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Glaucoma Flashcards

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1
Q

What is glaucoma

A

Glaucoma is caused by a disorder in the normal flow of aqueous humour. It is important to understand aqueous humour in detail.

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2
Q

Revise

A
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3
Q

Physiology of glaucoma

A

Aqueous humour supplies nutrients to the cornea and lens

  • It flows from the posterior chamber to the anterior chamber via the pupil.
  • It fills the anterior chamber at 0.25mL (larger than the posterior chamber)
  • It is composed of 99% water and has a lower glucose and protein concentration than plasma.
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4
Q

Production and secretion of aqueous

A

Aqueous humour is formed by the non-pigmented inner epithelium of the ciliary processes at the pars plicata

The inner non-pigmented epithelium is continuous with the neural retina

Most secretion occurs by active transport which is under sympathetic control:

  • Stimulation of beta-2 receptors increase secretion
  • Stimulation of alpha-2 receptors decreases secretion
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5
Q

What structure is continous with the RPE

A

The ciliary body also has an outer pigmented epithelium that is posteriorly continuous with RPE

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6
Q

Drainage of AQH

A

AQH travels from the posterior chamber to the anterior chamber via the pupil (the hole in the iris centre). There are 2 main pathways for AQH to drain from the eye:

  1. Trabecular path (90%)
  2. Uveoscleral path
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7
Q

Compare Trabecular vs Uveoscleral drainage of AQH

A

Trabecular path (90%)

  • Also known as the conventional route
  • AQH flows through the trabecular meshwork → Schlemm’s canal → episcleral veins
  • Contraction of ciliary muscle increases trabecular outflow

Uveoscleral path

  • AQH passes directly outward through ciliary muscle → suprachoroidal space → choroidal veins → vortex veins
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8
Q

What is the Trabecular Meshwork (TM)

A

The TM is a band of cellular sheets which form a sieve-like structure. It is triangular in cross-section and is found at the anterior chamber angle

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9
Q

What are the 3 parts of the TM

A
  • Innermost → uveal meshwork with large holes
  • Middle → corneoscleral meshwork with smaller holes
  • Outermost → juxtacanalicular meshwork connects TM to Schlemm canal
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10
Q

What area confers the largest resistance to AQH flow

A

The juxtacanalicular meshwork contains the narrowest spaces and confers the largest resistance to normal AQH outflow via the conventional route

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11
Q

Scleral Spur

A

A fibrous projection from the sclera.

  • Longitudinal ciliary muscles insert onto its posterior surface.
  • It is an important landmark in gonioscopy.
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12
Q

Anterior Chamber (AC) Angle

A

Extends from Schwalbe’s line (termination of Descemet’s membrane of the cornea) to the TM, scleral spur and ciliary body.

Clinically significant because the closure of the angle will impede AQH outflow via the conventional route.

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13
Q

What is the glaucoma TRIAD

A

Diagnosis is based on the ‘glaucoma triad’:

Raised IOP, abnormal disc, and visual field defects.

The latter 2 signs are most important.

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14
Q

Gold standard way to measure IOP

A

Goldmann tonometry

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15
Q

IOP normal values and variations

A
  • Normal range is 11-21 mmHg
  • Diurnal variation of up to 5 mmHg is normal.
  • Peaks in the morning
  • Supine positioning leads to higher IOP than sitting
  • IOP measurement is affected by corneal thickness, astigmatism and the axial length of the eyeball.
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16
Q

Is raised IOP required to diagnose glaucoma?

A

NO!

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17
Q

Optic Disc Changes in glaucoma

A
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18
Q

What finding may raise suspicion of optic nerve damage?

A

Decreased nerve fibre layer (NFL) thickness readings on OCT

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19
Q

What investigation is used to measure Visual Fields?

A

Perimetry

The best test for monitoring glaucoma is Humphrey 24-2 perimetry

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20
Q

Why do visual field defects occur in glaucoma?

A

Glaucomatous visual field defects occur as a result of damage to the retinal nerve fibres

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21
Q

Gonioscopy

A

Gonioscopy is a method of visualizing the anterior chamber angle, it is important in identifying angle-closure glaucoma.

Peripheral anterior synechiae might be found in angle closure, this is the iris bowing forward and closing off the angle.

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22
Q

Lable the structures seen on gonioscopy

A
  1. Schwalbe’s line, 2. Trabecular meshwork (TM), 3. Scleral spur, 4. Ciliary body, 5. Iris.
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23
Q

List all structures seen on gonioscopy (superficial to deep)

A
  1. Posterior corneal surface
  2. Schwalbe’s line
  3. Non-pigmented trabecular meshwork
  4. Pigmented trabecular meshwork
  5. Scleral spur
  6. Ciliary body
  7. Iris
  8. Pupil
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24
Q

How much can medical treatment lower IOP in glaucoma

A

Medical treatment can on average lower IOP by 20-30% (5-7mm Hg)

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25
Drugs used in glaucoma (in order of use)
1. Latanoprost 2. Timolol 3. Brinzolamide 4. Brimonidine
26
Exceptions to glaucoma drugs in pregnancy/peadiatrics
No eye drops are licensed for children or pregnant women. Use brimonidine in first the trimester and switch to timolol in 3rd
27
Biggest issue with prescribing mutiple eye drops?
Compliance
28
MoA, SE and CI of all glaucoma drugs
29
3 major locations of beta receptors
1. heart 2. lungs 3. adipose
30
What procedure can be performed in chronic glaucoma where medications have failed to control IOP
Trabeculectomy
31
Trabeculectomy
The creation of a fistula from the anterior chamber to the sub-tenon space - creating a bleb (elevation of the conjunctiva where the aqueous gathers) Antimetabolites can be used adjunctively to slow the healing process and prevent bleb failure * 5-FU: pyrimidine analogue which inhibits fibroblasts by blocking DNA synthesis * Mitomycin C: alkylating agent which inhibits fibroblasts
32
Blebitis
33
Types of laser surgery, indications and laser types used
34
List 2 causes of Iatrogenic Glaucoma
1. Post-Vitreoretinal Surgery 2. Post-Cataract Surgery
35
What is Primary Open Angle Glaucoma (POAG)
Chronic glaucomatous change due to optic nerve damage with an open anterior chamber angle
36
Pathology of POAG
This is a ‘primary’ disease, meaning there is no identifiable cause of the glaucomatous change Risk Factors * MYOC and OPTN gene mutations * Steroids * Smoking * Myopia * Afro-Caribbean race * Increasing age
37
Why is Afro-Caribbean a risk factor for POAG
People of Afro-Caribbean origin a more likely to be myopic (longer eyes) and are at risk of open-angle glaucoma, compared to east Asians who are more likely to be hyperopic (shorter eyes) and at risk of angle-closure glaucoma
38
Presentation of POAG
* Asymptomatic at first but will develop visual field defects * Typical presentation is a 60-year-old black myope with a history of vascular risk factors.
39
Investigations for POAG
* Tonometry: IOP > 21mmHg * Slit-lamp examination: no signs of precipitating diseases * Gonioscopy: open angle * Fundoscopy: glaucomatous optic disc changes * Perimetry: visual field defects
40
Management of POAG
41
List the 4 clinical varients of Primary Angle Closure Glaucoma (PACG)
1. **Anatomically narrow drainage angle (ANDA)**: On gonioscopy the AC angle is narrow and the person is likely to be at higher risk of angle-closure 2. **Iridotrabecular contact (ITC)**: on gonioscopy the AC angle is closed 3. **Acute primary angle closure (APAC)**: ITC + acute symptomatic elevated IOP 4. **Primary angle-closure glaucoma**: ITC + Glaucomatous damage + elevated IOP or PAS or APAC episodes
42
Pathology of PACG
Pupil block mechanism (Majority): * Apposition of iris to lens → abnormal AQH through the pupil → increase in pressure difference between the posterior and anterior chambers → anterior bowing of the peripheral iris leading → peripheral anterior synechiae (PAS) → angle closure → obstructed aqueous outflow → elevated IOP → glaucomatous optic nerve damage Plateau iris configuration (East Asian): * Flat iris + anteriorly positioned ciliary processes → iris is pushed forward → angle closure.
43
What drug is associated with bilateral PACG
Topiramate
44
Diagnosis of PACG
45
Management of APAC
The aim is to stabilize IOP quickly to prevent blindness * First line: urgent admission + IV acetazolamide * Adjuncts: timolol + apraclonidine + steroids + pilocarpine + lie the patient supine * Monitor and consider systemic hyperosmotics (IV mannitol) * Definitive treatment is bilateral peripheral iridotomy, with either ND:YAG laser or surgery.
46
Management of PACG
* The aim is to control IOP over time * Bilateral peripheral iridotomy * The same medication protocol as POAG * Cataract extraction is effective in acute and chronic stages
47
Why is peripheral iridotomy done bilaterally in PACG?
Peripheral iridotomy is done bilaterally because angle closure in one eye, drastically increases the risk of angle-closure in the fellow eye (other eye).
48
Primary Congenital Glaucoma
49
Normal Tension Glaucoma (NTG)
50
What defines Ocular Hypertension (OHT)?
Raised IOP (>21 mmHg) without glaucomatous damage.
51
Can OHT convert to POAG
* Some OHT patients convert to POAG within several years. * Risk factors for conversion: older, higher IOP, larger cup/disc ratio, thinner cornea * Aim of treatment is to prevent conversion and control IOP. Achieved by topical IOP lowering medications following the same protocol as for POAG
52
What causes Secondary Open Angle Glaucoma
Conditions which cause clogging of the trabecular meshwork where the angle is still open. This blocks aqueous outflow and leads to increased IOP, which subsequently leads to glaucoma.
53
List 7 causes of secondary open angle glaucoma
1. Posner-schlossman Syndrome 2. Pseudoexfoliation Syndrome 3. Pigment Dispersion Syndrome 4. Phacolytic Glaucoma 5. Angle Recession Glaucoma 6. Red Cell and Ghost Cell 7. GlaucomaSturge-weber Syndrome
54
Posner-schlossman Syndrome
55
Pseudoexfoliation Syndrome
56
Pigment Dispersion Syndrome
57
Phacolytic Glaucoma
58
Angle Recession Glaucoma
59
Red Cell and Ghost Cell Glaucoma
60
Sturge-weber Syndrome
61
What causes secondary closed angle glaucoma
Conditions which generally involve changes to the ocular structure where the anterior chamber angle is compromised.
62
List 4 causes of secondary closed angle glaucoma
1. Neovascular Glaucoma 2. Lens Related Glaucoma 3. Aqueous Misdirection Syndrome 4. Iridocorneal Endothelial Syndrome
63
Neovascular Glaucoma
64
Lens Related Glaucoma
65
Aqueous Misdirection Syndrome
66
Iridocorneal Endothelial Syndrome
67
Acute Glaucoma Summary
68
Chronic Glaucoma Summary
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