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53 Cards in this Set

  • Front
  • Back
Muscarinic Receptors
5 subtypes (M1-M5). Stimulated by Ach (and muscarine), blocked by atropine.
Location of M1 receptors
Location of M2 receptors
Nerves, cardiac & smooth muscle cells
Location of M3 receptors
Endothelium, exocrine glands, and smooth muscle
Location of N1 receptors
Autonomic ganglia
Location of N2 receptors
skeletal muscle cells (neuromuscular junction)
Cholinergic neurotransmission steps
1. Synthesis
2. Storage
3. Release
4. Binding to receptor
5. Degradation of Ach
6. Recycling choline
Blocks the sodium/choline cotransporter at the pre-synaptic neruon cell membrane.
Inhibits packaging of acetylcholine into synaptic vesicles (also in vesicle is ATP & proteoglycan) by blocking the transporter.
Botulinum toxin (Botox)
Prevents synaptic vesicle from fusing with membrane, thereby preventing release of Ach at synaptic cleft.
Necessary for initiation of vesicle docking - initiated by the propagation of action potential down the nerve axon; the calcium channel is a N-type voltage-dependent calcium channel.
Glycoprotein enzyme found at synapse (on post-synaptic membrane) - specific for Ach, hydrolyzes the ester:
Ach --(ach_ase)--> choline + acetate
Choline Acetyl Transferase
Enzyme that synthesizes Ach:

AcetylCoA + choline --(ChAT)--> Ach
Nicotinic receptors
Two basic clinical subtypes: N1, blocked by hexamethonium, and N2, blocked by curare. Both are stimulated by Ach (and nicotine).
Glycoprotein enzyme found at synapse (on post-synaptic membrane) - specific for Ach, hydrolyzes the ester:
Ach --(ach_ase)--> choline + acetate
Choline Acetyl Transferase
Enzyme that synthesizes Ach:

AcetylCoA + choline --(ChAT)--> Ach
Nicotinic receptors
Two basic clinical subtypes: N1, blocked by hexamethonium, and N2, blocked by curare. Both are stimulated by Ach (and nicotine).
Direct-acting cholinergic agonists
Mimic effect of Ach by binding directly to Ach receptors. Some are specific for muscarinic receptors. All direct-acting cholinergic agonists have longer duration of action than Ach.
-THE cholinergic neurotransmitter
-binds to nicotinic & muscarinic receptors (cholinoreceptors).
-Quickly degraded by Ach-ase (no therapeutic use)

1. Decrease heart rate & C.O.
-mimics vagal stimulation
2. Decreasein BP
-via NO synthesis in vascular endothelium
3. Increases salivation, intestinal secretions, GI motility, stimulates bronchoconstriction & bronchial secretions, increase tone of detrussor muscle, ciliary muscle & pupillae constrictor muscle (miosis)
Bethanechol (Urecholine)
-direct-acting cholinergic agonist
-specific for muscarinic receptors
-duration of ~1 hour
-primary action is on smooth musculature of bladder & GI tract
-poor substrate for Ach-ase, though is degraded by other esterases
1. Increased GI motility & secretion
2. Detrussor muscle stimulation (& trigone/sphincter relaxation)

-used to stimulate the atonic bladder
-adverse effects - general cholinergic stimuli effects (sweating, salivation, flushing, decr BP, nausea, abd. pain, diarrhea, bronchospasm)
Carbachol (Carbacol)
-Direct-acting cholinergic agonist
-poor substrate for Ach-ase
-1 administration lasts ~1 hour
-agonizes both muscarinic and nicotinic receptors
1. Increases GI motility & secretions, mimics Ach effects in eye (miosis, accomodation)
2. due to nicotinic agonism, may stimulate ganglia to secrete NE, causing first stimulation, then depression of these systems
-therapeutic use - rarely used, except as a miotic agent
-inhibits synthesis (therefore, release) of Ach
Tetrodotoxin & saxitoxin
inhibition of Na+ channels, therefore inhibits nerve impulses
Methacholine (Mecholyl)
-direct-acting cholinergic agonists:
-used for diagnosis of asthma
Pilocarpine (Salagen)
-Direct-acting cholinergic agonist
-tertiary amine (alkaloid), stable to hydrolysis by Ach-ase
-exhibits selective muscarinic acitvity
1. applied to cornea, causes miosis & accomodation.
-Used to lower intraocular pressure emergently; used to treat glaucoma, and increase salivation
Cevimeline (Evoxac)
-Direct-acting cholinergic agonist
-specific for muscarinic receptors
-used for treatment of dry mouth (in Sjogren's syndrome)
What do you give to counteract the side-effects of direct-acting cholinergic agonists?
Atropine (muscarinic antagonist)
anticholinesterase agents
drugs that inhibit the action of acetylcholinesterase (Ach-ase), thereby prolonging the lifetime/intensifying the effect of Ach and/or cholinergic agonists (at both muscarinic & nicotinic receptor sites)
mechanism of action of Ach-ase
2 sites of activity on Ach-ase: 1)Anionic site (holds the quartenary amine/positive charged site in place electrostatically)
2)Esteratic site (covalently bonds with substrate)

Cleaves the compound by reducing the ester bond.
Edrophonium (Tensilon)
-Reversible inhibitor of Ach-ase
-binds at both anionic and esteratic site of Ach-ase
-rapid onset, short duration of action
-USED FOR DIAGNOSIS OF MYASTHENIA GRAVIS (in MG, relieves symptoms; in normal individual, causes cholinergic crisis)
-the antidote for cholinergic crisis is ATROPINE
Physostigmine (Eserine)
-reversible anticholinesterase agent
-readily absorbed from GI tract, SC tissue, mucous membranes
-produces both muscarinic and nicotinic activities; CROSSES INTO CNS (IMPORTANT ANTIDOTE TO ATROPINE TOXICITY)
-due to CNS effects, causes stimulation followed by depression
-used for treatment of glaucoma
Neostigmine (Prostigmin)
-reversible anticholinesterase agent, that also has DIRECT nicotinic agonist effects
-no CNS effects
-used for Tx/Dx of myasthenia gravis, postoperative atony of gut & bladder
-used for curare poisoning
Pyridostigmine (Mestinon)
-reversible anticholinesterase agent
-longer acting than others (3-6 hours), with fewer side effects
-used for Tx of myasthenia gravis, antidote for curare poisoning
-IRREVERSIBLE anticholinesterase agent
-used in treatment of glaucoma
Acetylcholinesterase re-activator:

if Ach-ase has been put out of commission, this drug can put it back into commission (used sometimes with atropine to counteract the effects of some toxic situations) by regenerating the Ach-ase enzyme if its been modified by some agent.
Isoflurophate (DFP)
-binds to Esteratic site (serine residue) of Ach-ase, inactivating it.
-if left untreated for long enough (6-8 hours in case of DFP), the agent will lose an alkyl group, making the enzyme IRREVERSIBLY inhibited (this is called aging)
Non-depolarizing neuromuscular blocking agents
Bind to nicotinic receptor at neuromuscular junction (N2 type), either reversibly or irreversibly, thereby preventing Ach-mediated muscle fiber depolarization. Counteracted by anticholinesterase agents (for reversible agents) or praloxime (for irreversible agents).
reversible non-depolarizing neuromuscular blocking agent (competitive)
-short onset (minutes), long acting (1.5-2 hours)
-order of paralysis: face/neck->limbs->trunk->intercostals->diaphragm;
recovery in reverse order
-overdose usually treated with assisted ventilation. Anticholinesterase agents sometimes used as adjunct therapy (ie, neostigmine, pyridostigmine)
-some blockade of autonomic ganglia @ therapeutic dose. DOES NOT CROSS BBB!
-causes some histamine release, so may cause decr C.O., hypotension, urticaria, bronchospasm
-low oral bioavailability, 30% renal elimination over several hours, limited hepatic metabolism
-used as muscle relaxant with general anesthesia
Pancuronium (Pavulon)
reversible non-depolarizing neuromuscular blocking agent
-no histamine effects, no hypotensive effects
-HR, C.O., minimally affected
-used as muscle relaxant for endotracheal intubation
-at 0.07 mg/kg, onset is short (3-5 min), duration is long (100 min)
-renal/hepatic elimination/metabolism
Vecuronium (Norcuron)
reversible non-depolarizing neuromuscular blocking agent
-congener (analogue) of pancuronium
- at 0.05 mg/kg, onset is short (2-3 min), duration is intermediate (1 hour)
-hepatic/renal elimination/metabolism
Atracurium (Tracrium)
reversible non-depolarizing neuromuscular blocking agent
-minimal histamine release at Tx doses
-at 0.2 mg/kg, onset is short (2-3 min), duration is intermediate (1 hour)
-cleared via Hoffman degradation (conversion of amide to amine)
Mivacurium (Mivacron)
reversible non-depolarizing neuromuscular blocking agent
-same as for atracurium
-at 0.08 mg/kg, onset is short (2-3 min), duration is short (5 min)
-degraded by plasma cholinesterase
Rocuronium (Zemuron)
reversible non-depolarizing neuromuscular blocking agent
-same as for atracurium
-at 0.3 mg/kg, onset is short (1-2 min), duration is intermediate (30 min)
-Hepatic/renal elimination/metabolism
Depolarizing neuromuscular blocking agents
-Activates & depolarizes MEP
-MEP repolarizes, but receptors have become "desensitized" to Ach
-two phases:
phase 1 - causes muscle fasciculations (antagonized by curare, intensified by anticholinesterase agents)
phase 2 - desensitization, effect varies with dose & affeced muscle
succinylcholine (anectine)
depolarizing neuromuscular blocking agent
-advantages: rapid onset of action, ultra-short duration of action, can be given via IM injection
-disadvantages: hyperkalemia (especially in patients suffering from burns, massive trauma, denervation), cardiac dysrhythmias (especially w/ hypoxia & hypercarbia), masseter spasm, malignant hyperthermia in susceptible patients
**Has both depolarizing & non-depolarizing neuromuscular blockade effects
-in addition, has considerable anticholinesterase effects
ether, halothane, isoflurane
inhalation anesthetics
-possess a curare-like action
-synergizes with competitive neuromuscular blocking agents
streptomycin, neomycin, polymyxin
-cause competitive neuromuscular blockade
-similar effects seen by colistin & kanamycin
venom from poison-arrow frog
-causes paralysis by competitive (reversible) neuromuscular blockade of nicotinic receptors
-may bind with the channel pore, but doesn't bind at the agonist site
-doesn't cross GI tract; to be effective, must be delivered at site to be blocked (ie, parenteral route)
1. Increased GI motility & secretions
2. decreased HR (acts on SA, AV nodes & on atrium via Vagus nerve)
3. Miosis
4. decrease urinary bladder sphincter tone, increase detrussor muscle tone
5. bronchial constriction, increased bronchial secretions
6. salivation
anticholinesterase agent
-used topically, treatment for lice
Trihexyphenidyl HCl
-antimuscarinic drug
-Used to treat parkinsonism