Ophthalmology Flashcards
What type of drug is acetazolamide and how does it work?
- carbonic anhydrase inhibitor
- reduces aqueous humour production
What type of drug is brimonidine and how does it work?
- selective alpha-2 adrenoceptor agonist
- works by reducing aqueous humour formation and increasing uveoscleral outflow.
What type of drug is cyclopentolate and how does it work?
- antimuscarinic
- used in refraction and dilates the pupil by paralysing the ciliary muscle
What type of drug is latanoprost and how does it work?
- prostaglandin analogue
- works by increasing uveoscleral outflow and thus reduces intraocular pressure
What type of drug is pilocarpine and how does it work?
- a miotic
- acts by opening the drainage channels in the trabecular meshwork.
Amiodarone can cause what visual side effect?
- most patients on amiodarone will develop corneal micro-deposits
- this is reversible on withdrawal of treatment
- they rarely interfere with vision but can cause drivers to be dazzled by headlights glare at night.
What does this image show? What are the symptoms? How is it treated?
- pterygium
- foreign body sensation over several months
- can bleed on rubbing eye
- heaped up hyperaemic area of the nasal side of conjunctiva
- assoc with excessive exposure to wind, sunlight, sand
- 2x more common in men
- Benign growth-only need surgical removal if covers pupil, obstructs vision or acute symptoms.
- can recur after surgery
- can give artificial tears to help
What does this fundoscopy image show? What are the presenting symptoms? What is the management?
- central retinal vein occlusion
- common, most are aged >65
- thrombus formation most common cause
- Occlusion of the vein results in retinal hypoxia, and the resultant endothelial cell damage leads to extravasation of blood.
- unilateral painless loss of vision, often starts on waking
- less abrupt than CRAO
- retinal veins tortuous, engorged, widespread dot-blot and flame haemorrhages, some disc swelling (margherita pizza)
- immediate Opth referral <24hrs
- complications - neovascularisation, secondary glaucoma
How is a person formally certified as sight impaired, or severely sight impaired? What benefits are available to them?
- **certificate of vision impairment (CVI) **must be completed by a **consultant ophthalmologist. **
- CVI formally certifies someone as sight impaired (partially sighted)or as severely sight impaired (blind).
- Assessment of visual acuity and visual fields
- CVI shared with pt consent - to local authority.
- After registration social services should contact pt to carry out needs assessment.
- Benefits:
- free eye examinations
- discounts on bus/rail
- reduction in TV licence fee
- concessions
- reductions in council tax
- may be able to claim welfare benefits.
- Blind Person’s Allowance is added to the tax-free Personal Allowance (must be registered with LA)
Note: loss of sight in one eye does not count for registration unless the individual has poor sight in their other eye
Squint (intermittent deviation of the eyes) is common in neonates (no concern). At what age should normal binocular coordination develop? Who should you refer a child to if they have persistent strabismus after this age?
- three months
- refer to opthalmologist
What eyelid condition does this image show? What are the symptoms? How is it treated?
- chalazion
- a cyst - focus of inflammation- in the eyelid due to blocked meibomian gland. Not infectious.
- subacute - gradually enlarging, non tender, usually painless
- can become inflamed
- inside the lid, not on the margin (different to stye). Styes more painful. Styes more acute onset and shorter 7-10 day duration.
- chalazia chronic
- Mx: BD warm compress, lid massage, clean lid margin. Takes several weeks. If gets larger/not resolving can refer - for incision under LA.
What does the image show? How does it commonly present? How is it treated?
- sub-conjunctival haemorrhage.
- painless red eye, flat bright red patch (bleeding under conjunctiva from conjunctival vessels). Normal VA.
- spontaneous - after cough/sneeze/vomiting. Consider HTN. Anticoags.
- If traumatic ?basal skull fracture, intracranial bleed, orbital roof fracture (esp if cannot see posterior margin)
- If recurrent/bodily bruising - check FBC and clotting.
- Take 10-14d to resolve.
What is a Relative afferent pupillary defect (RAPD)?
a.k.a Marcus Gunn Pupil
- Light shone into the eyes alternately for 2–3 seconds with approximately one second in between.
- If afferent impulses on the left side are delayed (e.g. due to optic neuritis) as light is swung into the affected eye the consensual dilation from the (normal) right eye is more powerful than the light reflex in the affected eye.
- Therefore, paroxysmal dilatation is seen on the swinging light test in the affected (i.e., the left) eye.
- It demonstrates an incomplete optic nerve lesion.
What can cause an RAPD?
- any UNILATERAL
optic nerve pathology before the chiasm and some severe retinal diseases (retina is extension of optic.N). - optic nerve: optic neuritis (e.g. MS), optic nerve compression (e.g. glioma, meningioma), ischaemic optic neuropathy, trauma to optic nerve, advanced unilateral glaucoma.
- retinal: large retinal detachment, CRVO, CRAO.
What is first line management for blepharitis?
lid hygiene (including hot compresses with lid massage, lid washing and artificial tears)
Which patients are more at risk of acute angle closure glaucoma?
- hypermetropia (long-sightedness) - as have a shallow anterior chamber.
- age >60
- females (3x more common than in men)
- family Hx
- asian ethnicity
- topical mydriatics e.g timolol, alpha adrenergic agonists
What visual acuity threshold qualifies a patient to be registered as severely sight impaired (formerly blind)?
- a visual acuity less than 3/60.
- may satisfy criteria for severely sight impaired with a visual acuity greater than 3/60 if there are contracted visual fields.
What are the causes of acute red painful eye?
- acute angle closure glaucoma
- acute anterior uveitis (can be bilateral)
- scleritis
- keratitis
- endopthalmitis
- trauma
In a red eye - significant pain is suggestive of serious pathology. Whereas no pain or mild pain- self-limiting.
Headache if unilateral & ipsilateral to the red eye - suggests significant pressure or inflammation.
What does this image show? What are the presenting symptoms? How is it treated?
- Acute anterior uveitis = inflammation of iris
(iritis) +/- the ciliary body (iridocyclitis). - acute painful red eye (may be bilateral)
- pain worse on trying to read (accomodating)
- onset in hours-days
- blurred vision - reduced visual acuity
- photophobia
- headache common
- history of inflammatory condition, young person.
- pupil abnormally shaped - usually small and non-dilating.
- ciliary injection
- cells in anterior chamber on slit lamp
- hypopyon if severe.
Refer opth urgently <24hrs.
What are the red flag clinical signs on examination in a red eye?
- non-reactive pupil - AACG, anterior uveitis
- proptosis - periorbital swelling due to cellulitis
- unilateral periorbital rash - opthalmic shingles. Hutchinson’s sign - vesicles on tip/lateral nose, with ocular involvement.
- corneal opacity - discrete lesion -infection, or clouding - oedema/severe inflammation
- eyeball tenderness on palpation - intense tenderness- scleritis (mild in episcleritis). Firm- AACG.
- systemic signs of infection
What features in the history make bacterial conjunctivitis likely? What is the management?
- redness of conjunctiva
- muco-purulent discharge
- morning matting of the eyes
- self limiting, self care.
- delay chloamphenicol ABX for 72 hrs -may not be needed
- avoid chloramphenicol if prenant/ breasfeeding, hx blood dyscrasia.
- refer if ongoing symptoms after Rx - esp contact lens wearers - acanthomoeba keratitis is Ddx.
What does the image show? What are the presenting symptoms? How is it managed?
- acute angle closure glaucoma
*severe pain - rapid onset - headache
- blurred vision- reduced VA (rapid blindness)
- Nausea and vomiting common
- see coloured haloes around lights
- comes on when pupil in mid-dialation e.g. dim light, after GA
- Exam: unwell, red eye, Ciliary injection (ring of redness spreading out from the cornea), hazy cornea - reduced red reflex. Non reactive mid-dilated pupil.
- tender, hard globe
- Mx: immediate emergency referral. Lie supine, topical timolol, topical pilocarpine, IV acetazolamide, IV mannitol. IV analgesia & antiemetics. Definitive - laser iridotomy (unaffected eye also treated)
What does the image show? What are the presenting symptoms? How is it managed?
- scleritis = scleral inflammation
- women>men
- assoc systemic disease- RA,SLE
- Acute painful red eye
- severe boring eye pain and tearing
- pain can radiate to forehead, brow, jaw
- gradual onset
- normal or reduced VA (progressive impairment)
- progressive photophobia
- pupil appears normal.
- deep conjunctival injection involving multiple quadrants - bluish tinge
- very tender globe
Mx: refer opth <24h
What does this image show? What are the symptoms? How is it managed?
- episcleritis = inflammation of eipscleral layer
- benign, self-limiting (7-10d)
- most idiopathic, some due to systemic inflammatory conditions
- young adults
- acute onset unilateral red eye
- injection confined to single quadrant
- mild pain
- no change in VA, no pupil changes, no significant tearing
- episcleral vessels can be moved with cotton bud
refer if increased pain, or not resolving after 7 days - need to exlude scleritis.
What are the symptoms of viral conjunctivitis? How is it treated?
- adenovirus 90% - highly infectious
- acute onset bilateral red eyes
- burning/gritty/FB sensation
- watery discharge
- normal VA
- normal pupils
- Hx URTI/contact with others
- pre-auricular lymphadenopathy
- self resolves <14d
- cool compress, artificial tears
- stop contact lenses
- strict hygeine
What is the treatment for allergic conjunctivitis?
- watery itchy eyes with mild redness, seasonal
- anithistamines, cool compress, topical sodium cromoglicate eye drops
What are the symptoms of keratitis? How is it managed?
- corneal inflammation
- contact lenses - risk factor
- after a corneal abrasion -> bacterial keratitis
- can be viral - herpetic
- can progress to endopthalmitis -blindness
- acute painful red eye
- photophobia
- foreign body sensation
- reduced VA/normal
- corneal defect on staining
Mx: urgent referral <24h
Endopthalmitis - emergency immediate referral. (red eye, decreasing VA, recent surgery/trauma/immune compromise, chemosis of conjunctiva, hypopyon, hazy anterior chamber, lid oedema)
What are the stages of diabetic retinopathy?
What condition does this retinal photograph show? What are the signs on fundoscopy?
- Background diabetic retinopathy
- microaneurysms are localised outpouchings of capillaries that leak plasma constituents into the retina.
- They may be clinically indistinguishable from small dot and blot haemorrhages
- dot and blot haemorrhages: arise from bleeding capillaries in the middle layers of the retina.
What condition does this retinal photograph show? What are the signs on fundoscopy?
- pre-proliferative diabetic retinopathy
- presence of retinal ischaemia represents progression from BDR to pre-proliferative stage
- Cotton wool spots: small, fluffy, whitish superficial lesions. Accumulations of dead nerve cells from ischaemic damage.
What condition does the retinal photo show? What are the signs on fundoscopy?
- proliferative diabetic retinopathy
- Insufficient retinal perfusion -> production of vascular endothelial growth factor (VEGF) -> development of new vessels on the retina (neovascularisation).
- new vessels may be at the disc, termed “new vessels at the disc” (NVD), or over the other areas of the retina “new vessels elsewhere” (NVE).
- new vessels fragile, cause haemorrhage - can cause painless loss of vision
What are the additional fundoscopy findings in advanced diabetic retinopathy?
- recurrent vitreous haemorrhage from bleeding areas of neovascularisation
- tractional retinal detachments neovascularisation grow into the vitreous and form fibrous bands suspending the retina
- Rubeosis as neovascularisation occurs at the iris and drainage angle resulting in increased intraocular pressure and progressive glaucoma
What condition does this image show? What are the fundoscopic features?
- diabetic maculopathy = presence of exudates and/or macular oedema at the macula.
- Hard exudates are waxy yellow lesions (lipid deposits from leaky capillaries) with distinct margins arranged in clumps or rings, often surrounding leaking microaneurysms
- called “hard exudates” to distinguish them from “soft exudates”, an older term for cotton wool spots
What are the stages of hypertensive retinopathy?
Grade 1 disease: subtle, with generalised arteriolar narrowing ‘copper wiring’
* Grade 2 disease: development of areas of focal narrowing - compression of venules at sites of arteriovenous crossing ‘AV nipping’
* Grade 3 disease: development of retinal flame haemorrhages, hard exudates and cotton wool spots.
* Grade 4: malignant HTN can present with grade 4 disease - all features of grade 3 plus papilloedema.
What condition does the photo show? What are the fundoscopic findings?
- malignant HTN
- extensive haemorrhages, cotton wool spots, optic disc swelling and a ring of exudates around the macula (macular star).
What is glaucoma? How is IOP maintained and controlled? What is the flow of aqueous humour?
= a progressive optic neuropathy (damage of the optic nerve head) that is associated with visual field loss and usually raised intraocular pressure (IOP).
Leading irreversible cause of sight loss globally. (cataract most common but reversible)
Aqueous humour maintains the IOP - balance between rate of production and drainage. Measured by tonometry. Pressures 11 - 21 mmHg normal.
Produced by ciliary body -> flows up though pupil, then out through trabecular meshwork. Some drained via alternative uveoscleral route - fluid absorbed into root of iris & ciliary muscle.
Autonomic control of IOP:
alpha-receptors- reduce IOP by reducing aqueous production, and increasing uveoscleral outflow
beta receptors - increase IOP by increasing aqueous production.
Which is the most common type of glaucoma? What is the epidemiology? What are the clinical features? What are the features on fundoscopy?
- Primary open angle glaucoma (>70%)
- no underlying cause
- adult onset, increases with age
- affects both genders equally
- usually bilateral
- IOP raised (>21)
- flow reduced through trabecular meshwork - chronic degenerative obstruction.
- Painless visual loss
- initial peripheral visual loss- gradually affects central vision
- routine eye check picks up raised IOP and reduced visual fields ‘arcuate scotoma’
- optic disc examination shows increased cup:disc ratio. Due to the irreversible loss of nerve fibres (pink neuro-retinal rim). Cup has no nerve fibres.
- OCT shows exact C:D
What is the management for primary (chronic) open angle glaucoma? How do the treatments work?
- education - lifelong treatment, no symptoms in early stages but irreversible vision loss, need to take drops daily to delay progression. Family members may wish to get tested. Most patients on treatment will have a good QoL and will not go blind.
- medical Mx: if IOP >24mmHg and suspected COAG
- Prostaglandin analogues first line e.g latanoprost. (stronger than Bblockers, less ADRs). Increase uveoscleral outflow. CI: uveitis, pregnant, breastfeeding
- Bblockers e.g. timolol. **Reduce aqueous secretion **by inhibiting B2 receptors in ciliary body. CI: bradycardia, asthma, heart block
- 3.** carbonic anhydrase inhibitors**. e.g brinzolamide (topical), acetazolamide (systemic). Reduce aqueous secretion by ciliary body. CI: renal imairment, breast feeding, severe hepatic impairment.
- Sympathomimetics - alpha-2-receptor agonists e.g brimonidine.** reduce aqueous secretion** by stimulating alpha receptors in ciliary body & increase outflow through trabecular meshwork. CI: angle closure (causes mydriasis).
- **Miotics **- parasympathomimetics e.g. pilocarpine. Cause ciliary muscle contraction - helps **open drainage channels in trabecular meshwork **to increase outflow. CI: uveitis. Poorly tolerated side effects, mainly for Acute Angle Closure.
- regular review in secondary care.
- Laser/surgery considered after 2 different medical agents.
- pt MUST inform DVLA if bilateral glaucoma
What sign does this image show? What can cause this?
- papilloedema or optic disc swelling.
- Papilloedema = optic disc swelling secondary to raised intracranial pressure.
- “Optic disc swelling”=any cause of a swollen optic disc.
- Causes of optic disc swelling: intracranial space-occupying lesions, optic neuritis (e.g. multiple sclerosis), malignant hypertension and uveitis (e.g. tuberculosis, sarcoidosis).
- Optic disc margins appear blurred and small haemorrhages may be noted.
What sign does the image show?
- optic nerve atrophy
- death of nerve fibres within the optic nerve.
- results in a pale optic disc instead of the usual pink appearance.
- Primary optic nerve atrophy is caused by inflammation (optic neuritis), glaucoma or general retinal ischaemia
- Secondary optic nerve atrophy is caused by longstanding papilloedema.
- requires neuroimaging to rule out life-threatening intracranial causes.
What condition does this image show? How does it present? What are the signs on examination?
- Central retinal artery occlusion
*sudden (instantaneous) painless, profound loss of vision. - most frequently caused by emboli obstructing the retinal artery (e.g. stroke). Occasionally caused by vasculitis (e.g. giant cell arteritis).
- Classical appearance is of a “cherry-red spot”. This occurs due to the intact reflex of the fovea standing out against a pale, ischaemic retina.
- marked RAPD
- Immediate referral (optimal treatment within 100mins) - massage, meds
- Rule out GCA (though GCA usually causes ischaemic optic neuropathy) - reversible
- poor prognosis otherwise.
- MUST inform DVLA
What condition does this image show?
- Central retinal vein occlusion
What condition does this image show?
- Age-related macular degeneration
(dry)
What is the pathophysiology of ARMD?
- Drusen in the macula. Drusen = undigested cellular debris drom degeneration of RPE (retinal pigment epithelium) cells (due to ageing) - this then accumulates as drusen.
- Drusen builds up between RPE and underlying membrane. Hard and soft drusen. Soft drusen are larger and lift the RPE - cause further hypoxia and inflammation.
- Drusen PLUS ‘geographic atrophy’ = DRY ARMD (most common - 90% of all AMD).
- Drusen PLUS ‘choroidal neovascularisation’ = WET ARMD.
What condition does the image show?
wet age related macular degeneration
What are the non glaucomatous visual field losses in this image?
What are the visual field defects shown?
- Superior / inferior arcuate defect
- The most common early to mid stage glaucomatous field. The reason these look like arcs and come off the blind spot is that they represent the loss of bundles of nerves as they come out of the optic nerve head.
What do these visual field defects show?
- Blind spot enlargement
- can be seen in glaucoma, but also can occur with papilledema and optic nerve head swelling. This would likely be seen in patients with idiopathic intracranial hypertension
What do these visual fields show?
- Severe constriction with a central island
- end stage glaucoma. At this point, many patients still have great central vision of 20/20 to 20/50, but peripheral vision is nearly gone.
What are the causes of sudden painless loss of vision?
What are the causes of gradual painless loss of vision?
What are the symptoms of retinal detachement? What are the signs on examination?
- painless loss of vision ‘like a curtain’ coming across the vision - progressive towards centre of vision (over hrs)
- rate of detachment can vary
- upper retinal detachment causes loss of lower part of vision.
- 50% have preceding symptoms: flashes/floaters
- if macula is detached - central vision is lost (may not recover even after reattachment surgery)
- examination: shows visual field loss, RAPD, grey retina which may balloon forwards, may be loss of red reflex, fall in visual acuity. CANNOT exclude RD with opthalmoscope - refer urgently for slit lamp Ax.
DDx for field loss: stroke (will be bilateral, stable, homonymous, macula spared)
TIA - may be unilateral but not persistent or progressive.
What are the risk factors and causes for retinal detachment?
- Causes: rhegmatogenous (most common) - tear in the neurosensory retina, usually due to PVD. Tractional - fibres full the sensory retina away from the RPE. Exudative - damage to RPE - fluid enters subretinal space.
- idiopathic
- Increasing age
- myopia (thin peripheral retina, prone to tears)
- previous cataract surgery (accelerates posterior vitreous detachment)
- proliferative diabetic retinopathy (causes tractional RD)
- eye trauma (tractional)
- retinopathy of prematurity (tractional)
- inflammatory (posterior uveitis - exudative RD)
What is dacrocystitis?
- inflammation of the lacrimal sac
- usually due to infection s.aureus
- can be acute or chronic.
- acute - acute infection of the lacrimal sac
- chronic (in middle aged/elderly) - watery eye which discharges mucus regularly.Eye does not look inflamed. Refer for syringing of lacrimal system/surgery.
How should a stye be managed?
- tender swelling within tarsal plate
- due to acute staphylococcal infection
- emergency admission if signs of periorbital/orbital cellulitis
- Otherwise: reassure, self care - usually self limiting, warm compress QDS until it drains/resolves.
- do not attempt to puncture
- avoid eye makeup/contact lenses
- if painful external stye - can pluck eyelash from infected follicle
- topical ABX only if signs of bacterial conjunctivitis
- refer to opth if not resolved
What are the differentiating signs of orbital cellulitis?
- fever, malaise
- increased pain, pain on moving the eye
- external eye muscle opthalmoplegia - cannot move the eye
- proptosis
- chemosis
- reduced visual acuity/blurred vision
Emergency admission.
