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Ophthalmology Flashcards

1
Q

What is glaucoma?

A

optic nerve damage caused by a rise in intra-ocular pressure by blockage in aqueous humour trying to escape eye
*peripheral vision loss then total

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2
Q

What is the path of travel for aqueous humour?

A
  • produced by ciliary body
  • flows through posterior chamber and around iris into anterior
  • drain through trabecular meshwork to canal of schlemm
  • eventually entering general circulation
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3
Q

What is the normal intra ocular pressure?

A

10-21 mmHg

*created by resistance to flow through trabecular meshwork

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4
Q

What is the pathophysiology of acute angle-closure glaucoma?

A

iris bulges forward and seals off trabecular meshwork from anterior chamber, preventing aqueous drainage

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5
Q

What is the pathophysiology of open angle glaucoma?

A

gradual increase in resistance to flow through the trabecular meshwork, pressure slowly builds up

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6
Q

What are some risk factors of open angle glaucoma?

A

increasing age
family history
black ethnic origin
myopia

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7
Q

What are some risk factors of close-angle glaucoma?

A

increasing age
family history
Chinese and was asian ethnic origin
shallow anterior chambers
female

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8
Q

What medications might precipitate acute angle-closure?

A
  • adrenergic eg: noradrenaline
  • anticholinergic eg: oxybutynin and solifenacin
  • tricyclic eg: amitriptyline
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9
Q

How does closed angle closure present?

A
  • severely painful red eye
  • blurred vision
  • halos around lights
  • associated headaches, N+V

o/e - red eye, hazy cornea, decreased visual acuity, mid-dilated pupil not reactive to light, hard eye on gentle palpation

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10
Q

How does open angle present?

A

fluctuating pain, headaches, blurred vision, halos around lights, particularly at night

*peripheral loss of vision, arcuate scotomoa, nasal step

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11
Q

What are some secondary causes of glaucoma?

A

iatrogenic, lens relates issues like cataracts, medicine related like steroids, neovascular, pigment related

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12
Q

How would you investigate suspected glaucoma?

A
  • measure intra-ocular pressure with non-contact tonometry or Goldmann
  • slit lamp for cup-disk ratio and angle
  • visual field
  • gonioscopy
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13
Q

How do you manage open-angle glaucoma?

A

360 degree selective laser trabeculoplasty
prostaglandin analogue - latanoprost
beta blocker - timolol
carbonic anhydrase inhibitor - dorzolamide
sympathomimetics
trabeculectomy

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14
Q

How do you manage closed angle glaucoma?

A

initial - pilocarpine, acetazolamide, other like timolol, latanoprost, analgesia

secondary - pilocarpine, acetazolamide, timolol, brimonidine

*Definitive - laser iridotomy

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15
Q

What is uveitis?

A

inflammation of uveal tract, comprising iris, ciliary body and choroid
*commonly uveitis

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16
Q

What is anterior uveitis?

A

iritis - which only affects the iris and iridocyclitis affects iris and ciliary body

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17
Q

What are some causes of iritis?

A

HLA-B27 conditions - AS, reactive arthritis, IBD
autoimmune - sarcoidosis, vasculitis
infection - herpes, herpes zoster
traumatic
iatrogenic - surgery, bisphosphonates
cancer - leukaemia, malignant melanoma

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18
Q

What is intermediate uveitis?

A

inflammation of ciliary body
*no pain, blurring vision, floaters

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19
Q

What is posterior uveitis?

A

inflammation of back of eye - retina or choroid

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20
Q

How does anterior uveitis present?

A

*over few hours or gradually over several

  • bilateral presentation - systemic conditions
  • unilateral - idiopathic or herpetic
  • painful, red eye with blurring of vision
  • photophobia
  • tearing
  • systemic - joint pain, back pain, flare up of IBD, infective sx

*chronic or intermediate and posterior - painless and decreased vision

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21
Q

How is anterior uveitis investigated?

A

general - ciliary injection, irregular pupil, cloudy cornea, hypopyon
slit lamp - ciliary flush, inflammatory cells in anterior chamber, flare, adhesions between lens and pupil
lab - bloods for HLA-B27, ANA, infectious diseases screen
OCT - macular oedema, CXR, spinal XR for AS

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22
Q

How is anterior uveitis managed?

A

*can be self limiting

  • ophthalmologist referral 24h assessment
  • aim to control inflammation, prevent visual loss, minimise long term complications
  • topical steroid drops to reduce inflammation
  • pupil dilating drops (cyclopentolate) to alleviate sx
  • treat underlying
  • systemic in severe - steroids and immunosuppressants
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23
Q

What are the complications of anterior uveitis?

A
  • severe - vision loss
  • macular oedema
  • secondary cataract
  • rise in intra-ocular pressure by inflammation of trabecular meshwork
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24
Q

What is conjunctivitis?

A

inflammation of the conjunctiva - thin layer of tissue that covers the inside of the eyelids and the sclera
*bacterial, viral or allergic

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25
Q

What is the pathophysiology of conjunctivitis?

A
  • bacterial - staphylococcus aureus,Streptococcus pneumoniae,Haemophilus influenzae
  • allergic - when in contact with allergens
  • also can be from irritation like smoke, dust, wearing contact lenses longer or without cleaning etc
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26
Q

What is the presentation of conjunctivitis?

A

*no pain, photophobia or reduced visual acuity
- red, blood shot eye
- itchy, gritty sensation
- discharge + blurry vision purulent for bacterial, clear for viral, muco-purulend for chlamydial, swelling of conjunctival sac for allergic

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27
Q

How might you investigate conjunctivitis?

A
  • contact lens wearers - topical fluoresceins to identify any corneal staining
  • swabs for viral or chlamydial
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28
Q

How can you manage conjunctivitis?

A

*1-2w without tx
- hygiene measures, avoid spread
- clean with cooled boiled water
- chloramphenicol or fusidic acid drops
- antihistamines for allergic
- nO CONTACTS worn

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29
Q

When would conjunctivitis be a red flag?

A

👁️ neonatal - <1m urgent ophthal assessment

  • gonococcal infection with permanent vision loss complications
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30
Q

What is scleritis?

A

inflammation of the sclera, which is the outer layer of connective tissue surrounding most of eye, except cornea

*RA, vasculitis like granulomatosis with polyangiitis or less commonly infection

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31
Q

How might scleritis present?

A
  • red, inflamed sclera - localised or diffuse
  • congested vessles
  • severe pain (boring pain)
  • pain with eye movement
  • photophobia
  • epiphoria - excessive tears
  • reduced visual acuity
  • tenderness to palpation of eye

*white patch on sclera if ischaemia and necrosis

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32
Q

How is scleritis managed?

A
  • MDT
  • NSAIDs oral
  • topical or systemic steroids
  • immunosuppression - for underlying condition eg:methotrexate
  • antimicrobials for infectious
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33
Q

How is episcleritis different?

A

localised area, outer layer of sclera

*associated with RA and IBD

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34
Q

How does episcleritis present?

A
  • localised or diffuse redness - patch in lateral sclera
    • triangle of redness
  • no pain or mild pain
  • dilated episcleral vessels
  • injected vessels are mobile when gentle pressure is applied on the sclera
  • NO photophobia or discharge and normal visual acuity - SCLERITIS
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35
Q

How might episcleritis be investigated?

A
  • apply phenylephrine eye drops - cause blanching of episcleral vessels causing redness to disappear
    • will NOT affect scleral vessels and will not impact this redness
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36
Q

How is episcleritis managed?

A
  • self limiting in 1-2w
  • analgesia like ibuprofen
  • lubricating eye drops
  • severe - steroid eye drops
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37
Q

What is the pathophysiology of a corneal ulcer?

A
  • bacterial
  • viral - HSV, HZO, adeno
  • other fungal, acanthamoeba
    • acathamoeba - tap water bourne
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38
Q

How does a corneal ulcer present?

A
  • pain - VERY, pain receptors
  • photophobia
  • contact lens and tap water contamination
  • facial cold sores
  • rash and vesicles
  • recent injury and abrasions

O/E

  • conjunctival injection
  • infiltrate
  • hypopyon
  • fluroscein showing up
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39
Q

How is a corneal ulcer managed?

A
  • bacterial - intensive hourly drops of fluroquinolones
  • viral - topical acyclovir for a week
  • fungal - intensive anti fungal and anti amoebic
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40
Q

What is the pathophysiology of herpes keratitis?

A

viral inflammation of the cornea caused by herpes simplex
- commonly epithelial layer of cornea
- primary or recurrent

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41
Q

How does herpes keratitis present?

A
  • primary - mild symptoms of blepharoconjuctivitis - eyelid margins and conjunctiva
  • recurrent
    • painful red eye
    • photophobia
    • vesicles
    • foreign body sensation
    • watery discharge
    • reduced visual acuity
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42
Q

How is herpes keratitis investigated?

A
  • slit lamp with fluorescein showing dendritic corneal ulcer
    • “branching” appearance of ulcer
  • corneal scrapings - viral testing
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43
Q

How is herpes keratitis managed?

A
  • urgent assessment
  • topical or oral antivirals eg: acyclovir
  • corneal transplant - treat permanent scarring and vision loss after keratitis
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44
Q

What is the common cause of bacterial keratitis?

A

Pseudomonas
Staphylococcus

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45
Q

How does bacterial keratitis present?

A
  • red eye: pain and erythema
  • photophobia
  • foreign body, gritty sensation
  • hypopyon may be seen
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46
Q

How might bacterial keratitis be investigated?

A

an accurate diagnosis can only usually be made with a slit-lamp,meaning same-day referral to an eye specialist is usually required to rule out microbial keratitis

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47
Q

How does bacterial keratitis manage?

A
  • topical antibiotics
    • typically quinolones are used first-line
  • cycloplegic for pain relief
    • e.g. cyclopentolate
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48
Q

What are the complications of keratitis?

A
  • corneal scarring
  • perforation
  • endophthalmitis
  • visual loss
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49
Q

What are some other causes of keratitis?

A
  • Fungalinfection (e.g.,CandidaorAspergillus)
  • Contact lens-induced acute red eye (CLARE)
  • Exposure keratitis, caused by inadequate eyelid coverage (e.g ectropion)
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50
Q

What is age related macular degeneration?

A

progressive loss of central vision associated with formation of drusen or angiogenesis and changes in retinal pigmentary epithelium
*dry or wet

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51
Q

What is characteristic of dry macular degeneration?

A

drusen in buch’s membrane - undigested cellular debris from degeneration of RPE (retinal pigment epithelium) cells as a part of normal ageing process

*accumulation leads to atrophy of retinal epithelium

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52
Q

What characterises wet macular age degeneration?

A

characterised by choroidal neovascularisation - VEGF (vascular endothelial growth factor) is a protein molecule that has critical role in angiogenesis so in wet AMD causes abnormal angiogenesis and vessel leakage
*fibrous scar tissue and central vision loss and leads to scotoma

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53
Q

What are some RF for AMD?

A
  • age
  • smoking
  • Caucasian ethnicity
  • high fat diet
  • drugs like aspirin
  • co-morbidities like CVS and HTN
  • ocular characteristics
    • light coloured iris
    • hyperopia
  • genetics
    • complement factor H
    • gene variant Y402H (drusen formation link)
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54
Q

How would you classify AMD?

A

early - few medium sized druse, mild pigmentary abnormalities
intermediate - >1 large drusen
advanced - gradual vision loss or advanced wet is rapid vision loss

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55
Q

How does dry AMD present?

A
  • visual changes unilateral with
    • gradual loss of central vision
    • reduced visual acuity
    • crooked or wavy appearance to straight lines (metamorphopsia)
  • gradually worsening ability to read small text
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56
Q

How does wet AMD present?

A

👁️ wet AMD - more acutely

  • visual loss within days and progress to complete within 2-3 years
  • often progresses to bilateral disease

</aside>

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57
Q

How is AMD investigated?

A
  • pinhole worsens
  • reduced visual acuity - snellen chart
  • scotoma - enlarged central area of vision loss
  • amsler grid test - assess for distortion of straight lines seen in AMD
  • drusen - fundoscopy
  • slit lamp - detailed view of retina and macula
  • optical coherence tomography - cross sectional view of retina
  • fluorescein angiography - fluorescein contrast and photographing the retina to assess the blood supply
    • oedema
    • neovascularisation in wet AMD
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58
Q

How is dry AMD managed?

A
  • no cure, ambler to monitor
  • vitamin supplements in early disease
  • registration with national centre for blind
  • social work involvement, OT, psychology involvement
  • informing DVLA if visual acuity poor
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59
Q

How is wet AMD managed?

A

*no cure - maintain functional sight, amsler grid to monitor

  • 2w referral for wet AMD
    • intravitreal anti-VEGF therapy - monthly
  • registration with national centre for blind
  • social work involvement, OT, psychology involvement
  • informing DVLA if visual acuity poor
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60
Q

What may cause gradual vision loss?

A

corneal abrasion
chemical injury
cataracts
diabetic eye disease
presbyopia

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61
Q

What could cause corneal abrasions?

A
  • damaged contact lenses
    • associated with pseudomonal infection
    • differential with herpes keratitis - antiviral
  • fingernails
  • foreign body - metal fragments
  • tree branches
  • makeup brushes
  • entropion - inward turned eyelid
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62
Q

How might a corneal abrasion present?

A
  • painful red eye
  • photophobia
  • foreign body sensation
  • epiphoria
  • blurred vision
63
Q

How would you investigate and manage corneal abrasion?

A
  • fluorescein stain - diagnose
    • yellow-orange colour and collects in abrasions or ulcers
      • when visualising in cobalt blue light
  • uncomplicated - heals in 2-3 days
  • complicated - ophthalmology
    • remove foreign bodies
    • simple analgesia eg:paracetamol
    • lubricating eye drops
    • antibiotic eye drops eg: chloramphenicol
    • close follow up
64
Q

Which type of chemical injury is worse - acid or alkali?

A

alkali - lipophilic, penetrate corneal stroma and destroy epithelium, releasing proteolytic enzymes which cause further damage

acid - denatures protein, and the coagulated proteins act as a barrier to prevent further penetration (except HCl)

65
Q

How might chemical injuries present and what is a worrying sign?

A

stinging, burning, redness, pain, swelling of eyelids, blurring of vision

*red eye, except for pallor of vessels in a certain patch - suggestive of limbal ischaemia → corneal scarring and limbal deficiency

66
Q

How would you manage chemical injuries?

A
  • IRRIGATION! to achieve physiological pH
  • remove foreign bodies
  • medically augment collagen synthesis
  • antibiotics, atropine, artificial tears
  • surgical debridement
67
Q

What is the role of the lens and ciliary body?

A

<aside>
👁️ focus light onto retina, held in place by suspensory ligaments attached to ciliary body

- ciliary body contracts to change shape of lens and thicken it
- lens has no blood supply and is nourished by aqueous humour
</aside>

68
Q

What is a cataract?

A

progressively opaque eye lens which reduces light entering eye and visual acuity
*can be congenital or progressive

69
Q

What are some causes of cataracts?

A
  • age related
  • pre-senile
    • steroids
    • DM
    • trauma
    • uveitis
  • congenital
70
Q

What are some risk factors of developing cataracts?

A
  • increasing age
  • smoking
  • alcohol
  • DM
  • steroids
  • hypocalcaemia
71
Q

How does cataracts present?

A

*asymmetrical
- change in glasses prescription - myopic shift with short sighted first as light converges as cataract hardens
- slow reduction in visual acuity
- progressive blurring of vision
- colours more faded - brown or yellow
- starbursts around lights at night especially
*loss of red reflex

72
Q

How are cataracts managed?

A
  • phacoemulsification - if vision 6/12 with sub-tenon block
    *important to treat as prevents detection of other pathology like AMD, DM retinopathy etc
73
Q

What is a complication of cataracts?

A

endophthalmitis - inflammation of vitreous and aqeous humour
mx: intravitreal abx

74
Q

What is the blood supply to the retina?

A

carotid → ophthalmic → central retinal and posterior ciliary artery

75
Q

What is the pathophysiology of diabetic retinopathy?

A
  • chronic hypoglycaemia damages retinal small vessels and endothelial cells
  • increases vascular permeability -> leaks and blot haemorrhages + hard exudates
  • neovascularisation etc
76
Q

What are some characteristic features of diabetic retinopathy?

A

hard exudates
micro-aneurysms and venous beading
cotton wool spots
intra-retinal microvascular abnormalities
neovascularisation

77
Q

What are the stages of diabetic retinopathy?

A

background retinopathy
pre-proliferative
proliferative
diabetic maculopathy
ischaemic diabetic maculopathy

78
Q

What is background diabetic retinopathy? and what does this mean for management?

A

micro-aneurysms
dot and blot haemorrhages
cotton wool spots
hard exudates

*no tx indicated, annual screening with digital photography

79
Q

What is pre-proliferative stage and what’s the management?

A

extensive blot haemorrhages and intra-retinal microvascular abnormalities (ischaemia)

*4-6m follow up with digital fundus colour photos + retinal laser tx

80
Q

what is proliferative stage and what is the management?

A

neovasuclarisation and vitreous haemorrhages

*pan retinal photocoagulation targeting new vessels, retinal laser

81
Q

Differentiate between diabetic maculopathy and ischaemic diabetic maculopathy and what is the management?

A

diabetic - exudates within macula and macular oedema!
ischaemic - angio needed to diagnose, occlusions within vessels

*mx - anti-VEGF bevacizumab, ranibizumab, intravitreal dexamethasone implant to reduce macular oedema

82
Q

What are some risk factors for diabetic retinopathy?

A
  • duration of diabetes - 50% at 7 years duration and 90% at 17-50
  • poor glycaemic control
  • hypertension
  • dyslipidaemia
  • obesity
  • pregnancy
83
Q

How might diabetic retinopathy present?

A

asymptomatic and most present with severe disease

  • floaters
  • blurred vision and distortion if macula affected
  • decreased visual acuity - gradual, painless reduction in quality
  • loss of vision - severe haemorrhage in results in sudden complete and painless vision loss
  • blindness in untreated and uncontrolled
84
Q

What is the diabetic eye screening programme?

A
  • for anyone with diabetes
  • every 1-2 years
    • depends on previous 2 scans
85
Q

How is diabetic retinopathy investigated?

A
  • visual acuity - logMAR
  • gold: fundoscopy with slit lamp or through fundus photography
  • OCT: non invasive and infrared
  • Fundus fluorescein angiography
    • dye into arm to see retinal blood vessels
86
Q

What is the general management options available for non-proliferative diabetic retinopathy?

A
  • close monitoring and careful diabetic control
  • pre-proliferative: 4-6m follow up with digital fundus colour photos
    • retinal laser treatment given if,
      • only one good eye left
      • attendance to clinic poor
      • prior cataract surgery
87
Q

What is the management for proliferative DM retinopathy?

A
  • Pan-retinal photocoagulation (PRP) - extensive laser treatment across the retina to suppress new vessels
    • aim to kill ischaemic retina so hypoxic drive and oxygen demand is lessened and supply focused to central retina
      *complications - visual field defects, impaired night vision, accidental macular burn
  • anti VEGF - medication intravitreal injection
    • bevacizumab, ranibizumab
  • surgery - vitrectomy in severe disease
  • macular oedema
    • intravitreal implant containing dexamethasone
88
Q

What is presbyopia?

A

age related nearsightedness - begins at 40 year old

  • secondary to loss of elasticity of the crystalline lens
    • results in decreased accommodating power when seeing objects at arm’s length or closer
    • image focuses behind retina

*presents as gradual loss of near vision eg: reading

89
Q

How is presbyopia managed?

A
  • corrective lenses
    • convex lenses
    • bifocal - bottom lens refracts light for close up vision, top refracts light to allow you to see distant objects
    • multifocals
  • corrective surgery
    • refractive surgery to achieve monovision
    • corneal inlays
90
Q

what conditions cause sudden loss of vision?

A

retinal detachment
central retinal artery occlusion
central retinal vein occlusion vitreous haemorrhage (due to diabetic retinopathy)

91
Q

what causes amaurosis fugax?

A

temporary loss of vision caused by a temporary interruption to the blood supply

92
Q

what is the pathophysiology of central retinal artery?

A

obstruction to blood flow through the central retinal artery, which was a brach of ophthalmic artery which is a brach of ICA

*cause atherosclerosis, GCA, vasculitis hence CVS RF

93
Q

how does central artery occlusion present?

A
  • sudden painless loss of vision: curtain coming down
  • RAPD
94
Q

what is relative afferent pupillary defect?

A
  • pupil in affected eye constricts more when light shone in other eye than when shone in itself
  • input not sensed by ischaemic retina when testing direct but sensed in consensual
95
Q

how is retinal artery occlusion investigated?

A
  • fundoscopy: pale retina with cherry red spot (fovea) due to lack of perfusion
  • GCA: ESR, temporal artery biopsy
    *refer immediately
96
Q

how is central artery occlusion managed?

A
  • GCA: potentially reversible so high dose prednisolone +/- IV Methylpred
  • attempt to dislodge blockage: ocular massage, anterior chamber paracentesis, inhaled carbogen, IV acetazolamide+mannitol etc
  • secondary prevention of CVS, treat reversible RF
97
Q

what is the pathophysiology of central vein occlusion?

A

thrombus forms in retinal veins and obstructs the venous drainage from retina

  • central retinal vein run through the optic nerve - responsible for draining retinal capillaries
  • atherosclerotic thickening of central retinal artery leading to vein compression
  • causes retinal tissue ischaemia, infarction, vessel leakage and neovascularisation
98
Q

what are some risk factors for central vein occlusion?

A
  • age
  • FHx of vascular
  • atherosclerosis
  • open angle glaucoma
  • inflammatory: sarcoidosis, Lyme
  • hyper coagulable state
  • myeloproliferative states
99
Q

what is the presentation of central vein occlusion?

A
  • sudden, painless unilateral visual loss (more gradual than artery occlusion)
  • relative afferent pupillary defect - ischaemia
  • visual field defect
100
Q

what is a differential for CRVO?

A

branch retinal vein occlusion (BRVO) - this occurs when a vein in the distal retinal venous system is occluded

101
Q

how is retinal venous occlusion investigated?

A
  • fundoscopy: widespread hyperaemia, severe retinal haemorrhages, macular oedema, cotton wool spots
  • BP
  • FBC, glucose, ESR
  • fundal photo
  • fundus fluorescein angio
102
Q

how is CRVO managed?

A
  • immediate ophthal referral
  • control BP
  • treatment aim to control complications
  • macular oedema: anti-VEGF, intravitreal steroid implant, laser
  • neovascular complications: pan-retinal photocoagulation
103
Q

what is a complication of CRVO?

A
  • Ischaemic carries poorer prognosis
    • retinal non-perfusion, capillary closure, retinal hypoxia which increases neovascularisation risk
  • may resolve spontaneously, cause vitreous haemorrhages or cystoid macular oedema
104
Q

what is retinal detachment?

A

involves the neurosensory layer of retina (containing photoreceptors and nerves) separating from the retinal pigment epithelium (base later attached to choroid)

105
Q

what is the consequence of a retinal detachment?

A
  • due to retinal tear -> vitreous fluid to get under the neurosensory retina and fill the space
  • neurosensory retina relies on blood vessels of the choroid for its blood supply
    • detachment disrupts this causing permanent damage to photoreceptors -> sight threat
106
Q

what are some RF for retinal detachment?

A
  • lattice degeneration (thinning of retina)
  • posterior vitreous detachment
  • trauma
  • diabetic retinopathy
  • retinal malignancy
  • family history
107
Q

how does retinal detachment present?

A
  • painless
  • peripheral vision loss - sudden, shadow coming across vision
  • blurred vision or distorted vision
  • flashes and floaters
  • RAPD if optic nerve involved
  • fundoscopy: red reflex might be lost
108
Q

how is retinal detachment managed?

A
  • aim to create adhesions between retina and choroid with laser and cryo
  • aim to reattach retina: vitrectomy, scleral buckle, pneumatic retinoplexy
109
Q

what is optic neuritis?

A

inflammatory condition of the optic nerve that leads to acute, unilateral, central loss of vision (over hours to days)

  • common in females 20-40
110
Q

what is the pathophysiology of optic neuritis?

A
  • immune-mediated demyelination of the optic nerve as an isolated incident or part of wider disorder
  • acute version of MS
  • also associated with DM, syphillis
111
Q

what is the presentation of optic neuritis?

A
  • acute, central vision loss - unilateral over hours to days
  • poor discrimination of colours - red desaturation
  • pain worse of eye movement
  • photopsia - flashes of light
  • relative afferent pupillary defect
  • visual field defects - central scotoma
  • optic atrophy - chronic
112
Q

how is optic neuritis investigated?

A
  • swinging light test: RAPD
  • ophthalmoscopy: mildly swollen disc
  • MRI brain and orbits with contrast: confirm demyelinating optic neuritis
  • LP: elevated protein, lymphocytes,oligoclonal bands
113
Q

how is optic neuritis managed?

A
  • high dose IV steroids - methylprednisolone
  • disease modifying therapies - MS?
  • recovery usually 4-6w
114
Q

what is the pathophysiology of third nerve palsy?

A
  • posterior communicating artery aneurysm
  • microvascular, pupil sparing DM, HTN
  • other: trauma, neoplasm, infection, migraine, congenital
115
Q

how does third nerve palsy present?

A
  • affects all EOM except lateral rectus and superior oblique
    • these act unopposed to give exotropia and hypotropia ie. down and out
  • dilated pupil + accommodation paralysis
116
Q

how is third nerve palsy investigated?

A
  • check BP
  • cranial nerve examination
  • fundoscopy - retinopathy and optic disc swelling
  • temporal artery examination
  • lid fatigue
  • eye movements and cover test - orthoptics
  • fasting glucose
  • CT, MRI if pupil sparing
  • MG antibodies
117
Q

how is third nerve palsy managed?

A
  • treat amblyopia in children <8 → prisms help in isolated muscles
  • surgery - achieves limited area of binocular single vision at best
  • occlusive contact lens - residual diplopia
118
Q

what is the pathophysiology of fourth nerve palsy?

A
  • acquired - head trauma, trochlear or orbital injury, ENT surgery, sinus infections or vascular
  • can be idiopathic or associated with HTN, DM, rarely demyelination, GCA, tumours and aneurysms
119
Q

how does fourth nerve palsy present?

A
  • vertical diplopia: defective downwards gaze
    *prominent when looking down
  • contralateral head tilt
  • ipsilateral hypertropia
120
Q

how is trochlear palsy managed?

A
  • prisms may control small deviations
  • hyperdeviation - surgery
    • SO tendon tuck etc
121
Q

what is the pathophysiology of a abducens palsy?

A
  • adults - microvascular HTN, DM, MS, neoplasm, head trauma, infection, raised ICP, GCA and idiopathic
  • children - microvascular unlikely, transient in neonates, benign palsy of childhood 1-3w after febrile illness
122
Q

what is the presentation of abducens palsy?

A
  • horizontal diplopia - greater when looking to affected side and distance
    • diplopia may be constant
  • head turn to same side
123
Q

how is abducens palsy investigated?

A
  • check for other CN signs - present when Pons (CN 7), cavernous sinus (CN 3,4, 5 trigeminal division) affected
  • orthoptic testing - prism cover test
  • hess chart
  • blood tests
  • MRI, CT → false localising signs in raised ICP
124
Q

how is abducens palsy managed?

A
  • childhood - resolve spontaneously
  • stable and symptomatic post 6m consider surgery
    • surgery selected based on abduction status (past midline)
125
Q

what is the pathophysiology of orbital floor fracture?

A

usually as a result of a direct blow to the orbit, typically involving the floor and or medial wall but with orbital rim intact
- this leads to sudden increase in intraorbital pressure

126
Q

what are the types of orbital floor fractures and the anatomical components involved?

A
  • inferior: most common, orbital fat prolapses into maxillary sinus, inferior rectus too?
  • medial: orbital fat, medial rectus into ethmoid air cells
  • superior: uncommon
  • lateral: associated with orbital rim, craniofacial injuries
127
Q

how does orbital blow out fracture present?

A

*excessive soft tissue swelling
- diplopia, restricted ocular motion
- enophthalmos
- diplopia as EOM entrapment
- orbital emphysema
- malar region numb: infraorbital nerve injury
- hypoglobus

128
Q

how might you manage an orbital blow out fracture?

A

*CT

  • ice for swelling, decongestants to aid drainage, avoid nose blowing, steroids for swelling, abx
  • surgery to release trapped tissue within 24-48h
129
Q

what is the significance of thyroid diseases in relation to ophthalmology?

A

autoimmune condition resulting in inflammation and swelling of extra-ocular muscle, fatty tissue and connective tissue within orbit

*follows acute phase for 6m to 2y where damage happens, inactive phase when sx remain

130
Q

how might thyroid related eye disease present?

A
  • excessive watering
  • ‘gritty’ sensation
  • photophobia
  • eye pain
  • ask - red eye, blurred vision, pressure sensation
  • systemic - pretibial myxoedema, goitre, acropachy
131
Q

what might thyroid eye disease exemption show?

A
  • eye lid retraction
  • proptosis
  • lig lag - von Graefe’s sign
  • lid oedema
  • diplopia due to restriction of inferior rectus
  • incomplete eyelid closure
  • strabismus
132
Q

what investigations are carried out for thyroid related eye disease?

A
  • measure proptosis
  • assess optic disc
  • visual acuity, colour vision, RAPD
  • TFT
  • antibody test
    • anti-thyroid peroxidase, anti-TSH
  • USS extra-ocular muscles
  • CT orbit - nerve involvement
  • MRI orbits
133
Q

how is thyroid related eye disease managed?

A
  • compressive optic neuropathy - Urgent IV methylprednisolone
  • Ophthal + endo review
  • correct thyroid hormone levels
  • smoking cessation
  • steroids to reduce swelling
134
Q

what are some complications of thyroid related eye disease?

A

*compressive optic neuropathy - reduced visual acuity, colour vision → sight-threatening

  • globe subluxation
  • gaze abnormalities
  • raised IOP → glaucoma
135
Q

what is the pathophysiology of amaurosis fugax?

A

result of ischaemia to the retina, choroid, or optic nerve from an arterial embolus, usually in the retinal artery (from ipsilateral carotid artery disease)

136
Q

what are some RF for amaurosis fugax?

A
  • over 50
  • vascular RF
    • HTN, HPL, smoking, previous TIA or stroke
137
Q

how does amaurosis fugax present?

A
  • transient vision loss in one or both eyes
    • abrupt, maximum severity within seconds lasting to minutes
    • full recovery
  • negative visual phenomenon - blackout or ‘greying out’ of vision
  • normal ophthal exam
138
Q

how is amaurosis fugax investigated?

A
  • inflammatory markers - rule out GCA
  • carotid imaging for stenosis
  • cardiac investigations - AF other stroke RF
  • neuro-imaging is needed
139
Q

how is amaurosis fugax managed?

A
  • 300mg of aspirin unless contraindicated
    • urgent TIA referral within 24h
  • secondary prevention - statin, antiplt, optimising BP etc
140
Q

what is blepharitis?

A

inflammation of the eyelid margins
- due to meibomian gland dysfunction (common, posterior bleph), or seborrhoeic dermatitis/ staphylococcal infection (less common, anterior bleph)

141
Q

how does blepharitis present?

A
  • bilateral symptoms
  • grittiness and burning discomfort - around lid margins
  • eyes sticky in the morning
  • results in dry eye which could cause redness
  • foreign body sensation
  • margins may be red - swollen in staphylococcal blepharitis
  • styes and chalazions common in these
  • secondary conjunctivitis
142
Q

what does blepharitis look like on examination?

A
  • anterior - eyelash deformity and depigmentation and loss
  • posterior - dilated and obstructed Meibomian glands
143
Q

how is blepharitis managed?

A

diagnosis - history, examination
- slit lamp
- swabs maybe done for cultures

hot compress
lid hygiene
artificial tears
abx
ophthal referral if painful

144
Q

how is lid hygiene done for blepharitis?

A
  • lid hygiene - mechanical removal of debris from margins
    • cotton wool buds dipped in mix of cooled boiled water and baby shampoo often used
    • alternative is sodium bicarb, teaspoonful in cup of cooled water recently boiled
145
Q

what is a meibomian cyst?

A
  • lipo-granulomatous lesion that forms in obstructed meibomian gland
  • non-infectious and associated with blepharitis and acne rosacea
146
Q

how does meibomian cyst present and how is it managed?

A
  • painless red eyelid cysts
    • in internal eyelid
  • when infected becomes internal hordeolum
  • not painful or tender to touch
  • resolves spontaneously
    • warm compress of eye lid to loosen gland
    • eyelid massage to express content 2x a day
  • if persistent referral for incision and curettage
147
Q

what is a subconjuctival haemorrhage?

A
  • small blood vessels within the conjunctiva ruptures, releasing blood into the space between the sclera and conjunctiva
    • after strenuous activity like coughing, weight lifting or straining
    • or trauma to eye
    • commonly idiopathic in otherwise healthy
148
Q

what are some risk factors for subconjuctival haemorrhage?

A

*may predispose

  • HTN
  • bleeding disorders - thrombocytopenia
  • whooping cough
  • medications eg: anti-plt, DOACs, warfarin
  • non-accidental injury
149
Q

how does subconjuctival haemorrhage present?

A
  • patch of bright red blood underneath conjunctiva - covering white of eye
  • painless
  • does NOT affect vision
  • precipitating event!
150
Q

how is subconjuctival haemorrhage investigated and managed?

A
  • simple history and examination, BP, INR - if on warfarin
  • spontaneous resolution
  • 2 weeks
  • lubricating eye drops - mild irritation
151
Q

what is the pathophysiology of posterior vitreous detachment?

A
  • vitreous body comes away from retina - common in older age
    • vitreous humour is gel inside the vitreous chamber of eye, maintain structure of eyeball and keeps retina pressed on choroid
  • with age, less firm and less able to maintain shape
152
Q

how does posterior vitreous detachment present?

A
  • painless
  • can be asymptomatic
  • floaters
  • flashing lights
  • blurred vision
153
Q

How is posterior vitreous detachment managed?

A

*exclude retinal detachement

  • brain adjusts overtime
  • safety net for retinal detachment as predisposes

Y4 NSS (11 decks)

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