Ophthalmology Flashcards
List the differentials for painless red eye
Episcleritis
Subconjunctival haemorrhage
conjunctivitis
List differential causes of a painful red eye
Acute angle closure glaucoma Anterior Uveitis Scleritis Keratitis Corneal ulcers/abrasions Foreign body Trauma Chemical injury
Describe cataract and it’s risk factors
Opacification and clouding of the lens (which is avascular)
Older age Congenital (TORCH infections) Smoking Alcohol (dehydration) Iatrogenic -> steroids, vitrectomy, IV injections
What are the S/S of cataract?
Change in colour vision (becomes more brown/yellow)
Vision worse at night -> glare and starbursts around lights
Myopic shift (become short sighted i.e. cannot see things far away)
Protein aggregation and lens opacification
Reduced VA
Loss of red reflex
Define phakic, aphakic and pseudophakic
Phakic = natural lens
Aphakic - eye has no lens
Pseudophakic - lens has been artificially replaced
What is the treatment for cataracts?
Conservative - do nothing if not severe
Phacoemulsification (uses USS) to emulsify lens and then replace with new one
Describe complications of cataract surgery
Endophthalmitis = inflammation of inner eye, 3-5 days post op, needs treated with intravitreal antibiotics
Retinal detachment
Acute angle closure glaucoma (cataract proteins can leak into the anterior chamber)
Define glaucoma
Group of eye diseases resulting in damage to the optic nerve, often due to increased IOP
Describe the production and flow of aqueous humour in the eye
Produced by the ciliary body, flows from the posterior chamber around the iris to the anterior chamber, drains through trabecular meshwork (through Canal of Schlemm) into general circulation
Describe the classifications of glaucoma and describe the pathophys behind each
Open or closed angle
Acure or chronic
Primary or secondary
Open = there is resistance to flow of aqueous humour through the trabecular network
Closed = Iris pushed forwards against the cornea and blocks flow of aqueous humour into the trabecular mesh
What are the risk factors for acute angle closure glaucoma?
Age Hypermetropia (long-sighted and having a smaller eye) FHx East Asian/Chinese Shallow anterior chamber
What are the risk factors for open angle glaucoma?
Age Black Myopic (short-sighted i.e. bigger eye) Smoking Diabetes HTN
What is the classical S/Sx of glaucoma?
How is glaucoma investigated?
Halos around lights at night
Peripheral vision affected
Increased cup:disc ratio >0.5
(Goldmann applanation) tonometry = measuring pressure
Fundoscopy - assess for disc cupping
Visual fields
How is open angle vs closed angle glaucoma treated?
Open angle:
- prostaglandins (latanoprost) to increase outflow of fluid
- beta blocker (timolol) to reduce fluid production
- carbonic anhydrase (dorzolamide) - reduce aqueous humour production
- Sympathomimetics (brimonidine) - increase outflow and reduce fluid production
(surgical = trabeculectomy)
Closed angle:
- pilocarpine (muscarinic receptor agonist which constrict pupil to open up the pathway for aqueous humour to flow)
- acetazolamide 500mg oral (carbonic anhydrase inhibitor) to reduce fluid production
- then same drugs as open ^^^
(surgical: Iridotomy, trabeculectomy)
Describe AMD and its subtypes
Age related macular degeneration
Progressive degenerative disease involving macula
Dry (atrophic) or wet (exudative - caused by choroidal neovascularisation)
Dry = 90%, Wet = 10%
What are the presenting features of macular degeneration?
Describe pathophysiology
Reduced VA
Central vision lost / metamorphopsia
Normal peripheral vision
Pathophysiology:
- Disruption of Bruch’s layer and RPE cells
What are the risk factors for AMD?
Smoking Increasing age HTN CVD FH Female Hypermetropia Caucasian
What are the fundoscopy findings in wet vs dry AMD?
Dry: macula drusen, RPE hyperpigmentation
Wet: haemorrhages, lipid exudates, neovascularisation…
How is AMD investigated?
What is the treatment for AMD?
VA
Fundoscopy (look for drusen vs neovascularisation)
Amsler chart (look for metamorphopsia)
Fluoroscein angiogram - to show neovascularisation
Dry - no treatment (reduce RFx e.g. stop smoking)
Wet - Intravitreal injections (Anti-VEGF)
Differentiate scleritis and episcleritis
Episclera = between conjunctiva and sclera
Sclera = the white outer coating of the eye (under the episclera)
Episcleritis = mild pain and self-limiting, blanches with phenylephrine
Scleritis = acute red eye, pain on movement and keeps awake at night, associated with RA and GPA, does not blanch with phenylephrine
What is Charles Bonnet syndrome?
Where visual hallucinations occur as a result of visual loss
Not related to psychosis/dementia
The patient is very aware that their hallucinations are not real
What are the S/Sx of acute angle closure glaucoma
Sudden onset painful red eye Blurry vision Photophobia Headache Halos around lights N&V
Hazy cornea (oedema) Mid-dilated fixed pupil Iris bombe Reduced VA Closed angle on gonioscopy
Describe endophthalmitis and how it may present
Infection of the aqueous +/- vitreous humour which causes inflammation in the eye
Most commonly occurs post-op from cataract surgery
Onset 1-7 days post-surgery Disproportionate/increasing post-operative inflammation Hypopyon Pain Worsening vision Posterior segment inflammation RAPD Lid swelling
Define central retinal artery occlusion and its risk factors
= blockage of the retinal artery which carried oxygen to the nerve fibres in the retina RFx: - HTN - ageing - glaucoma - DM
How is CRAO caused?
Atherosclerosis
Suggestive if: HTN, diabetes, hypercholesterolaemia, smoking
Embolism: Carotid artery disease, valvular disease
Inflammatory: GCA
Medications: OCP, cocaine
Sickle cell disease
What are the clinical features of CRAO?
Sudden onset, unilateral, PAINLESS vision loss White swollen retina with a ‘cherry red spot’ RAPD Visible emboli (25%)
How is CRAO investigated and treated?
Fundoscopy ESR/CRP – rule out GCA OCT: inner retinal atrophy with outer retinal preservation Fluorescein angiography Carotid artery US
Mgx: depends on cause
Distinguish between pre-septal and orbital cellulitis
Pre-septal cellulitis: Inflammation of eyelid/ soft tissues, ANTERIOR to the orbital septum
Usually from Trauma/ bacteraemia (e.g. bite, penetrating injury, foreign body)
Orbital cellulitis: inflammation of the soft tissue within the orbit POSTERIOR to the orbital septum (i.e. muscles, fat and connective tissue)
Often secondary to paranasal sinusitis (as sinuses surround orbit)
Orbital septum = membranous sheath which acts as the anterior boundary of the orbit, connecting orbital rims to eyelids
How do pre-septal and orbital cellulitis present
Pre-septal: Lid erythema, inflammation, tenderness, warmth, rarely fever, NO VISUAL CHANGE
Orbital: same as above + fever, conjunctival swelling (chemosis), proptosis, painful/ limited eye movement + diplopia (due to inflammation of muscles/ cranial nerves), reduced VA/ RAPD (due to optic nerve involvement)
What are the complications of orbital cellulitis
Sepsis Orbital compartment syndrome Central spread of infection Meningitis – Spread to meninges Cavernous sinus thrombosis Cerebral abscess Blindness – due to pressure on optic nerve/ thrombotic ischemia of optic nerve vessels
When the eyeball is looking medially, which muscle controls upwards gaze?
Inferior oblique
What is the most common cause of a 3rd nerve palsy?
ANEURYSM - vasculopathic patient
What is the most common cause of a 4th nerve palsy?
Congenital or trauma
What is the most common cause of a 6th nerve palsy?
Raised ICP
What is the most common type of retinal detachment?
Rhegmatogenous = separation of the vitreous from the retina -> retinal tear then occurs -> wallpaper theory -> separation of neurosensory retina from RPE
What are the risk factors for a retinal tear
Cataract surgery
Trauma
DM
Myopia (larger eyes when short sighted, increased stretching of retina)
What are the signs/symptoms of retinal detachment
4F’s
- flashes
- floaters
- field loss (corresponding to area of detachment)
- fall in VA
List the differentials for ‘flashing lights’
Posterior vitreous detachment Retinal tear Retinal detachment Occular migraine Postural hypotension TIA etc...
List the differentials for ‘sudden painless visual loss’
Vitreous haemorrhage Retinal vein occlusion Retinal artery occlusion Retinal detachment Amaurosis fugax CVA Anterior ischaemic optic neuropathy
Describe the pathophysiology of diabetic retinopathy
Microvascular changes
Basement membrane thickening
VEGF response
Neovascularisation and leaky vessels
How is diabetic eye disease classified?
Can get retinopathy (non-proliferative or proliferative)
Can get maculopathy
Non-proliferative retinopathy can be:
- mild = microaneurysms
- moderate = hard exudates and cotton wool spots
- severe = dot haemorrhages in 4 quadrants
Proliferative retinopathy = neovascularisation
Describe the treatment of DR
Non-invasive:
- BP, lipid and BM control
- smoking cessation
Invasive (once neovascularisation has occurred):
- anti-VEGF injections
- laser treatment
- vitrectomy
What are the complications of DR
Retinal detachment Vitreous haemorrhage Cataracts Optic neuropathy Rebeosis iridis
Describe the types of conjunctivitis, how they present and their treatment
Bacterial - usually unilateral, green discharge, good hygiene and self limiting or treat with topical Abx
Viral - bilateral, pre-auricular LNs often involved, clear discharge, self-limiting/use lubricating drops
Allergic - bilateral, swollen, itchy eyes. No LN. Treat with antihistamines/anti-inflammatories
What is keratitis
Inflammation of the cornea
Compare and contrast bacterial vs viral vs fungal keratitis
Bacterial
- caused by staph/strep/pseudomonas
- rapid onset, photophobia, reduced VA, hypopyon sometimes
- treat with Abx
- circular on fluoroscein staining
Viral
- insidious onset
- pain, reduced VA, vesicles around eye
- commonly caused by herpes simplex ( = herpes keratitis) or VZV
- look for Huchinson’s sign = nose vesicles are a predictor of optic ZOSTER involvement
- Treat with PO aciclovir
- will see dentritic spiky ulcers on fluoroscein staining
Fungal -> shows cloudy, white, spreading fluffy lesions, caused by vegetative matter getting into the eye
Compare and contrast scleritis vs episcleritis
The coverings of the eye from outer to inner are:
- conjunctiva
- episcleritis
- scleritis
Scleritis
- painful, severe, awake at night
- diffuse red eye
- associated with RA/SLE/granulomatosis + PA
- does NOT blanch with phenylephrine
- treat with NSAIDs/steroids
Episcleritis
- mild pain
- sectoral red eye
- DOES blanch with phenylephrine
- usually self-limiting but NSAIDs/steroids may be required
Describe uveitis and the features of anterior uveitis
Uveitis = inflammation of uveal tract = iris + ciliary body + choroid
Anterior uveitis = mainly inflammation of iris. Associated with HLA-B27 diseases. Fts: - painful red eye - photophobia - small fixed pupil (synechiae form and pupil may be abnormal shape) - hypopyon in anterior chamber Treatment: - steroids - mydriatics (dilating drops)
What are the complications of anterior uveitis
Cataract
Glaucoma
Macular oedema
Describe a retrobulbar haemorrhage and the signs/symptoms
Emergency Bleeding within the orbit Causes orbital compartment syndrome Fts: - pain - reduced VA - RAPD - increased IOP - proptosis - reduced eye mobility
How is retrobulbar haemorrhage treated?
Lateral canthotomy procedure -> emergency decompression by cutting open eyelid
Describe the nerve control and neurotransmitters behind
a) pupil constriction
b) pupil dilation
a) constriction = parasympathetic, CN3, uses ACh
b) dilation = sympathetic, uses NA/A
List causes of abnormal pupil shape
Anterior uveitis and synechiae formation
Acute angle closure glaucoma (causes ischaemic damage to iris muscles)
Coloboma (congenital malformation)
Tadpole pupil (temporary spasm of segment of pupil seen in migraine)
List causes of mydriasis
Dilated pupil
- Holmes Ades pupil
- 3rd nerve palsy
- anticholinergics (oppose ACh in the parasympathetic system)
- cocaine
- raised ICP
List causes of miosis
- Horners syndrome
- Argyll-Robertson pupil
- Pilocarpine (muscarinic receptor agonist used to treat acute angle closure glaucoma)
Describe features of a 3rd nv palsy
ptosis
dilated, non-reactive pupil
down and out position of the eye
Describe the differences between medical and surgical 3rd nv palsy
Medical = pupil sparing, as outer parasympathetic fibres are spared. Usually a microvascular cause e.g. diabetes, HTN, ischaemia
Surgical = pupil affected, usually a physical compressive cause which affects the outer parasympathetic fibres e.g. tumour, trauma, raised ICP, cavernous sinus thrombosis, posterior communicating artery aneurysm
What are the features of Horner’s syndrome and list causes based on the 3 regions of the sympathetic tract which can be affected
= ptosis, miosis, anhidrosis - damage to the sympathetic supply to the eye which can be: CENTRAL - S - cyst in spinal cord (syringomyelia) - Stroke - MS - Swelling (tumour)
Pre-ganglionic = THORACIC - T
- Tumour (pancoast)
- Trauma
- Thyroidectomy
- Top (cervical) rib
Post-ganglionic (CERVICAL) - C
- carotid aneurysm
- carotid artery dissection
- cavernous sinus thrombosis
- cluster headache
How can the site of the sympathetic lesion be worked out?
Based on the presence of anhidrosis!
Central lesion - anhidrosis of face, arms and trunk
Pre-ganglionic - anhidrosis of face
Post-ganglionic - no anhidrosis
How can you test for Horner’s syndrome
Cocaine eye drops
Stop noradrenaline reuptake at the NMJ and make it hand around for longer
This would cause a normal eye to DILATE as more NA stimulates iris dilator muscles
In Horner’s syndrome, there is no NA in the first place, so cocaine eye drops DO NOT CAUSE DILATION
Describe a Holmes-Adie pupil and what is Holmes-Adie syndrome
- unilateral dilated pupil
- cause unclear ?viral
- damage of post-ganglionic sympathetic fibres
Holmes-Adie syndrome = HA pupil + absent knee and ankle reflexes
Describe an Argyll-Robertson pupil
- specific finding in neurosyphilis
- constricted pupil
- accommodates but does not react to light
Describe the cause and presentation of central retinal vein occlusion
*Central retinal artery vs vein occlusion cannot be distinguished from history -> both present with sudden painless visual loss!
Cause - usually atherosclerotic Features on examination: - tortuous vessels - disc swelling/oedema - flame haemorrhages on the retina - macular oedema
Describe the presentation of posterior vitreous detachment
Vitreous humour detached from retina
PAINLESS
Spot of visual loss
Flashing and floaters
No treatment needed, brain adjusts to areas of visual loss over time
Describe what can progress from posterior vitreous detachment
Posterior vitreous detachment -> retinal tears (where vitreous fluid can travel under the retina) -> retinal detachment
Describe the presentation of retinal detachment
SIGHT THREATENING as the retina is detached from the choroid, and the retina gets its blood supply via diffusion from the choroid
Fts:
- painless
- peripheral visual loss (like a curtain coming)
- blurred/distorted vision
- flashes and floaters
