drug management Flashcards
what are they symptoms of glaucoma
optic nerve damage, visual field loss, eventual blindness
risk factors
high IOP >21, family history, race, systemic hypertension, cvd, migraine, previous ocular disease.
what is the cause of glaucoma
impaired drainage of aqueous humour
where are the sites of aqueous outflow
trabecular meshwork, sclera and ciliary body.
what are the main Aims of antiglaucoma treatment
to reduce IOP to <16-20, preserves visual field, compatibility with other treatments and no topical or systemic se.
how is prostaglandins involved in aq humour outflow
it decreased IOP
which receptors do the prostaglandin analogues act via
FP receptors
where are FP receptors present
ciliary body, muscle and sclera, trabecular meshwork
3 examples of prostaglandin analogues
latanaprost, tafluprost, travoprost
what is the moa of prostamide analogues
FP receptor agonist. increases uveoscleral and trabecular outflow
how is IOP lowered
increase in uvoscleral outflow and reduced resistance by degradation of collagen and extracellular metric and decreases resistance of ciliary muscle and sclera
side effects of prostaglandin and prostamide analogues
red eye, eyelash growth, sensitivity to light
why can’t prostaglandin and prostamide analogues be used in pregnancy
effects on cell division
how do beta blockers decrease aqueous humour production
blocks cAMP production which prevents ion transport in the ciliary epithelium preventing aqueous humour production due to lack of osmotic gradient.
what are the disadvantaged of using beta blockers to decrease IOP
effects are seen on untreated eye too, systemic se are also observed