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  • 2020–2021 BCSC Basic and Clinical Science Course™

    Go to Academy Store Learn more and Purchase.

    2 Fundamentals and Principles of Ophthalmology

    Part V: Ocular Pharmacology

    Chapter 16: Ocular Pharmacotherapeutics*

    Cholinergic Drugs

    Several commonly used ophthalmic medications affect the activity of acetylcholine receptors in synapses of the somatic and autonomic nervous systems (Fig 16-1). These receptors are found in

    • the motor end plates of the extraocular and levator palpebrae superioris muscles (supplied by somatic motor nerves)

    • the cells of the superior cervical (sympathetic) ganglion and the ciliary and sphenopalatine (parasympathetic) ganglia (supplied by preganglionic autonomic nerves)

    • parasympathetic effector sites in the iris sphincter and ciliary body and in the lacrimal, accessory lacrimal, and meibomian glands (supplied by postganglionic parasympathetic nerves)

    Although all cholinergic receptors are by definition responsive to acetylcholine, they are not homogeneous and can be classified by their responses to 2 drugs: muscarine and nicotine (Table 16-3). Muscarinic receptors are found in the end organs of the parasympathetic autonomic system. Nicotinic receptors are found in the postganglionic neurons of both the sympathetic and parasympathetic systems, in striated muscle (the end organ of the somatic system), and in the adrenal medulla. Cholinergic drugs may be further divided into the following groups (Fig 16-2):

    Figure 16-1 Summary of the neurotransmitters released and the types of receptors found within the autonomic and somatic nervous systems.

    (Reproduced with permission from Mycek MJ, Harvey RA, Champe PC, eds. Pharmacology. 2nd ed. Lippincott’s Illustrated Reviews. Philadelphia: Lippincott-Raven; 1997:32.)

    Table 16-3 Cholinergic and Adrenergic Receptors

    • direct-acting agonists, which act on the receptor to elicit an excitatory postsynaptic potential

    • indirect-acting agonists, which increase endogenous acetylcholine levels at the synaptic cleft by inhibiting acetylcholinesterase

    • antagonists, which block the action of acetylcholine on the receptor

    Muscarinic Drugs

    Direct-acting agonists

    Topically applied, direct-acting agonists have 3 actions:

    • They cause contraction of the iris sphincter, which not only constricts the pupil (miosis) but also changes the anatomical relationship of the iris to both the lens and the chamber angle.

    • They cause contraction of the circular fibers of the ciliary muscle, relaxing zonular tension on the lens equator and allowing the lens to shift forward and assume a more spherical shape (accommodation).

    • They cause contraction of the longitudinal fibers of the ciliary muscle, producing tension on the scleral spur (opening the trabecular meshwork) and facilitating aqueous outflow. Contraction of the ciliary musculature also produces tension on the peripheral retina, occasionally resulting in a retinal tear or even rhegmatogenous detachment.

    Acetylcholine does not penetrate the corneal epithelium well, and it is rapidly degraded by acetylcholinesterase (Fig 16-3). Thus, it is not used topically. Acetylcholine, 1%, and carbachol, 0.01%, are available for intracameral use in anterior segment surgery. These drugs produce prompt and marked miosis.

    Figure 16-2 A, Neurotransmitter binding triggers an intracellular response. B, Summary of cholinergic agonists.

    (Reproduced with permission from Harvey RA, Champe PC, eds. Pharmacology. Lippincott’s Illustrated Reviews. Philadelphia: Lippincott; 1992:30, 35.)

    The onset of intracameral acetylcholine, 1%, is more rapid than that of intracameral carbachol; acetylcholine acts within seconds of instillation, but the effect is short-lived. The drug is not stable in aqueous form and, as mentioned previously, is rapidly broken down by acetylcholinesterase in the anterior chamber. When administered similarly, intracameral carbachol, 0.01%, is 100 times more effective and longer lasting than acetylcholine, 1%. Maximal miosis is achieved within 5 minutes and lasts for 24 hours. In addition, carbachol, 0.01%, is an effective hypotensive drug that lowers intraocular pressure (IOP) during the crucial 24-hour period after surgery.

    Figure 16-3 Synthesis and release of acetylcholine from the cholinergic neuron. AcCoA = acetyl coenzyme A.

    (Reproduced with permission from Mycek MJ, Harvey RA, Champe PC, eds. Pharmacology. 2nd ed. Lippincott’s Illustrated Reviews. Philadelphia: Lippincott-Raven; 1997:37.)

    Pilocarpine, 0.12%, is used diagnostically to confirm an Adie tonic pupil, a condition in which the parasympathetic innervation of the iris sphincter and ciliary muscle is defective because of the loss of postganglionic fibers. Denervated muscarinic smooth muscle fibers in the affected segments of the iris exhibit supersensitivity and respond well to this weak miotic, whereas the normal iris does not.

    Pilocarpine, 0.25%, 0.5%, 1%, 2%, 3%, or 4% (4 times daily), and carbachol, 1.5% or 3% (2 times daily), are used in the treatment of primary open-angle glaucoma (POAG) because they lower IOP by facilitating outflow (Table 16-4). Use of pilocarpine beyond 2% is not more effective and may even cause a paradoxical increase in IOP in some cases of angle-closure glaucoma because this strong miotic may induce anterior movement of the lens–iris diaphragm. This is a concern particularly in cases of secondary angle closure attributed to anterior rotation of the ciliary body and choroidal edema (eg, malignant glaucoma [also referred to as aqueous misdirection] and topiramate-induced angle closure, respectively).

    Table 16-4 Miotics

    Miotic therapy can also be used (1) to treat elevated IOP in patients with primary angle-closure glaucoma in which the anterior chamber angle remains occludable despite laser iridotomy; and (2) as prophylaxis for angle closure before iridotomy, but not as a long-term substitute for laser iridotomy (see BCSC Section 10, Glaucoma, for additional information).

    Miosis, cataractogenesis, and induced myopia are generally unwelcome adverse effects of muscarinic therapy. Although the broad range of retinal dark adaptation usually compensates sufficiently for the effect of miosis on vision during daylight hours, patients taking these drugs may be visually incapacitated in dim light. In addition, miosis often compounds the effect of axial lenticular opacities; thus, many patients with cataracts are unable to tolerate miotics. Furthermore, older patients with early cataracts have visual difficulty in scotopic conditions, and the miosis induced by cholinergic drugs may increase the risk of falls. Younger patients may have difficulty with miotics as well. For example, patients younger than 50 years may manifest disabling myopia and induced accommodation because of drug-induced contraction of the ciliary body, which increases the convexity of the lens and shifts the lens forward. Other complications observed with use of higher concentrations of miotics include iris cysts and retinal detachment due to ciliary body contraction and traction on the pars plana.

    Systemic adverse effects of muscarinic agonists include salivation, diarrhea, urinary urgency, vomiting, bronchial spasm, bradycardia, and diaphoresis. However, systemic adverse effects are rare following topical use of direct-acting agonists. For example, a slowly dissolving pilocarpine gel used at bedtime minimizes the unwanted adverse effects of the agent and is useful for younger patients, patients with symptoms of variable myopia or intense miosis, older patients with lens opacities, and patients who have difficulty complying with more frequent dosing regimens.

    Ciliary muscle stimulation can help manage accommodative esotropia. The near response is a synkinesis of accommodation, miosis, and convergence. As discussed previously, muscarinic agonists contract the ciliary body and induce accommodation as an adverse effect. Therefore, the patient does not need to accommodate at near, which decreases not only the synkinetic convergence response but also the degree of accommodative esotropia.

    Indirect-acting agonists

    Indirect-acting muscarinic agonists (cholinesterase inhibitors) have the same actions as direct-acting muscarinic agonists, although they have a longer duration of action and are frequently more potent. These medications react with the active serine hydroxyl site of cholinesterases, forming an enzyme–inhibitor complex that renders the enzyme unavailable for hydrolyzing acetylcholine.

    There are 2 classes of cholinesterase inhibitors:

    • reversible inhibitors, such as physostigmine (available as a powder for compounding and as a solution for injection), neostigmine, and edrophonium

    • irreversible inhibitors, such as echothiophate (phospholine iodide, no longer available for ophthalmic use in the United States); diisopropyl phosphorofluoridate (no longer available for ophthalmic use in the United States), which phosphorylates both the acetylcholinesterase of the synaptic cleft and the butyrylcholinesterase (pseudocholinesterase) of plasma; and demecarium bromide (no longer available for ophthalmic use in the United States)

    The duration of inhibitory action is determined by the strength of the bond between the inhibitor and the enzyme. Inhibitors that are organic derivatives of phosphoric acid (eg, organophosphates such as echothiophate) undergo initial binding and hydrolysis by the enzyme, forming a phosphorylated active site. Such a covalent phosphorus–enzyme bond is extremely stable and hydrolyzes very slowly. Because of the marked differences in their duration of action, organophosphate inhibitors are irreversible inhibitors.

    The action of phosphorylating cholinesterase inhibitors can be reversed by treatment with oxime-containing compounds. Oxime pralidoxime—though useful in the treatment of acute organophosphate poisoning (eg, insecticide exposure)—is of little value in reversing the marked reduction of plasma butyrylcholinesterase activity that occurs with long-term irreversible cholinesterase-inhibitor therapy.

    Patients receiving long-term irreversible cholinesterase-inhibitor therapy such as echothiophate may experience toxic reactions from systemic absorption of local anesthetics containing ester groups (eg, procaine), which are normally inactivated by plasma cholinesterase. Administration of the muscle relaxant succinylcholine during induction of general anesthesia is also hazardous in these patients because the drug will not be metabolized and will prolong respiratory paralysis.

    Phosphorylating cholinesterase inhibitors may also cause local ocular toxicity. In children, cystlike proliferations of the iris pigment epithelium may develop at the pupil margin, which can block the pupil. For unknown reasons, cyst development can be minimized by concomitant use of phenylephrine (2.5%) drops. In adults, cataracts may develop, or preexisting opacities may progress. Interestingly, such cataracts are rare in children, and significant epithelial cysts are rare, if they occur at all, in adults.

    Antagonists

    Topically applied muscarinic antagonists, such as atropine, react with postsynaptic muscarinic receptors and block the action of acetylcholine. Paralysis of the iris sphincter, coupled with the unopposed action of the dilator muscle, causes pupillary dilation, or mydriasis (Table 16-5). Mydriasis facilitates examination of the peripheral lens, ciliary body, and retina. Muscarinic antagonists are approved for therapeutic use in the treatment of anterior uveitis in adults because they reduce contact between the posterior iris surface and the anterior lens capsule, thereby preventing the formation of iris–lens adhesions, or posterior synechiae. Topically applied muscarinic antagonists also reduce permeability of the blood–aqueous barrier and are useful for treating ocular inflammatory disease. Atropine and cyclopentolate have been approved by the FDA for use in pediatric patients but not for all indications.

    Muscarinic antagonists also paralyze the ciliary muscles, which helps relieve pain associated with iridocyclitis; inhibit accommodation for accurate refraction in children (cyclopentolate, atropine); and treat ciliary block (malignant) glaucoma. However, use of cycloplegic drugs to dilate the pupils of patients with POAG may elevate IOP, especially in patients who require miotics for pressure control. Therefore, use of short-acting medications and monitoring of IOP in patients with severe optic nerve damage are advised.

    Table 16-5 Mydriatics and Cycloplegics

    In situations requiring complete cycloplegia, such as the treatment of iridocyclitis (scopolamine, homatropine, or atropine for adults) or the full refractive correction of accommodative esotropia, more potent drugs are preferred. Although a single drop of atropine has some cycloplegic effect that lasts for days, 2 or 3 instillations a day may be required to maintain full cycloplegia for pain relief from iridocyclitis. It may become necessary to change medications if atropine elicits a characteristic local irritation with swelling and maceration of the eyelids and conjunctival injection (hyperemia). When mydriasis alone is necessary to facilitate examination or refraction, drugs with a shorter residual effect are preferred because they allow faster return of pupil response and reading ability.

    Systemic absorption of topical muscarinic antagonists can cause dose-related toxicity, especially in children, for whom the dose is distributed within a smaller body mass. A combination of central and peripheral effects, including flushing, fever, tachycardia, constipation, urinary retention, and even delirium, can result. Mild cases may require only discontinuation of the drug, but severe cases can be treated with intravenous physostigmine (approved for adults and children), slowly titrated until the symptoms subside. Physostigmine is used because it is a tertiary amine (uncharged) and can cross the blood–brain barrier.

    Administration of atropine for systemic effect blocks the oculocardiac reflex, a reflex bradycardia that is sometimes elicited during ocular surgery by manipulation of the conjunctiva, the globe, or the extraocular muscles. The reflex can also be prevented at the afferent end by retrobulbar anesthesia, although it can occur during administration of the retrobulbar block.

    Excerpted from BCSC 2020-2021 series: Section 2 - Fundamentals and Principles of Ophthalmology. For more information and to purchase the entire series, please visit https://www.aao.org/bcsc.

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    Presbyopia-Correcting IOLs
    2022 Codequest - Multistate (Recorded March 29)
    2022 Codequest Virtual (Multistate)
    Retina Patient Education Video Collection
    Cataract and Refractive Surgery Patient Education Video Collection
 
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