Lippincott Cholinergic Agonists Flashcards
4.1 Botulinum toxin blocks the release of acetylcholine from
cholinergic nerve terminals. Which of the following is a
possible effect of botulinum toxin?
A. Skeletal muscle paralysis.
B. Improvement of myasthenia gravis symptoms.
C. Increased salivation.
D. Reduced heart rate.
Correct answer = A. Acetylcholine released by cholinergic
neurons acts on nicotinic receptors in the skeletal muscle
cells to cause contraction. Therefore, blockade of ACh release
causes skeletal muscle paralysis. Myasthenia gravis is an
autoimmune disease where antibodies are produced against
nicotinic receptors and inactivate nicotinic receptors. A reduc-
tion in ACh release therefore worsens (not improves) the
symptoms of this condition. Reduction in ACh release by botu-
linum toxin causes reduction in secretions including saliva (not
increase in salivation) causing dry mouth and an increase (not
reduction) in heart rate due to reduced vagal activity.
4.2 A dentist would like to reduce salivation in a patient in
preparation for an oral surgical procedure. Which of the
following strategies will be useful in reducing salivation?
A. Activate nicotinic receptors in the salivary
glands.
B. Block nicotinic receptors in the salivary glands.
C. Activate muscarinic receptors in the salivary
glands.
D. Block muscarinic receptors in the salivary glands.
Correct answer = D. Salivary glands contain muscarinic
receptors, not nicotinic receptors. Activation of muscarinic
receptors in the salivary glands causes secretion of saliva.
Blocking muscarinic receptors, using drugs such as atro-
pine, reduces salivary secretions and makes the mouth dry.
4.3 Which of the following is a systemic effect of a
muscarinic agonist?
A. Reduced heart rate (bradycardia).
B. Increased blood pressure.
C. Mydriasis (dilation of the pupil).
D. Reduced urinary frequency.
E. Constipation.
Correct answer = A. A muscarinic agonist binds to and
activates muscarinic receptors in the heart, endothelial
cells (blood vessels), the gut, and iris sphincter (eye) and
urinary bladder wall muscles, in addition to several other
tissues. Activation of muscarinic receptors by an agonist
causes a reduction in heart rate, constriction of circular
muscles in the iris sphincter leading to constriction of the
pupil (miosis), increased GI motility (hence, diarrhea, not
constipation), and contraction of bladder muscles leading
to an increase (not decrease) in urination frequency. In the
endothelial cells of blood vessels, muscarinic activation pro-
duces release of nitric oxide that causes vasorelaxation and
a reduction (not increase) in blood pressure
4.4 If an ophthalmologist wants to dilate the pupils for an
eye examination, which of the following drugs/classes
of drugs could be theoretically useful?
A. Muscarinic receptor activator (agonist).
B. Muscarinic receptor inhibitor (antagonist).
C. Acetylcholine.
D. Pilocarpine.
E. Neostigmine.
Correct answer = B. Muscarinic agonists (for example,
ACh, pilocarpine) contract the circular smooth muscles
in the iris sphincter and constrict the pupil (miosis).
Anticholinesterases (for example, neostigmine, physostig-
mine) also cause miosis by increasing the level of ACh.
Muscarinic antagonists, on the other hand, relax the circu-
lar smooth muscles in the iris sphincter and cause dilation
of the pupil (mydriasis).
4.5 In Alzheimer’s disease, there is a deficiency of
cholinergic neuronal function in the brain. Theoretically,
which of the following strategies will be useful in treating
the symptoms of Alzheimer’s disease?
A. Inhibiting cholinergic receptors in the brain.
B. Inhibiting the release of acetylcholine in the brain.
C. Inhibiting the acetylcholinesterase enzyme in the brain.
D. Activating the acetylcholinesterase enzyme in the
brain.
Correct answer = C. Since there is already a deficiency in
brain cholinergic function in Alzheimer’s disease, inhibiting
cholinergic receptors or inhibiting the release of ACh will
worsen the condition. Activating the acetylcholinesterase
enzyme will increase the degradation of ACh, which will
again worsen the condition. However, inhibiting the acetyl-
cholinesterase enzyme will help to increase the levels of
ACh in the brain and thereby help to relieve the symptoms
of Alzheimer’s disease.
4.6 An elderly female who lives in a farm house was brought
to the emergency room in serious condition after
ingesting a liquid from an unlabeled bottle found near
her bed, apparently in a suicide attempt. She presented
with diarrhea, frequent urination, convulsions, breathing
difficulties, constricted pupils (miosis), and excessive
salivation. Which of the following is correct regarding
this patient?
A. She most likely consumed an organophosphate
pesticide.
B. The symptoms are consistent with sympathetic
activation.
C. Her symptoms can be treated using an
anticholinesterase agent.
D. Her symptoms can be treated using a cholinergic
agonist.
Correct answer = A. The symptoms are consistent with that
of cholinergic crisis. Since the elderly female lives on a farm
and since the symptoms are consistent with that of cho-
linergic crisis (usually caused by cholinesterase inhibitors),
it may be assumed that she has consumed an organo-
phosphate pesticide (irreversible cholinesterase inhibitor).
Assuming that the symptoms are caused by organophos-
phate poisoning, administering an anticholinesterase agent
or a cholinergic agonist will worsen the condition. The symp-
toms are not consistent with that of sympathetic activation,
as sympathetic activation will cause symptoms opposite to
that of cholinergic crisis seen in this patient.
4.7 Sarin is a volatile nerve agent that inhibits cholinesterase
enzymes. Which of the following symptoms would you
expect to see in a patient exposed to sarin?
A. Urinary retention.
B. Tachycardia.
C. Constriction of pupils (miosis).
D. Dilation of the pupils (mydriasis).
E. Dry mouth.
Correct answer = C. Sarin is an organophosphate nerve gas
that inhibits cholinesterase enzymes and increases ACh
levels. Therefore, symptoms of cholinergic crisis (increased
urination, bradycardia, excessive secretions, constriction
of pupils, etc.) should be expected in patients exposed to
sarin. Urinary retention, tachycardia, mydriasis, and dry
mouth are usually seen with muscarinic antagonists
4.8 Head and neck irradiation in cancer patients can
decrease salivary secretion and cause dry mouth. All of
the following drugs or classes of drugs are theoretically
useful in improving secretion of saliva in these patients
except:
A. Muscarinic antagonists.
B. Muscarinic agonists.
C. Anticholinesterase agents.
D. Pilocarpine.
E. Neostigmine.
Correct answer = A. Activation of muscarinic receptors in
the salivary glands causes secretion of saliva. This can be
achieved in theory by using a muscarinic agonist such as
pilocarpine or an anticholinesterase agent such as neo-
stigmine (increases levels of ACh). Muscarinic antagonists
(anticholinergic drugs) will reduce salivary secretion and
worsen dry mouth.
4.9 Which of the following drugs or classes of drugs will be
useful in treating the symptoms of myasthenia gravis?
A. Nicotinic antagonists.
B. Muscarinic agonists.
C. Muscarinic antagonists.
D. Anticholinesterase agents
Correct answer = D. The function of nicotinic receptors in
skeletal muscles is diminished in myasthenia gravis due to
the development of antibodies to nicotinic receptors in the
patient’s body (autoimmune disease). Any drug that can
increase the levels of ACh in the neuromuscular junction
can improve symptoms in myasthenia gravis. Thus, cholin-
esterase inhibitors help to improve the symptoms of myas-
thenia gravis. Muscarinic drugs have no role in myasthenia
gravis, and nicotinic antagonists will worsen the symptoms.
4.10 Atropa belladonna is a plant that contains atropine (a
muscarinic antagonist). Which of the following drugs or
classes of drugs will be useful in treating poisoning with
belladonna?
A. Malathion.
B. Physostigmine.
C. Muscarinic antagonists.
D. Nicotinic antagonists.
Correct answer = B. Atropine is a competitive muscarinic
receptor antagonist that causes anticholinergic effects.
Muscarinic agonists or any other drugs that can increase the
levels of ACh will be able to counteract the effects of atropine.
Thus, anticholinesterases such as malathion and physostig-
mine can counteract the effects of atropine in theory. However,
malathion being an irreversible inhibitor of acetylcholinester-
ase is not used for systemic treatment in patients. Muscarinic
antagonists will worsen the toxicity of atropine. Nicotinic antag-
onists could worsen the toxicity by acting on parasympathetic
ganglionic receptors and thus reducing the release of ACh.
