen disc with splinter haemorrhages

management:
- commence secondary prevention e.g. aspirin, statin
- smoking cessation advice and BP check

34
Q

describe scleritis

A

associated with rheumatoid arthritis, granulomatosis with polyangiitis

features
- red, inflamed sclera (localised or diffuse)
- congested vessels
- severe pain especially at night
- pain with eye movement
- photophobia
- epiphora (excessive tear production)
- reduced visual acuity
- tenderness to palpation of globe

management of scleritis
- NSAIDs
- oral steroids 1mg/kg
- immunosuppression appropriate to systemic condition

35
Q

describe the symptoms, risk factors and management of acute angle closure glaucoma

A

risk factors
- increasing age
- hypermetropia
- family history
- female
- Chinese and East Asian ethnic origin
- Shallow anterior chamber

investigations
- tonometry: assess elevated IOP
- gonioscopy: visualise angle

management
- acute
> lie patient on their back without pillow

> eye drops
> pilocarpine: direct parasympathomimetic (miotic, muscarinic receptor agonist)
> timolol: beta-blocker
> apraclonidine: alpha 2 agonist

> IV acetazolamide

  • definitive treatment
    > laser peripheral iridotomy
36
Q

list medications which can precipitate acute angle closure glaucoma

A

mydriatic eye drops

adrenergic medications e.g. noradrenaline

anticholinergic medications e.g. oxybutinin and solifenacin

tricyclic antidepressants e.g. amitriptyline - anticholinergic effects

37
Q

describe the symptoms and risk factors for primary open angle glaucoma

A

progressive optic neuropathy due to a rise in intraocular pressure with optic disc and visual field changes

gradual increase in IOP due to increase in resistance to flow of aqueous humour through trabecular meshwork

fundoscopy
- optic disc cupping
- optic disc haemorrhage
- optic disc notch

risk factors: age, family history, Black ethnic origin, myopia

symptoms
- usually asymptomatic
- peripheral visual loss (tunnel vision)
- fluctuating pain
- headache
- blurred vision
- halos around lights, esp nighttime

investigations
- Goldmann applanation tonometry
- Slit lamp
- Gonioscopy

38
Q

list diabetic eye diseases

A
  • susceptability to infection: preseptal cellulitis, keratitis, blepharitis, chalazion
  • dry eyes / neurotrophic cornea
  • anterior uveitis
  • cataracts
  • diabetic papillitis
  • diabetic retinopathy / maculopathy
  • cranial nerve palsies
39
Q

describe blepharitis

A

inflammation of eyelid margins

symptoms
- dry, gritty, itchy eye
- can lead to styes and chalazions

management
- warm compresses
- gentle cleaning of eyelid margins

40
Q

describe diabetic retinopathy

A
  • non-proliferative diabetic retinopathy
    > microaneurysms in retinal arterioles
    > blot haemorrhages
    > hard exudates
    > cotton wool spots: infarctions in retinal fibre layer
    > venous beading

> treatment: regular observation, if very severe consider panretinal laser photocoagulation (often leads to reduction in visual fields)

  • proliferative diabetic retinopathy

> VEGF-driven: new vessels on the disc (NVDs) or new vessels elsewhere (NVEs)

> predisposes to sight-threatening conditions
> vitreous haemorrhage
> retinal detachment
> neovascular glaucoma

> treatment:
> panretinal laser photocoagulation
> intravitreal VEGF inhibitors
> vitreoretinal surgery if severe or vitreous haemorrhage

41
Q

describe diabetic maculopathy

A

more common in T2DM (retinopathy more common in T1DM)

most common cause of decreased vision in diabetic patients

leakage (exudates, haemorrhages) in macula leads to macular oedema

treatment: anti-VEGF injections, intraocular steroid implants

42
Q

describe hypertensive retinopathy

A

can happen slowly with chronic hypertension or quickly with malignant hypertension

features
- arteriovenous nipping
- cotton wool spots caused by ischaemia/infarction
- retinal haemorrhages
- hard exudates
- papilloedema

Keith-Wagener Classification
- Stage 1: mild narrowing of arterioles
- Stage 2: focal constriction of blood vessels and AV nicking
- Stage 3: cotton wool patches, exudates and haemorrhages
- Stage 4: papilloedema

management: control blood pressure and manage risk factors

43
Q

describe giant cell arteritis and its management

A

systemic vasculitis classically causing ischaemic optic neuropathy, central retinal artery occlusion, cranial nerve palsies

consider in
> 50 years old
new temporal headache
scalp tenderness/jaw claudication
visual loss (fleeting/permanent)
stroke / retinal artery occlusion / cranial nerve palsies
weight loss / myalgia / night sweats / polymyalgia rheumatica
raised inflammatory markers

diagnosis: doppler ultrasound for temporal artery, axillary artery and carotids OR temporal artery biopsy

treatment - high dose steroids
> start 3 days IV methylprednisolone
> taper onto high dose oral prednisolone, consider tocilizumab to prevent recurrence

44
Q

describe thyroid eye disease

A

orbital inflammation affecting 40% of patients with abnormal thyroid status

most hyperthyroid (Graves), some hypothyroid, few euthyroid

features
- swollen lids
- lid lag / lid retraction / scleral show
- swollen injected conjuctivae
- proptosis
- restricted eye movements
- sight threatening features
> compressive optic neuropathy
> exposure keratopathy

squint (esotropia) eye turns inwards

treatment
- optimise TFTs
- artificial tears and lubrication
- stop smoking
- oral selenium if mild disease
- systemic steroids if sight-threatening
- external beam radiation
- surgery
> orbital decompression surgery
> eye muscle surgery
> eye lid surgery

45
Q

describe visual milestones

A

6 weeks - fix and follow light source
3 months - fix and follow slow target
6 months - reaches out accurately for toys
2 years - picture matching
3 years - letter matching, single letters
5 years - Snellen/logmar chart

46
Q

describe amblyopia

A

halting of visual development due to reduced visual input

usually monocular

develops up to the age of 8

types
- strabismic
- refractory
- stimulus deprivation (sensory amblyopia)
> e.g. ptosis, congenital cataract

treatment
- glasses
- penalise non-ambylopic eye: patching, atropine (pupil dilation and blurring of good eye)
- surgery if cause is squint
- earlier treatment of amblyopia correlates with a greater chance of reversal

47
Q

describe conjunctivitis of the newborn

A

conjunctivitis of the newborn

gonococcal infection
- typically day 1-3
- copious pus
- systemic antibiotics per GUM

chlamydia
- typically day 4-28
- can cause pneumonitis
- oral erythromycin

herpes simplex
- can cause systemic upset and encephalitis
- usually HSV1
- treatment: IV aciclovir

48
Q

nasolacrimal duct obstruction

A

imperforate distal valve of nasolacrimal duct

features
- frequent watery eye
- eye discharge
- infection

majority spontaneously open within 12 months

medial canthal massage is thought to increase the chance of opening

surgical options available if symptoms persist after 12 months

49
Q

describe strabismus

A

aka squint
> misalignment of visual axes

types
- concomitant
> imbalance in extraocular muscles
> convergent more common than divergent

  • paralytic
    > paralysis of extraocular muscles

features
- can be intermittent
- can have a refractive element
- assess cranial nerve palsies in case of SOL
- uncorrected can lead to amblyopia

inwards - esotropia
outwards - exotropia
up - hypertropia
down - hypotropia

investigations
- light shone in eye is in centre of cornea (hirschberg test)

50
Q

describe retinopathy of prematurity

A

babies born before 32 weeks or under 1.5kg

screening by ophthalmologist every 2 weeks

management
- transpupillary laser photocoagulation
- cryotherapy
- injections of intravitreal VEGF inhibitors

51
Q

describe leukocoria

A

white pupil

screened at newborn check and at 6 week check

causes
- retinoblastoma
- congenitl cataract

refer urgently to ophthalmology clinic

52
Q

describe signs of non-accidental injury in eyes in children

A

multiple retinal layer haemorrhages

caused by violent shaking or abuse

53
Q

list causes of anterior uveitis

A
  • idiopathic
  • HLA-B27 genotype associated diseases: inflammatory arthropathies, IBD
  • infections: toxoplasmosis, HSV, HZV, CMV, TB, Lyme disease, HIV, syphilis
  • other autoimmune/inflammatory diseases
  • traumatic
  • iatrogenic
  • cancer
54
Q

explain the treatment for primary open angle glaucoma

A

medication:
- prostaglandin analogues e.g. latanoprost (first-line in heart block)
- beta blockers e.g. timolol
- carbonic anhydrase inhibitors e.g. dorzolamide
- sympathomimetics e.g. brimonidine

laser: 360 selective laser trabeculoplasty (SLT)
> first-line when IOP >=24 mmHg

surgery: refractory cases
- trabeculectomy
- tube shunt
- minimal invasive glaucoma surgery (MIGS) e.g. eye stent

55
Q

describe retinitis pigmentosa

A

genetic condition causing degeneration of the photoreceptors in the retina (especially rods)

features
- night blindness
- peripheral visual loss

fundoscopy
- bone spicule pigmentation
- pigmentation most concentrated around mid-peripheral area of retina
- waxy / pale disc

management
- genetic counselling
- vision aids
- sunglasses to protect retina from accelerated damage

56
Q

describe posterior vitreous detachment

A

vitreous body comes away from retina

common in older age

presentation
- asymptomatic
- floaters/flashers
- blurred vision

management
- no treatment, improves as brain adjusts
- can predispose to retinal tears/detachment

57
Q

describe symptoms of age-related macular degeneration

A

symptoms (usually unilateral)

  • gradual loss of central vision (scotoma)
  • reduced visual acuity
  • crooked or wavy appearance to straight lines (metamorphopsia)
  • difficulties in dark adaptation, worse vision at night
  • photopsia (flickering/flashing lights), glare around objects
58
Q

list causes of Horner’s syndrome

A

4S, 4T, 4C

4S: Sentral (anhidrosis of face, arm and trunk)
- stroke
- multiple sclerosis
- swelling (tumours)
- syringomyelia

4T: torso (pre-ganglionic: anhidrosis of face)
- tumour (pancoast)
- trauma
- thyroidectomy
- top rib (cervical rib)

4C: cervical (post-ganglionic: no anhidrosis)
- carotid aneurysm
- carotid artery dissection
- cavernous sinus thrombosis
- cluster headache

also congenital horner’s syndrome (associated with heterochromia)

59
Q

list features of Horner’s syndrome

A
  • ptosis
  • miosis
  • anhidrosis
  • enophthalmos
60
Q

describe herpes zoster ophthalmicus and its management

A

reactivation of varicella zoster virus in area supplied by ophthalmic branch of trigeminal nerve (CN V)

features
- vesicular rash around eye
- Hutchinson’s sign: rash on tip/side of nose (strong risk factor for ocular involvement)

management
- oral antiviral treatment 7-10 days
> IV antivirals if immunocompromised
- topical corticosteroids if secondary inflammation of eye

complications
- ocular: conjunctivitis, keratitis, episcleritis, anterior uveitis
- ptosis
- post-herpetic neuralgia

61
Q

describe the mechanism of action and give an example for each of the following groups of drugs

  • carbonic anhydrase inhibitors
  • prostaglandin analogues
  • alpha 2 adrenoceptor agonist
  • beta blockers
  • muscarinic receptor agonist
A

carbonic anhydrase inhibitor e.g. dorzolamide
> decreases production of aqueous humour in eye so reduces IOP
> used to treat glaucoma
> side-effect: sulphonamide-like reaction

prostaglandin analogues e.g. latanoprost
> increase uveoscleral outflow which reduces IOP
> side-effect: increased eyelash length, iris pigmentation and periocular pigmentation

alpha 2 adrenoceptor agonists e.g. brimonidine
> decrease production of aqueous humour and increase outflow, thereby reducing IOP

beta blockers e.g. timolol
> decrease aqueous humour production
> side-effect: worsen asthma / heart block

muscarinic receptor agonists e.g. pilocarpine
> constrict ciliary muscles which opens trabecular meshwork and increases outflow of aqueous humour, reducing IOP

62
Q

describe nasolacrimal duct obstruction

A

most common cause of persistent watery eyes in infants

caused by imperforate membrane at lower end of lacrimal duct

management
- teach parents to massage duct
- symptoms resolve in 95% by one year
- refer unresolved cases to ophthalmology for consideration of probing

63
Q

describe a Homes-Adie pupil

A

features
> benign variant in women
> anisocoria worse in bright light
> slowly reactive to light with normal accommodation
> dilated pupil that remains small for an abnormally long time when it has constricted
> accompanied by absent knee/ankle jerks

64
Q

describe relative afferent pupillary defect (RAPD)

A

aka Marcus-Gunn pupil

caused by lesion anterior to optic chiasm

  • optic nerve: optic neuritis
  • retina: retinal detachment

swinging light test shows that the affected and normal eye appear to dilate when light is shone into the affected eye

65
Q

describe side-effects of pilocarpine

A

pupillary constriction, blurred vision, headaches

66
Q

What is the treatment for patients with suspected visual loss secondary to temporal arteritis?

A

IV methylprednisolone

67
Q

describe a fourth nerve palsy

A

CN IV

Clinical features
- vertical diplopia (worse when looking down and nasally)
> classically when reading a book or going down stairs

  • subjective tilting of objects (torsional diplopia)
  • when looking straight ahead the affected eye deviates upwards and outwards
68
Q

describe Holmes Adie syndrome

A

features
- dilated pupil, usually unilateral
- 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
- females
- absent leg reflexes

due to loss of parasympathetic innervation

69
Q

describe an Argyll-Robertson pupil

A

features
> associated with neurosyphilis and T2DM
> accommodation reflex present (ARP) but pupillary reflex absent
> both pupils small, irregular and unreactive to light but still accommodate

70
Q

describe a Hutchinson’s pupil

A

features
- unilaterally dilated pupil unresponsive to light
- due to ipsilateral oculomotor nerve compression
> haematoma
> tumour

71
Q

describe acanthamoeba keratitis

A

associated with contact lens use in bodies of water e.g. sea or swimming pools.

clinical features
- eye pain out of proportion to clinical findings
- reduced visual acuity
- redness, photophobia, and discharge

treatment
- antiamoebic: combined biguanide and diamidine therapy

Phase 4 (14 decks)

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