Lippincott Cholinergic antagonists Flashcards
5.1 During an ophthalmic surgical procedure, the surgeon
wanted to constrict the pupil of the patient using a miotic
drug. However, he accidentally used another drug that
caused dilation of the pupil (mydriasis) instead. Most
likely, which of the following drugs did he use?
A. Acetylcholine.
B. Pilocarpine.
C. Tropicamide.
D. Phentolamine.
E. Bethanechol.
Correct answer = C. Muscarinic agonists such as ACh, pilo-
carpine, and bethanechol contract the circular muscles of
iris sphincter and cause constriction of the pupil (miosis),
whereas muscarinic antagonists such as atropine and tropi-
camide prevent the contraction of the circular muscles of the
iris and cause dilation of the pupil (mydriasis). α-Adrenergic
antagonists such as phentolamine relax the radial muscles
of the iris and cause miosis.
5.2 Sarin is a nerve gas that is an organophosphate
cholinesterase inhibitor. Which of the following could be
used as an antidote to sarin poisoning?
A. Pilocarpine.
B. Carbachol.
C. Atropine.
D. Physostigmine.
E. Nicotine.
Correct answer = C. Sarin is an organophosphate cholines-
terase inhibitor. It causes an increase in ACh levels in tissues
that leads to cholinergic crisis by the activation of musca-
rinic as well as nicotinic receptors. Most of the symptoms
of cholinergic crisis are mediated by muscarinic receptors
and, therefore, the muscarinic antagonist atropine is used
as an antidote for sarin poisoning. Cholinergic agonists such
as pilocarpine, carbachol, physostigmine (indirect agonists),
and nicotine will worsen the symptoms of sarin poisoning.
5.3 Atropine is one of the ingredients in the antidiarrheal
combination diphenoxylate/atropine available in the
United States. Which of the following effects is produced
by atropine that contributes to its antidiarrheal effect?
A. Increase in gastrointestinal motility.
B. Reduction in gastrointestinal motility.
C. Increase in salivation.
D. Increase in acid secretion.
Correct answer = B. Muscarinic agonists produce an
increase in gastrointestinal motility, salivation, and acid
secretion. Atropine is a muscarinic antagonist and therefore
causes a reduction in gastrointestinal motility that contrib-
utes to its antidiarrheal effect.
5.4 A patient with chronic obstructive pulmonary disease
(COPD) was prescribed a β2
agonist for the relief of
bronchospasm. However, the patient did not respond to
this treatment. Which of the following drugs or classes
of drugs would you suggest for this patient as the next
option?
A. β1
Agonist.
B. Muscarinic agonist.
C. Physostigmine.
D. Ipratropium.
E. Phentolamine.
Correct answer = D. Major receptors present in the bron-
chial tissues are muscarinic and adrenergic-β2
receptors.
Muscarinic activation causes bronchoconstriction, and β2
receptor activation causes bronchodilation. Therefore, direct
or indirect (physostigmine) muscarinic agonists will worsen
bronchospasm. Ipratropium is a muscarinic antagonist that
can relax bronchial smooth muscles and relieve broncho-
spasm in patients who are not responsive to β2
agonists.
α1
and β1
receptors are not commonly present in bronchial
tissues and, therefore, β1
agonists or α antagonists (phentol-
amine) do not have any significant effects on bronchospasm.
5.5 Which of the following drugs would be the most effective
anti–motion sickness drug for a person planning to go
on a cruise?
A. Atropine.
B. Tropicamide.
C. Scopolamine.
D. Darifenacin.
E. Tiotropium.
Correct answer = C. All muscarinic antagonists (anticho-
linergic drugs) listed above are theoretically useful as
anti–motion sickness drugs; however, scopolamine is the
most effective in preventing motion sickness in practice.
Tropicamide mostly has ophthalmic uses, and tiotropium is
used for respiratory disorders (COPD). Darifenacin is used
for overactive bladder.
5.6 Which of the following is correct regarding ganglion-
blocking drugs?
A. Blockade of sympathetic ganglia could result in
reduced blood pressure.
B. Blockade of parasympathetic ganglia could result in
reduced heart rate.
C. Nicotine is a nondepolarizing ganglion blocker.
D. Atropine is a nondepolarizing ganglion blocker.
Correct answer = A. Selective blockade (in theory) of the
sympathetic ganglion causes reduction in norepinephrine
release and therefore reduction in heart rate and blood pres-
sure. Selective blockade (in theory) of the parasympathetic
ganglion causes reduction in ACh release and therefore an
increase in heart rate. Receptors at both sympathetic and
parasympathetic ganglia are of the nicotinic type. Nicotine is
an agonist at nicotinic receptors and produces a depolarizing
block in the ganglia. Atropine is a muscarinic antagonist and
has no effect on the nicotinic receptors found in the ganglia
5.7 Which of the following is correct regarding the
neuromuscular blockers (NMBs)?
A. Nondepolarizing NMBs are administered orally.
B. Cholinesterase inhibitors reduce the effects of
nondepolarizing NMBs.
C. Nondepolarizing NMBs affect diaphragm muscles
first.
D. Effects of depolarizing neuromuscular blockers can
be reversed using cholinesterase inhibitors
Correct answer = B. Nondepolarizing NMBs such as cisa-
tracurium and vecuronium are highly polar compounds
and are poorly absorbed from the GI tract. Therefore, they
are administered parenterally, not orally. Nondepolarizing
NMBs are competitive antagonists at nicotinic recep-
tors. Therefore, increasing the levels of ACh at the neu-
romuscular junction reduces the effects of these agents.
Cholinesterase inhibitors increase the levels of ACh at the
neuromuscular junction and reduce the effects of nondepo-
larizing NMBs, but may enhance (not reverse) the effects
of depolarizing NMBs. Nondepolarizing NMBs first affect
rapidly contracting muscles seen in the face and eyes and
affect the diaphragm muscles last
5.8 Which of the following is correct regarding drug interactions
with nondepolarizing neuromuscular blockers (NMBs)?
A. Desflurane reduces the effects of nondepolarizing
NMBs.
B. Cholinesterase inhibitors increase the effects of
nondepolarizing NMBs.
C. Aminoglycosides increase the effects of
nondepolarizing NMBs.
D. Calcium channel blockers reduce the effects of
nondepolarizing NMBs.
Correct answer = C. Halogenated hydrocarbon anesthetics
such as desflurane enhance the effects of nondepolarizing
NMBs by exerting a stabilization effect at the neuromuscular
junction (NMJ). Acetylcholinesterase inhibitors increase the
levels of ACh at the NMJ and reduce the effects of nonde-
polarizing NMBs. Aminoglycoside antibiotics increase the
effects of nondepolarizing NMBs by reducing the release of
ACh from the cholinergic neurons. Calcium channel block-
ers increase the effects of nondepolarizing NMBs, possibly
by affecting ion transport at the NMJ
5.9 A patient was administered a neuromuscular blocker
(NMB) prior to a surgical procedure to produce skeletal
muscle paralysis. This NMB drug affected small, rapidly
contracting muscles of the face and eyes first and
diaphragm muscles last. The effect of this drug was
easily reversed with neostigmine. Which of the following
neuromuscular blockers was most likely administered
to this patient?
A. Rocuronium.
B. Succinylcholine.
C. Diazepam.
D. Tubocurarine
Correct answer = A. There are two types of NMBs: depo-
larizing and nondepolarizing NMBs. Depolarizing NMBs are
agonists at the nicotinic receptors, whereas nondepolarizing
NMBs are antagonists at the nicotinic receptors. Both types
of NMBs affect the rapidly contracting muscles (face, eye,
etc.) first and diaphragm muscles last. However, cholinester-
ase inhibitors such as neostigmine increase ACh levels in the
NMJ and reverse the effects of nondepolarizing NMBs, but
not those of depolarizing NMBs. Therefore, the NMB admin-
istered to this patient is most probably rocuronium, which is
a nondepolarizing NMB. Tubocurarine is also a nondepolar-
izing NMB, but it is not used in practice. Succinylcholine is a
depolarizing NMB, and diazepam is a benzodiazepine that
does not cause paralysis of skeletal muscles.
5.10 A patient was administered a neuromuscular blocker
(NMB) prior to a surgical procedure to produce skeletal
muscle paralysis. This NMB drug caused initial skeletal
muscle fasciculations before the onset of paralysis.
The effect of this drug could not be reversed with
neostigmine. Which of the following neuromuscular
blockers was most likely administered to this patient?
A. Cisatracurium.
B. Succinylcholine.
C. Diazepam.
D. Tubocurarine.
Correct answer = B. Depolarizing NMBs cause muscle
fasciculations before causing paralysis, and their effects
cannot be reversed using cholinesterase inhibitors such
as neostigmine. Nondepolarizing NMBs do not cause mus-
cle fasciculations, and their effects can be reversed using
cholinesterase inhibitors. Therefore, the NMB used in this
patient is succinylcholine, which is a depolarizing NMB.
Cisatracurium and tubocurarine are nondepolarizing NMBs,
and diazepam does not cause paralysis of skeletal muscles.
