Ophthalmology Flashcards
Give 3 common differentials for a red eye.
Common and treatable in primary care: blepharitis conjunctivitis, dry eye, episcleritis, styes, chalazion
Give 3 differentials for a red unilateral painful eye.
These are all red flags.
Iritis, corneal ulcers and foreign bodies, scleritis, acute angle glaucoma. Unilateral - tumour
What is blepharitis and how does it present?
Blepharitis = inflammation of the eyelid margin
Sx: sore, gritty, itchy eyes, hard to open in morning, bilateral, intermittent. May have lumps - chalazia, styes
May have dry eye syndrome: watery eyes, blurred vision, dry eyes and intolerance of contact lenses.
Associated seborrheic dermatitis: dandruff, oily skin, facial rashes.
Associated rosacea: facial flushing, redness or telangiectasia.
How would you diagnose blepharitis?
Hx - exclude tumour, red flags are unilateral, painful. Localised lash loss could be sebacious gland carcinoma - ask if unsure.
Ex: mild conjunctival redness, loss of eyelashes, in-growing eyelashes (scraping eyelid),
seborrheic –> lashes stuck together, greasy appearance of anterior lid margin
staphylococcal –> collarettes (crusting on base of eyelashes), hard scales
Posterior –> meibomian gland orifices covered with small oil globules/foam. lid lumps (chalazia and styes)
How is blepharitis managed?
Not curable but manageable. Lid hygiene - clean using sterilised water and cotton wool
Warm compress
Lubricating eye drops eg polyvinyl alcohol
Give 3 differential diagnosis for acute visual loss.
Think inflammation, vascular occlusion, haemorrhage.
retinal artery and vein occlusions, giant cell arteritis, optic neuritis, retinal detachment, vitreous haemorrhage, visual field loss due to stroke and intracranial tumours
Give 3 differentials for gradual visual loss.
Think degenerative, neuropathy, vasculopathy.
refractive error, cataract, macular degeneration, open angle glaucoma
What is a cataract?
Cataracts are where the lens in the eye becomes cloudy and opaque. This reduces visual acuity by reducing the light that enters the eye
How does central retinal artery occlusion present? What would you see on fundoscopy?
Sudden painless loss of vision like a curtain coming down.
Relative afferent pupillary defect
Fundoscopy will show a pale retina (due to lack of perfusion) with cherry-red spot (macula)
How is central retinal artery occlusion managed?
Refer to ophthal
If GCA is the cause treat that - ESR, temporal artery biopsy, prednisolone 60mg.
No evidence for intervention as artery is too small - vision will be lost.
Manage risk factors for atherosclerosis
Can try ocular massage, inhaling carbogen to dilate the artery, or sublingual isosorbide dinitrate
How does central retinal vein occlusion present? What would you see on fundoscopy?
Sudden painless loss of vision.
Pooling of blood –> macular and optic disc oedema, retinal flame and blot haemorrhages, VEGF and neovascularisation.
How is central retinal vein occlusion managed?
Refer to ophthal for treatment of macular oedema, prevent neovascularisation and glaucoma. This is done with laser photocoagulation, intravitreal steroids, and/or anti-VEGF eg ranibizumab.
Manage risk factors for atherosclerosis, check for associated conditions - ESR (SLE), FBC (leukaemia), BP (htn), glucose (diabetes)
How does diabetic retinopathy present and what would you see on fundoscopy?
Asymptomatic (found on screening), can cause haemorrhage.
Fundoscopy:
Cotton wool spots = nerve fibre damage
Microaneurysms = bulges in blood vessel walls
Hard exudates = lipid deposits
Blot haemorrhages
Neovascularisation
IntraRetinal Microvascular Abnormalities - dilated tortuous retinal capillaries/AV fistula
How would an optic melanoma present and what would you see on fundoscopy?
Asymptomatic. no pain or field defect.
Large grey raised blotch on fundoscopy.
Mx - often not treated if not causing problems.
How does retinitis pigmentosa present? What would you see on fundoscopy?
Night blindness, starting in childhood (hereditary), loss of peripheral vision before central vision (may have good acuity).
Fundoscopy shows ‘bone-spicule’ pigmentation around the mid-peripheral area, pale optic disc.
What is the pathophysiology of retinitis pigmentosa?
Congenital inherited condition involving degeneration of the rods and cones in the retina. More degeneration of rods than cones –> night blindness.
Asso syndromes eg:
Usher’s syndrome (+hearing loss),
Bassen-Kornzweig syndrome (+neurological symptoms)
Refsum’s disease (+neuro + hearing + skin problems)
What is glaucoma?
Optic nerve damage caused by significant rise in intraocular pressure, caused by blockage in aqueous humour.
Open angle = gradual increase in resistance through the trabecular meshwork, so aqueous humour cannot exit the eye.
How does glaucoma present?
Asymptomatic - found on routine eye check
Peripheral visual loss (tunnel vision)
Pain, headache, blurred vision, halos around lights
How is glaucoma diagnosed?
Visual fields
Tonometry:
Non-contact - puff of air. Less accurate
Goldmann applanation tonometry = gold standard, actually makes contact with cornea, accurate IOP
Fundoscopy - cupping of optic disc >0.5 cup:disc ratio
Give 3 risk factors for glaucoma other than older age.
FHx
Black ethnicity
Shortsightedness (myopia)
What is the management of open-angle glaucoma?
Reduce IOP
Treat if IOP >24mmHg, follow up
First line: Prostaglandin analogue eye drops eg latanoprost. These increase uveoscleral outflow. SEs - eyelash growth, eyelid pigmentation and iris pigmentation.
Beta blocker eg timolol - reduce production of aquous humour
Carbonic anhydrase inhibitors eg acetazolamide - reduce production of aquous humour
Sympathomimetics eg brimonidine - reduce production of aqueous fluid and increase uveoscleral outflow.
Trabeculectomy
What is acute angle closure glaucoma?
Iris bulges forward and seals off trabecular meshwork from the anterior chamber, preventing aqeuous humour from being able to drain away. Optic nerve damage, ophthalmology emergency - sight threatening.
Give 4 risk factors for acute angle closure glaucoma.
Increasing age
FHx
Females are affected around 4 times more often than males
Chinese and East Asian ethnic origin. Unlike open-angle glaucoma, it is rare in people of black ethnic origin.
Shallow anterior chamber
Give 3 medications that can precipitate acute angle-closure glaucoma.
Adrenergic medications such as noradrenalin
Anticholinergic medications such as oxybutynin and solifenacin
Tricyclic antidepressants such as amitriptyline, which have anticholinergic effects
How does acute angle closure glaucoma present?
Unwell, acute onset Severely painful red eye Blurred vision Halos around lights Associated headache, nausea and vomiting Red, teary eye Unilateral fixed dilated pupil Firm eyeball Hazy cornea Reduced visual acuity
What is the management of acute angle closure glaucome?
Same day referral to ophthalmology for laser iridotomy.
While waiting:
Lie on back without a PILOw
PILOcarpine eye drops (2% blue, 4% brown). This is a muscarinic agonist –> miotic =constricts pupil, and causes ciliary muscle contraction.
Acetazolamide 500mg PO (carbonic anhydrase inhibitor)
Analgesia, antiemetic if required
Hyperosmotic agents eg mannitol
Timolol to reduce aquous humour
Sympathomimetic eg Brimonidine
What is ARMD? What are the types?
Age related macular degeneration: most common cause of blindness in UK.
10% wet, worse prognosis, treatable
90% dry, untreatable
What are drusen?
Yellow deposits of proteins and lipids between the retinal pigment epithelium and Bruch’s membrane in the macula.
Can be normal, but larger and more drusen indicated MD (wet and dry)
Give 3 similarities and 3 differences between wet and dry AMD.
Both: Worsening central visual field loss, reduced visual acuity, crooked or wavy lines. Drusen, atrophy of retinal pigment epithelium, degeneration of the photoreceptors.
Wet: VEGF –> Neovascularisation from choroid layer of the macula into the retina, causing oedema and more rapid visual loss, may have bilateral disease, can treat with anti-VEGF eg ranibizumab
Dry: Gradual, no treatment - control RFs
Give 4 RFs for ARMD.
Age, smoking, white or Chinese ethnic origin, FHx, CVD
How is ARMD diagnosed?
Reduced acuity using a Snellen chart
Scotoma (a central patch of vision loss)
Amsler grid test can be used to assess the distortion of straight lines
Fundoscopy. Drusen are the key finding.Slit-lamp biomicroscopic fundus examination by a specialist can be used to diagnose AMD.
Optical coherence tomography is a technique used to gain a cross-sectional view of the layers of the retina. It can be used to diagnose wet AMD.
Fluorescein angiography involves giving a fluorescein contrast and photographing the retina to look in detail at the blood supply to the retina. It is useful to show up any oedema and neovascularisation. It is used second line to diagnose wet AMD if optical coherence tomography does not exclude wet AMD.
What is the management of ARMD?
Refer to ophtho Dry: Avoid smoking Control blood pressure Vitamin supplementation has some evidence in slowing progression
Wet:
Anti-VEGF eg ranibizumab, bevacizumab and pegaptanib to slow the development of new vessels. They are injected directly into the vitreous chamber of the eye once a month. They slow and even reverse the progression of the disease. They typically need to be started within 3 months to be beneficial.
How is diabetic retinopathy classified?
Proliferative =neovascularisation, vitreous haemorrage
Non-proliferative =
Mild - microaneurysms
Moderate - + blot haemorrhages, hard exudates, cotton wool spots and venous beading
Severe: + microaneurysms in 4 quadrants, venous beading in 2 quadrants, IMRA
Diabetic maculopathy: oedema, ischemia
Give 4 complications of diabetic retinopathy.
Retinal detachment
Vitreous haemorrhage (bleeding in to the vitreous humour)
Rebeosis iridis (new blood vessel formation in the iris)
Optic neuropathy
Cataracts
What is the management of diabetic retinopathy?
Laser photocoagulation
Anti-VEGF medications such as ranibizumab and bevacizumab
Vitreoretinal surgery (keyhole surgery on the eye) may be required in severe disease
Give 5 signs of hypertensive retinopathy.
Silver wiring or copper wiring: arterial wall sclerosis causing increased reflection of the light.
Arteriovenous nipping: the arterioles cause compression of the veins where they cross due to arteriosclerosis
Cotton wool spots: ischaemia and infarction in the retina causing damage to nerve fibres.
Hard exudates: damaged vessels leaking lipids into the retina.
Retinal haemorrhages: damaged vessels rupturing and releasing blood into the retina.
Papilloedema: ischaemia to the optic nerve resulting in optic nerve swelling (oedema) and blurring of the disc margins.
How is hypertensive retinopathy classified?
Keith-Wagener Classification
Stage 1: Mild narrowing of the arterioles
Stage 2: Focal constriction of blood vessels and AV nicking
Stage 3: Cotton-wool patches, exudates and haemorrhages
Stage 4: Papilloedema
Give 4 risk factors for cataracts other than age.
Smoking Alcohol Diabetes Steroids Hypocalcaemia
How do cataracts present?
Asymmetrical as compensate with unaffected eye
Slow reduction in vision, progressive blurring, change of colour vision (sepia tinge), starbursts around lights
Loss of red reflex
What is the management of cataracts?
If the symptoms are manageable then no intervention may be necessary.
Cataract surgery - drilling and breaking the lens into pieces, removing the pieces and then implanting an artificial lens into the eye. This is usually done as a day case under local anaesthetic.
Cataracts can prevent the detection of other pathology such as macular degeneration or diabetic retinopathy. Once cataract surgery is performed these conditions may be detected. Therefore, the surgery may treat the cataract but they may still have poor visual acuity due to other causes.
What complication of cataract surgery do you need to warn patients about?
Endophthalmitis - rare. Inflammation of the inner contents of the eye, usually caused by infection. It can be treated with intravitreal antibiotics injected into the eye. This can lead to loss of vision and loss of the eye itself.
What causes miosis?
Circular muscles in iris cause pupil constrIction when stimulated by PNS fibres traveling along CN III via acetylcholine.
Causes:
Horners syndrome (ptosis, miosis, anhidrosis)
Cluster headaches
Argyll-Robertson pupil (accommodation reflex but no light reflex, neurosyphilis)
Opiates
Nicotine
Pilocarpine
What causes mydriasis?
Dilator muscles of pupil cause pupil Dilation when stimulated by SNS fibres via adrenalin.
Causes:
Third nerve palsy (+ptosis, down and out eye position)
Holmes-Adie syndrome (damage to post-ganglionic parasympathetic fibres –> unopposed action of SNS, + absent lower limb reflexes)
Raised intracranial pressure
Congenital
Trauma
Stimulants such as cocaine
Anticholinergics
What causes abnormal pupil shape?
Trauma to the sphincter muscles in the iris can cause an irregular pupil. This could be caused by cataract surgery and other eye operations.
Anterior uveitis –> posterior synechiae = adhesions that cause irregularly shaped pupil
Acute angle closure glaucoma can cause ischaemic damage to the muscles of the iris causing an abnormal pupil shape, usually a vertical oval.
Rubeosis iridis (neovascularisation in the iris) can distort the shape of the iris and pupil. This is usually associated with poorly controlled diabetes and diabetic retinopathy.
Coloboma is a congenital malformation in the eye. This can cause a hole in the iris causing an irregular pupil shape.
Tadpole pupil is where there is spasm in a segment of the iris causing a misshapen pupil. This is usually temporary and associated with migraines.
What causes third nerve palsy?
Idiopathic
‘Medical’ = Microvascular eg diabetes, htn, ischemia –> sparing of parasympathetic fibres, so pupil is normal but you get ptosis and ophthalmoplegia
‘Surgical’ = PNS fibres compressed by tumour, trauma, cavernous sinus thrombosis (compression at the cavernous sinus), posterior communicating artery aneurysm, raised ICP
What causes Horner’s syndrome?
The sympathetic innervation enters the spinal cord from the brain, enter sympathetic ganglia, and exit through neck alongside internal carotid artery to the face.
Central lesions (sentral): S – Stroke S – Multiple Sclerosis S – Swelling (tumours) S – Syringomyelia (cyst in the spinal cord)
Pre-ganglionic lesions (torso): T – Tumour (Pancoast’s tumour) T – Trauma T – Thyroidectomy T – Top rib (a cervical rib growing above the first rib above the clavicle)
Post-ganglionic lesion (cervical): C – Carotid aneurysm C – Carotid artery dissection C – Cavernous sinus thrombosis C – Cluster headache
Congenital –> heterochromia
How is Horner’s syndrome diagnosed?
Cocaine eye drops stop noradrenalin re-uptake at the neuromuscular junction. This causes a normal eye to dilate because there is more noradrenalin stimulating the dilator muscles of the iris. In Horner syndrome, the nerves are not releasing noradrenalin to start with so blocking re-uptake does not make a difference and there is no reaction of the pupil.
Alternatively, a low concentration adrenalin eye drop (0.1%) won’t dilate a normal pupil but will dilate a Horner syndrome pupil.
What is a stye?
Hordeolum externum = infection of glands of Zeis (sweat glands) or glands of Moll (sebacious), base of eyelashes. Tender red lump on eyelid
Hordeolum internum = Meibomian gland infection - deeper, more painful
How is stye treated?
Hot compress
Analgesia
Chloramphenicol (abx) eye drops if persistent or with conjuctivities
What is a chalazion?
Blocked Meibomian gland/cyst –> non-tender (non-infective) eyelid swelling.
How is chalazion treated?
Hot compress + analgesia
Chloramphenicol drops if acutely inflamed
What is entropion and how do you manage it?
Eyelid turning inwards, lashes may brush against eyeball resulting in pain, corneal damage and ulceration.
Tape down eyelid, lubricating eye drops
Surgical intervention
Urgent if risk to sight
What is ectropion and how is it managed?
Eyelid turns outwards, inner aspect exposed –> risk of exposure keratopathy.
Lubricating eye drops
Refer if risk to sight
Surgery may be needed
What is Trichiasis and how is it managed?
Inward growth of eyelashes, causes pain, corneal damage and ulceration. Management = epilation - remove eyelash.
What is the difference between peri-orbital and orbital cellulitis?
Involvement of tissues behind the orbital septum in orbital cellulitis. Pain on eye movement, reduced eye movement and vision, abnormal pupil reactions and proptosis. Admit and IV abx, surgical drainage if abscess. Always consider CT in facial/peri-orbital cellulitis.
What is conjunctivitis and how does it present?
Inflamed conjunctiva (thin covering inside of eyelids and sclera). Bacterial, Viral or Allergic Bilateral red, bloodshot eyes, itchy, gritty, discharge. - purulent in bacterial, clear in viral.
How is conjunctivitis managed?
Exclude pain or visual loss (except for discharge causing blurryness)
Self-resolves 1-2 weeks
Bacterial very contagious - avoid sharing towels, wash hands, don’t use contact lenses
Clean eyes with cooled boiled water and cotton wool
admit neonates for gonococcal conjunctivitis - sight-threatening
Allergic –> antihistamines, avoid allergens, mast-cell stabilisers for chronic seasonal sx
What is anterior uveitis and how does it present?
Inflammation of anterior part of uvea (iris, ciliary body, choroid).
Can be acute or chronic.
Unilateral dull, aching, painful red eye
Ciliary flush (a ring of red spreading from the cornea outwards)
Reduced visual acuity
Floaters and flashes
Sphincter muscle contraction causing miosis (constricted pupil)
Photophobia due to ciliary muscle spasm
Pain on movement
Excessive tear production (lacrimation)
Abnormally shaped pupil due to posterior synechiae (adhesions) pulling the iris into abnormal shapes
A hypopyon is a collection of white blood cells in the anterior chamber, seen as a yellowish fluid collection settled in front of the lower iris, with a fluid level
Acute asso with HLA B27 - Ank spond, IBD, RA.
Give 4 associations with chronic anterior uveitis.
Sarcoidosis, syphilis, lyme disease, TB, herpes
What is the management of anterior uveitis?
Acute --> same day referral to ophthalmology Slit lamp exam Steroids Antimuscarinic cyloplegic-mydriatic medications: Cycloplegic - cyclopentolate Mydriatic - atropine Immunosuppressants Laser therapy, cryotherapy or vitrectomy
What is episcleritis? How does it present?
Benign, self limiting inflammation of episclera (beneath conjunctiva). Common in young and middle aged adults, asso inflammatory disorders eg RA, IBD
Acute unilateral segmental redness, foreign body sensation, eye watering, may have mild pain
What is scleritis? How does it present?
Inflammation of sclera.
Unilateral or bilateral acutely painful red eye, pain on eye movements, photophobia, tenderness
50% have associated systemic condition: RA, IBD, SLE, sarcoidosis, GPA
What is the main complication of scleritis?
Necrotising scleritis - painless visual loss, can lead to scleral perforation.
What is the management of scleritis?
Same day referral
Treat/consider dx underlying condition
NSAIDs, steroids, immunosuppression as needed
What causes corneal abrasions?
Contact lenses - consider pseudomonas Foreign bodies Fingernails Eyelashes Entropion (inward turning eyelid) Chemicals
How are corneal abrasions diagnosed?
Fluoroscein stain
Slit lamp if more significant
exclude herpes keratitis
How are corneal abrasions managed?
Same day referral if sight threatening.
Remove foreign body in primary care if appropriate (mild, uncomplicated, sufficient experience)
Analgesia, lubricating eye drops, chloramphenicol, 24h follow up
Cyclopentolate (mydriatic eye drops) may relieve photophobic sx
Chemical - irrigation, urgent referral
Uncomplicated abrasions heal 2-3 days
What is keratitis?
Inflammation of the cornea.
usually viral infection with herpes simplex
Bacterial infection with pseudomonas or staphylococcus
Fungal infection with candida or aspergillus
Contact lens acute red eye (CLARE)
Exposure keratitis is caused by inadequate eyelid coverage (e.g. eyelid ectropion)
What is the difference between herpes keratitis and stromal keratitis?
Herpes keratitis usually only affects epithelial layer of cornea. Stromal involvement is associated with stromal necrosis, vascularisation and scarring –> risk of corneal blindness.
How is keratitis diagnosed?
Staining with fluorescein will show a dendritic corneal ulcer. Dendritic describes the appearance of branching and spreading of the ulcer.
Slit-lamp examination is required to find and diagnose keratitis.
Corneal swabs or scrapings can be used to isolate the virus using a viral culture or PCR.
How is herpes keratitis managed?
Same day referral for:
Aciclovir (topical or oral)
Ganciclovir eye gel
Topical steroids may be used alongside antivirals to treat stromal keratitis
What is subconjunctival haemorrhage?
Common rupture of small blood vessel in conjunctiva, releasing blood between the sclera and conjunctiva, which looks like a bright red patch, no pain or visual loss.
Give 5 causes of subconjunctival haemorrhage.
Usually idiopathic but consider:
Hypertension
Bleeding disorders
whooping cough
medications (warfarin, NOACs, antiplatelets)
Non-accidental injury
Also triggered by straining - coughing fit, heavy lifting
What is the management of subconjunctival haemorrhage?
Self-resolve in 2 weeks. If foreign body sensation can use lubricating eye drops.
What is posterior vitreous detachment?
Separation of vitreous gel from retina. Common in older people, painless, +/- visual changes, floaters and flashes. Not harmful but may predispose to retinal tear/detachment so refer to ophthalmology to assess retina.
What is retinal detachment? How does it present?
Retina separates from choroid, usually due to a retinal tear which allows vitreous fluid to get under the retina and fill the space between the retina and the choroid.
Presents with painless peripheral visual loss, like a shadow coming across the vision, blurring, distortion, flashes and floaters
What is the management for retinal detachment?
Same day referral
Fix the tear eg laser therapy
Reattach the retina eg pneumatic retinopexy or vitrectomy, reducing traction.
What is the management for retinitis pigmentosa?
General:
Refer routinely to ophtho
Genetic counselling
Vision aids
Sunglasses
Driving limitations and informing the DVLA
Regular follow up to assess vision and check for other potentially reversible conditions that may worsen the vision such as cataracts
Limited evidence: Vitamin and antioxidant supplements Oral acetazolamide Topical dorzolamide Steroid injections Anti-VEGF injections
Future - Gene therapy?
