Glaucoma

Question 1

What is glaucoma?

Answer 1

Intraocular pressure too high for normal functioning of optic nerve head

Question 2

What is a common cause of glaucoma?

Answer 2

Often associated with a disturbance in circulation of aqueous humour in the eye

Question 3

How is aqueous humour formed?

Answer 3

Clear fluid formed from blood, filtered in ciliary process arterioles, rate of formation 2-3 microlitres/min, total volume of aqueous humour = 125 microlitres, ATPase and carbonic anhydrase involved in formation

Question 4

Aqueous humour circulation

Answer 4

Filtered in ciliary body, flows into posterior chamber then into anterior chamber, passes through trabecular meshwork, drains via canal of Schlemm into ocular veins, also uveoscleral outflow

Question 5

What is normal intraocular pressure and what controls it?

Answer 5

Normal pressure in 10-21 mmHg

Balance between secretion and drainage

Question 6

What happens if there is too much aqueous humour secretion?

Answer 6

If drainage cannot keep pace with secretion, pressure is increased, restriction of blood supply to optic nerve through back pressure, optic nerve atrophy (wasting away), reduces field of vision

Question 7

What determines the types of glaucoma?

Answer 7

Depends on poor aqueous humour drainage:
i) degeneration and subsequent collapse of trabecular meshwork
ii) mechanical blockage of trabecular meshwork by peripheral role of iris (flapping back)
Increase infiltration pressure (rare)

Question 8

Primary open angle glaucoma

Answer 8

Most common, ~0.5% of population, chronic simple glaucoma, slow onset, commonly high IOP, pathological changes in trabecular meshwork may occur, > 40 years, short sighted, more common in Afro-Caribbeans, possible association with diabetes mellitus

Question 9

Primary closed angle glaucoma

Answer 9

Acute glaucoma
Caused by blockage of trabecular meshwork, sudden onset, can be ocular emergency
Symptoms include dilated pupils, inflamed eyes, blurred vision, reflex nausea and vomiting
Bad cases will have loss of vision (24 hrs), blindness (2-3 days), can be drug induced (atropine), long lasting mydriasis for 2 days- 3 weeks, medical emergency

Question 10

Secondary glaucomas

Answer 10

Inflammation e.g. uveitis
Pigmentary granules shed from iris and ciliary epithelium
Exfoliative: flakes peel off iris and block meshwork,
Iris bombe: iris adheres to lens, increased posterior pressure, iris bulges forward
Lens related e.g. cataract lens may swell and from synechiae
Some drugs e.g. vasodilators, cortisone, compression trauma can cause bleeding that blocks trabecular meshwork
Tumours

Question 11

Congenital glaucomas

Answer 11

Deformity, usually present at birth, onset may be in first two years of life, requires surgery

Question 12

Diagnosis of glaucomas

Answer 12

Examine optic disc, measure intraocular pressure, gonioscopy

Question 13

Ophthalmascopic examination

Answer 13

Optic disc appears cupped, white due to nerve fibre degeneration, increased pressure may restrict blood supply and anoxia causes degeneration

Question 14

Measurement of intraocular pressure

Answer 14

Contact tonometry with local anaesthetic, air jet tonometry with fine air jet

Question 15

Goniscopy

Answer 15

Viewing the irideocorneal angle via a mirror or prism, angle normally masked by total internal reflection from the ocular tissue

Question 16

Prostaglandin analogues

Answer 16

Most powerful topical ocular hypotensive agents available
Mechanism is to increase uveoscleral outflow
E.g. latanoprost, used for unresponsive open angle glaucoma and OHT, instilled in the evening,
Side effects include possible change in eye pigmentation, eye lash thickening or lengthening

Question 17

Prostamide

Answer 17

E.g. bimatoprost (Lumigan)- increases trabecular and uveoscleral outflow

Question 18

Beta blockers

Answer 18

Used for chronic open angle glaucoma, e.g. timolol, no selective antagonist, enhances antiglaucoma effects of prostaglandins, CA inhibitors and pilocarpine

Question 19

Mechanism of beta blockers

Answer 19

Block B2 receptors in afferent ciliary BVs, vasoconstriction and decreased inflow, reduced IOP
Side effects include bradycardia, palpitation, hypotension and bronchial asthma
Ocular effects include corneal anaesthesia and allergic blepharoconjunctivitis

Question 20

Sympathetic agonists mechanism

Answer 20

A1 afferent ciliary vasoconstriction (reduces inflow) and increases trabecular drainage
A2 decreases aqueous secretion and increased uveoscleral outflow
E.g. dipevephrine is an adrenaline prodrug but more lipid soluble, penetrates cornea then converted to adrenaline, fewer systemic side effects

Question 21

A2 adrenoceptor agonists

Answer 21

Brimonidine used in open angle glaucoma/ocular hypertension, may be used as adjunct to B blockers

Question 22

Carbonic anhydrase inhibitors

Answer 22

Prevent bicarbonate and water passage into aqueous humour, decreasing IOP, used in open angle glaucoma and secondary glaucoma, e.g. dorzolamide, brinzolamide

Question 23

Miotic (parasympathomimetic)

Answer 23

Used in closed angle glaucoma
Opens up drainage channels in trabecular meshwork, contracts constrictor pupillae, pulls iris away from trabecular meshwork
Side effects include poor night vision, transient headache, irritation on instillation
Avoid use in inflammatory conditions e.g. acute iritis, uveitis and secondary glaucoma

Question 24

Osmotic agents

Answer 24

Hyperosmotic agents increase extracellular osmolarity- aqueous humour decreases IOP e.g. mannitol
Given in emergency or before surgery

Question 25

Important points for ophthalmic preparations

Answer 25

Sterility, tonicity- eye will tolerate NaCl (0.7-2.0%), hypertonic solutions rapidly diluted by tears, pH range 3.5-10.5 well tolerated in eye
Stability- depends on pH and temperature