, Test Bank For Pharmacology for Nurses A
Pathophysiologic Approach 7th Edition By Michael
Adams, Norman Holland, Shanti Chang (All
Chapters, 100% Original .
1. A patient with chronic heart failure (NYHA class III) is being managed with a regimen
including an angiotensin receptor-neprilysin inhibitor (ARNI). Which of the following best
describes the mechanism by which this drug class improves outcomes compared to an ACE
inhibitor alone?
A. Inhibition of neprilysin increases natriuretic peptide levels, promoting vasodilation and natriuresis,
while blocking AT1 receptors reduces aldosterone secretion.
B. Combined inhibition of ACE and neprilysin leads to accumulation of bradykinin, causing cough
and angioedema, which paradoxically reduces preload.
C. Selective blockade of angiotensin II type 2 receptors enhances nitric oxide production, offsetting the
vasoconstrictor effects of neprilysin inhibition.
D. Neprilysin inhibition prevents degradation of endothelin-1, augmenting inotropic effects, while AT1
blockade reduces afterload.
Answer: A
Rationale: ARNIs (e.g., sacubitril/valsartan) inhibit neprilysin, increasing levels of natriuretic
peptides (ANP, BNP, CNP) which cause vasodilation, natriuresis, and inhibit fibrosis and
hypertrophy. Concurrent AT1 receptor blockade by valsartan suppresses the RAAS. Option A
correctly describes this dual mechanism. Option B is incorrect because ARNIs do not inhibit
ACE; bradykinin accumulation is associated with ACE inhibitors. Option C is false; ARNIs
block AT1, not AT2. Option D is incorrect; neprilysin degrades endothelin-1, so inhibition
increases endothelin-1, which is vasoconstrictive and detrimental.
2. A researcher is studying a novel drug that acts as a positive allosteric modulator at
GABA-A receptors. Which of the following effects is most likely to be observed in animal
models?
A. Increased seizure threshold and anxiolysis without direct receptor activation.
B. Direct opening of chloride channels leading to rapid sedation.
C. Antagonism of benzodiazepine binding sites, reducing inhibitory neurotransmission.
D. Upregulation of GABA synthesis via feedback inhibition.
Answer: A
Rationale: Positive allosteric modulators (e.g., benzodiazepines) enhance the effect of GABA
when it binds, but do not directly activate the receptor. They increase the frequency of chloride
channel opening, leading to anxiolysis and anticonvulsant effects. Option A is correct. Option B
Page 1
,describes direct agonists like barbiturates. Option C describes inverse agonists. Option D is not
a known effect of allosteric modulation.
3. A patient with type 2 diabetes has an eGFR of 35 mL/min/1.73m² and is currently on
metformin. According to current FDA guidelines, which of the following is the most
appropriate recommendation?
A. Continue metformin at the same dose but monitor renal function monthly.
B. Discontinue metformin due to increased risk of lactic acidosis.
C. Reduce metformin dose by half and add a sulfonylurea.
D. Switch metformin to a sodium-glucose cotransporter-2 (SGLT2) inhibitor.
Answer: B
Rationale: Metformin is contraindicated when eGFR falls below 30 mL/min/1.73m² due to risk of
lactic acidosis. At eGFR 30-45, dose reduction is recommended, but below 30, it should be
discontinued. Option B is correct. Option A is not safe. Option C is not the best immediate
action. Option D is incorrect because SGLT2 inhibitors require eGFR 30 for initiation and are
not recommended below 45 for glycemic efficacy.
4. Which of the following pharmacodynamic interactions is most likely to occur when a
patient taking warfarin is started on a broad-spectrum antibiotic that reduces gut flora?
A. Decreased warfarin absorption due to antibiotic-induced diarrhea.
B. Enhanced warfarin effect due to reduced vitamin K synthesis by gut bacteria.
C. Competitive displacement of warfarin from plasma proteins by the antibiotic.
D. Inhibition of warfarin metabolism via CYP450 enzyme competition.
Answer: B
Rationale: Broad-spectrum antibiotics reduce vitamin K-producing gut flora, leading to
decreased vitamin K availability. This potentiates warfarin's anticoagulant effect (by reducing
synthesis of clotting factors). Option B is correct. Option A is not the primary mechanism;
diarrhea may affect absorption but is less significant. Option C is a pharmacokinetic interaction
but not typical for most antibiotics. Option D is possible for some antibiotics (e.g.,
metronidazole) but not all; the most consistent mechanism is reduction of vitamin K.
5. A patient with opioid use disorder is started on methadone maintenance therapy. Which
of the following best describes the rationale for using methadone over other full opioid
agonists?
A. Methadone has a shorter half-life, allowing for more flexible dosing and lower risk of overdose.
B. Methadone produces less euphoria due to its antagonist activity at kappa opioid receptors.
C. Methadone's long half-life and slow onset reduce withdrawal symptoms and craving without
significant euphoria.
D. Methadone is a partial agonist at mu receptors, producing a ceiling effect on respiratory depression.
Answer: C
Page 2
, Rationale: Methadone has a long elimination half-life (24-36 hours) and slow onset of action, which allows once-daily
dosing to suppress withdrawal and craving with minimal euphoria. Option C is correct. Option A is false; methadone has a
long half-life. Option B is incorrect; methadone has no significant kappa antagonist activity. Option D describes
buprenorphine, which is a partial agonist.
6. A patient is receiving vancomycin for a methicillin-resistant Staphylococcus aureus
(MRSA) infection. Which of the following monitoring parameters is most critical for
preventing nephrotoxicity?
A. Peak serum concentration maintained between 20-40 mcg/mL.
B. Trough serum concentration maintained between 15-20 mcg/mL.
C. Area under the curve (AUC) to minimum inhibitory concentration (MIC) ratio > 400.
D. Serum creatinine measured only at the end of therapy.
Answer: B
Rationale: Vancomycin trough levels correlate with nephrotoxicity; current guidelines
recommend targeting trough concentrations of 15-20 mcg/mL for serious MRSA infections.
Higher troughs increase risk of acute kidney injury. Option B is correct. Option A is incorrect;
peak monitoring is not standard. Option C is a pharmacodynamic target for efficacy, not
nephrotoxicity prevention. Option D is insufficient; renal function should be monitored
regularly.
7. A patient with bipolar disorder is being treated with lithium. After 6 months of therapy,
the patient develops polyuria and polydipsia. Which of the following is the most likely
explanation?
A. Lithium-induced nephrogenic diabetes insipidus due to downregulation of aquaporin-2 channels.
B. Lithium-induced central diabetes insipidus due to decreased antidiuretic hormone (ADH) release.
C. Compulsive water drinking due to lithium-induced activation of the thirst center.
D. Osmotic diuresis from lithium-induced glucosuria.
Answer: A
Rationale: Lithium can cause nephrogenic diabetes insipidus by interfering with the action of
ADH on the collecting ducts, specifically by downregulating aquaporin-2 water channels. This
leads to inability to concentrate urine, causing polyuria and polydipsia. Option A is correct.
Option B is incorrect; lithium does not affect ADH release. Option C is not a known direct
effect. Option D is incorrect; lithium does not cause glucosuria.
8. A patient is prescribed a drug that is a substrate of CYP3A4 and has a narrow
therapeutic index. Which of the following co-administered drugs would most likely require
a dose reduction of the substrate?
A. Phenytoin, a CYP3A4 inducer.
B. Ketoconazole, a CYP3A4 inhibitor.
C. Warfarin, a substrate of CYP2C9.
D. Metformin, which is excreted renally unchanged.
Page 3
Pathophysiologic Approach 7th Edition By Michael
Adams, Norman Holland, Shanti Chang (All
Chapters, 100% Original .
1. A patient with chronic heart failure (NYHA class III) is being managed with a regimen
including an angiotensin receptor-neprilysin inhibitor (ARNI). Which of the following best
describes the mechanism by which this drug class improves outcomes compared to an ACE
inhibitor alone?
A. Inhibition of neprilysin increases natriuretic peptide levels, promoting vasodilation and natriuresis,
while blocking AT1 receptors reduces aldosterone secretion.
B. Combined inhibition of ACE and neprilysin leads to accumulation of bradykinin, causing cough
and angioedema, which paradoxically reduces preload.
C. Selective blockade of angiotensin II type 2 receptors enhances nitric oxide production, offsetting the
vasoconstrictor effects of neprilysin inhibition.
D. Neprilysin inhibition prevents degradation of endothelin-1, augmenting inotropic effects, while AT1
blockade reduces afterload.
Answer: A
Rationale: ARNIs (e.g., sacubitril/valsartan) inhibit neprilysin, increasing levels of natriuretic
peptides (ANP, BNP, CNP) which cause vasodilation, natriuresis, and inhibit fibrosis and
hypertrophy. Concurrent AT1 receptor blockade by valsartan suppresses the RAAS. Option A
correctly describes this dual mechanism. Option B is incorrect because ARNIs do not inhibit
ACE; bradykinin accumulation is associated with ACE inhibitors. Option C is false; ARNIs
block AT1, not AT2. Option D is incorrect; neprilysin degrades endothelin-1, so inhibition
increases endothelin-1, which is vasoconstrictive and detrimental.
2. A researcher is studying a novel drug that acts as a positive allosteric modulator at
GABA-A receptors. Which of the following effects is most likely to be observed in animal
models?
A. Increased seizure threshold and anxiolysis without direct receptor activation.
B. Direct opening of chloride channels leading to rapid sedation.
C. Antagonism of benzodiazepine binding sites, reducing inhibitory neurotransmission.
D. Upregulation of GABA synthesis via feedback inhibition.
Answer: A
Rationale: Positive allosteric modulators (e.g., benzodiazepines) enhance the effect of GABA
when it binds, but do not directly activate the receptor. They increase the frequency of chloride
channel opening, leading to anxiolysis and anticonvulsant effects. Option A is correct. Option B
Page 1
,describes direct agonists like barbiturates. Option C describes inverse agonists. Option D is not
a known effect of allosteric modulation.
3. A patient with type 2 diabetes has an eGFR of 35 mL/min/1.73m² and is currently on
metformin. According to current FDA guidelines, which of the following is the most
appropriate recommendation?
A. Continue metformin at the same dose but monitor renal function monthly.
B. Discontinue metformin due to increased risk of lactic acidosis.
C. Reduce metformin dose by half and add a sulfonylurea.
D. Switch metformin to a sodium-glucose cotransporter-2 (SGLT2) inhibitor.
Answer: B
Rationale: Metformin is contraindicated when eGFR falls below 30 mL/min/1.73m² due to risk of
lactic acidosis. At eGFR 30-45, dose reduction is recommended, but below 30, it should be
discontinued. Option B is correct. Option A is not safe. Option C is not the best immediate
action. Option D is incorrect because SGLT2 inhibitors require eGFR 30 for initiation and are
not recommended below 45 for glycemic efficacy.
4. Which of the following pharmacodynamic interactions is most likely to occur when a
patient taking warfarin is started on a broad-spectrum antibiotic that reduces gut flora?
A. Decreased warfarin absorption due to antibiotic-induced diarrhea.
B. Enhanced warfarin effect due to reduced vitamin K synthesis by gut bacteria.
C. Competitive displacement of warfarin from plasma proteins by the antibiotic.
D. Inhibition of warfarin metabolism via CYP450 enzyme competition.
Answer: B
Rationale: Broad-spectrum antibiotics reduce vitamin K-producing gut flora, leading to
decreased vitamin K availability. This potentiates warfarin's anticoagulant effect (by reducing
synthesis of clotting factors). Option B is correct. Option A is not the primary mechanism;
diarrhea may affect absorption but is less significant. Option C is a pharmacokinetic interaction
but not typical for most antibiotics. Option D is possible for some antibiotics (e.g.,
metronidazole) but not all; the most consistent mechanism is reduction of vitamin K.
5. A patient with opioid use disorder is started on methadone maintenance therapy. Which
of the following best describes the rationale for using methadone over other full opioid
agonists?
A. Methadone has a shorter half-life, allowing for more flexible dosing and lower risk of overdose.
B. Methadone produces less euphoria due to its antagonist activity at kappa opioid receptors.
C. Methadone's long half-life and slow onset reduce withdrawal symptoms and craving without
significant euphoria.
D. Methadone is a partial agonist at mu receptors, producing a ceiling effect on respiratory depression.
Answer: C
Page 2
, Rationale: Methadone has a long elimination half-life (24-36 hours) and slow onset of action, which allows once-daily
dosing to suppress withdrawal and craving with minimal euphoria. Option C is correct. Option A is false; methadone has a
long half-life. Option B is incorrect; methadone has no significant kappa antagonist activity. Option D describes
buprenorphine, which is a partial agonist.
6. A patient is receiving vancomycin for a methicillin-resistant Staphylococcus aureus
(MRSA) infection. Which of the following monitoring parameters is most critical for
preventing nephrotoxicity?
A. Peak serum concentration maintained between 20-40 mcg/mL.
B. Trough serum concentration maintained between 15-20 mcg/mL.
C. Area under the curve (AUC) to minimum inhibitory concentration (MIC) ratio > 400.
D. Serum creatinine measured only at the end of therapy.
Answer: B
Rationale: Vancomycin trough levels correlate with nephrotoxicity; current guidelines
recommend targeting trough concentrations of 15-20 mcg/mL for serious MRSA infections.
Higher troughs increase risk of acute kidney injury. Option B is correct. Option A is incorrect;
peak monitoring is not standard. Option C is a pharmacodynamic target for efficacy, not
nephrotoxicity prevention. Option D is insufficient; renal function should be monitored
regularly.
7. A patient with bipolar disorder is being treated with lithium. After 6 months of therapy,
the patient develops polyuria and polydipsia. Which of the following is the most likely
explanation?
A. Lithium-induced nephrogenic diabetes insipidus due to downregulation of aquaporin-2 channels.
B. Lithium-induced central diabetes insipidus due to decreased antidiuretic hormone (ADH) release.
C. Compulsive water drinking due to lithium-induced activation of the thirst center.
D. Osmotic diuresis from lithium-induced glucosuria.
Answer: A
Rationale: Lithium can cause nephrogenic diabetes insipidus by interfering with the action of
ADH on the collecting ducts, specifically by downregulating aquaporin-2 water channels. This
leads to inability to concentrate urine, causing polyuria and polydipsia. Option A is correct.
Option B is incorrect; lithium does not affect ADH release. Option C is not a known direct
effect. Option D is incorrect; lithium does not cause glucosuria.
8. A patient is prescribed a drug that is a substrate of CYP3A4 and has a narrow
therapeutic index. Which of the following co-administered drugs would most likely require
a dose reduction of the substrate?
A. Phenytoin, a CYP3A4 inducer.
B. Ketoconazole, a CYP3A4 inhibitor.
C. Warfarin, a substrate of CYP2C9.
D. Metformin, which is excreted renally unchanged.
Page 3
