High Yield Opthal and Derm Flashcards
What is normal intraocular pressure?
10-21 mmHg
It is created by the resistance to flow of aqueous humour through the trabecular meshwork
Raised intraocular pressure causes cupping of the optic disc.
What is this?
In the centre of the optic disc is an indent called the optic cup, which is usually less than 50% of the size of the optic disc.
Raised intraocular pressure causes this indent to become wider and deeper, described as “cupping”. A cup-disk ratio greater than 0.5 is abnormal.
Risk factors for open-angle glaucoma include:
Increasing age
Family history
Black ethnic origin
Myopia (nearsightedness)
Hypertension
Diabetes mellitus
Corticosteroids
In open-angle glaucoma, the rise in IOP may be asymptomatic for a long time and diagnosed by routine eye testing.
How may it present if symptomatic?
Peripheral visual field loss
Decreased visual acuity (blurred vision)
Fluctuating pain
Headaches
Halos around lights, particularly at night
How does open-angle glaucoma present on fundoscopy?
- Optic disc cupping - cup-to-disc ratio >0.7, loss of disc substance makes optic cup widen and deepen
- Optic disc pallor - indicating optic atrophy
- Bayonetting of vessels - vessels have breaks as they disappear into the deep cup and re-appear at the base
When is treatment initiated for open-angle glaucoma?
at an intraocular pressure of 24 mmHg or above
How can open-angle glaucoma be managed?
Prostaglandin analogue eye drops (e.g., latanoprost) are the first-line medical treatment - increase uveoscleral outflow
360° selective laser trabeculoplasty - laser is directed at the trabecular meshwork, improving drainage
Other than prostaglandin analogues, what eye drops may be used in the mx of open angle glaucoma?
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 the uveoscleral outflow
Risk factors for acute angle-closure glaucoma include:
Increasing age
Family history
Female (four times more likely than males)
Chinese and East Asian ethnic origin
Shallow anterior chamber
How do patients with acute angle-closure glaucoma present?
Severely painful red eye
Decreased visual acuity (blurred vision)
Halos around lights
Associated headache, nausea and vomiting
Symptoms worse with mydriasis (e.g. watching TV in a dark room)
What may be seen on examination of patients with acute angle-closure glaucoma?
Red eye
Hazy cornea
Semi-dilated non-reactive pupil
Hard eyeball on gentle palpation
Decreased visual acuity
How can acute angle closure glaucoma be managed in the community?
Acute angle-closure glaucoma requires immediate admission!
Measures while waiting for an ambulance are:
Lying the patient on their back without a pillow
Pilocarpine eye drops (2% for blue and 4% for brown eyes)
Acetazolamide 500 mg orally
Analgesia and an antiemetic, if required
How can acute angle closure glaucoma be managed in secondary care?
Pilocarpine eye drops
IV Acetazolamide
Hyperosmotic agents (e.g. IV mannitol)
Timolol, Dorzolamide - both reduce the production of aqueous humour via different mechanisms
Brimonidine - reduces aqueous humour production and increases uveoscleral outflow
What is the most common cause of blindness in the UK?
Age-related macular degeneration (AMD)
Give some risk factors for AMD?
Older age
Family history
Smoking (x2 risk)
Cardiovascular disease (e.g., hypertension)
Obesity
Poor diet (low in vitamins and high in fat)
How does AMD typically present?
Visual changes associated with AMD tend to be unilateral, with:
Gradual loss of central vision
Reduced visual acuity
Crooked or wavy appearance to straight lines (metamorphopsia)
Worsening night vision
Patients often present with a gradually worsening ability to read small text.
What are the key examination findings for AMD?
Reduced visual acuity using a Snellen chart
Scotoma (an enlarged central area of vision loss)
Amsler grid test can be used to assess for the distortion of straight lines seen in AMD
Drusen may be seen during fundoscopy
What is the pathophysiology of diabetic retinopathy?
Hyperglycaemia (high blood sugar) damages the retinal small vessels and endothelial cells.
Damage to the blood vessel walls leads to microaneurysms and venous beading
Increased vascular permeability leads to leaking blood vessels, blot haemorrhages and hard exudates
Damage to nerve fibres in the retina causes fluffy white patches called cotton wool spots to form on the retina
What are the potential complications of diabetic retinopathy?
Vision loss
Retinal detachment
Vitreous haemorrhage (bleeding into the vitreous humour)
Rubeosis iridis (new blood vessel formation in the iris) – this can lead to neovascular glaucoma
Optic neuropathy
Cataracts
Give some risk factors for developing cataracts
Increasing age
Smoking
Alcohol
Diabetes
Steroids
Hypocalcaemia
How do cataracts present?
Symptoms are usually asymmetrical, as both eyes are affected separately.
It presents with:
Slow reduction in visual acuity
Progressive blurring of the vision
Colours becoming more faded, brown or yellow
Starbursts can appear around lights, particularly at night
Give a complication of cataract surgery
Endophthalmitis : inflammation of the inner contents of the eye, usually caused by infections
Can lead to vision loss
Treated with intravitreal antibiotics injected directly into the eye
Give some causes of Mydriasis (Dilated Pupil)
Trauma
Third nerve palsy
Raised ICP
Acute angle-closure glaucoma
Stimulants (e.g., cocaine)
Anticholinergics (e.g., oxybutynin)
Holmes-Adie syndrome
Give some causes of Miosis (Constricted Pupil)
Horner syndrome
Cluster headaches
Argyll-Robertson pupil (neurosyphilis)
Opiates
Nicotine
Pilocarpine
