Module 3C Ophthalmology - Conditions Flashcards
What 3 parts is the uvea made up of?
Uvea = middle layer of the eye, located between the retina and the sclera, it consists of the:
- iris
- ciliary body
- choroid (layer between retina and sclera)
What usually causes anterior uveitis + what genotype is anterior uveitis usually associated with?
- usually caused by an autoimmune process
- particularly HLA-B27 - associated with ankylosing spondylitis and reactive arthritis
Anterior uveitis - symptoms and signs O/E
Symptoms:
- Painful red eye
- Reduced visual acuity
- photophobia - due to ciliary muscle spasm
- excessive lacrimation
Signs O/E:
- ciliary flush - ring of red spreading from cornea outwards
- abnormally shaped pupil (posterior synechiae)
- hypopyon - pus and inflammatory cells in the anterior chamber
Anterior uveitis - investigations
- Slit-lamp biomicroscopy - key for diagnosis
- IOP measurement + dilated fundus examination - to assess posterior segment involvement and for complications
(3. Serology for underlying cause can be done in addition)
Anterior uveitis - management
- Topical corticosteroids (eg. prednisolone acetate, dexamethasone) - to relieve inflammation/pain
- Cytoplegics (eg. cyclopentolate or atropine eye drops) - helps relieve ciliary spasm and pain
(3. recurrent cases may require biologics - DMARDs or anti-TNFs)
what are the 2 types of glaucoma?
- open-angle glaucoma (chronic glaucoma)
- acute angle-closure glaucoma
What is (primary) open-angle glaucoma?
- chronic, progressive optic nerve damage caused by a rise in intraocular pressure - characterised by the degeneration of retinal ganglion cells and their axons, leading to irreversible visual field loss
- raised IOP is caused by a blockage in aqueous humour trying to escape the eye
What is the function of aqueous humour, where is it produced, and how is it drained?
- function - supplies nutrients to the cornea + lens
- produced by the ciliary body
- drains through the trabecular meshwork to the canal of Schlemm at the angle between the cornea and iris
Open VS Acute angle-closure glaucoma - anatomy
- Open glaucoma - there is a gradual increase in resistance to flow through the trabecular meshwork
- Acute angle-closure glaucoma - iris bulges forward and seals off trabecular meshwork from anterior chamber - preventing aq humour from draining –> continual build-up of pressure and acute onset of symptoms
What effect does a raised intraocular pressure have on the optic disc?
- Raised IOP causes cupping of the optic disc
- optic cup is usually < 50% of the size of the optic disc - raised IOP causes this indent to become wider and deeper (“cupping”)
(primary) Open-angle glaucoma - symptoms and signs O/E
Symptoms:
- Peripheral visual field loss - nasal scotomas progressing to ‘tunnel vision’
- decreased visual acuity - blurred vision +/- halos around lights (particularly at night)
Fundoscopy signs:
- optic disc cupping - cup-to-disc ratio > 0.5 (due to increased IOP)
- optic disc pallor (indicating optic atrophy)
How is intraocular pressure (IOP) measured?
Goldmann applanation tonometry
- gold-standard test to measure IOP
Open-angle glaucoma - investigations
Diagnosis is based on:
- Goldmann applanation tonometry - measures IOP
- Slit lamp with pupil dilation - assess cup-disc ratio and optic nerve/fundus health
- Visual fields (automated perimetry)
- Gonioscopy - to assess angle between iris and cornea
- Central corneal thickness measurement
Open-angle glaucoma - management
Aim of treatment is to lower IOP and prevent progressive visual field loss:
1. IOP lowering:
- 360° selective laser trabeculoplasty - 1st-line to pts with an IOP ≥ 24 mmHg
- Prostaglandin analogue eye drops (eg. latanoprost) - increases uveoscleral outflow
- Reduction of aq humour:
- beta-blockers (timolol)
- carbonic anhydrase inhibitors
- sympathomimetics (eg. Brimonidine) - Trabeculoectomy (new channel created for aq humour to drain)
Adverse effects of prostaglandin analogues (eg. latanoprost)
- eyelash growth
- eyelid pigmentation
- iris pigmentation
Acute angle closure glaucoma - pathophysiology
- iris bulges forward and blocks off trabecular meshwok from the anterior chamber –> preventing aq humour from draining and leading to a continual increase in intraocular pressure
- as pressure builds in posterior chamber, iris is further pushed forward and exacerbates the angle closure
Open-angle glaucoma VS Acute angle closure glaucoma - difference in at risk ethnic groups?
- Open-angle glaucoma - black ethnic origin
- Acute angle closure glaucoma - female + Asian
Acute angle closure glaucoma - Symptoms + Signs O/E
Symptoms:
- severely painful red eye +/- headache
- decreased visual acuity - blurred vision +/- halos around lights
Signs O/E:
- Red eye
- Hazy cornea
- fixed + dilated pupil
Acute angle closure glaucoma - investigations
- Gonioscopy - to assess iridocorneal angle –> a closed angle is diagnostic of AACG
- Tonometry - elevated IOP is a hallmark of AACG
Acute angle closure glaucoma - management
Immediate admission required, initial management:
1. Lie pt supine
2. Pilocarpine eye drops (2% for blue eyes, 4% for brown eyes) - causes pupil constriction + ciliary muscle contraction –> opens up trabecular meshwork for drainage of aq humour
3. IV acetazolamide - reduces aq humour production
(+/- IV mannitol +/- timolol +/- dorzolamide +/- brimonidine)
Definitive management:
1. Laser peripheral iridotomy - creates tiny hole in peripheral iris
What is the most common cause of blindness in the UK?
Age-related macular degeneration
Wet VS Dry age-related macular degeneration
Dry (non-neovascular) - 90% cases:
- characterised by Drusen deposits in Bruch’s membrane
Wet (neovascular/exudative) - 10% cases:
- characterised by choroidal neovascularization - VEGF stimulates the development of new vessels
- these vessels can leak fluid - causing oedema and vision loss (worse prognosis)
What stimulates development of new vessels in wet AMD (age-related macular degeneration)?
Vascular endothelial growth factor (VEGF)
Age-related macular degeneration (AMD) - Presentation/findings on examination
- Reduced visual acuity (gradual in dry AMD, subacute in wet AMD)
- CENTRAL SCOTOMA - gradual loss of central vision
- Struggle with vision at night/dark adaptation
- Metamorphopsia (wavy appearance to straight lines)
O/E:
- Fundoscopy - Drusen deposits in dry AMD
- Fluorescein angiography to view retina - shows oedema and neovascularization in wet AMD
- Ocular coherence tomography - gives cross-sectional view of layers of retina
What test is used to assess for metamorphosis in AMD?
Amsler grid test
Age-related macular degeneration (AMD) - Management
Dry AMD - no specific treatment, management involves reducing risk of progression by:
1. Avoiding smoking
2. Controlling BP
3. Vitamin supplementation (A, C, and E) + Zinc
Wet AMD:
1. intravitreal anti-VEGF injections (eg. ranibizumab, aflibercept) - block VEGF and slow development of new vessels
What does the term cataracts mean?
- Cataracts describe a progressively opaque eye lens, which reduces the light entering the eye and visual acuity
What is the role of the lens and how does it receive its nourishment?
- role of the lens is to focus light on the retina - ciliary body contracts and relaxes to change the shape of the lens
- the lens has no blood supply and is nourished by the aqueous humour
Presentation of cataracts and signs O/E
Symptoms are usually asymmetrical:
- slow reduction in visual acuity
- progressive blurring of vision
- colours becoming more faded, brown, or yellow
- ‘starbursts’ can appear around lights (particularly at night)
O/E:
- loss of red reflex
- lens can appear grey or white using an ophthalmoscope
Cataracts - management
- if symptoms manageable - no intervention needed
- Cataract surgery - lens replaced with an artificial lens
Endophthalmitis describes inflammation of the inner contents of the eye, usually caused by infections, and is a rare but serious complication of cataract surgery (it can lead to vision loss) - how is this treated?
intravitreal antibiotics injected directly into the eye
Central retinal artery occlusion - aetiology
- Carotid artery stenosis/atherosclerosis - most common cause
- the central retinal artery is a branch of the ophthalmic artery, which is a branch of the internal carotid artery - GCA can also be a cause (where vasculitis affecting the ophthalmic or central retinal artery reduces blood flow)
- Cardiac emboli - most common cause under 40 yrs
Central retinal artery occlusion - risk factors
CVD risk factors (atherosclerosis):
- smoking
- hypertension
- diabetes
- raised cholesterol
Central retinal artery occlusion - presentation + signs O/E
Symptoms:
- sudden painless loss of vision - like a “curtain coming down”
O/E:
- Swinging right test - RAPD
- Fundoscopy - ‘cherry red spot’ + pale retina
Differentials for a sudden painless vision loss
- retinal detachment
- central retinal artery occlusion
- central retinal vein occlusion
- vitreous haemorrhage (due to diabetic retinopathy)
Fundoscopy findings in central retinal artery occlusion
- ‘cherry red spot’
- pale retina - due to ischaemia
Central retinal artery occlusion - management (acute and long-term)
Immediate referral (vision-threatening emergency) - management aims to remove/dislodge the blockage:
1. Ocular massage (to improve blood flow and potentially dislodge a clot)
2. Intra-arterial thrombolysis: urokinase administered via ophthalmic artery (risk VS benefit)
3. Reduction of IOP: IV acetazolamide OR IV mannitol +/- topical timolol
4. Vasodilator therapy: sublingual isosorbide dinitrate OR inhaled carbogen (95% oxygen + 5% carbon dioxide) –> aimed to reperfuse retina
(5. GCA is a reversible cause - ESR + temporal artery biopsy –> high dose steroids)
(6. Long-term management - treat reversible risk factors + secondary prevention of CVD)
What rheumatological condition is GCA associated with?
Polymyalgia rheumatica (PMR)
Giant cell arteritis - clinical features + signs O/E
Symptoms:
- unilateral headache - typically severe and around temple and forehead
- scalp tenderness, jaw claudication, blurred/double vision
O/E:
- temporal artery may be tender and thickened to palpation (with reduced or absent pulsation)
(50% have associated PMR symptoms too - eg. shoulder and pelvic girdle pain and stiffness)
Giant cell arteritis - investigations
- Raised inflammatory markers - ESR > 50 mm/hr
- Temporal artery biopsy - multinucleated giant cells
- Duplex USS - “halo” sign and stenosis of temporal artery
Giant cell arteritis - Management
- Immediate high-dose steroids (to prevent vision loss) - prednisolone OR methylprednisolone
- Adjunctive therapy - Aspirin 75mg OD (decreases stroke risk) +/- PPI (for GI protection while on steroids) + Bisphosphonates and Adcal D3 (for bone protection while on steroids)
(3. MDT approach - rheumatology, vascular surgeons, ophthalmology)
In GCA, vision loss is the most feared and serious complication - what is this due to?
Anterior ischaemic optic neuropathy
Central VS Branch retinal vein occlusion
- occurs when a blood clot (thrombus) forms in the retinal veins, blocking drainage of blood form the retina
- the branch retinal veins drain into the central retinal vein which runs through the optic nerve to drain into either the superior ophthalmic vein or cavernous sinus
- blockage of one of the branch veins affects the area drained by that branch
- blockage in the central vein causes problems with the whole retina
- there are 4 branch retinal veins that drain about 1/4 of the retina each
Retinal vein occlusions - which sites are at a higher risk of occlusion?
sites where the retinal arteries cross over the top of the veins can cause narrowing of the vein - these sites ar more vulnerable to occlusion
Retinal vein occlusion - pathology of vision loss
- Blockage (thrombus) of a retinal vein causes increased pressure in the vessels draining the eye
- this results in fluid and blood leaking into the retina, causing macular oedema and retinal hemorrhages –> this results in retinal damage and vision loss
Retinal vein occlusions - what are the 2 types and which is worse (what can it lead to?)
- Ischaemic or non-ischaemic
- Retinal ischaemia leads to release of vascular endothelial growth factor (VEGF) - resulting in new blood vessel development (neovascularisation)
Retinal vein occlusion - clinical features + signs O/E
Symptoms:
- painless reduciton of vision or vision loss
- branch occlusion - vision loss corresponds to affected area of retina
- if involves branch draining macula - central vision is lost
O/E:
- Fundoscopy (more so in ischaemic CRVO) - cotton wool spots, venous tortuosity, retinal oedema, flame-shaped hemorrhages)
- Snellen chart - < 6/60
- RAPD
Branch retinal vein occlusion - fundoscopy
Retinal vein occlusion - management
Refer immediately to ophthalmologist, management aims to treat macular oedema and prevent neovascularization:
1. Anti-VEGF therapies (eg. ranibizumab and aflibercept)
2. Intravitreal dexamethasone
3. Laser photocoagulation (to get rid of new vessels)
Corneal abrasions - Clinical features + O/E
- painful, red eye
- photophobia
- decreased visual acuity in affected eye - blurred vision
- foreign body sensation
O/E - usually visible to naked eye, but a fluorescein stain can be applied to the eye to aid diagnosis
Corneal abrasions - management
Usually heal over 2-3 days, more serious may need treatment:
1. Antibiotic eye drops
(2. remove foreign body if there is one)
3. Simple analgesia - paracetamol
4. lubricating eye drops
Give 3 examples of lubricating eye drops in order of their viscosity (least viscous to most viscous)
- Hypromellose drops (least viscous) - effects last around 10 mins
- Polyvinyl alcohol drops (middle viscous choice)
- Carbomer drops (most viscous) - effects last 30-60 mins
Corneal foreign body - management (include post-removal care)
- Anaesthesia
- Foreign body removals - irrigation OR needle technique OR Jeweller’s forceps OR Alger brush (if residual rust rings or iron deposits)
- Post-removal care - antibx prophylaxis +/- cycloplegics +/- analgesia +/- tetanus prophylaxis
- Follow-up - 24-48hrs post-procedure
Retinal detachment - pathophysiology + why this can be sight-threatening
- neurosensory layer (photoreceptor - rods/cones) separates from the retinal pigment epithelium (base layer attached to the choroid)
- usually due to a retinal tear - allowing vitreous fluid to get under the neurosensory retina and fill the space between the layers
- the neurosensory retina relies on the blood vessels of the choroid for its blood supply - therefore, retinal detachment can disrupt the blood supply and cause permanent damage to the photoreceptors
Posterior vitreous detachment - pathology + most common aetiology
- when the vitreous body comes away from the retina - common in older age
- vitreous humour = gel inside the vitreous chamber of the eye, it maintains the structure of the eyeball and keeps the retina pressed on the choroid
- with age it becomes less firm and less able to maintain its shape
Retinitis pigmentosa - presentation + O/E
Usually symptoms start in childhood:
- Night blindness
- Peripheral vision loss
(rods degenerate more than cones - rods are responsible for night vision and peripheral vision)
O/E:
- Fundoscopy - pigmentation (“bone-spicule” pigmentation)
Conjunctivitis (“pink eye”) - Presentation + bacterial VS viral
Symptoms:
- Red, bloodshot eye
- itchy or gritty sensation
- no pain
.
- Bacterial –> purulent discharge (“eyes stuck together in morning”)
- Viral –> clear discharge (associated with other viral symptoms + preauricular lymph nodes)
Episcleritis - Presentation + O/E (appearance)
Acute-onset unilateral features:
- localised or diffuse redness (often a patch of redness in the lateral sclera)
- no pain
O/E:
- dilated episcleral vessels
Subconjunctival haemorrhage - Presentation + appearance (what typically precipitates a subconjunctival haemorrhage.)
- bright red blood underneath conjunctiva
- painless + does not affect vision
- Precipitating event - coughing fit or heavy lifting
Vitreous haemorrhage - Clinical features + O/E
Symptoms:
- sudden, painless vision loss or floaters
- +/- decreased visual acuity
O/E:
- Fundoscopy - absent or diminished red reflex
(image shows vitreous hemorrhage on fundoscoy, pt has a background of treated diabetic retinopathy)
- Slit-lamp examination - assess for retinal tears/detachment
- B-scan ultrasonography - used if fundus is obscured by the haemorrhage on fundoscopy
Diabetic retinopathy - Pathophysiology
Due to chronic hyperglycaemia:
- Blot haemorrhages (due to increased vascular permeability)
- Hard exudates (yellow-white deposits of lipids and proteins in the retina)
- Microaneurysms - damage to blood vessel walls leads
- Cotton wool spots (due to damage to nerve fibres in the retina)
- Intraretinal microvascular abnormalities (IRMA) (dilated and tortuous capillaries in the retina)
- Neovascularization can occur too
Diabetic retinopathy - Clinical features + O/E (fundoscopy)
Symptoms:
- early stages often asympomatic
- as progresses - pt may experience blurred vision, floaters, dark areas in their visual field, and eventually vision loss
Dilated Fundoscopy:
- microaneurysms
- cotton wool spots
- hard exudates
- intraretinal microvascular abnormalities in NPDR
- Neovascularisation +/- vitreous haemorrhage in PDR
What does this image show?
diabetic retinopathy previously treated with pan-retinal laser photocoagulation
Hypertensive retinpoathy - features on fundoscopy
- Silver wiring (walls of arterioles become thickened and sclerosed - reflect more light on examination)
- AV nipping (where arterioles cause compression of the veins where they cross)
- Cotton wool spots (caused by ischaemia and infarction of the retina)
- Hard exudates (caused by damaged vessels leaking lipids/proteins onto the retina)
- Retinal haemorrhages (caused by damaged vessels rupturing)
- Papilloedema (caused by ischaemia to the optic nerve - results in optic nerve swelling)
What muscles are involved in pupil constriction and dilation + which NS (symp or parasymp) is involved in each?
Sphincter pupillae (circular muscles) –> pupil constriction
- stimulated by parasympathetic NS (using acetylcholine as a neurotransmitter)
.
Dilator pupillae (radial muscles) –> pupil dilation
- stimulated by sympathetic NS (using adrenaline as a neurotransmitter)
What are the two categories of third nerve pasly based on the presence of pupil involvement
- Ischaemic (microvascular):
- Pupil sparing - as parasympathetic fibres are spared
- Causes - diabetes, ischaemia
- tend to be more benign and spontaneously resolve - Compressive (mass lesion):
- Pupil involved - as parasympathetic fibres are compressed
- Causes - tumour, PCOM tumour, cavernous sinus thrombosis
(the oculomotor nerve travels directly from the brainstem to the eye in a straight line - travels through cavernous sinus and close to the posterior communicating artery)
(The parasympathetic fibres/pupillary fibres are on the outside of the nerve, therefore compression/tumour affects them but ischaemia does not)
Holmes-Adie pupil - caused by damage to what fibres and why does this cause the symptoms of holmes adie pupil (dilated pupil that reacts poorly to light and relatively well to accommodation) ?
- Post-ganglionic parasympathetic fibres
- arise from the ciliary ganglion (where pre-ganglionic parasympathetic fibres (from the Edinger-Westphal nucleus) synapse)
- they innervate the iris sphincter muscle (pupil constriction) + the ciliary muscle (lens accommodation for near vision)
What are the 2 types of stye (hordeolum)?
Infection or inflammation of the eyelids - particularly the oil glands - causes a tender red lump along the eyelid that may contain pus
- Hordeolum externum - infection of the glands of Zeis (sebaceous glands at the base of the eyelashes) or glands of Moll (sweat glands at the base of the eyelashes)
- Hordeolum internum - infection of the Meibomian glands - they are deeper, tend to be more painful
Entropion - what is it + management
- Entropion = when the eyelid turns inwards with lashes pressed against the surface of the eye
- this causes pain and can result in corneal damage and ulceration
.
management:
1. taping eyelid down + lubricating drops (to prevent drying out)
2. definitive –> surgical
Ectropion - what is it + complication + management
- Ectropion = when the eyelid turns outwards, exposing the inner aspect
- usually affects the bottom lid - can result in exposure keratopathy, as eyeball is exposed and not adequately lubricated and protected
.
management:
1. regular lubricating eye drops to protect surface of eye
2. surgery - if more severe
Trichiasis - what is it + management
- Trichiasis = inward growth of the eyelashes
- It results in pain and can cause corneal damage and ulceration
.
management:
1. removing affected eyelashes
2. recurrent cases - electrolysis, cryotherapy, or laser treatment to prevent from regrowing
Periorbital cellulitis - what is it + presentation
- eyelid and skin infection in front of the orbital septum
- presents with swollen, red, hot skin around the eyelid and eye
Herpes simplex keratitis - clinical features + O/E
Symptoms:
- painful red eye
- photophobia
- watery discharge (epiphora)
- reduced visual acuity
O/E:
- Slit lamp examination - required to diagnose
- Fluorescein staining - dendritic corneal ulcer (dendritic describes the branching appearance of the ulcer)
What are these definitions + match the relevant term to the photo
- Esotropia
- Exotropia
- Hypertropia
- Hypotropia
- Esotropia: inward positioned squint (affected eye towards the nose)
- Exotropia: outward positioned squint (affected eye towards the ear)
- Hypertropia: upward moving affected eye
- Hypotropia: downward moving affected eye
What is hyperopia (farsightedness) + main cause
- distant objects seen more clearly than near ones - because light focuses behind the retina rather than directly on it
- the eye is too short, or the cornea/lens is too flat, leading to insufficient focusing power
What is myopia (nearsightedness) + main cause
- near objects are seen more clearly than distant ones - because light focuses in front of the retina
- eye is too long, or the cornea/lens is too steep, leading to excessive focusing power
Pseudosquint
- A pseudosquint (also known as pseudostrabismus) refers to the appearance of a squint (strabismus) when the eyes are actually properly aligned
- This condition is typically caused by facial or structural features around the eyes rather than an actual misalignment
- It is common in children and does not require treatment.
. - causes: wide nasal bridge
(this is why corneal light reflex is an important test for strabismus (squint)
What term is used to describe the redness of the white part of the eye
Ciliary injection
3 types of cataracts
- Nuclear - affects central nucleus of lens
- Cortical - affects outer edge (cortex) of lens
- Posterior subcapsular - affects back surface of lens
Name of this sign and what is the most serious cause?
Leukocoria (aka. white pupillary reflex)
- retinoblastoma (malignant tumour of retina)
(congenital cataract is also a cause)
