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Session 2 Pharm7
Pharm -7- Cholinergic Agents
| Question | Answer |
|---|---|
| What do cholinomimetics, parasympathomimetics, muscarinic agonists have in common | they are all cholinergic agonists |
| What are acetylcholine, methacholine, carbacol and Bethanechol | Choline Esters |
| What are muscarine, pilocarpine | Natural Alkaloids |
| What is the new M1/M3 specific agonist | Cevimeline |
| Why would you use other choline esters in place of just admnisitering acetylcholine | Acetylcholine is very susceptible to cholinesterase and gets broken down faster than other choline esters |
| Drug used for disorders associated with decreased Parasymp tone, used postoperative and postpartum for urinary retention and/or inadequate emptying of bladder. Helps correct abdominal distention and GI tract atony after surgery | Bethanchol |
| What is the MOA of bethanechol | acts at the muscarinic receptors to contract detrusor muscle and increase GI motility |
| What drug is used in acute and chronic glaucoma to reduce intraocular pressure and is better tolerated than AChE inhibitors. Also used to counteract atropine used in pupillary dilation and to treat dry mouth | Pilocarpine, |
| What is the MOA of pilocarpine | acts on M1/M3 receptor of constrictor pupillae to cause constriction of pupil and acts on M1/M3 receptors of salivary gland to increase secretion to combat xerostomia(dry mouth) |
| Why do you need to be careful in administering pilocarpine in the eye | it is a tertiary amine and can cross the conjunctiva leading to systemic effects |
| Drug that is used to treat Xerostomia(dry mouth) following head and neck irradiation, or associated with Sjoogren's syndrome | Cevimeline (evoxac) |
| What is the MOA of Cevimeline (evoxac) | newer M3 receptor agonist selective potent action at salivary glands and lacrimal glands, with fewer side effects than pilocarpine |
| What are the muscarinic agonists s/e | SLUD, salivation, lacrimation, urination urgency, defecation (diarhhea). Can cause hypotension and reduce coronary blood blow |
| What are some of the s/e of pilocarpine | CNS disturbances, excess salvation |
| why are muscarinic agonists contraindicated in asthma patients | they can cause bronchoconstriction and increase mucus secretions, |
| Why are muscarinic agonists contra ind in hyperthyroidism | they can cause hypotension which can trigger reflex increase in sympathetic activity to heart leading to arrythmia |
| What do the following have in common- atropine, scopolamine, homatropine, pirenzepine, ipratropium, tiotropium, and tolterodine | All are muscarinic Receptor Antagonists |
| What are the belladona alkaloids | atropine, scopolamine and homatropine |
| What are the synthetic and semisynthetic derivates of belladona alkaloids that are muscarinic receptor antagonists | Pirenzepine, ipratropium, tiotropium, tolterodine |
| What are the clinical uses of atropine | produces mydriasis and cycloplegia for eye exam antispasmodic treat organophosphate insecticide poisoning suppress respiratory secretions prior to surgery |
| What is the MOA of atropine | non selective muscarinic antagonist in the Eye- blocks all parasympathetic effects on the eye causing mydriasis and cycloplegia(loss of accomodation) GI- Reduces GI motility Salivary, sweat and lacrimal glands- reduces all secretions |
| What problems do you start to see as you increase the dose of atropine | low dose you get cardiac slowing, dryness of mouth and inhibition of sweating. But as dose increases you get rapid heart rate, palpitation, marked dryness of mouth and some blurring of near vision and with high dose you get hallucinations and coma |
| What are the clincial uses of scopolamine a muscarinic receptor antagonist | prophylactic for motion sickness, adjunct drug in anesthesia to produce sedation and amnesia |
| Which drug cross the BBB better at clinical doses atropine or scopolamine | Scopolamine crosses much more than atropine (which barely crosses in therapeutic doses) |
| What are the s/e of scopolamine | CNS depression, drowsiness, amnesia, fatigue, loss of REM sleep |
| Drug used in asthma & COPD to cause bronchodilation either as an adjunct to albuterol or instead of albuterol in patients who can't take adrenergic agonists | Ipratropium Bromide (atrovent) |
| What is the MOA of Ipratropium Bromide (atrovent) | Blocks muscarinic receptors and reduces bronchoconstriction mediated by parasympathetic system, Less CNS effects and minimal inhibitory effect on mucocilary clearance |
| What are the clinical uses of Tiotropium Bromide (spiriva) | used in COPD and asthma alot more bronchoselective greater affinity for M1/M3 than M2 |
| What are the clincal uses for tolterodine (detrol) | treatment of overactive bladder, Reduces number of incontinent episodes, increase amount of urine the bladder can hold, reduces frequency of urniation and urgency |
| what is the MOA of tolterodine (detrol) | Blocks M3 receptors on detrusor muscle reducing PSNS mediated contraction of the Bladder, Also Block M2 receptors and presynaptic SNS terminal enhancing SNS B2 relaxation of the detrusor -Also act on the trigone and internal sphincer preventing leaks |
| What are Solifenacin (Vesicare) Darifenacin (Enablex) Oxybutynin (Ditropan) | they are M3 antagoinists like Tolterodine |
| When are M3 antagonists like Tolterodine and Solifenacin (Vesicare), Darifenacin (Enablex),Oxybutynin (Ditropan) Contraindicated | they slow voiding and therefor are not appropriate in individuals with urinary retention such as Benign Prostatic Hyperplasia, |
| what are the s/e of muscarinic antagonists | blurred vision, confusion, mydriasis, constipation, urinary retention |
| Are ganglionic blockers if nicotinic receptors widely used | NO very few drugs in this category are clinically used |
| Since nicotinic ganglionic blockers are widely used where would you use nicotinic blockers | neuromuscular junction |
| What do NMJ blockers do | block cholinergic transmission between somatic motor nerve endings and the nicotinic receptors of skeletal muscles |
| What are the clinical uses of neuromuscular juction nicotinic blockers | skeletal muscle relaxants/ used in surgery to produce complete muscle relaxation |
| What type of NMJ blocker is succinyl choline | depolarizing blocker |
| what are the two types of NMJ blockers | non-depolarizing and depolarizing blockers |
| what type of NMJ blocker are | Atracurium Cistracurium Vecuronium Rocuronium Pancuronium Tubocurarine |
| are non-depolarizing NMJ blockers competitive or non-competitive blockers | competitive |
| What is succinyl choline made of | two acetylcholine molecules linked end to end |
| What is the onsent and duration of succinyl choline | rapid onset but short duration because it gets metabolized by plasma cholinesterase |
| What is a phase 1 block of NMJ nicotinic receptors | membrane depolarizes resulting in initial discharge that produces fasciculation followed by falccid paralysis |
| Can A phase 1 block be reversed by AchE inhibitors | NO |
| What is a Phase II block of NMJ nicotinic receptors | membrane repolarized but is desensitized to the effect of acetylcholine |
| What are the s/e of using succinylcholine NMJ depolarizing blocker | muscle pain postoperatively due to damaged muscle by hyperkalemia, at high doses can block ganglionic nicotinic receptors (decreasing heart rate and increased IOP) -serious s/e is malignant hyperthermia |
| What is the MOA of AchE (acetylcholine esterase) inhibitors | Inhibit acetylcholineesterase and prolong enhance actions of acetylcholine |
| What are the potential sites of action of AchE inhibitors | all effector organs innervated by PSNS, NMJ and all autonomic ganglia |
| What are the three main types of AchE inhibitors | Short, Intermediate, Irreversible |
| What are the clinical uses of AchE inhibitors | tx of myasthenia gravis, hypotonia of bladder and GI and glaucoma |
| What is the clinicla use of Physostigmine an AchE inhibitor | used to treat Glaucoma, or as an antidote to atropine and other anticholinergic drug poisonings |
| What problems can physostigmine an AchE inhibitor cause at high doses | convulsions, bradycardia leading to fall in cardiac output and muscle paralysis |
| What is the clinical use of Neostigmine | cannot cross BBB and has greater effect at NMJ so is used to treat myasthenia Gravis |
| what are the adverse effects of neostigmine an AchE inhibitor | generalized cholinergic stimulation and drop in b/p overdosage can cause cholinergic crisis and muscle paralysis |
| What can be administerd in organophosphate poisoning | pralidoxime which can reactivate acetylcholinesterase cannot penetrate BBB |
| Review Slide 52 | review Slide 52 |
Created by:
smaxsmith
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