glaucoma Flashcards

1
Q

Define glaucoma

A

Optic neuropathy with characteristic progression of field defects

usually associated with ocular hypertension (intra-ocular pressure >21mmHg)

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2
Q

What is acute closed angle (closure) glaucoma

A

reversible (appositional) or adhesional (synechial) closure of the anterior-chamber angle resulting in raised intra-ocular pressure (IOP)

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3
Q

Aetiology of Acute closed angle glaucoma

A

Blocked drainage due to approximation of iris to cornea from the anterior chamber via the canal of Schlemm/trabecular meshwork → increased IOP → compression of the retinal nerve fibres → scotoma and visual field loss

  • thick cataractous lens
  • Ectoptic lens
  • DM
  • Ocular ischaemia
  • Trauma
  • Uveitis
  • Steroid use
  • Rubeosis iridis (DM, central retinal vein occlusion)
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4
Q

Risk factors for acute closed angle glaucoma

A

Female
Hyperopia
Shallow peripheral anterior chamber
Afro-Caribbean
Older age
Family history
DM
Medications that induce angle narrowing e.g. anticholinergics - atropine, sulphonamide, phenothiazines

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5
Q

Symptoms of acute closed angle glaucoma

A

Severe pain (ocular/headache)
REDUCED visual acuity , usually unilateral
Eye redness
Halos around lights
Aching eye or brow pain
Headache
Nausea & vomiting
Symptoms worse with mydriasis (e.g. watching tv in dark room)

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6
Q

Signs of acute closed angle glaucoma on examination

A

Red eye
Fixed and dilated pupil
Loss of red reflex
Corneal oedema: hazy cornea
Eye tender and hard on palpation
Cupped optic disc
Visual field defect (arcuate scotoma)

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7
Q

Investigations for acute closed angle glaucoma

A

Fundoscopy: Cupped optic disc

Gonioscopy: Trabecular meshwork is not visible in angle closure, because the peripheral iris is in contact with it
Slit-lamp: shallow anterior chamber, large optic cup, narrowing of neuroretinal rim
Automatic static perimetry: visual field defects

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8
Q

Management for acute closed angle glaucoma

A
  1. Urgent referral to ophthalmology
  2. Medication: Combination of eye drops, for example:
    - 4% topical pilocarpine (direct parasympathomimetic → causes contraction of the ciliary muscle → opening the trabecular meshwork → increased outflow of the aqueous humour)
    - Dorzolamide (topical carbonic anhydrase inhibitor → reduces aqueous formation)
    - Acetazolamide (IV/PO carbonic anhydrase inhibitor → reduces aqueous formation)
    - Timolol (beta-blocker→ decreases aqueous humour production)
    - Apraclonidine (alpha-2 agonist → dual mechanism, decreasing aqueous humour production and increasing uveoscleral outflow)
  3. Definitive management: Laser peripheral iridotomy
    - creates a tiny hole in the peripheral iris → aqueous humour flowing to the angle
    - Both eyes
  4. Lens extraction
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9
Q

Define open angle glaucoma

A

Characterised by an anatomically open angle but with an obstructed and slowed drainage system outflow

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10
Q

Aetiology for open angle glaucoma

A

Resistance to outflow through trabecular meshwork e.g. blood, inflammatory cells→ Increased intra-ocular pressure >21 → reduced blood flow → damage to the optic nerve → optic disc atrophy and cupping

  • neurodegenerative process where retinal ganglion cells degenerate
  • Associated with GLC1A and myocilin mutations
  • Trauma
  • Uveitis
  • Steroids
  • Rubeosis iridis (DM, central retinal vein occlusion)
  • Buphthalmos
  • Inherited ocular disorders
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11
Q

Risk factors for open angle glaucoma

A

Asian
Female
Myopia
Shallow peripheral anterior chamber
Older age
Family history
DM
Medications that induce angle narrowing e.g. anticholinergics - atropine, sulphonamide, phenothiazines

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12
Q

Symptoms of open angle glaucoma

A

Usually asymptomatic
Peripheral visual field loss may be noted
Usually bilateral
Halo arounds lights

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13
Q

Signs of open angle glaucoma on examination

A

Optic disc may be cupped Usually no signs
Cup to disc ratio > 0.4
Notching of optic nerve cup
Peripheral vision loss
Increased IOP
Scotoma - tunnel vision
Loss of nerve fibre layer
Retinal haemorrhages

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14
Q

Investigations for open angle glaucoma

A

Field testing: scotoma (indicates loss of nerve fibre layer)
Fundoscopy: cupped optic disc

Tonometry: IOP >21mmHg, Goldmann prism semi-circle ends do NOT line up
Direct/indirect ophthalmoscopy: Cup-to-disc ratio over 0.6, flame haemorrhages in late disease
Slit-lamp biomicroscopy: drainage angle open, cornea clear, deep anterior chamber

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15
Q

Management for open angle glaucoma

A

Long term (topical hypotensives)

1st line (one → the other → a combination of both):
Beta-blocker → aqueous production: timolol, betaxolol
Prostaglandin analogue→uveoscleral outflow: latanoprost

2nd line:
Topical alpha-2 agonist → aqueous production: brimonidine tartrate
Carbonic anhydrase-I → aqueous production: acetazolamide
Topical miotic (M3 agonist) → uveoscleral outflow: pilocarpine

Surgical (can be used 1st line over medical if desired [NEW, 2019]) → laser trabeculoplasty
- Laser treatment: Laser trabeculoplasty for POAG | iridotomy for ACAG
- Conventional: Trabeculectomy | Canaloplasty | Iridectomy facilitates outflow of aqueous humour
- 5-fluorouracil or Mitomycin may be used to reduce scarring

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16
Q

Who is screened for open angle glaucoma

A

> 35yo
Afro-Caribbean
FHx
Steroid treatment
DM
HTN
Migraines
Myopia

17
Q

Complications of glaucoma

A

Congenital: Amblyopia | Visual loss
POAG: Visual loss
ACAG: Visual loss | Anterior synechiae