content Flashcards
definition of glaucoma
optic nerve damage due to a significant rise in intraocular pressure caused by a blockage in aqueous humour trying to escape the eye
anatomy of the chambers of the eye
- anterior = between cornea and iris
- posterior = between iris and lens
- vitreous = between lens and optic nerve
normal intraocular pressure
10-21mmHg
anatomy of the aqueous humour in the eye
- produced by ciliary body
- flows around lens and under iris, through anterior chamber and through trabecular meshwork into the canal of schlemm
- then enters general circulation
pathophysiology of open-angle glaucoma
gradual increase in resistance through trabecular meshwork making it more difficult for aqueous humour to flow through and exit the eye
-> slow and chronic onset of glaucoma
pathophysiology of acute angle-closure glaucoma
iris bulges forward and seals off trabecular meshwork from the anterior chamber, preventing aqueous humour being able to drain away
-> continual build-up of pressure = emergency
ophthalmoscopy finding in glaucoma
cupping of the optic disc (centre of the normal optic disc usually <1/2 size of disc but pressure on eye in glaucoma causes it to increase to >1/2 size)
risk factors for open-angle glaucoma
- increasing age
- FHx
- Black ethnic origin
- nearsightedness (myopia)
presentation of open-angle glaucoma
- may be picked up on routine screening
- gradual loss of peripheral vision -> tunnel vision
- gradual onset of fluctuating pain, headaches, blurred vision and halos around lights
how to measure intraocular pressure
- non-contact tonometry -> puff of air at cornea and measuring corneal response
- golwmann applanation tonometry -> contact with cornea and apply different pressures
diagnosis of glaucoma ix
- goldmann applanation tonometry
- fundoscopy
- visual field assessment
medical management of open-angle glaucoma
aim to reduce pressure
- prostaglandin analogue eye drops (latanoprost) increase uveoscleral outflow
- beta-blockers to reduce production of aqueous humour
- carbonic anhydrase inhibitors reduce production
- sympathomimetics reduce production and increase outflow
when to treat open-angle glaucoma
pressure of 24mmHg or above
surgical management of open-angle glaucoma
trabeculectomy -> creating new channel from anterior chamber, through sclera to location under conjunctiva
produces ‘bleb’ where aqueous humour drains
risk factors for closed-angle glaucoma
- increasing age
- female: male = 4:1
- FHx
- Chinese and East Asian (rare in Black ethnic origin)
- shallow anterior chamber
medications which can precipitate angle-closure glaucoma
- adrenergic meds e.g. noradrenaline
- anticholinergic meds e.g. oxybutynin
- tricyclic antidepressants e.g. amitriptyline
presentation of angle-closure glaucoma
- generally unwell
- severely painful red eye
- blurred vision
- halos around lights
- associated headache, nausea and vomiting
examination findings in angle-closure glaucoma
- red eye
- teary
- hazy cornea
- decreased visual acuity
- dilation of affected pupil
- fixed pupil size
- firm eyeball on palpation
initial mx of angle-closure glaucoma in primary care
- lie patient on their back without a pillow
- pilocarpine eye drops: 2% for blue eyes, 4% for brown eyes (mitotic agent)
- acetazolamide 500mg PO
- analgesia and antiemetic if required
secondary care medical mx of angle-closure glaucoma
- pilocarpine
- acetazolamide
- hyperosmotic agents e.g. glycerol, mannitol
- timolol
- dorzolamide
- sympathomimetics
definitive tx of angle-closure glaucoma
laser iridectomy -> laser to make hole in iris to allow aqueous humour to flow from posterior chamber into anterior chamber
definition of age-related macular degeneration
degeneration in macular causing progressive deterioration in vision
types of macular degeneration
wet (10%) -> worse prognosis
dry (90%)
key finding on fundoscopy in macular degeneration
drusen = yellow deposits of proteins and lipids appear between retinal pigment epithelium and Bruch’s membrane
features of both types of macular degeneration
- drusen on fundoscopy
- atrophy of retinal pigment epithelium
- degeneration of photoreceptors
pathophysiology of wet macular degeneration
- development of new vessels growing from choroid layer into retina
- vessels leak fluid or blood and cause oedema and more rapid loss of vision
- chemical stimulating vessel development = vascular endothelial growth factor (VEGF)
risk factors for macular degeneration
- age
- smoking
- white or Chinese ethnic origin
- FHx
- CVD
presentation of macular degeneration
- gradual worsening central visual field loss
- reduced visual acuity
- crooked/wavy appearance to straight lines
examinations in suspected macular degeneration
- snellen chart (reduced acuity)
- scotoma (central patchy of vision loss)
- amsler grid test (distortion of straight lines)
- fundoscopy (drusen)
ix in suspected macular degeneration
- slit-lamp biomicroscopic fundus exam
- optical coherence tomography
- fluorescein angiography (see blood supply to retina)
mx of dry macular degeneration
lifestyle measures to slow progression:
- avoid smoking
- control BP
- vitamin supplementation
mx of wet macular degeneration
- anti-VEGF (vascular endothelial growth factor) e.g. ranibizumab, bevacizumab, pegaptanib
- injected directly into vitreous chamber once a month
- slow and even reverse progression by blocked neovascularization
definition of diabetic retinopathy
blood vessels in the retina are damaged by prolonged exposure to hyperglycaemia
pathophysiology of diabetic retinopathy
hyperglycaemia causes damage to retina small vessels and endothelial cells
increased vascular permeability leaks to leakage, blot haemorrhages and formation of hard exudates
what are cotton wool spots
fluffy white patches on the retina due to damaged nerve fibres e.g. diabetic or hypertensive retinopathy
fundoscopy findings in proliferative diabetic retinopathy
- cotton wool spots
- microaneurysms
- hard exudates
- blot haemorrhages
- neovascularization
classification of diabetic retinopathy
non-proliferative:
- mild: microaneurysms
- moderate: microaneurysms, blot haemorrhages, hard exudates, cotton wool spots and venous beading
- severe: blot haemorrhages and microaneurysms in 4 quadrants, venous beading in 2 quadrants, intraretinal microvascular abnormality
proliferative:
- neovascularization
- vitreous haemorrhage
complications of diabetic retinopathy
- retinal detachment
- vitreous haemorrhage
- rebeosis iridis (blood vessel formation in iris)
- optic neuropathy
- cataracts
mx of diabetic retinopathy
- laser photocoagulation
- anti-VEGF
- vitreoretinal surgery
definition of hypertensive retinopathy
damage to small blood vessels in the retina relating to systemic hypertension (either chronic or malignant hypertension)
fundoscopy findings in hypertensive retinopathy
- cotton wool spots
- silver wiring
- hard exudates
- arteriovenous nipping
- retinal haemorrhages
- papilloedema
classification of hypertensive retinopathy
Keith-Wagener classification
- stage 1 = mild narrowing of arterioles
- stage 2 = focal constriction of blood vessels and AV nipping
- stage 3 = cotton wool patches, exudates and haemorrhages
- stage 4 = papilloedema
mx of hypertensive retinopathy
control BP and other risk factors such as smoking and lipid levels
definition of cataracts
lens in the eye becomes cloudy and opaque leading to reduced visual acuity
risk factors for cataracts
- increasing age
- smoking
- alcohol
- diabetes
- steroids
- hypocalcaemia
presentation of cataracts
symptoms usually asymmetrical
- very slow reduction in vision
- progressive blurring
- change of colour vision (become more brown)
- starbursts appear around lights
mx of cataracts
- no intervention if manageable symptoms
- cataract surgery -> drilling and breaking lens into pieces and replacing with artificial lens
complication of cataract surgery
endophthalmitis -> inflammation of inner contents of the eye, usually caused by infection
can lead to loss of vision and loss of the eye itself
mechanism of pupil constriction
circular muscles in the iris cause constriction via stimulation by parasympathetic nerves (CN III) using ACh
mechanism of pupil dilation
dilator muscles stimulated by sympathetic nervous system using adrenaline
causes of mydriasis (dilated pupil)
- CN III palsy
- raised ICP
- congenital
- trauma
- stimulants such as cocaine
- anticholinergics
causes of miosis (constricted pupil)
- Horners syndrome
- cluster headaches
- opiates
- nicotine
- pilocarpine
presentation of third nerve palsy
- ptosis (drooping of upper eyelid)
- dilated, non-reactive pupil
- divergent strabismus (squint) causing down and out position of eye
causes of third nerve palsy
- idiopathic
- tumour
- trauma
- cavernous sinus thrombosis
- posterior communicating artery aneurysm
- raised ICP
what is a partial third nerve palsy
sparing of the pupil -> indicates microvascular cause as the parasympathetic fibres are spared
may be due to: diabetes, hypertension, ischaemia
triad of horners syndrome
- ptosis
- miosis
- anhidrosis
may be enopthalmos (sunken eye)
anatomy of sympathetic nerves to the face
- arise from spinal cord in the chest (pre-ganglionic)
- enter sympathetic ganglion at base of neck and exit as post-ganglionic
- post-ganglionic travel to the head alongside internal carotid artery
how to differentiate between pre-ganglionic, central and post-ganglionic causes of horners syndrome
central lesions cause anhidrosis of arm and trunk as well as face
pre-ganglionic lesions cause anhidrosis of only the face
post-ganglionic lesions cause no anhidrosis
causes of horners syndrome and mnemonic
4 Ss (Sentral), 4 Ts (Torso - pre-ganglionic), 4 Cs (Cervical - post-ganglionic)
- S = stroke, mS, swelling (tumour), syringomyelia
- T = tumour (pancoast), trauma, thyroidectomy, top rib (cervical rib)
- C = carotid aneurysm, carotid artery dissection, cavernous sinus thrombosis, cluster headache