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Therapeutics > The pathogenesis of primary open angle glaucoma > Flashcards

The pathogenesis of primary open angle glaucoma Flashcards

1
Q

what is the definition of glaucoma

A

a progressive optic neuropathy having characteristic morphological changes of the optic nerve head and retinal nerve fibre layer
in the absence of other ocular disease and their congenital abnormalities

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2
Q

what 2 components does glaucoma cause damage to and what does this damage result in

A
  • the optic nerve head
  • the peripapillary retinal nerve fibre layer

results in a characteristic visual field defect

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3
Q

how common is glaucoma as a cause of blindness in the UK

A

2nd/3rd most common cause

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4
Q

__________ registration from glaucoma continues to ________

A

blindess registration from glaucoma continues to increase

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5
Q

what are the 2 classifications of glaucoma

A
  • primary glaucoma

- secondary glaucoma

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6
Q

what are the 2 types of primary glaucoma

A
  • open angle

- closed angle

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7
Q

what is secondary glaucoma the result of

A

due to underlying medical condition or injury to the eye

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8
Q

how much of all glaucomas encountered does POAG account for

A

the majority - 85%

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9
Q

what is POAG due to

A

the resistance in the aqueous outflow pathway

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10
Q

what are the 2 routes which aqueous leaves the eye

A
  • trabecular meshwork

- uveoscleral outflow

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11
Q

list the steps of production of aqueous to when in reaches the anterior chamber

A
  • aqueous humour is produced by the ciliary epithelium
  • it percolates out into the posterior chamber
  • it passes through the pupil
  • and into the anterior chamber, where it circulates
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12
Q

what is the role of aqueous humour

A

to provide nutrients to the lens and cornea (particularly the corneal endothelium) and to remove metabolic waste product from these 2 areas

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13
Q

what are the 2 classes of outflow pathways of aqueous humour

A
  • conventional - trabecular meshwork

- unconventional - eveoscleral

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14
Q

explain how aqueous drains from the eye via the conventional pathway

A

aqueous leaves through the trabecular meshwork into schlemm’s canal and then into collector channels and episcleral veins

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15
Q

explain how aqueous drains from the eye via the unconventional pathway

A

aqueous passes through interstitial spaces of ciliary muscle and choroid, or suprachoroidal space transclerally

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16
Q

majority ____% of aqueous will leave through the ___________ ____________

A

majority ~90% of aqueous will leave through the trabecular meshwork

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17
Q

what is the trabecular meshwork composed of

A

primarily of collagen beams which interlace with each other

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18
Q

how is the trabecular meshwork constructed and why

A

the collagen beams leaves spaces/pores at which the aqueous passes

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19
Q

how many anatomical regions are there of the trabecular meshwork and describe each one

A

1st region: uveal meshwork - here the spaces between the trabecular beams/pores are quite large, therefore when aqueous passes through here, theres very little resistance to its flow

2nd region: corneoscleral meshwork - here the pore sizes/spaces formed by the beams are much smaller, therefore causes a slightly more resistance to flow of aqueous to this region

3rd region: juxtacanalicular meshwork - which lines schlemm’s canal, at this point this is where aqueous is at its most resistance

aqueous collects into schlemm’s canal through the formation of giant vacuoles, the aqueous then goes through the collector channels and drains into the epi scleral veins

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20
Q

what is the 1st region of the trabecular meshwork called and what happens with the aqueous here

A

uveal meshwork

here the spaces between the trabecular beams/pores are quite large, therefore when aqueous passes through here, theres very little resistance to its flow

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21
Q

what is the 2nd region of the trabecular meshwork called and what happens with the aqueous here

A

corneoscleral meshwork

here the pore sizes/spaces formed by the beams are much smaller, therefore causes a slightly more resistance to flow of aqueous to this region

22
Q

what is the 3rd region of the trabecular meshwork called and what happens with the aqueous here

A

juxtacanalicular meshwork

which lines schlemm’s canal, at this point this is where aqueous is at its most resistance

23
Q

how does the aqueous drain away once it has reached schlemm’s canal

A

aqueous collects into schlemm’s canal through the formation of giant vacuoles, the aqueous then goes through the collector channels and drains into the epi scleral veins

24
Q

list the stages of where the aqueous drains through via the unconventional pathway

A
  • the aqueous bypasses the trabecular meshwork
  • there is no epithelial barrier between the anterior chamber and supraciliary space
  • so the aqueous collects into this space
  • it then goes through into the inter muscular spaces of the ciliary body which is filled with lose connective tissue
  • then it goes through the suprachoroidal space which also has lose connective tissue and is considered largely as a potential space
  • the aqueous they gradually diffuses through the M scleral channels of the sclera
25
Q

what is the supraciliary space

A

its space just above the ciliary body

26
Q

what is the inter muscular spaces of the ciliary body

A

it is space between the 3 layers of the ciliary muscle which is filled with lose connective tissue and some ground substance which makes it potential for aqueous to collect there

27
Q

what is the suprachoroidal space

A

space just above the choroid, also another space for aqueous to collect

28
Q

what happens to the aqueous in glaucoma that results in a patient having increased IOP

A
  • aqueous is produced as normal

- there is increased resistance to drainage

29
Q

what 2 factors can cause an increased resistance to drainage

A
  • increases with age - due to hardening of the trabecular meshwork
  • genetic factors - affect the composition of the collagen beams of the trabecular meshwork, may predispose px from getting glaucoma
30
Q

in open angle glaucoma, the build up of ______ __________ in the anterior chamber has the effect of building up the _________ ____________ in the eye that causes damage to the _______ ________ and ____________________ and this damage in the _____ will manifest as a ________ _________ _________

A

in open angle glaucoma, the build up of fluid pressure in the anterior chamber has the effect of building up the overall pressure in the eye that causes damage to the optic nerve and retinal nerve fibre layer and this damage in the NFL will manifest as a visual field defect

31
Q

damage to the _________ ONH and RNFL manifests as a __________ ___________ visual field defect

A

damage to the inferior ONH and RNFL manifests as a superior paracentral visual field defect

32
Q

where is the primary sight of insult from raised IOP

A

optic nerve head

33
Q

what structure does the damage of the ONH subsequently damage

A

retinal ganglion axons - irreversible permanent damage

34
Q

what is the environment of the retina important for

A

helping the RGCs stay viable and healthy with its support cells

35
Q

what support cells does the retina have in order to keep RGCs healthy and how do they support provide this support

A
  • muller cells
  • amacrine cells
  • astrocytes
    they all provide nutrition and help to maintain glutamate homeostasis in the retina
36
Q

why is glutamate needed in the retina

A

to ensure that nerve cells will fire

glutamate homeostasis has recently been shown to play a role in RGC viability

37
Q

what are the 2 features that contribute to the glaucomatous optic neuropathy

A
  • microcirculation - which provides nutrition and removes waste products of the ONH and retrobulbar ON
  • the lamina cribrosa/ONH itself - how the axons pass through here

these two features can potentially contribute to causing damage to the RGC axons and causing glaucoma

38
Q

what are the 2 theories of glaucoma

A
  • mechanical theory

- vascular theory

39
Q

what is the lamina cribrosa and what exits the eye via this structure

A
  • a series of perforated collagenous sheets, like a sieve
  • retinal ganglion cell axonal bundles which leave the eye from the ONH, have to go through the lamina cribrosa before they get to the bulbar optic nerve
40
Q

how is the lamina cribrosa structures in humans

A

the pore sizes are varied by region, with the inferior and superior poles have pores which are much larger, so larger bundles go through these pores, compared to those passing through the nasal and temporal poles

41
Q

how are the path of the RGC axons when they go through the sieve of the lamina cribrosa

A

the path of the axons are not straight as each axon bundle has to go a convoluted way through the lamina cribrosa before it reached the retro bulbar space

42
Q

how does raised IOP have a direct effect on the lamina cribrosa
which forms the basis of the mechanical theory of glaucoma damage

A

it causes compression of the lamina cribrosa plates and a shearing/stretching of the pores, so as the bundles pass through the pores, they get damaged (i.e. stretched, sheared and compressed)

this forms the basis of the mechanical theory of glaucoma damage

43
Q

what happens to the RNFL as the axon bundles get damaged

A

the axon bundles start to die off and in the RNFL they start to coalesce to form larger wedge defects if they pressure remains uncontrolled and the lamina remains damaged

this regional pore size helps to explain why in glaucoma, you have damage to the inferior and superior RNFL first, because the pores in these areas are larger so theres more axon bundles going through these areas hence causing more stretching, shearing and damage

44
Q

what is the appearance of the ONH like as a result of glaucoma and the associated structures

A
  • the lamina cribrosa which is in the optic cup have slightly striated and distorted pores
  • there can be a notch = a complete loss of the inferior NRR
  • the calibre of the blood vessel is going to go into the exasperated cup and coming out again in the inferior retinal surface
45
Q

what does the vascular theory of glaucoma describe

A

how the microcirculation changes and how this will contribute to RGC damage and RGC axon damage

if the blood vessels supplying the RGC axons are poorly perfused/theres not enough blood passing through these blood vessels, then that axon bundle will not get nutrition or removal of waste therefore the axon bundle gradually gets damaged and will die

46
Q

what is the appearance of a healthy ONH and retro bulbar ON

A

they are well perfused = have millions of micro capillaries that will supply nutrients to the optic nerve and RGC axons as they leave the retina and pass through the ONH

47
Q

there is no direct contact between the _________ _________ and __________ __________ as each axon bundle is protected by a layer of __________, but each bundle has its own ________ _________

A

there is no direct contact between the blood vessels and axonal bundles as each axon bundle is protected by a layer of astrocytes, but each bundle has its own vascular supply

48
Q

list 3 causes of potential mechanisms of poor ocular blood flow/perfusion

A
  • local resistance to ocular blood flow
  • reduced ocular perfusion pressure
  • blood hyper viscosity
49
Q

what 2 things can cause local resistance to ocular blood flow

A
  • atherosclerosis - at the level of the ONH or bulbar ON which can be caused by systemic diseases
  • defective auto regulation - instead of bv’s dilating, they constrict
50
Q

what 3 things causes reduced ocular perfusion pressure

A
  • increase in IOP or decrease in BP or both
  • microvascular disease, peripheral vasospasm (Raynaud’s, migraine), systemic hypotension

has a direct affect on the calibre of the blood vessels = almost like a compression of those capillaries therefore not enough nutrition is getting to the optic nerve. so raised IOP has a direct affect on ocular blood flow

Therapeutics (19 decks)

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