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Ophthalmology Flashcards

1
Q

OPEN ANGLE GLAUCOMA

What is glaucoma in general?

A
  • Optic neuropathies associated with raised intraocular pressure (IOP)
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2
Q

OPEN ANGLE GLAUCOMA

What is the pathophysiology of primary open angle glaucoma?

A
  • Gradual increased resistance to aqueous humour outflow through the trabecular meshwork leading to increased IOP
  • The iris is CLEAR of the meshwork
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3
Q

OPEN ANGLE GLAUCOMA

What are some risk factors for primary open angle glaucoma?

A
  • Increasing age + FHx
  • Black ethnic origin
  • Myopia
  • HTN + DM
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4
Q

OPEN ANGLE GLAUCOMA

What is the clinical presentation?

A
  • Insidious onset + may be Dx via routine screening at optometrist
  • Peripheral vision loss = tunnel vision
  • Halos around lights (esp. at night)
  • Decreased visual acuity
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5
Q

OPEN ANGLE GLAUCOMA
How is primary open angle glaucoma investigated?
What is gold standard?

A
  • Visual field assessment for peripheral vision loss
  • Fundoscopy
  • Measuring IOP (non-contact tonometry vs. GOLD STANDARD Goldmann applanation tonometry)
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6
Q

OPEN ANGLE GLAUCOMA

What might fundoscopy reveal in primary open angle glaucoma?

A
  • Optic disc cupping = cup:disc >0.7 (0.4–0.7) as IOP makes optic cup widen + deepen
  • Optic disc pallor = optic atrophy
  • Bayonetting of vessels = sharp kink as pass over edge of cup
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7
Q

OPEN ANGLE GLAUCOMA
What is the difference between the two methods of measuring IOP?
What is normal IOP and when is it treated?

A
  • Non-contact = screening, estimates IOP by shooting air at cornea
  • Goldmann applanation = device on slit lamp directly applies various pressures to cornea
  • Normal 10–21mmHg, treat when ≥24mmHg
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8
Q

OPEN ANGLE GLAUCOMA
What is the first line management of primary open angle glaucoma?
What is the mechanism of action?
What are some side effects?

A
  • Prostaglandin analogue eye drops = latanoprost
  • Increases uveoscleral outflow
  • Eyelash growth + brown iris pigmentation
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9
Q

OPEN ANGLE GLAUCOMA

In terms of second line management of primary open angle glaucoma, how can the drugs be categoried?

A
  • Drugs that reduce aqueous humour production = beta-blockers (timolol) and carbonic anhydrase inhibitors (dorzolamide)
  • Drugs that increase uveoscleral outflow = muscarinic receptor agonist/miotic (pilocarpine)
  • Drugs that do both = sympathomimetics/alpha-2-agonists (brimonidine)
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10
Q

OPEN ANGLE GLAUCOMA
What conditions would you avoid timolol in?
When would you avoid using brimonidine and what is an adverse effect?

A
  • Asthma + heart block

- Avoid if MAOI/TCA, can cause ocular hyperaemia

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11
Q

OPEN ANGLE GLAUCOMA
What is the mechanism of action of pilocarpine?
What is are some side effects?

A
  • Rapid miosis + contraction of ciliary muscles open trabecular meshwork so increased aqueous humour outflow
  • Miosis, headache + blurred vision
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12
Q

OPEN ANGLE GLAUCOMA

If medical management fails in primary open angle glaucoma, what option may be trialled?

A
  • Trabeculectomy = bleb creates new channel for aqueous humour to drain from anterior chamber
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13
Q

ACUTE ANGLE CLOSURE GLAUCOMA

What is the pathophysiology of acute angle closure glaucoma?

A
  • Iris bulges forward + seals off the trabecular meshwork from the anterior chamber preventing drainage of aqueous humour = acute raised IOP
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14
Q

ACUTE ANGLE CLOSURE GLAUCOMA
What are some risk factors of acute angle closure glaucoma?
What medications can precipitate it?

A
  • Hypermetropia, female, Eastern Asian, FHx, cataracts

- Adrenergics (noradrenaline), anticholinergics = both cause mydriasis

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15
Q

ACUTE ANGLE CLOSURE GLAUCOMA

What symptoms may a patient experience in acute angle closure glaucoma?

A
  • Acute, severely painful red eye
  • Blurred vision
  • Halos around lights
  • Headache
  • N+V
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16
Q

ACUTE ANGLE CLOSURE GLAUCOMA

What are some signs of acute angle closure glaucoma on examination?

A
  • Dull/hazy cornea due to corneal oedema
  • Semi-dilated non-reacting pupil
  • Firm eyeball on palpation
  • Decreased visual acuity
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17
Q

ACUTE ANGLE CLOSURE GLAUCOMA

How do you manage someone with acute angle closure glaucoma initially?

A
  • EMERGENCY = same-day ophthalmologist assessment
  • Combination of eye drops = pilocarpine, timolol, brimonidine
  • IV acetazolamide
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18
Q

ACUTE ANGLE CLOSURE GLAUCOMA

What is the definitive management of acute angle closure glaucoma?

A
  • Laser peripheral iridotomy = hole in peripheral iris allows aqueous humour to flow posterior > anterior chamber which relieves pressure pushing iris against cornea
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19
Q

AGE-RELATED MACULAR DEGENERATION
What are the two types of age-related macular degeneration (AMD)?
What is the epidemiology?

A
  • Dry (90%) and wet (10%)

- Most common cause of blindness in the UK

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20
Q

AGE-RELATED MACULAR DEGENERATION

What is the pathophysiology of dry AMD?

A
  • Drusen in Dry
  • Caused by atrophy of the retinal pigment epithelium + retinal photoreceptor degeneration > protein/lipid deposits (drusen)
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21
Q

AGE-RELATED MACULAR DEGENERATION

What is the pathophysiology of wet AMD?

A
  • Choroidal neovascularisation into retina where leakage of serous fluid + blood can lead to rapid loss of vision
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22
Q

AGE-RELATED MACULAR DEGENERATION
What is the biggest risk factor of AMD?
What are some other risk factors?

A
  • Advancing age

- Smoking, FHx, CVD risk factors

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23
Q

AGE-RELATED MACULAR DEGENERATION
What is the clinical presentation of AMD?
How may this differ in wet AMD?

A
  • Gradual worsening CENTRAL visual loss = central scotoma
  • Reduced visual acuity, esp. low lighting + near field objects
  • Fluctuations in visual disturbance which vary day-to-day
  • Crooked/wavy appearance of straight lines
  • Wet = ACUTE vision loss
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24
Q

AGE-RELATED MACULAR DEGENERATION

What are some tests you would do when examining someone with suspected AMD?

A
  • Snellen chart = reduced visual acuity
  • Amsler grid test = assess distortion of straight lines
  • Fundoscopy
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25
Q

AGE-RELATED MACULAR DEGENERATION
What would you see on fundoscopy for dry AMD?
What would you see on fundoscopy for wet AMD?

A
  • Drusen in macular area

- Demarcated red patches = intra-retinal or sub-retinal fluid leakage or haemorrhage

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26
Q

AGE-RELATED MACULAR DEGENERATION
What is the first line specialist investigation in AMD?
What investigation is mandatory for diagnosis + follow-up?
What other investigation is there and when would you use it?

A
  • Slit-lamp microscopy
  • Optical coherence tomography = X-sectional view of layers of retina
  • Fluorescein angiography = if ?neovascularisation, detects leakage
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27
Q

AGE-RELATED MACULAR DEGENERATION
How do you manage AMD in general?
What is the management of dry AMD?

A
  • Urgent referral to ophthalmology

- Avoid smoking, control BP, vitamin supplementation (zinc + vitamins A/C/E)

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28
Q

AGE-RELATED MACULAR DEGENERATION

What is the definitive management of wet AMD?

A
  • Anti-vascular endothelial growth factor (VEGF) medications (ranibizumab, bevacizumab) 4/52 intravitreous injection
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29
Q

AGE-RELATED MACULAR DEGENERATION
What treatment may be considered in AMD if there is neovascularisation?
What is an important risk of this treatment?

A
  • Laser photocoagulation to slow progression of AMD

- Risk of acute visual loss after treatment

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30
Q

CATARACTS
What is the pathophysiology of cataracts?
What is the epidemiology?

A
  • Gradual lens opacification reducing visual acuity by reducing the light that reaches the retina
  • Leading cause of curable blindness worldwide, more common in women
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31
Q

CATARACTS
What is the most common cause of cataracts?
What are some risk factors and what type of cataracts do they relate to?

A
  • Normal ageing process (nuclear type)
  • CVD = smoking, alcohol, DM (dot opacities type)
  • Steroids (Subcapsular type)
  • Hypocalcaemia
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32
Q

CATARACTS

What is the clinical presentation of cataracts?

A
  • Asymmetrical gradual reduction in visual acuity + progressive blurring
  • Glare + halos around lights, esp. at night
  • Faded colour vision = colours more brown/yellow
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33
Q

CATARACTS

What investigations would you do in cataracts?

A
  • Fundoscopy = loss of red reflex (grey/white) but normal fundus + optic nerve
  • Slit-lamp examination reveals visible cataract
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34
Q

CATARACTS
What is the initial management of cataracts?
What is the definitive management of cataracts?

A
  • Prescribing stronger lenses, encourage bright lights

- Cataract surgery = replace lens with artificial one (only effective treatment)

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35
Q

CATARACTS

Before referring someone for cataracts surgery, what factors should be considered?

A
  • Impact on vision + QOL
  • If they’re uni or bilateral
  • Risk/benefits
  • Patient choice
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36
Q

CATARACTS

What are some complications of cataract surgery?

A
  • Endophthalmitis
  • Posterior capsule opacification = thickening of lens capsule
  • Retinal detachment
  • Posterior capsule rupture
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37
Q

CATARACTS
What is endophthalmitis?
What can it progress to?
How is it managed?

A
  • Rare but serious inflammation of inner eye contents often 2º to infection
  • Can progress to vision or even eye loss
  • Intravitreal Abx
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38
Q

CRAO

What is the pathophysiology of central retinal artery occlusion (CRAO)?

A
  • Occlusion > reduced central retinal artery blood flow which supplies the retina
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39
Q

CRAO
What is the most common cause of CRAO?
What are some other causes?
What are some risk factors?

A
  • Atheroscelrosis
  • Emboli or vasculitis (GCA)
  • CVD = smoking, HTN, alcohol, DM, obesity
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40
Q

CRAO

What is the clinical presentation and examination findings in CRAO?

A
  • Sudden painless monocular loss of vision
  • RAPD due to ischaemic retina not sensing input
  • Fundoscopy = pale retina (reduced perfusion) + cherry red spot at macula
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41
Q

CRAO

What is the management of CRAO?

A
  • Immediate ophthalmologist assessment

- Long-term = optimise CVD risk factors

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42
Q

CRVO
What is the pathophysiology of central retinal vein occlusion (CRVO)?
What is a potential consequence of this?

A
  • Thrombus blocks drainage of blood from retinal veins causing pooling of blood in retina + so macular oedema + retinal haemorrhages
  • May lead to release of VEGF > neovascularisation
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43
Q

CRVO

What are some risk factors of CRVO?

A
  • CVD = smoking, alcohol, HTN, DM, obesity

- Thrombophilias = polycythaemia

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44
Q

CRVO

What is the clinical presentation of CRVO?

A
  • Sudden painless monocular loss of vision
  • RAPD
  • Fundoscopy = widespread flame haemorrhages “stormy sunset” + optic disc swelling
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45
Q

CRVO
What is a key differential of CRVO?
What is it?

A
  • Branch retinal vein occlusion

- Vein in distal retinal venous system is occluded so more limited area of fundus affected

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46
Q

CRVO

How does branch retinal vein occlusion present?

A
  • Blurring of vision or field defect rather than total loss

- Flame haemorrhages in region of occlusion on fundoscopy

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47
Q

CRVO

What is the management of CRVO?

A
  • Immediate ophthalmologist assessment
  • Majority conservative
  • Macular oedema = intravitreal anti-VEGF (ranibizumab)
  • Retinal neovascularisation = laser photocoagulation
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48
Q

AION
What is anterior ischaemic optic neuropathy (AION)?
What are the two types?

A
  • Optic nerve damage due to lack of blood supply

- Arteritic (most commonly GCA) or non-arteritic

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49
Q

AION

What is the clinical presentation and exam findings of AION?

A
  • Sudden onset monocular vision loss
  • RAPD
  • Fundoscopy = optic disc swelling (acute phase) + pale (chronic phase)
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50
Q

AION

What is the management of AION?

A
  • Immediate ophthalmology assessment
  • Always check FBC, CRP/ESR, ?temporal artery biopsy if GCA
  • GCA = high dose steroids to prevent vision loss
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51
Q

POSTERIOR VITREOUS DETACHMENT
What is the pathophysiology of posterior vitreous detachment?
What is a consequence of this?

A
  • Vitreous gel separates from the retina due to natural changes to the vitreous fluid of the eye with ageing (less firm + able to maintain shape)
  • Predisposes to retinal tears or detachment
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52
Q

POSTERIOR VITREOUS DETACHMENT
What is the clinical presentation of posterior vitreous detachment?
What are some risk factors?

A
  • Can be asymptomatic, more common in F
  • Sudden onset flashes + floaters
  • Painless blurred vision
  • Age, highly myopic pts
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53
Q

POSTERIOR VITREOUS DETACHMENT

What is a key investigation in posterior vitreous detachment and what may it show?

A
  • Ophthalmoscopy = Weiss ring

- Detachment of vitreous membrane around the optic nerve to form a ring-shaped floater

54
Q

POSTERIOR VITREOUS DETACHMENT

What is the management of posterior vitreous detachment?

A
  • Ophthalmology assessment within 24h > rule out retinal tear or detachment
  • Improves without treatment over 6m
  • Surgery if associated retinal tear or detachment
55
Q

RETINAL DETACHMENT

What is the pathophysiology of retinal detachment?

A
  • Retina separates from choroid underneath usually due to retinal tear allowing vitreous fluid to get under retina + fill space between retina/choroid
  • Outer retina relies on choroidal vessels for blood supply > emergency
56
Q

RETINAL DETACHMENT
What are the two main causes of retinal detachment?
What are some risk factors?

A
  • Retinal tear
  • Vitreous collapse (with age) > posterior vitreous detachment
  • Age, eye trauma, FHx
57
Q

RETINAL DETACHMENT

What is the clinical presentation of retinal detachment?

A
  • New onset flashes + floaters
  • Painless blurred vision
  • Peripheral>central vision loss “sudden + like a shadow coming across vision”
58
Q

RETINAL DETACHMENT

What is the management of retinal detachment?

A
  • Immediate ophthalmology referral
  • Retinal tears = laser therapy or cryotherapy > create adhesions between retina/choroid to prevent detachment
  • Retinal detachment = vitrectomy > surgery to reattach retina
59
Q

VITREOUS HAEMORRHAGE
What is a vitreous haemorrhage?
What are some causes?

A
  • Bleeding from retinal vessels into vitreous gel

- Proliferative diabetic retinopathy in 50%, ocular trauma (#1 paeds/young adults), retinal tear/detachment

60
Q

VITREOUS HAEMORRHAGE

What is the clinical presentation of vitreous haemorrhage?

A
  • Painless monocular vision loss
  • Red hue in vision
  • Blurred vision with floaters or black dots
  • NO RAPD, absent red reflex
61
Q

VITREOUS HAEMORRHAGE

What investigations would you do in vitreous haemorrhage?

A
  • Fundoscopy
  • Slit lamp examination
  • USS eye to rule out retinal tear/detachment
62
Q

VITREOUS HAEMORRHAGE

What is the management of vitreous haemorrhage?

A
  • Clears spontaneously within 6–8w
  • ?Vitrectomy
  • Laser photocoagulation in proliferative diabetic retinopathy
63
Q

CONJUNCTIVITIS

What is conjunctivitis?

A
  • Inflammation of the conjunctiva either allergic, viral or bacterial
64
Q

CONJUNCTIVITIS
What are the causes of conjunctivitis that is…

i) allergic?
ii) viral?
iii) bacterial?

A

i) Seasonal (pollen) or perennial (dust mite, detergents)
ii) HSV, adenovirus
iii) H. influenzae, staph. aureus, strep pneumoniae

65
Q

CONJUNCTIVITIS

What is the clinical presentation of allergic conjunctivitis?

A
  • BILATERAL conjunctival erythema

- Allergic Sx = nasal congestion, sneezing, eyelid swelling, itch

66
Q

CONJUNCTIVITIS

How can you differentiate the clinical presentation of infective conjunctivitis?

A
  • Bacterial = PURULENT discharge, eyes stuck together in morning
  • Viral = SEROUS discharge, recent URTI, pre-auricular lymphadenopathy
67
Q

CONJUNCTIVITIS

What is the management of allergic conjunctivitis?

A
  • First line = avoid allergens, topical/systemic antihistamines
  • Second line = topical mast-cell stabilisers to prevent histamine release
68
Q

CONJUNCTIVITIS

What is the management of infective conjunctivitis?

A
  • Often self-limiting, no contact lenses, avoid sharing towels
  • Topical chloramphenicol if bacterial
  • Topical fusidic acid is alternative in pregnant women
69
Q

EPISCLERITIS
What is episcleritis?
What conditions is it associated with?

A
  • Inflammation of outermost layer of sclera, just underneath the conjunctiva
  • Inflammatory disorders = rheumatoid arthritis, IBD
70
Q

EPISCLERITIS

What is the clinical presentation of episcleritis?

A
  • Painless red eye (may be mild pain)
  • Episcleral injected vessels are MOBILE with gentle scleral pressure
  • Watering of eye
71
Q

EPISCLERITIS

What investigation can be done to confirm the diagnosis and differentiate it from the main differential?

A
  • Phenylephrine drops blanch conjunctival + episcleral but NOT scleral vessels
  • Eye redness improves after drops = episcleritis
72
Q

EPISCLERITIS

What is the management of episcleritis?

A
  • Conservative with analgesia, cold compresses + safety netting
  • Artificial tears may be used
73
Q

SCLERITIS
What is scleritis?
What is the most serious type and why?

A
  • Inflammation of the full thickness of the sclera

- Necrotising scleritis = visual impairment but NO pain, risk of scleral perforation

74
Q

SCLERITIS

What is scleritis associated with?

A
  • 50% systemically unwell with rheum conditions such as RA, SLE, granulomatosis with polyangiitis + IBD
75
Q

SCLERITIS

What is the clinical presentation of scleritis?

A
  • PAINFUL red eye with NO response to phenylephrine drops
  • Injected vessels are NOT mobile with scleral pressure as deeper
  • Reduced visual acuity
76
Q

SCLERITIS

What is the management of scleritis?

A
  • Same day ophthalmology referral
  • NSAIDs (topical/systemic)
  • Steroids (topical/systemic)
77
Q

ANTERIOR UVEITIS

What is anterior uveitis?

A
  • Inflammation in the anterior part of the uvea (iris + ciliary body)
78
Q

ANTERIOR UVEITIS

What are the causes of acute and chronic anterior uveitis?

A
  • Acute (HLA B27) = ankylosing spondylitis, reactive arthritis, psoriatic arthritis, IBD
  • Chronic = sarcoidosis, infections (TB, syphilis, herpes)
79
Q

ANTERIOR UVEITIS

What is the clinical presentation of anterior uveitis?

A
  • Unilateral painful red eye + ophthalmoplegia
  • Photophobia (ciliary muscle spasm)
  • Abnormal pupil shape (posterior synechiae/adhesions)
  • Ciliary flush (red ring spreading from cornea outwards)
  • Hypopyon (pus collection in anterior chamber = yellow fluid with a level)
  • Floaters + flashers
80
Q

ANTERIOR UVEITIS

What is the management of anterior uveitis?

A
  • Same day ophthalmology referral
  • Cycloplegic-mydriatic eye drops = cyclopentolate, atropine (antimuscarinics)
  • Steroid eye drops
81
Q

ANTERIOR UVEITIS

How do cycloplegic-mydriatic eye drops help in anterior uveitis?

A
  • Paralyses ciliary body + causes mydriasis to reduce pain associated with ciliary muscle spasm
82
Q

KERATITIS
What is keratitis?
What are the two main types?

A
  • Inflammation of the cornea

- Herpes keratitis + bacterial keratitis

83
Q

KERATITIS
What causes herpes keratitis?
What often precipitates bacterial keratitis?

A
  • Reactivation of HSV1 which lies dormant in trigeminal ganglion
  • Often precipitated by minor trauma due to corneal abrasion or contact lens use
84
Q

KERATITIS

What is the main cause of bacterial keratitis and how may this differ?

A
  • Usually Staph. aureus

- Pseudomonas aeruginosa or amoebic (acanthamoebic keratitis, contaminated water) in contact lens wearers

85
Q

KERATITIS

What is the clinical presentation of keratitis?

A
  • Red eye with pain + photophobia
  • Foreign body/gritty sensation
  • Bacterial = may have hypopyon
  • Reduced visual acuity (may have corneal opacification)
86
Q

KERATITIS

What is a pathognomonic sign of herpes keratitis?

A
  • Dendritic ulcers seen on slit lamp with fluorescein
87
Q

KERATITIS

What are some complications of keratitis?

A
  • Corneal scarring > blindness (#1 form of corneal blindness in developed world)
  • Endophthalmitis
  • Perforation
88
Q

KERATITIS

What is the management of keratitis?

A
  • Contact lens wearers with red eye = same day ophthalmology slit-lamp to rule out microbial keratitis
  • Bacterial = topical Abx
  • HSV = topical aciclovir as untreated > corneal scarring (?transplant)
89
Q

CORNEAL ABRASIONS

What is a corneal abrasion and what causes it?

A
  • Damage to corneal epithelium often 2º to trauma to the eye (contact lenses, foreign body, entropion) or occupational (sheet metal working)
90
Q

CORNEAL ABRASIONS
What is the clinical presentation of a corneal abrasion?
How would you investigate this?

A
  • Painful red eye, foreign body sensation, watering eye
  • May develop corneal ulcer (deeper breach in corneal epithelium)
  • Fluorescein stain applied to eye = stain collects in abrasion highlighting it
91
Q

CORNEAL ABRASIONS

What is the management of corneal abrasions?

A
  • Same day ophthalmology referral for slit lamp exam

- Uncomplicated = simple analgesia, lubricating eye drops, follow-up in 24h

92
Q

SUBCONJUNCTIVAL HAEMORRHAGE

What is a subconjunctival haemorrhage?

A
  • Small blood vessels within conjunctiva ruptures + releases blood into the space between the sclera + conjunctiva
93
Q

SUBCONJUNCTIVAL HAEMORRHAGE

What causes a subconjunctival haemorrhage?

A
  • Often after episodes of strenuous activity or trauma
  • Whooping cough
  • Sneezing
  • HTN
  • NAI
  • Bleeding disorders + anticoagulants
94
Q

SUBCONJUNCTIVAL HAEMORRHAGE
What is the clinical presentation of subconjunctival haemorrhage?
What is the management?

A
  • Painless patch of bright red blood

- Spontaneous recovery in about 2w

95
Q

PERIORBITAL/ORBITAL CELLULITIS
What is periorbital cellulitis?
What is orbital cellulitis?

A
  • Infection of soft tissues anterior to orbital septum (eyelids, skin, subcut tissues) but NOT contents of orbit
  • Infection affecting fat + muscles posterior to orbital septum within the orbit but NOT involving globe
96
Q

PERIORBITAL/ORBITAL CELLULITIS
What usually causes periorbital cellulitis?
What usually causes orbital cellulitis?

A
  • Spread from superficial tissue injury (chalazion, insect bite)
  • Spreading infection from URTI or sinusitis
97
Q

PERIORBITAL/ORBITAL CELLULITIS
What are some common bacterial causes of periorbital cellulitis?
What are some common bacterial causes of orbital cellulitis?
What are some risk factors for orbital cellulitis?

A
  • Staph aureus, staph epidermidis, streptococci
  • Staph aureus, HiB, streptococci
  • Paeds, previous sinusitis, no HiB vaccine, periorbital cellulitis
98
Q

PERIORBITAL/ORBITAL CELLULITIS
What is the clinical presentation of periorbital cellulitis?
How is this differentiated from orbital cellulitis?

A
  • Symptoms = acute onset red, swollen + painful eye, fever

- Signs = erythema + oedema of eyelids, ptosis due to swelling (signs differentiate from orbital cellulitis)

99
Q

PERIORBITAL/ORBITAL CELLULITIS
What is the clinical presentation of orbital cellulitis?
What are some potential major complications of orbital cellulitis?

A
  • Symptoms = acute onset red, swollen + painful eye, fever
  • Signs = ophthalmoplegia, proptosis, decreased acuity, RAPD
  • Cavernous sinus thrombosis or intracranial infection
100
Q

PERIORBITAL/ORBITAL CELLULITIS

What are some investigations you would do in periorbital and orbital cellulitis?

A
  • Bloods = FBC (raised WCC), CRP raised, blood cultures + swab MC&S
  • Contrast CT orbits, sinuses + brain scan to look for inflammation of orbital tissues deep to septum to Dx
101
Q

PERIORBITAL/ORBITAL CELLULITIS
What is the management of pre-orbital cellulitis?
What is the management of orbital cellulitis?

A
  • Urgent ophthalmology referral, PO/IV Abx, ?admit if paeds

- Ophthalmology emergency > admit for IV Abx

102
Q

BLEPHARITIS
What is blepharitis?
What are some causes?

A
  • Inflammation of the eyelid margins
  • Meibomian gland dysfunction (common, posterior)
  • Seborrhoeic dermatitis/staph infection (less common, anterior)
  • Rosacea
103
Q

BLEPHARITIS
What is the usual function of the Meibomian gland?
What occurs in dysfunction?

A
  • Secrete oil onto eye surface to prevent rapid evaporation of tear film
  • Drying + irritation
104
Q

BLEPHARITIS

What is the clinical presentation of blepharitis?

A
  • Bilateral grittiness + dryness
  • Eyelid margins red + itchy
  • Swollen eyelids in staph blepharitis
  • Styes + chalazions more common
105
Q

BLEPHARITIS

What is the management of blepharitis?

A
  • Hot compress BD to soften lid margin
  • Lid hygiene to mechanically remove debris = cotton wool buds dipped in cooled boiled water or baby shampoo
  • Lubricating eye drops for symptomatic control
106
Q

EYELID DISORDERS – STYE

What is the classification of styes?

A
  • Hordeolum externum = infection of glands of Zeis (sebum producing) or glands of Moll (sweat glands) at base of eyelashes, usually staphyloccal
  • Hordeolum internum = infection of Meibomian glands, may result in chalazion
107
Q

EYELID DISORDERS – STYE
How do styes present?
How are they managed?

A
  • Tender red lump along eyelid ±pus
  • Hot compresses + analgesia
  • ?Topical chloramphenicol if associated with conjunctivitis
108
Q

EYELID DISORDERS – CHALAZION
What is a chalazion?
What can cause it?

A
  • Meibomian gland becomes blocked and swells > Meibomian cyst
  • Hordeolum internum
109
Q

EYELID DISORDERS – CHALAZION
How do chalazions present?
How are they managed?

A
  • Firm, non-tender swelling in eyelid (often upper)
  • Hot compresses + analgesia
  • ?Topical chloramphenicol if acutely inflamed
  • Few require surgical drainage
110
Q

EYELID DISORDERS – ENTROPION
What is entropion?
How does this present?

A
  • Eyelid turns inwards with lashes against the eyeball

- Pain which can lead to corneal damage (abrasions) + ulceration

111
Q

EYELID DISORDERS – ENTROPION

What is the initial management of entropion?

A
  • Same-day ophthalmology referral if risk to sight

- Taping eyelid down to prevent inwards turning (with lubricating eye drops to prevent eye drying out)

112
Q

EYELID DISORDERS – ENTROPION

What is the definitive management of entropion?

A
  • Surgical intervention
113
Q

EYELID DISORDERS – ECTROPION
What is ectropion?
What is a consequence of this?

A
  • Eyelid turns outwards with inner aspect of eyelid exposed (often bottom lid)
  • Exposure keratopathy as eyeball exposed + not adequately lubricated + protected
114
Q

EYELID DISORDERS – ECTROPION

What is the management of ectropion?

A
  • Same-day ophthalmology referral if risk to sight
  • Mild = may only need regular lubricating eye drops
  • Significant cases = surgery
115
Q

EYELID DISORDERS – TRICHIASIS

What is trichiasis?

A
  • Inward growth of eyelashes > pain + can lead to corneal damage (abrasion)/ulceration
116
Q

EYELID DISORDERS – TRICHIASIS

What is the management of trichiasis?

A
  • Same-day ophthalmology referral if risk to sight
  • Eyelash removal (epilation)
  • Recurrent cases = electrolysis, cryotherapy or laser treatment to prevent lash regrowth
117
Q

HERPES ZOSTER OPHTHALMICUS

What is herpes zoster ophthalmicus?

A
  • Reactivation of the varicella zoster virus in the area supplied by the ophthalmic division of the trigeminal nerve
118
Q

HERPES ZOSTER OPHTHALMICUS
What is the clinical presentation of herpes zoster ophthalmicus?
What is an important sign?

A
  • Painful red eye
  • Vesicular rash around eye ± actual eye involvement
  • Hutchinson’s sign = rash on tip/side of nose > nasociliary involvement + strong indicator for ocular involvement
119
Q

HERPES ZOSTER OPHTHALMICUS

What are some potential complications of herpes zoster ophthalmicus?

A
  • Ocular involvement = conjunctivitis, keratitis, episcleritis, anterior uveitis
  • Post-herpetic neuralgia
120
Q

HERPES ZOSTER OPHTHALMICUS

What is the management of herpes zoster ophthalmicus?

A
  • Ocular involvement = same day ophthalmology review
  • PO aciclovir 7–10d started within 72h (IV if severe or immunocompromised)
  • Do NOT Rx top steroids without ophthalmology guidance
121
Q

HORNER’S SYNDROME
What are the three main causes of Horner’s syndrome?
How can they be differentiated by clinical presentation?

A
  • Central lesions (S–entral) = anhidrosis of face, arm + trunk
  • Pre-ganglionic lesions (T–orso) = anihydrosis of the face
  • Post-ganglionic lesions (C-ervical) = no anhidrosis
122
Q

HORNER’S SYNDROME
What are some causes of…

i) central Horner’s syndrome?
ii) pre-ganglionic Horner’s syndrome?
iii) post-ganglionic Horner’s syndrome?

A

i) Stroke, Syringomelia, multiple Sclerosis
ii) pancoast Tumour, Thyroidectomy, Trauma
iii) Carotid artery dissection + aneurysm, Cavernous sinus thrombosis, Cluster headache

123
Q

HORNER’S SYNDROME
What is the classic clinical presentation of Horner’s syndrome?
What other features may be present?

A
  • Triad = miosis, ptosis + unilateral anihidrosis
  • Enophthalmos (sunken eye)
  • Heterochromia (difference in iris colour) in congenital Horner’s
124
Q

HORNER’S SYNDROME
What test can be used in Horner’s syndrome to confirm?
What happens?

A
  • Apraclonidine (alpha adrenergic agonist) drops
  • Pupillary dilation in Horner’s (hypersensitive) but mild miosis in normal pupil as down-regulates noradrenaline release
125
Q

HYPERTENSIVE RETINOPATHY
What is hypertensive retinopathy?
What classification is used?

A
  • Damage to small blood vessels in the retina due to systemic HTN
  • Keith-Wagener classification
126
Q

HYPERTENSIVE RETINOPATHY

What are the various stages of hypertensive retinopathy?

A
  • I = arteriolar narrowing + tortuosity, increased light reflex (silver wiring as arterioles sclerosed)
  • II = arteriovenous nipping (compression of veins where sclerosed arterioles cross)
  • III = cotton-wool spots, hard exudates + retinal haemorrhages
  • IV = papilloedema (ischaemia to optic nerve > oedema + blurred margins)
127
Q

RETINITIS PIGMENTOSA

What is retinitis pigmentosa?

A
  • Congenital inherited condition with degeneration of rods + cones in retina
  • Often rods degenerate more than cones > night blindness
128
Q

RETINITIS PIGMENTOSA
What is the clinical presentation of retinitis pigmentosa?
When does it normally present and who in?

A
  • Peripheral vision lost first = tunnel vision
  • Night blindness may be first Sx
  • Sx start in childhood in those with positive FHx
129
Q

RETINITIS PIGMENTOSA

What might you see on fundoscopy in retinitis pigmentosa?

A
  • Black “bone-spicule” pigmentation in peripheral retina
  • Optic disc pallor
  • Retinal vessel narrowing
130
Q

RETINITIS PIGMENTOSA

What is the management of retinitis pigmentosa?

A
  • Ophthalmology referral for assessment + diagnosis

- Vision aids + sunglasses to protect retina from accelerated damage

FINALS (20 decks)

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