Primary Open Angle Glaucoma

Question 1

What is glaucoma?

Answer 1

Chronic progressive optic neuropathy caused by a group of ocular conditions.
- Traditionally characterized by elevated intraocular pressure
- Associated with visual field loss as damage progresses

Question 2

Consequences of glaucoma?

Answer 2

The elevated pressure causes optic nerve damage in the following ways:
1. Mechanical dysfunction via compression of the axons at the lamina cribrosa
2. Vascular dysfunction which later leads to ischemia of the optic nerve

Question 3

Normal inraocular pressure?

Answer 3

10-20 mmHg

Question 4

Key feature to ascertain whether it is glaucoma or not?

Answer 4

↑ IOP is not always = glaucoma
- There must be features of optic nerve neuropathy to ascertain presence of the disease

Question 5

Flow of aqueous humor?

Answer 5

ciliary processes > aqueous humor in posterior chamber flows over the lens and through the pupil > anterior chamber > trabecular meshwork > Schlemm’s canal > collector channels > episcleral veins

Question 6

Classification of acquired glaucoma?

Answer 6

1. Primary
   - elevated IOP is not associated with any other ocular disorder
2. Secondary
   - there is a recognizable ocular (e.g., uveitis) and non ocular (e.g., diabetes) disorders which alters aqueous outflow

Question 7

Types of primary glaucoma?

Answer 7

1. OAG: angle between the iris and the cornea is normal
2. CAG: angle between iris and the cornea is narrow

Question 8

What is primary open angle glaucoma?

Answer 8

A subset of the glaucoma’s defined by an open, normal appearing anterior chamber angle and raised intraocular pressure, with no other underlying disease

Question 9

Characteristics of open angle glaucoma?

Answer 9

1. peripheral visual field loss followed by central field loss corresponding to the cupping of the optic disc
2. Intraocular Pressure > 21mmHg
3. May occur bilaterally but may not be symmetrical

Question 10

Epidemiology of OAG?

Answer 10

• Second leading cause of blindness in the world
• Leading cause of irreversible blindness and leading cause of blindness among Black Americans
• More common in Africans
• Usually, adult onset and increases with age (mostly above 40)
• It affects both genders equally

Question 11

Pathophysiology of OAG?

Answer 11

↑ IOP → Glaucomatous optic nerve damage

Question 12

Pathophysiology of raised intraocular pressure?

Answer 12

1. Proliferation of endothelial lining with thickening of basement membrane
2. Narrowed intertrabecular spaces and obstruction by accumulated material
3. Loss of trabecular endothelial cell (resulting in trabecular beam fusing)
4. These increase the resistance to aqueous outflow; drainage is impaired → ↑ IOP

Question 13

Pathophysiology of optic nerve damage in OAG?

Answer 13

1. Due to sustained ↑ IOP; progressive damage
2. Direct mechanical damage and ischemic damage
3. Optic nerve cupping

Question 14

What is optic nerve cupping?

Answer 14

• The optic nerve head has a shallow depression at the center and raised edges in the peripherally
• This forms a cup shaped appearance of the optic head.
• The cup is small and the surrounding neuroretina tissues are pink in a healthy eye
• In POAG, the nerve cells surrounding the cup are lost which makes the cup to increase in size more than normal; the neuroretina tissues become pale

Question 15

Risk factors of OAG?

Answer 15

1. Raised IOP → glaucomatous optic neuropathy
2. Age – prevalence ↑ with older age
3. Race – Black
4. Positive family history of POAG
   - 1st degree relative; ↑ if sibling
5. Myopia – more susceptible to glaucomatous damage
6. Thin central corneal thickness – measurement error

Question 16

Clinical symptoms of OAG?

Answer 16

1. Painless loss of vision
2. Headache
3. Visual field changes
   - Due to its slow progression, patients may not know that they have the disease in the early stages

Question 17

Clinical signs of OAG?

Answer 17

1. Reduced visual acuity
2. Normal anterior chamber depth
3. Sluggish pupil

Question 18

Ddx for OAG?

Answer 18

1. Primary angle closure glaucoma
2. Ocular hypertension
3. Normal tension glaucoma
4. Steroid induced glaucoma

Question 19

Diagnosis of OAG?

Answer 19

1. Raised intraocular pressure
   – by Goldmann tonometer
2. Cupping of optic disk
   – fundoscopy
3. Visual field defects
   - Central measured by automated perimetry
   - Peripheral measured by listers Goldmann perimetry
4. Normal anterior angles on gonioscopy
5. Exaggerated diurnal fluctuation of IOP
   - >5mmHg is suspected of glaucoma; - >8mmHg is confirmation of glaucoma

Question 20

History in OAG?

Answer 20

1. Visual changes
2. Previous ophthalmic history
3. Family history
4. Past medical history
5. Allergies
6. Any current medications

Question 21

Examination in OAG?

Answer 21

1. Visual acuity
2. Colour
3. Slit lamp exam
4. Fundoscopy
5. Tonometry

Question 22

Investigations in OAG?

Answer 22

1. Perimetry
2. Gonioscopy
3. Pachymetry
4. Optic coherence tomography of the optic disc

Question 23

Management of OAG?

Answer 23

The main target is to reduce intraocular pressure
1. Medical
2. Surgical
3. Laser therapy

Question 24

Medical therapy for OAG?

Answer 24

1. prostaglanins - first line
2. beta adrenergic blockers
3. carbonic anhydrous inhibitors
4. alpha adrenergic agonists
5. cholinergic agonists

Question 25

Prostaglandin use in OAG?

Answer 25

e.g. Latanaprost, Travoprost, Bimatoprost MOA: Increase uveal scleral outflow Side effects: 1. Eyelash lengthening 2. Eyelid pigmentation 3. Iris pigmentation

Question 26

Beta adrenergic blockers use in OAG?

Answer 26

e.g. Timolol, Bexatolol, Levobunolol MOA: Reduce production of aqueous humor Side effects: 1. Bradycardia 2. Shortness of breath 3. Bronchospasm

Question 27

Carbonic anhydrase inhibitors use in OAG?

Answer 27

e.g. Dorzolamide, Brinzolamide MOA: 1. Increase uveal scleral drainage 2. Reduce production of aqueous humor Side effects: 1. Stinging 2. Burning 3. Depression

Question 28

Alpha adrenergic agonists use in OAG?

Answer 28

e.g. Brimonoidine MOA: 1. Increase uveal scleral drainage 2. Reduce production of aqueous humor Side effects: 1. Increased salivation 2. Increased sweating

Question 29

Cholinergic agonists use in OAG?

Answer 29

e.g. Pilocapine MOA: Increase trabecular flow Side effects: 1. Dim vision (small pupil) 2. Iris cyst

Question 30

Laser therapy in OAG?

Answer 30

Laser therapy trabeculoplasty 1. Argon laser trabeculoplasty 2. Selective laser trabeculoplasty

Question 31

Surgical treatment for OAG?

Answer 31

Trabeculectomy - A channel is created from the anterior chamber through the sclera to a subconjunctival space referred to as filtering bleb - Used as first line approach only for patient with severe visual field loss at baseline - Second line approach for patients with advanced OAG who have not responded to medications or laser therapy

Question 32

Prognosis of OAG?

Answer 32

1. Good if diagnosed and treated early – most patients recover well. 2. Untreated POAG lead to irreversible blindness

Question 33

Complications of POAG?

Answer 33

1. Absolute glaucoma 2. Irreversible visual loss

Question 34

Post op complications of POAG?

Answer 34

1. Post – op shallow AC 2. Hyphaema 3. Iritis 4. Cataract due to accidental injury to the lens 5. Endophthalmitis