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MSRA > Ophthalmology > Flashcards

Ophthalmology Flashcards

1
Q

What is the pathophysiology of acute angle closure glaucoma?

A

OPHTHALMOLOGICAL EMERGENCY

the iris bulges forward and seals off the trabecular meshwork from the anterior chamber, preventing aqueous humour from draining and leading to a continual increase in intraocular pressure

The pressure builds in the posterior chamber, pushing the iris forward and exacerbating the angle closure

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2
Q

What are some medications that can precipitate acute angle closure glaucoma?

A
  • Adrenergic medications (e.g., noradrenaline)
  • Anticholinergic medications (e.g., oxybutynin and solifenacin)
  • Tricyclic antidepressants (e.g., amitriptyline), which have anticholinergic effects
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3
Q

What are some signs on examination of acute angle closure glaucoma?

A
  • Red eye
  • Hazy cornea
  • Decreased visual acuity
  • Mid-dilated pupil
  • Fixed-size pupil
  • Hard eyeball on gentle palpation
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4
Q

What is the initial management of acute angle closure glaucoma?

A

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
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5
Q

How does pilocarpine work?

A

Pilocarpine acts on the muscarinic receptors in the sphincter muscles in the iris and causes pupil constriction (it is a miotic agent). It also causes ciliary muscle contraction.

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6
Q

How does acetazolamide work?

A

Acetazolamide is a carbonic anhydrase inhibitor that reduces the production of aqueous humour.

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7
Q

What are some secondary care management in acute angle closure glaucoma?

A
  • Pilocarpine eye drops
  • Acetazolamide (PO/IV)
  • Hyperosmotic agents (e.g., IV mannitol) increase the osmotic gradient between the blood and the eye
  • Timolol is a beta blocker that reduces the production of aqueous humour
  • Dorzolamide is a carbonic anhydrase inhibitor that reduces the production of aqueous humour
  • Brimonidine is a sympathomimetics that reduces aqueous humour production and increases uveoscleral outflow
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8
Q

What is the definitive management in acute angle closure glaucoma?

A

Laser iridotomy

This involves making a hold in the iris using a laser, which allows the aqueous humour to flow directly from the posterior chamber to the anterior chamber. This relieves the pressure pushing the iris forward against the cornea and opens the pathway for the aqueous humour to drain.

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9
Q

What is glaucoma?

A

Glaucoma refers to the optic nerve damage caused by a rise in intraocular pressure. Raised intraocular pressure is caused by a blockage in aqueous humour trying to escape the eye.

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10
Q

What is normal intraocular pressure?

A

10-21 mmHg

Treatment is for 24mmHg and above

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11
Q

What is the pathophysiology of open-angle glaucoma?

A

gradual increase in resistance to flow through trabecular meshwork, intraocular pressure slowly builds up within the eye

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12
Q

How does raised intraocular pressure affect the optic disc?

A

cupping of the optic disc

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13
Q

How does open-angle glaucoma usually present?

A

May be asymptomatic - Dx by routine eye testing

Affects peripheral vision first => gradual onset peripheral vision loss/tunnel vision

Also may cause:
- fluctuating pain
- headaches
- blurred vision
- halos around lights, esp at night

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14
Q

How to measure intraocular pressure? What is the gold standard?

A

Non-contact tonometry (air puff thing)

Goldmann applanation tonometry - gold-standard
:::::::device acc touches the cornea and applies pressure

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15
Q

How is open-angle glaucoma usually diagnosed?

A

Diagnosis is based on:

  • Goldmann applanation tonometry for the intraocular pressure
  • Slit lamp assessment for the cup-disk ratio and optic nerve health
  • Visual field assessment for peripheral vision loss
  • Gonioscopy to assess the angle between the iris and cornea
  • Central corneal thickness assessment
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16
Q

What is the management of open-angle glaucoma?

A

360° selective laser trabeculoplasty for all pts

1st line Rx: Prostaglandin analogue eye drops (e.g., latanoprost) - increase uveoscleral outflow

other eye drops:
- 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

Surgical: trabeculectomy

17
Q

How do prostaglandin analogues work? What are some notable side effects?

A

e.g. latanoprost

work by increasing uveoscleral outflow

S/E: eyelash growth, eyelid pigmentation, iris pigmentation (browning)

18
Q

What is anterior uveitis?

A

inflammation of the anterior uvea. The uvea consists of the iris, ciliary body and choroid. The choroid is the layer between the retina and the sclera. Intermediate uveitis and posterior uveitis are less common.

usually caused by autoimmune process, but can be infection, trauma, ischaemia, malignancy

19
Q

What are some associated autoimmune conditions with anterior uveitis?

A
  • seronegative spondyloarthropathies
  • IBD
  • sarcoidosis
  • Behcet’s disease
20
Q

What are the symptoms of anterior uveitis?

A
  • painful red eye (dull,aching pain)
  • reduced visual acuity
  • photophobia
  • excessive lacrimation
21
Q

What are some signs/examination findings in anterior uveitis?

A
  • ciliary flush - ring of red spreading from cornea outwards
  • miosis (constricted pupils) - sphincter muscle contraction
  • abnormally shaped pupil - posterior adhesions pulling iris
  • hypopyon (inflammatory cells fluid collection)
22
Q

What is the management of anterior uveitis?

A

urgent assessment and management by ophthalmologist

1st line: steroids (eye drops/PO/IV) and cycloplegic eye drops (cyclopentolate or atropine) ::: cycloplegics dilate pupil and reduce pain due to spasms by paralysing ciliary muscles

23
Q

What is retinal vein occlusion?

A

thrombus in retinal veins - centra or branch retinal veins
branch veins drain into central vein, branch blockage affects that area, central vein affects whole retina

=> venous congestion in retina => blood leakage into retina => macular oedema and retinal haemorrhages => retinal damage and vision loss

classified into:
- ischaemic - leads to release of VEGF (vascular endothelial growth factor) => neovascularisation
- non-ischaemic

24
Q

How does retinal vein occlusion present?

A
  • painless blurred vision/vision loss
25
Q

What are the findings on fundoscopy in retinal vein occlusion?

A
  • dilated tortuous retinal veins
  • flame and blot haemorrhages
  • retinal oedema
  • cotton wool spots
  • hard exudates

“blood and thunder” appearance

26
Q

What is the management of retinal vein occlusion?

A

immediate referral to opthalmologist

  • Anti-VEGF therapies (e.g., ranibizumab and aflibercept)
  • Dexamethasone intravitreal implant (to treat macular oedema)
  • Laser photocoagulation (to treat new vessels)
27
Q

What are some causes of central retinal artery occlusion?

A

most common - Atherosclerosis

GCA - vasculitis affects ophthalmic or central retinal artery

28
Q

How does central retinal artery occlusion present?

A

Sudden painless loss of vision “curtains coming down”

Relative Afferent Pupillary Defect - affected pupil constricts LESS with light than other eye

29
Q

What can be seen on fundoscopy in central retinal artery occlusion?

A

Pale retina
Cherry red spot (fovea thinner showing red-coloured choroid below)

30
Q

What are some differentials for sudden painless vision loss?

A
  • Central retinal artery occlusion
  • Central retinal vein occlusion
  • Retinal detachment
  • Vitreous haemorrhage (diabetic retinopathy)
31
Q

What is the management of central retinal artery occlusion?

A

vision-threatening emergency = immediate referral

if GCA, test with ESR and temporal artery biopsy, treat with high-dose systemic steroids

Immediate management options attempt to dislodge/resolve the blockage. There is no consensus, guidelines or solid evidence base for these options:
- Ocular massage (massaging the eye)
- Anterior chamber paracentesis (removing fluid from the anterior chamber to reduce the intraocular pressure)
- Inhaled carbogen (5% carbon dioxide and 95% oxygen) (to dilate the artery)
- Sublingual isosorbide dinitrate (to dilate the artery)
- Oral pentoxifylline (to dilate the artery)
- Intravenous acetazolamide (to reduce the intraocular pressure)
- Intravenous mannitol (to reduce the intraocular pressure)
- Topical timolol (to reduce the intraocular pressure)

32
Q

How does conjunctivitis present?

A
  • red, bloodshot eye
  • itchy, gritty sensation
  • discharge

No pain/photophobia/reduced visual acuity

33
Q

What is the difference in presentation between bacterial and viral conjunctivitis?

A

Bac - purulent discharge, worse in morning (eyes stuck together), contagious, spread to other eye

Viral - clear discharge, assoc w/ other symptoms of viral infection (dry cough, sore throat, blocked nose), may have tender pre-auricular lymph nodes, contagious

34
Q

What are some differentials of painful red eye?

A
  • Acute angle-closure glaucoma
  • Anterior uveitis
  • Scleritis
  • Corneal abrasions or ulceration
  • Keratitis
  • Foreign body
  • Traumatic or chemical injury
35
Q

What are some differentials for painless red eye?

A
  • Conjunctivitis
  • Episcleritis
  • Subconjunctival haemorrhage
36
Q

What is the management of conjunctivitis?

A

Resolves in 1-2 weeks without treatment
Hygiene to stop spreading
Cleaning eyes with cooled boiled water and cotton wool

Chloramphenicol or fusidic acid for bac

Neonates under 1 m/o need URGENT assessment - maybe gonococcal infection which can cause permanent vision loss

37
Q
A

MSRA (16 decks)

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