Ophthalmology Flashcards
What is glaucoma
optic nerve damage caused by a significant rise inintraocular pressure
What is the normal range of intraocular pressure
10-21 mmHg
Describe the flow of aqueous humour
The aqueous humour is produced by the ciliary body. The aqueous humour flows from the ciliary body, around the lens and under the iris, through the anterior chamber, through the trabecular meshwork and into the canal of Schlemm. From the canal of Schlemm it eventually enters the general circulation.
What creates intraocular pressure
the resistance to flow through the trabecular meshwork into the canal of Schlemm
Pathophysiology of open-angle glaucoma
gradual increase in resistance through the trabecular meshwork -> more difficult for aqueous humour to flow through the meshwork -> pressure slowly builds within the eye and this gives a slow and chronic onset of glaucoma
Effect of raised intraocular pressure on optic disk
Increased pressure in the eye causes cupping of the optic disc (indent becomes wider and deeper)
Risk factors of open-angle glaucoma
Increasing age
Family history
Black ethnic origin
Nearsightedness (myopia)
Presentation of open-angle glaucoma
The rise in pressure is often asymptomatic
As glaucoma worsens the peripheral vision gradually closes in (tunnel vision)
Can present with gradual onset of fluctuating pain, headaches, blurred vision and halos appearing around lights, particularly at night time
How is intraocular pressure measured
Non-contact tonometry commonly used
Goldmann applanation tonometry is the gold standard
Investigations to diagnose glaucoma
Goldmann applanation tonometry/ non-contact tonometry can be used to check the intraocular pressure
Fundoscopy assessment to check for optic disc cupping and optic nerve health.
Visual field assessment to check for peripheral vision loss.
Management of open-angle glaucoma
1st line: Prostaglandin analogue eye drops (e.g. latanoprost) - increase uveoscleral outflow
Beta-blockers (e.g. timolol) reduce the production of aqueous humour
Carbonic anhydrase inhibitors (e.g. dorzolamide) reduce the production of aqueous humour
Sympathomimetics (e.g. brimonidine) reduce the production of aqueous fluid and increase uveoscleral outflow
If medical mx fails: trabeculectomy surgery
Pathophysiology of acute closed-angle glaucoma
the iris bulges forward and seals off the trabecular meshwork from the anterior chamber preventing aqueous humour from being able to drain away -> continual build-up of pressure in the eye -> pressure builds up particularly in the posterior chamber, which causes pressure behind the iris and worsens the closure of the angle
Risk factors of closed-angle glaucoma
Increasing age
Females are affected around 4 times more often than males
Family history
Chinese and East Asian ethnic origin. Unlike open-angle glaucoma, it is rare in people of black ethnic origin.
Shallow anterior chamber
Medications that precipitate closed-angle glaucoma
Adrenergic medications such as noradrenalin
Anticholinergic medications such as oxybutynin and solifenacin
Tricyclic antidepressants such as amitriptyline, which have anticholinergic effects
Closed-angle glaucoma: presentation
Short history of:
Feeling unwell in themselves
Severely painful red eye
Blurred vision
Halos around lights
Associated headache, nausea and vomiting
Closed angle glaucoma: examination
Red-eye
Teary
Hazy cornea
Decreased visual acuity
Dilatation of the affected pupil
Fixed pupil size
Firm eyeball on palpation
Closed-angle glaucoma: initial mx
same-day assessment by an ophthalmologist, while waiting:
Lie patient on their back without a pillow
Give pilocarpine eye drops (2% for blue, 4% for brown eyes)
Give acetazolamide 500 mg orally
Given analgesia and an antiemetic if required
Closed-angle glaucoma: secondary care mx
Pilocarpine - constricts pupil, opens up flow pathway
Acetazolamide (oral or IV)
Hyperosmotic agents such as glycerol or mannitol increase the osmotic gradient between the blood and the fluid in the eye
Timolol is a beta-blocker that reduces the production of aqueous humour
Dorzolamide is a carbonic anhydrase inhibitor that reduces the production of aqueous humour
Brimonidine is a sympathomimetic that reduces the production of aqueous fluid and increase uveoscleral outflow
Definitive mx: laser iridotomy
Age-related macular degeneration: definition
degeneration in the macula that cause a progressive deterioration in vision
Age-related macular degeneration: types
90% of cases are dry and 10% are wet. Wet age-related macular degeneration carries a worse prognosis
Age-related macular degeneration: common findings
Larger/ greater numbers of Drusen
Atrophy of the retinal pigment epithelium
Degeneration of the photoreceptors
Age-related macular degeneration: wet pathophysiology
development of new vessels growing from the choroid layer into the retina
These vessels can leak fluid or blood and cause oedema and more rapid loss of vision
key chemical that stimulates the development of new vessels is vascular endothelial growth factor (VEGF) and this is the target of medications to treat wet AMD
Age-related macular degeneration: risk factors
- Age
- Smoking
- White or Chinese ethnic origin
- Family history
- Cardiovascular disease
Age-related macular degeneration: presentation
- Gradual worsening central visual field loss
- Reduced visual acuity
- Crooked or wavy appearance to straight lines
- Wet presents more acutely - loss of vision over days and progress to full loss of vision over 2-3 years, often progresses to bilateral disease
Age-related macular degeneration: examination
- Reduced acuity using a Snellen chart
- Scotoma (a central patch of vision loss)
- Amsler grid test can be used to assess the distortion of straight lines
- Fundoscopy. Drusen are the key finding
- Slit-lamp biomicroscopic fundus examination by a specialist can be used to diagnose AMD
- Optical coherence tomography to diagnose AMD
- Fluorescein angiography to show up any oedema and neovascularisation - used if OCT is inconclusive
Age-related macular degeneration: dry mx
- no specific tx
- lifestyle changes to slow progression (smoking, BP, vitamins)
Age-related macular degeneration: wet mx
- Anti-VEGF medications - Vascular endothelial growth factor is involved in the development of new blood vessels in the retina
- ranibizumab, bevacizumab and pegaptanib
- injected directly into the vitreous chamber of the eye once a month
- can slow and even reverse the progression of the disease
- typically need to be started within 3 months to be beneficial
Diabetic retinopathy: definition
blood vessels in the retina are damaged by prolonged exposure to high blood sugar levels (hyperglycaemia) causing a progressive deterioration in the health of the retina
Diabetic retinopathy: pathophysiology
- Hyperglycaemia leads to damage to the retinal small vessels and endothelial cells -> Increased vascular permeability -> leakage from the blood vessels, blot haemorrhages and the formation of hard exudates (lipid deposits)
- Microaneurysms - weakness in the wall causes small bulges
- Venous beading - walls of the veins are no longer straight and parallel and look more like a string of beads or sausages
- **Damage to retinal nerve fibres **- fluffy white patches form on the retina (cotton wool spots)
* Intraretinal microvascular abnormalities (IMRA) - dilated and tortuous capillaries in the retina that can act as arteriovenous shunts - Neovascularisation - growth factors are released in the retina causing the development of new blood vessels
Diabetic retinopathy: classification
- non-proliferative and proliferative depending on whether new blood vessels have developed
- Non-proliferative (background or pre-proliferative) can develop in to proliferative retinopathy
- classified based on the findings on fundus examination
Diabetic retinopathy: features
non-proliferative
- Mild: microaneurysms
- Moderate: microaneurysms, blot haemorhages, hard exudates, cotton wool spots and venous beading
- Severe: blot haemorrhages plus microaneurysms in 4 quadrants, venous beading in 2 quadrates, intraretinal microvascular abnormality (IMRA) in any quadrant
Diabetic retinopathy: features
proliferative
- Neovascularisation
- Vitreous haemorrhage
Diabetic Maculopathy: features
- Macular oedema
- Ischaemic maculopathy
Diabetic Retinopathy: complications
- Retinal detachment
- Vitreous haemorrhage (bleeding in to the vitreous humour)
- Rebeosis iridis (new blood vessel formation in the iris)
- Optic neuropathy
- Cataracts
Diabetic Retinopathy: mx
* Laser photocoagulation
* Anti-VEGF medications such as ranibizumab and bevacizumab
* **Vitreoretinal surgery **(keyhole surgery on the eye) may be required in severe disease
Hypertensive retinopathy: definition
the damage to the small blood vessels in the retina relating to systemic hypertension
can be the result of years of chronic hypertension or can develop quickly in response to malignant hypertension.
Hypertensive retinopathy: findings
Silver wiring or copper wiring - the walls of the arterioles become thickened and sclerosed causing increased reflection of the light.
Arteriovenous nipping - the arterioles cause compression of the veins where they cross. This is again due to sclerosis and hardening of the arterioles.
Cotton wool spots -caused by ischaemia and infarction in the retina causing damage to nerve fibres.
Hard exudates - caused by damaged vessels leaking lipids into the retina.
**Retinal haemorrhages ** - caused by damaged vessels rupturing and releasing blood into the retina.
Papilloedema - caused by ischaemia to the optic nerve resulting in optic nerve swelling (oedema) and blurring of the disc margins.
Hypertensive retinopathy: classification
Keith-Wagener Classification
Stage 1: Mild narrowing of the arterioles
Stage 2: Focal constriction of blood vessels and AV nicking
Stage 3: Cotton-wool patches, exudates and haemorrhages
Stage 4: Papilloedema
Hypertensive retinopathy: mx
Management is focused on controlling the blood pressure and other risk factors such as smoking and blood lipid levels.
