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
Iopidine (apraclonidine)
glaucoma drug- adrenergic agonist
decreases aqueous production; predominant MOA: reduction of aqueous production via stimulation of alpha-2 receptors; secondary MOA: increased uveoscleral outflow; relatively selective alpha-2 agonist
Alphagan-P (brimonidine)
glaucoma drug- adrenergic agonist
decreases aqueous production; predominant MOA: reduction of aqueous production via stimulation of alpha-2 receptors; secondary MOA: increased uveoscleral outflow; highly selective alpha-2 agonist (30x more affinity than iopidine)
Azopt (brinzolamide)
glaucoma drug- topical carbonic anhydrase inhibitor (CAI)
decreases aqueous production; carbonic anhydrase plays a central role in aqueous production by generating bicarbonate ions; Type II enzymes found in NPCE; inhibition of CA II; decreases bicarbonate; decreases aqueous secretion; decreases IOP
Trusopt (dorzolamide)
glaucoma drug- topical carbonic anhydrase inhibitor (CAI)
decreases aqueous production; carbonic anhydrase plays a central role in aqueous production by generating bicarbonate ions; Type II enzymes found in NPCE; inhibition of CA II; decreases bicarbonate; decreases aqueous secretion; decreases IOP
Diamox (acetazolamide)
glaucoma drug- oral carbonic anhydrase inhibitor (CAI)
decreases aqueous production; carbonic anhydrase plays a central role in aqueous production by generating bicarbonate ions; Type II enzymes found in NPCE; inhibition of CA II; decreases bicarbonate; decreases aqueous secretion; decreases IOP
Neptazane (methazolamide)
glaucoma drug- oral carbonic anhydrase inhibitor (CAI)
decreases aqueous production; carbonic anhydrase plays a central role in aqueous production by generating bicarbonate ions; Type II enzymes found in NPCE; inhibition of CA II; decreases bicarbonate; decreases aqueous secretion; decreases IOP
Cosopt
glaucoma drug- dorzolamide/timolol
dorzolamide: decreases aqueous production; carbonic anhydrase plays a central role in aqueous production by generating bicarbonate ions; Type II enzymes found in NPCE; inhibition of CA II; decreases bicarbonate; decreases aqueous secretion; decreases IOP
timolol: decreases aqueous production by blocking beta receptors in the eye
Combigan
glaucoma drug- brimonidine/timolol
brimonidine: decreases aqueous production; predominant MOA: reduction of aqueous production via stimulation of alpha-2 receptors; secondary MOA: increased uveoscleral outflow; highly selective alpha-2 agonist (30x more affinity than iopidine)
timolol: decreases aqueous production by blocking beta receptors in the eye
Simbrinza
glaucoma drug- brinzolamide/brimonidine
brinzolamide: decreases aqueous production; carbonic anhydrase plays a central role in aqueous production by generating bicarbonate ions; Type II enzymes found in NPCE; inhibition of CA II; decreases bicarbonate; decreases aqueous secretion; decreases IOP
brimonidine: decreases aqueous production; predominant MOA: reduction of aqueous production via stimulation of alpha-2 receptors; secondary MOA: increased uveoscleral outflow; highly selective alpha-2 agonist (30x more affinity than iopidine)
AREDS 1 and 2 vitamins
reduce risk of progressing to advanced AMD
Lucentis (ranibizumab)
intravitreal anti-VEGF agent
binds to free-floating VEGF molecules to prevent attachment of VEGF to endothelial surface receptors (VEGFR) responsible for the neovascular “growth” signal;
inhibits all isoforms of VEGF-A
Avastin (beavcizumab)
intravitreal anti-VEGF agent
binds to free-floating VEGF molecules to prevent attachment of VEGF to endothelial surface receptors (VEGFR) responsible for the neovascular “growth” signal;
inhibits all isoforms of VEGF-A
Eylea (aflibercept)
intravitreal anti-VEGF agent
binds to free-floating VEGF molecules to prevent attachment of VEGF to endothelial surface receptors (VEGFR) responsible for the neovascular “growth” signal;
inhibits all isoforms of VEGF-A; higher affinity for VEGF than Avastin; also blocks placental growth factor
Beovu (brolucizumab)
intravitreal anti-VEGF agent
binds to free-floating VEGF molecules to prevent attachment of VEGF to endothelial surface receptors (VEGFR) responsible for the neovascular “growth” signal
Jetrea (ocriplasmin)
viterolytic agent
dissolves protein matrix of vitreoretinal interface; breaks down bonds between superficial retina and collagen fibrils, laminin, and fibronectin
