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Neuro & Special Senses > Ophthalmology Conditions > Flashcards

Ophthalmology Conditions Flashcards

1
Q

What is the action of atropine?

A

Parasympatholytic
Anticholinergic
Blocks the response of the iris sphincter muscles and accommodative muscles of the ciliary body

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2
Q

What are mydriatics and cycloplegics and examples?

A

Dilate the pupil and paralyse the ciliary muscle

Atropine
Cyclopentolate
Tropicamide
Phenylephirine

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3
Q

What are uses of mydriatics and cycloplegics?

A

Dilate pupil for visualisation of the retina
Management of children with amblyopia - lazy eye
Use in refraction of children for prescription of glasses

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4
Q

What is the action of cyclopentolate?

A

Parasympatholytic
Anticholinergic
Blocks response of iris sphincter muscles and accommodative muscles of ciliary body

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5
Q

What is the action of tropicamide?

A

Parasympatholytic
Anticholinergic
Blocks response of iris and ciliary muscle

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6
Q

What is the action of phenylephirine?

A

Sympathetic agonist

Stimulation of iris dilation muscle

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7
Q

What are the side effects of mydriatic/cycloplegic drops?

A

Whitening of eyelids due to vasoconstriction (resolves when drops wear off)
Atropine can cause redness of face and warm sensation to touch (so consider lower dose)
Sting eyes for few seconds after instillation
Cannot drive until blurring effect has worn off

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8
Q

What are the uses of fluorescein drops?

A

Diagnostically to highlight defects in corneal epithelium
Diagnostically to assess tear drainage in children with congenital nasolacrimal duct obstruction
Investigation when measuring IOP (tonometry)
Administered with local anaesthetic as 0.25% solution with oxybuprocaine HCl or proxymetacaine HCl

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9
Q

What is the mechanism of fluorescein drops?

A

Precursor of eosins
Temporarily stains any cell it enters
Marks damaged areas

Skin discolouration may last 6-12 hours
Contraindicated in an allergy

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10
Q

How long can atropine last?

A

1-2 weeks

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11
Q

How long can cyclopentolate last?

A

Effect in 25-75 mins

Recovery over 6-24 hrs

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12
Q

How long can tropicamide last?

A

Effect within 15-20 mins

Recovery over 4-8 hours

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13
Q

How long can phenylephirine drops last?

A

3-6 hours

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14
Q

When are mydriatic and cycloplegic drops contraindicated?

A

Untreated narrow angle glaucoma

Atropine - not in HTN
Avoid phenylephirine in children

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15
Q

What is glaucoma?

A

Optic nerve damage caused by a significant rise in intraocular pressure
Due to blockage in aqueous humour trying to escape

Pressure due to resistance to flow through the trabecular meshwork into the canal of Schlemm

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16
Q

What is the pathophysiology of open angle glaucoma?

A

Gradual increase in resistance through the trabecular meshwork
Slow and chronic onset, as pressure slowly builds up in eye

Increased pressure causes cupping of optic disc
Normal indent (optic cup) becomes larger due to pressure (>0.5 of the sixe of the optic disc - abnormal)
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17
Q

What are some of the risk factors for open-angle glaucoma?

A

Increasing age
Family history
Black ethnic origin
Nearsightedness (myopia)

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18
Q

What is the presentation of open-angle glaucoma?

A

Can be asymptomatic for long period of time
Diagnosed on routine check
Affects peripheral vision first, closes in until tunnel vision

Can present with gradual onset of fluctuating pain
headache
blurred vision
halos appearing around lights, particularly at night time

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19
Q

How can intraocular pressure be measured?

A

Non-contact tonometry - puff of air at cornea and measuring corneal response

Goldmann applanation tonometry - gold standard
Special device mounted on slip lamp, makes contact with cornea and applies different pressures

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20
Q

What investigations enable a diagnosis of open angle glaucoma?

A

Goldmann applanation tonometry
Fundoscopy to check for optic disc cupping and optic nerve health
Visual field assessment to check for peripheral vision loss

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21
Q

What is the management of open-angle glaucoma?

A

Treatment started at an IOP of 24mmHg or above

First line - latanoprost prostaglandin eye drops
Increase uveosacral outflow

Or
Beta blockers, timolol
Carbonic anhydrase inhibitors, dorzolamide
Sympathomimetics, brimonidine

Trabeculectomy surgery when eye drops ineffective:
new channel from anterior chamber, through sclera to under conjunctiva
causes a bleb under conjunctiva (reabsorbed)

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22
Q

What are some of the types of glaucoma?

A

Open angle
Acute angle
Developmental - congenital or Reiters
Secondary - trauma, uveitic, steroid

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23
Q

What occurs in acute angle closure glaucoma?

A

Iris bulges forwards
Seals off trabecular meshwork, so cannot drain
Aqueous humour cannot leave anterior chamber

Pressure builds up in posterior chamber, causing pressure behind the iris
Worsens closure of angle

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24
Q

What are the risk factors for angle closure glaucoma?

A

Increasing age
Females affected 4x more often than males
Family history
Chinese and East Asian ethnic origin, rare in black
Shallow anterior chamber

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25
Q

What medications can precipitate acute angle closure glaucoma?

A

Adrenergic medications e.g. noradrenalin
Anticholinergic medications e.g. oxybutynin and solifenacin
TCAs e.g. amitriptyline as have anticholinergic effects (inhibits parasympathetic effect, causing glaucoma in those with narrow anterior chambers by dilating pupil and causing pupillary block)

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26
Q

What is seen on examination in acute angle glaucoma?

A 
Severely painful red eye
Teary
Hazy cornea
Decreased visual acuity
Dilatation of the affected pupil
Fixed pupil size
Firm eyeball on palpation

Halos around lights
Associated headache, nausea, vomiting

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27
Q

What is the initial management of acute angle glaucoma?

A

Same day assessment
Lie patient on back, no pillow
Give pilocarpine eye drops - 2% for blue, 4% brown eyes
Give acetazolamide (carbonic anhydrase inhibitor reduces production of aqueous humour)
Give analgesia
Anti-emetic if needed

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28
Q

What secondary management of acute angle glaucoma is required?

A 
Pilocarpine
Acetazolamide IV/PO
Hyperosmotic agents e.g. glycerol, mannitol to increase osmotic gradient between blood and fluid
Timolol - beta-blocker
Dorzolamide
Brimonidine

Definitive treatment - laser iridotomy; hole in iris for humour to flow from posterior chamber to anterior
Relieves pressure pushing iris against the cornea

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29
Q

What is the leading cause of blindness in the UK?

A

Age related macular degeneration

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30
Q

What are the two types of age related macular degeneration?

A

Wet - 10% cases
Dry - 90%

Wet carries a worse prognosis

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31
Q

What is a key finding in association with macular degeneration?

A

Drusen on fundoscopy

Yellow deposits of proteins and lipids that appear between the retinal pigment epithelium and Bruch’s membrane

Normal drusen - <63 micrometres and hard

Large and greater numbers early sign, common to both wet and dry

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32
Q

What other features, aside from drusen are common to both wet and dry AMD?

A

Atrophy of the retinal pigment epithelium

Degeneration of the photoreceptors

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33
Q

What are the layers of the macula?

A

Choroid layer at bottom - contains blood vessels
Bruch’s membrane
Retinal pigment epithelium
Photoreceptors

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34
Q

What is the pathophysiology of wet AMD?

A

Development of new vessels growing from the choroid layer into the retina
These vessels can leak fluid/blood, cause oedema
VEGF released

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35
Q

What are the risk factors for AMD?

A 
Age
Smoking
White or chinese
Family history
CVD, HTN
Ocular characteristics - light iris
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36
Q

What is the presentation of AMD?

A

Gradual worsening central visual field loss
Reduced visual acuity
Crooked or wavy appearance to straight lines

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37
Q

What is the importance of the presentation of wet AMD?

A

Presents more acutely
Presents with loss of vision over days
Progresses to full loss of vision over 2-3 years
Often progresses to bilateral disease

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38
Q

What is seen on examination in AMD?

A

Snellen - reduced acuity
Scotoma - central patch of vision loss
Amsler grid test - distortion of straight lines
Fundoscopy - Drusen

Slit lamp biomicroscopic fundus exam

Optical coherence tomography - cross section of retina for wet AMD

Fluorescein angiography - second line for wet AMD

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39
Q

What is the management of dry AMD?

A

Focus on lifestyle measures to slow progression
Avoid smoking
Control BP
Vitamin supplements - zinc and antioxidants (not recommended to smokers due to increase in lung ca)

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40
Q

What is the management of wet AMD?

A

Anti-VEGF e.g.
ranibizumab, bevacizumab, pegaptanib
slows development of new vessels
injected into vitreous chamber once a month

Photodynamic therapy with Verteperfin - light activated compound, taken up by dividing cells inc neovascular tissue
Injected IV, activated by illumination, is sparing of healthy tissue

Need to be started within 3 months to be beneficial

If untreated can become functionally blind within 2 years
Is a treatable disease

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41
Q

How large is the macula?

A

5.5mm in diameter with the fovea at the centre

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42
Q

What is the function of the retinal pigment epithelium RPE?

A

Outer blood retinal barrier
Prevents leak of ECF from choriocapillaries to subretinal space
Actively pumps ions and water out of subretinal space
Absorbs stray light
Storage, metabolism and transport of Vitamin A in visual cycle

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43
Q

What are signs of dry AMD?

A

Drusen

RPE hyperplasia and atrophy

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44
Q

What is drusenoid RPE detachment?

A

Soft drusen enlarge, become more numerous and coalesce giving a localised elevation of the RPE

Lifts it away from Bruch’s membrane
Results in hypoxic state and inflammation

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45
Q

What occurs in advanced stages of dry AMD?

A

Confluent drusen
Central and paracentral degeneration of the macula
Atrophy of choriocapillaries, RPE and photoreceptors
Geography atrophy - map like area of atrophy extending from foveal centre

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46
Q

What is the classification of wet AMD?

A

Based on location of lesion in relation to fovea:
subfoveal
juxtafoveal
extrafoveal

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47
Q

What is the fundus fluorescein angiogram classification?

A

For Wet AMD
Characterised by angiographic
Classic - CNV clearly visible
Occult - obscured, not visible

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48
Q

What clinical features have been associated with an even greater risk of developing wet AMD?

A

More than 5 drusen
Large - soft and confluent drusen
Pigment clumping in the RPE
Systemic hypertension

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49
Q

What is Charles Bonnet syndrome?

A

Visual hallucinations due to visual loss

Common in those with wet AMD

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50
Q

What is hypertensive retinopathy?

A

Damage to small blood vessels in retina

Chronic hypertension or malignant HTN

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51
Q

What is silver/copper wiring?

A

Walls of the arterioles become thickened and sclerosed increasing reflection of light

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52
Q

What is arteriovenous nipping?

A

Arterioles cause compression of the veins where they cross

Due to sclerosis and hardening of the arterioles

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53
Q

What are cotton wool spots?

A

Due to ischaemia and infarction in the retina, causing damage to nerve fibres
Appear as fluffy white patches on the retina
Result of accummulation of axoplasmic material within the nerve fibre layer

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54
Q

What are the findings in hypertensive retinopathy?

A

Cotton wool spots
Retinal haemorrhages - rupture and release of blood into the retina
Papilloedema - ischaemia to optic nerve, causes optic nerve swelling and blurring of disc margins
Silver wiring
Hard exudates
Arteriovenous nipping

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55
Q

What is the pathophysiology of diabetic retinopathy?

A

Hyperglycaemia damages retinal small vessels and endothelial cells.
Increased vascular permeability leads to leakage from the blood vessels, blot haemorrhages and hard exudates.

Damage to blood vessel wall - microaneurysms and venous bleeding.

Damage to nerve fibres in retina - cotton wool spots

Intraretinal microvascular abnormalities - dilated and tortuous capillaries
Shunt between arterial and venous vessels

Neovascularisation - growth factors released in the retina, development of new blood vessels

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56
Q

What is the classification of diabetic retinopathy?

A

Non-proliferative - background, can develop into proliferative
Proliferative - new blood vessels have developed, vitrous haemorrhages

Diabetic maculopathy

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57
Q

What are the findings of non-proliferative diabetic retinopathy?

A

Mild - microaneurysms

Moderate - microaneurysms, blot haemorrhages, hard exudates, cotton wool spots, venous bleeding

Severe - blot haemorrhages, microaneurysms in 4 quadrants
venous beating in 2 quadrants
intraretinal microvascular abnormality

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58
Q

What are the findings in diabetic maculopathy?

A

Ischaemic maculopathy

Macular oedema

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59
Q

What are the complications of diabetic retinopathy?

A

Retinal detachment
Vitreous haemorrhage - bleeding into the vitreous humour
Rebeosis iridis - new blood vessel formation in the iris
Optic neuropathy
Cataracts

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60
Q

What is the management of diabetic retinopathy?

A

Laser photocoagulation
Anti VEGF medications - ranibizumab, bevacizumab
Vitreoretinal surgery

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61
Q

What does damage to retinal capillaries lead to in diabetic retinopathy?

A

Microvascular occlusion

Microvascular leakage

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62
Q

What are predictive risk factors for progression of diabetic retinopathy?

A 
Duration of DM
Hyperglycaemia
HTN. hyperlipidaemia
Nephropathy
Pregnancy

Obesity, smoking, alcohol, physical inactivity

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63
Q

What is rubeosis iridis?

A

Neovascularisation - new blood vessels found on the surface of the iris
often associated with diabetes in advanced proliferative retinopathy

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64
Q

What are cataracts?

A

When the lens in the eye becomes cloudy and opaque, describes any opacity or reduction in clarity of the crystalline lens

Lens focuses light onto the retina

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65
Q

How are congenital cataracts screened for?

A

They occur before birth

Screened for red reflex during neonatal examination

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66
Q

What are the risk factors for cataracts?

A

Most develop over years with advanced age in the presence of risk factors

Increasing age
Smoking
Alcohol
Diabetes
Steroids 
Hypoglycaemia
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67
Q

What is the difference in the loss of vision in cataracts compared with other pathologies?

A

Cataracts cause generalised reduction in visual acuity, starbursts around light

Glaucoma - peripheral loss of vision, halos around lights

Macular degeneration - central loss of vision, crooked or wavy appearance to straight lines

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68
Q

What is the clinical presentation of cataracts?

A

Usually asymmetrical, as both eyes affected separately

Very slow reduction in vision
Progressive blurring of vision
Change of colour of vision, colours becoming more brown or yellow
Starbursts around lights, particularly at night time

Loss of red reflex - can appear white or grey, show up on photographs

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69
Q

What is the management of cataracts?

A

Surgery - drill and break lens into pieces, remove and implant artificial lens into the eye

or lens extraction by phacoemulsification - ultrasound energy

Cataracts can mean other conditions e.g. AMD or diabetic retinopathy can go undetected, until after surgery and still have poor visual acuity

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70
Q

What is endophthalmitis?

A

Rare but serious complication
Inflammation of inner contents of the eye
Usually due to infection
Treated with intravitreal antibiotics

Otherwise loss of vision and loss of the eye

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71
Q

What are the causes of cataracts?

A 
Congenital
Age
Drugs - systemic steroids or steroid eye drops
Systemic disease - diabetes, down's
Other ocular disease - uveitis
Trauma
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72
Q

What are the complications of cataract surgery?

A

Per-operatively - posterior capsular rupture, vitreous loss
Early-post op - endophthalmitis
Late post-op - posterior capsule opacification

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73
Q

What can cause abnormal pupil shape?

A

Trauma to sphincter muscles in the iris, e.g. cataract surgery

Anterior uveitis causing adhesions

Acute angle glaucoma causing ischaemic damage - vertical oval pupil

Rubeosis iridis - neovascularisation of the iris
in diabetic retinopathy

Coloboma - congenital malformation, hole in the iris causing irregular pupil shape

Tadpole pupil - spasm in a segment of the iris, temporary, associated with migraines

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74
Q

What are causes of mydriasis - dilated pupil?

A 
Third nerve palsy
Holmes-Aide syndrome
Raised ICP
Congenital
Trauma
Stimulants such as cocaine
Anticholinergics
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75
Q

What are causes of miosis - constricted pupil?

A 
Horner's syndrome
Cluster headaches
Argyll Robertson pupil - neurosyphilis
Opiates
Nicotine
Pilocarpine
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76
Q

What is the presentation of a third nerve palsy?

A

Ptosis - levator palpebrae superioris
Dilated non-reactive pupil
Divergent strabismus - down and out eye

Oculomotor supplies all muscles except lateral rectus and superior oblique - so down and out from these

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77
Q

What are causes of a third nerve palsy?

A

Oculomotor nerve travels through cavernous sinus close to posterior communicating artery

Therefore cavernous sinus thrombosis or posterior communicating aneurysm can compress

Idiopathic
Tumour
Trauma
Cavernous sinus thrombosis
Posterior communicating aneurysm
Raised ICP
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78
Q

What is the difference between a sparing and full third nerve palsy?

A

Sparing - microvascular because parasympathetic fibres spared - spares the pupil - diabetes, HTN, ischaemia

Full - surgical third due to physical compression

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79
Q

What is the triad of Horner’s?

A

Ptosis
Miosis
Anhidrosis

May also have enopthalmos - sunken eye
Light and accommodation not affected

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80
Q

What are the causes of Horner’s?

A

Central - 4 Ss
Stroke, MS, swelling (tumour), syringomyelia

Pre-ganglionic - 4Ts
Tumour (pancoast), trauma, thyroidectomy, top rib - cervical rib growing above first rib

Post-ganglionic - 4Cs
Carotid aneurysm, carotid artery dissection, cavernous sinus thrombosis, cluster headache

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81
Q

What is congenital Horner’s associated with?

A

Heterochromia - difference in colour of the iris on the affected side

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82
Q

What is the pathway of nerves affected in Horner’s?

A

Sympathetic arise from spinal cord
These are pre-ganglionic

Enter into sympathetic ganglion at the base of the neck

Exit as post-ganglionic, travel to the head, run alongside internal carotid artery

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83
Q

How can Horner’s be tested for?

A

Cocaine eye drops
Stops noradrenalin re-uptake at the NMJ
Causes normal eye to dilate as more noradrenaline available so causes dilation, but in Horner’s there is no release initially
So no reaction

Or - adrenaline eye drops won’t dilate a normal pupil, but will dilate a Horner’s

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84
Q

What is a Holmes Adie pupil? (tonic pupil)

A

Unilateral dilated pupil
Sluggish to react to light
Slow dilation of the pupil following constriction, over time pupil will get smaller

Damage to post-ganglionic parasympathetic fibres

Holmes Adie syndrome also has absent ankle and knee reflexes

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85
Q

What is Argyll Robertson pupil?

A

Specific to neurosyphilis

Constricted pupil, accommodates when focusing on near object but does not react to light

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86
Q

What is blepharitis?

A

Inflammation of the eyelid margins

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87
Q

What is the presentation of blepharitis?

A

Gritty, itchy, dry sensation in the eyes

Associated with dysfunction of the Meibomian glands

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88
Q

What is the management of blepharitis?

A

Hot compress
Gentle cleaning of eyelid margins to remove debris

Lubricating eye drops:
Hypromellose
Polyvinyl alcohol
Carbomer

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89
Q

What is a stye?

A

Infection of glands of zeis or glands of moll

Sebaceous glands at the base of the eyelashes

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90
Q

What is the management of a stye?

A

Hot compresses and analgesia

Topical antibiotics e.g. chloramphenicol if associated with conjunctivitis or persist

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91
Q

What is a chalazion?

A

Blockage of Meibomian gland

Swelling in the eyelid, typically not tender

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92
Q

What is the treatment of chalazion?

A

Hot compress, analgesia

Topical antibiotics if actuely inflamed

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93
Q

What is the presentation of a stye?

A

Tender red lump along eyelid

May contain pus

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94
Q

What is entropion?

A

Eyelid turns inwards with the lashes against the eyeball

Results in pain, can cause corneal damage and ulceration

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95
Q

What is the management of entropion?

A

Taping eyelid down
Use regular lubricating drops to prevent eye drying out

Definitive management with surgical intervention

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96
Q

What rheumatology pathology is common in uveitis?

A

Ank spon

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97
Q

What are the features of ank spon?

A

HLA-B27 associated

Apical fibrosis
Anterior uveitis
Aortic regurgitation
Achilles tendonitis
AV node block
Amyloidosis
And cauda equina syndrome

Peripheral arthritis

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98
Q

What should be asked in a patient with acute red eye?

A

Vision - normal or reduced
Painful or painless
Check IOP

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99
Q

What causes painful red eye?

A 
Conjunctivitis
Scleritis
Keratitis
Corneal foreign body
Episcleritis
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100
Q

What are causes of painless red eye?

A

Subconjunctival haemorrhage

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101
Q

What is crucial to the history of subconjunctival haemorrhage?

A

Hypertension
On any anticoagulation

Check INR - if raised, needs to be addressed ASAP

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102
Q

What is ectropion?

A

Eyelid turns outwards
Inner aspect of the eyelid exposed, usually affects bottom lid

Can lead to exposure keratopathy as eyeball is exposed

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103
Q

What is trichiasis?

A

Inward growth of the eyelashes, can result in corneal damage and ulceration

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104
Q

What is the management of trichiasis?

A

Remove the eyelash - epilation

Recurrent cases may require electrolysis, cryotherapy or laser treatment to prevent lash regrowing

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105
Q

What is periorbital cellulitis?

A

Eyelid and skin infection in front of the orbital septum
In front of the eye

Presents with swelling, redness, hot skin around the eyelids and eye

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106
Q

What is the treatment of periorbital cellulitis?

A

Systemic antibiotics

May require observation if vulnerable to prevent development into orbital

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107
Q

What is orbital cellulitis and its clinical features?

A

Infection around the eyeball, behind the orbital septum

Sight threatening emergency

Pain on eye movement
Reduced eye movements
Changes in vision
Abnormal pupil reactions
Forward movement of the eyeball - proptosis
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108
Q

What is the treatment of orbital cellulitis?

A

Medical emergency
Requires admission
IV antibiotics
Surgical drainage if abscess

MRI/CT helpful in diagnosis and planning treatment

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109
Q

How does the lens change shape?

A

Ciliary body contract –> pull suspensory ligaments –> flatten lens –> less refraction

vice versa if ciliary body relax

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110
Q

What are common causes of cataracts in younger patients?

A

Trauma

Drugs - steroids, amiodarone, allopurinol

Systemic disease - Diabetes, myotonic dystrophy, neurofibromatosis type 2

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111
Q

What is conjunctivitis?

A

Inflammation of the conjunctiva

the tissue that covers the inside of eyelids and sclera

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112
Q

What are the main types of conjunctivitis?

A

Bacterial
Viral
Allergic

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113
Q

What is the main presentation of conjunctivitis?

A 
Unilateral or bilateral
Red eyes
Bloodshot
Itchy or gritty sensation
Discharge from the eye

Does not cause pain, photophobia or reduced visual acuity

Vision may be blurry due to discharge

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114
Q

What are the features of bacterial conjunctivitis?

A

Purulent discharge
Inflamed conjunctiva

Typically worse in the morning, eye stuck together
Starts in one eye, spread to the other

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115
Q

What are the features of viral conjunctivitis?

A

Clear discharge
Other symptoms of viral infection e.g. dry cough, sore throat, blocked nose
Contagious

Preauricular lymph nodes

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116
Q

What is the management of conjunctivitis?

A

Usually resolves without treatment after 1-2 weeks

Good hygiene
Avoid contact lenses

Abc - chloramphenicol and fusidic acid

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117
Q

What is a consideration in conjunctivitis under 1 month?

A

Neonatal conjunctivitis
Gonococcal infection
Can cause loss of sight
Complications e.g. pneumonia

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118
Q

What is allergic conjunctivitis and its management?

A

Contact with allergens
Causes swelling of conjunctival sac and eyelid
Significant watery discharge, itchy

Antihistamines
Topical mast cell stabilisers - preventing mast cells releasing histamines

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119
Q

What is anterior uveitis?

A

Inflammation in the anterior uvea - iritis

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120
Q

What is the uvea?

A

Iris, ciliary body, choroid

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121
Q

What is the difference between acute and chronic uveitis?

A

Chronic - more granulomatous - more macrophages, less severe

Lasts more than 3 months

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122
Q

What conditions are associate with acute anterior uveitis?

A

HLA B27 conditions
Ankylosing spondylitis
Inflammatory bowel disease
Reactive arthritis

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123
Q

What conditions are associated with chronic anterior uveitis?

A 
Sarcoidosis
Syphilis
Lyme's disease
TB
Herpes virus
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124
Q

What is the presentation of anterior uveitis?

A

Unilateral
Starts spontaneously
Without a hx of trauma or precipitating events

May occur with a flare of an associated disease e.g. reactive arthritis

Dull aching painful red eye
Ciliary flush - ring of red spreading from cornea
Reduced visual acuity
Floaters, flashes
Miosis - constriction due to sphincter contraction
Photophobia - ciliary muscle spasm
Pain on movement
Excessive tears
Posterior synechiae - adhesions pulling iris, abnormally shaped
Hypopyon - collection of white blood cells in anterior chamber

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125
Q

What is the management of anterior uveitis?

A

Referral for same day assessment due to emergency red eye

Refer to rapid access clinic for topical steroids

Steroids
Cycloplegic-mydriatic medications e.g. cyclopentolate or atropine
(antimuscarinic, block iris sphincter and ciliary body)
Immunosuppressants e.g. DMARDs, TNF inhibitors
Laser therapy, cryotherapy, vitrectomy

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126
Q

What is episcleritis?

A

Inflammation of episclera
Outermost layer of sclera
Underneath conjunctiva

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127
Q

Who is episcleritis seen in?

A

Young and middle aged adults
Not usually due to infection
Associated with inflammatory disorders e.g. RA or IBD

128
Q

What is the presentation of episcleritis?

A 
Acute onset, unilateral
Typically not painful
Can have mild pain
Segmental redness - lateral sclera
Foreign body sensation
Dilated episcleral vessels
Watering of eye
No discharge
129
Q

What is the management of episcleritis?

A 
Usually self limiting
Will recover in 1-4 weeks
Lubricating eye drops
Simple analgesia
Cold compresses
Systemic NSAIDs naproxen
130
Q

What are the most common causes of ophthalmia neonatorum?

A

Conjunctivitis in the first 30 days of life
Bacteria - strep, staph
Neisseria gonorrhoea
Chlamydia

131
Q

What is scleritis?

A

Inflammation of the full thickness of the sclera

Most severe is necrotising scleritis, can lead to perforation of the sclera

132
Q

What are associated systemic conditions with scleritis?

A 
Rheumatoid arthritis
SLE
Inflammatory bowel disease
Sarcoidosis
Granulomatosis with polyangiitis
133
Q

What is the presentation of scleritis?

A 
Acute onset
50% cases bilateral
Severe pain
Pain with eye movement
Photophobia
Eye watering
Reduced visual acuity
Abnormal pupil reaction to light
Tenderness to palpation

Severe 8-9/10 boring pain

May have diffuse or nodular swelling

134
Q

What is the management of scleritis?

A

Consider underlying systemic condition
NSAIDs - topical/systemic
Steroids
Immunosuppression - appropriate to the underlying condition e.g. methotrexate for RA

Refer to eye emergency dept

135
Q

What can complicate the management of scleritis?

A 
Scleromalacia perforans - diffuse scleral thickening seen in rheumatoid
Keratitis - persistent ulceration
Uveitis
Cataract formation
Glaucoma
136
Q

What causes scleritis?

A

Immune complex dependent microangiopathy

137
Q

What are corneal abrasions and common causes?

A

Scratches or damage to the cornea, cause of red, painful eye

Contact lenses - assoc. infection with pseudomonas
Foreign bodies
Fingernails
Eyelashes
Entropion - inward turning eyelid
138
Q

What is an important differential to consider with corneal abrasions?

A

Herpes keratitis

Requires antiviral drops

139
Q

What is the presentation of corneal abrasions?

A 
History of contact lenses or foreign body
Painful red eye
Foreign body sensation
Watering eye
Blurring vision
Photophobia
140
Q

How can a corneal abrasion be diagnosed?

A

Fluorescein stain
Collects in abrasions - yellow-orange colour
Slit-lamp examination

141
Q

What is the management of corneal abrasions?

A

Same day assessment
Mild in primary care

Removal of foreign bodies
Simple analgesia
Lubricating eye drops
Antibiotic drops - chloramphenicol
FU after 24 hours

Chemical abrasions - immediate irrigation for 20-30 minutes, urgent referral

Mild uncomplicated usually heal over 2-3 days

142
Q

What are some of the causes of keratitis?

Inflammation of the cornea

A 
Viral infection - herpes
Bacterial - pseudomonas, staph
Fungal - candida, aspergillus
CLARE - contact lens acute red eye
Exposure keratitis - inadequate eye lid covering, e.g. ectropion
143
Q

Where does herpes simplex keratitis most commonly affect?

A

The epithelial layer of the cornea

If inflammation of the stroma - stromal keratitis

144
Q

What complications is stromal keratitis associated with?

A

Stromal necrosis
Vascularisation and scarring
Can lead to corneal blindness

145
Q

What is the presentation of herpes keratitis?

A 
Painful red eye
Photophobia
Vesicles around the eye
Foreign body sensation
Watering eye
Reduced visual acuity

Fever, vesicular lid lesions
Follicular conjunctivitis
Preauricular lymphadenopathy

146
Q

How can herpes keratitis be diagnosed?

A

Staining with fluorescein
Shows dendritic corneal ulcer (branching and spreading of the ulcer)
Slit-lamp examination
Corneal swabs, scrapings

147
Q

What is the management of herpes keratitis?

A

Same day assessment

Aciclovir - topical or oral
Ganciclovir eye gel
Topical steroids for stromal keratitis

Corneal transplant may be required after infection to treat corneal scarring caused by stromal keratitis

148
Q

What causes herpes simplex keratitis?

A

Type 1 HSV common important cause of ocular disease

Usually acquired in early life from close contact e.g kissing

Primary infection may cause a conjunctivitis, then resolution and latency in trigeminal ganglion

Risk of reactivation if immunosuppression, systemic illness

149
Q

What is herpes zoster ophthalmicus?

A

Ophthalmic shingles
Affects ophthalmic division of the trigeminal nerve

Prodromal period, unwell
Pain and vesicles in nerve distribution

Lid swelling, may be bilateral
Keratitis
Iritis
Secondary glaucoma

150
Q

What bacteria can cause bacterial keratitis?

A

Staph epidermidis
Staph aureus
Strep pneumonia
Pseudomonas

151
Q

What are predisposing causes of bacterial keratitis?

A

Keratoconjunctivitis sicca - dry eye
Breach in corneal epithelium e.g. trauma or surgery
Contact lens wear
Prolonged use of topical steroids

152
Q

What is the presentation of bacterial keratitis?

A

Pain - severe
Purulent discharge
Visual loss
Hypopyon - mass of white cells collected in anterior chamber
White corneal opacity - site of polymorphonuclear infiltration of the stroma

153
Q

What are other types of keratitis?

A

Fungal

Interstitial - any vascular keratitis that affects the corneal stroma without epithelial involvement

154
Q

What are causes of a painful eye with vision loss?

A 
Angle closure glaucoma
Corneal ulcer/keratitis
Uveitis
Endophthalmitis
Retrobulbar optic neuritis
Orbital cellulitis
Giant cell arteritis
155
Q

What are causes of a painless eye with fleeting vision loss?

A

Embolic retinal artery occlusion
Migraine and aurea
Raised intracranial pressure
Prodromal in GCA

156
Q

What are causes of a painless eye with persistent vision loss?

A 
Vitreous haemorrhage
Retinal artery occlusion
Retinal detachment
AMD
Other macular disease
Optic neuritis
Ischaemic optic neuropathy
Orbital disease affecting the optic nerve
Intracranial disease affecting the visual pathway
157
Q

What are some causes of ocular pain?

A

Discomfort - blepharitis, dry eye, conjunctivitis, allergy

Pain on movement - optic neuritis

Pain around the eye - GCA, migraine, cellulitis, headache

Severe pain - keratitis, abrasion, foreign body, uveitis, angle closure glaucoma, endophthalmitis, scleritis, myositis of extraocular muscles

158
Q

What are causes of diplopia?

A

Neurogenic - nerve palsies, failure to control squint, visual field defects

Myogenic - thyroid eye disease, myasthenia, myositis, myopathy

Orbital - trauma, SOLs

Monocular - corneal disease, cataracts

159
Q

What are the causes of myopia?

A

(Short sightedness)

Parallel rays of light brought to a point of focus before they reach the retina

Eye too long/large - axial
Optical focusing apparatus of the eye is too powerful

160
Q

What are the causes of hypermetropia?

A

Long sightedness

Eye is too short
Focusing apparatus too weak (lens and cornea)

Treated with a convex lens

161
Q

What is aphakia?

A

After a cataract extraction, the eye is rendered highly hypermetrophic

Because the lens provides one third of the refractive power of the eye

162
Q

How can aphakia be corrected?

A

Insertion of an intraocular lens at the time of surgery
Contact lenses
Aphakic spectacles

163
Q

What is the risk of orbital cellulitis?

A

Can spread to cause a brain abscess

164
Q

What tumours may produce signs of orbital disease?

A

Lacrimal gland tumours
Optic nerve gliomas - in neurofibromatosis type 1
Meningiomas
Lymphomas
Rhabdomyosarcomas
Mets e.g. neuroblastomas in kids, breast, lung, prostate

165
Q

What can cause ptosis?

A

Mechanical - large lid lump, lid oedema, downward tethering due to scarring, structural abnormalities

Neurological - third nerve palsy, Horner’s, Marcus Gunn jaw winking syndrome

Myogenic - myasthenia gravis, muscular dystrophy, ophthalmoplegia

166
Q

What is myasthenia gravis?

A

Autoimmune disease of the voluntary muscles
Weakness triggered by periods of muscle activity
Relieved by rest

Circulating antibodies block the action of acetylcholine at post synaptic nicotinic neuromuscular kunctions

167
Q

What tests are completed to diagnose myasthenia gravis?

A

Repeated upgaze, downgaze movements
results in fatigue and increased ptosis

Look fown for 15s then look at elevated target, lid overshoots then falls
Ice applied reduces ptosis
Weakness of eyelid closure

168
Q

What can cause evaporative dry eye?

A

Inadequate meibomian oil delivery
Ectropion - not adequately apposed
Incomplete lid closure e.g. seventh nerve palsy
Infrequent blinking - parkinson’s

169
Q

What can cause ectopia lentis (disorder of lens position)?

A

Weakness of zonule - subluxation

After ocular trauma
Homocystineuria - lens displaced downwards
Marfan’s

170
Q

What signs are seen on examination in uveitis?

A

Visual acuity reduced

Eye inflamed - mostly around the limbus - ciliary flush

171
Q

What may a patient complain of with macular dysfunction?

A

Blurred central vision
Distorted vision - metamorphopsia
Reduction or enlargement of an object
Loss of the central visual field

172
Q

What can macular oedema be associated with?

A

Intraocular surgery
Uveitis
Retinal vascular disease - diabetic retinopathy and retinal vein occlusion
Retinitis pigmentosa

173
Q

What is a retinoblastoma?

A

Commonest malignant tumour of the eye in childhood
Due to germinal mutations or somatic mutations

If the eye can be salvaged - systemic chemo and local treatment e.g. cryo
Removal of the eye

174
Q

What are the features of a retinoblastoma?

A

White pupillary reflex
Squint due to reduced vision
Occasionally if advanced; painful red eye

175
Q

What is the cause of cotton wool spots?

A

At margins of ischaemic retinal infarct

Due to obstruction of axoplasmic flow, build up of axonal debris in the nerve fibre layer of the retina

176
Q

What are the stages of diabetic retinopathy?

A

None - no signs, vision normal

Background - signs of leakage, microaneurysms, haemorrhage, exudates away from the macula

Maculopathy - exudates, haemorrhage in macula region, central oedema, vision reduced, sight threatening

Preproliferative retinopathy - evidence of arteriolar occlusions, RMA, cotton wool spots, veins irregular, vision normal

Proliferative retinopathy - release of vasoproliferative substance, new vessel growth on disc or retina, vision normal, sight threatening

Advanced retinopathy - bleeding into vitreous, pulling of overlying pigment epithelium

177
Q

What is a subconjunctival haemorrhage?

A

One of the small blood vessels in the conjunctiva ruptures

Releases blood into space between sclera and conjunctiva

178
Q

What can cause subconjunctival haemorrhages?

A

Idiopathic - otherwise healthy
After a period of strenuous activity e.g. heavy coughing, weight lifting, straining when constipated
Trauma to the eye

179
Q

What factors can predispose a patient to subconjunctival haemorrhage?

A 
Hypertension
Bleeding disorders e.g. thrombocytopenia
Whooping cough
Medications e.g. warfarin, NOACs, antiplatelets
Non accidental injury
180
Q

What is the presentation of a subconjunctival haemorrhage?

A 
Patch of bright red blood underneath the conjunctiva
In front of the sclera
Painless
Does not affect vision
May be history of strenuous event
181
Q

What is the management of a subconjunctival haemorrhage?

A

Harmless, resolve spontaneously
Within 2 weeks
Investigate precipitating factors
If there is foreign body sensation, lubricating eye drops can help

182
Q

What is the vitreous body?

A

Gel inside the eye that maintains the structure of the eyeball, keeps the retina pressed on the choroid
Made up of collagen and water

183
Q

What is posterior vitreous detachment?

A

Vitreous gel comes away from the retina, very common, particularly in older patients

184
Q

What is the presentation of posterior vitreous detachment?

A 
Painless condition
Can be completely asymptomatic
Spots of vision loss
Floaters
Flashing lights
185
Q

What is the management of posterior vitreous detachment?

A

No treatment necessary
Symptoms improve over time as brain adjusts
Can predispose a patient to developing retinal tears or detachment

Exclude and assess risk of this, thorough assessment of the retina

186
Q

What is retinal detachment?

A

Sight-threatening emergency
Outer retina relies on blood vessels of the choroid for its blood supply

Retina separates from choroid underneath
Usually due to retinal tear
Allows vitreous fluid to get under the retina, fills space

187
Q

What are the risk factors for retinal detachment?

A 
Posterior vitreous detachment
Diabetic retinopathy
Trauma to the eye
Retinal malignancy
Older age
Family history
188
Q

What is the presentation of retinal detachment?

A 
Painless
Peripheral vision loss
Sudden, shadow like curtain coming across vision
Blurred or distorted vision
Flashes and floaters
189
Q

What is the management of retinal detachment?

A

Reattach retina, reduce traction or pressure which may cause it to recur

Vitrectomy - removing relevant parts of vitreous body and replacing with oil or gas

Scleral buckling - silicone buckle to put pressure on outside of eye/sclera so outer eye indents and brings choroid inwards to make contact with retina

Pneumatic retinopexy - inject gas bubble into vitreous body and position patient so gas bubble creates pressure and flattens retina

190
Q

What is the management of retinal tears?

A

Create adhesions between the retina and choroid
Laser therapy
Cryotherapy

191
Q

What occurs in central retinal vein occlusion?

A

When a blood clot forms in the retinal veins

Central retinal vein runs through optic nerve, drains blood from retina

One of four branched veins blocked causes problems in area, whereas central vein causes problems for whole retina

Blood in retina = leakage of fluid and blood
Causes macular oedema and retinal haemorrhages
Damages retinal tissue
Loss of vision
Release of VEGF to stimulate neovascularisation

192
Q

What is the presentation of central retinal vein occlusion?

A

Sudden painless loss of vision

193
Q

What are the risk factors for central retinal vein occlusion?

A 
Hypertension
High cholesterol
Diabetes
Smoking
Glaucoma
Systemic inflammatory conditions such as SLE
194
Q

What is seen on fundoscopy in central retinal vein occlusion?

A

Flame and blot haemorrhages
Optic disc oedema
Macula oedema

195
Q

What other investigations are useful in central retinal vein occlusion?

A 
Full medical history
FBC for leukaemia
ESR for inflammatory disorders
BP for hypertension
Serum glucose for diabetes
196
Q

What is the management of central retinal vein occlusion?

A

Referral immediately
Treatment of macular oedema and prevent complications e.g. neovascularisation, galucoma

Laser photocoagulation
Intravitreal steroids e.g. dexamethasone intravitreal implant
Anti-VEGF therapies e.g. rituximab, bevacizumab

197
Q

What are the risk factors of central retinal artery occlusion?

A 
Risk factors for atherosclerosis
Older age
Family history
Smoking
Alcohol consumption
Hypertension
Diabetes
Poor diet
Inactivity
Obesity
198
Q

Who is at a higher risk of central retinal artery occlusion secondary to giant cell arteritis?

A

White patients over 50
Particularly females
And those already affected by GCA or polymyalgia rheumatica

199
Q

What is the presentation of central retinal artery occlusion?

A

Sudden painless loss of vision
Relative afferent pupillary defect
Fundoscopy - pale retina, cherry-red spot, due to lack of perfusion

200
Q

What is the relative afferent pupillary defect?

A

Pupil in the affected eye constricts more when light is shone in the other eye, compared to when it is shone in the affected eye.

Because the input is not being sensed by the ischaemic retina, but is being sensed by the normal retina causing consensual reflex

201
Q

What is the management of central retinal artery occlusion?

A

Referral immediately
Check for GCA - ESR and temporal artery biopsy, give steroids - prednisolone 60mg

If presents shortly after symptoms, try to dislodge thrombus:
Occular massage
remove fluid from anterior chamber to reduce IOP
Inhaling carbogen (5% carbon dioxide, 95% oxygen) to dilate artery
sublingual isosorbide Dinitrate to dilate the artery

Long term management reduce reversible risk factors

202
Q

What is optic neuritis?

A

Inflammation of the optic nerves

203
Q

What are some of the types of optic neuritis and causes?

A

Acute demyelinating - most common, due to MS

Ischaemic - GCA, diabetic papillopathy

Corticosteroid-responsive - autoimmune diseases, SLE

Infections - TB, mycoplasma,
Lyme’s

Nutritional - B12 deficiency

Drugs - Amiodarone, ethambutol, isoniazid, methanol intoxication

204
Q

What are the differentials for optic neuritis?

A

Posterior scleritis
Maculopathy
Retinopathy
Big blind spot syndrome

205
Q

What is the usual presentation of optic neuritis?

A

Visual impairment
Pain around the eye
Dyschromatopsia - impairment of colour vision

Light flashes
Increased symptoms with raised body temperature

Decreased pupillary light reaction in the affected eye

206
Q

What are the investigations for optic neuritis?

A

Full ophthalmological examination
Testing visual acuity, contrast and colour vision, visual field testing
MRI - developing MS

Bloods - FBC, ESR, TFTs, autoantibodies, syphilis
Serological testing
CXR - infection
LP

207
Q

What is the management of optic neuritis?

A

Consider corticosteroids in acute phase - methylprednisolone

208
Q

What does Hutchinson’s sign indicate?

A

Lesion to the tip of the nose
Increased chance of ocular involvement

Treatment is with aciclovir

209
Q

What are the stages of thyroid eye disease?

A

Inflammatory phase
Followed by ‘inactive’ fibrotic phase
Sight loss can occur when delay in start of treatment

Onset of hyperthyroidism and TED usually within 18 months of each other

210
Q

How does blepharitis present?

A 
Bilateral
Burning watery eyes (with foreign body sensation if cornea involved)
Worse in morning - eyes may stick
Red inflamed eyelid
Crusts/scales along eyelashes
Tear film deficiency
211
Q

Why are corticosteroids used for uveitis?

A

Reduce inflammation

Prevent adhesions

212
Q

What complications are associated with uveitis?

A

Relapse
Posterior synechiae (adhesions from lens to iris)
Cataract
Glaucoma (due to steroids)

213
Q

What must you examine for if a patient has uveitis?

A 
Back pain - ank spond
Rash/bite - lyme
Resp. Symptoms - Sarcoidosis
GI symptoms - IBD
Cold sore - herpes
Oral/genital ulcers - Behcet's
214
Q

What features are associated with intermediate uveitis?

A

Painless floaters
Decreased vision
Minimal redness and pain

215
Q

What is affected in posterior uveitis?

A

Retina and choroid

216
Q

What happens in herpetic keratitis?

What is the hallmark feature on examination?

A

Virus travel along trigeminal nerve to ophthalmic division to corneal nerve

Dendritic ulcer pattern seen

217
Q

What investigations would you request for someone with a corneal abrasion?

A

None normally needed
CT = 1st choice
X-ray if metallic FB
MRI contraindicated for metallic FB

Fluorescein examination

218
Q

What are the ADR’s associated with anti-VEGF injections?

A

Retinal detachment
Endophthalmitis
Allergic reaction

219
Q

What is retinitis pigmentosa?

A

Inherited eye disease that is characterised by black pigmentation and gradual degeneration of the retina

220
Q

How does retinitis pigmentosa present?

A

Night blindness
Ring scotoma - loss of all peripheral vision –> tunnel vision –> blindness
Black bone spicule pigmentation of the peripheral retina
Mottling of retinal pigmented epithelium
Waxy looking disc

221
Q

What is the pathogenesis of retinitis pigmentosa?

A

Photoreceptor death - rods first

Cell death lead to inflammation of vitreous humour

222
Q

Why do you not get a relative afferent pupillary defect in Retinitis Pigmentosa?

A

Some cases X linked - more men

Peak ages - 7.5, 17 and >50yo

223
Q

How is Retinitis pigmentosa managed?

A

Visual rehab
Counselling

No way to stop disease progression

224
Q

What is the pathogenesis of thyroid eye disease?

A

Autoimmune reaction to thyroid stimulating hormone receptors

Infiltration of lymphocytes into orbital tissue, release of cytokines
Hyperosmotic shift causing oedema

225
Q

What are the risk factors of thyroid eye disease?

A 
Current smoking
Female sex
Middle age
Autoimmune thyroid disease
Uncontrolled thyroid function
Radio-iodine therapy
226
Q

What is the presentation of thyroid eye disease?

A 
Occular irritation
Ache - worse in mornings
Red eyes
Diplopia - restricted ocular mobility
Change in appearance of eyes, bulging eyes
Dry or watery
Mild photophobia
Dyschromatopsia - colour deficiency

Proptosis - lid retraction, lid lag, orbital fat prolapse

Exposure keratopathy - photophobia, tearing, grittiness, pain, due to incomplete lid closure

227
Q

What are the investigations for thyroid eye disease?

A

TSH
Free thyroxine - T4
Anti-TSH receptor autoantibodies, TPO
Thyroid uptake scan

228
Q

What are some complications of thyroid eye disease?

A

Superior limbic keratoconjunctivitis
Conjunctival injection - over rectus muscles - enlargement of conjunctival vessels

Glaucoma may result from decreased episcleral venous outflow

Strabismus - presents as hypotropia or esotropia due to involvement of inferior and medial rectus

Optic nerve compression

229
Q

What is examined in thyroid eye disease?

A 
Visual acuity
Ishihara colour assessment
Exophthalmometry
Assess lid lag, lid retraction
Corneal exposure
Intraocular pressure
Orthoptic assessment
230
Q

What is the clinical activity score for thyroid eye disease?

A

Pain - feeling on globe, or with movement
Redness - eyelids, conjunctiva
Swelling - lids, chemosis (swelling of conjunctiva)
Impaired function - decrease in eye movements, acuity

231
Q

What are the types of thyroid eye disease?

A

Type I - minimal inflammation and restrictive myopathy – mainly fat expansion

Type II - significant orbital inflammation and restrictive myopathy

232
Q

What is the treatment of thyroid eye disease?

A 
Optimise endocrine control
Stop smoking
Avoid radioiodine
Lubricants
(Ocular Hypotensives)
NSAIDS
Selenium, rituximab
Steroids
Steroid sparing agents
Radiotherapy
Surgery - orbital decompression, strabismus surgery, blepharoplasty
Botulinum toxin to reduce upper lid swelling
Prisms to control diplopia
233
Q

What is a squint (strabismus)?

A

Eyes don’t point in the same direction

Misalignment of the visual axis of the eyes

234
Q

What are the different causes of proptosis?

A

Protrusion of the eye

Displaced directly forwards in a SOL within the extraocular muscle cone - intra-conal lesion e.g. optic nerve sheath meningioma

Displaced to one side - extra-conal lesion
e.g. tumour of lacrimal glands displaces to nasal side

Transient proptosis - valsalva manoeuvre increases cephalic venous pressure

Presence of pain with proptosis suggests infection

235
Q

What cause cause pupil irregularity and alter pupil reactions?

A

Anterior uveitis - posterior synechiae - appearance
Sequelae of intraocular surgery
Blunt trauma to the eye - may rupture sphincter muscle - trauma mydriasis
Acute and severe rise in intraocular pressure e.g. glaucoma

236
Q

What can cause a disruption of the sympathetic pathway and Horner’s?

A

Syringomyelia - expanding cavity in the spinal cord, sometimes extends into medulla
Small cell carcinoma of the lung apex - cervical chain
Neck injury
Cavernous sinus disease - catching sympathetic carotid plexus in the sinus

237
Q

What are the features of Horner’s?

A

Small pupil on affected side
Loss of dilator function
Recession of the globe into the orbit - enophthalmos
Lack of sweating if the pathway is affected proximal to the base of the skull

238
Q

What are important clues of raised intracranial pressure?

A

Headache worse on waking and coughing
Nausea, retching
Diplopia - sixth nerve palsy
If due to e.g. SOL - visual field loss, cranial nerve palsy
Hx of head trauma suggesting subdural haemorrhage, history of medications e.g. oral contraceptives, tetracyclines

239
Q

What are the visual signs of raised intracranial pressure?

A

Optic disc swollen, edges blurred, superficial capillaries are dilated
Large blind spot
Abnormal neurological signs may indicate space occupying lesion

240
Q

What is idiopathic intracranial hypertension?

A

Usually presents in overweight women
Headache, obscurations of vision and sixth nerve palsies
Raised intracranial pressure and disc swelling present

Treatment with medications e.g. oral acetazolamide
Ventriculoperitoneal shunting
Optic nerve decompression

241
Q

What is the presentation of giant cell arteritis?

A

Autoimmune vasculitis

Sudden loss of vision
Scalp tenderness e.g. on combing
Pain on chewing, jaw claudication
Shoulder pain
Malaise
242
Q

What are the investigations for GCA?

A

ESR and CRP usually grossly elevated
Temporal artery biopsy
BP check, blood glucose check

243
Q

What is the management of GCA?

A

High dose steroids immediately, oral and IV

Dose tapered over ensuing weeks

244
Q

What are causes of a pale optic disc?

A 
Compression of optic nerve
Retinal artery occlusion
Glaucoma
RICP
Optic neuritis
Inherited optic nerve/retinal disease
Toxic optic neuropathy
Tobacco/alcohol
245
Q

What are most common causes of compression of the optic chiasm?

Causing a bitemporal hemianopia - compression of the nasal retina (temporal field)

A

Pituitary tumour
Meningioma
Craniopharyngioma

246
Q

What defect do lesions of the optic tract and radiation cause?

Usually vascular or neoplastic

A

Homonymous hemianopia

Loss confined to the right or left hand side of the field in both eyes

247
Q

What are the types of squint?

A

Congenital/acquired - onset before/after 6 months
Concomitant/incomitant
Manifest/latent

248
Q

What is the function of the different extraoccular muscles?

A

Superior rectus - abduction and elevation
Lateral rectus - abduction
Inferior rectus - abduction and depression
Inferior oblique - adduction and elevation
Medial rectus - adduction
Superior oblique - adduction and depression

249
Q

Define Hyphaema

A

When blood enters anterior chamber between cornea and iris

250
Q

How does a Hyphaema present?

A

Decrease/ Loss of vision (may improve as gravity pulls the blood down)
Red tinge to eye

251
Q

Name 5 causes of a Hyphaema

A 
Intraocular Surgery 
Blunt trauma
Lacerating Trauma
Leukaemia
Retinoblastoma
252
Q

How are Hyphaemas managed?

A

Small - Outpatient basis, antifibrinolytics, corticosteroids, mitotics, asparin

Non resolving - surgical clean out

Pain relief - avoid aspirin and NSAIDs due to platelet interaction

253
Q

Name three requirements of the accommodation reflex

A

Eyes converging
Pupil size reducing
Lens changing shape and pattern

254
Q

Name six causes of sudden visual loss

A 
CRAO
Anterior Ischaemic Optic Neuropathy
Vitreous Haemorrhage
Retinal Vein Occlusion
Retinal Detachment
Optic Neuritis
255
Q

Give 5 causes of Endopthalmitis

A 
Trauma,
Eye Surgery,
VEGF injections,
Endogenous seeding,
Extension of Corneal infection
256
Q

Describe the likely pathogens of Endopthalmitis with each cause

A

Surgery - Coag neg Staph (epidermis),
Trauma - bacillus cereus,
Endogenous - S.Aureus,Klebsiella

257
Q

Orbital Cellulitis is generally a clinical diagnosis. What investigations could you do, and what would they show?

A

FBC - leukocytosis

Blood cultures - negative

LP (if focal signs)

Swabs

CT sinus and orbit - extension

258
Q

Orbital Cellulitis is an emergency and requires urgent antibiotics and four hourly monitoring. What are the Abx of choice?

A

1) Co Amoxiclav
If pen allergic - Clindamycin and Metronidazole

MRSA - Vancomycin

259
Q

What is the immediate management for Ocular Chemical Injury?

A

1) Check pH with universal indicator
2) Administer topical anaesthetic and remove contact lenses
3) 1L saline irrigation continued until pH is 7
4) Rechecked every 15 minutes

260
Q

If the Chemical Injury of the eye was moderate or severe, how would it be managed?

A

Dexamethasone 1-2 hourly
Vitamin C (topically and orally)
Citrate and Tetracyclines

261
Q

Name three associations of Anterior Uveitis and Chronic Anterior Uveitis respectively

A

Anklyosing Spondylitis, IBD, Reactive Arthritis

Sarcoidosis, Syphilis, TB

262
Q

What can be seen on examination of a Keratitic eye?

A

Oedema
White cell infiltration
Epithelial defect

263
Q

What is Presbyopia?

A

Gradual loss of accommodation response due to decline in elasticity, becoming apparent when amplitude is insufficient to carry out near tasks

264
Q

How does Presbyopia present?

A

Difficulty carrying out near tasks

Accommodative lag (from distance to near vice versa)

Tiring with continuous close work

265
Q

How is Presbyopia treated?

A

OTC glasses are normally sufficient

If pre-existing refractive error - prescription glasses

266
Q

If Presbyopia happens prematurely, what is the likely cause?

A

Accommodative Insufficiency (Associated with encephalitis and enclosed head trauma)

Inability to maintain binocular enlargment as object becomes closer (aka eye strain)

267
Q

Define Anterior Ischaemic Optic Neuropathy

A

Loss of vision as a result of damage to optic nerve from ischaemia

Involves the 1mm head of optic nerve (AKA disc)

268
Q

How does Arteritic Anterior Ischaemic Optic Neuropathy present?

A

Rapid onset unilateral visual loss and decreased acuity

Chalky white pallor of optic disc

Amaurosis fugax?

GCA signs?

269
Q

How is Arteritic Ischaemic Optic Neuropathy investigated?

A

GCA - ESR/CRP, Temporal Artery Biopsy

MRI/USS - between Arteritic and non

OCT

270
Q

Describe the management options for Arteritic Anterior Ischaemic Optic Neuropathy

A

IV Methylpred for 3 days (switch to oral and taper)

MAB against IL6 (Tocilizumab)

Methotrexate

271
Q

Vitreous haemorrhage is one of the most common causes of sudden painless visual loss. Describe the possible aetiologies

A

Proliferative diabetic retinopathy (fragile vessels)
Posterior vitreous detachment
Ocular Trauma

272
Q

How does Vitreous Haemorrhage present?

A
  • Sudden painless visual loss
  • Red Hue (may turn green after breakdown)
  • New onset floaters/cobwebs
  • May be worse in the morning if blood settles during sleep
273
Q

Name four investigations for Vitreous Haemorrhage

A

IOP
Slit Lamp - Red Cells in anterior vitreous
Rule out retinal detachment
USS

274
Q

Describe the general management of Vitreous Haemorrhage

A

Exclude retinal detachment

Rest with head elevated and re- evaluate in 3-7 days for source

275
Q

Name four definitive treatment options for Vitreous Haemorrhage

A

Laser Photocoagulation (for proliferative vasculopathies)

Anterior Retinal Cryotherapy

Vitrectomy

VEGF

276
Q

Diplopia can be monocular or binocular, what is the difference?

A

Monocular - doesn’t disappear with one eye closed, likely opthalmological aetiology

Binocular - with one eye closed it disappears, likely neurological aetiology

277
Q

Describe the anatomical course of CNIII

A 
Emerges from midbrain
Travels close to PCA
Pierces dura near tentorium cerebelli
Lateral cavernous sinus
Superior orbital fissure
278
Q

Name four causes of Oculomotor nerve lesions

A

Diabetes
GCA
Raised ICP
PCA Aneurysm

279
Q

How do Oculomotor nerve lesions present?

A

Fixed dilated pupil that doesn’t accommodate

Ptosis

Unopposed lateral deviation

Intortion on looking down

Microvascular - pupil sparing

280
Q

How do Oculomotor nerve lesions present (sympathetics involved)?

A

Pupil will be fixed but not dilated

281
Q

Trochlear Nerve lesions are rare, give three causes

A

Orbital trauma
Diabetes
Infarction secondary to hypertension

282
Q

Name 6 causes of Diplopia

A 
CNIII lesion
CNIV lesion
CNVI lesion
Orbital Blow Out #
Thyroid Eye Disease
MG
283
Q

How do Trochlear Nerve Lesions present?

A

Vertical Diplopia

Weakness of downward and intortion

Compensatory head tilt away from affected side

284
Q

How does a CNVI lesion appear?

A

Inability to look laterally

285
Q

Give three causes of a CNVI lesion

A

MS
Pontine Cerebrovascular incident
Raised ICP (due to long course)

286
Q

Describe the pathophysiology of an Orbital Blow Out Fracture

A

Usually from an object <5cm

Force transmits along rim and into orbital floor

Force is transmitted into three buttresses (infraorbital, displacement of zygomaticofrontal suture, fracture of zygomatic arch)

287
Q

Name five clinical features of Orbital Blow Out Fractures

A 
Periorbital bruising
Surgical Emphysema
Vertical Diplopia (worse on looking up)
Endopthalmos
Infraorbital Paraesthesia
288
Q

What investigations should you do for a suspected Orbital Blow Out?

A

Plain XRay - Facial, Occipitomental, Submentovertical (droplet sign in maxillary sinus)

CT

289
Q

How are Orbital Blow Out Fractures managed?

A

Don’t blow nose for 10 days

Some can be managed with just broad spec abx

Surgery

290
Q

The onset of Thyroid Eye Disease is normally within 18 months of diagnosis. Describe the pathophysiology

A

Initial inflammatory phase lasting 6-24 months (expansion of extraocular muscles and orbital fat resulting in proptosis and optic neuropathy)

Followed by inactive fibrotic phase

Infiltration of lymphocytes stimulate cytokine release and polysaccharide release from fibroblasts - leads to oedema

291
Q

What are the important receptors in Thyroid Eye Disease?

A

TSH

IGF1

292
Q

Name four risk factors for Thyroid Eye Disease

A

Current smoker
Female
Middle Aged
Radioiodine therapy

293
Q

Describe the pathophysiology of Myasthenia Gravis

A
  • Receptor sites at NMJ are destroyed
  • Not enough stimulation to trigger action potential
  • Increased fatiguability with use (reduced ACh) and improvement with rest
294
Q

Name some signs of Myasthenia Gravis

A

Ptosis
Cogan Lid Twitch (down gaze followed by up gaze, eye saccades and lid overshoots)
Incomitant strabismus
Raised eyebrows

Pupils never involved

295
Q

Name three diagnostic tests for MG

A

Tensilon Test (inhibits AChesterase, only useful when they have measurable findings)

Repetitive Nerve Stimulation Test (decline in compound muscle action potentials within the first 4-5 stimuli)

Single Fibre EMG

296
Q

Name two laboratory tests for MG

A

Serum Anti ACh Receptor Titre

Serum Anti Muscle Specific Kinase AB titre

297
Q

What is the main differential for MG?

A

Lambert Eaton Syndrome

Improvement of symptoms with repeated stimulation

298
Q

Describe the management of MG

A

Med - Steroids, Pyridostigmine, Immunomodulators (if refractory)

Surgery - Removal of thymus

299
Q

What is Amaurosis Fugax?

How does Amaurosis Fugax present?

A

Hypoperfusion of optic nerve, normally secondary to carotid artery atherosclerosis and secondary thromboemboli

Precedes stroke so urgent investigations required

Curtain descending down over vision
If provoked by gaze - optical lesion

300
Q

Other than carotid pathology, give three causes of Amaurosis Fugax

A

GCA
Retinal Migraine
Papilledema

301
Q

How is Amaurosis Fugax investigated?

A

Inflammatory markers
Carotid imaging and cardiac evaluation
MRI/MRA

302
Q

How is Amaurosis Fugax managed?

A

TIA - stroke work up
GCA - Emperic steroids and temporal artery biopsy
Antiplatelets/Anticoag

303
Q

What is Papilledema?

A

Optic disc swelling secondary to raised ICP

Oedema, continued pressure and optic nerve atrophy

304
Q

Name three investigations you would do to define the underlying cause of Papilledema

A

BP
CT/MRI
LP with opening pressure

305
Q

Name three ways Papilloedema can present

A

Asymptomatic
Signs of raised ICP
Abducens Palsy

306
Q

The gold standard management for Papilloedema is to treat underlying cause and reduced ICP. How should IIH be managed?

A

Weight reduction
Acetazolamide

?CSF Shunt, Duran Venous Stenting

307
Q

Dry eyes can cause a gritty, foreign body sensation worse at the end of the day. What are some red flags?

A

Severe eye pain
Significant visual loss
Photophobia

308
Q

What is the treatment of dry AMD?

A

Supplementation with Vitamin C, Vitamin E, Zinc, Copper, Lutein and Zeaxanthin

309
Q

What is pan-retinal photocoagulation used for?

A

Proliferative diabetic retinopathy
Sacrificing the peripheral retina to reduce the production of VEGF by the ischaemic retina and preventing neovascularisation

310
Q

What is an important investigation and complication of rubeosis iridis?

A

Serious complication of severe proliferative diabetic retinopathy - new vessels grow on the iris and in the anterior chamber.
These vessels have the potential to cause a raised intraocular pressure and a secondary glaucoma and therefore measuring this patient’s intraocular pressure is very important.

311
Q

What are two important sign’s in thyroid eye disease?

A 
Lid retraction (Dalrymple's sign)
Lid lag on down gaze (Von Graefe's sign)
312
Q

What is the treatment of endopthalmitis?

A

The treatment is intravitreal vancomycin as the most common causative organisms after surgery are gram positive.

Cultures are taken from the vitreous, either by a tap, or by doing a vitrectomy and antibiotic therapy should be tailored according to culture and sensitivities.

313
Q

What can be given for the treatment of allergic conjunctivitis?

A

mast cell stabilisers such as Sodium Cromoglycate

314
Q

What is a systemic cause of cataracts?

A

Myotonic dystrophy

315
Q

What is the treatment for gonorrhoeal conjunctivitis in infants?

A

Ceftriaxone IV, bacitracin ointment and hourly saline lavage

Neuro & Special Senses (12 decks)

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