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OD3 (S1&2) > DIS - Glaucoma Histopathology II - Week 2 > Flashcards

DIS - Glaucoma Histopathology II - Week 2 Flashcards

1
Q

Between apoptosis and necrosis, which is more likely to be associated with open angle glaucoma and closed angle glaucoma?

A

Open angle - apoptosis
Closed angle - necrosis

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2
Q

What produces aqueous humour? How does it flow once made?

A

Produced by the ciliary body and flows around the lens to the anterior chamber, nourishes the lens and corneal endothelium

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3
Q

Describe what two structures drain the aqueous humour (and percentages).

A

5-15% drains via the trabecular meshwork into schlemms canal
85-95% drains via the uveo-scleral route

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4
Q

What structures allow rapid, fine control of aqueous outflow and where are they found exactly?

A

Giant vacuoles found on the endothelial surface of schlemms canal

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5
Q

What do trabecular cells cover, what do they produce, and what does this substance do?

A

They cover beams of cribiform meshwork, producing a gel filler of GAGs, glycoproteins, and fibrillar material
It is thought to slow down flow and stick to debris

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6
Q

What do trabecular cells do to debris?

A

They are highly phagocytic and clean debris from the meshwork

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7
Q

List three things that can cause meshwork blockage

A

Pigment blockage
Debris
Vacuole dysfunction

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8
Q

What two post-trabecular dysfunctions can cause an angle compromise?

A

Decreased venous drainage
Increased venous backpressure

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9
Q

What is irido-corneal endothelial (ICE) syndrome?

A

Anterior membrane overgrowth, causing angle closure
The PTM is occluded by the iris

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10
Q

What is the abnormality in congenital glaucoma?

A

Malformed trabecular structures

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11
Q

List three possible causes of secondary open-angle glaucoma.

A

Resistance to outflow
Increased debris in the TM exceeding phagocytic capacity
GAGs in connective tissue block flow

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12
Q

List two causes of resistance to trabecular meshwork outflow.

A

Pigment dispersion
Pseudoexfoliation

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13
Q

List a cause of TM debris exceeding phagocytic capacity.

A

Steroid use

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14
Q

List a cause of GAGs in connective tissue blocking flow.

A

Steroid response TIGR gene

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15
Q

What kind of mode of inheritance does congential glaucoma causing malformed TM have? Why does it occur (briefly)?
What are the two most common results of this mutation? Is a large CDR seen?

A

Autosomal recessive
A protein needed for proper cleavage of the anterior chamber is abnormal
Gies impaired or no drainage
Often anterior insertion of the iris onto the cornea is seen
Large CDR is seen

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16
Q

Name the two expressions of congenital glaucoma and note their severity.
List four characteristics of these expressions.
Note whether or not they are bilateral.

A

Axenfeldt-Rieger (minor to moderate)
Peter’s (severe)
Child (0-2) has high to very high IOP
Abnormal iris/lens/cornea
Buthalmos (large eyeball) with leukocoria (white pupil)
Asymmetry between the eyes (colour and size)
Are often bilateral (75%)

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17
Q

List 5 common signs and symptoms of Axenfeldt-Reigers syndrome.

A

Photophobia
Epiphora
Hard eye
Large cloudy cornea
Anterior schwalbes line

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18
Q

What is common in 15% of Axenfeldt-Rerigers syndrome and what is IOP like?

A

Posteiror embryotoxin common in the nasal margin
IOP is generally normal, major disorder gives high IOP

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19
Q

What is the mechanism of cause behind peters syndrome?`

A

Incomplete cleavage of the lens from the ris

20
Q

True or false
Peters syndrome will always lead to congential glaucoma.

A

True

21
Q

Does peters syndrom have a good or poor prognosis?

A

Poor

22
Q

What sign can often be seen with peters syndrome?

A

Central cornea-lens dysgenesis, appearing as a white plaque

23
Q

Does juvenile glaucoma tend to have a strong family history?

A

Strong history - need to monitor x2 yearly

24
Q

What is IOP like in juvenile glaucoma?

A

Large diurnal IOP fluctuation

25
Q

Are large cups found in those with juvenile glaucoma? Does this make diagnosis easy or difficult?

A

They usually have large cups
Makes diagnosis on appearance hard

26
Q

Is surgery for juvenile glaucoma often successful?

A

Yes

27
Q

What are three things that generally occur with age that contribute to increased TM resistance in primary open angle glaucoma?

A

Decreased giant vacuole formation
Increased GAG/debris
Collapse of cribiform structures

28
Q

What age, gender, and ametropic status does pigment dispersion syndrome/glaucoma tend to affect most?

A

Young myopic males

29
Q

Lidt four iris anomalies that can cause blockage of the cribiform trabecular meshwork.

A

Posterior insertion
Backwards bowing of the iris
Hypoplasia/vascular dysgenesis of the iris
Pigment shower after exercise due to IOP spike

30
Q

What interaction between the iris and zonules can cause pigment loss?

A

Backward iris rubs on zonules and lens in the midperiphery to release pigment

31
Q

On what three surfaces can pigment collect on? Name them if it is applicable.

A

Corneal endothelium (krukenberg spindle)
Iris surface
Cribiform TM

32
Q

What kind of disorder is pseudoexfoliative syndrome/glaucoma?

A

Vascular disorder at the collar

33
Q

What kind of deposits can be seen in pseudoexfoliative syndrome/glaucoma, where do they come from, and on what three structures do they deposit on?

A

White fluffy deposits from the ciliary body deposit on the lens, corneal endothelium, and trabecular meshwork

34
Q

What forms in the central zone in pseudoexfoliative syndrome/glaucoma, and why? How does it appear a the pupil margin? What two appearances can it have and what slitlamp setup is best to see it?

A

Due to iris sweeping motion, plug dandruff flakes on the pupil margin, can be in sheets or flakes
Best seen in red reflex

35
Q

Where does pseudoexfoliative material seem to arise from? Is it found exclusively in the eye?

A

Abnormal metabolism of ECM
Can be found throughout the body, in the lungs, heart, liver, joints etc

36
Q

Does steroid use generally result in a fast/quick IOP rise? What happens with long term use? Is the effect of steroids on IOP greatest with intraocular/topical medications or systemic?

A

Up to 15% of normal people and 50% of glaucoma patients will give a fast/quick rise in IOP
Everyone else will do so with long term use
IOP rise greatest with intraocular/topical eye medications

37
Q

What effect can the use of dexmethasone for >1 month have on IOP?

A

A 100% increase to IOP

38
Q

Give the mechanism for steroid glaucoma, including percentages (3).

A

Genetic tendency enhances presponse in 50%
35% trabecular-meshwork inducible glucocorticoid response (TIGER)
15% myocilin gene (MYOC)

39
Q

What two things can stertoids produce in the meshwork?

A

Decreased phagocytosis by trabecular cells
Increase in trabecular mucopolysaccharides (GAGs)

40
Q

What effect do steroids have on schlemms canal (note the cell and effect)?

A

Changes to endothelial cells in schlemms canal, resulting in the suppression of giant vacuole formation

41
Q

Give the IOP response order for the following:
Red forte
Flarex
Maxidex
From highest to lowest.

A

Maxidex > Pred forte&raquo_space; Flarex

42
Q

List four possible causes of primary angle closure glaucoma, and give 2 examples for each.

A

Lens related
-pupil block
-swelling
Vitreous
-tumour
-haemorrhage
Malignant glaucoma
-surgery-scleral buckle procedure
Iris/ciliary body
-cysts
-tumours

43
Q

At what IOP levels is the AC generally affected? Why so? What happens following this (2)?

A

Affected at moderate IOP (30-40mmHg)
Aqueous is stagnant
Corneal endothelial compromise gives oedema and epithelial defects in the cornea

44
Q

With high IOP, explain what happens at the anterior pole, the iris, and the limbus.

A

Ocular hypoxia at the anterior pole, leading to:
Iris ischaemia, iris atrophy, and limbal flush

45
Q

List two consequences of high IOP at the retina.

A

Backward bow of the lamina
Axonal and NFL dysfunction

OD3 (S1&2) (114 decks)

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