Ocular pharmacology Flashcards
How do the eyes constrict?
Parasympathetic nerves innervate the sphinteric muscle
Pupils are generally rather small hence there is a high basal level of activity
Muscarinic agonists will therefore constrict the eye (miosis) and antagonists will dilate the eye
How might the eyes dilate?
Radial muscles in the iris are innervated by sympathetic nerves
Their contraction will dilate the eyes (mydriasis)
Agonists will dilate and antagonists will constrict the eyes
What do the ciliary muscles do and how do they work?
They have parasympathetic innervation
When they contract, the ligaments attached to the lens go slack and allows for focus on near objects
When they are relaxed, the ligaments go taut and stretch the lens out allowing for focus on far objects
Very little adrenergic innervation
What does the ciliary body epithelium do?
Produces aqueous humour which:
Maintains intraocular pressure
Provides nutrient to eye
Released into posterior chamber
How can we control the formation of aqueous humour?
alpha1 agonists: constrict blood flow thereby by reducing blood supply and pressure to ciliary body
alpha2 agonists: reduces cAMP which reduces the vol of AH produced
beta1 agonists: increases the amount of AH produced
Hence to limit the amount of AH produced we use alpha agonists (clonidine) or beta blockers (timolol)
Dipiveferin
Pro-drug of adrenaline
Consists of adrenaline ester bonded to lipd molecule
Esterase breaks the ester bond allowing adrenaline to interact with receptors
Not very selective hence not licensed in UK
Acetazolamide- How does it work?
Production of AH is dependent on the active transport of HCO3- hence if you can inhibit the production of HCO3- you can reduce production of AH
Acetazolamide inhibits carbonic anhydrase reducing production of HCO3-
Brinzolamide is same mechanism but has long half life
How can we improve the drainage of AH?
Muscarinic agonists constrict the ciliary muscle as when it is relaxed the extra bulk can block the drainage
Uveosclereal flow can be improved via use of prostoglandin analogues (Latanoprost)
What abnormality causes closed angle glaucoma?
The iris deforms and blocks the trabecular network and uveosclereal canal
While open angle glaucoma is slow onset and progressive, closed angle is rapid onset and can cause irreversible damage
More common amoungst asians and inuits
Treatment for closed angle glaucoma
Osmotic drugs to remove water from aqueous humour reducing its vol. thereby reducing intraocular pressure however it is only a temporary fix
The only permanent treatment is surgery
The 2 types of age related macular degeneration (AMD)
Macula necessary for sharp vision
Dry AMD- slow onset, caused by degeneration of one area, no treatment
Wet AMD- rapid onset, can be treated by reducing leakage of local vasculature
Wet AMD
Caused by growth of leaky blood vessels under retina
Treatment with photodynamic therapy
-verteporforin photoactivated by red low energy laser
Causes occlusion of vasculature meaning that they don’t leak anymore
Vascular endothelial growth factor (VEGF) causes such leakge so can be used as a target for inhibition (anti-VEGF)
Screening for glaucoma
If 35-50yrs then eye check every 4 yrs If>50yrs the eye check every 2yrs Also consider at risk groups: afro/carribean family history short sightedness diabetes
First line treatment for chronic open angle glaucoma (COAP)
Generic PGA (eg. Latanoprost) if there is risk of COAP in their lifetime Offer additional topical treatment if not sufficiently controlled with monotherapy If not controlled with double therapy then refer to specialist Do not offer treatment to those with intraoculaar pressure less than 24mmHg
Pharmacological augmentation in surgery
Mitomycin C to prevent scar tissue from blocking drainage tubes