BIOL 110 Pharmacology 2026/2027 HESI RN Test Bank HESI RN Pharmacology Examination Preparation
BIOL 110 Pharmacology 2026/2027 HESI RN Test
Bank
Comprehensive 150-Question Examination Aligned with 2026-2027 HESI RN Pharmacology Standards
BSN 315 / HESI RN Pharmacology V2 Blueprint | Next Generation NCLEX (NGN) Item Format | Expert-Verified Rationales
Section Content Domain Question Range Weight
1 Pharmacokinetics and Pharmacodynamics Q1 - Q26 17%
2 Medication Administration and Safety Q27 - Q50 20%
3 Therapeutic Uses and Drug Classifications Q51 - Q80 20%
4 Adverse Effects and Contraindications Q81 - Q105 16%
5 Patient Teaching and Monitoring Q106 - Q125 13%
6 Clinical Judgment and NGN-Style Scenarios Q126 - Q150 14%
Cognitive Distribution: 25% Recall — 50% Application — 25% Analysis | 75% Scenario-Based (including NGN case studies) | 25%
Direct Recall/Classification | Format: Multiple Choice, 4 Options (A-D), One Correct Answer
SECTION 1: Pharmacokinetics and Pharmacodynamics (17%)
Absorption, Distribution, Metabolism, Excretion, Receptor Theory, Drug Interactions | Q1 - Q26
Q1: An 82-year-old patient with heart failure is prescribed oral furosemide 40 mg daily. The patient has
peripheral edema and a serum albumin of 2.8 g/dL (normal 3.5-5.0). Which pharmacokinetic change best
explains why this patient may experience a greater-than-expected diuretic response?
A. Decreased gastric motility slows the rate of absorption, prolonging the drug effect.
B. Reduced plasma protein binding increases the free (active) fraction of furosemide. [CORRECT]
C. Increased hepatic blood flow accelerates first-pass metabolism, lowering drug levels.
D. Decreased glomerular filtration rate enhances tubular reabsorption of the drug.
Correct Answer: B
Rationale: Furosemide is highly protein-bound (95-98%), and in hypoalbuminemia the free fraction rises sharply, producing
an exaggerated diuretic response at the loop of Henle even when total plasma concentration appears therapeutic. Decreased
gastric motility affects rate but not extent of absorption for an actively secreted loop diuretic. Increased hepatic blood flow
would actually reduce first-pass effects for high-extraction drugs but furosemide is not high-extraction. Decreased GFR
reduces renal clearance of furosemide but the dominant clinical issue in hypoalbuminemia is the rise in free drug.
Evidence-based practice in older adults with low albumin calls for lower initial dosing and close monitoring for volume
depletion and electrolyte disturbances.
Q2: A patient receives an oral dose of a medication. The nurse understands that 70% of the drug is
metabolized by the liver on its first pass through the portal circulation before reaching systemic circulation.
Page 1 | BIOL 110 / HESI RN Pharmacology 2026-2027
,BIOL 110 Pharmacology 2026/2027 HESI RN Test Bank HESI RN Pharmacology Examination Preparation
Which pharmacokinetic concept does this scenario illustrate?
A. Volume of distribution
B. First-pass effect [CORRECT]
C. Steady-state concentration
D. Therapeutic index
Correct Answer: B
Rationale: The first-pass effect (presystemic metabolism) describes hepatic metabolism of a fraction of an orally
administered drug before it reaches systemic circulation, reducing bioavailability. Drugs with high first-pass metabolism (e.g.,
propranolol, morphine, nitroglycerin) require substantially higher oral doses than parenteral doses to achieve equivalent effect.
Volume of distribution describes drug distribution into tissues. Steady state describes accumulation over multiple doses.
Therapeutic index compares toxic and therapeutic doses. Recognizing first-pass metabolism is critical for nurses because it
explains route-dependent potency differences and informs decisions about route selection when oral effect is inadequate.
Q3: A drug has a half-life of 12 hours. Assuming no loading dose is given and dosing occurs at regular
intervals consistent with the half-life, approximately how long will it take for the medication to reach
steady-state concentration?
A. 12 hours
B. 24 hours
C. 48 hours
D. 60 hours (approximately 5 half-lives) [CORRECT]
Correct Answer: D
Rationale: Steady state is reached after approximately 4-5 half-lives regardless of dose or dosing interval, because
accumulation and elimination equilibrate at this point. With a half-life of 12 hours, steady state is achieved in about 60 hours.
A loading dose may be used to achieve therapeutic levels more rapidly in drugs with long half-lives (e.g., amiodarone, digoxin,
phenytoin). The other options represent 1, 2, and 4 half-lives respectively, at which the drug concentration is only 50%, 75%,
and about 94% of steady state. This principle is fundamental to therapeutic drug monitoring and timing of serum drug levels.
Q4: A patient is started on intravenous heparin for acute deep vein thrombosis. The drug has a half-life of
approximately 90 minutes. Why is a continuous IV infusion preferred over intermittent bolus administration
in this scenario?
A. Heparin has poor oral bioavailability due to extensive first-pass metabolism.
B. Continuous infusion maintains steady therapeutic plasma levels and avoids peaks and troughs.
[CORRECT]
C. Bolus administration would irreversibly bind antithrombin III.
D. Continuous infusion bypasses the need for aPTT monitoring.
Correct Answer: B
Rationale: Heparin's short half-life (~60-90 minutes) means intermittent boluses would produce wide swings between
supratherapeutic peaks and subtherapeutic troughs, increasing both bleeding risk and clot recurrence risk. Continuous IV
infusion maintains steady-state concentration within the therapeutic window, requiring aPTT monitoring to titrate to goal.
Heparin is not given orally because of poor absorption and degradation by heparinase, not first-pass metabolism. Heparin
reversibly binds antithrombin III; protamine sulfate provides chemical antagonism. The aPTT is essential and is monitored
every 6 hours initially and at least daily thereafter while on infusion.
Page 2 | BIOL 110 / HESI RN Pharmacology 2026-2027
,BIOL 110 Pharmacology 2026/2027 HESI RN Test Bank HESI RN Pharmacology Examination Preparation
Q5: A 68-year-old patient is taking warfarin 5 mg daily for atrial fibrillation. The patient is newly prescribed
amiodarone for rhythm control. The nurse anticipates which pharmacokinetic interaction, and what action is
most appropriate?
A. Amiodarone induces CYP2C9, increasing warfarin metabolism; warfarin dose should be increased.
B. Amiodarone inhibits CYP2C9, decreasing warfarin metabolism; warfarin dose should be reduced and INR
monitored closely. [CORRECT]
C. Amiodarone displaces warfarin from plasma proteins only, with no effect on metabolism.
D. Amiodarone and warfarin have no clinically significant interaction.
Correct Answer: B
Rationale: Amiodarone is a potent inhibitor of CYP2C9 (the primary enzyme metabolizing S-warfarin) and to a lesser extent
CYP3A4 (R-warfarin). Inhibition reduces warfarin clearance, dramatically increasing INR and bleeding risk. The interaction
may persist for weeks to months after amiodarone discontinuation due to its long half-life and active metabolite
(desethylamiodarone). The nurse should anticipate a 30-50% warfarin dose reduction, more frequent INR monitoring, and
patient education about bleeding signs. CYP induction would lower INR; pure protein displacement alone is not the
mechanism. This is a classic HESI high-yield drug-drug interaction.
Q6: A patient is prescribed a medication that acts as a competitive antagonist at the beta-1 receptor. Which
pharmacodynamic effect should the nurse anticipate, and what clinical finding supports receptor antagonism
rather than agonism?
A. Increased heart rate and contractility due to receptor stimulation.
B. Decreased heart rate and blood pressure due to receptor blockade. [CORRECT]
C. Increased bronchial smooth muscle relaxation.
D. Increased renin release from the kidneys.
Correct Answer: B
Rationale: A competitive antagonist binds the receptor without activating it, blocking endogenous ligands (e.g.,
norepinephrine) from producing their effect. Beta-1 blockade in the heart and juxtaglomerular cells produces decreased heart
rate, decreased contractility, and decreased renin release, lowering blood pressure. Increased heart rate, contractility, and
bronchodilation reflect beta-1 or beta-2 agonism. Renin release is also reduced by beta-1 blockade. This pharmacodynamic
principle explains why beta-blockers are useful in hypertension, heart failure with reduced ejection fraction, and rate control
in atrial fibrillation, and why abrupt cessation causes rebound tachycardia due to upregulated receptor density.
Q7: A patient receiving long-term opioid therapy develops tolerance to the analgesic effects of morphine,
requiring escalating doses to achieve the same pain relief. Which pharmacodynamic mechanism best explains
this phenomenon?
A. Increased first-pass metabolism of morphine due to hepatic enzyme induction.
B. Receptor downregulation and desensitization at the mu-opioid receptor. [CORRECT]
C. Accelerated renal elimination of morphine active metabolites.
D. Decreased blood-brain barrier permeability to morphine.
Correct Answer: B
Rationale: Tolerance to opioids is primarily pharmacodynamic, resulting from downregulation and desensitization of
mu-opioid receptors and downstream signaling adaptations (e.g., increased cAMP pathway activity, beta-arrestin recruitment).
Pharmacokinetic changes such as enzyme induction are minor contributors. M6G (morphine-6-glucuronide) is an active
metabolite that contributes to analgesia; accelerated elimination is not the mechanism. The blood-brain barrier permeability is
not significantly altered. Tolerance differs from physical dependence (withdrawal on cessation) and addiction (compulsive use
Page 3 | BIOL 110 / HESI RN Pharmacology 2026-2027
, BIOL 110 Pharmacology 2026/2027 HESI RN Test Bank HESI RN Pharmacology Examination Preparation
despite harm); nurses must distinguish these to provide safe, compassionate, and effective pain management.
Q8: A drug has a therapeutic index of 2.5. How should the nurse interpret this value when administering this
medication?
A. The drug has a wide safety margin; routine dosing changes are unlikely to cause toxicity.
B. The drug has a narrow safety margin; small dosing errors or changes in clearance can produce toxicity.
[CORRECT]
C. The drug is eliminated almost entirely by the kidneys.
D. The drug requires no serum level monitoring.
Correct Answer: B
Rationale: The therapeutic index (TI) is the ratio of the toxic dose to the therapeutic dose (TD50/ED50). A low TI (close to
1-5, such as digoxin, lithium, warfarin, aminoglycosides) indicates a narrow margin between therapeutic and toxic effects;
small dosing errors, drug interactions, or changes in renal/hepatic function can produce toxicity. A high TI (e.g., >10 for many
antibiotics) allows wide dosing latitude. Drugs with low TI typically require serum drug level monitoring and individualized
dosing. The TI does not indicate route of elimination, and narrow-TI drugs almost always require serum concentration
monitoring for safe use.
Q9: A patient on long-term phenytoin therapy for seizure control is admitted with ataxia, nystagmus, and
diplopia. The serum phenytoin level is 32 mcg/mL (therapeutic 10-20). Which pharmacokinetic property of
phenytoin explains why small dose increases disproportionately raise serum levels in this patient?
A. Linear (first-order) kinetics at all concentrations.
B. Michaelis-Menten (saturation) kinetics, where metabolism saturates near the therapeutic range.
[CORRECT]
C. Zero-order kinetics at low concentrations only.
D. Renal tubular secretion saturation with increased reabsorption.
Correct Answer: B
Rationale: Phenytoin exhibits Michaelis-Menten (dose-dependent, saturable) kinetics: at low concentrations elimination is
first-order, but as concentrations approach and exceed the therapeutic range, the metabolic enzymes saturate and elimination
switches toward zero-order, so small dose increases cause disproportionate plasma level elevations and toxicity. This is why
phenytoin dosing must be individualized and levels monitored, particularly above 15 mcg/mL. Ataxia, nystagmus, and diplopia
are classic dose-related neurotoxicity signs. The other choices are incorrect: first-order kinetics would produce proportional
changes; zero-order kinetics at low doses is the opposite; renal secretion saturation is not the mechanism for phenytoin, which
is primarily hepatic.
Q10: A nurse is preparing to administer oral levothyroxine to a patient. Which medication-food interaction
should the nurse teach the patient to avoid, and why is timing critical?
A. Take levothyroxine with grapefruit juice to enhance absorption.
B. Take levothyroxine on an empty stomach at least 30-60 minutes before breakfast, because food (especially
fiber, calcium, and iron) significantly reduces absorption. [CORRECT]
C. Take levothyroxine with a high-fat meal to slow absorption and prolong effect.
D. Take levothyroxine at bedtime with a calcium supplement to improve thyroid function.
Correct Answer: B
Page 4 | BIOL 110 / HESI RN Pharmacology 2026-2027
BIOL 110 Pharmacology 2026/2027 HESI RN Test
Bank
Comprehensive 150-Question Examination Aligned with 2026-2027 HESI RN Pharmacology Standards
BSN 315 / HESI RN Pharmacology V2 Blueprint | Next Generation NCLEX (NGN) Item Format | Expert-Verified Rationales
Section Content Domain Question Range Weight
1 Pharmacokinetics and Pharmacodynamics Q1 - Q26 17%
2 Medication Administration and Safety Q27 - Q50 20%
3 Therapeutic Uses and Drug Classifications Q51 - Q80 20%
4 Adverse Effects and Contraindications Q81 - Q105 16%
5 Patient Teaching and Monitoring Q106 - Q125 13%
6 Clinical Judgment and NGN-Style Scenarios Q126 - Q150 14%
Cognitive Distribution: 25% Recall — 50% Application — 25% Analysis | 75% Scenario-Based (including NGN case studies) | 25%
Direct Recall/Classification | Format: Multiple Choice, 4 Options (A-D), One Correct Answer
SECTION 1: Pharmacokinetics and Pharmacodynamics (17%)
Absorption, Distribution, Metabolism, Excretion, Receptor Theory, Drug Interactions | Q1 - Q26
Q1: An 82-year-old patient with heart failure is prescribed oral furosemide 40 mg daily. The patient has
peripheral edema and a serum albumin of 2.8 g/dL (normal 3.5-5.0). Which pharmacokinetic change best
explains why this patient may experience a greater-than-expected diuretic response?
A. Decreased gastric motility slows the rate of absorption, prolonging the drug effect.
B. Reduced plasma protein binding increases the free (active) fraction of furosemide. [CORRECT]
C. Increased hepatic blood flow accelerates first-pass metabolism, lowering drug levels.
D. Decreased glomerular filtration rate enhances tubular reabsorption of the drug.
Correct Answer: B
Rationale: Furosemide is highly protein-bound (95-98%), and in hypoalbuminemia the free fraction rises sharply, producing
an exaggerated diuretic response at the loop of Henle even when total plasma concentration appears therapeutic. Decreased
gastric motility affects rate but not extent of absorption for an actively secreted loop diuretic. Increased hepatic blood flow
would actually reduce first-pass effects for high-extraction drugs but furosemide is not high-extraction. Decreased GFR
reduces renal clearance of furosemide but the dominant clinical issue in hypoalbuminemia is the rise in free drug.
Evidence-based practice in older adults with low albumin calls for lower initial dosing and close monitoring for volume
depletion and electrolyte disturbances.
Q2: A patient receives an oral dose of a medication. The nurse understands that 70% of the drug is
metabolized by the liver on its first pass through the portal circulation before reaching systemic circulation.
Page 1 | BIOL 110 / HESI RN Pharmacology 2026-2027
,BIOL 110 Pharmacology 2026/2027 HESI RN Test Bank HESI RN Pharmacology Examination Preparation
Which pharmacokinetic concept does this scenario illustrate?
A. Volume of distribution
B. First-pass effect [CORRECT]
C. Steady-state concentration
D. Therapeutic index
Correct Answer: B
Rationale: The first-pass effect (presystemic metabolism) describes hepatic metabolism of a fraction of an orally
administered drug before it reaches systemic circulation, reducing bioavailability. Drugs with high first-pass metabolism (e.g.,
propranolol, morphine, nitroglycerin) require substantially higher oral doses than parenteral doses to achieve equivalent effect.
Volume of distribution describes drug distribution into tissues. Steady state describes accumulation over multiple doses.
Therapeutic index compares toxic and therapeutic doses. Recognizing first-pass metabolism is critical for nurses because it
explains route-dependent potency differences and informs decisions about route selection when oral effect is inadequate.
Q3: A drug has a half-life of 12 hours. Assuming no loading dose is given and dosing occurs at regular
intervals consistent with the half-life, approximately how long will it take for the medication to reach
steady-state concentration?
A. 12 hours
B. 24 hours
C. 48 hours
D. 60 hours (approximately 5 half-lives) [CORRECT]
Correct Answer: D
Rationale: Steady state is reached after approximately 4-5 half-lives regardless of dose or dosing interval, because
accumulation and elimination equilibrate at this point. With a half-life of 12 hours, steady state is achieved in about 60 hours.
A loading dose may be used to achieve therapeutic levels more rapidly in drugs with long half-lives (e.g., amiodarone, digoxin,
phenytoin). The other options represent 1, 2, and 4 half-lives respectively, at which the drug concentration is only 50%, 75%,
and about 94% of steady state. This principle is fundamental to therapeutic drug monitoring and timing of serum drug levels.
Q4: A patient is started on intravenous heparin for acute deep vein thrombosis. The drug has a half-life of
approximately 90 minutes. Why is a continuous IV infusion preferred over intermittent bolus administration
in this scenario?
A. Heparin has poor oral bioavailability due to extensive first-pass metabolism.
B. Continuous infusion maintains steady therapeutic plasma levels and avoids peaks and troughs.
[CORRECT]
C. Bolus administration would irreversibly bind antithrombin III.
D. Continuous infusion bypasses the need for aPTT monitoring.
Correct Answer: B
Rationale: Heparin's short half-life (~60-90 minutes) means intermittent boluses would produce wide swings between
supratherapeutic peaks and subtherapeutic troughs, increasing both bleeding risk and clot recurrence risk. Continuous IV
infusion maintains steady-state concentration within the therapeutic window, requiring aPTT monitoring to titrate to goal.
Heparin is not given orally because of poor absorption and degradation by heparinase, not first-pass metabolism. Heparin
reversibly binds antithrombin III; protamine sulfate provides chemical antagonism. The aPTT is essential and is monitored
every 6 hours initially and at least daily thereafter while on infusion.
Page 2 | BIOL 110 / HESI RN Pharmacology 2026-2027
,BIOL 110 Pharmacology 2026/2027 HESI RN Test Bank HESI RN Pharmacology Examination Preparation
Q5: A 68-year-old patient is taking warfarin 5 mg daily for atrial fibrillation. The patient is newly prescribed
amiodarone for rhythm control. The nurse anticipates which pharmacokinetic interaction, and what action is
most appropriate?
A. Amiodarone induces CYP2C9, increasing warfarin metabolism; warfarin dose should be increased.
B. Amiodarone inhibits CYP2C9, decreasing warfarin metabolism; warfarin dose should be reduced and INR
monitored closely. [CORRECT]
C. Amiodarone displaces warfarin from plasma proteins only, with no effect on metabolism.
D. Amiodarone and warfarin have no clinically significant interaction.
Correct Answer: B
Rationale: Amiodarone is a potent inhibitor of CYP2C9 (the primary enzyme metabolizing S-warfarin) and to a lesser extent
CYP3A4 (R-warfarin). Inhibition reduces warfarin clearance, dramatically increasing INR and bleeding risk. The interaction
may persist for weeks to months after amiodarone discontinuation due to its long half-life and active metabolite
(desethylamiodarone). The nurse should anticipate a 30-50% warfarin dose reduction, more frequent INR monitoring, and
patient education about bleeding signs. CYP induction would lower INR; pure protein displacement alone is not the
mechanism. This is a classic HESI high-yield drug-drug interaction.
Q6: A patient is prescribed a medication that acts as a competitive antagonist at the beta-1 receptor. Which
pharmacodynamic effect should the nurse anticipate, and what clinical finding supports receptor antagonism
rather than agonism?
A. Increased heart rate and contractility due to receptor stimulation.
B. Decreased heart rate and blood pressure due to receptor blockade. [CORRECT]
C. Increased bronchial smooth muscle relaxation.
D. Increased renin release from the kidneys.
Correct Answer: B
Rationale: A competitive antagonist binds the receptor without activating it, blocking endogenous ligands (e.g.,
norepinephrine) from producing their effect. Beta-1 blockade in the heart and juxtaglomerular cells produces decreased heart
rate, decreased contractility, and decreased renin release, lowering blood pressure. Increased heart rate, contractility, and
bronchodilation reflect beta-1 or beta-2 agonism. Renin release is also reduced by beta-1 blockade. This pharmacodynamic
principle explains why beta-blockers are useful in hypertension, heart failure with reduced ejection fraction, and rate control
in atrial fibrillation, and why abrupt cessation causes rebound tachycardia due to upregulated receptor density.
Q7: A patient receiving long-term opioid therapy develops tolerance to the analgesic effects of morphine,
requiring escalating doses to achieve the same pain relief. Which pharmacodynamic mechanism best explains
this phenomenon?
A. Increased first-pass metabolism of morphine due to hepatic enzyme induction.
B. Receptor downregulation and desensitization at the mu-opioid receptor. [CORRECT]
C. Accelerated renal elimination of morphine active metabolites.
D. Decreased blood-brain barrier permeability to morphine.
Correct Answer: B
Rationale: Tolerance to opioids is primarily pharmacodynamic, resulting from downregulation and desensitization of
mu-opioid receptors and downstream signaling adaptations (e.g., increased cAMP pathway activity, beta-arrestin recruitment).
Pharmacokinetic changes such as enzyme induction are minor contributors. M6G (morphine-6-glucuronide) is an active
metabolite that contributes to analgesia; accelerated elimination is not the mechanism. The blood-brain barrier permeability is
not significantly altered. Tolerance differs from physical dependence (withdrawal on cessation) and addiction (compulsive use
Page 3 | BIOL 110 / HESI RN Pharmacology 2026-2027
, BIOL 110 Pharmacology 2026/2027 HESI RN Test Bank HESI RN Pharmacology Examination Preparation
despite harm); nurses must distinguish these to provide safe, compassionate, and effective pain management.
Q8: A drug has a therapeutic index of 2.5. How should the nurse interpret this value when administering this
medication?
A. The drug has a wide safety margin; routine dosing changes are unlikely to cause toxicity.
B. The drug has a narrow safety margin; small dosing errors or changes in clearance can produce toxicity.
[CORRECT]
C. The drug is eliminated almost entirely by the kidneys.
D. The drug requires no serum level monitoring.
Correct Answer: B
Rationale: The therapeutic index (TI) is the ratio of the toxic dose to the therapeutic dose (TD50/ED50). A low TI (close to
1-5, such as digoxin, lithium, warfarin, aminoglycosides) indicates a narrow margin between therapeutic and toxic effects;
small dosing errors, drug interactions, or changes in renal/hepatic function can produce toxicity. A high TI (e.g., >10 for many
antibiotics) allows wide dosing latitude. Drugs with low TI typically require serum drug level monitoring and individualized
dosing. The TI does not indicate route of elimination, and narrow-TI drugs almost always require serum concentration
monitoring for safe use.
Q9: A patient on long-term phenytoin therapy for seizure control is admitted with ataxia, nystagmus, and
diplopia. The serum phenytoin level is 32 mcg/mL (therapeutic 10-20). Which pharmacokinetic property of
phenytoin explains why small dose increases disproportionately raise serum levels in this patient?
A. Linear (first-order) kinetics at all concentrations.
B. Michaelis-Menten (saturation) kinetics, where metabolism saturates near the therapeutic range.
[CORRECT]
C. Zero-order kinetics at low concentrations only.
D. Renal tubular secretion saturation with increased reabsorption.
Correct Answer: B
Rationale: Phenytoin exhibits Michaelis-Menten (dose-dependent, saturable) kinetics: at low concentrations elimination is
first-order, but as concentrations approach and exceed the therapeutic range, the metabolic enzymes saturate and elimination
switches toward zero-order, so small dose increases cause disproportionate plasma level elevations and toxicity. This is why
phenytoin dosing must be individualized and levels monitored, particularly above 15 mcg/mL. Ataxia, nystagmus, and diplopia
are classic dose-related neurotoxicity signs. The other choices are incorrect: first-order kinetics would produce proportional
changes; zero-order kinetics at low doses is the opposite; renal secretion saturation is not the mechanism for phenytoin, which
is primarily hepatic.
Q10: A nurse is preparing to administer oral levothyroxine to a patient. Which medication-food interaction
should the nurse teach the patient to avoid, and why is timing critical?
A. Take levothyroxine with grapefruit juice to enhance absorption.
B. Take levothyroxine on an empty stomach at least 30-60 minutes before breakfast, because food (especially
fiber, calcium, and iron) significantly reduces absorption. [CORRECT]
C. Take levothyroxine with a high-fat meal to slow absorption and prolong effect.
D. Take levothyroxine at bedtime with a calcium supplement to improve thyroid function.
Correct Answer: B
Page 4 | BIOL 110 / HESI RN Pharmacology 2026-2027
