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Brody’s Human Pharmacology 6th Edition
Wecker Test Bank
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COVERS ALL CHAPTERS.
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Appendix
2. C. The HLA complex has been linked to drug hypersensitivity
ANSWERS TO SELF-ASSESSMENT QUESTIONS reactions including Stevens-Johnson syndrome and toxic epidermal
necrolysis. Several different HLA gene polymorphisms have been
Chapter 1 linked specifically to severe adverse effects for certain drugs including
No questions carbamazepine.
3. B. The SLCO1B1 Val174Ala polymorphism can lead to reduced
Chapter 2 simvastatin transport to the liver, leading to higher simvastatin plasma
1. B. Binding usually involves multiple weak bonds. It is rarely covalent, concentrations and thereby increasing the risk for simvastatin-induced
is usually stereoselective, and may or may not occur with a high myopathy.
affinity (KD). 4. C. Close to 50% of metastatic melanoma cases have mutations in
2. A. Chronic antagonist exposure will often increase receptor sensitivity. the v-raf murine sarcoma viral oncogene homolog B (BRAF), with
The other answers all refer to decreased receptor sensitivity. the primary mutation resulting in glutamic acid substituted for valine
3. C. Agonist drugs are specific for various classes of receptors but at codon 600, termed V600E. Patients with this mutation respond
may not be specific for each receptor subtype within a class. to the ATP inhibitor vemurafenib.
4. E. Intracellular signaling can occur through any of the mechanisms 5. A. Patients with nonfunctional DYPD variants and treated with
listed. 5-FU or capecitabine are at an increased risk for myelosuppression,
5. B. Based on the information given, one can conclude only that the gastrointestinal toxicities, mucositis, and hand-foot syndrome. They
potencies are different. No conclusions can be made about structure, are not at an increased risk for peripheral neuropathy.
types of receptors involved, whether they are directly acting agonists,
or whether they cause the same extent of relaxation. NURSINGTChapter
B.COM 5
6. D. The affinity constant describes how well a drug binds to a 1. C. Phase I studies determine safe drug dosages and pharmacokinetics
particular receptor and thus depends on both the drug and the on a small number of human volunteers.
binding site. It is the ratio of the reverse to forward rate constants. 2. A. As defined by the DEA, Schedule I drugs, substances, or chemicals
The rate of diffusion of drug in the plasma is unrelated to affinity are defined as drugs with no currently accepted medical use and a
constant. high potential for abuse.
3. C. Target validation is an important step in the drug discovery
Chapter 3 process that provides verification and confidence that modula-
1. D. Cell membranes are composed of phospholipids; they do not tion of a specific target with the drug will produce a desired
contain DNA. Receptor proteins may be embedded in the therapeutic effect.
membrane. 4. B. The DEA defines a generic drug as identical or bioequivalent to
2. B. Tubular reabsorption increases plasma levels of a drug. Biotrans- the brand name drug in dosage form, safety, strength, route of
formation, plasma protein binding, and renal or biliary excretion administration, quality, performance characteristics, and intended
all lower plasma drug concentrations. use.
3. D. In general, drugs that have high lipid solubility cross membranes 5. B. The Latin abbreviation q.i.d. means four times a day.
better than those with low lipid solubility. The larger the lipid:water
partition coefficient, the greater the lipid solubility. Chapter 6
4. A. The percent of the unionized form (HA) of a weak acid would 1. B. The parasympathetic nervous system uses ACh as the neuro-
be greatest in an environment with the highest H+ concentration, transmitter at both ganglia and the neuroeffector junction. Post-
which is the lowest pH (A + H+ ↔ HA). ganglionic parasympathetic neurons are short and located near the
5. E. The Therapeutic Index (TI) of a drug is equal to the ratio of the organ innervated, preganglionic cell bodies are located in the cra-
toxic dose to the therapeutic dose. The larger the TI of a drug, the niosacral divisions of the spinal cord, and parasympathetic neurons
less potential for adverse or toxic effects. innervating the respiratory system mediate bronchoconstriction.
6. D. By definition, the half-life (t1/2) of a drug is defined as the time 2. B. The neurotransmitter at postganglionic sympathetic neurons is
it takes for the concentration of a drug in the circulation to decrease NE. Sympathetic ganglia use ACh as the neurotransmitter and are
by half. located primarily in paravertebral chains. Nicotinic receptors are
present at all autonomic ganglia.
Chapter 4 3. A. Nicotinic receptors are ligand-gated ion channels; all the others
1. A. Clopidogrel is a prodrug that needs to be activated to be effec- are GPCRs.
tive. The enzyme responsible is CYP2C19. Individuals who are 4. D. The stimulation of prejunctional α2 adrenergic receptors on
CYP2C19 poor metabolizers have a reduced ability to activate postganglionic sympathetic neurons results in inhibition of NE
clopidogrel. release.
650
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, Brody's Human Pharmacology 6th Edition Wecker Test Bank
WWW.NURSYLAB.COM
APPENDIX 651
5. C. Activation of the parasympathetic nervous system results in administered with halogenated inhalational anesthetics, can precipitate
constriction of airway smooth muscle, decreased heart rate, decreased malignant hyperthermia.
renin secretion, and contraction of the GI tract. The blood vessels 2. C. Ganglionic blocking agents block the predominant sympathetic
do not receive parasympathetic innervation. or parasympathetic tone of organs and lead to dry mouth, tachycardia,
constipation, and urinary retention, as well as excessive hypotension
Chapter 7 and impotence.
1. B. Pilocarpine is a cholinergic agonist that acts on ACh receptors 3. E. Neuromuscular blockers are useful in several clinical situations
to constrict the pupil. when skeletal muscle relaxation can be beneficial, including as a
2. A. The patient exhibits typical parasympathetic symptoms with surgical adjunct, for orthopedic procedures, endotracheal intubation,
little neuromuscular involvement; consequently the muscarinic scoping procedures, and electroconvulsive therapy.
antagonist atropine is administered to antagonize the actions of the 4. A. Nicotinic receptors at ganglia are neuronal receptors composed
anticholinesterase insecticide. Atropine is preferred over the qua- of α or α and β subunits, whereas nicotinic receptors at the neu-
ternary ammonium muscarinic antagonist propantheline because romuscular junction are composed of α1, β1, δ, and ε (γ during
atropine enters the brain. development) subunits. Differences in subunit composition underlie
3. C. The respiratory depression that ensues following exposure to differences in the responses of these receptors to pharmacological
this insecticide may lead to death. All other options listed can be agents.
managed pharmacologically and are not typically lethal.
4. D. Bethanechol activates muscarinic receptors, causing a decrease Chapter 11
in heart rate, peripheral vasodilation, and constriction in the airways 1. B. DA produces complex dose-dependent peripheral actions with
of the lung. Bethanechol does not activate nicotinic receptors at the low doses relaxing smooth muscle in various vascular beds, including
neuromuscular junction. renal, mesenteric, and coronary, due to of D1 receptor activation;
5. C. It is likely that these individuals ate mushrooms containing the these doses do not activate α1 or β1 receptors.
fungal alkaloid muscarine, which activates muscarinic cholinergic 2. B. Epinephrine can reduce the bronchospasm associated with
receptors and leads to parasympathomimetic effects including miosis, anaphylaxis and counter the hypotension of anaphylactic shock by
blurred vision, lacrimation, excessive salivation and bronchial secre- promoting vasoconstriction in some vascular beds and increasing
tions, sweating, bronchoconstriction, bradycardia, abdominal cardiac output.
cramping, increased gastric acid secretion, diarrhea, and polyuria. 3. C. Dobutamine is used clinically for the short-term management
Atropine antagonizes all of these effects and is a useful antidote. of cardiac decompensation in patients with refractory heart failure
(American Heart Association Stage D).
Chapter 8
ChapterM12
NURSINGTB.C
1. E. The adverse effects of muscarinic receptor antagonists include
constipation, tachycardia, dry mouth, mydriasis, blurred vision,
O
1. C. Carvedilol is an α /β /β 1 1 2 receptor antagonist. Propranolol is a
inhibition of sweating, and urinary retention; thus it is contraindicated competitive antagonist at both β1 and β2 receptors. In combination
in patients with urinary retention. with doxazosin, which is a selective α1 receptor antagonist, these
2. C. The symptoms described are all consistent with the ingestion of drugs will antagonize the same receptors as carvedilol alone.
a muscarinic antagonist such as atropine. 2. A. Phentolamine blocks α1 and α2 adrenergic receptors, and thus
3. B. Muscarinic receptor antagonists that do not cross the blood-brain the effects of epinephrine after phentolamine will reflect effects only
barrier are useful for the treatment of COPD. Among the choices, by β1 receptors, most closely resembling the effects of the β1/β2
only ipratropium is such a drug. agonist isoproterenol.
4. D. The topical application of muscarinic receptor antagonists to a 3. B. Epinephrine-induced renin release is mediated by activation of
patient with narrow ocular angles can cause acute angle-closure β1 receptors. Thus, this action will be blocked by the relatively selective
glaucoma and are contraindicated in such patients. β1 receptor antagonist metoprolol; the other responses to epinephrine
5. B. Atropine is a muscarinic receptor antagonist and, as such, will are mediated by different receptor subtypes.
not counteract the effects of the cholinesterase inhibitors at nicotinic
receptors that mediate skeletal muscle transmission. Chapter 13
1. A. ACh is the only neurotransmitter whose action is terminated
Chapter 9 by hydrolysis via the action of acetylcholinesterase; the actions
1. E. High doses of nicotine, or prolonged exposure of receptors to of all the other amine neurotransmitters listed are terminated by
agonist, lead to desensitization of nicotinic receptors, which depresses reuptake.
ganglionic transmission. 2. A. All of the biogenic amine neurotransmitters are synthesized in
2. C. All studies indicate that agents used in cessation programs are nerve terminals and transported into vesicles by an active process;
more successful when counseling accompanies drug therapy. Lobeline their concentration in vesicles is 10 to 100 times that in the cytosol.
has not been shown to be effective for smoking cessation. 3. C. The long-term administration of agonists leads to a down regula-
3. E. Neuronal nicotinic receptors in autonomic ganglia, the adrenal tion of receptors in the postsynaptic cell membrane.
gland, the brain, and immune cells are composed of α or α and β 4. C. Dopaminergic neurons originate in the substantia nigra and
subunits. Muscle-type nicotinic receptors are composed of α1, β1, hypothalamus; the other types of neurons listed originate in other
δ, and ε (γ during development) subunits. brain regions.
5. B. A high degree of lipophilicity will facilitate the ability of drugs
Chapter 10 to cross the blood-brain barrier; the other choices would hinder it.
1. B. Genetic variations in butyrylcholinesterase activity resulting in 6. C. Ethanol, a CNS depressant, produces an initial stage of excitation
either lower concentrations of normal enzyme or an abnormal enzyme by reducing the activity of tonically active inhibitory brain systems.
may lead to prolonged actions of succinylcholine and, when It has none of the other effects listed.
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NURSINGTB.COM
, Brody's Human Pharmacology 6th Edition Wecker Test Bank
WWW.NURSYLAB.COM
652 APPENDIX
2. D. Ketamine is unique in its action as an antidepressant because
Chapter 14 its intravenous administration tempers suicidal thoughts and depres-
1. A. A loss of memory in an elderly individual may represent sion within a few hours.
Alzheimer’s disease. Donepezil is an acetylcholinesterase inhibitor 3. C. All amine reuptake inhibitors have the potential to precipitate
that preserves brain acetylcholine, a major neurotransmitter involved serotonin syndrome when used with other agents that also increase
in learning and memory thought to decline in Alzheimer’s disease. serotonin in the brain including many over-the-counter cough
There is no rationale for the use of any other drug listed. preparations containing dextromethorphan. Serotonin syndrome is
2. E. Alzheimer’s disease involves the loss of basal forebrain cholinergic characterized by fever, chills, diarrhea, myoclonus, tremor, motor
neurons, with primary therapy directed at increasing the levels of weakness, ataxia, and behavioral alterations.
acetylcholine in the brain. 4. C. Bupropion is contraindicated for use in any patient with a history
3. C. Early-onset Alzheimer’s disease may be linked to mutations in of seizures.
the genes coding for amyloid precursor protein (APP) or presenilins, 5. A. Although this woman has been in remission for 2 years, based
which are proteins involved in APP processing. on her history of alcohol use disorder, it would be unwise to provide
4. C. Alzheimer’s disease is a progressive neurodegenerative disorder, a prescription for a benzodiazepine.
and thus one would expect to see more atrophy. These is no evidence
that drug therapy slows the progression of neuronal loss. Chapter 18
5. B. The cognitive benefits of drug therapy vary from individual to 1. B. Although the exact pathophysiology of attention deficit hyper-
individual and, although statistically significant, are clinically modest. activity disorder is unclear, it is believed to involve suboptimal
Not all patients benefit, and those who do typically show only a norepinephrine and dopamine neurotransmission in the frontal
slight improvement in abilities. lobe.
6. B. Galantamine is an acetylcholinesterase inhibitor and a positive 2. E. Common adverse effects associated with the use of the stimulants
allosteric modulator at neuronal nicotinic receptors. Donepezil and include headaches, insomnia, anorexia, tic exacerbation, dry mouth,
rivastigmine only inhibit acetylcholinesterase, and memantine is a GI upset, weight loss, and reduced growth velocity.
glutamate receptor antagonist. 3. E. Although atomoxetine is less efficacious than the stimulants for
the treatment of attention deficit hyperactivity disorder, it is typically
Chapter 15 prescribed for children of low weight or stature.
1. C. Carbidopa is a peripheral aromatic amino acid decarboxylase 4. D. Adverse reactions to guanfacine include hypotension, somnolence,
inhibitor that does not cross the BBB and prevents the peripheral bradycardia, and syncope.
metabolism of l-DOPA. 5. D. Lisdexamfetamine is a prodrug that is converted to dextroam-
2. B. After 5 to 7 years of continued drug treatment, as many as 75% phetamine by enzymatic hydrolysis by red blood cells.
NURSINGTB.COM
of patients experience l-DOPA–induced dyskinesias, characterized 6. C. The effects of the amphetamines are attributed primarily to
by chorea and dystonia. enhanced dopamine and norepinephrine release.
3. B. Apomorphine is the only injectable drug for use in patients with
advanced Parkinson’s disease who experience episodes of immobility Chapter 19
(“off ” times) despite l-DOPA therapy. 1. E. Suvorexant is the only agent approved for both sleep-onset and
4. C. Tetrabenazine is a reversible inhibitor of the vesicular monoamine sleep-maintenance insomnia.
transport 2 (VMAT2) and prevents the uptake of dopamine into 2. D. The benzodiazepines depress REM sleep, and chronic REM
vesicles in the presynaptic neuron, leading to dopamine depletion. deprivation can lead to psychotic-like behaviors.
3. A. Ramelteon is the first and only selective melatonin receptor
Chapter 16 agonist approved for the treatment of insomnia.
1. A. Lithium is filtered by the kidneys, with 95% of an administered 4. E. The benzodiazepines may lead to CNS depression, dependence,
dose excreted in the urine in 24 hours. Any drug that interferes with daytime sedation, anterograde amnesia, headache, and dizziness and
glomerular filtration can increase plasma levels of lithium. thus are not ideal drugs for the treatment of insomnia.
2. B. The chronic administration of dopamine receptor antagonists 5. A. Suvorexant blocks orexin neuropeptides from binding to orexin
such as haloperidol can lead to an increased density of receptors, receptors and inhibits arousal signaling.
which underlies the development of tardive dyskinesia, a drug-induced
disorder characterized by abnormal facial movements. Chapter 20
3. B. The phenothiazine antipsychotics block muscarinic cholinergic 1. C. Orlistat is the only agent listed whose action is localized to
receptors, leading to many anticholinergic effects including dry the gastrointestinal tract. All the other agents readily enter the
mouth, urinary retention, and memory impairment. systemic circulation and may adversely affect the cardiovascular
4. D. Clozapine has the potential to produce agranulocytosis, requiring system.
blood cell counts for all patients taking this drug. 2. A. The only drug approved for binge-eating disorder is lisdexam-
5. E. Some atypical antipsychotics may temper negative symptoms of fetamine.
schizophrenia as a consequence of their antagonist actions at serotonin 3. D. Orlistat acts locally within the intestines to reduce the absorption
receptors. of dietary fat via inhibition of intestinal lipase, which decreases the
production of free fatty acids from triglycerides.
Chapter 17 4. C. Dronabinol, which is used for cachexia, stimulates appetite through
1. B. The β-adrenergic receptor antagonists such as propranolol are agonist actions at the cannabinoid receptor located in both the eating
useful for the short-term relief of performance anxiety because centers in the brain and in the gastrointestinal tract.
they suppress sympathetically mediated somatic manifestations of 5. C. Liraglutide is a long-acting GLP-1 receptor agonist approved for
anxiety. both type 2 diabetes and the treatment of obesity.
WWW.NURSYLAB.COM
NURSINGTB.COM
Brody’s Human Pharmacology 6th Edition
Wecker Test Bank
Test Bank Directly From The publisher, 100% Verified Answers.
COVERS ALL CHAPTERS.
Download Immediately After the Order.
, Brody's Human Pharmacology 6th Edition Wecker Test Bank
WWW.NURSYLAB.COM
Appendix
2. C. The HLA complex has been linked to drug hypersensitivity
ANSWERS TO SELF-ASSESSMENT QUESTIONS reactions including Stevens-Johnson syndrome and toxic epidermal
necrolysis. Several different HLA gene polymorphisms have been
Chapter 1 linked specifically to severe adverse effects for certain drugs including
No questions carbamazepine.
3. B. The SLCO1B1 Val174Ala polymorphism can lead to reduced
Chapter 2 simvastatin transport to the liver, leading to higher simvastatin plasma
1. B. Binding usually involves multiple weak bonds. It is rarely covalent, concentrations and thereby increasing the risk for simvastatin-induced
is usually stereoselective, and may or may not occur with a high myopathy.
affinity (KD). 4. C. Close to 50% of metastatic melanoma cases have mutations in
2. A. Chronic antagonist exposure will often increase receptor sensitivity. the v-raf murine sarcoma viral oncogene homolog B (BRAF), with
The other answers all refer to decreased receptor sensitivity. the primary mutation resulting in glutamic acid substituted for valine
3. C. Agonist drugs are specific for various classes of receptors but at codon 600, termed V600E. Patients with this mutation respond
may not be specific for each receptor subtype within a class. to the ATP inhibitor vemurafenib.
4. E. Intracellular signaling can occur through any of the mechanisms 5. A. Patients with nonfunctional DYPD variants and treated with
listed. 5-FU or capecitabine are at an increased risk for myelosuppression,
5. B. Based on the information given, one can conclude only that the gastrointestinal toxicities, mucositis, and hand-foot syndrome. They
potencies are different. No conclusions can be made about structure, are not at an increased risk for peripheral neuropathy.
types of receptors involved, whether they are directly acting agonists,
or whether they cause the same extent of relaxation. NURSINGTChapter
B.COM 5
6. D. The affinity constant describes how well a drug binds to a 1. C. Phase I studies determine safe drug dosages and pharmacokinetics
particular receptor and thus depends on both the drug and the on a small number of human volunteers.
binding site. It is the ratio of the reverse to forward rate constants. 2. A. As defined by the DEA, Schedule I drugs, substances, or chemicals
The rate of diffusion of drug in the plasma is unrelated to affinity are defined as drugs with no currently accepted medical use and a
constant. high potential for abuse.
3. C. Target validation is an important step in the drug discovery
Chapter 3 process that provides verification and confidence that modula-
1. D. Cell membranes are composed of phospholipids; they do not tion of a specific target with the drug will produce a desired
contain DNA. Receptor proteins may be embedded in the therapeutic effect.
membrane. 4. B. The DEA defines a generic drug as identical or bioequivalent to
2. B. Tubular reabsorption increases plasma levels of a drug. Biotrans- the brand name drug in dosage form, safety, strength, route of
formation, plasma protein binding, and renal or biliary excretion administration, quality, performance characteristics, and intended
all lower plasma drug concentrations. use.
3. D. In general, drugs that have high lipid solubility cross membranes 5. B. The Latin abbreviation q.i.d. means four times a day.
better than those with low lipid solubility. The larger the lipid:water
partition coefficient, the greater the lipid solubility. Chapter 6
4. A. The percent of the unionized form (HA) of a weak acid would 1. B. The parasympathetic nervous system uses ACh as the neuro-
be greatest in an environment with the highest H+ concentration, transmitter at both ganglia and the neuroeffector junction. Post-
which is the lowest pH (A + H+ ↔ HA). ganglionic parasympathetic neurons are short and located near the
5. E. The Therapeutic Index (TI) of a drug is equal to the ratio of the organ innervated, preganglionic cell bodies are located in the cra-
toxic dose to the therapeutic dose. The larger the TI of a drug, the niosacral divisions of the spinal cord, and parasympathetic neurons
less potential for adverse or toxic effects. innervating the respiratory system mediate bronchoconstriction.
6. D. By definition, the half-life (t1/2) of a drug is defined as the time 2. B. The neurotransmitter at postganglionic sympathetic neurons is
it takes for the concentration of a drug in the circulation to decrease NE. Sympathetic ganglia use ACh as the neurotransmitter and are
by half. located primarily in paravertebral chains. Nicotinic receptors are
present at all autonomic ganglia.
Chapter 4 3. A. Nicotinic receptors are ligand-gated ion channels; all the others
1. A. Clopidogrel is a prodrug that needs to be activated to be effec- are GPCRs.
tive. The enzyme responsible is CYP2C19. Individuals who are 4. D. The stimulation of prejunctional α2 adrenergic receptors on
CYP2C19 poor metabolizers have a reduced ability to activate postganglionic sympathetic neurons results in inhibition of NE
clopidogrel. release.
650
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NURSINGTB.COM
, Brody's Human Pharmacology 6th Edition Wecker Test Bank
WWW.NURSYLAB.COM
APPENDIX 651
5. C. Activation of the parasympathetic nervous system results in administered with halogenated inhalational anesthetics, can precipitate
constriction of airway smooth muscle, decreased heart rate, decreased malignant hyperthermia.
renin secretion, and contraction of the GI tract. The blood vessels 2. C. Ganglionic blocking agents block the predominant sympathetic
do not receive parasympathetic innervation. or parasympathetic tone of organs and lead to dry mouth, tachycardia,
constipation, and urinary retention, as well as excessive hypotension
Chapter 7 and impotence.
1. B. Pilocarpine is a cholinergic agonist that acts on ACh receptors 3. E. Neuromuscular blockers are useful in several clinical situations
to constrict the pupil. when skeletal muscle relaxation can be beneficial, including as a
2. A. The patient exhibits typical parasympathetic symptoms with surgical adjunct, for orthopedic procedures, endotracheal intubation,
little neuromuscular involvement; consequently the muscarinic scoping procedures, and electroconvulsive therapy.
antagonist atropine is administered to antagonize the actions of the 4. A. Nicotinic receptors at ganglia are neuronal receptors composed
anticholinesterase insecticide. Atropine is preferred over the qua- of α or α and β subunits, whereas nicotinic receptors at the neu-
ternary ammonium muscarinic antagonist propantheline because romuscular junction are composed of α1, β1, δ, and ε (γ during
atropine enters the brain. development) subunits. Differences in subunit composition underlie
3. C. The respiratory depression that ensues following exposure to differences in the responses of these receptors to pharmacological
this insecticide may lead to death. All other options listed can be agents.
managed pharmacologically and are not typically lethal.
4. D. Bethanechol activates muscarinic receptors, causing a decrease Chapter 11
in heart rate, peripheral vasodilation, and constriction in the airways 1. B. DA produces complex dose-dependent peripheral actions with
of the lung. Bethanechol does not activate nicotinic receptors at the low doses relaxing smooth muscle in various vascular beds, including
neuromuscular junction. renal, mesenteric, and coronary, due to of D1 receptor activation;
5. C. It is likely that these individuals ate mushrooms containing the these doses do not activate α1 or β1 receptors.
fungal alkaloid muscarine, which activates muscarinic cholinergic 2. B. Epinephrine can reduce the bronchospasm associated with
receptors and leads to parasympathomimetic effects including miosis, anaphylaxis and counter the hypotension of anaphylactic shock by
blurred vision, lacrimation, excessive salivation and bronchial secre- promoting vasoconstriction in some vascular beds and increasing
tions, sweating, bronchoconstriction, bradycardia, abdominal cardiac output.
cramping, increased gastric acid secretion, diarrhea, and polyuria. 3. C. Dobutamine is used clinically for the short-term management
Atropine antagonizes all of these effects and is a useful antidote. of cardiac decompensation in patients with refractory heart failure
(American Heart Association Stage D).
Chapter 8
ChapterM12
NURSINGTB.C
1. E. The adverse effects of muscarinic receptor antagonists include
constipation, tachycardia, dry mouth, mydriasis, blurred vision,
O
1. C. Carvedilol is an α /β /β 1 1 2 receptor antagonist. Propranolol is a
inhibition of sweating, and urinary retention; thus it is contraindicated competitive antagonist at both β1 and β2 receptors. In combination
in patients with urinary retention. with doxazosin, which is a selective α1 receptor antagonist, these
2. C. The symptoms described are all consistent with the ingestion of drugs will antagonize the same receptors as carvedilol alone.
a muscarinic antagonist such as atropine. 2. A. Phentolamine blocks α1 and α2 adrenergic receptors, and thus
3. B. Muscarinic receptor antagonists that do not cross the blood-brain the effects of epinephrine after phentolamine will reflect effects only
barrier are useful for the treatment of COPD. Among the choices, by β1 receptors, most closely resembling the effects of the β1/β2
only ipratropium is such a drug. agonist isoproterenol.
4. D. The topical application of muscarinic receptor antagonists to a 3. B. Epinephrine-induced renin release is mediated by activation of
patient with narrow ocular angles can cause acute angle-closure β1 receptors. Thus, this action will be blocked by the relatively selective
glaucoma and are contraindicated in such patients. β1 receptor antagonist metoprolol; the other responses to epinephrine
5. B. Atropine is a muscarinic receptor antagonist and, as such, will are mediated by different receptor subtypes.
not counteract the effects of the cholinesterase inhibitors at nicotinic
receptors that mediate skeletal muscle transmission. Chapter 13
1. A. ACh is the only neurotransmitter whose action is terminated
Chapter 9 by hydrolysis via the action of acetylcholinesterase; the actions
1. E. High doses of nicotine, or prolonged exposure of receptors to of all the other amine neurotransmitters listed are terminated by
agonist, lead to desensitization of nicotinic receptors, which depresses reuptake.
ganglionic transmission. 2. A. All of the biogenic amine neurotransmitters are synthesized in
2. C. All studies indicate that agents used in cessation programs are nerve terminals and transported into vesicles by an active process;
more successful when counseling accompanies drug therapy. Lobeline their concentration in vesicles is 10 to 100 times that in the cytosol.
has not been shown to be effective for smoking cessation. 3. C. The long-term administration of agonists leads to a down regula-
3. E. Neuronal nicotinic receptors in autonomic ganglia, the adrenal tion of receptors in the postsynaptic cell membrane.
gland, the brain, and immune cells are composed of α or α and β 4. C. Dopaminergic neurons originate in the substantia nigra and
subunits. Muscle-type nicotinic receptors are composed of α1, β1, hypothalamus; the other types of neurons listed originate in other
δ, and ε (γ during development) subunits. brain regions.
5. B. A high degree of lipophilicity will facilitate the ability of drugs
Chapter 10 to cross the blood-brain barrier; the other choices would hinder it.
1. B. Genetic variations in butyrylcholinesterase activity resulting in 6. C. Ethanol, a CNS depressant, produces an initial stage of excitation
either lower concentrations of normal enzyme or an abnormal enzyme by reducing the activity of tonically active inhibitory brain systems.
may lead to prolonged actions of succinylcholine and, when It has none of the other effects listed.
WWW.NURSYLAB.COM
NURSINGTB.COM
, Brody's Human Pharmacology 6th Edition Wecker Test Bank
WWW.NURSYLAB.COM
652 APPENDIX
2. D. Ketamine is unique in its action as an antidepressant because
Chapter 14 its intravenous administration tempers suicidal thoughts and depres-
1. A. A loss of memory in an elderly individual may represent sion within a few hours.
Alzheimer’s disease. Donepezil is an acetylcholinesterase inhibitor 3. C. All amine reuptake inhibitors have the potential to precipitate
that preserves brain acetylcholine, a major neurotransmitter involved serotonin syndrome when used with other agents that also increase
in learning and memory thought to decline in Alzheimer’s disease. serotonin in the brain including many over-the-counter cough
There is no rationale for the use of any other drug listed. preparations containing dextromethorphan. Serotonin syndrome is
2. E. Alzheimer’s disease involves the loss of basal forebrain cholinergic characterized by fever, chills, diarrhea, myoclonus, tremor, motor
neurons, with primary therapy directed at increasing the levels of weakness, ataxia, and behavioral alterations.
acetylcholine in the brain. 4. C. Bupropion is contraindicated for use in any patient with a history
3. C. Early-onset Alzheimer’s disease may be linked to mutations in of seizures.
the genes coding for amyloid precursor protein (APP) or presenilins, 5. A. Although this woman has been in remission for 2 years, based
which are proteins involved in APP processing. on her history of alcohol use disorder, it would be unwise to provide
4. C. Alzheimer’s disease is a progressive neurodegenerative disorder, a prescription for a benzodiazepine.
and thus one would expect to see more atrophy. These is no evidence
that drug therapy slows the progression of neuronal loss. Chapter 18
5. B. The cognitive benefits of drug therapy vary from individual to 1. B. Although the exact pathophysiology of attention deficit hyper-
individual and, although statistically significant, are clinically modest. activity disorder is unclear, it is believed to involve suboptimal
Not all patients benefit, and those who do typically show only a norepinephrine and dopamine neurotransmission in the frontal
slight improvement in abilities. lobe.
6. B. Galantamine is an acetylcholinesterase inhibitor and a positive 2. E. Common adverse effects associated with the use of the stimulants
allosteric modulator at neuronal nicotinic receptors. Donepezil and include headaches, insomnia, anorexia, tic exacerbation, dry mouth,
rivastigmine only inhibit acetylcholinesterase, and memantine is a GI upset, weight loss, and reduced growth velocity.
glutamate receptor antagonist. 3. E. Although atomoxetine is less efficacious than the stimulants for
the treatment of attention deficit hyperactivity disorder, it is typically
Chapter 15 prescribed for children of low weight or stature.
1. C. Carbidopa is a peripheral aromatic amino acid decarboxylase 4. D. Adverse reactions to guanfacine include hypotension, somnolence,
inhibitor that does not cross the BBB and prevents the peripheral bradycardia, and syncope.
metabolism of l-DOPA. 5. D. Lisdexamfetamine is a prodrug that is converted to dextroam-
2. B. After 5 to 7 years of continued drug treatment, as many as 75% phetamine by enzymatic hydrolysis by red blood cells.
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of patients experience l-DOPA–induced dyskinesias, characterized 6. C. The effects of the amphetamines are attributed primarily to
by chorea and dystonia. enhanced dopamine and norepinephrine release.
3. B. Apomorphine is the only injectable drug for use in patients with
advanced Parkinson’s disease who experience episodes of immobility Chapter 19
(“off ” times) despite l-DOPA therapy. 1. E. Suvorexant is the only agent approved for both sleep-onset and
4. C. Tetrabenazine is a reversible inhibitor of the vesicular monoamine sleep-maintenance insomnia.
transport 2 (VMAT2) and prevents the uptake of dopamine into 2. D. The benzodiazepines depress REM sleep, and chronic REM
vesicles in the presynaptic neuron, leading to dopamine depletion. deprivation can lead to psychotic-like behaviors.
3. A. Ramelteon is the first and only selective melatonin receptor
Chapter 16 agonist approved for the treatment of insomnia.
1. A. Lithium is filtered by the kidneys, with 95% of an administered 4. E. The benzodiazepines may lead to CNS depression, dependence,
dose excreted in the urine in 24 hours. Any drug that interferes with daytime sedation, anterograde amnesia, headache, and dizziness and
glomerular filtration can increase plasma levels of lithium. thus are not ideal drugs for the treatment of insomnia.
2. B. The chronic administration of dopamine receptor antagonists 5. A. Suvorexant blocks orexin neuropeptides from binding to orexin
such as haloperidol can lead to an increased density of receptors, receptors and inhibits arousal signaling.
which underlies the development of tardive dyskinesia, a drug-induced
disorder characterized by abnormal facial movements. Chapter 20
3. B. The phenothiazine antipsychotics block muscarinic cholinergic 1. C. Orlistat is the only agent listed whose action is localized to
receptors, leading to many anticholinergic effects including dry the gastrointestinal tract. All the other agents readily enter the
mouth, urinary retention, and memory impairment. systemic circulation and may adversely affect the cardiovascular
4. D. Clozapine has the potential to produce agranulocytosis, requiring system.
blood cell counts for all patients taking this drug. 2. A. The only drug approved for binge-eating disorder is lisdexam-
5. E. Some atypical antipsychotics may temper negative symptoms of fetamine.
schizophrenia as a consequence of their antagonist actions at serotonin 3. D. Orlistat acts locally within the intestines to reduce the absorption
receptors. of dietary fat via inhibition of intestinal lipase, which decreases the
production of free fatty acids from triglycerides.
Chapter 17 4. C. Dronabinol, which is used for cachexia, stimulates appetite through
1. B. The β-adrenergic receptor antagonists such as propranolol are agonist actions at the cannabinoid receptor located in both the eating
useful for the short-term relief of performance anxiety because centers in the brain and in the gastrointestinal tract.
they suppress sympathetically mediated somatic manifestations of 5. C. Liraglutide is a long-acting GLP-1 receptor agonist approved for
anxiety. both type 2 diabetes and the treatment of obesity.
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