Opthalmology Flashcards
What is the vitreous chamber of the eye? Describe the anatomy.
The largest chamber of the eye, located behind the lens and in front of the optic nerve. It is filled with vitreous humour.
What is the anterior chamber of the eye? Describe the anatomy.
Located between the cornea and iris. It is filled with aqueous humour.
What is the posterior chamber of the eye? Describe the anatomy.
Located between the lens and iris. It is filled with aqueous humour.
Where is aqueous humour produced?
Ciliary body.
Describe the flow of aqueous humour in the eye.
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.
What is normal intraocular pressure?
10-21 mmHg.
Define glaucoma.
Optic nerve damage secondary to raised intraocular pressure.
Describe the pathophysiology of open-angle glaucoma.
Gradual increase in resistance through the trabecular meshwork. It is more difficult for aqueous humour to exit the eye and pressure increases within the eye.
Give examples of risk factors for the development of open-angle glaucoma.
Increasing age, family history, black ethnicity, near-sightedness.
How does open-angle glaucoma present clinically?
Loss of peripheral vision that eventually develops into tunnel vision. Fluctuating pain, headaches, blurred vision and halos.
Open-angle glaucoma: What are halos?
Bright circles of light that surround lights, particularly at night.
How is open-angle glaucoma diagnosed?
Measure intraocular pressure by non-contact tonometry or contact tonometry.
What investigations (other that tonometry) should be performed in suspected open-angle glaucoma?
Visual field assessment.
Fundoscopy.
Open-angle glaucoma: What is the difference between non-contact tonometry and contact tonometry?
Non-contact tonometry uses air to estimate pressure whereas contact tonometry makes direct contact with the cornea.
What might fundoscopy reveal in open-angle glaucoma?
Optic disc cupping.
What is the first-line management of open-angle glaucoma?
Prostaglandin analogue drops such as latanoprost.
Describe how latanoprost treats open-angle glaucoma.
Increases uveoscleral outflow.
Open-angle glaucoma: What are two side effects of latanoprost use?
Eyelash growth.
Eye discolouration.
What medications (other than latanoprost) can be used in the management of open-angle glaucoma?
Beta-blockers (timolol).
Carbonic anhydrase inhibitors (acetazolamide).
Describe how timolol and acetazolamide treat open-angle glaucoma.
Reduces production of aqueous humour.
What is acute angle-closure glaucoma?
Ophthalmology emergency. Optic nerve damage secondary to raised intraocular pressure.
Describe the pathophysiology of acute angle-closure glaucoma?
The iris bulges forward and seals of the trabecular meshwork from the anterior chamber, preventing drainage of aqueous humour and resulting in a continual build-up of pressure in the eye.
Give examples of risk factors for acute angle-closure glaucoma.
Increasing age, female sex, family history, East-Asian ethnicity.
Give examples of medications which increase the risk of developing acute angle-closure glaucoma?
Adrenergic medications (noradrenaline). Anticholinergic medications (oxybutynin, solifenacin). Tricyclic antidepressants (amitriptyline).
How does acute angle-closure glaucoma present clinically?
Short history of severely painful red eye.
What does examination reveal in acute angle-closure glaucoma?
Hazy cornea, decreased visual acuity, fixed dilated pupil, firm eyeball.
How is acute angle-closure glaucoma managed?
Lay the patient flat. Give pilocarpine eye drops. Give acetazolamide. Give timolol. Definitive management - laser iridotomy.
Describe how pilocarpine, acetazolamide and timolol treat acute angle-closure glaucoma.
Pilocarpine causes pupil constriction.
Acetazolamide and timolol both reduce production of aqueous humour.
Describe how laser iridotomy is used in the treatment of acute angle-closure glaucoma.
A hole is made in the iris to allow aqueous humour to flow from the posterior chamber into the anterior chamber.
What is the most common cause of blindness in the UK?
Age-related macular degeneration (AMD).
What is the pathophysiology of age-related macular degeneration?
Macular degeneration that causes progressive deterioration in vision.
Describe the structure of the macula (from bottom to top).
Choroid layer containing blood vessels.
Bruch’s membrane.
Retinal pigment epithelium.
Photoreceptors.
Give examples of risk factors for the development of age-related macular degeneration.
Increasing age, smoking history, family history, cardiovascular disease.
What is the presentation of age-related macular degeneration?
Gradually worsening central vision loss, reduced visual acuity and crooked/wavy appearance of straight lines.
What are the two types of AMD?
Dry age-related macular degeneration (90% of cases).
Wet age-related macular degeneration (more severe).
Describe the pathophysiology of dry AMD.
Characterised by the degeneration of retinal photoreceptors and the formation of drusen.
What are drusen and where in the macula do they form?
Yellow deposits of lipids and proteins. Deposition occurs between Bruch’s membrane and the retinal pigment epithelium.
How is dry AMD managed?
Reduce progression. Encourage smoking cessation, control blood pressure and supplement vitamins.
Describe the pathophysiology of wet AMD?
Development of new vessels from the choroid layer into the retina. The vessels leak fluid or blood and cause oedema.
How does the presentation of wet AMD differ from dry AMD?
Patients complain of more rapid vision loss in wet AMD.
How is wet AMD managed?
Anti-vascular endothelial growth factor (anti-VEGF) injections such as ranibizumab… which block VEGF and and the development of new blood vessels.
What investigations are performed in AMD?
Snellen chart.
Automated visual field testing.
Amsler grid test.
Fundoscopy.
What does Snellen chart reveal in AMD?
Reduced visual acuity.
What does automated visual field testing reveal in AMD?
Scotoma (central patch of vision loss).
What does Amsler grid test reveal in AMD?
Distortion of straight lines.
What does fundoscopy reveal in AMD?
Presence of drusen.
What is diabetic retinopathy?
Complication of prolonged exposure to high blood glucose.
Describe the pathophysiology of diabetic retinopathy.
High blood sugar leads to damage of the retinal small vessels and endothelial cells… increased vascular permeability leads to leakage, blot haemorrhages and the formation of hard exudates (yellow/white deposits of lipids in the retina).
What investigation is performed in the assessment of diabetic retinopathy?
Fundoscopy.
What might fundoscopy show in diabetic retinopathy?
Blot haemorrhages. Hard exudates. Cotton wool spots. Microaneurysms. Intraretinal microvascular abnormalities. Neovascularisation.
What do cotton wool spots represent in diabetic retinopathy?
Damage to nerve fibres.
How is diabetic retinopathy classified?
Non-proliferative diabetic retinopathy.
Proliferative diabetic retinopathy.
What is the difference between proliferative and non-proliferative diabetic retinopathy?
Proliferative includes neovascularisation and vitreous haemorrhage (presents as sudden vision loss).
What is the management of diabetic retinopathy?
Laser photocoagulation.
Ranibizumab (anti-VEGF).
Vitreoretinal surgery.
Give examples of complications of diabetic retinopathy.
Retinal detachment.
Vitreous haemorrhage.
Optic neuropathy.
Cataracts.
What is hypertensive retinopathy?
Damage to the small blood vessels of the retina relating to systemic hypertension. Can develop due to years of chronic hypertension or quickly as a result of malignant hypertension.
What investigation is performed in the assessment of hypertensive retinopathy?
Fundoscopy.
What might fundoscopy reveal in hypertensive retinopathy?
Silver wiring. Arteriovenous nipping. Cotton wool spots. Hard exudates. Retinal haemorrhage. Papilloedema.
Hypertensive retinopathy: What is silver wiring (on fundoscopy)?
Arteriole wall thickening, sclerosis… increased reflection of light.
Hypertensive retinopathy: What is arteriovenous nipping (on fundoscopy)?
Arteriole sclerosis leads to compression of adjacent veins.
Hypertensive retinopathy: What is retinal haemorrhage (on fundoscopy)?
Damaged vessels rupture and leak blood into the retina.
Hypertensive retinopathy: What is papilloedema (on fundoscopy)?
Optic nerve ischaemia leads to swelling and blurring of the optic disc margins.
How is hypertensive retinopathy managed?
Control blood pressure.
Control blood lipid levels.
Encourage smoking cessation.
Describe the pathophysiology of cataracts.
Condition of reduced visual acuity that occurs as the lens becomes cloudy and opaque (reducing the amount of light that can enter).
What is the normal function of the lens in the eye?
To focus light onto the retina. Held in place by suspensory ligaments attached to the ciliary body, which contract and relax to focus the lens.
What are risk factors for the development of cataracts?
Increasing age, smoking, alcohol consumption, diabetes, steroid use, hypocalcaemia.
How do cataracts present clinically?
Asymmetrical, slow reduction in vision with progressive blurring. Patients complain of change in colour vision (more brown/yellow) and starburst that appear around lights.
What does examination reveal in people with cataracts?
Loss of red reflex.
What is the definitive management of cataracts?
Surgery - removal of diseased lens and implantation of artificial lens into the eye.
What is a rare complication of cataract surgery?
Endophthalmitis (inflammation of the inner contents of the eye, typically due to infection).
What muscles control pupil constriction?
Circular muscles in the iris.
What neurotransmitter stimulates the circular muscles of the eyes as part of the parasympathetic nervous system?
Acetylcholine.
What muscles control pupil dilation?
Dilator muscles.
What neurotransmitter stimulates the dilator muscles of the eyes as part of the sympathetic nervous system?
Adrenaline.
Give examples of causes of mydriasis (dilated pupil).
Third nerve palsy Holmes-Adie syndrome Raised ICP Trauma Stimulants (cocaine) Anticholinergics
Give examples of causes of miosis (constricted pupil).
Horners syndrome. Cluster headaches Neurosyphilis (Argyll-Robertson pupil) Opiates Nicotine Pilocarpine
How does third nerve palsy present?
Ptosis.
Dilated non-reactive pupil
Divergent strabismus (down and out position).
Give two causes of third nerve palsy.
Cavernous sinus thrombosis
Posterior communicating artery aneurysm
What is the triad of Horner syndrome?
Ptosis
Miosis
Anhidrosis