Glaucoma Flashcards
What is glaucoma?
Intraocular pressure too high for normal functioning of optic nerve head
What is a common cause of glaucoma?
Often associated with a disturbance in circulation of aqueous humour in the eye
How is aqueous humour formed?
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
Aqueous humour circulation
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
What is normal intraocular pressure and what controls it?
Normal pressure in 10-21 mmHg
Balance between secretion and drainage
What happens if there is too much aqueous humour secretion?
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
What determines the types of glaucoma?
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)
Primary open angle glaucoma
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
Primary closed angle glaucoma
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
Secondary glaucomas
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
Congenital glaucomas
Deformity, usually present at birth, onset may be in first two years of life, requires surgery
Diagnosis of glaucomas
Examine optic disc, measure intraocular pressure, gonioscopy
Ophthalmascopic examination
Optic disc appears cupped, white due to nerve fibre degeneration, increased pressure may restrict blood supply and anoxia causes degeneration
Measurement of intraocular pressure
Contact tonometry with local anaesthetic, air jet tonometry with fine air jet
Goniscopy
Viewing the irideocorneal angle via a mirror or prism, angle normally masked by total internal reflection from the ocular tissue
Prostaglandin analogues
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
Prostamide
E.g. bimatoprost (Lumigan)- increases trabecular and uveoscleral outflow
Beta blockers
Used for chronic open angle glaucoma, e.g. timolol, no selective antagonist, enhances antiglaucoma effects of prostaglandins, CA inhibitors and pilocarpine
Mechanism of beta blockers
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
Sympathetic agonists mechanism
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
A2 adrenoceptor agonists
Brimonidine used in open angle glaucoma/ocular hypertension, may be used as adjunct to B blockers
Carbonic anhydrase inhibitors
Prevent bicarbonate and water passage into aqueous humour, decreasing IOP, used in open angle glaucoma and secondary glaucoma, e.g. dorzolamide, brinzolamide
Miotic (parasympathomimetic)
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
Osmotic agents
Hyperosmotic agents increase extracellular osmolarity- aqueous humour decreases IOP e.g. mannitol
Given in emergency or before surgery
Important points for ophthalmic preparations
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
