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47 Cards in this Set
- Front
- Back
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Bethanechol
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- muscarinic agonist: resistant to ChE
- stimulant of GI tract and bladder; few CV effects - also: methacholine, carbachol |
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Muscarine
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- reversible muscarinic agonist
- treat by administering antagonist |
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Pilocarpine
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- muscarinic agonist
- used to treat glaucoma and dry mouth (xerostomia); oral administration |
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Nicotine
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- nicotinic agonist (depolarizing blocker)
- only therapeutic use is to help people quit smoking |
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Edrophonium
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- reversible anti-ChE
- shortest-acting of the anti-ChEs - use to diagnose myasthenia gravis |
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Physostigmine (eserine)
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- carbamate; reversible anti-ChE
- similar structure to ACh; reacts with ChE similarly but yields carbamylated (as opposed to acetylated) enzyme, which is only very slowly regenerated to original form - use to treat glaucoma and anti-muscarinic poisoning |
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Neostigmine
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- carbamate; reversible anti-ChE
- more potent than physostigmine - no CNS penetration |
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Diisopropyl phosphorofluoridate (DFP)
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- organophosphorus (irreversible) anti-ChE
- treat poisoning with pralidoxime |
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Pralidoxime
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- cholinergic reactivator; use to treat anti-ChE poisoning at nicotinic synapses (skeletal paralysis)
- has nucleophilic oxygen that pulls phosphorus away from nucleophilic oxygen of ChE’s active center - works unless enzyme-organophosphate complex is “aged” (1-2 hours) |
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Botulinum toxin
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- blocks ACh release
- very toxic (LD50 = 3x10^(-8) mg/kg) - injected in very dilute concentrations to locally paralyze muscles |
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Atropine
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- competitive muscarinic antagonist
- little/no CNS effects - use to treat anti-ChE poisoning |
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Benztropine
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- competitive muscarinic antagonist
- can be used as adjunct with L-DOPA to treat Parkinson’s |
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Scopolamine
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- competitive muscarinic antagonist
- use to prevent motion sickness - has CNS effects (drowsiness, amnesia; with increased doses, restlessness, hallucination) |
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d-tubocurarine
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- competitive nicotinic blocker
- 2 N+ widely separated in bulky, rigid structure - acts mostly at skeletal NMJ but also at ganglia; causes histamine release - reduces sympathetic input to vasculature; side effects on heart (arrhythmias) - similar to: rocuronium, pancuronium, atracurium, vecuronium |
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Metocurine
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- competitive nicotinic blocker
- synthetic, more potent derivative of d-tubocurarine - muscle relaxant for long surgical procedures (~120 min) |
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Pancuronium
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- competitive nicotinic blocker
- affects NET and M2 receptor as well - steroid derivative |
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Atracurium
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- competitive nicotinic blocker
- intermediate time course bet. succinylcholine and metocurine with fewer CV effects - also: vecuronium |
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Hexamethonium
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- competitive nicotinic blocker
- selective blockade of ganglia |
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Decamethonium
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- depolarizing nicotinic blocker
- selective blockade of skeletal NMJ |
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Succinylcholine
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- depolarizing nicotinic blocker
- very short acting; used for brief surgical procedures (like tracheal intubation) - acts mostly at skeletal NMJ but also at ganglia |
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Clonidine
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- α2 agonist
- used as antihypertensive; also for pain and drug withdrawal - acts centrally to produce inhibition of sympathetic vasomotor centers; also has peripheral effects; inhibits pain neurotransmission in spinal cord - similar to methyldopa |
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Brimonidine
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- α2 agonist
- used to treat glaucoma |
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Isoproterenol
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- β1 and β2 agonist (strong)
- vasodilation and relaxation of bronchial and GI smooth muscle, but also cardiac effects (avoid by using specific β2 agonists for asthma) - metabolized mostly by COMT (large isopropyl on amino group renders it resistant to MAO) |
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Tyramine
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- sympathomimetic (indirect action)
- dopamine without 3-OH on ring - acts indirectly to cause dumping of NE into synaptic cleft; also acts as false transmitter - metabolized by MAO --> can trigger hypertensive crisis in pts taking MAO inhibitors - present in aged cheese and wine |
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Amphetamine
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- sympathomimetic (indirect action)
- no OH groups --> highly lipid soluble --> CNS stimulant - synthetic - can be administered in nebulized form - used to treat narcolepsy; ADHD in kids (methylphenidate used more often) - used in military to enhance/prolong performance - amphetamine is a good substrate for both NET and VMAT --> enters storage vesicle where it degrades the proton gradient that VMAT relies on, so that NE flows out of storage vesicle, out of nerve terminal, and into synapse |
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Ephedrine
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- α and β agonist that also causes NE release
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Phenylephrine
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- α1 agonist
- used as pressor agent in hypotensive states; induces mydriasis; aids nasal decongestion - also: pseudoephedrine |
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Terbutaline
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- β2 agonist used to treat asthma
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Albuterol
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- β2 agonist used to treat asthma
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Salmeterol
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- β2 agonist
- slower and longer-acting than albuterol - use to treat COPD |
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Dobutamine
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- beta-1 agonist
- activates beta-1 > beta-2 >> alpha-1 receptors (increases contractility and output more than HR) - use to treat heart failure and cardiogenic shock |
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Metaraminol
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- α agonist that also causes NE release
- can act as false transmitter - resistant to MAO and COMT - given with local anesthetics to keep them restricted to injection area |
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Ritodrine
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- β2 agonist used to stop premature labor
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Phenoxybenzamine
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- irreversible α blocker (1 and 2)
- alkylates the receptor, blocking it permanently - decreased peripheral resistance --> baroreceptor response --> sympathomimetic cardiac stimulation - causes orthostatic hypotension |
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Phentolamine
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- competitive α blocker (1 and 2)
- cardiac effects similar to phenoxybenzamine - parasympathomimetic GI tract stimulation (prevented by atropine) - causes release of histamine from mast cells |
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Prazosin
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- α1 blocker (binds α2 also, but weakly)
- acts peripherally (lowers blood pressure without increasing HR) - 95% bound to plasma protein - causes postural hypotension, syncope |
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Yohimbine
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- α2 blocker (opposite of clonidine, the α2 agonist)
- increases sympathetic outflow from CNS to increase BP and HR (blocks postsynaptic α2 receptors) - also has peripheral sympathomimetic effect by blocking inhibitory presynaptic α2 receptors |
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Timolol
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- β blocker (1 and 2)
- short-acting - used to treat glaucoma: aqueous humor is produced in the ciliary epithelium, which has β2 receptors |
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Propranolol
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- β blocker (1 and 2; first pure β antagonist)
- derived from isoproterenol (β agonist) - lipid-soluble, well absorbed from gut, largely metabolized by liver (like timolol and pindolol, other 1st generation β blockers) |
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Carvedilol
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- α1 and β1 blocker
- third generation β blocker: produces vasodilation in addition to cardiac effects caused by β1 block - other third generation β blockers: celiprolol, nebivolol |
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Atenolol
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- β1 blocker
- long-acting and more water soluble (relative to non-selective β blockers) - preferable to non-selective β blockers because it has CV effects without causing bronchoconstriction |
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Metyrosine
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- inhibits tyrosine hydroxylase (which catalyzes Tyr --> DOPA), greatly decreasing synthesis of catecholamines
- can be used to treat pheochromocytoma (tumor cells will produce less NE) |
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Methyldopa
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- methylated version of DOPA; competes with DOPA for enzyme (dopa decarboxylase)
- produces methylnorepinephrine, which is a false transmitter that acts as an α (mostly α2) agonist - has anti-hypertensive effects due to α2 stimulation |
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Reserpine
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- irreversible blocker of VMAT; long-lasting effect
- NE can still enter nerve terminal, but it can’t enter storage vesicle --> inactivated in cytoplasm by MAO --> NE (and 5-HT) stores are depleted in CNS and PNS |
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Cocaine
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- blocks NET
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Imipramine
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- tricyclic antidepressant; blocks NET
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Pyridostigmine
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- reversible anti-ChE
- long acting; use to treat myasthenia gravis - no CNS penetration |
