pharmacology of glaucoma drugs Flashcards
pharmacology of muscarinic agonist
drug binds to the muscarinic M3 acetylcholine receptors as an agonist in the muscle constrictor. Binding activates the muscle which results in an increase in tension in the ciliary muscle improving drainage and lowering of intraocular pressure.
example of muscarinic agonist
pilocarpine
what does pilocarpine do
- contracts the ciliary muscles
- constricts pupil
- relaxes lens
- improves drainage
ADE of muscarinic agonists
- blurred vision and ocular irritation (burning, itching)
- headache
- also cause miosis which could be permanent in long-term use
lacrimation is infrequent, retinal detachment is rare
pharmacology of beta blockers
- used to be first line treatments but are now adjunctive therapy
- binds as an antagonist to beta-adrenoreceptors present in the ciliary epithelium to stop production of aq humour, although precise mechanism of action is unknown
examples of beta-blockers
- timolol
- betaxolol
ADE of beta-blockers
- systemic effects: bradycardia, hypotension (fainting), bronchospasm
- may experience stinging sensation and blurred vision
what does timolol do
- non selective (can bind to beta 1 and 2 receptors)
- drops IOP by 25%
- fewer local effects
- could have systemic effects
what does betaxolol do
- cardioselective
- drops IOP by 20%
- less likely to have systemic ADE
pharmacology of adrenergic agonists
- agonists for alpha2-receptors located within ciliary muscles
examples of adrenergic agonists
- apraclonidine
- brimonidine (long-term use)
what do adrenergic agonists do
- decrease synthesis of aq humour
- increase amount of drains from eye through uveoscleral outflow
ADE of adrenergic agonists
- ocular irritation, dry mouth and nose
- taste disturbances
- can decrease sympathetic tone resulting in lowering of BP, fainting, systemic hypotension and dizziness
pharmacology of carbonic anhydrase inhibitors
- inhibit carbonic anhydrase 2 (CAMII) enzyme, the major subtype of this enzyme is found in the eye. This prevents HCO3- from forming
- under normal physiological conditions, HCO3- will cross into aq humour, causing sodium to follow. Then, via osmosis, water follows.
- therefore blockage of carbonic anhydrase II will stop this process reducing aq humour formation and thus IOP
dorzolamide and brinzolamide are both water and lipid-soluble therefore can easily penetrate corneal
examples of carbonic anhydrase inhibitors
- azetazolamide
- dorzolamide
- brinzolamide
ADE of carbonic anhydrase inhibitors
- acetazolomide cannot tolerate drug - diuresis, loss of appetite, tingling and neutropenia
- topical drugs: ocular irritation, sensation of foreign body in eye = uncomfortable + blurred vision
- corneal staining can occur
pharmacology of prostaglandin analogues
- safest and most effective, first line treatment for glaucoma
- binds as an agonist to the prostaglandin F receptor in trabecular meshwork, ciliary muscle and sclera of eye
- these tissues are aq humour outflow pathways. Their extracellular matrix becomes degraded, leading to uveoscleral outflow of aq humour
examples of prostaglandin analogues
- latanoprost
- bimatoprost
- travaprost
- tafluprost
ADE of prostaglandin analogues
- iris hyperpigmentation (occur gradually and is mostly irreversible)
- eyelash changes (gradually become dark, lengthened and thickened. But reversible upon cessation of treatment)
- conjunctival hyperaemia (redness in sclera of eye)
- eye irritation, blurred vision, allergies and headaches
what do prostaglandin analogues do?
- decrease IOP
