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  • Created by: z
  • Created on: 13-03-16 16:06

Definition and classification

  • "a condition characterised by optic disc cupping and visual fiel dloss, in which intraocular pressure (IOP) is sufficiently raised to impair normal optic nerve function"
  • Classification:
    • primary or secondary > open or closed angle
      • primary open angle glaucoma (POAG) - commonest
      • primary acute angle closure glaucoma
        • sudden closure of angle reuslting in suddern icr IOP e.g. in hypermetropic eyes
      • secondary glaucoma 
          • e.g. inflammatory, traumatic, neovascular, drug induced (steroids)
        • congenital glaucoma
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  • POAG is a syndrome, must have:
    • IOP > 21 mmHg (norm= 10-21)
    • open aqueuos drainage (i.e. no macroscopic bloackage of outflow)
    • pathologically cupped disc
    • glaucomatuous visual field loss
  • POAG prevalence: 65 million worlwide w/ 7 million blind
  • pathogenesis: 2 theories
    • "direct mechanical" theory - raised IOP mechanically damages optic nv
    • "indirect ischaemic" theory - raised IOP stops microcirculation as perfusion pr too low
  • POAG causes: ageing (rare <40yr), corticosteroids (topical and systemic), FHx (multigenetic)
  • associations - FHx, ocular probs (highy myopia, central venous occlusion), DM
  • symptoms - asymptomatic until advanced (painless, no redness, unnoticed periph. visual loss)
  • If criteria not met, may be:
    • ocular hypertension - IOP > 21 mmHg but normal optic disc and field
    • normotensive glaucoma - IOP normal but cupped disc and vsua field loss
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POAG examination

  • visual acuity - decr in advanced disease
  • raised IOP -  use Goldman applanation tonometer (inject LA then prod eye to find pr)
  • open drainage angle inspection - gonioscopy
  • inspect optic disc by ophthalmoscopy
    • pathologically cupped disc ("cup"=dead fibres, some degree is normal but incr in glauoma)
      • cup:disc ratio >0.5
      • C:D asymmetry
      • nasal shift of vessels
      • haemorrhages
    • NB disc still pinkish- if pale it's not glaucoma
  • use Goldman fields (human) or Humphrey fields (computerised) to generate picture of visual fields (shaded=loss); glaucomatous field loss is progressive:
    • initially nasal
    • then superior and inferior arcuate scotoma
    • temporal and central islands
    • complete field los= blindness
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Assessment of glaucoma

  • monitoring of:
    • IOP
    • optic disc
    • visual fields (w/ Goldma/Humphrey perimetry) every 6/12 or 12/12 (NB Humphrey more reproducable so easier to detect progression)
  • problems w/ glaucoma
    • not curable (can only slow/stop progression)
    • incr prevalence w/ aging pop
  • hard to predict who will develop
    • regular check ups for >40yrs esp if FHx, or regular steroid use (e.g. RA pts)
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Treatment of glaucoma

  • medical
    • topical (eye drops= fewer s/e but still there)
      • prostaglandin F2alpha analogues e.g. latanoprost - cause incr uveoscleral outflow
      • beta-blockers e.g. timolol - cause decr aqueous production
      • carbonic anhydrase inhibitors e.g. dorzolamide - decr aqueous prod
      • alpha-2 agonists e.g. brimonidine cause incr uveoscleral drainage and decr aqu prod
    • systemic (only if v high IOP)
      • carbonic anhydrase inhibitor (acetazolamide) given orally POAG, IV for angle closure, only short term b/c lots of s/e
  • surgical (only for young pt or aggressive glaucoma)
    • trabeculectomy - surgical cretaion of fistula b/w ant chamber and subconjuctival space, provides alternative path for aqueous escape
      • add augmentation so fistula doesn't heal - topical chemoRx (mitomycin-C, 5-fluourouracil)
    • laser to trabecular meshwork (incr drainage)
    • drainage tubes - tube +/- valve to relase humour into subconjunctival space
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