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OCULAR PHARMACOLOGY

OCULAR PHARMACOLOGY. DR: Mahmoud Saeed Lecturer Of Clinical Pharmacy BMC. Anatomical & Physiological considerations. 1. Iris and Pupil . A-Constrictor pupillae muscle : Parasympathetic supply. Muscarinic M3 receptors. Miosis (constriction of pupil). 1. Iris and Pupil .

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OCULAR PHARMACOLOGY

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  1. OCULAR PHARMACOLOGY DR: MahmoudSaeed Lecturer Of Clinical Pharmacy BMC

  2. Anatomical & Physiological considerations

  3. 1. Iris and Pupil • A-Constrictor pupillae muscle : • Parasympathetic supply. • Muscarinic M3 receptors. • Miosis (constriction of pupil).

  4. 1. Iris and Pupil • B-Dilator pupillae muscle: • Sympathetic supply. • α1 receptors. • Mydriasis (dilation of pupil).

  5. 2.Ciliary body • Functions: • Secretion of aqueous humor by ciliary epithelium ( mainly β2 & some β1 receptors). • Accommodation of the vision by contraction of ciliary muscle ( loss of accommodation = Cycloplegia ). • Uveoscleral outflow.

  6. Intraocular pressure(IOP) • Normal IOP: 15-25 mm Hg. • Glaucoma = ↑ IOP. • To ↓ IOP : 1- ↓ Formation of aqueous humor. 2- ↑ Drainage of aqueous humor.

  7. Miotic Drugs • Drugs that constrict the pupil . • A – Parasympathomimetics: 1. Direct acting : e.g. pilocarbine , carbachol & bethanecol . 2. Indirect acting : e.g. physostigmine .

  8. Miotic Drugs • Actions of Parasympathomimetics: • Miosis : Through M3 receptors → contraction of Constrictor Pupillae Muscle 2. Accommodation for near vision . 3. ↓ IOP due to opening of canal of Schlemm.

  9. Miotic Drugs • B – Sympatholytics: e.g. Guanethidine . • C – Central acting : e.g. Morphine .

  10. Mydriatic Drugs • Drugs which produce dilation of the pupil. • A- Active Mydriatics : • Stimulate dilator pupillae muscle via α1 R. 1- Sympathomimetics : • Direct effect : e.g. Phenylephrine. • Indirect effect : e.g. Amphetamine . • Dual action : e.g. Ephedrine .

  11. Mydriatic Drugs • A- Active Mydriatics : • 1- Sympathomimetics : • Actions : 1. Contraction of dilator pupillae muscle. (Light & corneal reflexes are present). 2. Vasoconstriction of blood vessels→ eye decongestant . 3. No cycloplegia . 4. Contra-indicated in closed angle glaucoma .

  12. Mydriatic Drugs • A- Active Mydriatics: • 2. Cocaine : • Local anesthetic for the cornea & conjunctiva. • Corneal & conjunctiva reflex are absent . • Light reflex is present.

  13. Mydriatic Drugs • B – Passive Mydriatics : • Parasympatholytics → M3 blocker → Paralysis of ciliary muscle → cycloplegia . • e.g. Atropine & homatropine.

  14. Mydriatic Drugs • B – Passive Mydriatics: • Parasympatholytics: • Actions : 1-Cycloplegia (accommodation for far vision). 2-↑ IOP . 3- Absolutely contraindicated in glaucoma .

  15. Glaucoma

  16. What is glaucoma? • Optic neuropathy that is the leading cause of irreversible blindness in the world • Major types are open angle and closed angle • Differences among various types of glaucoma complicate the nomenclature • Glaucoma is commonly associated with elevated intraocular pressure (IOP), but the disease can occur in the context of normal IOP • Our understanding and treatment of the disease is very focused on IOP

  17. Open Angle Glaucoma • Obstruction at the level of the trabecular meshwork. • Progressive loss of visual field over time from periphery to center. • Majority of patients have IOP > 21 mmHg, asymptomatic. • Treatment: • 1-β-Blockers. • 2-α2 Agonist. • 3-Prostaglandin analogues. • 4-Miotic drops. • 5-Non specific adrenergic agonist. • 6-Carbonic anhydrase inhibitors.

  18. Closed Angle Glaucoma • Apposition of iris and trabecular meshwork • Parasympatholytics (pupillary dilation) can precipitate attack • Increase risk with age, increase in volume of lens • Acute onset, patient complains of nausea, headache (rather than eye ache), malaise, general distress • Requires surgery . • We must decrease IOP before surgery by:1- Osmotic agents. • 2- Miotic drops. • 3-Carbonic anhydrase inhibitors. • 4-α2 agonist.

  19. REVIEW: Autonomic NS Effect on the Eye

  20. TREATMENT RATIONALE LOWER IOP BY: Decreasing Production of Aqueous Humor Increasing Outflow of Aqueous Humor

  21. DRUGS THAT DECREASE AQUEOUS PRODUCTION • Beta-Blockers [levobunolol, timolol, carteolol, betaxolol] -Mechanism: Act on ciliary body to  production of aqueous humor -Administration: Topical drops to avoid systemic effects -Side Effects: Cardiovascular (bradycardia, asystole, syncope), bronchoconstriction (avoided by b1-selective betaxolol), depression • Alpha-2 Adrenergic Agonists[apraclonidine, brimonidine] -Mechanism:  production of aqueous humor -Administration: Topical drops -Side Effects: Lethargy, fatigue, dry mouth [apraclonidine is a derivative of clonidine (antihypertensive) which cannot cross BBB to cause systemic hypotension] • Carbonic Anhydrase Inhibitors[acetazolamide, dorzolamide] -Mechanism: Blocks CAII enzyme production of bicarbonate ions (transported to posterior chamber, carrying osmotic water flow), thus  production of aqueous humor -Administration: Oral, topical -Side Effects: malaise, kidney stones, possible (rare) aplastic anemia

  22. DRUGS THAT INCREASE AQUEOUS OUTFLOW • Nonspecific Adrenergic Agonists [epinephrine, dipivefrin] -Mechanism: uveoscleral outflow of aqueous humor -Administration: Topical drops -Side Effects: Can precipitate acute attack in patients with narrow iris-corneal angle, headaches, cardiovascular arrhythmia, tachycardia • Parasympathomimetics [pilocarpine, carbachol, echothiophate] -Mechanism:  contractile force of ciliary body muscle,  outflow via TM -Administration: Topical drops or gel, (slow-release plastic insert) -Side Effects: Headache, induced miopia. Few systemic SE for direct-acting agonists vs. AchE inhibitors (diarrhea, cramps, prolonged paralysis in setting of succinylcholine). Why isn’t Ach used? • Prostaglandins[latanoprost] -Mechanism: May  uveoscleral outflow by relaxing ciliary body muscle -Administration: Topical drops -Side Effects: Iris color change

  23. Rx GLAUCOMA: ADDITIONAL CONSIDERATIONS • No single medication can be used in all patients • Compliance • Critical: Rx often requires several agents, • multiple times a day, everyday • Role of slow-release drug delivery devices (Langer) • Non-pharmacologic ways to lower IOP: • Laser (argon laser trabeculoplasty)  aqueous outflow, loses effectiveness over time • Surgical (trabeculectomy) • Creates alternative path for aqueous outflow • Only definitive therapy for closed angle • Effectiveness of Rx measured by ability to lower IOP, but other factors may be (more) important: Neuroprotection/increased blood flow to optic nerve

  24. GLAUCOMA:Key Points • Glaucoma: -Visual loss from optic neuropathy -Open angle chronic, Closed angle acute -Final common pathway:  IOP (usually) • Drug Rx: All directed towardsIOP either via: • -  aqueous production: Beta blockers • Alpha-2 agonists • Carbonic anhydraseinhibitors • -  aqueous outflow:(Adrenergic agonists, nonspecific) • Parasympathomimetics • Prostaglandins • Treatment slows progression • Understanding ANS effect on the eye is critical for reasoning through drug mechanisms of action • Understanding ANS effect on the whole body is critical for predicting and avoiding dangerous side effects

  25. Thank You

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