10 - Pathogenesis of Glaucoma Flashcards
most common features of glaucoma
- loss of retinal ganglion cells
- thinning of retinal nerve fibre layer
- cupping of disc
when does secondary glaucoma occur
when there is an underlying condition
what is open angle glaucoma
- extracellular material becomes depositied in trabecular meshwork
- gives rise to increased resistance to outflow - raise IOP
risk factors of glaucoma
- black
- IOP > 26mmHg
- myopia (>3D)
- diabetes
- FH
clinical features of glaucoma
- extensive inferior visual field loss
- subtle changes in NRR
- disc cupping
primary angle closure glaucoma
- pupil block
role of IOP
represnts primary risk factor for developing glaucoma
- both incidence + progression of glauc can be controlled by decreasing IOP
what is increased IOP due to in OPEN ANGLE glaucoma
- increased resistance ot outflow
what is increased IOP due to in CLOSED ANGLE glaucoma
pupillary block
how is impact of IOP on pathogenesis of glaucoma explained
2 theories
- mechanical (direct)
- vascular (indirect)
what is aqeous produced by
ciliary epithelium
where does aqeous drainage occur
irido- corneal angle via conventinal + uveo scleral pathways
what is IOP determined by
the balance between aqueous production and drainage
mechanism of aqueous production
- pigmented and non-pigmented cells of ciliary epithelium make aqeuous
- ions move around in the aqeous and are transported from stroma to pigment cells, through gap junctions to NPE
- active transport of ions from NPE to posterior chamber
what is the catalyser of this mechanism (aqueous production)
- carbonic anhydrase
aquous outflow pathways
- majority drains through trabecular meshwork/canal of schlemm (conventional pathway)
- some drains through uveo-scleral pathway
what are the 3 distinct layers of aqueous outflow pathway ( conventional)
- uveo trabeucli
- corneal-scleral trabeculi
- juxta canicular - adjacent to canal of schlemm
glaucoma is associated with an increased?
- resistance to outflow
in open angle glaucoma, where is resistance higher than normal
-JCT (INNER WALL REGION)
changes occur to the cells of the JCT - what does this do
slows the rate of aqueous production, so higher IOP
how do you differentiate changes in outflow pathway (POAG) to normal ageing changes
plaque like deposits in the JCT
how can secondary glaucomas arise
- intertrabecular spaces being blocked by cellular or non-cellular material
aqueous outflow pathway - uveo scleral
- this area is good for drugs like prostoglandin analogs
- aqueous enters ciliary body + leaves through vascular roots
mechanism of optic nerve damage (direct)
- loss of retinal ganglion cells, optic nerve head
- high IOP = stress and strain to eye = changes to lamina cribosa
- this remodelling leads to axonal damage + disruption of axonal transport
- essential factors not delivered = shrinkage + atrophy of RGC axons
why is axoplasmic flow important
- delivers essential topic factors to neural cell body
- interfering with pathway leads to death of retinal ganglion cells
Mechanism of optic nerve damage (indirect)
IOP can stress the nerves
- this stress can have acute and chronic effects on delivery of nutrients in blood to axons in lamina cribosa
when can ischaemia still occur
in predisposed indivudals with normal IOP
pharmacological regulation of IOP
trabecular outflow
- muscarinic agonists
uveoscleral outflow
- prostaglandin agonists
aqueous humour inflow
- beta blockers
-carbonic anhydrase inhibtors
- alpha agonists
surgery to improve drainage in glaucoma
-Selective laser trabeculoplasty
-Trabeculectomy- to open up pathway
-Minimally invasive glaucoma surgery (MIGS)
how can IOP be lowered
pharmacologically using drugs that reduce aqueous production or enhance drainage
