List I - Act Core Conditions Flashcards

1
Q

What is glaucoma?

A
  • Group of eye diseases that cause progressive optic neuropathy and in which IOP is a key modifiable factor
  • Glaucoma is commonly associated with raised IOP and is characterised by:
  • Visual field defects
  • Changes to the optic nerve such as pathological cupping or as a late sign, pallor of the optic disc
  • Ocular hypertension is where there is consistently or recurrently elevated IOP (greater than 21 mmHg) but with no signs of glaucoma
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2
Q

What is the anterior chamber?

A
  • Fluid filled space between the iris and the cornea
  • Anterior chamber angle is the angle between the iris and the cornea where they join the sclera towards the outside of the eye
  • Trabecular meshwork is situated in the apex of the anterior chamber angle and is the main outflow route for the aqueous humour
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3
Q

What is the aqueous humour?

A
  • Fluid produced from plasma by the ciliary epithelium of the ciliary body (the circular structure just behind the iris) - carbonic anhydrase plays a key role in its production
  • Aqueous humour is secreted into the posterior chamber between the lens and the iris, it then flows through the pupil into the trabecular meshwork, a small amount drains out via the venous circulation of the iris, ciliary body, choroid, and sclera
  • Secretion of the aqueous humour is increased by stimulation of beta-2 receptors and decreased by stimulation of alpha-2 receptors of the sympathetic nervous system that are located on cells of the ciliary body
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4
Q

What is the role of intra ocular pressure in the eye?

A
  • IOP keeps the eye in the shape of a globe and is maintained by the balance between production and outflow of aqueous humour
  • Raised IOP is the main risk factor for developing glaucoma as the raised IOP may damage nerve fibres of the optic nerve or blood vessels supplying these nerve fibres
  • A pressure of between 11-21 mmHg is considered normal - some develop glaucoma at pressures below 21 mmHg and some have pressures well above this without showing signs of glaucoma
  • Drugs used to treat glaucoma aim to reduce IOP and work by either reducing the production of aqueous humour or increasing its outflow
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5
Q

What is glaucoma classified according to?

A
  • Age of onset - congenital, infantile, juvenile or adult
  • Cause - primary (no known cause) or secondary with a known underlying cause
  • Rate of onset - acute, subacute or chronic
  • The anterior chamber angle between the iris and cornea - either open or closed
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6
Q

What are the features of open angle glaucoma?

A
  • Angle between the iris and the cornea is normal
  • Primary open angle glaucoma is by far the most common type of glaucoma
  • Mainly affects people over the age of 40
  • Usually insidious onset and follows a chronic course
  • Usually affects both eyes but one may be more affected than the other
  • Is typically associated with raised IOP
  • Normal tension (pressure) glaucoma occurs in a significant minority of people with POAG where glaucoma develops with normal IOP
  • Suspect POAG is when the appearance of the optic nerve head is suggestive of glaucoma but the visual fields appear normal, or conversely, where a visual field defect exists yet the optic nerve appears healthy
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7
Q

What are the features of closed angle glaucoma?

A
  • Angle between the iris and the cornea is at least partially closed
  • Primary angle closure glaucoma (PACG) is the most common type of angle closure glaucoma
  • Onset may be acute, subacute or chronic
  • Mainly affects older people occurring in about 0.4% of people in the UK over 40 years
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8
Q

In which people should acute angle closure (which may progress to glaucoma) be suspected?

A

In a person with an acute painful red eye and in particular who:

  • Is female, Asian, long sighted or of older age
  • Has a history of episodes of blurred vision, headaches or eye pain associated with nausea and seeing halos around lights; these symptoms typically occur in the evening and are relieved by sleeping
  • May also have headache, nausea, vomiting, lights are seen around halos - caused by an oedematous cornea, semi-dilated and fixed pupil, tender, hard eye, impaired visual acuity
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9
Q

If acute angle glaucoma is suspected, what is the action?

A
  • Admit the person for ophthalmology assessment
  • If not possible, emergency treatment should start in primary care
  • Lie the person flat with their face up and head not supported by pillows
  • If available, pilocarpine drops should be administered - one drop of 2% in blue eyes or 4% in brown eyes, acetazolamide 500 mg given orally (if no contraindications) and analgesia and an anti-emetic provided if required
  • If chronic glaucoma is suspected the person should be referred to an optometrist or ophthalmologist
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10
Q

What is the main complication of untreated glaucoma?

A
  • Irreversible loss of vision (partial or complete)
  • Appropriate treatment reduces the risk of progression of the disease
  • Treatment of all types of glaucoma and of ocular hypertension when indicated is normally initiated and monitored by specialists
  • Mainstay of treatment is to reduce IOP
  • Usually done with eye drops but sometimes laser or surgical treatments are required
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11
Q

What is the initial presentation of primary open angle glaucoma?

A
  • May present insidiously and for this reason is often detected during routine optometry appointments
  • Features include:
  • Peripheral visual field loss - nasal scotomas progressing to tunnel vision
  • Decreased visual acuity
  • Optic disc cupping
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12
Q

What are the signs on fundoscopy of primary open angle glaucoma?

A
  1. Optic disc cupping - cup-to-disc ratio >0.7 (normal = 0.4-0.7), occurs as loss of disc substance makes optic cup widen and deepen
  2. Optic disc pallor - indicating optic atrophy
  3. Bayonetting of vessels - vessels have breaks as they disappear into the deep cup and re-appear at the base
  4. Additional features - Cup notching (usually inferior where vessels enter disc), Disc haemorrhages
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13
Q

How is diagnosis of POAG made?

A
  • Case finding and provisional diagnosis is done by an optometrist
  • Optic nerve head damage visible under the slit lamp
  • Visual field defect
  • IOP > 24 mmHg as measured by Goldmann-type applanation tonometry
  • Referral to the ophthalmologist is done via the GP
  • Final diagnosis is done by investigations as below
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14
Q

What investigations are done for diagnosing POAG?

A
  • Automated perimetry to assess visual field
  • Slit lamp examination with pupil dilatation to assess optic neve and fundus for a baseline
  • Applanation tonometry to measure IOP
  • Central corneal thickness measurement
  • Gonioscopy to assess peripheral anterior chamber configuration and depth
  • Assess risk of future visual impairment, using risk factors such as IOP, central corneal thickness (CCT), family history, life expectancy
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15
Q

What is the NICE guidance for managing primary open angle glaucoma?

A
  • First line: prostaglandin analogue (PGA) eye drop
  • Second line: beta blocker, carbonic anhydrase inhibitor or sympathomimetic eyedrop
  • More advanced surgery or laser treatment can be tried

Reassessment

  • Important to exclude progression and visual field loss
  • Needs to be done more frequently if IOP uncontrolled, the patient is high risk, or there is progression
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16
Q

What is the mechanism of prostaglandin analogues in the treatment of POAG?

A
  • Latanoprost
  • Increases uveoscleral outflow
  • Once daily administration
  • Adverse effects include brown pigmentation of the iris, increased eyelash length
17
Q

What is the mechanism of beta blockers in the treatment of POAG?

A
  • Timolol
  • Reduces aqueous production
  • Should be avoided in asthmatics and patients with heart block
18
Q

What is the mechanism of sympathomimetics in the treatment of POAG?

A
  • Brimonidine, an alpha2 adrenoceptor agonist
  • Reduces aqueous production and increases outflow
  • Avoid if taking MAOI or tricyclic antidepressants
  • Adverse effects include hyperaemia
  • Cannot give with acute angle glaucoma due to risk of myadritic effects
19
Q

What is the mechanism of carbonic anhydrase inhibitors in the treatment of POAG?

A
  • Dorzolamide
  • Reduces aqueous production
  • Systemic absorption may cause sulphonamide like reactions
20
Q

What is the mechanism of miotics in the treatment of POAG?

A
  • Pilocarpine - muscarinic receptor agonist
  • Increases uveoscleral outflow
  • Adverse effects included a constricted pupil, headache and blurred vision