OCULAR DRUGS (Cholinomimetics, Non-Selective α Agonist and α2 Selective Agonist. Carbonic Anhydrase Inhibitor) Flashcards
What is the mechanism of action of Pilocarpine?
Direct muscarinic cholinergic agonist that stimulates ciliary muscle contraction, increases trabecular meshwork outflow, causes miosis, and reduces intraocular pressure.
What are the clinical uses of Pilocarpine?
Testing for anisocoria and treatment of glaucoma.
What are the side effects of Pilocarpine?
Corneal edema, miosis, induced myopia, brow ache, retinal detachment, and decreased vision (especially in patients with cataracts).
What is the mechanism of action of Physostigmine?
Reduces intraocular pressure by ciliary muscle contraction, opening of trabecular meshwork, and increasing outflow of aqueous humor.
What are the clinical uses of Physostigmine?
Treatment of glaucoma.
What are the side effects of Physostigmine?
Reduced visual acuity in poor lighting, ciliary spasm, headache, lacrimation, myopia, blurred vision, retinal detachment, iris cysts, and cataracts.
What is the mechanism of action of Carbachol?
Reduces intraocular pressure by ciliary muscle contraction, opening of trabecular meshwork, and increasing outflow of aqueous humor.
What are the clinical uses of Carbachol?
Miosis during surgery and treatment of glaucoma.
What are the side effects of Carbachol?
Corneal edema, miosis, induced myopia, decreased vision, brow ache, and retinal detachment.
What is the mechanism of action of Epinephrine in glaucoma?
Increases outflow via uveoscleral veins and reduces intraocular pressure by increasing outflow and slightly decreasing aqueous humor production.
What are the side effects of Epinephrine in glaucoma?
Conjunctival constriction, slight mydriasis, localized burning, irritation, allergic reactions, melanin granule accumulation, and risk of hypertensive crisis or ventricular arrhythmias if systemically absorbed.
What is the mechanism of action of Dipivefrin?
Transformed into epinephrine in the eye, increasing uveoscleral outflow and reducing intraocular pressure.
What are the clinical uses of Dipivefrin?
Treatment of glaucoma.
What are the side effects of Dipivefrin?
Photosensitivity, conjunctival hyperemia, hypersensitivity, and reduced systemic side effects compared to epinephrine.
What is the mechanism of action of Dapiprazole?
α-adrenergic antagonist effective in reversing sympathomimetic-induced mydriasis and enhancing recovery of accommodation after cycloplegics.
What are the clinical uses of Dapiprazole?
Treatment of glaucoma, ocular hypertension, and reversal of mydriasis.
What are the side effects of Dapiprazole?
Conjunctival irritation.
What is the mechanism of action of Apraclonidine?
Decreases aqueous secretion and reduces intraocular pressure.
What are the clinical uses of Apraclonidine?
Treatment of glaucoma and ocular hypertension.
What are the side effects of Apraclonidine?
Photosensitivity, conjunctival hyperemia, and hypersensitivity.
What is the mechanism of action of Brimonidine?
Reduces production of aqueous humor and increases its outflow.
What are the clinical uses of Brimonidine?
Treatment of glaucoma and ocular hypertension.
What are the side effects of Brimonidine?
Burning, stinging of the eye, blurred vision, photosensitivity, conjunctival hyperemia, and hypersensitivity.
What is the mechanism of action of Acetazolamide?
Inhibits carbonic anhydrase II in the ciliary epithelium, blocking the formation of bicarbonate and attracting sodium, which increases aqueous humor outflow and decreases intraocular pressure.
What are the clinical uses of Acetazolamide?
Treatment of glaucoma and ocular hypertension.
What are the side effects of Acetazolamide?
Diuresis, loss of appetite, tingling, neutropenia, paresthesias, GI disturbances, anorexia, drowsiness, confusion, metabolic acidosis, hypokalemia, urolithiasis.
What is the pharmacokinetics of Acetazolamide?
PO, completely absorbed, 90% bioavailability, duration of action 4-12 hours, t1/2 = 4 hours, excreted via active renal tubular secretion.
What is the mechanism of action of Dorzolamide?
Inhibits carbonic anhydrase II in the ciliary epithelium, blocking bicarbonate formation and increasing aqueous humor outflow.
What are the clinical uses of Dorzolamide?
Treatment of glaucoma and ocular hypertension.
What are the side effects of Dorzolamide?
Bitter taste, burning sensation, occasional headache, nausea, fatigue.
What is the pharmacokinetics of Dorzolamide?
Topical ophthalmic drops with onset of action <2 hrs, peak effect 2-4 hrs, duration of action 6-8 hrs.
What is the mechanism of action of Brinzolamide?
Inhibits carbonic anhydrase II in the ciliary epithelium, blocking bicarbonate formation and increasing aqueous humor outflow.
What are the clinical uses of Brinzolamide?
Treatment of glaucoma and ocular hypertension.
What are the side effects of Brinzolamide?
Diuresis, loss of appetite, tingling, bitter taste, burning sensation, occasional headache, nausea, fatigue.
What is the pharmacokinetics of Brinzolamide?
Topical ophthalmic drops with onset of action <2 hrs, peak effect 2 hrs, duration of action >12 hrs.
What is the mechanism of action of Dichlorphenamide?
Inhibits carbonic anhydrase II in the ciliary epithelium, blocking bicarbonate formation and increasing aqueous humor outflow.
What are the clinical uses of Dichlorphenamide?
Treatment of glaucoma and ocular hypertension.
What are the side effects of Dichlorphenamide?
Diuresis, loss of appetite, tingling, bitter taste, burning sensation, occasional headache, nausea, fatigue.
What is the pharmacokinetics of Dichlorphenamide?
PO, t1/2 = 2 hours.
What is the mechanism of action of Methazolamide?
Inhibits carbonic anhydrase II in the ciliary epithelium, blocking bicarbonate formation and increasing aqueous humor outflow.
What are the clinical uses of Methazolamide?
Treatment of glaucoma and ocular hypertension.
What are the side effects of Methazolamide?
Diuresis, loss of appetite, tingling, bitter taste, burning sensation, occasional headache, nausea, fatigue, paresthesias, GI disturbances, anorexia, drowsiness, confusion, metabolic acidosis, hypokalemia, urolithiasis.
What is the pharmacokinetics of Methazolamide?
PO, well absorbed, onset of action 1-2 hrs, peak effect 4-6 hrs, duration of action 12-24 hrs, t1/2 = 14-15 hrs, 25% eliminated unchanged in urine.
