"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
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
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
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