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OD3 - Clin. Optometry Sem 1 and Preacademic Period > D - Glaucoma Histopath 1 - Week 2 > Flashcards

D - Glaucoma Histopath 1 - Week 2 Flashcards

1
Q

Define ocular perfusion

A

amount of blood getting to the nerve

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2
Q

Define papilloedema

A

oedema in the discs of BOTH eyes. (so has to be bilateral. If unilateral oedema, it’s not papilloedema)

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3
Q

How does papilloedema occur?

A

only occurs from brain/neural causes (e.g. brain tumour)

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4
Q

Does the disc in a patient with only glaucoma (glaucoma optic neuropathy) present with swelling or palor?

A

NO

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5
Q

What is the major cause of demyelination of nerves in the eye?

A

Multiple sclerosis

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6
Q

List 6 causes of optic neuropathy that present with swelling/pale/vision afected

A 
Inherited ON
Inflammatory/infectious ON
Demyelinating ON
Toxic ON
Compressive ON
Ischemic ON
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7
Q

Is vision normal in glaucoma optic neuropathy?

A

yes

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8
Q

Describe how the nerve appearance typically changes as optic neuropathy progresses

A

Starts with oedema at 1 week. By 2 months, the oedema gets paler, and by 3 months, oedema goes away and is replaced with just palor.

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9
Q

Why can diagnosing optic neuropathy be difficult if a patient has had it for 6 months?

A

By 6 months, you can’t tell the cause of the disc palor in fundus examination. You would need contact from GP or something from previous appointment to help determine the cause of the pallor

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10
Q

What are the 2 main types of glaucoma? Describe typical IOP levels for each

A

POAG: may or may not have high IOP
PCAG: always has high IOP (>30mmHg at some stage)

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11
Q

List two mechanisms for angle closure glaucoma. Can they be seen with VH?

A
  1. Pupil block/iris impeding angle - can be identified with VH
  2. Gunk in eye causing TM blockage - need gonio to see this
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12
Q

What is the normal number of RGCs lost per eye per year with normal ageing?

A

~5000 cells/eye/year (due to apoptosis)

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13
Q

How does GON impact the number of RGCs lost over time?

A

accelerates loss of neurons by apoptosis.

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14
Q

How does ischemia impact the number of RGCs lost over time? Explain what happens to the RGCs.

A

Ischemia triggers a sudden/massive loss of RGCs. This results in creating so much gunk etc. that the remaining neurones can no longer survive, causing them to undergo autophagy (a slower loss).

(So a fast big loss, followed by a smaller slower loss)

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15
Q

What aspects of the optic nerve makes it susceptible to neuropathy?

A
  1. High mitochondrial density
  2. Dense capillary plexus in lamina & about the nerve
  3. Complex pressure gradients on tissues/axons
  4. Axons, RGC soma & microglia susceptible to increase in IOP
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16
Q

Where is high mitochondrial density found in the optic nerve? Why?

A

Very dense mitochondria in prelamina region due to the high energy demand of axons going through the lamina to the brain.

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17
Q

What does mitochondrial abnormality promote? (2)

A

Oxidative damage + inflammation
Energy depletion

Both promote apoptosis

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18
Q

What does “axoplasmic stasis” refer to?

A

A cease in axonal transport due to energy depletion/mitochondrial abnormality

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19
Q

What is the role of the capillary plexus? What happens if it’s compromised?

A

delivers oxygen & metabolites to axons + mitochondria. If compromised, you can get hypoxia/ischaemia

20
Q

What pressure gradient exists for the optic nerve?

A

Translaminar Pressure Gradient. (TLPG)
This gradient is created at the lamina cribrosa and is a gradient between the IOP and intracranial pressure (ICP). Can be defined as the difference between IOP and ICP per unit thickness of the lamina cribrosa

TLPG = (IOP/ICP) /thickness of LC

i.e. it’s IOP vs ICP

(or alternatively, you could say IOP + BP vs TP, where TP = the post lamina tissue pressure, which is equivalent to ICP)

21
Q

How can an imbalance of the translaminar pressure gradient affect the optic nerve?

A

Imbalance can cause lamina bowing &/or scleral stretch

i.e. the lamina starts stretching out as the pressure increases. “It’s like putting too much air in a soccer ball”

22
Q

How can lamina bowing & scleral stretch affect the appearance and function of the optic nerve?

A

Distorts lamina pores which breaks capillaries, thus reducing capillary perfusion to the lamina and peripapillary choroid (scleral) region (hypoxia)

23
Q

What does an imbalance of the translaminar pressure gradient ultimately lead to?

A

promotes neuroinflammatory processes and axonal and RGC apoptosis

24
Q

Where in the optic nerve do nerve fibres become myelinated?

A

in the post-laminar region

25
Q

How can an increase in IOP affect axons, RGC soma and microglia of the optic nerve? (6)

A

Increased IOP activates RGC pressure receptors
RGCs get stressed - can’t sustain axoplasmic flow through LC
Glial cells become reactive - increase production of TNFalpha
Inflammatory cascades activate - damage lamina axons
Damage stops neurotrophins (FOOD) flowing to axons
Axons get sick.

26
Q

What does axonal damage at the lamina lead to? (4)

A 
RGC apoptosis (b/c no neurotrophins/food)
Leads to thinning in RNFL
Loss of axons weakens lamina integrity causing lamina to bow backwards (cup deepens)
Capillaries break etc.
27
Q

What happens to the optic nerve in advanced stages of IOP damage? (3)

A

Apoptosis + neuroinflammation ==> soma/axon death
Lamina weakens further (b/c large loss of axons) + remodels
Lamina bows even further backward

28
Q

Which kind of glaucoma is likely responsible for acute cell death? What about programmed cell death?

A

Acute cell death: PACG

Programmed cell death: POAG

29
Q

Describe the histological changes in:
A: Early GON (glaucomatous optic neuropathy)
B: Advanced GON

[NB: the images from this slide are practically guaranteed on exam!]

A

A: Clean loss of NFL and GCL = apoptosis. INL is ok
B: increased thickness of NFL due to gliosis. INL thins

(*gliosis = activation of glia cells. e.g. astrocytes)

30
Q

How does RGC loss manifest clinically? (2) Explain

A

Loss of neural rim. Via 1. loss of ganglion cell and 2. loss of axons or NFL
This expresses as increased CDR

31
Q

Is CDR a good indicator of GON? What do we consider a normal CDR?

A

Poor indicator of GON due to large variation in disc size. Normal CDR = 0.7

32
Q

What aspect of the optic nerve appearance is a good indicator of GON?

A

NRR thickness!

—ISNT rule is a moderate indicator for GON

33
Q

Briefly describe how visual field defects progress with glaucoma in 4 steps

A
  1. Little blind spots in arcuate regions (b/w 10 and 20 deg)
  2. Blind spots join up to form arcuate scotoma
  3. Inferior seidel scotoma formation
  4. Central Ronne’s step (a nasal step) formation
34
Q

What are the 3 tests for counting RGC numbers? And which is better in general?

A

O.N (NRR photos)
NFL (TSNIT)
Macula GCC

In general, NFL > GCC > NRR

35
Q

Which test for counting RGCs is good for myopes? Why not use NFL for myopes?

A

ON is good for myopes.

NFL not as good b/c NFL is thinner in myopes

36
Q

How many of the 3 tests for counting RGCs are needed to make a diagnosis?

A

all of them

37
Q

List 4 apoptotic triggers for GON induced RGC death

A

prolonged IOP elevation
loss of mitochondrial capacity
reduced perfusion
neuroinflammatory induction

(technically this has been covered earlier in lecture)

38
Q

List 3 necrotic triggers for GON induced RGC death

A

very high IOP
low sBP
loss of blood (shock)

(causing acute trauma/ischemia)

39
Q

What apoptotic mechanisms are there? (3)

A 
Pressure dependent mechanisms (mechanical)
Neuroinflammatory mechanisms (FAS, TNFalpha)
Mechanisms secondary to mitochondrial aging
40
Q

What are the 2 pressure dependent mechanisms of apoptosis? Explain them

A

Stretch mechanism: Potassium influx via TRAAK/TRASK alters NMDA channel causing Ca+ influx
Tension mechanism: Tension on the membrane alters NMDA causing Ca+ influx

Too much calcium = apoptosis

41
Q

How do the 2 pressure dependent mechanisms alter the NMDA channel?

A

By dislodging the Mg-ion

42
Q

What inflammatory responses can cause apoptosis? (2)

A

Direct pressure effect on microglia or
Reduced perfusion (BP-IOP)
— i.e. chronic imbalance of IOP and blood supply at optic nerve

43
Q

What does a chronic imbalance of IOP and blood supply at the optic nerve lead to? (3)

A

Reduced mitochondrial function
Increased inflammatory cytokines
Reduced axoplasmic flow (leading to reduced bDNF)

44
Q

What does mitochondrial aging generally do? (2)

A 
Produces oxidative stress
Reduced ATP (energy) (therefore harder to do axonal transport, therefore reduced neurotrophic/food support)
45
Q

What 2 mechanisms from mitochondrial aging promote apoptosis

A
  1. Lack of bDNF due to axoplasmic stasis
  2. Lack of lamina derived neurotrophic factors (LDNF) due to elevated IOP

*bDNF = brain derived neurotrophic factor

46
Q

How can IOP independently affect the lamina?

A

the actual lamina pores get larger and move further away from each other

OD3 - Clin. Optometry Sem 1 and Preacademic Period (25 decks)

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