Opthamology Flashcards
How is aqueous humour produced and how does it drain
Aqueous humour is produced by ciliary bodies behind the iris. It flow through the lens to the anterior chamber and drains through the trabecular network between the iris and cornea via the canal of schlemm.
What is the pathophysiology of acute -closed angle glaucoma
Blocked drainage of the aqueous humour from the anterior chamber via the canal of schlemm causing a sudden increase in intra-occular pressure.
What is the pathophysiology of chronic- open angle glaucoma
Slow blockage of the drainage of the aqueous fluid - causing a gradual increase in intra-ocular pressure.
Risk factors for acute-closed angle glaucoma
- hypermetropia
- shallow anterior chamber
- female
- FH
- > 50 y/o
- Drugs –> anti-cholinergics; sympathomimetics; TCA’s; anti-histamines
Risk factors for chronic-open angle glaucoma
- Myopia
- DM/HTN/ Migraine
- FH
- African/asian
- increasing age
- systemic steroids
- ocular hypertension (increased IOP on 2 occasions - monitor every 6-12m)
Compare the presentation of closed v open angle glaucoma
CLOSED
- sudden onset
- prodrome (rainbow haloes around lights at night)
- severe deep, boring pain
- +- n&v +- headache
- reduced acuity and blurred vision
- fixed, dilated, irregular pupil
- eye feels hard +- red eye
OPEN
- can be asymptomatic
- peripheral visual field defect (superior nasal first) - see as parts of page missing
- central field intact until optic nerve damage is irreversible
Investigations for glaucoma
- Tonometry –> (>21 for open; can be >40 for closed)
(thick cornea affects reading) - slit lamp - OPEN (cup:disc ration increased); CLOSED (corneal oedema; iris atrophy)
- Gonioscopy - shows whether open/closed angle
- fundoscopy - CLOSED (cloudy cornea +- circumcorneal injection); OPEN (cupping of optic disc)
- Visual field assessment/OCT for OPEN
Management of acute - closed angle glaucoma
- refer urgently to ophthalmology
- pilocarpine 2-4% - drops stat (miosis opens blockage)
- topical BB (timolol - to reduce aq. formation)
- acetazolamide IV (500mg STAT)
- analgesia +- anti-emetics
Once reduced IOP-> bilateral peripheral iridotomy
OR surgical iridectomy/lensectomy
Management of chronic open-angle glaucoma
- life-long mx; INFORM DVLA
- control of conditions e.g. DM/HTN
Medical - eyedrops
1) timolol
2) Latanoprost
3) brimonidine
4) dorzolamide/ acetazolamide (PO)
5) pilocarpine
Surgical - laser trabeculoplasty
- trabeculectomy (create new channel to increase drainage)
- artificial shunt
Eye drops available for use in glaucoma, MOA, S.E & CI
1) BB (timolol)
MOA - I. adrenoreceptors in ciliary body to reduce aq. production
S.E - irritation, dry eyes, bronchospasm
CI - asthma, HF, bradycardia
2) PG analogue (Latanoprost)
MOA - increase uveroscleral outflow
S.E - uveitis, photophobia, bradycardia, increased eyelash length, iris and periocualr pigmentation
CI - Pregnancy, acute uveitis
3) a-agonist (brimonidine)
MOA - reduced aq. production and increases uveroscleral outflow
S.E - dizzy, dry mouth, headache, red eye, skin reactions
CI - raynaud’s, CVD
4) Carbonic anhydrase I (Dorzolamide - drops; acetazolamide PO)
MOA - reduces aq. secretion
SE - uveitis, headaches
CI - renal/hepatic impairment
5) Miotics (pilocarpine)
MOA - contract ciliary muscles to open drainage ch.
SE - eye pain, bradycardia
CI - uveitis
S.E of trabeculectomy and how to prevent it
- reduces IOP - can cause retinal damage (contact lenses reduce leakage)
Complications of glaucoma
- loss of vision
- retinal A/V occlusion
- affects other eye
Presentation of conjunctivitis
Often bilateral; purulent discharge - Bacterial: sticky; crusty lid - Viral: watery, no itch - allergic: watery, itcy, lid swelling Discomfort Conjunctival injection (Vessels moved over sclera) Acuity, pupil responses and cornea are unaffected. blurring of vision - clears when blink if cornea involved - photophobia red eye
Risk factors for conjunctivitis
- contact exposure
- contact lenses
- trauma
- chemical/UV exposure
- AI disease
- Allergies
Causes of conjunctivitis
Viral: adenovirus; HSV
Bacterial: s.aureus, step, haemophilus, chlamydia, gonococcus
Allergic - hayfever (may - aug); dust allergy (worse in AM)
Ix for conjunctivitis
- O/E - papillae (allerguy); follice formation (viral)
- measure visual acuity)
- ?swab
- inflamed LN (viral)
Rx of conjunctivitis
ALL –> no contact lenses, lid hygiene 3 x d
Bacterial: chloramphenicol 0.5% ointment (can return to school 24h after starting)
Allergic: anti-histamine drops: e.g. emedastine (or PO) allergen avoidance; cold compress; sodium cromoglycate (mast cell stabiliser); severe -steroids
Viral - self-limiting
What is giant papillary conjunctivitis and its rx
- conjunctivitis caused by iatrogenic FB (contact lenses, prostheses, sutures)
- shows giant papillae on tarsal conjunctivae
Rx - remove FB; cromoglycate
Vernal keratoconjunctivitis - presentation and rx
- in male children with a hx of atopy
- itchy, photophobia, lacrimation, papillary conjunctivitis on upper tarsal plate (giant cobblestones), limbal follicles and white spots, punctate lesions on corneal epithelium.
SEVERE - opaque oval plaque replacing upper zone of corneal epi
Rx - olopatadine (Anti-hist + mast cell stab)
What is contact dermatoconjunctivitis
- allergic conjunctivitis caused by eyedrops/ cosmetics
- np response to anti-hist/mast cell stab
What is the pathophysiology of retinal detachment
Holes/tears in retina allow fluid to separate sensory retina from retinal pigmented epithelium
Causes of retinal detachment and risk factors
- MAIN - pre-existing posterior vitreous detachment causing traction on retina –> adhesions –> tears
- secondary to retinal surgery, trauma, DM/HTN,
Other risks –> myopia, FH, previous PVD< glaucoma, ca/inflamm eye disease
Presentation of retinal detachment
4 F’s Floaters: numerous, acute onset, “spiders-web” Flashes (photopsia) Field loss (curtain) Fall in acuity (macular involved) Painless
Presentation of Posterior vitreous detachment
- monochromatic photpsia in peripheral temporal field
- no change in vision yet
Ix for retinal detachment
- visual acuity (reduced when macula involed - +- vitreous haemmorrhage)
- visual fields (defect correlates to detached area)
- pupil reflexes (RAPD if involved macula)
- slit-lamp (visualise detachment +- tears)
- OCT - access extent
- fundoscopy - grey, opalescent retina, ballooning forward
Rx for retinal detachment
If macula still intact can save vision - if exudate - ix cause > Urgent surgery - Vitrectomy + gas tamponade +- laser coagulation to secure the retina - early tears can seal with laser/cryo - restrict head movements POST -OP - abx and steroids
Differentials of transient visual loss
Vascular: TIA, migraine MS Subacute glaucoma Papilloedema optic neuritis
Pathophysiology of vitreous haemorrhage
- small extravasations of blood which produce vitreous floaters can be from new vessels (DM) or retinal detachment/ tears/trauma
Presentation of vitreous haemorrhage
Small bleeds → small black dots / ring floaters
Large bleed can obscure vision → no red reflex, retina can’t be visualised
Ix and Mx of vitreous haemorrhage
Ix - B scan US to identify cause
Mx -VH undergoes spontaneous absorption
Vitrectomy may be performed in dense VH
Risk factors for age-related macular degeneration
Smoking ↑age Genetic factors/FH hx cataract surgery CVD/HTN ethnicity
Dry v WET ARMD
Dry (Geographic Atrophy)
Drusen: fluffy white spots around macula
Degeneration of macula (changed to retinal pigmented epi)
Slow visual decline over 1-2yrs - difficulty reading
Wet ( Subretinal Neovascularisation)
Aberrant vessels grow into retina from choroid and → haemorrhage (via VEGF)
Rapid visual decline (sudden / days / wks) - distortion
Fundoscopy shows macular haemorrhage → scarring –> central vision loss
Amsler grid detects distortion
Presentation of ARMD
Elderly pts. Central visual loss reduced contract sensitivity (abnormal dark adaptation) reduced acuity ?photopsia
Ix of ARMD
OCT (optical coherence tomography)
- Gives high resolution images of the retina
- Wet –> (subretinal and intra-retinal oedema)
- dry –> (drusen, geographic atrophy)
Visual acuity
fundoscopy - drusen, scars, bleeds
Amsler grid - distortion in wet
fluroscein angiography (inject to visualise vasculature) - wet allows to assess for neovascularisation and haemorrhages
Mx of ARMD
smoking cessation, inform DVLA, visual rehab, regular check-ups, correct other optic illness and risk factors
- Antioxidant vitamins (C,E) + zinc may help early ARMD
Wet --> anti-VEGF injections (avastatin/lucentis) - monthly for 3m intravitreally (reduces neovascularisation SE - endophthalmitis OR photodynamic therapy (destroys neovac membrane)
Eye conditions associated with DM
- cataracts (lens absorbs glucose and converts to sorbitol via aldose reductase)
- glaucoma
- occular motos nerve palsy (CN 3&6)
- diabetic retinopathy
Pathogenesis of diabetic retinopathy
Microangiopathy (narrowing A) → occlusion
Occlusion → ischaemia → new vessel formation in retina
Bleed → vitreous haemorrhage
Carry fibrous tissue ̄c them → retinal detachment
Occlusion also → cotton wool spots (ischaemia)
Vascular leakage → oedema and lipid exudates
Rupture of microaneurysms → blot haemorrhage
Screening for eye disease in DM
All diabetics should be screened annually (in T1DM for 12 y/o)
Fundus photography
Refer those with maculopathy, NPDR and PDR to ophthalmologist
30% NPDR develop PDR in 1yr
Ix for diabetic retinopathy
Fluorescein angiograph
Visual acuity
slit lamp/ fundoscopy
OCT (macula oedema?_
Mx of diabetic retinopathy
Good BP and glycaemic control
Rx concurrent disease: HTN, dyslipidaemia, renal disease, smoking, anaemia
Laser photocoagulation
- Maculopathy: focal or grid
- Proliferative disease: pan-retinal (macula spared)
+- IV triamcinolone and anti-VEGF if macular oedema
vitrectomy if vitreous haemorrhage
- if proliferative left untreated would lose vision in 2 years
Grading of diabetic retinopathy
Background Retinopathy: Leakage
Dots: microaneurysms
Blot haemorrhages
Hard exudates: yellow lipid patches
Pre-proliferative Retinopathy: Ischaemia Cotton-wool spots (infarcts) Venous beading Dark Haemorrhages Intra-retinal microvascular abnormalities
Proliferative Retinopathy
New vessels
Pre-retinal or vitreous haemorrhage
Retinal detachment
Maculopathy
Caused by macular oedema
↓ acuity may be only sign
Hard exudates w/i one disc width of macula
feature of horner’s syndrome
Ptosis (partial)
Miosis
Anhidrosis
+- Enophthalmos
Causes of horners syndrome
Central
MS; stroke; syringomyelia
Pre-ganglionic (neck)
Tumour: (pancoast)T1 nerve root lesion
Trauma: CVA insertion or CEA
Thyroidectomy
Post-ganglionic Cavernous sinus thrombosis (2O to spreading facial infection via the ophthalmic vein) CN 3, 4, 5, 6 palsies Carotid A dissection
What is an argyll robertson pupil
Small, irregular pupils
Accommodate but doesn’t react to light
Atrophied and depigmented iris
Causes –> DM/ syphilis