Pharmacotherapy II: Ophthalmic Diseases 2025 PDF

Pharmacotherapy II: Ophthalmic Diseases Augsburg PA Program, 2025 Miranda LaCroix, MSPAS, PA-C  Objectives 1. Describe the physiology and treatment approaches of primary open-angle and angle- closure glaucoma. 2. Identify the first and second-line agents (by c...

Pharmacotherapy II: Ophthalmic Diseases Augsburg PA Program, 2025 Miranda LaCroix, MSPAS, PA-C  Objectives 1. Describe the physiology and treatment approaches of primary open-angle and angle- closure glaucoma. 2. Identify the first and second-line agents (by class) for the treatment of open-angle glaucoma. 3. Given a patient scenario, select the best medication considering the pharmacologic effects and patient-care concerns across the lifespan for glaucoma. 4. Summarize the key prescribing considerations and patient education for a patient receiving treatment for glaucoma. 5. Explain the physiology of allergic conjunctivitis, dry eye, and bacterial conjunctivitis. 6. Summarize the key prescribing considerations and patient education for allergic conjunctivitis and bacterial conjunctivitis. 7. Identify at least 2 drugs from each class of commonly prescribed topical ophthalmic antibacterial agents to prescribe for bacterial conjunctivitis or eye trauma.  Glaucoma Glaucoma is a group of eye disorders characterized by progressive optic nerve damage in part due to a relative increase in intraocular pressure (IOP) that can lead to irreversible loss of vision. Second leading cause of blindness behind cataracts (1st in irreversible blindness) Progression of Vision Loss in Glaucoma Normal Anterior Eye  Glaucoma Primary Open Angle Glaucoma (POAG) leads to progressive optic nerve damage with eventual impairment of vision. Visual loss develops first in the peripheral visual field. As the disease advances, loss occurs in the central visual field. Acute Angle-Closure Glaucoma is precipitated by displacement of the iris such that it covers the trabecular meshwork, thereby preventing exit of aqueous humor from the anterior chamber. Causes acute vision loss.  Glaucoma Open Angle- Angle Closure  POAG Risk Factors Elevated IOP Medications African or Hispanic descent Corticosteroids Family history of glaucoma Ophthalmic Older age Systemic Thinner central corneal Inhaled/Nasal thickness Ophthalmic anticholinergics Myopia Vasodilators Type 2 diabetes Cimetidine  POAG: Treatment Goals of Treatment Target IOP is chosen based on Control IOP patient baseline IOP and the amount of existing visual field loss Stabilize the status of the optic Initial target is at least 25% nerve and retinal fiber layer lower than baseline Prevent further vision loss Greater reductions (30-50%) Minimize adverse effects of may be indicated for patients therapy and impact on with severe disease, risk factors patients' vision, general health, for disease progression, or normal tension glaucoma and quality of life POAG Treatment First Line (Topical): Beta blockers Prostaglandin analogs Alpha2 adrenergic agonists Second Line Carbonic anhydrase inhibitors Cholinergics Rho Kinase inhibitors Class Mechanism Common Adverse Effects First-Line Agents Decreased aqueous humor Nonselective: Heart block, bradycardia, bronchospasm β Blockers formation β1-Selective: Heart block, bradycardia, hypotension Prostaglandin Increased aqueous humor Heightened brown pigmentation of the iris and eyelid Analogs outflow α2-Adrenergic Decreased aqueous humor Headache, dry mouth, dry nose, altered taste, Agonists formation conjunctivitis, lid reactions, pruritus Second-Line Agents Increased aqueous humor Muscarinic agonists: Miosis and blurred vision Cholinergic Drugs outflow Cholinesterase inhibitors: Miosis and blurred vision Carbonic Anhydrase Decreased aqueous humor Ocular stinging, bitter taste, conjunctivitis, lid reactions Inhibitors formation Increased aqueous humor Eye discomfort, hyperemic conjunctiva, conjunctival Rho Kinase Inhibitor outflow hemorrhage  β-blockers Example drugs: Timolol, Betaxolol MOA: lower IOP by decreasing production of aqueous humor. Adverse Effects: transient ocular stinging. Occasionally cause conjunctivitis, blurred vision, photophobia, and dry eyes. Systemic: ↓ HR and BP, bronchospasm, hypoglycemia, CNS sedation Contraindications: AV heart block, sinus bradycardia, and cardiogenic shock, Caution in heart failure, asthma and end-stage COPD Betaxolol: only ophthalmic β blocker that is β1-selective à preferred choice for patients with pulmonary disease  Prostaglandin Analogues Example drugs: latanoprost, bimatoprost, tafluprost MOA: lowers IOP by facilitating aqueous humor outflow, in part by relaxing the ciliary muscle. IOP lowering up to ~30%. Adverse Effects: Increased brown pigmentation of the iris, eyelid Increase the length, thickness, and pigmentation of the eyelashes Blurred vision, burning, stinging, conjunctival hyperemia, conjunctival edema, and punctate keratopathy. Rarely: macular edema.  α2-Adrenergic Agonist Example Drugs: Brimonidine (Alphagan P) MOA: lowers IOP by reducing the production of aqueous humor and perhaps by increasing outflow; may delay optic nerve degeneration and protect retinal neurons from death. Adverse Effects: are dry mouth, ocular hyperemia, local burning and stinging, headache, blurred vision, foreign body sensation, and itching. Systemic: headache, dry mouth, fatigue  Cholinergics Example Drugs: Pilocarpine MOA: stimulates cholinergic receptors in eye causing increase of aqueous humor by: (1) miosis (constriction of the pupil secondary to contraction of the iris sphincter) (2) contraction of the ciliary muscle (an action that focuses the lens for near vision). Adverse Effects: Miosis, retinal detachment, local irritation, eye pain, and brow ache. Rare Systemic: bradycardia, bronchospasm, hypotension, urinary urgency, diarrhea, hypersalivation, and sweating. Systemic toxicity can be reversed with a muscarinic antagonist (e.g., atropine)  Carbonic Anhydrase Inhibitors Example Drugs: Dorzolamide (Trusopt) MOA: decrease production of aqueous humor Oral option (acetazolamide) can reduce production by 50% Adverse Effects: bitter aftertaste, transient blurred vision, burning/stinging Wait 15 minutes after administration before inserting contact lenses. Oral (systemic) effects: malaise, anorexia, fatigue, and paresthesias. Contraindicated with sulfa allergy, renal impairment  Glaucoma Patient Education Take medications as directed. If days are skipped or if prescriptions are not refilled, loss of vision may occur. Notify of any vision loss, severe eye pain, headache, or nausea and vomiting (angle-closure glaucoma). If photophobia: wear sunglasses, wide-brimmed hats, visors, or baseball caps Caution if medication contains benzalkonium as a preservative Wait 15 min before inserting contacts Do not to touch the dropper with hand or to the eye (infection risk) Close the eye(s) for 3 minutes after administering and lightly press a thumb or finger over the medial canthus = increase absorption Patient Centered Care Across the Lifespan Children: greater systemic absorption, most drugs not approved. Pilocarpine is used in congenital glaucoma Elderly: β blockers may worsen heart failure α2 agonists can cause orthostatic hypotension (falls) Caution with carbonic anhydrase inhibitors in renal impairment Cholinesterase inhibitors may cause bradycardia and hypotension.  Key Prescribing Considerations Therapeutic Goal: Reduce elevated IOP and prevent loss of vision. Baseline Data: IOP measurement, fundoscopic exam, visual field testing. Monitoring: IOP every 1 to 3 months initially then prn. β blockers = hypotension, bradycardia, AV block, and wheezing due to bronchoconstriction. α2 agonist = CNS effects (e.g., excessive drowsiness) and hypotension. Pilocarpine = visual acuity check, monitor for wheezing, slowed heart rate, decreased blood pressure, urinary urgency, diarrhea, excessive salivation, and excessive perspiration. Minimizing Adverse Effects: All agents can cause eye discomfort and itching. Artificial tears – wait 30 min. Warm compresses.  Angle Closure Glaucoma ≤ 5% of 1◦ glaucoma Mechanical obstruction by AH outflow through trabecular meshwork Increased IOP à loss of vision in hours to days Treat emergently to avoid vision loss Medical therapy to lower IOP, reduce pain, and reverse corneal edema before surgery BB, α2 agonist, prostaglandin analog, systemic CAI, or hyperosmotics Treatment: laser iridotomy  Acute Conjunctivitis Bacterial Viral Allergic  Allergic Conjunctivitis Symptoms: itching, increased lacrimation/discharge, conjunctival Allergic hyperemia (redness) Conjunctivitis: Diagnosis: Clinical Acute or chronic conjunctival inflammation secondary to airborne allergens Allergic Conjunctivitis  Allergic Conjunctivitis Management Treatment Class Mechanism Onset of Action Ophthalmic Demulcents Isotonic solutions used as substitutes for Immediate (artificial tears) natural tears to dilute or remove allergen H1-Receptor Antagonists Provide immediate symptomatic relief by Immediate (Antihistamines) blocking histamine response Activate α1-adrenergic receptors on blood Immediate redness and edema Ocular Decongestants vessels, causing vasoconstriction reduction Benefits take several days to Prevent release of inflammatory mediators Mast Cell Stabilizers develop; 2 or more weeks to be (e.g., cromolyn, lodoxamide) maximally effective Inhibit cyclooxygenase, required for NSAIDs Reduces symptoms prostaglandin synthesis Inhibit production of prostaglandins, Varies (inhibition of inflammatory Glucocorticoids leukotrienes, and thromboxane pathways)  Key Prescribing Considerations Therapeutic Goal: Relief of ocular pruritis, watery discharge, and redness. Prevention of associated complications that occur secondary to eye irritation or vigorous eye rubbing. Baseline Data & Monitoring: assess for evidence of eye infection. Identifying High-Risk Patients: Ocular decongestants are contraindicated in angle- closure glaucoma. Long-term glucocorticoids may increase IOP and lead to cataracts. Minimizing Adverse Effects: Mast cell stabilizers—take days to weeks to work Glucocorticoids—Reserve for short-term therapy of severe conditions. Establish that symptoms are caused by allergies and that there is no underlying viral infection. Decongestants—Reserve for short-term therapy (no longer than 2 weeks) to avoid rebound congestion.  Patient Education Allergen avoidance can reduce the severity of symptoms Artificial tears or other eye lubricants may provide relief from dryness and the associated discomfort AND help flush out allergens Application of cold compresses for 5–10 min at a time may help if discomfort is severe. Avoid rubbing eyes and wearing contact lenses, Wait at least 5 min between multiple drugs so that the second drug administered doesn't flush out the first drug administered.  Bacterial Conjunctivitis Highly contagious Etiology: Staphylococcus Spread by direct contact w/ patient aureus, Streptococcus & their secretions or with pneumoniae, Haemophilus contaminated objects & surfaces. influenzae, and Moraxella catarrhalis Presentation: redness and purulent discharge of eye(s) Bacterial Conjunctivitis Management Class and Generic Formulation Duration Name - Ciprofloxacin (Ciloxan) typically 7–14 days Fluoroquinolones - Ofloxacin (Ocuflox) typically 7–14 days Aminoglycosides - Tobramycin (Tobrex) typically 7–14 days Macrolides - Erythromycin (Ilotycin) typically 7–14 days Tetracyclines - Doxycycline (Vibramycin) typically 7–14 days Polymyxin B/ - Polymyxin B/Trimethoprim (Polytrim) typically 7–14 days Trimethoprim  Key Prescribing Considerations & Patient Education Infected individuals should not share handkerchiefs, tissues, towels, cosmetics, linens, or eating utensils. Most ԁаусаre centers and schools require that students receive 24 hours of treatment before returning to school. Patients should not use contact lenses while they have any eye infection. If they wear contacts and are diagnosed with bacterial conjunctivitis, need to cover for pseudomonal infection (oxofloxacin, ciprofloxacin)  Dry Eye Systemic Medications Most commonly idiopathic Aqueous tear deficiency Associated with older age Diuretics Can be caused by connective Anticholinergics tissue disorders Antidepressants Sjogren syndrome BB Rheumatoid arthritis Antihistamines Lupus Decongestants OCPs Inadequate eye closure Evaporative dry eyes Bell/FN Palsy Isotretinoin, antiandrogens Insufficient blink rate Poor eyelid closer Parkinson’s disease Major antipsychotics, adrenergic agonists, Botox  Dry Eye Management Ophthalmic Demulcents (artificial tears) Isotonic solutions used as substitutes for natural tears. Ocular Decongestants (adrenergic) Phenylephrine, naphazoline, oxymetazoline, brimonidine, and tetrahydrozoline. Adverse effects: stinging, burning, and reactive hyperemia Topical Cyclosporine Ophthalmic Emulsion (Restasis) For dry eyes from inflammation Suppresses the immune response, thereby promoting resumption of tear production. Adverse effects: burning, stinging, foreign body sensation, pruritus, conjunctival hyperemia, and blurred vision. Steroids Only used in absence of infection Most providers avoid in a non-acute setting Key Prescribing Considerations & Patient Education Stay hydrated Use humidifiers Avoid dry, drafty environments Avoid smoking, secondary smoke exposure Aggravating medication avoidance as possible