o What is the rate limiting step of acetylcholine synthesis? How does the rate of nerve firing
affect synthesis and what is the mechanism?
o What is Ach not synthesized inside the neuron?
o What are the two types of choline active transporters? Which type is used to reuptake broken
o What neutralizes Ach in the synaptic cleft? What is the time frame from Ach release to
o How is choline taken up into the cells? What drug blocks it?
o What drug inhibits vesicle packaging?
o What drug inhibits vesicle membrane fusion? How is inhibition achieved?
o Where are the three places where muscarine work? What drug will block these areas?
o Do muscarine agonists have a sympathetic or parasympathetic effect? What type of
receptors do they use?
o Where are the places that nicotine acts? What is the other name for each type? What drugs
o What are nicotinic receptors located on? What happens when ligand binds and what is the
affect on the cell? How does high Ach affect nicotinic receptors?
o What is the order of affinity of muscarine, Ach, and nicotine for muscarinic and nicotinic
o Under what conditions will antagonists have no effect?
o What is NO synthesized from and what enzyme converts it? Where does arginine come from?
o What are the two endothelium-dependent vasodilators that trigger NO synthesis? What is the
mechanism of this signaling? How does NO then affect smooth muscle? How does NO
affect endothelial cells?
o What is the strongest vasodialator? What is the most potent vasoconstrictor?
o Why are endothelial derived vasoconstrictors important for maintaining blood pressure?
How will injecting Ach affect NO formation? What are two other molecules formed by
endothelial cells to trigger vasodilation?
o How does a low dose of Ach affect BP? A high dose? What if you give a large dose of Ach
with atropine? What about low dose Ach with atropine?
o How does IV nicotine affect BP? How do alpha blockers affect BP?
o What are the subtypes of muscarinic receptors? Where is each located? What is the post-
receptor mechanism of each?
o What are the classifications of nicotinic receptors? What subunit is unique to the embryonic
o What is Botox used to treat? How does it work?
o How does the parasympathetic nervous system affect the eyes, lungs, GI, heart, and bladder?
o Do muscarinic agonists produce sympathetic or parasympathetic effects?
o What are the two ganglia that control eye constriction/dilation? What neurotransmitter does
each release? What action does each cause?
o What affect does high levels of Ach have on Ach receptors?
o What is Horner’s syndrome? What is Holmes-Adie syndrome?
o What are the two muscles that affect pupil diameter and focusing?
o What innervates the ciliary muscle? Does parasympathetic action cause near or far site?
Does it make the lens more or less convex? What combination of pupil movement and
focusing does atropine make?
o What is cycloplegia? What drug can cause it?
o How do the action potentials differ in the SA&AV node, atrial cell, bundle cell, and
o What are the five phases of an AP? What causes each phase? Which phase is diastolic?
o How does parasympathetic input affect heart rate, AV node conduction velocity, and
excitability of latent pacemakers?
o How does Ach affect atrial cells? How does it affect AV nodal cells?
o What are the affects of muscarinic agonists on the lungs?
o Which choline esters are not degraded by cholinesterase? Which does not work on nicotinic
o What is sickle syndrome? Xerophthalmia? Xerostomia?
o How are choline esters administered? Why?
o What are some of the side effects of parasympathomimetics? What is the antidote for these
o What are the contraindications of parasympathomimetics?
o Where do muscarinic receptor antagonists work?
o What function is most sensitive to muscarinic blockade?
o What are the naturally occurring muscarinic antagonists?
o What is the only quaternary ammonia synthetic muscarinic antagonist? What route can it not
o How do muscarinic antagonists affect blood vessels? What effect do they have on the CNS?
o How well are antimuscarinic drugs absorbed and distributed in the body? How about
o Will atropine cause a larger change in old people or young people? Why?
o Are there cholinergic and adreno receptors in the superior cervical ganglion? Does atropine
affect these receptors? What drug can block these receptors?
o How do small doses of nicotine affect heart rate? Large doses? How does nicotine affect
blood pressure? Skeletal muscle? GI system? CNS?
o How do nicotine replacement therapies work? Why are they not addictive?
o What is the only ganglionic blocker that crosses the blood-brain barrier?
o What are the only three sites under sympathetic tone? What are the only two sites under
o What is the mneumonic for a perons with a ganglionic block?
o What are the three types of locally acting muscle relaxants?
o How do non-depolarizing agents work? Is it reversible? What part of the NMJ is blocked?
What drug can counter the blocking action?
o What is the onset and duration of d-tubocurarine? What is the order that it causes paralysis?
What order does recovery occur in?
o Do NMJ blockers cross the blood brain barrier? Can they be used as analgesics?
o What secondary effect does d-tubocurarine have? What is d-tubocurarine used to treat?
o How quick is the onset for the NMJ blockers?
o What two NMJ blockers have no CNS effects?
o What are the ultra short, short, intermediate, and long acting drugs?
o How do depolarizing NMJ blockers work? What are the two phases? Does the end plate
remain depolarized? What can be used to intensify and antagonize the phase 1 effects?
What reaction is seen in phase 1? What determines the duration of phase 2?
o What are the three tests to assess neuromuscular transmission? What are the responses in
non-depolarizing block, phase I depolarizing block, and phase II depolarizing block?
o What are the advantages of succinylcholine? What are the disadvantages? What is the major
o What is the drug with combined NMJ blocking action? What other activity does this drug
o What are two types of drugs that can enhance an NMJ block? What are examples of each?
How do they work?
o What sites do anticholinesterases work at?
o What are the two sites on the acetylcholinesterase? What kind of bond occurs at each site?
o What are the two AA’s at the esterotic site?
o How is acetylcholine hydrolyzed and the enzyme regenerated?
o How do anticholinesterases work? Organophosphates?
o What sites does edrophonium bind? How does it stimulate skeletal muscle? What is it used
o What are the two drugs used for the diagnosis of myasthenia gravis? What do they have in
o What causes myasthenia gravis? How can achetylcholinesterase counter it?
o What are the clinical manifestations of myasthenia gravis?
o What sites does physostigmine bind to? Where is it absorbed from? What neurotransmitter
actions does it produce? What is it used to treat?
o Does neostigmine produce muscarinic or nicotinic actions? Does it have CNS effects? What
is it used to treat?
o What is the advantage of pyridostigmine? What is it used to treat?
o How is myasthenia gravis treated?
o What are the clinically used organophosphorus compounds?
o Why do insecticides not affect humans?
o Do the nerve gasses have muscarinic or nicotinic action? What can they be hydrolyzed by?
o What are the therapeutic uses of irreversible acetylcholinesterase inhibitors? How do you
o What is the drug that reactivates alkylphosphorylated acetylcholinesterases?