10 - Pathogenesis of Glaucoma Flashcards

1
Q

most common features of glaucoma

A
  • loss of retinal ganglion cells
  • thinning of retinal nerve fibre layer
  • cupping of disc
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2
Q

when does secondary glaucoma occur

A

when there is an underlying condition

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3
Q

what is open angle glaucoma

A
  • extracellular material becomes depositied in trabecular meshwork
  • gives rise to increased resistance to outflow - raise IOP
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4
Q

risk factors of glaucoma

A
  • black
  • IOP > 26mmHg
  • myopia (>3D)
  • diabetes
  • FH
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5
Q

clinical features of glaucoma

A
  • extensive inferior visual field loss
  • subtle changes in NRR
  • disc cupping
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6
Q

primary angle closure glaucoma

A
  • pupil block
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7
Q

role of IOP

A

represnts primary risk factor for developing glaucoma
- both incidence + progression of glauc can be controlled by decreasing IOP

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8
Q

what is increased IOP due to in OPEN ANGLE glaucoma

A
  • increased resistance ot outflow
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9
Q

what is increased IOP due to in CLOSED ANGLE glaucoma

A

pupillary block

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10
Q

how is impact of IOP on pathogenesis of glaucoma explained

A

2 theories
- mechanical (direct)
- vascular (indirect)

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11
Q

what is aqeous produced by

A

ciliary epithelium

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12
Q

where does aqeous drainage occur

A

irido- corneal angle via conventinal + uveo scleral pathways

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13
Q

what is IOP determined by

A

the balance between aqueous production and drainage

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14
Q

mechanism of aqueous production

A
  • 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
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15
Q

what is the catalyser of this mechanism (aqueous production)

A
  • carbonic anhydrase
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16
Q

aquous outflow pathways

A
  1. majority drains through trabecular meshwork/canal of schlemm (conventional pathway)
  2. some drains through uveo-scleral pathway
17
Q

what are the 3 distinct layers of aqueous outflow pathway ( conventional)

A
  1. uveo trabeucli
  2. corneal-scleral trabeculi
  3. juxta canicular - adjacent to canal of schlemm
18
Q

glaucoma is associated with an increased?

A
  • resistance to outflow
19
Q

in open angle glaucoma, where is resistance higher than normal

A

-JCT (INNER WALL REGION)

20
Q

changes occur to the cells of the JCT - what does this do

A

slows the rate of aqueous production, so higher IOP

21
Q

how do you differentiate changes in outflow pathway (POAG) to normal ageing changes

A

plaque like deposits in the JCT

22
Q

how can secondary glaucomas arise

A
  • intertrabecular spaces being blocked by cellular or non-cellular material
23
Q

aqueous outflow pathway - uveo scleral

A
  • this area is good for drugs like prostoglandin analogs
  • aqueous enters ciliary body + leaves through vascular roots
24
Q

mechanism of optic nerve damage (direct)

A
  • 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
25
why is axoplasmic flow important
- delivers essential topic factors to neural cell body - interfering with pathway leads to death of retinal ganglion cells
26
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
27
when can ischaemia still occur
in predisposed indivudals with normal IOP
28
pharmacological regulation of IOP
**trabecular outflow** - muscarinic agonists **uveoscleral outflow** - prostaglandin agonists **aqueous humour inflow** - beta blockers -carbonic anhydrase inhibtors - alpha agonists
29
surgery to improve drainage in glaucoma
-Selective laser trabeculoplasty -Trabeculectomy- to open up pathway -Minimally invasive glaucoma surgery (MIGS)
30
how can IOP be lowered
pharmacologically using drugs that reduce aqueous production or enhance drainage
31