Final Exam Drugs to Know Flashcards
pilocarpine
glaucoma drug- direct acting cholinergic agonist
increases aqueous outflow; muscarinic cholinergic agonist; iris sphincter contraction- pupil constriction; ciliary muscle contraction- accommodation and increased aqueous outflow
Xalatan (latanoprost 0.005%)
glaucoma drug- prostaglandin analog
increases aqueous outflow; prodrugs are hydrolyzed in cornea –> active “free acids”; free acids bind to FP receptors in the ciliary body; activation of FP receptors up-regulates matrix metalloproteinases (MMPs) which degrade extracellular (i.e., collagen) in the uveoscleral pathway; makes the uveoscleral meshwork more porous; results in an increase in uveoscleral outflow and a lowering of IOP (main effect); may also enhance outflow through the TM
Travatan Z (travaprost 0.004%)
glaucoma drug- prostaglandin analog
increases aqueous outflow; prodrugs are hydrolyzed in cornea –> active “free acids”; free acids bind to FP receptors in the ciliary body; activation of FP receptors up-regulates matrix metalloproteinases (MMPs) which degrade extracellular (i.e., collagen) in the uveoscleral pathway; makes the uveoscleral meshwork more porous; results in an increase in uveoscleral outflow and a lowering of IOP (main effect); may also enhance outflow through the TM
Lumigan (bimatoprost 0.01%)
glaucoma drug- prostaglandin analog
increases aqueous outflow; prodrugs are hydrolyzed in cornea –> active “free acids”; free acids bind to FP receptors in the ciliary body; activation of FP receptors up-regulates matrix metalloproteinases (MMPs) which degrade extracellular (i.e., collagen) in the uveoscleral pathway; makes the uveoscleral meshwork more porous; results in an increase in uveoscleral outflow and a lowering of IOP (main effect); may also enhance outflow through the TM
Zioptan (tafluprost 0.0015%)
glaucoma drug- prostaglandin analog
increases aqueous outflow; prodrugs are hydrolyzed in cornea –> active “free acids”; free acids bind to FP receptors in the ciliary body; activation of FP receptors up-regulates matrix metalloproteinases (MMPs) which degrade extracellular (i.e., collagen) in the uveoscleral pathway; makes the uveoscleral meshwork more porous; results in an increase in uveoscleral outflow and a lowering of IOP (main effect); may also enhance outflow through the TM
Vyzulta (latanoprostene bunod 0.024%)
glaucoma drug- prostaglandin analog
increases aqueous outflow; prodrugs are hydrolyzed in cornea –> active “free acids”; free acids bind to FP receptors in the ciliary body; activation of FP receptors up-regulates matrix metalloproteinases (MMPs) which degrade extracellular (i.e., collagen) in the uveoscleral pathway; makes the uveoscleral meshwork more porous; results in an increase in uveoscleral outflow and a lowering of IOP (main effect); may also enhance outflow through the TM
nitric oxide-donating PGA; NO causes relaxation of TM; TM becomes more porous
Rescula (unoprostone isopropyl 0.15%)
glaucoma drug- prostone
increases aqueous outflow; active ingredient has a local effect on K and chloride channels in the TM; aqueous outflow through the TM is increased
Rhopressa (netarsudil 0.02%)
glaucoma drug- rho kinase inhibitors (ROCK inhibitors)
increases aqueous outflow; cytoskeletal reorganization in TM; rho proteins regulate cell shape and proliferation; elevated levels of rho kinase noted in glaucoma patients; loss of rho kinase function in the TM is associated with micromechanical relaxation of tissue, specifically in the juxtacanalicular portion of TM; bottom line: ROCK inhibitors make the TM more porous
combines ROCK inhibitor with norepinephrine transmitter (NET) inhibitor; increases TM outflow; decreases episcleral venous pressure; decreases aqueous production
Rocklatan (netarsudil 0.02%/ latanoprost 0.005%)
glaucoma drug- combination ROCK inhibitor and PGA
ROCK inhibitor: increases aqueous outflow; cytoskeletal reorganization in TM; rho proteins regulate cell shape and proliferation; elevated levels of rho kinase noted in glaucoma patients; loss of rho kinase function in the TM is associated with micromechanical relaxation of tissue, specifically in the juxtacanalicular portion of TM; bottom line: ROCK inhibitors make the TM more porous
PGA: increases aqueous outflow; prodrugs are hydrolyzed in cornea –> active “free acids”; free acids bind to FP receptors in the ciliary body; activation of FP receptors up-regulates matrix metalloproteinases (MMPs) which degrade extracellular (i.e., collagen) in the uveoscleral pathway; makes the uveoscleral meshwork more porous; results in an increase in uveoscleral outflow and a lowering of IOP (main effect); may also enhance outflow through the TM
timolol maleate (Timoptic, Timoptic XE, Istalol)
glaucoma drug- beta blocker
decreases aqueous production by blocking beta receptors in the eye; majority of choices are non-selective (B1 and B2)
timolol hemihydrate (betimol)
glaucoma drug- beta blocker
decreases aqueous production by blocking beta receptors in the eye; majority of choices are non-selective (B1 and B2)
Betagan (levobunolol)
glaucoma drug- beta blocker
decreases aqueous production by blocking beta receptors in the eye; majority of choices are non-selective (B1 and B2)
OptiPranolol (metipranolol)
glaucoma drug- beta blocker
decreases aqueous production by blocking beta receptors in the eye; majority of choices are non-selective (B1 and B2)
Ocupress (carteolol)
glaucoma drug- beta blocker
decreases aqueous production by blocking beta receptors in the eye; majority of choices are non-selective (B1 and B2)
Betoptic-S (betaxolol)
glaucoma drug- beta blocker
decreases aqueous production by blocking beta receptors in the eye; beta-1 selective
