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
Management of retinal detachment
cryotherapy/laser photocoagulation (permanent adhesion of RPE & retina)
vitrectomy (removes traction)
pneumatic retinopexy
Central retinal artery occlusion
an ophthalmic emergency characterised by occlusion of the retinal artery essentially an ischaemic stroke of the eye
one of the more common causes of severe visual impairment in elderly pts
pts usually >60y/o, more common in men
Aetiology of Central retinal artery occlusion
thrombotic emboli from carotid artery atherosclerosis = most common
embolism
thrombosis
vasculitis
arteritis
Presentation of central retinal artery occlusion
sudden unilateral painless visual loss (mostly reduced to finger counting, often described as ascending curtain)
+
relative afferent pupil defect
history of amaurosis fugax (transient loss of vision i.e. angina of the eye)
if branches affected = scoots
Investigations of central retinal artery occlusion
ophthalmoscopy (greyish white retinal discolouration - pale), cherry red spot on macula, retinal plaques/emboli, segmentation of blood column in arteries)
Bruits over carotids (on carotid doppler)
ESR/CRP (to rule out temporal arteritis)
Management of central retinal artery occlusion
ophthalmologic emergency, must reperfuse tissue asap
firm ocular massage
artery dilation (sublingual nitrites, carbon therapy)
hyperbaric oxygen
Central retinal vein occlusion
an interruption of the normal venous drainage from the retinal tissue affecting either the central retinal vein or its branches
one of the most common causes of painless unilateral vision loss
usually seen in pts >65 yrs
more common than central retinal artery occlusion
Risk factors for central retinal vein occlusion
atherosclerosis HTN diabetes smoking cardiovascular disease glaucoma COCP use sickle cell disease ↑ age
presentation of central retinal vein occlusion
sudden reduction/loss of visual acuity (unilateral)
blurred vision
afferent pupillary defect
Investigations for central retinal vein occlusion
ophthalmoscopy (dot-and-blot and/or flame haemorrhages in all 4 quadrants, cotton wool spots, macular oedema, papilloedema, venous dilation & tortiosity)
fluorescin angiography (to differentiate ischaemic & non ischaemic)
OCT (macular oedema)
Management of central retinal vein occlusion
emergency opthalmic presentation
pan retinal photocoagulation (prevents neovascularisation) ± intravitreal anti-VEGF agents
Diabetic retinopathy
the retinal consequence of chronic progressive diabetic microvascular leakage & occlusion, a potentially sight threatening disease, almost all diabetic pts well develop some degree of retinopathy
most common cause of blindness in those aged 35-65
Presentation of diabetic retinopathy
generally asymptomatic until late stages
progressive blindness & visual impairment (gradual)
Ophthalmological finding for non proliferative diabetic retinopathy
most common form of diabetic retinopathy
intraretinal microvascular abnormalities, micro aneurysms, intraretinal haemorrhage, hard exudates, cotton wool spots, retinal oedema, dot-and-blot haemorrhages
Ophthalmological finding for proliferative diabetic retinopathy
pre retinal neovascularisation, vitreous haemorrhages, plus finding of non proliferative retinopathy
Ophthalmological finding for diabetic maculopathy
macula oedema, dot haemorrhages, macular ischaemia, hard exudates on macula
more common in T2DM
Investigating diabetic retinopathy
OCT (for macula oedema)
generally fundoscopy sufficient
Management of diabetic retinopathy
improved diabetic control
intravitreal anti-VEGF injections
pan retinal photocoagulation / focal photocoagulation
Vitreous haemorrhage
extravasation of blood in & around the vitreous body, one of the most common causes of painless visual loss
caused include proliferative diabetic retinopathy (accents for ~50% of cases), posterior vitreous detachment, ocular trauma, retinal vein occlusion
Risk factors for vitreous haemorrhage
neovascularisation
trauma
anticoagulants/antiplatelets
high myopia
Presentation of vitreous haemorrhage
sudden onset of unilateral painless visual loss
red-hue to vision (haze may turn green as Hb breaks down)
floaters & cobwebs
symptoms generally worse in mornings
Investigations of vitreous haemorrhage
slit lamp (RBCs in anterior vitreous) dilated fundoscopy (haemorrhage in vitreous cavity)
fluorescein angiography (to identify neovascularisation)
USS (to rule out retinal tear/detachement)
OCT
Management of vitreous haemorrhage
observation (haemorrhage may resolve spontaneous)
treat underlying cause
photocoagulation (for vitreous tears & neovascularisation)
Macular degeneration/age related macular degeneration
potentially progressive maculopathy i.e. progressive degenerative changes of the macula,
most common cause of blindness in the UK
Types of age related macular degeneration (AMD)
Dry AMD: (~90%)
also referred to as non-exudative
characterised by drusens (yellow round spots), on retinal pigment epithelium (RPE) + hyper/hypopigmentation of RPE
gradual progression of visual loss
Wet AMD (~10%) also referred as exudative/neovascular characterised by choroidal neovascularisation with leakage of serous fluid & blood between RPE & Bruch's membrane leads to sudden or rapid visual loss worse prognosis
Risk factors of age related macular degeneration (AMD)
↑ age smoking family history of AMD obesity caucasian ethnicity cardiovascular disease risk factors (HTN, Diabetes, dyslipidaemia)
Presentation of age related macular degeneration (AMD)
painless central/pericentral visual impairement (dry: usually over years/decades, wet: acute/weeks to months)
scotomas
loss/↓ contrast sensitivity
photopsia
Investigations/examinations age related macular degeneration (AMD)
Ampler grid (focal area of distortion) OCT (intra/subretinal fluid, RPE detachement/loss) fluorescein angiography ( to identify neovascularisation) fundoscopy (dry: drusens, RPE atrophy/hypertrophy) (wet: sub/intraretinal haemorrhage/exudate, scarring, retinal discolouration)
Management of dry age related macular degeneration (AMD)
lifestyle modifications pt education & advice dietary supplements smoking cessation must inform DVLA
Management of wet age related macular degeneration (AMD)
1st line: anti-VEGF injections e.g. ranibizumab
2nd line: laser photocoagulation
Giant cell arteritis
type of autoimmune vasculitis causing chronic inflammation of large & medium sized arteries particularly the carotids and its major branches (common carotid, ICA, ECA)
most common form of systemic vasculitis in adults
2-3x more common in females, usually aged >50 yrs
Presentation of giant cell arteritis
recent onset temporal headaches, myalgia, malaise, fever jaw claudication scalp tenderness on palpation double vision/blurred vision visual loss (scotoma, amaurosis fungal)
Investigations for giant cell arteritis
CRP/ESR (↑) FBC (normochromic normocytic anaemia) LFTs (mildly ↑ ALP & AST/ALT) temporal artery biopsy (gold standard) temporal artery USS
Management of giant cell arteritis
high dose corticosteroids (can be given even if negative’ biopsy if high suspicion due to skip lesions)
low dose aspirin
NB visual loss often irreversible
Conjunctivitis (pink eye)
inflammation of the conjunctiva (the lining of the eyelids & eyeball) caused by bacteria/viruses/allergies/immunological reactions/mechanical irritation
if corneal involvement: keratoconjunctivitis
Presentation of conjunctivitis
conjunctival injections (conjunctival hyperaemia with blood vessel dilation = ocular hyperaemia & reddening)
discharge & crust formation
chemises (oedema of eyelids and/or conjunctiva)
photophobia
itching (mainly in allergic types)
Viral conjunctivitis
most common type of conjunctivitis usually caused by adenovirus
presents with unilateral symptoms but quickly spreads bilaterally
clear watery discharge, ↑ lacrimation
normal vision
often recent history of URTI
mangement:
supportive (cold compresses, lubricants) topical steroids if adenospots, topical antiviral e.g. ganciclovir if HSV