Test Flashcards
Sarin is a nerve gas that is an organophosphate
cholinesterase inhibitor. Which of the following could be
used as an antidote to sarin poisoning?
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.
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.
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.
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.
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.
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.
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.
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.
Which of the following is correct regarding adrenergic
neurotransmission?
A. Epinephrine is the major neurotransmitter released
from sympathetic nerve terminals.
B. Norepinephrine is mainly released from the adrenal
glands.
C. Tricyclic antidepressants and cocaine prevent
reuptake of norepinephrine into the nerve terminals.
D. Monoamine oxidase (MAO) converts dopamine to
norepinephrine in the nerve terminal.
Correct answer = C. Tricyclic antidepressants (TCAs) and
cocaine inhibit the transporter protein that prevents the
reuptake of norepinephrine into the sympathetic nerve ter-
minals. Norepinephrine, not epinephrine, is the major neu-
rotransmitter released from sympathetic nerve terminals.
Epinephrine, not norepinephrine, is mainly released from
the adrenal glands. Dopamine is converted to norepineph-
rine by dopamine β-hydroxylase, not by MAO.
All of the following are correct regarding adrenergic
receptors, except:
A. α1 Receptors are primarily located on the
postsynaptic membrane in the effector organs.
B. α2 Receptors are primarily located on the
presynaptic sympathetic nerve terminals.
C. β1 Receptors are found mainly in the heart.
D. β2 Receptors are found mainly in adipose tissue.
Correct answer = D. α1 Receptors are located on the post-
synaptic membrane in the effector organs such as blood
vessels. α2 Receptors are mainly found on the presynaptic
sympathetic nerve terminals, where they inhibit the release
of norepinephrine when activated. β1 Receptors are found
in the heart, in addition to some other tissues, and cause
increase in heart rate and contractility when activated. β2
receptors are found in the lungs, in addition to some other
tissues, and cause relaxation of bronchial smooth muscles
when activated. β3 Receptors are found in adipose tissue
and are involved in lipolysis.
A hypertensive patient was accidentally given an α2
agonist instead of an α1 blocker. Which of the following
is correct in this situation?
A. α2 Agonists can increase the release of
norepinephrine from sympathetic nerve terminals.
B. α2 Agonists can reduce blood pressure in this
patient.
C. α2 Agonists can increase blood pressure in this
patient.
D. α2 Agonists will not affect blood pressure in this
patient.
Correct answer = B. α2 Agonists activate α2 receptors
located in the presynaptic terminal of sympathetic neurons
and cause a reduction in the release of norepinephrine from
sympathetic nerve terminals. This leads to a reduction in
blood pressure. α2 Agonists such as clonidine and methyl-
dopa are therefore used as antihypertensive agents.
Which of the following is correct regarding responses
mediated by adrenergic receptors?
A. Stimulation of α1 receptors increases blood
pressure.
B. Stimulation of α1 receptors reduces blood pressure.
C. Stimulation of sympathetic presynaptic α2 receptors
increases norepinephrine release.
D. Stimulation of β2 receptors increases heart rate
(tachycardia).
E. Stimulation of β2 receptors causes
bronchoconstriction
Correct answer = A. Stimulation of α1 receptors, mostly
found in the blood vessels, causes vasoconstriction and
increase in blood pressure. Stimulation of α2 receptors on
the sympathetic presynaptic terminal reduces the release
of norepinephrine. β2 receptors are not found in the heart,
so activation of β2 receptors does not affect heart rate.
Stimulation of β2 receptors found in the bronchial tissues
causes bronchodilation, not bronchoconstriction.
An asthma patient was given a nonselective β agonist
to relieve bronchoconstriction. Which of the following
adverse effects would you expect to see in this patient?
A. Bradycardia.
B. Tachycardia.
C. Hypotension (reduction in blood pressure).
D. Worsening bronchoconstriction.
Correct answer = B. A nonselective β agonist activates both
β1 as well as β2 receptors. β1 activation causes an increase
in heart rate (tachycardia), contractility, and subsequent
increase in blood pressure. It relieves bronchoconstriction
because of the β2 receptor activation.
Which of the following adrenergic agonists is most
likely to cause CNS side effects when administered
systemically?
A. Epinephrine.
B. Norepinephrine.
C. Isoproterenol.
D. Dopamine.
E. Ephedrine.
Correct answer = E. Ephedrine is more lipophilic compared
to the other drugs listed and therefore is more likely to
cross the blood–brain barrier when administered systemi-
cally. Therefore, ephedrine is more likely to cause CNS side
effects compared to other listed drugs.
A 70-year-old patient was brought to the emergency
room with a blood pressure of 76/60 mm Hg,
tachycardia, and low cardiac output. He was diagnosed
with acute heart failure. Which of the following drugs
would be the most appropriate to improve his cardiac
function?
A. Epinephrine.
B. Fenoldopam.
C. Dobutamine.
D. Isoproterenol.
Correct answer = C. Among the choices, the ideal drug to
increase contractility of the heart in acute heart failure is
dobutamine, since it is a selective β1-adrenergic agonist.
Fenoldopam is a dopamine agonist used to treat severe
hypertension. Other drugs are nonselective adrenergic
agonists that could cause unwanted side effects.
A 12-year-old boy who is allergic to peanuts was brought
to the emergency room after accidentally consuming
peanuts contained in fast food. He is in anaphylactic
shock. Which of the following drugs would be most
appropriate to treat this patient?
A. Norepinephrine.
B. Phenylephrine.
C. Dobutamine.
D. Epinephrine.
Correct answer = D. Norepinephrine has more α agonis-
tic effects and activates mainly α1, α2, and β1 receptors.
Epinephrine has more β agonistic effects and activates
mainly α1, α2, β1, and β2 receptors. Phenylephrine has pre-
dominantly α effects and activates mainly α1 receptors.
Dobutamine mainly activates β1 receptors and has no signif-
icant effects on β2 receptors. Thus, epinephrine is the drug
of choice in anaphylactic shock that can both stimulate the
heart (β1 activation) and dilate bronchioles (β2 activation).
Which of the following adrenergic agonists is commonly
present in nasal sprays available over-the-counter
(OTC) to treat nasal congestion?
A. Clonidine.
B. Albuterol.
C. Oxymetazoline.
D. Dobutamine.
E. Norepinephrine.
Correct answer = C. Drugs with selective α1 agonistic activ-
ity are commonly used as nasal decongestants because of
their ability to cause vasoconstriction in the nasal vessels.
Oxymetazoline is an α1 agonist and therefore the preferred
drug among the choices as a nasal decongestant. Clonidine
is an α2 agonist, albuterol is a β2 agonist, dobutamine is a
β1 agonist, and norepinephrine is a nonselective adrenergic
agonist.
One of your patients who is hypertensive and gets mild
asthma attacks occasionally bought an herbal remedy
online to help with his asthma. He is not on any asthma
medications currently but is receiving a β1-selective
blocker for his hypertension. The herbal remedy seems
to relieve his asthma attacks, but his blood pressure
seems to increase despite the β-blocker therapy. Which
of the following drugs is most likely present in the herbal
remedy he is taking?
A. Phenylephrine.
B. Norepinephrine.
C. Dobutamine.
D. Ephedrine.
E. Salmeterol.
Correct answer = D. Two drugs among the choices that
could relieve asthma are ephedrine and salmeterol, as they
activate β2 receptors in the bronchioles and cause broncho-
dilation. However, salmeterol is a selective β2 agonist and
should not cause an increase in blood pressure. Ephedrine
on the other hand stimulates the release of norepinephrine
and acts as a direct agonist at α- and β-adrenergic receptors,
thus causing an increase in blood pressure. Phenylephrine
(a nonselective α agonist) does not cause bronchodilation.
Norepinephrine is a nonselective adrenergic agonist that
does not have any stimulatory effects on β2 receptors. Also,
norepinephrine is not active when given orally.
60-year-old female patient started on a new
antihypertensive medication recently. Her blood
pressure seems to be under control, but she complains
of fatigue, drowsiness, and fainting when she gets up
from the bed (orthostatic hypotension). Which of the
following drugs is she most likely taking?
A. Metoprolol.
B. Propranolol.
C. Prazosin.
D. Clonidine.
Correct answer = C. α-Blockers (prazosin) are more likely
to cause orthostatic hypotension compared to β-blockers
(metoprolol, propranolol) and α2 agonists (clonidine).
A 30-year-old male patient was brought to the ER with
amphetamine overdose. He presented with high blood
pressure and arrhythmia. Which of the following is
correct regarding this patient?
A. Amphetamine can activate all types of adrenergic
receptors.
B. β-Blockers are the ideal antidotes for amphetamine
poisoning.
C. α-Blockers can normalize the blood pressure in this
patient.
D. Miosis could be a possible symptom of
amphetamine poisoning.
Correct answer = A. Amphetamine is an indirect adrenergic
agonist that mainly enhances the release of norepinephrine
from peripheral sympathetic neurons. Therefore, it activates
all types of adrenergic receptors (that is, α and β receptors)
and causes an increase in blood pressure. Since both α
and β receptors are activated by amphetamine, α-blockers
or β-blockers alone cannot relieve the symptoms of amphet-
amine poisoning. Since amphetamine causes sympathetic
activation, it causes mydriasis, not miosis.
A new antihypertensive drug was tested in an animal
model of hypertension. The drug when given alone
reduces blood pressure in the animal. Norepinephrine
when given in the presence of this drug did not cause
any significant change in blood pressure or heart
rate in the animal. The new drug is similar to which
of the following drugs in terms of its pharmacological
mechanism of action?
A. Prazosin.
B. Clonidine.
C. Propranolol.
D. Metoprolol.
E. Carvedilol
Correct answer = E. Norepinephrine activates both α1
and β1 receptors and causes an increase in heart rate
and blood pressure. A drug that prevents the increase in
blood pressure caused by norepinephrine should be simi-
lar to carvedilol that antagonizes both α1 and β1 receptors.
Prazosin is an α1 antagonist, clonidine is an α2 agonist, and
propranolol and metoprolol are β antagonists, and these
drugs cannot completely prevent the cardiovascular effects
of norepinephrine.
A β-blocker was prescribed for hypertension in a female
asthma patient. After about a week of treatment, the
asthma attacks got worse, and the patient was asked
to stop taking the β-blocker. Which of the following
β-blockers would you suggest as an alternative in this
patient that is less likely to worsen her asthma?
A. Propranolol.
B. Metoprolol.
C. Labetalol.
D. Carvedilol.
Correct answer = B. The patient was most likely given a
nonselective β-blocker (antagonizes both β1 and β2 recep-
tors) that made her asthma worse due to β2 antagonism.
An alternative is to prescribe a cardioselective (antagonizes
only β1) β-blocker that does not antagonize β2 receptors in
the bronchioles. Metoprolol is a cardioselective β-blocker.
Propranolol, labetalol, and carvedilol are nonselective
β-blockers and could worsen the asthma.
A 70-year-old male needs to be treated with an
α-blocker for overflow incontinence due to his enlarged
prostate. Which of the following drugs would you
suggest in this patent that will not affect his blood
pressure significantly?
A. Prazosin.
B. Doxazosin.
C. Phentolamine.
D. Tamsulosin.
E. Terazosin
Correct answer = D. Tamsulosin is an α1 antagonist that is
more selective to the α1 receptor subtype (α1A) present in
the prostate and less selective to the α1 receptor subtype
(α1B) present in the blood vessels. Therefore, tamsulosin
does not affect blood pressure significantly. Prazosin, doxa-
zosin, terazosin, and phentolamine antagonize both these
subtypes and cause significant hypotension as a side effect.
A 50-year-old male was brought to the emergency room
after being stung by a hornet. The patient was found to
be in anaphylactic shock, and the medical team tried
to reverse the bronchoconstriction and hypotension
using epinephrine. However, the patient did not fully
respond to the epinephrine treatment. The patient’s wife
mentioned that he is taking a prescription medication
for his blood pressure, the name of which she does not
remember. Which of the following medications is he
most likely taking that could have prevented the effects
of epinephrine?
A. Doxazosin.
B. Propranolol.
C. Metoprolol.
D. Acebutolol.
Correct answer = B. Epinephrine reverses hypotension by
activating β1 receptors and relieves bronchoconstriction by
activating β2 receptors in anaphylaxis. Since epinephrine
was not effective in reversing hypotension or bronchocon-
striction in this patient, it could be assumed that the patient
was on a nonselective β-blocker (propranolol). Doxazosin
(α1-blocker), metoprolol, or acebutolol (both β1-selective
blockers) would not have completely prevented the effects
of epinephrine.
