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Glaucoma > POAG > Flashcards

POAG Flashcards

1
Q

Explain what prevalence is?

A

Estimate of the number of people with a specific disease in the population

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2
Q

Which age range does POAG mostly occur in?

A

Over 40s

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3
Q

What’s the estimated percentage of people with POAG?

A

1-2%

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4
Q

Explain what incidence is ?

A

Number of new cases in a specific timeframe

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5
Q

What’s the incidence of POAG in the Netherlands?

A

4/1000

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6
Q

What’s the incidence of POAG is Australia?

A

2.2/1000

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7
Q

What’s the incidence of POAG in the US?

A

6.6/1000

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8
Q

Why is incidence more difficult to carry out?

A

Because it requires follow up over a long period of time

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9
Q

What’s the incidence of POAG in the U.K.?

A

11,000

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10
Q

Why is it difficult detecting POAG and why does it go undiagnosed in 9/10?

A

Because there’s a lack of symptoms in the early stages

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11
Q

What is the prevalence of POAG in 43-54?

A

0.9%

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12
Q

What is the prevalence of POAG in 75 years+?

A

4.7%

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13
Q

What is the incidence of POAG in 80 years+

A

4x

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14
Q

What is the

Risk factor of people with African ancestry to get POAG?

A

1.33x increased risk

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15
Q

What is the risk factor for African px over 80 to get POAG?

A

5x

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16
Q

What is the incidence of African px that are 40+ to get POAG?

A

8.5%

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17
Q

What is the incidence of Latino px to get POAG in over 40s?

A

4.74%

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18
Q

What is the risk of POAG from other ethnic backgrounds? (Which ethnicity is more at risk?)

A

Singapore px, Bangladesh, holland and U.K.

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19
Q

Who in the family increases the risk of POAG?

A

Siblings because they share a greater proportion of genetic material than parents

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20
Q

What is the risk of getting POAG when your sibling has it?

A

3.70x

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21
Q

What is the risk factor of getting POAG when your parent has it?

A

2.17x

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22
Q

Which gender is more at risk of POAG? And by how much?

A

Men by 1.37x

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23
Q

Is a myope or hyperope more at risk of POAG? And by how much? And what increases the risk?

A

Myopes are at risk by 3x. The greater the refractive error, the higher the risk of getting POAG. 1-3D: 2.33x
3D+: 3.3x

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24
Q

Why are myopes more at risk of POAG?

A

Because hy have an increased axial length which increases the stress on walls which increases iop which increases the stress on the onh which increases the chance of NFL damage

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25
Q

Is increased iop a risk factor for glaucoma or a diagnostic feature?

A

It’s a risk factor. It’s not a diagnostic factor because 50% of POAG px have an iop that’s normal

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26
Q

Is there a specific amount iop should be in order not to develop POAG? And what’s the associated between developing POAG and increased iop?

A

No there isn’t. There’s no safe level. The higher the iop is, the higher the risk of developing POAG

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27
Q

What happens when you modify iop?

A

Lowering IOP reduces the risk of POAG. Lowering POAG by 20% halved the risk of developing POAG

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28
Q

What influence does the corneal thickness have on IOP?

A

The thinner cornea leads to an underestimation of iop and thinner corneas have an increased risk of developing POAG

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29
Q

What is the risk factor of a px with a corneal thickness 540 of getting POAG?

A

3x

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30
Q

What tests need to be performed to check corneal thickness?

A

Pachymetry

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31
Q

Is a px who has a corneal thickness of 600 at risk of POAG?

A

No

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32
Q

Do systemic risk factors such as migraines, hbp and diabetes increase the risk of POAG?

A

Maybe a little but definitely not significantly

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33
Q

What, Why and how are px with raynauds at risk of POAG?

A

Raynauds is when the arteries spasm which leads to reduced compromised vascular circulation leading to reduced perforation to the she

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34
Q

Explain what POAG is in terms of its pathophysiology:

A

It’s a progressive prix neuropathy associated with iop related changes to the optic nerve head resulting in loss of vision

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35
Q

Explain light being processed in the eye with retinal ganglion cells

A

Light first enters the photoreceptors and then goes to the hz cells, bipolar cells and then amacrine cells (in the INL) and then to the ganglion cells which transmit light as electrical signals which then are sent to the brain

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36
Q

What is the procedure of RGC synapsing in the LGN?

A

The RGC dendrites collect signals via their dendrites and the signals are processed in the cell body and transmitted down the axon towards the ONH down the optic nerve and synapses at the LGN

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37
Q

Why does vision loss occur with ganglion cell damage?

A

Because it’s the final output signal from the retina and any damage to this leads to vision loss

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38
Q

When does vision loss due to RGC death/damage start to occur?

A

In very advanced cases

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39
Q

Why is POAG difficult to detect?

A

Because early onh changes are difficult to see and in the early stages it’s not got many sx

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40
Q

Why are visual field results very variable?

A

Due to the lack of sensitivity needed to detect early onh damage

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41
Q

When do visual fields pick up on the field defects?

A

When at least 50% of the field is lost

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42
Q

How do RGCs get nutrients?

A

1- proteins are delivered from the LGN to the RGC via RGC axons
2- from the fine capillary network fibres in the superficial layers of the retina and the onh
-they leave the rgcs exposed to glauc

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43
Q

Explain the association of the px’s age and developing glaucoma?

A

Normal ageing brings around a loss of neurons throughout the central nervous system. In the elderly eye, there can be a loss of RGCs that is close to the threshold where glauc causes visual field loss and NFL damage and RGC damage and you can’t distinguish this vf loss from the vf loss from glaucoma

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44
Q

Besides checking whether oedema is significant, what else can OCT do?

A

It allows us to meaure the thickness of RNFL which then correlates with cognitive function.

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45
Q

Explain the relationship

Between RNFL and RGC loss:

A

The thinner the RNFL, the greater the RGC loss

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46
Q

Explain the relationship between RNFL and RGC loss on cognitive function

A

The thinner the RNFL, the greater the loss of RGCs which show a reduction in performances on cognitive tests

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47
Q

What can oct predict besides oedema?

A

Age related conditions such as dementia

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48
Q

Explain how aqueous is produced?

A

The ciliary body produces aqueous which then circulates throughout the anterior chamber and drains via the trabecular into the canal of schlem or drains via the uveo scleral pathway

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49
Q

in relation to mechanical damage, what causes the increase of iop?

A

Restricted drainage

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50
Q

Does POAG occur due to restricted drainage?

A

yes, but there’s no obstruction that’s visible but drainage is compromised.

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51
Q

What does the aqueous exiting via the trab need in order to work efficiently?

A

It’s a pumping process therefore needs functioning endo and mito cells

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52
Q

Explain the drainage via the uveoscleral pathway:

A

Aqueous drains into the uvea via the ciliary body and exits via the sclera

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53
Q

Does iop increase of reduce with age?

A

Both routes of drainage are compromised and aqueous production reduces with age which shows no there won’t be an increase of iop with age

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54
Q

What is it called when px’s have high and differing iop but no glauc damage?

A

Ocular hypertensives

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55
Q

Does increased iop cause onh damage?

A

No it’s not a causative factor but iop needs only to be above the px’s safety level iop to increase the risk of RGC death

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56
Q

With iop why is the testing not very effective?

A

Because there’s spikes throughout the day with eye movements and blinking that could increased iop above the safe level and increase damage but we’re not able to capture it

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57
Q

What is the correlation between onh damage and iop

A

Iop is positively correlated with onh damage

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58
Q

Explain the relationship between increased iop and the risk or progression from oht to POAG

A

1mmHg is associated with a 10% increase risk of progression from oht to POAG

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59
Q

What is the risk of an untreated an untreated OHT px’s risk of progression from oht to unilateral blindness?

A

1.5-10.5%

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60
Q

What’s the risk in a treated oht of developing unilateral blindness?

A

0.3-2.4%

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61
Q

What treatment is there for OHT?

A

Iop lowering meds

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62
Q

Explain what happens with RNF at the lamina?

A

They converge into bundles at the onh where they exit via the sclera at the lamina

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63
Q

What is the lamina made of and what does it do?

A

It’s made of a network of collagen and provides a scaffold for RGC axons

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64
Q

Why does elevated iop cause deformation of the lamina?

A

Because the lamina is more flexible than the sclera

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65
Q

What happens when the lamina goes through deformation?

A

It bows posteriorly which places mechanical strain on the RGCs passing through

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66
Q

What does mechanical distortion limit the ability of RGC axons to transport?

A

BDNF: brain derived neurotrophic factor- protein which is critical for RGC health and without it, the RGC will die

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67
Q

Where does the bdnf get transported from?

A

From the LGN to the RGC cell body

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68
Q

What shape is the RGC axon bundle?

A

It reflects the shape of RNFL

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69
Q

If there was damage to a specific bundle at the lamina, what shape will the defect be?

A

Arcuate scotoma shape

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70
Q

Which meridian of the lamina is larger

A

Vertical

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71
Q

Which meridian of the lamina has less support?

A

Vertical

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72
Q

What is the majority of glauc damage attributable to?

A

Iop induced axonal damage at the onh or just compromised due to raised iop

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73
Q

If the RGC death occurs anywhere on the retina and not tied to a specific bundle, what can field defects look like?

A

They don’t just be arcuate scotomas bye can be diffused field loss too

74
Q

What is sensitive to vascular interruptions?

A

Neural tissue

75
Q

Explain what occurs with non-myelinated tissue:

A

They have an increased metabolic demand which then makes them specially sensitive to vascular interruptions

76
Q

What does compromised blood flow cause?

A

Localised ischemia leading to loss of RGC function and RGC death

77
Q

In glaucoma px’s what occurs affecting their blood supply?

A

They have below normal blood flow amongst px’s and reduced blood flow is observed at the onh, choroid and retinal vessels. They also have incomplete filling of vessels supplying onh which leads to reduced perfusion

78
Q

What does reduced perfusion correlate with?

A

Field defects

79
Q

What does localised ischemia cause?

A

RGC death

80
Q

Does reduced perfusion occur in OHT or just POAG with normal iop px’s?

A

Normal iop px’s

81
Q

What causes changes to the appearance of the RNFL at the onh?

A

Vascular factors/changes and mechanical damage

82
Q

What do changes to the RNFL and ONH case?

A

Field defects

83
Q

Will px’s wit RNFL and ONH changes have any symptoms?

A

No but it will eventually lead to field defects which would cause sx when an extensive part of the field is affected

84
Q

When will POAG start to show sx?

A

When an extensive part of the field is affected

85
Q

If field loss is monocular and in the non dominant eye, will you get sx?

A

No

86
Q

Why is there a lack of sx in POAG?

A

Because the acuity is driven by function of RGCs that serve the macula region and the RGCs form to make the papillomacular bundle which is spared till later stages of the disease

87
Q

When do we start seeing noticeable changes in the onh?

A

When significant RGC atrophy has occurred

88
Q

Where does the nerve fibre tissue loss occur in the lamina?

A

Anterior lamina - prelamiar

89
Q

What occurs at the posterior lamina?

A

Bowing (posterior bowing)

90
Q

What are the structural changes that occur in glaucoma?

A
  • thinning of the RNFL
  • thinning of the NRR
  • excavation (deepening of the cup)
91
Q

What causes an increase of cup death?

A

Loss of nerve fibre tissue

92
Q

What do we use to look at the cup depth?

A

Dilated pupil on the slit lamp

93
Q

If it’s not possible to check the depth with dilation what do we do?

A

See the angle on which the vessels go down from the NRR into the cup

94
Q

Explain what bayoneting is?

A

This is where the rim is lost and the vessels change direction and pass under the edge of the cup (sharp direction change and seem like a Z shape)

95
Q

Besides looking at the angle of which the vessels go in, how else can we see the depth of the cup?

A

By seeing whether the floor of the cup is in focus or not. If it’s out of focus and looks like it’s in another layer then it’s a deep cup

96
Q

How does the cd ratio increase?

A

The cup expands posteriorly and becomes deeper and expands away from the centre of the onh

97
Q

Is cd ratio useful?

A

No because all the cd ratios are different for different people

98
Q

Is a small disc and a large cup suspicious? If so why is it?

A

Yes because it signifies atrophy

99
Q

Is a small cup and large disc suspicious? If so why?

A

No. A large disc provides a large aperture for a fixed amount of nerve fibres to pass

100
Q

What are the correction factors for 66D, 78D and 90D lenses?

A

1x, 1.2x, 1.33x

101
Q

When a ON disc is classified, what’s the size of the disc after correction and what is the cd ratio of normal discs in that category?

A

<1.5mm and CD ratio <0.55

102
Q

What is the classification of a medium disc after the size correction has been applied and the cd ratio of normal discs in that category?

A

1.5-2.0 size and cd ratio: <0.65

103
Q

What is the classification of a large disc size after the correction factor has been calculated and the cd ratio of the normal discs in that category?

A

> 2.00 and cd ratio: <0.75

104
Q

With regards to the classification table of cd ratios and disc size, how do we know what’s not normal?

A

If it falls outside of the normal limits mentioned of THAT particular size

105
Q

Describe pathological cupping:

A

Cup becomes larger in comparison to optic disc

106
Q

What leads to pathological cupping?

A

Loss of neuro retinal rim

107
Q

Where does cupping start?

A

Inferior temporal then superior temporal (isn’t rule)

108
Q

Describe focal notching:

A

Nerve fibre atrophy in NRR

109
Q

How do we detect the presence of notching?

A

The thickness of the NRR declines (isn’t)

110
Q

What does it mean when the NRR doesn’t follow the isn’t rule?

A

There could be glaucomatous thinning (glauc damage)

111
Q

What if the NRR doesn’t follow the isn’t rule and never did? Is this a sign of long term of damage or just normal?

A

It’s normal because many eyes may not follow the isn’t rule and if the eye never followed it, then it doesn’t show glaucomatous damage

112
Q

If the px had always followed the isn’t rule but for this app they seem to not follow the isn’t rule then is this suspicious?

A

Yes because if they were previously following it but now not, we now start to suspect glaucoma due to the thinning of NRR due to atrophy

113
Q

What is focal notching associated with?

A

Flame haemorrhages at the onh

114
Q

What is the difference between flame haemorrhages and splinter haemorrhages?

A

They’re both the same and have same appearances but splinter haemorrhages are called splinter because theyre flame haemorrhages found at the onh

115
Q

Besides at the onh, where else are splinter haemorrhages found?

A

Near focal NRR notches

116
Q

What do splinter haemorrhages reflect?

A

Glaucomatous damage to RNFL due to atrophy of the RGC axons leading to support loss for the capillaries

117
Q

Are splinter haemorrhages a risk factor of imminent onh damage?

A

No, they’re a sign of ongoing glauc progression

118
Q

What can focal notching be associated with?

A

Peri papillary atrophy

119
Q

Where is PPA mostly found?

A

On the onh’s temporal side

120
Q

Where is ppa restricted to?

A

The area with the most RNFL thinning

121
Q

Besides being associated with focal notching, who else is at risk of ppa?

A

Elderly and myopic px’s

122
Q

When and why shouldn’t ppa be considered a risk for some people?

A

It’s more common amongst elderly and myopes if it’s circumferential or at the temporal margin

123
Q

What are all glaucomatous onh changes associated with increasing?

A

Pallor

124
Q

Define pallor?

A

Paleness of the NRR

125
Q

What happens as RGC atrophy progresses?

A

The cup gets larger and and an increasing amount of the disc takes on te cups colour

126
Q

What colour does the cup floor be?

A

The colour of the lamina cribrosa (white/grey)

127
Q

What overlays and obscures the lamina cribrosa?

A

RNFL

128
Q

What colour is a healthy NRR?

A

Yellow/pink/orange

129
Q

What does onh atrophy cause in regards to pallor?

A

Less light to be absorbed by thin RNFL which then produces more pallor as more light reaches the lamina

130
Q

In a healthy eye where is pallor greatest?

A

Temporal where NRR is thinnest

131
Q

What’s a sign of glaucomatous damage regarding pallor?

A

Irregularity around the cup margin

132
Q

Describe the formation of an acquired optic disc:

A

It’s linked to RNFL atrophy and is a discrete area of depression within the optic cup at the level of the lamina

133
Q

What is an oct used to see?

A

Measure RNFL thickness or see whether oedema is significant or not

134
Q

Why is good for glauc px’s?

A

Because it detracts field defects 8 years before fields

135
Q

What are the limitations of slit lamp based onh assessments?

A

1) - RGC atrophy causing structural changes occurs slowly so a single exam can’t provide an accurate snapshot of the px’s onh and can’t confirm or deny whether they have glaucoma. Observations over a few appointments show the presence or absence of the progressive disease
2) - there’s a subjective nature in the measurements and variability across different clinicians and they may also be carried out under poor img quality
3) - myopic eyes ace tilted discs and ppa which make NRR assessing challenging

136
Q

Define the threshold in fields:

A

The minimum light intensity needed for reliable detection at multiple points within the vf

137
Q

Which part of the visual field does glaucoma affect?

A

Central 30 deg before going to more peripheral areas

138
Q

Why is it unnecessary to do a field test on more peripheral areas?

A

Because first it affects central and doesn’t affect the outer periphery till after

139
Q

Why aren’t fields very useful?

A

Because it doesn’t show damage of the field until extensive damage is done and they may have limited screening programs with only a pass fail criteria

140
Q

If you have a right eye, which side is the blind spot on?

A

Temporal side

141
Q

If there’s glaucomatous damage to the px’s ganglion cells in the temporal field, where will the field defect be?

A

Nasal defect

142
Q

If there’s damage at specific RGC axons in the onh, what defects are produced?

A

Localised actuate defects

143
Q

What kind of field defects are associated with glaucoma?

A

Arcuate defects, paracentral defects and diffused loss

144
Q

Where do arcuate field defects begin and where do they last effect?

A

Superior nasal, inferior nasal, inferior temporal, superior temporal

145
Q

Why don’t arcuate and paracentral defects cross the midline?

A

Because they’re bundles that serve specific regions

146
Q

What is it called when the defects become more dense?

A

Altitudinal defects

147
Q

What happens when field defects in glaucoma become more extensive?

A

Inferior and superior facts merge to form field defects that will cross the midline

148
Q

If visual loss in glaucoma is monocular or bilateral but asymmetrical, what will occur?

A

+RAPD

149
Q

What happens if RGC cell bodies are effected?

A

RGC function will be compromised across scattered areas causing a diffuse loss of field

150
Q

If the field loss of diffused, should we be concerned about glaucoma damage?

A

Yes, any visual loss should be taken serious with or without suspicious signs

151
Q

Can you have arcuate, paracentral and diffused loss altogether?

A

Yes, multiple defects can occur

152
Q

What induces a defect that’s visible binoculary?

A

If the defects are close to fixation in either eye or defects in opposite eyes overlap

153
Q

When would you get sx in px with glaucoma?

A

When the defects are very close to fixation

154
Q

What do we need to do to ensure an extensive amount of field isn’t lost before the px gets referred?

A

We need to aid early detection by combining results with other assessment information and the px’s risk factors instead of just relying on field results and field loss

155
Q

When should to px be referred?

A

If the optom identifies one or more of the following:

  • onh damage consistent with glaucoma (change in the isn’t rule, notching, bayoneting, ppa) with or without raised iop
  • iop exceeds 24mmHg
  • field defect consistent with glaucoma
  • narrow drainage angle (pcag)
  • conditions associated with glaucoma (pds, pseudo)
156
Q

What if acquired optic pathology has been found?

A

It requires ophthalmological opinion due to the possibility of progressive onh damage

157
Q

What if iop over 24 is only found and nothing else?

A

Then we should refer only if it was measured via Goldman

158
Q

If the iop was only

Measured via nct and it was over 24, what should we do?

A

We should first refer them to a referral refinement clinic and remeasure it with Goldman

159
Q

What would you do if your px had an iop above 24 but there was no referral refinement clinics?

A

Then you’d have to refer them regardless of

How it was measured and the referral letter should indicate the referral is in a sense of a repeat readings scheme

160
Q

What protocol should be followed if referring only on nct?

A
  • take four readings per eye and take the mean
  • only when the mean result is 24 should you refer for further tests because if there’s not 4 tests carried out then the chance of getting a mean number is higher
161
Q

What should you do with oht px’s?

A

Treating them isn’t cost effective and they won’t
Be treated for glauc damage anyway because they have no signs of glauc. The only treatment they should have is iop lowering meds

162
Q

What is the referral threshold for raised iop?

A

24mmHg

163
Q

When px’s with iop over 24 are referred with no other signs but haven’t been diagnosed with oht, what tests are carried out?

A
  • iop using Goldman
  • cct with pachymetry
  • ac depth with gonioscopy
  • field tests with sap
  • optic nerve assessment with dilation
164
Q

If your view is obscured of the fundus but it’s risky dilating the px, what would you do?

A

Make a judgement as to whether glaucoma is more dangerous for them or the original pathology

165
Q

When is it obvious that a field defect has occurred due to glaucoma?

A

When the fields is repeated and the same defect appears removing the chance of human error or anomaly

166
Q

If you see a field defect, when should you refer?

A

If it’s a repeatable defect, recent or progressive, it should be referred even if there’s no link to glaucoma (raised iop or onh damage) but before doing so you need io repeat it to make sure its field loss and not an error or in the incorrect place

167
Q

If you had a px who had onh changes that were associated with glaucoma damage, iop over 24 measured with Goldman and field defects that had been repeated and showed the same thing, what would the referral be?

A

Routine/non-urgent referral (and it could be months so inform the px)

168
Q

If the iop is over 35 and there’s field loss, what would the referral be?

A

Same day phone call to hes

169
Q

Who should we routinely do fields testing and iop checks on?

A
  • px from ethnic groups that are at a higher risk
  • px’s over 40s
  • family history (first relative)
  • if the px has been taking steroids
170
Q

What do shared care schemes introduce?

A

“In house triages” which reduce false positives

171
Q

Who falls into the false positive groups with (glaucoma specific shared care schemes)?

A
  • px’s who meet some criteria for oht (raised iop) but normal discs etc and then have Goldman and get iops below 24
  • px who have some criteria for POAG e.g. Field defects and after triage they’re found to be inconsistent or absent and everything else is normal
172
Q

What are false positives in fields caused by?

A

They can be cause by lens artefacts or poor px understanding/cooperation

173
Q

If an optom comes across a suspicious onh appearance and suspects glauc, what happens with referral?

A

They can be referred to hes, glaucoma specialist or triaged by another optom at another practise, the same practise can’t provide an in house triage

174
Q

Who are these shared schemes commissioned by?

A

Commissioning groups who work with the loc to implement schemes

175
Q

Explain a tier 1 iop app:

A
  • Goldman needs to be done firstly
  • if the iop is less than 24, then we don’t need to treat it
  • if it’s more than 24, then we need to repeat it
  • if repeated and it’s still 24, then additional tests need to be done in hes
176
Q

Describe a tier 2 fields and iop app:

A
  • Goldman and fields need to be repeated

- field defects consistent and still there when repeated and iop is still more than 24 then we need to refer to hes

177
Q

Besides repeating iop and fields, why else can a tier 2 app be used to carry out?

A

Dilation of onh

178
Q

If theres no referral refinement, what do we refer px’s on?

A

Nct readings but hes may request Goldman

179
Q

What is the inclusion criteria for oht px’s?

A
  • px diagnosed with oht and don’t require treatment
  • px diagnosed with oht who are on iop lowering drops but who’s treated iop is within target
  • psudo/pigment syndrome with iop greater than 24 mmHg but no other signs
180
Q

What’s the oht monitoring service exclusion criteria?

A
  • POAG (with pseudo/pds)
  • suspect glaucoma
  • raised iop with angles in danger of closing
181
Q

What does an oht monitoring service involve (test wise)?

A
  • re ask new sx and compliance with drops if provided
  • VA
  • threshold perimetery
  • Goldman
  • van herick
  • volk
  • decision to continue on oht monitoring or refer back to glauc clinic in hes if iop not within target or problems with drops
182
Q

What’s the criteria for referring back to hes glauc clinic?

A
  • iop over 32
  • iop over target
  • field defect
  • change in optic disc appearance
  • repeat gonioscopy
  • repeat cct
  • poor compliance or adverse reactions to meds
  • other indications of a change in condition

Glaucoma (7 decks)

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