Opthamology fifth yr Flashcards
Summary of cataracts?
lens of the eye gradually opacifies i.e. becomes cloudy
Difficult for light to reach the retina, causing reduced/blurred vision
leading cause of curable blindness
F>M, increases with age
causes - normal ageing process
RF for cataracts?
Increasing age
Smoking
Increased alcohol consumption
Trauma
DM
Long-term corticosteroids
Radiation exposure
Myotonic dystrophy
Metabolic disorders - hypocalcaemia
Features of cataracts?
Sx - gradual onset
Reduced visual acuity
Faded colour vision
Glare - lights brighter than usual - “starbursts”
Halos
Asymmetrical
Signs
Defect in red reflex
Ix
Opthalmoscopy - after pupil dilation - normal fundus and optic nerve
Slit-lamp examination - visible cataract
Classification of cataracts?
Nuclear: change lens refractive index, common in old age
Polar: localized, commonly inherited, lie in the visual axis
Subcapsular: due to steroid use, just deep to the lens capsule, in the visual axis
Dot opacities: common in normal lenses, also seen in diabetes and myotonic dystrophy
Tx of cataracts?
Non-surgical - stronger glasses/contact lens, brighter lighting
Surgery - removing cloudy lens and replacing this with an artificial one.
NICE suggests that referral for surgery should be dependent upon whether a visual impairment is present, impact on quality of life, and patient choice.
Complications following cataract surgery?
Posterior capsule opacification: thickening of the lens capsule
Retinal detachment
Posterior capsule rupture
Endophthalmitis: inflammation of aqueous and/or vitreous humour - treat with intravitreal antibiotics
Summary of open angle glaucoma?
Glaucoma refers to optic nerve damage due to significant rise in intraocular pressure
This is caused by a block in aqueous humour trying to escape the eye
2 types - open-angle and closed-angle
Normal intraocular pressure?
10-21 mmHg - caused by resistance to flow through the trabecular meshwork into the canal of Schlemm
Pathophysiology of open-angle glaucoma?
Gradual increase in resistance through trabecular meshwork.
More difficult for aqueous humour to flow through meshwork and exit eye. Pressure SLOWLY builds - slow and chronic onset of glaucoma
Pathophysiology of acute angle-closure glaucoma?
Iris bulges forward and seals off the trabecular meshwork from the anterior chamber - preventing aqueous humour from being able to drain away
Leads to a continual build-up of pressure - opthalmology emergency
Increased pressure = cupping of optic disc. Indent in optic disc (optic cup) larger - ‘cupping’
RFs for open angle glaucoma?
Increasing age
FHx
Black ethnic origin
Myopia
Presentation of open angle glaucoma?
Rise in IOP for long time
It is diagnosed by routine screening when attending optometry for an eye check.
Peripheral vision loss - closes in to cause tunnel vision
It can present with gradual onset of fluctuating pain, headaches, blurred vision and halos appearing around lights, particularly at night time.
Ix for open angle glaucoma?
Non-contact tonometry - via opticians
Goldmann applanation tonometry - gold standard way
Visual field assessment - check for peripheral vision loss
Management of open-angle glaucoma?
Aims to reduce intraocular pressure - start at pressure of 24 mmHg or above
Prostaglandin analogue eye drops (e.g. latanoprost) are first line. Increase uveoscleral outflow. SE = eyelash, eyelid pigmentation, iris pigmentation (browning)
BB - timolol - reduce the production of aqueous humour
Carbonic anhydrase inhibitors - dorzolamide - reduce the production of aqueous humour
Sympathomimetics - brimonidine - reduce production of aqueous fluid and increase uveoscleral outflow
Trabeculoectomy surgery - required where eye drops are ineffective. Creates new channel from anterior chamber, through the sclera to a location under the conjunctiva. Causes a bleb
Management of open-angle glaucoma?
Aims to reduce intraocular pressure - start at pressure of 24 mmHg or above
Prostaglandin analogue eye drops (e.g. latanoprost) are first line. Increase uveoscleral outflow. SE = eyelash, eyelid pigmentation, iris pigmentation (browning)
BB - timolol - reduce the production of aqueous humour
Carbonic anhydrase inhibitors - dorzolamide - reduce the production of aqueous humour
Sympathomimetics - brimonidine - reduce production of aqueous fluid and increase uveoscleral outflow
Trabeculoectomy surgery - required where eye drops are ineffective. Creates new channel from anterior chamber, through the sclera to a location under the conjunctiva. Causes a bleb
Pathophysiology of diabetic retinopathy?
Condition where blood vessels in retina are damaged by prolonged exposure to hyperglycaemia
Hyperglycaemia leads to damage to the retinal small vessels and endothelial cells.
Increased vascular permeability leads to leakage from the blood vessels, blot haemorrhages, and formation of hard exudates. Hard exudates are yellow/white deposits of lipids in the retina
Damage to blood vessels lead to micro aneurysms and venous beading.
Damage to nerve fibres in retina - cotton wool spots
Intraretinal microvascular abnormalities (IMRA) - dilated and tortuous capillaries in the retina. Shunt between arterial and venous vessels in the retina.
Neovascularisation - growth factors released in the retina causing the development of new blood vessels
Findings of diabetic retinopathy?
Cotton wool spots
Neovascularisation
Microaneurysms
Venous beading
Hard exudates
Blot haemorrhages
Staging of diabetic retinopathy?
Non-proliferative and proliferative
Diabetic maculopathy
Non-proliferative
Mild - microaneurysms
Moderate - microaneurysms, blot haemorrhages, hard exudates, cotton wool spots, venous beading
Severe - blot haemorrhages plus microaneurysms in 4 quadrants, venous beading in 2 quadrants, intreretinal microvascular abnormality (IMRA) in any quadrant
Proliferative
Neovascularisation
Vitreous haemorrhage
Diabetic maculopathy
Macular oedema
Ischaemic maculopathy
Complications of diabetic retinopathy?
Retinal detachment
Vitreous haemorrhage (bleeding in to the vitreous humour)
Rebeosis iridis (new blood vessel formation in the iris)
Optic neuropathy
Cataracts
Management of diabetic retinopathy?
Optimise glycemic control, BP and hyperlipidaemia
Regular opthalmology review
Maculopathy - VEGF inhibitors
Non-proliferative retinopathy - regular observation, severe/very severe consider panretinal laser photocoagulation
Proliferative retinopathy
- panretinal laser photocoagulation - SE - reduction in visual fields
- intravitreal VEGF inhibitors - combination with panretinal laser photocoagulation, e.g., ranibizumab
- severe or vitreous haemorrhage - vitreoretinal surgery
Signs in retina due to hypertensive retinopathy?
As a result of chronic HTN or rapidly due to malignant HTN
Silver wiring or copper wiring - where the walls of the arterioles become thickened and sclerosed causing increased reflection of the light
AV nipping - arterioles cause compression of veins where they cross - 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 - due to lipids leaking from damaged vessels
Retinal haemorrhages - damaged vessels rupturing and releasing blood into the retina
Papilloedema - by ischaemia to the optic nerve resulting in optic nerve swelling (oedema) and blurring of the disc margins
Classification of hypertensive retinopathy?
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
Management of hypertensive retinopathy?
controlling the blood pressure and other risk factors such as smoking and blood lipid levels.
Management of hypertensive retinopathy?
controlling the blood pressure and other risk factors such as smoking and blood lipid levels.
