Ophthalmology Flashcards
Visual Loss
Give Differentials
Sudden Painless Loss
- Retinal Detachment (w/ flashes/floaters)
- Central retinal vein occlusion
- Central retinal artery occlusion
- Vitreous haemorrhage
- posterior uveitis
- Wet Age-related macular degeneration
- Amaurosis fugax
- Cortical blindness
- Migraine aura
Sudden Painful Loss
- Acute angle-closure glaucoma
- Giant Cell arteritis
- Optic neuritis
- Anterior uveitis
- Trauma
- Keratitis
Gradual Painless Loss
- Cataract
- Open angle glaucoma
- Diabetic retinopathy/maculopathy
- Dry age related macular degeneration
- Retinitie pigmentosa (B/L concentric field loss, optic disc pallor)
- Optic nerve compression
- Keratoconus
- Chronic papilledema (-> permanent optic nerve dysfunction)
Acute Angle Close Glaucoma
- Pathophysiology
- Presentation
- Management
- Complications
Pathophysiology
- Glaucoma = optic nerve damage/disc changes PLUS visual field defects
- Normally associated w/ raised IOP
- Acute angle closure: reduced aqueous humour outflow as the lens pushes the iris against the trabecular meshwork, blocking it.
Risk factors:
- shallow ant. chamber (e.g. hypermetropia), dilated pupil
Presentation
- Sudden onset red, painful eye + blurred vision
- N+V, headache, eye feels hard, hazy cornea, semi-dilated fixed pupil
Management
- Immediate ophthalmology ref
- IV acetazolamide 500mg (carbonic anhydrase inhibitor)
- PLUS combination of eye drops: pilocarpine 4% drops (cholinergic parasymp - constricts pupil), B-blocker (e.g. timolol), alpha-2-agonist (e.g. apraclonidine)
- Definitive Tx: laser peripheral iridotomy (done bilaterally - tiny hole in peripheral iris)
Primary Open Angle Glaucoma
Pathophysiology
Presentation
Management
Pathophysiology
- Reduced aqeuous humour outflow through trabecular meshwork (clogged w/ debris)
- RFs: age, race (black), fam Hx, myopia, HTN, DM
Presentation
- gradual onset, insidious, painless loss of peripheral vision (central preserved -> tunnel vision), reduced visual acuity
- O/E:
- optic disc cupping (enlarged cup (light bit in middle of optic disc) - ration >0.7 (normal 0.4-0.7))
- Optic disc pallor (indicates optic atrophy)
- Bayonetting of vessels
Management - eye drops
- 1st line: PG analogue (eg. latanoprost - increases aqueous outflow)
- SEs: brown pigmentation of iris, increased lash length
- 2nd line: B-blocker (eg. timolol - reduced production of aqeuous - avoid in asthma + heart block); Carbonic anhydrase inhibitor (eg. acetzolamide) OR alpha agonist (e.g. brimonidine - avoid if taking tricyclic antidepressant or MAOI)
-Other:
- Selective laser trabeculoplasty or trabeculectomy (pathway cut through sclera to drain aqeous under conjunctiva)
Age Related Macular Degeneration
- Pathophysiology
- Presentation
- Investigations
- Management
(N.B. this is the most common cause of blindness in the UK)
Pathophysiology
- Degeneration of central retina (macula) - specifically: degeneration of retinal photoreceptors (-> drusen) + atrophy of retinal pigment epithelium
- Risk factors: age, smoking, family hx, HTN, DM, hyperlipiaemia
Two forms
- Early ARMD (dry): drusen + alterations/atrophy to RPE
- Late ARMD (wet) - choroidal neovascularisation, can -> subretinal haemorrhage or fluid leak (well demarcated red patches) + scar formation
Presentation
- Early/Dry - more gradual onset:
Reduced VA. Worse for near objects + at night.
Photopsia (perception of flickering lights) + glare around objects
Visual hallucinations can -> charles bonnet syndrome
- Wet - often slow progression over months then speeds up over week or so. - > central scotoma
Investigations
- Fundoscopy:
- Dry: Drusen (lipofuscin deposits - yellow round spots, can become confluent later -> macular scar)
- Wet: well demarcated red patches (intra or subretinal fluid leak/haemorrhage)
- Distortion of line perception on Amsler grid
For diagnosis:
- Slit lamp microscopy + colour fundus photography
- Fluroscein angiography (urgent) if neovascular ARMD suspected - to confirm diagnosis + guide treatment
- Ocular coherence tomography: drusen (areas of RPE elevation), RPE hyperpigmentation + geographic atrophy
Management
Both need urgent (within 1/52 referral to ophthalmology to rule out wet ARMD
Early/Dry
-counselling, support groups, visual aids
-stop smoking
- Diet: Zinc and anti-oxidant vitamins (A,C,E)
- Amsler grid to monitor
Late/Wet
- Intra-vitreal anti-VEGF (Urgent- within 2/12) e.g. ranibizimab, aflibercept.
- Other: laser photocoagulation (slows progression BUT risk of acute visual loss)
- Monitor w/ OCT (initially monthly)
Episcleritis
- Pathophysiology
- Presentation
- Management
Pathophysiology
- Inflammation of episclera. Not normally associated w/ any systemic disease.
- more common in young women
Presentation
- Sudden onset red eye: sectoral or diffuse
- mild discomfort, tearing +/- mild photophobia
- vessels mobile on gentle pressure AND blanch w/ phenylephrine (topical vasoconstrictor)
- Resolves spontaneously in 1-2w
Management
- Reassure +/- cold compress + topical lubricant
Scleritis
-Pathophysiology
-Presentation
- Investigations
-Management
Pathophysiology
- Inflammation of sclera. potentially site threatening.
- 50% associated w/ underlying disease: RA, vasculitis, SLE, Sarccoid, IBD, TB, syphylis etc.
Presentation
- Red eye +/- tearing + photophobia
- Severe, boring, retrobulbar pain (can radiate to forehead/temporal area)
- Doesn’t blanch w/ topical phenyleprine + vessels not mobile on pressure
Can be:
- Non-necrotising
- Necrotising - white avasc areas surrounded by red sclera (necrosis can -> translucency + visible blue/back uveal tissue)
Investigations
- Rheum/inflam bloods for underlying cause
Management
- Non-necrotising: NSAID +/- immunpsupression
- Necrotising - IV pred (then taper + switch to PO) + then maintenance immune supression
Keratitis
- Pathophysiology
- Presentation
- Management
- Complications
Pathophysiology
Corneal inflammation - Sight Threatening
Causes:
-Bacterial: staph aureus OR pseudomonas (in contact wearers)
-fungal
-Amoebic (acanthamoebic keratitis) - pain out of keeping w/ findings. risk if exposure to soil or contaminated water
-Parasitic
- HSV
Presentation
- FB sensation, pain, photophobia, lacrimation, mucopurulent discharge, red eye, reduced VA
- May have hypopyon
Management
- Contact lens wearers: same day ophthalmology ref for slit lamp
- Topical abx - quinolones
- Cycloplegic for pain releif e.g. cyclopentolate
Complications
- Corneal scarring, perforation, endophthalmitis, visual loss
Conjunctivitis
- Pathophysiology
- Presentation
- Management
Bacterial
- purulent discharge, eyes ‘stuck together’ in morning, sore/gritty eyes, normally b/l
- chloramphenicol eye drops or fusidic acid eye drops (fusidic acid in pregnancy)
Gonococcal: rapid onset, copious discharge, chemosis, lid oedema - within days post-birth in neonates
–> PO + topical penicillin
Chlamydia: slow onset mild discomfort for weeks, red eye w/ scanty mucopurulent discharge + palpable preauricular node - in neonates 2/52 post birth
Adults –> topical erythromycin + GUM ref
Neonate -> topical erythromycin + paeds ref
Viral
- Serous discharge, recent URTI, preauricular lymph nodes
- Commonly adenovirus - self-limiting - manage w/ cold compress, strict hygeine - if corneal involvement (e.g. reduced VA) - topical steroids
- Herpes simplex conjunctivitis- normally unilateral + associated w/ cutaneous vesicles around eye
- Manage w/ topical aciclovir as 50% develop herpes simplex keratitis, can –> dendritic corneal ulcer. If presenting w/ ulcer give topical aciclovir AND immediate opthalmology ref
Allergic
- B/L erythema, itch +/- eyelid swelling
- 1st line: topical/systemic antihistamines
- 2nd: topical mast cell stabilisers e.g. sodium cromoglicate
Extra
- contact lens users should have fluoroscein to look for corneal staining/ulcers
Retinitis Pigmentosa
- Pathophysiology
- Presentation
- Investigation
- Management
Pathophysiology
- Inherited, chronic, degenerative disease of retina
- Photoreceptor cells affected 1st (rods, then cones) then other cell layers
- Can be in isolation of associated w/ weird conditions: Usher syndrome, Lawrence-Moon-Biedl syndrome, Alport’s
Presentation
- Typically in early adulthoood
- Nyaltopia (reduced vision in dim light)
- Tunnel vision
- Decreased VA
- Photophobia
- Photopsia
Investigation
- Fundoscopy: black bone spicule desposits in peripheral retina
-Electroretinography- reduced electrical response of light sensitive cells
- VF: progressive constriction
Management
- Supportive - genetic + psych counselling
- Visual impairment registration/low vision aids
- If macular oedema can give carbonic anhydrase inhibitors (topical dorzolamide or PO acetazolamide)
Uveitis = inflammation of the uveal tract (iris, ciliary body, choroid, retina)
Anterior Uveitis
- Pathophysiology
- Presentation
- Management
**Pathophysiology **
- Inflammation of iris +/- ciliary
- Associated conditions: those w/ HLA B27 - ankylosing spondylitis, juvenile idiopathic arterhitis, IBD, psoriatc arthritis, reactive arthritis
Presentation
- Irregular pupil
- Red eye (general or limbal)
- Ciliary flush - ring of redness spreading out
- Pain
- Photophobia
- Normal or blurred vision
- Anterior chamber inflammation -> hypopyon, cells + flare
Management
- Topic steroids e.g. dexamathason
- Dilate pupil w/ cyclopentolate (prevents synechiae formation + paralyses ciliary muscle to reduces pain)
- If raised IOP: B-blockers, PG analgoues, acetazolamide
- Refer ophthalmology
Posterior Uveitis
- Pathophysiology
- Presentation
- Management
Pathophysiology
- Inflammation of choroid, optic nerve head, retina (if choroid + retina = chorioretinitis)
- Causes: syphilis, CMV, toxoplasmosis, sarcoidossis, TB, HIV (always test for this)
Presentation
- Painless blurred vision
- Floaters
- Scotoma
- Blind spots in visual field
- Can -> severe visual loss
Management
Steroids -PO or injected
+/- biologics/immunosupressants long term
Diabetic Eye Disease
- Pathophysiology
- Presentation
- Investigation
- Management
Pathophysiology
- Hyperglycaemia -> increased retinal blood flow -> endothelial dysfunction, increased vasc permeability, retinal ischaemia
Classification
- Non-proliferative Diabetic Retinopathy
- Proliferative
- Maculopathy
Presentation
- Gradually worsening vision, floaters, blurred vision
Investigations
Non-proliferative:
- mild: 1+ microaneurysm
- Mod: microaneurysms, blot haemorrhages, hard exudate, soft exudates (cotton wool spots), venous beading
- Severe:
4 quadrants: blot haemorrhages + microaneurysms
2 quadrants: venous beading
1 quadrant: Intraretinal microvasc abnormalities (IRMA)
Proliferative:
- Retinal neovascularisation (can -> vitreous haemorrhage)
- Fibrous tissue ant. to retinal disc
- (more common in T1DM)
Maculopathy
- Based on location rather than severity
-more common in T2
Management
- All patients: optimise glycaemic control, BP, lipids + reg ophthalmology r/v
- Non-proliferative: reg observation
- Proliferative: panretinal laster photocoagulation (leaves all little yellow dots on retina after), intravitreal VEGF inhibitors, vitreoretinal surgery if severe/or vitreous haemorrhage
- Maculopathy: if any change in VA then intravitreal VEGF inhibitor
Central Retinal Vein Occlusion
Pathophysiology
Presentation
Investigation
Management
Pathophysiology
- thrombosis of central retinal vein - obstructs outflow -> rise in intravasc pressure
- more common than arterial occlusion
- Risk factors: age, HTN, CVS disease, DM, glaucoma, polycythemia, blood dyscrasia, vasculitis
Presentation
- profound, sudden, painless loss of vision
- In severe cases can get RAPD (suggests ischaemic variant)
Investigation
- severe retinal haemorrhage + widespread hyperaemia on fundoscopy
Management
- Manage underlying cause, most managed conservatively
- Refer to ophthalmology to monitor, can –>
- Macular oedema (intravitreal VEGF)
- Retinal neovascularisation (laser photocoagulation)
Central Retinal
Central Retinal Artery Occlusion
- Pathophysiology
- Presentation
- Investigation
- Management
Pathophysiology
- Most = thromboembolic atherosclerosis (e.g. diseased valves, arteritis (GCA) –> infarction of inner 2/3rd of retina
Presentation
- Sudden onset, painless, severe loss of vision
- RAPD normally present (unlike vein when it is rare)
Investigation
- Retinal oedema (pale) w/ cherry red spot at fovea
Management
- Ophthlamic emergency -> immediate ref
Management options:
- Treat underlying conditions
- Ocular massage + acetazolamide, poss intra-arterial thrombolysis
