Ophthalmology Flashcards
Glaucoma
a group of eye disease associated with acute or chronic damage to the optic nerve head with progressive loss of retinal ganglion feels & their axons leading to progressive visual field loss
one of the most common eye conditions
Types of glaucoma
open angle (90%)
angle-closure
Open angle glaucoma
generally bilateral progressive loss of optic nerve fibres with open chambre angles (ie the trabecular meshwork not obstructed) but obstructed & slowed drainage system outflow leads to ↑IOP (intraoccqular pressure)
most common form of glaucoma
prevalence ↑ with age
Risk factors for open angle glaucoma
↑ age Family history ↑ IOP (ocular hypertension) afro-carribbean race myopia (short-sightedness) HTN diabetes corticosteroids
Presentation of open angle glaucoma
vast majority of pts are asymptomatic
very insidious onset
may be detected at routine optometry appointment
↓visual acuity
bilateral peripheral visual field loss (nasal scotoma progressing to tunnel vision)
mild headaches
impaired adaption to darkness
NB pts often only notice visual loss once severe & permanent damage has occurred
Investigating open angle glaucoma
ophthalmoscopy (↑ cup-to-disc ratio, >0.7, disc cupping optic disc pallor, bayoneting of vessels, cup notching, disc haemorrhages)
slit lamp (normal appearing anterior chamber angle)
tonometry (↑IOP)
nerve fibre layer analysis (loss/thinning of nerve fibre layer)
Optical coherence tomography (OCT) & automated perimetry
Management of open angle glaucoma
Eye drops/pharmacological:
1st line: prostaglandin analogues e.g. latanoprost
Beta blockers e.g. timolol
Sympathomimetics e.g. brimodine
carbonic anhydrase inhibitors e.g. donzolamide
meiotic e.g. pilocarpine
laser treatment/surgery (considered in refractory cases)
Driving with open angle glaucoma
the pt must inform the DVLA who will asses pt to see if they are fit to continue driving
if pt does not inform DVLA despite clear advice you can break confidentiality & inform the DVLA in public interest but you are advised to inform the pt of your intentions to do so
Angle-closure glaucoma
a group of disease where there is a reversible (appositional) or adhesion (synechial) closure of the anterior chamber angle resulting in ↑ IOP
more common in females
Types of angle-closure glaucoma
Acute: rapid rise in IOP due to relatively sudden blockage of the trabecular meshwork by the iris via the pupillary block mechanism
chronic: may develop after acute form where synechial closure of the angle persists for it may develop over time as angle closes from prolonged/repetitive contact between peripheral iris & the trabecular meshwork
Risk factors for angle-closure glaucoma
female sex hyperopia (far-sightedness) southeast asian/inuit/asian heritage ↑ age family history mydriasis (e.g. drug induced via anticholinergics)
Presentation of angle closure glaucoma
chronic: similar to open-angle glaucoma
acute:
sudden onset unilateral reddened & severely painful eye
↓ visual acuity, blurred vision
coloured haloes around lights, symptoms worse in dark (due to mydriasis)
hard-red eye
corneal oedema (dull/hazy cornea)
non reactive mid dilated pupil
Investigating angle closure glaucoma
vision threatening emergency requiring emergency treatment as soon as clinically suspected
gonioscopy (trabecular meshwork not visible) slit lamp (shallow anterior chamber, signs of glaucoma e.g. large cup, nerve fibre loss) automatic static perimetry (visual field defect) tonometry (↑IOP, typically >40mmHg)
Treatment of angle closure glaucoma
Pharmacological :
1st line: IV acetazolamide + supine position + topicals (e.g. beta blockers (timolol), steroids (prednisolone), pilocarpine, phenylephrine)
definitive management:
surgery/laser treatment e.g. laser peripheral iridotomy or surgical iridotomy
Cataracts
an opacification of the crystalline lens due to protein aggregation, leading cause of visual impairment & blindness world wide
very common (>50% aged >65) more common in women
Aetiology of cataracts
congenital (<1%):
hereditary congenital cataracts associated with Trisomy 13/18/21, Marfan’s, Neurofibromatosis 2
acquired (>99%): age related (>90%), Diabetes, glucocorticoid use, eye infections
Presentation of cataracts
depend on size & location of opacity
gradual painless visual loss (blurred, cloudy, dim vision)
glare (associated with halos around lights)
washed out colour vision
grey/yellow/brownish clouding visible in lens
↓ red reflex
Investigations for cataracts
fundoscopy (normal fungus & optic nerve) slit lamp (visible cataract)
Management of cataracts
Early stages: conservative (not frequently used)
Cataract surgery (lens removal & replacement, most pts >60y/o)
Retinal detachement
typically a progressive condition in which the neuroretina separates (detaches) from the retinal pigment epithelium (RPE)
most retinal detachments are preceded by posterior virtuous detachment causing traction on the retina
incidence ↑ with age, average age of presentation ~40yrs
Risk factors for retinal detachment
myopia (↑ risk of posterior virtuous detachment)
Family history of retinal break/detachment
personal history or retinal break
Classification of retinal detachment
Rhegmatogenous RD:
most common, due to retinal break e.g. posterior vitreous detachment allowing retinal fluid formed y vitreous degeneration to seep in between RPE & neuroretina
Non-rhegmatogenous RD:
exudative: sub retinal fluid accumulation without retinal tears
tractional: uncommon, fibres in vitreous contract pulling retina away
Presentation of retinal detachment
Posterior vitrous detachment (PVD) as prodrome: floaters, flashes of light in vision, blurred vision, cobwebs across vision, dark curtain descending down vision
Weiss ring on ophthalmology
floaters, flashes of light (photopsia), scotoma, veil/curtain over vision
sudden painless visual loss
Investigations of retinal detachment
visual acuity (↓)
slit lamp (shows retinal detachment/defect)
indirect opthalmoscopy
USS or OCT