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Y4 Neuro and SS > Opthalmology > Flashcards

Opthalmology Flashcards

1
Q

State 4 RFs for cataracts

A
  • age- affects 50% of those over age 65
  • smoking
  • diabetes
  • systemic corticosteroids
  • eye trauma, female, uveitis, UV exposure, poor nutrition, alcohol are smaler RFs
  • retinitis pigmentosa lol- pt in 20s w/ night vision loss, feild defect, fhx and black peripheries on fundoscopy (google it)
  • Downs
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2
Q

Describe the pathophys of catartacts in adult and what may cause in a child?

A
  • There is deposition of new crystallin lens fibres with age, old ones are not removed
  • New deposition disruption of the carefully composed structure leading to protein aggregation and so clouding and light scattering
  • 2nd factor= accumulation of yellow- brown pigement making reading more difficult as affects contrast
  • Paediatric cataracts may be caused by galactosaemia, genetic, TORCH infection, diabetes, traumatic or post radiotherapy
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3
Q

Describe the clinical features of cataracts

A
  • gradual painless loss of vision- not improved by viewing through pinhole
  • haloes around lights and problems watching tv
  • problems recognising faces and diplopia in one eye
  • defects in red reflex
  • lens appears brown or white when bright white light shone on eye
  • pupillary reactions normal
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4
Q

How is cataracts managed?

A
  • extracapsular lens extraction or phacoemulsification (lens liquidied with USS probe and then aspirated before replacing it with artificial lens)
  • decision to treat depends on affect on QoL an risk vs benefit rather than specific acuity
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5
Q

State 4 early complications of cataracts surgery

A
  • poor vision (inadequate correction of refractive error or pre- exisitng eye condition)
  • capsular rupture with vitreous loss- endopathalmitis risk
  • protruding or broken sutures
  • trauma to iris
  • wound gape or iris prolapse
  • anterior chamber haemorrhage
  • vitreous or choroidal haemorrhage
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6
Q

State 4 late complications of cataracts surgery

A
  • posterior chamber opacification: vision can usually be restored with laser capsulotomy
  • cystoid macular odema
  • uveitis
  • retinal detachment
  • open or closed angle glaucoma
  • ARMD
  • dysphotopsias: unwanted optic phenomena due to light artefacts reflecting off IOL
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7
Q

What is primary open angle glaucoma

A

Progressive, chronic condition characteristed by:

  • Adult onset
  • Intraocular pressure >21mmHg- however 20-52% have normal tension glaucoma
  • Open iridocorneal angle- flow is simply reduced through the trabecular meshwork
  • Glaucomatous optic neuropathy
  • Visual field loss compatible with nerve fibre damage
  • Absence of underlying cause
  • Usually bilateral but asymmetrical
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8
Q

Give 4 RFs for primary open angle glaucoma

A
  • age (rare before 40)
  • fhx
  • afrocarribean
  • ocular htn
  • myopia, retinal disease diabetes, systemic htn
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9
Q

describe the clinical features of primary open angle glaucoma

A
  • Most asymptomatic as vision loss is initially to peripheral vision so when they notice it is too late and damage is permenant
  • May be picked up on checking IOP and part of visual fields by optician or by GP looking at optic disc
  • Gonioscopy is used to measure angle between cornea and iris
  • Corneal thickness needs to be done as will increase IOP reading falsely
  • Goldmann tonometry is used to measure IOP- usually raised (9-21 is normal)
  • Optic disc exam- increase in cup size in relation to disc ( ratio >0.7)
  • Loss of peripheral visual fields (measure with perimetry)
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10
Q

How is primary open angle glaucoma managed?

A
  • topical beta blocker (timolol) or prostaglandin analogue (latanoprost) 1st to reduce IOP
  • miotics and sympathmiometics can also be used
  • laser and surgical management if 2 of these fail (selective laser trabeculoplasty)
  • Even if IOP isnt raised they’re still given medication to lower it
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11
Q

What can cause angle closure glaucoma?

A
  • insidious/ primary
  • hypermetropia
  • lens bulging forward as a result of swelling eg blood(hyphaema), blood vessels (diabetic eye disease) or protein (hypertensive uveitis)
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12
Q

describe the clinical features of acute angle closure glaucoma

A
  • severe rapidly progressive pain in and around the eye
  • blurred vision/ visual loss
  • marked red eye- reddest around cornea
  • pupil fixed and dilated, sometimes hazy cornea
  • hard globe (press with eye lids closed and will be hard and tender)
  • IOP raised (often 50s or more)
  • N+V common
  • attacks often start when something dilates pupil
  • coloured haloes around lights (subacute attacks)
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13
Q

How should acute angle closure glaucoma be managed?

A
  • give all glaucoma meds that arnt contraindicated (timolol, lantoprost, pilocarpine, maxidex etc)
  • IV acetazolamide (500mg over 10 mins) and lay supine
  • if no response in 1 hr and U&E normal give hyperosmotics such as mannitol
  • If this fails or U&E abnormal, iridoplasty can be done
  • systemic analgesia and antiemetics
  • laser peripheral iridotomy within a few weeks of the attack, sometimes lensectomy
  • top steroids often given bc eye becomes inflammed
  • pilocarpine drops often given to constrict the pupil and help unblock the drainage
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14
Q

Give 3 complications of acute angle closure glaucoma

A
  • permanent visual loss
  • repetition of attacks
  • attack in other eye
  • central retinal vein or artery occlusion
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15
Q

Describe and explain the 5 retinal findings in diabetic retinopathy

A
  • Microvascular occlusion causes retinal ischaemia and leds to AV shunts and NEOVASCULARISATION .
  • Leakage results in intraretinal haemorrhages and MACULAR ODEMA
  • MICROANEURYSMS: physical weakening of capillary walls which predispose them to leakages
  • HARD EXCUDATES precipitates of lipoproteins leaking from retinal blood vessels
  • HAEMORRHAGES: rupture of weakened capillaries, appearing as small dots/ larger blots or flame haemorrhages that track along nerve- fibre budles in superficial retinal layers
  • COTTON WOOL SPOTS- axonal debris build up due to poor axonal metabolism at margin of ischaemic infarcts
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16
Q

Describe the grading of diabetic retinopathy

A
  • Non proliferative (MILD (<2 microaneurysm) MOD (mciroa + intraretinal haemorrhages +/- cotton wool spots, venous bleeds) SEVERE/ PRE-PROLIFERATIVE (number of change in number of quadrants)
  • Proliferative (non high risk (no changes within 1 diameter of optic disc) and high risk (large new vessels on disc or everywhere, retinal detachment or pre retinal haemorrhage)
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17
Q

Describe the grading of diabetic maculopathy

A
  • focal or diffuse macular odema
  • ischaemic maculopathy (normal but reduced acuity and ischaemia seen on fluorescein angiography)
  • clinically significant macular odema: thickening or hard exudates which are of certain size/ distance from the fovea
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18
Q

Describe the clinical features of diabetic eye disease

A
  • Painless gradual reduction in central vision
  • Haemorrhages result in sudden onset dark painless floaters which may resolve over several days
  • Severe haemorrhages result in painless visual loss
  • Spots within the red reflex suggest vitreous haemorrhage
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19
Q

How is diabetic retinopathy managed?

A
  • laser photocoagulation treatment if neovascularisation to induce regression and also helps reduce central macula thickening
  • diabetes, BP, lipid control
  • sometimes vitrectomy after preretinal/intravitreal bleeds
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20
Q

How is diabetic maculopathy managed?

A
  • anti VEGF injections

- intravitreal triacinolone (steroid) injections

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21
Q

give 4 complications of diabetic eye disease

A
  • macular ischaemia
  • vitreous haemorrhage
  • retinal detachment
  • glaucoma
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22
Q

Describe the pathophys of dry and wet ARMD

A

Dry: soft drusen in macula + atropy of retinal pigment epithelium causing gradual vision loss
Wet: new blood vessels grow in choriocapillaries under the retina, they lead to haemorrhage and scarring, progression varies from 3 months to 3 yrs. end point is scar formation known as disciform macular degeneration

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23
Q

Describe the clinical features of ARMD

A
  • painless deterioration in central vision (esp near vision) in person age >55
  • loss of contrast sensitivity
  • size or colour of objects appear differnt in each eye
  • flashing or flickering lights and glare
  • In wet ARMD straight lines appear crooked or wavey (due to macula odema) and visual deterioration is much quicker, often get profound sudden loss, flashers and floaters in event of a bleed
  • yellow deposits called drusen seen in macula area on opthalmoscop
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24
Q

How is ARMD diagnosed?

A

Ocular coherence tomography (OCT), fluorescein angiography if wet ARMD suspected

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25
Q

How is dry ARMD managed?

A
  • no treatment but slow progress:
  • stop smoking
  • visual rehab
  • nutritional supplements (vitamins A,C,E, lutein, zinc, copper
  • lots of leafy greens and fresh fruit
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26
Q

how is wet ARMD managed?

A
  • intravitreal injections of VEGF if macula odema
  • laser photocoagulation for neovasc
  • photodynamic therapy
  • macular translocation (NICE doesn’t recommend)
  • implanted lens systems in future
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27
Q

Describe the pathophys to retinal vein occlusion

A
  • Commonest cause is thombus formation
  • Other causes inc vein wall disease and external compression (arteriole thickening compresses the vein within the same sheath)
  • Backlog of stagnated blood + hypoxia = extravasation of blood futher stagnation
  • Ischaemic damage stimulates VEGF
    leading to neovascularisation so haemorrhage + glaucoma (clogs drainage system)
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28
Q

Describe the clinical features of branch and central retinal vein occlusion

A

Branch:
- unilateral painless blurred vision + altitudinal visual field defect and visual distortion. Fundoscopy= vascular dilation and tortuosity of vessles and haemorrhages in one area
Central:
- sudden unilateral painless loss of vision
- flame haemorrhages and disc odema on fundoscopy
- if ischaemic: marked pupillary defect, cotton wool spots, occasionally detachment

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29
Q

How is retinal vein occlusion managed?

A

Branch: panretinal photocoagulation if develop macula odema or neovascularisation, dexamethasone, anti VEGF, triamcinolone injections
Central: no proven treatment, modify RFs and keep pain free, non ischaemic will get pan retinal photocoagulation if neovascularisation occurs

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30
Q

Describe the pathophys of retinal artery occlusion

A
  • Central retinal artery is branch of ophthalmic artery (brach of internal carotid)
  • It supplies optic disc and then branches into superior and inferior and then again into temporal and nasal which supplies the 4 quadrants of the retina
  • Cilioretinal artery is present in 30% ppl and can help preserve macular in some people after CRAO
  • Aetiology is same as any stoke but most are embolic from carotid artery disease, some are retrobulbar masses leading to optic nerve and CRA compression
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31
Q

Describe the clinical features of retinal artery occlusion

A
  • Central retinal artery: sudden unilateral acute painless loss of vision, usually to counting fingers (if worse - ophthalmic artery affected)
  • 10% get amarosis fugax- curtain coming down
  • Examination= afferent pupillary defect + pale retina and cherry red spot + attenuation of vessels + carotid bruits/ murmers/ AF/ HTN
  • Branch: defect in one quadrant/ half of vision, retinal pallor only in area affected
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32
Q

How is central retinal artery occlusion managed?

A
  • If present within 90-100 mins= firm ocular massage (may dislodge obstruction but rarely works)
  • Lowering IOP within anterior chamber paracentesis + acetazolamide
  • Dilation of artery (GTN, inhaled carbogen or hyperbaric oxygen)
  • Intra arterial fibrinolysis through local injection or urokinase into proximal part of ophthalmic artery
  • Long term: identify an treat underlying cause, manage RFs, carotid endarterectomy, vision aids, DVLA notification
  • Prognosis is poor
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33
Q

Describe the pathophys of retinal detachment

A

Most are preceeded by posterior vireous detachment (PVD), which causes traction on retina and a tear, liquefied vitreous seeps under retina and causes it to detach.
Can be rhegmatougenous (commonest, as above, tear is between the sensory and pigment epithelium) or non- can be exudative (primary damage of RPE causes subretinal fluid in and pushes retina off) or tractional (rare)

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34
Q

Give 5 RFs for retinal detachment

A
  • Mypoia (short sightedness- increased PVD risk)
  • Fhx
  • Previous history of RD in either eye
  • Age
  • Marfans
  • Diabetic retinopathy, eye injury, retinal vein occlusion, retinopathy of prematurity increase risk of non rhegmatogenous tractional RD
  • Inflammatory condition, vascular disease, maculopathy and malignancy increase risk of non rhegmatogenous exudative RD
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35
Q

describe the clinical features of retinal detachment

A
  • new sudden onset floaters (often a shower) indicate a PVD has occured
  • then they get new onset flashes of light as the vitreous pulls the retina away
  • then sudden onset painless progressive visual field loss (described as shadow)- starts peripheral but comes in
  • if macula detaches, visual acuity is reduced
  • RAPD if macular or half of non macula retina detaches
  • grey or folded red reflex
  • see a sheet of sensory retina billowing towards centre of globe, or a visible tear, on fundoscopy
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36
Q

how is retinal detachment managed?

A
  • vitrectomy and scleral buckling for detachment repair
  • cryotherapy or laser photocoagulation to repair retinal holes/ tears
  • most RDs not involving macular are repaired same day- if macula involved within 5 days
  • strict bed rest and hold head in particular position to stop progression before surgery
  • prevention: protective eyewear for severely mypoic pts playing contact sports, repair tears/ holes, recognise PVD early
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37
Q

What words are used to describe a strabismus (squint)

A

eso- inward deviation
exo- outward deviation
hypo- downward
hyper- upward

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38
Q

What is the difference between a concomitant or incomitant (paralytic) squint?

A 
concomitant= the squinted eye can move normally if tested separately from the good eye. 
Incomitant= cannot move even when good eye is covered
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39
Q

what is the leading cause of a squint in adult and child?

A

adult- stroke (then thyroid eye disease)

child- refractive errors (then cerebral palsy, downs, hydrocephalus, SOLs etc)

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40
Q

How are concomitant squints managed?

A

Almost all due to refractive errors- correct these first.
If <8yrs, eye patching +/- cycloplegic drops in good eye can bring bad eye in and force it to work- takes up to 18 weeks.
If treatment fails, surgical realignment with recess and resect- cosmetic effect isn’t permanent and rarely restores binocular vision

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41
Q

What is the difference between monocular and binocular dipolopia? List common causes for each

A

Monocular- when double vision remains on occulsion of uninvolved eye-> NOT STRABISMUS- usually refractive error or cataracts.
Binocular- double vision corrected when either eye is occluded. CONCOMITANT malalignment= strabismus. INCOMITANT malalignment= CN palsy, NMJ disorder (MG), restrictive disease (thyroid or blow out #), ocular myopathy, ocular myositis, supranuclear palsy.
No malalignment= MS/MG, physiologic/ non organic

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42
Q

State 4 causes of a incomitant strabismus

A
  • CN palsy
  • ocular myositis: idiopathic nonspecific inflammation of extraocular muscle, presents in early adulthood, also get pain on moving eye. Resolves spontaneously in 6 weeks
  • ocular myopathy: rare genetic progressive bilateral reduction in eye movement, starts before age 20, often ptosis also.
  • thyroid eye disease
  • myasthenia gravis: worse at end of day, intermittent, ptosis, fatiguability
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43
Q

Describe the CFs and causes of a CNIII palsy

A

CFs: down and out eye, ptosis, USUALLY large pupil w/ partial/ completely impaired pupil response- direct & consensual reflexes affected (pupils not always affected)
Causes: ischaemic microvascular disease or cavernous sinus syndrome (usually pupil sparing), aneurynsm (CT angio URGENTLY), tumours, trauma, pituitary apoplexy, herpes zoseter, leukaemia, ophthalmoplegic migraine, raised ICP

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44
Q

Describe a CNIV palsy and state 3 causes

A

Eye up and out a bit, cant move down and in, binocular vertical diplopia, difficulty reading, tilted head. Causes inc trauma, vasculopathy, demyelinating disease, congenital or idiopathic

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45
Q

Describe the CFs and causes of a CNVI palsy

A

horizontal diploia- worse for distance than near vision and on lateral gaze. Cant move eye outwards. Causes inc vasculopathy, trauma and idiopathic. Less common causes inc raised ICP, cavernous sinus syndrome, MS, GCA, inflammation, infections

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46
Q

What are entropians and extropians?

A 
entropian= lower eyelid turns in 
extropian= lower eyelid turns out
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47
Q

what is lagopthalamos and when is it an emergency and what causes it

A

Lagopathalmos is inability to fully close eye. If bells phenomenon present, cornea is protected so not emergency. Cause is often bells palsy sometimes secondary to trauma, infections. Could also be due to proptosis (thyroid eye disease, orbital tumours, lacrimal gland tumours, orbital inflammatory pseudotumour)

48
Q

give 4 differentials for ptosis

A

aponeurotic/ old age, MG, MS, horners, CNIII palsy, botox injections, lid tumours, bells, chalazion, cellulitis, exopthalmos, lyme disease, uveitis, stroke

49
Q

How is aponeurotic ptosis managed?

A

Levator muscle suspension or frontalis suspension

50
Q

Describe the key differences between viral, bacterial and allergic conjunctivitis

A

Viral: watery eye, lymph nodes up, sometimes itchy, morning crusting, URTI recently, follicles sometimes
Bacterial: mucopurulent discharge, eyes stuck on waking, rarely itchy, papillae +/- follicles
Allergic: very itchy, lid swelling, nasal conjection, sneezing, seasonal, not conganeous, rarely get discharge or gritty feeling, papillae

51
Q

What viruses and bacteria commonly cause conjunctivitis

A
  • Viral: adenovirus, HSV, hepes zoster opthalmicus, mulluscum contagiosum
  • Bacterial: staph, step P, h. influenza, gonococcal conjunctivitis (fast onset, lid odema, profuse discharge- high risk as invades cornea), chlamydia (low grade + urethritis, in newborns)
52
Q

How should bacterial conjunctivitis be managed?

A

Treat with abx if contact lens wearer (Chlorampenicol or fusidic acid), chlamydia (topical tetracyline + systemic doxy) or gonococcal (IM ceftriaxone) infection. Otherwise self limiting and resolves in 1-2 weeks, lubricant eye drops OTC may help discomfort, avoid sharing pillows and towels, wash hands often.

53
Q

How is viral conjunctivitis managed?

A

supportive: cool compress, artificial tears, can take 4-6 weeks to improve, don’t wear contacts, lubricant eye drops, wash hands, avoid sharing towels and pillows, don’t exclude from school

54
Q

How is allergic conjunctivitis managed?

A

topical mast cell stabilisers (lodoxamide), topical antihistamines (antazoline) – don’t use for >6 weeks, diclofenac eye drops for seasonal use, oral antihistamines (chlorphenamine), topical or oral steroids if very severe and sure of diagnosis. Avoid rubbing eyes, cool compress, avoid contacts, avoid allergens, artificial tears can dilute antigens

55
Q

give 4 complications of conjunctivitis

A
  • Corneal ulcer esp if contact lens wearer
  • Blepharitis (meibomian gland inflame)
  • Otitis externa
  • Meningococcal disease
  • Pneumonia after chlamydia inf
56
Q

What is the difference in clinical features between scleritis and episcleritis

A

Scleritis: subacute/ gradual onset, boring eye pain worse on eye movement, localised or diffuse redness, watering, gradual vision loss and diplopia, systemic disease, redness decreases w/ phenylephrine drops
Episcleritis: acute onset, redness and discomfort (rarely marked pain), symptoms more mild, watering, acuity normal
Photophobia mild and more common in scleritis, however if marked photophobia, think uveitis

57
Q

What disease are associated with scleritis and episcleritis?

A

Scleritis: 50% have underling cause eg RA, wegners, SLE, reactive arthritis, PAN, ank spond, gout, sphillis
Episcleritis: mostly idiopathic, 30% have underling disease: IBD, hyperuriceaemia, CT disease (RA, SLE, PAN), thryoid eye disease, foreign body or chemical insult

58
Q

How should scleritis and episcleritis be managed?

A

Scleritis: adress underling disease (DMARDs, immunosurpression), abx if infectious, oral NSAIDs/ pred
Episcleritis: lubricating eye drops, topical corticosteroids or oral anti inflammatory agents if severe

59
Q

When are subconjunctival haemorrhages concerning?

A

Eye trauma as could indicate globe injury esp if severe or diffuse. If track posteriorly it may indicate fracture.

60
Q

How should corneal abrasions be assessed and managed?

A
  • Seidels test- with fluorescein and blue light - check aqueous fluid isnt leaking though a corneal laceration
  • paincontrol with NSAIDs and prevention of infection with abx (chloramphenicol)
  • no patching or contact lens use
61
Q

How are corneal foreign bodies removed?

A
  • under local anaestheic
  • irriagate
  • then use wetted cotton wool bud/ triangle of card
  • then try 25 guage needle or bore if experienced
  • dont remove if penetrating as could prolapse contents- fix eye shield, don’t valsalva and go straight to surgery
62
Q

How does bacterial keratitis present? what organisms cause it>

A
  • usually in contact lens wearer or after trauma to eye causing abrasion
  • red eye, pain, photophobia, foreign body sensation
  • reduced visual acuity
  • epithelial defect (green under fluorscein dye +blue light), white cell infiltrate and odema
  • staph (commonest), acanthamoeba (suspect if initial treatment not working), psuedomonas and gonoccocus (suspect these if profuse discharge, these carry risk of corneal perforation)
63
Q

How should bacterial keratitis be managed?

A
  • refer to eye casualty

- needs intensive topical abx +/- cycloplegics then steroids after healing phase

64
Q

How does herpes simplex keratitis (HSV) present?

A

mild, early childhood, URTI then red eye with pain and photophobia, corneal clouding and profuse tearing

65
Q

How does herpes zoster opthalmicus (VZV) present?

A

Year to decades after chicken pox, influenza like illness: Neuralgia, macular- papular rash over ophthalmic branch of trigeminal nerve, keratitis develops in 65%. Corneal ulcers, uveitis, extraocular nerve palsy, reitnal or optic nerve involvement.
Rash on tip of nose indicated nasociliary involvement (hutchinson sign)
May be precipitated by trauma, surgery, immunosurpression and systemic illness

66
Q

How should viral keratitis (VZV or HSV) be managed?

A

Both need referral for assessment of degree of corneal involvement
- HSV may need topical cycloplegics and topical gangciclovir,
- Varicella zoster opthalmicus needs systemic antiviral (aciclovir) and topical steroids.
Most pts benefit from lubricants and analgesia

67
Q

When is fungal ketatitis seen and how is it managed?

A
  • Aspergillus and fusarium seen in agricultural setting + injury to eye, candida sometimes seen in AIDS
  • similar to bacterial but more gradual and no abx response
  • needs antimycotic therapy and corneal scrape, treatment may last weeks and require systemic therapy or keratoplasty
68
Q

List 7 things that predispose you to contact lens problems

A
  • dry eyes
  • blepharitis
  • poor lens care/ inexperienced
  • prolonged and night time use
  • smoking
  • immunosurpression
  • ageing
  • systemic disease
  • trauma or surgery
69
Q

Give 5 complications of contact lens use

A
  • bacterial keratitis
  • corneal abrasions
  • corneal hypoxia (rare not as better lenses)
  • allergic conjunctivitis (preservative in the lens solution)
  • giant papillary conjunctivitis (intolerance to lens itself)
  • toxic conjunctivitis (esp with soft lenses)
  • tight lens syndrome (corneal odema as lens cant move, epithelial erosions and neovascularisation)
70
Q

Give 4 causes of granulomatous and non granulomatous anterior uveitis

A 
- granulomatous/ chronic= inflammatory- autoimmune, sarcoid, bechets, SLE, HLA B27 disorders
Non granulomatous/ acute= 
- infectious- TB, HIV/ AIDs, herpes zoster opthalmicus, leprosy
- paraneoplastic, intraocular lymphoma
- trauma
- iatrogenic
- ischaemic 
- idiopathic
71
Q

Describe the clinical features of anterior uveitis

A
  • Unilateral pain redness and photophobia which progresses over hrs- days
  • headache
  • blurred vision
  • perilimbal injection
  • hypopyon if significant inflammation
  • pupil shape change
  • excess tears
  • KPs- white inflammatory cells clumped togogether on posterior part of cornea on slit lamp
  • cells in anterior chamber on slit lamp
72
Q

How should anterior uveitis be managed?

A
  • refer to opthalmologist within 24hrs
  • cycloplegic drugs to relieve pain and prevent adhesions between iris and lens
  • steroids
  • immunosurpression if macula odema occurs and visual acuity reduced
  • antimicrobirals if infectious (rare)
  • severe or chronic: phototherapy, cryotherapy or vitrectomy
73
Q

Give 3 complications of anterior uveitis

A
  • cyrstoid macula odema
  • secondary cateract
  • glaucoma
  • vitreous opacities
  • retinal detachment
  • neovascularisation
  • macular ischaemia, vascular occlusions or optic neuropathy can occur with posterior uveitis
74
Q

What can cause anterior ischaemic optic neuropathy

A

Giant cell arteritis (AAION) or small vessel disease (NAAION)

75
Q

Describe the clinical features of anterior ischaemic optic neuropathy

A
  • Typically presents suddenly upon waking
  • Poor vision in one eye- often have dark shadow involving just upper or lower half of vision and nasal area.
  • No pain
  • Visual acuity improves after 6 months of infarct
  • Other features of GCA may be present in AAION (temporal headache/ tendereness, pmr symptoms, age >50, systemic symptoms)
  • NAAION pts often younger (around 70) and have many risk factors
  • reduced direct but normal consensual reflex , RAPD
  • often red desaturation
  • pale swollen optic disc +/- flame haemorrhages and blood vessel swelling
76
Q

How is non arteritic AION managed?

A

manage vascular risk factors, no specific management

77
Q

Describe the clinical features of optic neuritis

A
  • Visual impairment (develops over hr- days, exaggerated by hot baths)
  • pain around eye (worse on movement)
  • dyschromatopsia (impaired colour vision-> central red desaturation)
  • other symptoms: flashing lights, altered perception of direction of movement, fatigue, RAPD, abnormal contrast sensitivity
78
Q

Give 5 causes for optic neuritis

A
  • multiple sclerosis
  • GCA
  • autoimmune diseases (sarcoid, sle, bechets, devics, non speficic autoimmune ON)
  • post infectious or vaccination
  • infectous causes: TB, syphilis, MMR, herpes
  • B12 deficiency
  • drugs: amiodarone, ethambutol, isoniazid, methanol intoxication
79
Q

How should optic neuritis be investigated?

A
  • MRI brain for MS

- if atypical then bloods and LP for autoimmune and infectious causes

80
Q

How should optic neuritis be managed?

A
  • corticosteroids in acute phase- IV methyl pred for 3 days can speed up recovery but no long term improvement in outcomes
  • further management depends on cause
81
Q

What is the commonest cause of sticky eye in children?

A
  • congenital nasolacrimal duct obstruction
  • however need to think about chlamydia conjunctivitis if in first 28 days
  • most resolve spontaneously and dont require investigtaion, lacrimal sac massage several times a day may help and refer if not resolved in a year
82
Q

What is the defect and name for short and long sightedness?

A 
Myopia= short sight= long eyeball= focus before retina (converging lens)
Hyperopia= long sight= short eyeball and focus after lens (diverging lens)
83
Q

What is ambylopia?

A

When one eye has weak vision which persists when refractive error or structural abnormality is corrected. There is oftn strabismus because the image from the weak eye is ignored. Causes inc persisting strabismus after correction of error, asymmetric refractive errors or orbital growths.
Presents with unilateral decreased visual acuity +/- squint.

84
Q

Describe the clinical features of retinoblastoma

A
  • presents before age 5, sometimes with fhx due to Rb1 gene mutation
  • leukocoria (white pupil on red reflex)- or absent red reflex
  • deterioration of vision
  • red irritable eye
  • faltering growth
  • unexplained squint
  • delayed development
  • nystagmus
  • iris colour change
  • redness of eye
85
Q

What is orbital compartment syndrome and what causes it?

A

When intraorbital pressure exceeds perfusion. usually caused by trauma leading to retrobulbar haemorrhage but less common causes inc local injections, post- septal cellulitis, abscess, foreign body

86
Q

What MRI change can be seen suggesting orbital compartment syndrome will be damaging the nerve

A

the optic nerve becomes straight (it naturally has S shape to allow 8mm proptosis, when straight axons will start to get damaged)

87
Q

Describe the features of orbital compartment syndrome

A
  • marked elevated IOP
  • proptosis
  • reduced acuity
  • tight orbit
  • decreased extraocular movements
  • cannot open eyelids and red desturation
88
Q

What is emergency treatment of orbital compartment syndrome

A
  • lateral canthotomy- make slit in lateral part of eye to relieve pressure
89
Q

Why are alkali burns worse than acid burns to the eye?

A

Acid precipitates tissue protein causing barrier to further ocular penetration. Alkali burns are more severe as lipophilic so penetrate eye more rapidly.

90
Q

How should toxic injuries to the eye be managed?

A
  • Manage with copious irrigation with normal saline (20L or more may be needed), may need local anaesthetic to keep eye open
  • Topical betablockers are continued to control IOP after the event
  • Steroids for 2 weeks to surpress inflammation, topical citrate and tetracylines are also used, cycloplegics provide comfort to the eye
  • Some surgical option inc tenonplasty, tissue adhesives, amniotic membrane transplant, corneal stem cell transplant
91
Q

What is pre retinal/ vitreous haemorrhage, what are the clinical features?

A

Leakage of blood into areas in and around vitrous humour. Symptoms: sudden onset floaters shower which over 10 mins or so is enough to obscure vision completely, reddish tint to vision, photopsia (brief flashes of light in the peripheral vision), can be seen on fundoscopy (look up a picture)

92
Q

What may cause vitrous haemorrhage

A
  • Diabetic retinopathy is commonest cause- new blood vessels that form are prone to haemorrhage
  • Trauma- leading cause in young ppl
  • wet ARMD
  • Retinal tear/ detachment
  • Posterior vitreous detachment
  • retinal artery macro aneurysms, proliferative sickle cell retinopathy, neovascularisation secondary to retinal vein occlusion
  • blood vessels cross below the haemorrhage area
93
Q

How is vitreous haemorrhage managed?

A
  • If unknown cause and no detachment then rest with head elevated to 30-45 degrees for 3-7 days and then reevaulate to find cause
  • may take weeks- months to settle
  • Sometimes patch eyes to limit movement prior to treatment so blood can settle
  • Stop taking blood thinners
  • Treatment depends on cause- if retinal detachment it requires laser surgery urgently
  • Body may take months to clear blood from retina and sometimes vitrectomy is needed to remove the standing blood
  • Laser photocoagulation is used ASAP in proliferative vasculopathies when retina is visible
  • Anterior retinal cryotherapy is used if vitreous haemorrhage is fresh as aids clearance of the blood
94
Q

Describe the features of post septal orbital cellulitis

A

Eyelid odema, erythema, chemosis (conjunctival inflammation)
+
orbital signs such as proptosis, ophthalmoplegia, RAPD, blurred or double vision
+ systemic signs such as fever

95
Q

How should postseptal orbital cellulitis be investigated?

A

CT/ MRI sinuses, orbit and brain to find cause and assess for complications such as abscess.
Swabs or skin breaks, throat and nasal secretions.
Sepsis 6 investigations eg bloods etc

96
Q

How should pre and post septal orbital cellulitis be managed?

A
  • Preseptal: often admit, give oral co-amoxiclav, check response to abx and CT scan normal, involve ENT if sinusitis present
  • Post septal: IV abx (cefotaxime, flucloxacillin), optic nerve function monitored four- hourly, surgery when; CT evidence of orbital collection, no response to abx, decreased visual acuity or atypical picture warranting biopsy
97
Q

Give 3 complications of pre and post septal orbital cellulitis

A

Preseptal: progression or postseptal, lagopathalmos, lid abscess, ectropian, lid necrosis (all rare)
Post septal:
o Ocular: exposure keratopathy, raised IOP, retinal artery/ vein occlusion, endopathlmitis, optic neuropathy
o Orbital abscess: more associated with post traumatic aetiology
o Subperiosteal abscess
o Intracranial (rare): abscess, meningitis, cavernous sinus thrombus

98
Q

Describe the clinical features of giant cell arteritis

A
  • AGE >50
  • Acute onset temporal headache + scalp tenderness
  • Jaw claudication
  • Visual disturbances: due to AION- blurred vision, amaurois fugax, transient or permenant visual loss, dipolopia (if CN palsy)
  • Abnormality on palpation of temporal artery: absent pulse, beaded, tender or enlarged
  • Myalgia, malaise or fever
  • PMR symptoms: proximal stiffness, soreness and pain
  • Fundoscopic evidence of ischaemic disease
99
Q

State the criteria for GCA diagnosis

A

(need 3 out of the 5):

  • Age >50
  • New headache
  • Temporal abnormality
  • ESR >50 mm/ hour
  • Abnormal artery biopsy
100
Q

how should GCA be investigated?

A
  • ESR and CRP
  • Normocytic normochromic anaemia and thrombocytosis are present
  • Autoantibody and complement levels usually normal
  • Temporal artery biopsy
  • Colour duplex ultrasonography also relatively accurate for diagnosing GCA
101
Q

How should GCA be managed?

A
  • 40mg pred daily unless ischaemic symptoms- in this cause use 60
  • If visual symptoms, admit and treat with IV methyl pred 1g
  • When asymptomatic and normal test results, reduce dose in 10mg steps every 2 weeks until 20mg then 2.5 mg steps
  • Start aspirin 75mg daily unless contraindicated
102
Q

List 3 complications of GCA

A
  • Loss of vision
  • Aneurysms, dissections of aorta and major branches
  • Steroid related complications
103
Q

What is endopthalmitis and what causes it?

A
  • inflammation of anterior and posterior chambers of the eye
  • usually due to eye surgery (inc cataracts), penetrating trauma or extension of corneal infection
  • treatment involved abx injection into eye and vitrectomy in severe cases
104
Q

How does endopthalmitis present?

A

-Presents with acute eye pain, reduce vision, red eye and ocular discharge and often eyelid swelling. Hypopyon is common finding. Usually 1-2weeks post op.

105
Q

Describe the eye development of thyroid disease

A
  • Begins as active inflammatory orbital phase lasting 6-12 months- during this expansion of extraocular muscles and orbital fat occurs
  • This leads to proptosis, compressive optic neuropathy and compromised extraocular muscle motility (can be asymmetric and affecting inferior rectus first and cause strabismus)
  • Progressive deterioration followed by a peak and then spontaneous improvement
  • Onset of hyperthyroidism and TED are usually within 18 months of each other but either can occur first
106
Q

other than thyroid eye disease, what can cause proptosis

A
  • Allergic conjunctivitis
  • Dry eye
  • Orbital myositis
  • Chronic progressive external opthalmoplegia
  • Idiopathic orbital inflammatory disease
  • Lymphoproliferative disorders
  • MG
  • Cushings
  • retrobulbar tumour/ abcess/ hameorrhage
107
Q

How should thyroid eye disease be managed?

A

-Stop smoking
- Acheieve and maintain eurthyroid state (wont help much as the autoantibodies cause the disease, not the T4 level)
- Lubricants if symptoms of corneal exposure
- Prisms to control diplopia
- Botulinum toxin for upper lid swelling
If mod- severe:
- Oral steroids, ciclosporin, Iv immunoglobulins
- Rituximab and infliximab emerging therapies
- Surgery if sight threatening: orbital decompression, strabismus surgery, lid lengthening surgery, blepharoplasty

108
Q

How can eye complications of MS be managed?

A
  • high dose methyl pred IV
  • IV Ig
  • plasmapheresis short term for severe attacks if steroids contraindicated or ineffective
  • Dimethyl fumerate, natalizumab, interfereon beta are also approved for MS
  • often no treatment given for ON as vision will recover over 6 weeks (to variable extents) and steroids will only speed up recovery (not final outcome) so side effects arnt worth it unless bilateral
109
Q

What eye diseases are associated with HIV?

A
  • conjunctival microvasculopathy
  • CMV retinitis
  • VZV retinitis
  • herpes zoster opthalmicus
  • molluscum contagiousum
  • keratitis
  • HIV retinopathy (microangiopathy w/ cotton wool spots)
110
Q

what causes sub retinal haemorrhage (can see blood vessels travelling over the haemorrhage site) and how are they managed?

A

Causes: choroidal neovascularization, retinal tear, Coat’s disease, sickle cell anemia, blunt trauma
Management: anit vegf only if small, expansile gas, intravetiral/ sub retinal tissue plasminogen activator

111
Q

name 3 most important causes of large and one of small pupil

A

Large: pharmacological (stimulants, psychotropics, atropine and phenylephrine drops), acute angle closure glaucoma, CNIII palsies, holmes adi
Small: horners, drugs (opiates)

112
Q

how are hyphaemas managed?

A
  • strict rest to avoid secondary bleed which should clog trabecular meshwork and cause glaucoma
  • monitor IOP
  • most resolve on their own but rarely surgical evacuation is needed
  • if eye has sustained enough trauma for this to occur it also needs thorough checking over for corneal abrasion, retinal tear/ detachment etc
113
Q

Describe the 4 opthalmic manifestations of MS

A
  • Uveitis more common
  • cranial nerve palsies- lid lag, pupil defects, diploia and incomitant squints
  • optic neuritis: red desat, reduced acuity, RAPD, eye pain on movement
  • intranucular opthalmoplegia: when 1 eye looks laterally the other doesnt turn medially or lags often w/ nystagmus of the laterally moving eye. Due to lesion of MLF between CN VI and IV, may be bilateral.
  • symptoms often worse w/ heat (shower, bath, summer)
114
Q

how is blepharitis managed?

A
  • lid hygene: cotton bud+ clenser along lid line, clean BD
  • wet warm compress for anterior blepharitis
  • dry warm compress for posterior
  • avoid mascara and eyeliner
  • anterior: chloramphenicol can be rubbed into lid line if hygene and warm compress not enough
  • oral abx can be given 2nd line for posterior
  • steroid ointment into lid margins if no corneal opacities
115
Q

Describe the differences between stye (hordeolum) and meibomian cyst (chalazion)?

A

STYE: at lash line (external) or localised inflamm of tarsal plate on everting eyelid (internal), tender, follicle often staph infected, either lid
MEIBOMIAN CYST: well defined nodule on everting eyelid, firm, usually painless, upper lid, found above lash line (blocked oil gland), develops slowly over weeks

116
Q

How are stye and meibomian gland cyst managed?

A

Stye: warm compress 15 mins 2-4x p day, if painful and external can remove lash from infected follicle or incise and drain w/ fine needle, abx if evidence of spreading infection (conjunctivitis, mucopurulent discharge)
MBC: warm compress + gentle massage after, othalmology for excision if persistent, recurrent, causing astigmatism, visual change or cosmetic dislike.

117
Q

What different types of blepharitis are there?

A
  • bacterial/ staph( anterior): eyelid inflam, lash loss, ulcers, stye, corneal epithelial defects
  • seborrhoeic (anterior): scales, greasy, no corneal defects, eyelid inflam, dermatitis common, lash loss rare
  • meibomian (posterior): chalazions, corneal epithelial defects (punctate erosions), foamy discharge, no lid inflam
    All: dry gritty feeling, crusting, burning/ itching, bilateral, worse in morn, recurrent conjunctivits

Y4 Neuro and SS (6 decks)

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