Ophthalmology Conditions Flashcards

(315 cards)

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
What medications can precipitate acute angle closure glaucoma?
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)
26
What is seen on examination in acute angle glaucoma?
``` 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
27
What is the initial management of acute angle glaucoma?
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
28
What secondary management of acute angle glaucoma is required?
``` 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
29
What is the leading cause of blindness in the UK?
Age related macular degeneration
30
What are the two types of age related macular degeneration?
Wet - 10% cases Dry - 90% Wet carries a worse prognosis
31
What is a key finding in association with macular degeneration?
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
32
What other features, aside from drusen are common to both wet and dry AMD?
Atrophy of the retinal pigment epithelium | Degeneration of the photoreceptors
33
What are the layers of the macula?
Choroid layer at bottom - contains blood vessels Bruch's membrane Retinal pigment epithelium Photoreceptors
34
What is the pathophysiology of wet AMD?
Development of new vessels growing from the choroid layer into the retina These vessels can leak fluid/blood, cause oedema VEGF released
35
What are the risk factors for AMD?
``` Age Smoking White or chinese Family history CVD, HTN Ocular characteristics - light iris ```
36
What is the presentation of AMD?
Gradual worsening central visual field loss Reduced visual acuity Crooked or wavy appearance to straight lines
37
What is the importance of the presentation of wet AMD?
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
38
What is seen on examination in AMD?
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
39
What is the management of dry AMD?
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)
40
What is the management of wet AMD?
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
41
How large is the macula?
5.5mm in diameter with the fovea at the centre
42
What is the function of the retinal pigment epithelium RPE?
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
43
What are signs of dry AMD?
Drusen | RPE hyperplasia and atrophy
44
What is drusenoid RPE detachment?
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
45
What occurs in advanced stages of dry AMD?
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
46
What is the classification of wet AMD?
Based on location of lesion in relation to fovea: subfoveal juxtafoveal extrafoveal
47
What is the fundus fluorescein angiogram classification?
For Wet AMD Characterised by angiographic Classic - CNV clearly visible Occult - obscured, not visible
48
What clinical features have been associated with an even greater risk of developing wet AMD?
More than 5 drusen Large - soft and confluent drusen Pigment clumping in the RPE Systemic hypertension
49
What is Charles Bonnet syndrome?
Visual hallucinations due to visual loss | Common in those with wet AMD
50
What is hypertensive retinopathy?
Damage to small blood vessels in retina | Chronic hypertension or malignant HTN
51
What is silver/copper wiring?
Walls of the arterioles become thickened and sclerosed increasing reflection of light
52
What is arteriovenous nipping?
Arterioles cause compression of the veins where they cross | Due to sclerosis and hardening of the arterioles
53
What are cotton wool spots?
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
54
What are the findings in hypertensive retinopathy?
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
55
What is the pathophysiology of diabetic retinopathy?
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
56
What is the classification of diabetic retinopathy?
Non-proliferative - background, can develop into proliferative Proliferative - new blood vessels have developed, vitrous haemorrhages Diabetic maculopathy
57
What are the findings of non-proliferative diabetic retinopathy?
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
58
What are the findings in diabetic maculopathy?
Ischaemic maculopathy | Macular oedema
59
What are the complications of diabetic retinopathy?
Retinal detachment Vitreous haemorrhage - bleeding into the vitreous humour Rebeosis iridis - new blood vessel formation in the iris Optic neuropathy Cataracts
60
What is the management of diabetic retinopathy?
Laser photocoagulation Anti VEGF medications - ranibizumab, bevacizumab Vitreoretinal surgery
61
What does damage to retinal capillaries lead to in diabetic retinopathy?
Microvascular occlusion | Microvascular leakage
62
What are predictive risk factors for progression of diabetic retinopathy?
``` Duration of DM Hyperglycaemia HTN. hyperlipidaemia Nephropathy Pregnancy ``` Obesity, smoking, alcohol, physical inactivity
63
What is rubeosis iridis?
Neovascularisation - new blood vessels found on the surface of the iris often associated with diabetes in advanced proliferative retinopathy
64
What are cataracts?
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
65
How are congenital cataracts screened for?
They occur before birth | Screened for red reflex during neonatal examination
66
What are the risk factors for cataracts?
Most develop over years with advanced age in the presence of risk factors ``` Increasing age Smoking Alcohol Diabetes Steroids Hypoglycaemia ```
67
What is the difference in the loss of vision in cataracts compared with other pathologies?
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
68
What is the clinical presentation of cataracts?
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
69
What is the management of cataracts?
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
70
What is endophthalmitis?
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
71
What are the causes of cataracts?
``` Congenital Age Drugs - systemic steroids or steroid eye drops Systemic disease - diabetes, down's Other ocular disease - uveitis Trauma ```
72
What are the complications of cataract surgery?
Per-operatively - posterior capsular rupture, vitreous loss Early-post op - endophthalmitis Late post-op - posterior capsule opacification
73
What can cause abnormal pupil shape?
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
74
What are causes of mydriasis - dilated pupil?
``` Third nerve palsy Holmes-Aide syndrome Raised ICP Congenital Trauma Stimulants such as cocaine Anticholinergics ```
75
What are causes of miosis - constricted pupil?
``` Horner's syndrome Cluster headaches Argyll Robertson pupil - neurosyphilis Opiates Nicotine Pilocarpine ```
76
What is the presentation of a third nerve palsy?
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
77
What are causes of a third nerve palsy?
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 ```
78
What is the difference between a sparing and full third nerve palsy?
Sparing - microvascular because parasympathetic fibres spared - spares the pupil - diabetes, HTN, ischaemia Full - surgical third due to physical compression
79
What is the triad of Horner's?
Ptosis Miosis Anhidrosis May also have enopthalmos - sunken eye Light and accommodation not affected
80
What are the causes of Horner's?
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
81
What is congenital Horner's associated with?
Heterochromia - difference in colour of the iris on the affected side
82
What is the pathway of nerves affected in Horner's?
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
83
How can Horner's be tested for?
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
84
What is a Holmes Adie pupil? (tonic pupil)
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
85
What is Argyll Robertson pupil?
Specific to neurosyphilis | Constricted pupil, accommodates when focusing on near object but does not react to light
86
What is blepharitis?
Inflammation of the eyelid margins
87
What is the presentation of blepharitis?
Gritty, itchy, dry sensation in the eyes Associated with dysfunction of the Meibomian glands
88
What is the management of blepharitis?
Hot compress Gentle cleaning of eyelid margins to remove debris Lubricating eye drops: Hypromellose Polyvinyl alcohol Carbomer
89
What is a stye?
Infection of glands of zeis or glands of moll | Sebaceous glands at the base of the eyelashes
90
What is the management of a stye?
Hot compresses and analgesia | Topical antibiotics e.g. chloramphenicol if associated with conjunctivitis or persist
91
What is a chalazion?
Blockage of Meibomian gland | Swelling in the eyelid, typically not tender
92
What is the treatment of chalazion?
Hot compress, analgesia | Topical antibiotics if actuely inflamed
93
What is the presentation of a stye?
Tender red lump along eyelid | May contain pus
94
What is entropion?
Eyelid turns inwards with the lashes against the eyeball Results in pain, can cause corneal damage and ulceration
95
What is the management of entropion?
Taping eyelid down Use regular lubricating drops to prevent eye drying out Definitive management with surgical intervention
96
What rheumatology pathology is common in uveitis?
Ank spon
97
What are the features of ank spon?
HLA-B27 associated ``` Apical fibrosis Anterior uveitis Aortic regurgitation Achilles tendonitis AV node block Amyloidosis And cauda equina syndrome ``` Peripheral arthritis
98
What should be asked in a patient with acute red eye?
Vision - normal or reduced Painful or painless Check IOP
99
What causes painful red eye?
``` Conjunctivitis Scleritis Keratitis Corneal foreign body Episcleritis ```
100
What are causes of painless red eye?
Subconjunctival haemorrhage
101
What is crucial to the history of subconjunctival haemorrhage?
Hypertension On any anticoagulation Check INR - if raised, needs to be addressed ASAP
102
What is ectropion?
Eyelid turns outwards Inner aspect of the eyelid exposed, usually affects bottom lid Can lead to exposure keratopathy as eyeball is exposed
103
What is trichiasis?
Inward growth of the eyelashes, can result in corneal damage and ulceration
104
What is the management of trichiasis?
Remove the eyelash - epilation Recurrent cases may require electrolysis, cryotherapy or laser treatment to prevent lash regrowing
105
What is periorbital cellulitis?
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
106
What is the treatment of periorbital cellulitis?
Systemic antibiotics | May require observation if vulnerable to prevent development into orbital
107
What is orbital cellulitis and its clinical features?
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 ```
108
What is the treatment of orbital cellulitis?
Medical emergency Requires admission IV antibiotics Surgical drainage if abscess MRI/CT helpful in diagnosis and planning treatment
109
How does the lens change shape?
Ciliary body contract --> pull suspensory ligaments --> flatten lens --> less refraction vice versa if ciliary body relax
110
What are common causes of cataracts in younger patients?
Trauma Drugs - steroids, amiodarone, allopurinol Systemic disease - Diabetes, myotonic dystrophy, neurofibromatosis type 2
111
What is conjunctivitis?
Inflammation of the conjunctiva | the tissue that covers the inside of eyelids and sclera
112
What are the main types of conjunctivitis?
Bacterial Viral Allergic
113
What is the main presentation of conjunctivitis?
``` 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
114
What are the features of bacterial conjunctivitis?
Purulent discharge Inflamed conjunctiva Typically worse in the morning, eye stuck together Starts in one eye, spread to the other
115
What are the features of viral conjunctivitis?
Clear discharge Other symptoms of viral infection e.g. dry cough, sore throat, blocked nose Contagious Preauricular lymph nodes
116
What is the management of conjunctivitis?
Usually resolves without treatment after 1-2 weeks Good hygiene Avoid contact lenses Abc - chloramphenicol and fusidic acid
117
What is a consideration in conjunctivitis under 1 month?
Neonatal conjunctivitis Gonococcal infection Can cause loss of sight Complications e.g. pneumonia
118
What is allergic conjunctivitis and its management?
Contact with allergens Causes swelling of conjunctival sac and eyelid Significant watery discharge, itchy Antihistamines Topical mast cell stabilisers - preventing mast cells releasing histamines
119
What is anterior uveitis?
Inflammation in the anterior uvea - iritis
120
What is the uvea?
Iris, ciliary body, choroid
121
What is the difference between acute and chronic uveitis?
Chronic - more granulomatous - more macrophages, less severe | Lasts more than 3 months
122
What conditions are associate with acute anterior uveitis?
HLA B27 conditions Ankylosing spondylitis Inflammatory bowel disease Reactive arthritis
123
What conditions are associated with chronic anterior uveitis?
``` Sarcoidosis Syphilis Lyme's disease TB Herpes virus ```
124
What is the presentation of anterior uveitis?
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
125
What is the management of anterior uveitis?
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
126
What is episcleritis?
Inflammation of episclera Outermost layer of sclera Underneath conjunctiva
127
Who is episcleritis seen in?
Young and middle aged adults Not usually due to infection Associated with inflammatory disorders e.g. RA or IBD
128
What is the presentation of episcleritis?
``` 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
What is the management of episcleritis?
``` Usually self limiting Will recover in 1-4 weeks Lubricating eye drops Simple analgesia Cold compresses Systemic NSAIDs naproxen ```
130
What are the most common causes of ophthalmia neonatorum?
Conjunctivitis in the first 30 days of life Bacteria - strep, staph Neisseria gonorrhoea Chlamydia
131
What is scleritis?
Inflammation of the full thickness of the sclera | Most severe is necrotising scleritis, can lead to perforation of the sclera
132
What are associated systemic conditions with scleritis?
``` Rheumatoid arthritis SLE Inflammatory bowel disease Sarcoidosis Granulomatosis with polyangiitis ```
133
What is the presentation of scleritis?
``` 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
What is the management of scleritis?
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
What can complicate the management of scleritis?
``` Scleromalacia perforans - diffuse scleral thickening seen in rheumatoid Keratitis - persistent ulceration Uveitis Cataract formation Glaucoma ```
136
What causes scleritis?
Immune complex dependent microangiopathy
137
What are corneal abrasions and common causes?
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
What is an important differential to consider with corneal abrasions?
Herpes keratitis | Requires antiviral drops
139
What is the presentation of corneal abrasions?
``` History of contact lenses or foreign body Painful red eye Foreign body sensation Watering eye Blurring vision Photophobia ```
140
How can a corneal abrasion be diagnosed?
Fluorescein stain Collects in abrasions - yellow-orange colour Slit-lamp examination
141
What is the management of corneal abrasions?
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
What are some of the causes of keratitis? | Inflammation of the cornea
``` 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
Where does herpes simplex keratitis most commonly affect?
The epithelial layer of the cornea If inflammation of the stroma - stromal keratitis
144
What complications is stromal keratitis associated with?
Stromal necrosis Vascularisation and scarring Can lead to corneal blindness
145
What is the presentation of herpes keratitis?
``` 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
How can herpes keratitis be diagnosed?
Staining with fluorescein Shows dendritic corneal ulcer (branching and spreading of the ulcer) Slit-lamp examination Corneal swabs, scrapings
147
What is the management of herpes keratitis?
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
What causes herpes simplex keratitis?
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
What is herpes zoster ophthalmicus?
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
What bacteria can cause bacterial keratitis?
Staph epidermidis Staph aureus Strep pneumonia Pseudomonas
151
What are predisposing causes of bacterial keratitis?
Keratoconjunctivitis sicca - dry eye Breach in corneal epithelium e.g. trauma or surgery Contact lens wear Prolonged use of topical steroids
152
What is the presentation of bacterial keratitis?
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
What are other types of keratitis?
Fungal | Interstitial - any vascular keratitis that affects the corneal stroma without epithelial involvement
154
What are causes of a painful eye with vision loss?
``` Angle closure glaucoma Corneal ulcer/keratitis Uveitis Endophthalmitis Retrobulbar optic neuritis Orbital cellulitis Giant cell arteritis ```
155
What are causes of a painless eye with fleeting vision loss?
Embolic retinal artery occlusion Migraine and aurea Raised intracranial pressure Prodromal in GCA
156
What are causes of a painless eye with persistent vision loss?
``` 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
What are some causes of ocular pain?
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
What are causes of diplopia?
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
What are the causes of myopia?
(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
What are the causes of hypermetropia?
Long sightedness Eye is too short Focusing apparatus too weak (lens and cornea) Treated with a convex lens
161
What is aphakia?
After a cataract extraction, the eye is rendered highly hypermetrophic Because the lens provides one third of the refractive power of the eye
162
How can aphakia be corrected?
Insertion of an intraocular lens at the time of surgery Contact lenses Aphakic spectacles
163
What is the risk of orbital cellulitis?
Can spread to cause a brain abscess
164
What tumours may produce signs of orbital disease?
Lacrimal gland tumours Optic nerve gliomas - in neurofibromatosis type 1 Meningiomas Lymphomas Rhabdomyosarcomas Mets e.g. neuroblastomas in kids, breast, lung, prostate
165
What can cause ptosis?
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
What is myasthenia gravis?
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
What tests are completed to diagnose myasthenia gravis?
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
What can cause evaporative dry eye?
Inadequate meibomian oil delivery Ectropion - not adequately apposed Incomplete lid closure e.g. seventh nerve palsy Infrequent blinking - parkinson's
169
What can cause ectopia lentis (disorder of lens position)?
Weakness of zonule - subluxation After ocular trauma Homocystineuria - lens displaced downwards Marfan's
170
What signs are seen on examination in uveitis?
Visual acuity reduced | Eye inflamed - mostly around the limbus - ciliary flush
171
What may a patient complain of with macular dysfunction?
Blurred central vision Distorted vision - metamorphopsia Reduction or enlargement of an object Loss of the central visual field
172
What can macular oedema be associated with?
Intraocular surgery Uveitis Retinal vascular disease - diabetic retinopathy and retinal vein occlusion Retinitis pigmentosa
173
What is a retinoblastoma?
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
What are the features of a retinoblastoma?
White pupillary reflex Squint due to reduced vision Occasionally if advanced; painful red eye
175
What is the cause of cotton wool spots?
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
What are the stages of diabetic retinopathy?
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
What is a subconjunctival haemorrhage?
One of the small blood vessels in the conjunctiva ruptures | Releases blood into space between sclera and conjunctiva
178
What can cause subconjunctival haemorrhages?
Idiopathic - otherwise healthy After a period of strenuous activity e.g. heavy coughing, weight lifting, straining when constipated Trauma to the eye
179
What factors can predispose a patient to subconjunctival haemorrhage?
``` Hypertension Bleeding disorders e.g. thrombocytopenia Whooping cough Medications e.g. warfarin, NOACs, antiplatelets Non accidental injury ```
180
What is the presentation of a subconjunctival haemorrhage?
``` 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
What is the management of a subconjunctival haemorrhage?
Harmless, resolve spontaneously Within 2 weeks Investigate precipitating factors If there is foreign body sensation, lubricating eye drops can help
182
What is the vitreous body?
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
What is posterior vitreous detachment?
Vitreous gel comes away from the retina, very common, particularly in older patients
184
What is the presentation of posterior vitreous detachment?
``` Painless condition Can be completely asymptomatic Spots of vision loss Floaters Flashing lights ```
185
What is the management of posterior vitreous detachment?
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
What is retinal detachment?
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
What are the risk factors for retinal detachment?
``` Posterior vitreous detachment Diabetic retinopathy Trauma to the eye Retinal malignancy Older age Family history ```
188
What is the presentation of retinal detachment?
``` Painless Peripheral vision loss Sudden, shadow like curtain coming across vision Blurred or distorted vision Flashes and floaters ```
189
What is the management of retinal detachment?
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
What is the management of retinal tears?
Create adhesions between the retina and choroid Laser therapy Cryotherapy
191
What occurs in central retinal vein occlusion?
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
What is the presentation of central retinal vein occlusion?
Sudden painless loss of vision
193
What are the risk factors for central retinal vein occlusion?
``` Hypertension High cholesterol Diabetes Smoking Glaucoma Systemic inflammatory conditions such as SLE ```
194
What is seen on fundoscopy in central retinal vein occlusion?
Flame and blot haemorrhages Optic disc oedema Macula oedema
195
What other investigations are useful in central retinal vein occlusion?
``` Full medical history FBC for leukaemia ESR for inflammatory disorders BP for hypertension Serum glucose for diabetes ```
196
What is the management of central retinal vein occlusion?
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
What are the risk factors of central retinal artery occlusion?
``` Risk factors for atherosclerosis Older age Family history Smoking Alcohol consumption Hypertension Diabetes Poor diet Inactivity Obesity ```
198
Who is at a higher risk of central retinal artery occlusion secondary to giant cell arteritis?
White patients over 50 Particularly females And those already affected by GCA or polymyalgia rheumatica
199
What is the presentation of central retinal artery occlusion?
Sudden painless loss of vision Relative afferent pupillary defect Fundoscopy - pale retina, cherry-red spot, due to lack of perfusion
200
What is the relative afferent pupillary defect?
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
What is the management of central retinal artery occlusion?
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
What is optic neuritis?
Inflammation of the optic nerves
203
What are some of the types of optic neuritis and causes?
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
What are the differentials for optic neuritis?
Posterior scleritis Maculopathy Retinopathy Big blind spot syndrome
205
What is the usual presentation of optic neuritis?
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
What are the investigations for optic neuritis?
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
What is the management of optic neuritis?
Consider corticosteroids in acute phase - methylprednisolone
208
What does Hutchinson's sign indicate?
Lesion to the tip of the nose Increased chance of ocular involvement Treatment is with aciclovir
209
What are the stages of thyroid eye disease?
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
How does blepharitis present?
``` 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
Why are corticosteroids used for uveitis?
Reduce inflammation | Prevent adhesions
212
What complications are associated with uveitis?
Relapse Posterior synechiae (adhesions from lens to iris) Cataract Glaucoma (due to steroids)
213
What must you examine for if a patient has uveitis?
``` Back pain - ank spond Rash/bite - lyme Resp. Symptoms - Sarcoidosis GI symptoms - IBD Cold sore - herpes Oral/genital ulcers - Behcet's ```
214
What features are associated with intermediate uveitis?
Painless floaters Decreased vision Minimal redness and pain
215
What is affected in posterior uveitis?
Retina and choroid
216
What happens in herpetic keratitis? | What is the hallmark feature on examination?
Virus travel along trigeminal nerve to ophthalmic division to corneal nerve Dendritic ulcer pattern seen
217
What investigations would you request for someone with a corneal abrasion?
None normally needed CT = 1st choice X-ray if metallic FB MRI contraindicated for metallic FB Fluorescein examination
218
What are the ADR's associated with anti-VEGF injections?
Retinal detachment Endophthalmitis Allergic reaction
219
What is retinitis pigmentosa?
Inherited eye disease that is characterised by black pigmentation and gradual degeneration of the retina
220
How does retinitis pigmentosa present?
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
What is the pathogenesis of retinitis pigmentosa?
Photoreceptor death - rods first | Cell death lead to inflammation of vitreous humour
222
Why do you not get a relative afferent pupillary defect in Retinitis Pigmentosa?
Some cases X linked - more men | Peak ages - 7.5, 17 and >50yo
223
How is Retinitis pigmentosa managed?
Visual rehab Counselling No way to stop disease progression
224
What is the pathogenesis of thyroid eye disease?
Autoimmune reaction to thyroid stimulating hormone receptors Infiltration of lymphocytes into orbital tissue, release of cytokines Hyperosmotic shift causing oedema
225
What are the risk factors of thyroid eye disease?
``` Current smoking Female sex Middle age Autoimmune thyroid disease Uncontrolled thyroid function Radio-iodine therapy ```
226
What is the presentation of thyroid eye disease?
``` 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
What are the investigations for thyroid eye disease?
TSH Free thyroxine - T4 Anti-TSH receptor autoantibodies, TPO Thyroid uptake scan
228
What are some complications of thyroid eye disease?
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
What is examined in thyroid eye disease?
``` Visual acuity Ishihara colour assessment Exophthalmometry Assess lid lag, lid retraction Corneal exposure Intraocular pressure Orthoptic assessment ```
230
What is the clinical activity score for thyroid eye disease?
Pain - feeling on globe, or with movement Redness - eyelids, conjunctiva Swelling - lids, chemosis (swelling of conjunctiva) Impaired function - decrease in eye movements, acuity
231
What are the types of thyroid eye disease?
Type I - minimal inflammation and restrictive myopathy – mainly fat expansion Type II - significant orbital inflammation and restrictive myopathy
232
What is the treatment of thyroid eye disease?
``` 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
What is a squint (strabismus)?
Eyes don't point in the same direction | Misalignment of the visual axis of the eyes
234
What are the different causes of proptosis?
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
What cause cause pupil irregularity and alter pupil reactions?
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
What can cause a disruption of the sympathetic pathway and Horner's?
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
What are the features of Horner's?
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
What are important clues of raised intracranial pressure?
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
What are the visual signs of raised intracranial pressure?
Optic disc swollen, edges blurred, superficial capillaries are dilated Large blind spot Abnormal neurological signs may indicate space occupying lesion
240
What is idiopathic intracranial hypertension?
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
What is the presentation of giant cell arteritis?
Autoimmune vasculitis ``` Sudden loss of vision Scalp tenderness e.g. on combing Pain on chewing, jaw claudication Shoulder pain Malaise ```
242
What are the investigations for GCA?
ESR and CRP usually grossly elevated Temporal artery biopsy BP check, blood glucose check
243
What is the management of GCA?
High dose steroids immediately, oral and IV | Dose tapered over ensuing weeks
244
What are causes of a pale optic disc?
``` Compression of optic nerve Retinal artery occlusion Glaucoma RICP Optic neuritis Inherited optic nerve/retinal disease Toxic optic neuropathy Tobacco/alcohol ```
245
What are most common causes of compression of the optic chiasm? Causing a bitemporal hemianopia - compression of the nasal retina (temporal field)
Pituitary tumour Meningioma Craniopharyngioma
246
What defect do lesions of the optic tract and radiation cause? Usually vascular or neoplastic
Homonymous hemianopia | Loss confined to the right or left hand side of the field in both eyes
247
What are the types of squint?
Congenital/acquired - onset before/after 6 months Concomitant/incomitant Manifest/latent
248
What is the function of the different extraoccular muscles?
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
Define Hyphaema
When blood enters anterior chamber between cornea and iris
250
How does a Hyphaema present?
Decrease/ Loss of vision (may improve as gravity pulls the blood down) Red tinge to eye
251
Name 5 causes of a Hyphaema
``` Intraocular Surgery Blunt trauma Lacerating Trauma Leukaemia Retinoblastoma ```
252
How are Hyphaemas managed?
Small - Outpatient basis, antifibrinolytics, corticosteroids, mitotics, asparin Non resolving - surgical clean out Pain relief - avoid aspirin and NSAIDs due to platelet interaction
253
Name three requirements of the accommodation reflex
Eyes converging Pupil size reducing Lens changing shape and pattern
254
Name six causes of sudden visual loss
``` CRAO Anterior Ischaemic Optic Neuropathy Vitreous Haemorrhage Retinal Vein Occlusion Retinal Detachment Optic Neuritis ```
255
Give 5 causes of Endopthalmitis
``` Trauma, Eye Surgery, VEGF injections, Endogenous seeding, Extension of Corneal infection ```
256
Describe the likely pathogens of Endopthalmitis with each cause
Surgery - Coag neg Staph (epidermis), Trauma - bacillus cereus, Endogenous - S.Aureus,Klebsiella
257
Orbital Cellulitis is generally a clinical diagnosis. What investigations could you do, and what would they show?
FBC - leukocytosis Blood cultures - negative LP (if focal signs) Swabs CT sinus and orbit - extension
258
Orbital Cellulitis is an emergency and requires urgent antibiotics and four hourly monitoring. What are the Abx of choice?
1) Co Amoxiclav If pen allergic - Clindamycin and Metronidazole MRSA - Vancomycin
259
What is the immediate management for Ocular Chemical Injury?
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
If the Chemical Injury of the eye was moderate or severe, how would it be managed?
Dexamethasone 1-2 hourly Vitamin C (topically and orally) Citrate and Tetracyclines
261
Name three associations of Anterior Uveitis and Chronic Anterior Uveitis respectively
Anklyosing Spondylitis, IBD, Reactive Arthritis Sarcoidosis, Syphilis, TB
262
What can be seen on examination of a Keratitic eye?
Oedema White cell infiltration Epithelial defect
263
What is Presbyopia?
Gradual loss of accommodation response due to decline in elasticity, becoming apparent when amplitude is insufficient to carry out near tasks
264
How does Presbyopia present?
Difficulty carrying out near tasks Accommodative lag (from distance to near vice versa) Tiring with continuous close work
265
How is Presbyopia treated?
OTC glasses are normally sufficient If pre-existing refractive error - prescription glasses
266
If Presbyopia happens prematurely, what is the likely cause?
Accommodative Insufficiency (Associated with encephalitis and enclosed head trauma) Inability to maintain binocular enlargment as object becomes closer (aka eye strain)
267
Define Anterior Ischaemic Optic Neuropathy
Loss of vision as a result of damage to optic nerve from ischaemia Involves the 1mm head of optic nerve (AKA disc)
268
How does Arteritic Anterior Ischaemic Optic Neuropathy present?
Rapid onset unilateral visual loss and decreased acuity Chalky white pallor of optic disc Amaurosis fugax? GCA signs?
269
How is Arteritic Ischaemic Optic Neuropathy investigated?
GCA - ESR/CRP, Temporal Artery Biopsy MRI/USS - between Arteritic and non OCT
270
Describe the management options for Arteritic Anterior Ischaemic Optic Neuropathy
IV Methylpred for 3 days (switch to oral and taper) MAB against IL6 (Tocilizumab) Methotrexate
271
Vitreous haemorrhage is one of the most common causes of sudden painless visual loss. Describe the possible aetiologies
Proliferative diabetic retinopathy (fragile vessels) Posterior vitreous detachment Ocular Trauma
272
How does Vitreous Haemorrhage present?
- 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
Name four investigations for Vitreous Haemorrhage
IOP Slit Lamp - Red Cells in anterior vitreous Rule out retinal detachment USS
274
Describe the general management of Vitreous Haemorrhage
Exclude retinal detachment Rest with head elevated and re- evaluate in 3-7 days for source
275
Name four definitive treatment options for Vitreous Haemorrhage
Laser Photocoagulation (for proliferative vasculopathies) Anterior Retinal Cryotherapy Vitrectomy VEGF
276
Diplopia can be monocular or binocular, what is the difference?
Monocular - doesn’t disappear with one eye closed, likely opthalmological aetiology Binocular - with one eye closed it disappears, likely neurological aetiology
277
Describe the anatomical course of CNIII
``` Emerges from midbrain Travels close to PCA Pierces dura near tentorium cerebelli Lateral cavernous sinus Superior orbital fissure ```
278
Name four causes of Oculomotor nerve lesions
Diabetes GCA Raised ICP PCA Aneurysm
279
How do Oculomotor nerve lesions present?
Fixed dilated pupil that doesn’t accommodate Ptosis Unopposed lateral deviation Intortion on looking down Microvascular - pupil sparing
280
How do Oculomotor nerve lesions present (sympathetics involved)?
Pupil will be fixed but not dilated
281
Trochlear Nerve lesions are rare, give three causes
Orbital trauma Diabetes Infarction secondary to hypertension
282
Name 6 causes of Diplopia
``` CNIII lesion CNIV lesion CNVI lesion Orbital Blow Out # Thyroid Eye Disease MG ```
283
How do Trochlear Nerve Lesions present?
Vertical Diplopia Weakness of downward and intortion Compensatory head tilt away from affected side
284
How does a CNVI lesion appear?
Inability to look laterally
285
Give three causes of a CNVI lesion
MS Pontine Cerebrovascular incident Raised ICP (due to long course)
286
Describe the pathophysiology of an Orbital Blow Out Fracture
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
Name five clinical features of Orbital Blow Out Fractures
``` Periorbital bruising Surgical Emphysema Vertical Diplopia (worse on looking up) Endopthalmos Infraorbital Paraesthesia ```
288
What investigations should you do for a suspected Orbital Blow Out?
Plain XRay - Facial, Occipitomental, Submentovertical (droplet sign in maxillary sinus) CT
289
How are Orbital Blow Out Fractures managed?
Don’t blow nose for 10 days Some can be managed with just broad spec abx Surgery
290
The onset of Thyroid Eye Disease is normally within 18 months of diagnosis. Describe the pathophysiology
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
What are the important receptors in Thyroid Eye Disease?
TSH | IGF1
292
Name four risk factors for Thyroid Eye Disease
Current smoker Female Middle Aged Radioiodine therapy
293
Describe the pathophysiology of Myasthenia Gravis
- Receptor sites at NMJ are destroyed - Not enough stimulation to trigger action potential - Increased fatiguability with use (reduced ACh) and improvement with rest
294
Name some signs of Myasthenia Gravis
Ptosis Cogan Lid Twitch (down gaze followed by up gaze, eye saccades and lid overshoots) Incomitant strabismus Raised eyebrows Pupils never involved
295
Name three diagnostic tests for MG
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
Name two laboratory tests for MG
Serum Anti ACh Receptor Titre | Serum Anti Muscle Specific Kinase AB titre
297
What is the main differential for MG?
Lambert Eaton Syndrome Improvement of symptoms with repeated stimulation
298
Describe the management of MG
Med - Steroids, Pyridostigmine, Immunomodulators (if refractory) Surgery - Removal of thymus
299
What is Amaurosis Fugax? | How does Amaurosis Fugax present?
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
Other than carotid pathology, give three causes of Amaurosis Fugax
GCA Retinal Migraine Papilledema
301
How is Amaurosis Fugax investigated?
Inflammatory markers Carotid imaging and cardiac evaluation MRI/MRA
302
How is Amaurosis Fugax managed?
TIA - stroke work up GCA - Emperic steroids and temporal artery biopsy Antiplatelets/Anticoag
303
What is Papilledema?
Optic disc swelling secondary to raised ICP Oedema, continued pressure and optic nerve atrophy
304
Name three investigations you would do to define the underlying cause of Papilledema
BP CT/MRI LP with opening pressure
305
Name three ways Papilloedema can present
Asymptomatic Signs of raised ICP Abducens Palsy
306
The gold standard management for Papilloedema is to treat underlying cause and reduced ICP. How should IIH be managed?
Weight reduction Acetazolamide ?CSF Shunt, Duran Venous Stenting
307
Dry eyes can cause a gritty, foreign body sensation worse at the end of the day. What are some red flags?
Severe eye pain Significant visual loss Photophobia
308
What is the treatment of dry AMD?
Supplementation with Vitamin C, Vitamin E, Zinc, Copper, Lutein and Zeaxanthin
309
What is pan-retinal photocoagulation used for?
Proliferative diabetic retinopathy Sacrificing the peripheral retina to reduce the production of VEGF by the ischaemic retina and preventing neovascularisation
310
What is an important investigation and complication of rubeosis iridis?
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
What are two important sign's in thyroid eye disease?
``` Lid retraction (Dalrymple's sign) Lid lag on down gaze (Von Graefe's sign) ```
312
What is the treatment of endopthalmitis?
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
What can be given for the treatment of allergic conjunctivitis?
mast cell stabilisers such as Sodium Cromoglycate
314
What is a systemic cause of cataracts?
Myotonic dystrophy
315
What is the treatment for gonorrhoeal conjunctivitis in infants?
Ceftriaxone IV, bacitracin ointment and hourly saline lavage