Ophthalmology Flashcards

1
Q

What is acute angle-closure glaucoma?

A

= an acute rise in intraocular pressure due to narrowing of the anterior chamber angle of the eye, causing optic nerve damage & sight loss.

  • Ophthalmological emergency
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2
Q

What are the risk factors of acute angle-closure glaucoma?

A
  • Increasing age → >65yrs
  • Anatomical predisposition → shallow anterior chamber, short eyeball length, hypermetropia (long-sightedness)
  • Family history
  • Female → 4x more likely than men
  • Chinese & East Asian ethnic origin
  • Pupil mid-dilation → precipitates pupillary block
    • Being in a dark room
    • Medications → anticholinergics (oxybutynin), SSRIs
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3
Q

How does acute angle closure glaucoma present?

A

History:

  • Symptoms develop over hours to days
  • Patient may have been in a dark room when symptoms began, or may be taking medications that cause pupil dilation.
  • Unilateral severe eye pain
    • Associated headache, nausea, & vomiting
  • Profound reduction in visual acuity or visual loss
  • Rainbow colour halos around bright lights
  • Red eye
  • Hazy cornea → due to raised IOP causing corneal oedema
  • Fixed, mid-dilated pupil which does not react to light
  • Hard eyeball on gentle palpation → ask patient to close their eye & gently palpate
  • Very high IOP → >30mmHg
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4
Q

What are the two key investigations for acute angle-closure glaucoma?

A
  • Tonometry → typically >30mmHg
  • Gonioscope → gold standard for assessing the angle between the iris & cornea. Mandatory for establishing the diagnosis
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5
Q

How is acute angle closure glaucoma managed?

A

Requires immediate admission & secondary care management. Conservative measures whilst waiting for an ambulance:

  • Lie patient flat on their back → gravity helps bring the lens away & open the anterior chamber angle.
  • Oral analgesia & antiemetic
  • Pilocarpine eye drops → acts on the muscarinic receptors in the sphincter muscles, causing pupil constriction, helping the flow of aqueous humour.
  • Acetazolamide → reduces the production of aqueous humour

Laser iridotomy → definitive treatment, where a hole is made in the iris using a laser, which allows the aqueous humour to drain directly from the posterior to anterior chamber.

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6
Q

What is retinal detachment, and what are the common causes?

A

= when the neurosensory layer of the retina (which contains the photoreceptors & nerves) separate from the retinal pigment epithelium.

  • Neurosensory retina relies on blood vessels of the choroid for its blood supply → detachment can lead to damage to the photoreceptors, making it sight-threatening.
  • Most commonly due to full-thickness retinal tear → allows the vitreous fluid behind the neurosensory retina.
  • Other types:
    • Tractional → vitreous membranes pull on the retina, causing it to separate. More common in patients with diabetic retinopathy.
    • Exudative → underlying retinal disease leads to the build-up of exudative fluid underneath the retina.
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7
Q

How does retinal detachment present?

A

Symptoms:

  • Painless loss of vision
  • Flashing lights & floaters
  • Cobwebs in peripheral vision
  • Shadow or grey curtain moving across visual field → loss of peripheral vision
  • Poor visual acuity
  • Relative afferent pupillary defect
  • Altered fundal reflex
  • Slit lamp → tobacco dust (Shafer’s sign)
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8
Q

How is a retinal detachment managed?

A
  • Vitrectomy
    • Most common treatment for RD.
    • Keyhole surgery on the eye, vitreous is drained, cryo/laser therapy is used to seal the retinal tear & the eye is then filled with an absorbing gas to hold it in place.
    • Patient must maintain a head position post-operatively & cannot fly for 3-6 months.
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9
Q

What is a normal intraocular pressure?

A

10-21 mmHg

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10
Q

How does glaucoma present?

A
  • May be asymptomatic & picked up on routine eye testing.
  • Glaucoma affects the peripheral vision first → gradual onset of peripheral vision loss (tunnel vision), particularly in the superior visual field.
  • Blurred vision
  • Headaches
  • Halos around lights, particularly at night
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11
Q

What is the gold-standard investigation for open-angle glaucoma?

A
  • Goldmann applanation tonometer → gold standard
    • Device is mounted on a slit lamp & makes brief contact with the cornea after using numbing eye drops.
    • Measures the pressure needed to indent the cornea.
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12
Q

At what point is treatment commenced for open-angle glaucoma, and what does that involve?

A

Treatment will commence when IOP>24mmHg.

360 degree selective laser trabeculoplasty (SLT) → recommended for all newly diagnosed patients requiring treatment.

Medical Management:

  • Involves a variety of eye drop preparations that either reduce the production or increases the outflow of aqueous humour.
  • 1st line → prostaglandin analogue, eg latanoprost
    • Increases uveoscleral outflow
    • Side effects → eyelash growth, eyelid pigmentation, iris pigmentation
  • Other eye drop options:
    • Beta-blockers → eg, timolol, reduce the production of aqueous humour
    • Carbonic anhydrase inhibitors → eg, dorzolamide, reduce production of aqueous humour

Surgical Management:

  • Trabeculectomy → required where other treatments are ineffective.
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13
Q

How does optic neuritis present?

A
  • Acute-subacute unilateral loss of vision
    • Visual acuity can vary from being normal to (rarely) becoming ‘no perception of light’.
    • Can be central scotoma or diffuse.
    • Worsens over hours to days → recovery starts within 2 weeks
  • Pain → retrobulbar & peri-ocular
    • > 90% of cases
    • Exacerbated by eye movements
    • Can precede or occur with visual loss.
  • Reduced contrast sensitivity & colour vision

Examination:

  • Relative afferent pupillary defect → positive for the affected eye unless there is pre-existing disease in the contralateral eye.
  • Optic nerve swelling & pallor
  • Normal extraocular muscle movement
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14
Q

How is optic neuritis managed?

A
  • High-dose corticosteroid therapy
    • IV methylprednisolone → reduces the risk of developing MS for the first 2 years
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15
Q

What are the symptoms of age-related macular degeneration?

A
  • Gradual loss of central vision
  • Reduced visual acuity
  • Metamorphopsia → crooked or wavy appearance to straight lines
  • Symptoms can be bilateral or unilateral
  • Wet AMD → presents more acutely, within days
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16
Q

What are the signs of age-related macular degeneration?

A
  • Reduced visual acuity on Snellen Chart
  • Scotoma → enlarged central area of vision loss
  • Amsler grid test → distortion of straight lines
  • Drusen on fundoscopy
  • Optical coherence tomography (OCT) → cross-sectional view of layers of the retina & is used for diagnosing & monitoring AMD.
  • Fluorescein angiography → involves giving fluorescein contrast & photographing the retina to assess the blood supply. Shows oedema & neovascularisation in wet AMD.
17
Q

How is age-related macular degeneration managed?

A

There is no cure for AMD. Aims → maintain functional sight for as long as possible & address QOL issues as they arrive.

  • Urgent ophthalmology referral is wet AMD is suspected.

Supportive:

  • Risk factor management → avoid smoking, control BP, vitamin supplementation (some evidence of slowing progression), reduce ocular UV exposure.
  • Register blind once appropriate
  • OT/social work involvement

Dry AMD:

  • In early, dry AMD then vitamins can be given. However in late dry AMD/neovascular disease there is no proven benefit

Wet AMD:

  • Intravitreal anti-VEGF therapy → blocks the development of new blood vessels in the retina.
    • Injected directly into the vitreous chamber of the eye every 4-6 weeks.
  • 2/3 of patients have stabilised vision loss, 1/3 has improvement.