Pharmacology for Nurses Test Bank | 2026 Updated
Questions & Answers
1. A patient with a history of chronic alcoholism is prescribed a high dose of
acetaminophen for acute pain. Which pathophysiological change most significantly
increases the risk of hepatotoxicity?
A. Induction of CYP2E1 leading to increased production of NAPQI
B. Decreased glucuronidation capacity due to liver enzyme inhibition
C. Reduced renal clearance of acetaminophen and its metabolites
D. Increased activity of glutathione S-transferase depleting glutathione
Answer: A
Rationale: Chronic alcohol consumption induces CYP2E1, which metabolizes acetaminophen to
the toxic metabolite NAPQI. With glutathione stores depleted, NAPQI accumulates, causing
hepatotoxicity. Option B is incorrect because glucuronidation is impaired in severe liver
disease, not typically induced by alcohol. Option C is incorrect as renal clearance is minor.
Option D is incorrect because glutathione S-transferase is not induced and glutathione depletion
results from NAPQI binding.
2. A patient on warfarin develops a subtherapeutic INR after starting a new medication.
Which drug most likely caused this interaction by inducing CYP450 enzymes?
A. Fluconazole
B. Carbamazepine
C. Amiodarone
D. Cimetidine
Answer: B
Rationale: Carbamazepine is a potent CYP450 inducer, increasing warfarin metabolism and
reducing its anticoagulant effect, leading to subtherapeutic INR. Fluconazole, amiodarone, and
cimetidine are CYP450 inhibitors that would potentiate warfarin and increase INR. Thus, only
carbamazepine causes the described interaction.
3. A patient receiving intravenous vancomycin develops redness and flushing of the face,
neck, and upper torso shortly after infusion. What intervention should the nurse prioritize?
A. Administer diphenhydramine and decrease the infusion rate
B. Discontinue the infusion immediately and obtain a serum vancomycin trough
C. Apply cool compresses and monitor vital signs every 5 minutes
D. Increase the infusion rate to complete the dose faster
Page 1
,Answer: A
Rationale: This describes vancomycin flushing reaction (red man syndrome) due to histamine
release. Slowing the infusion rate and administering antihistamines like diphenhydramine is the
appropriate intervention. Discontinuation is not necessary unless severe. Increasing rate would
worsen symptoms. Cool compresses are supportive but not the priority.
4. A patient on digoxin develops nausea, vomiting, and visual disturbances. Lab results
show potassium 3.1 mEq/L. How does hypokalemia contribute to digoxin toxicity?
A. Increases digoxin absorption from the gastrointestinal tract
B. Reduces competition between potassium and digoxin at the Na+/K+ ATPase pump
C. Enhances renal excretion of digoxin leading to electrolyte imbalance
D. Increases protein binding of digoxin, raising free drug concentration
Answer: B
Rationale: Hypokalemia reduces the competition between potassium and digoxin for binding to
the Na+/K+ ATPase pump, allowing more digoxin to bind and increasing its toxic effects. It does
not affect absorption or protein binding significantly, and renal excretion is not enhanced but
rather may be decreased due to hypokalemia-induced renal effects.
5. A patient with type 2 diabetes is prescribed metformin. Which laboratory value should
be monitored to assess the risk of lactic acidosis?
A. Hemoglobin A1c
B. Serum creatinine
C. Fasting blood glucose
D. Liver function tests
Answer: B
Rationale: Metformin is contraindicated in patients with renal impairment because it
accumulates and can cause lactic acidosis. Serum creatinine is used to estimate renal function.
Hemoglobin A1c and fasting glucose monitor glycemic control but not risk of lactic acidosis.
Liver function tests are not directly related.
6. A patient on a selective serotonin reuptake inhibitor (SSRI) is prescribed linezolid for a
bacterial infection. What is the primary concern with this combination?
A. Increased risk of serotonin syndrome due to MAO inhibition by linezolid
B. Reduced antibacterial efficacy of linezolid due to hepatic enzyme induction
C. Additive QT prolongation leading to cardiac arrhythmias
D. Decreased SSRI effectiveness due to competitive protein binding
Answer: A
Rationale: Linezolid is a reversible non-selective MAO inhibitor, which can precipitate serotonin
syndrome when combined with SSRIs that increase serotonin levels. Option B is incorrect
because linezolid is not a CYP inducer. Option C is less specific and not the primary concern;
linezolid has minimal QT effect. Option D is not clinically significant.
Page 2
,7. A patient with a history of opioid use disorder is started on buprenorphine/naloxone.
What is the rationale for including naloxone in the formulation?
A. To enhance the analgesic effect of buprenorphine through synergy
B. To prevent diversion by causing withdrawal symptoms if injected
C. To increase the half-life of buprenorphine by inhibiting its metabolism
D. To reduce the risk of respiratory depression by antagonizing mu receptors
Answer: B
Rationale: Naloxone has poor oral bioavailability but is active when injected. In the combination
tablet, naloxone is included to deter misuse by injection; if crushed and injected, naloxone
precipitates withdrawal. It does not enhance analgesia, alter buprenorphine metabolism, or
significantly reduce respiratory depression when taken sublingually as directed.
8. A patient receiving IV heparin develops a platelet count drop from 250,000 to 90,000
over 4 days. Which antibody is most likely responsible?
A. IgG anti-heparin-PF4 complex antibody
B. IgM anti-heparin antibody
C. IgE anti-heparin antibody
D. IgA anti-platelet antibody
Answer: A
Rationale: This presentation suggests heparin-induced thrombocytopenia (HIT), caused by IgG
antibodies against the heparin-platelet factor 4 (PF4) complex. These antibodies activate
platelets, leading to thrombocytopenia and thrombosis risk. IgM and IgE are not implicated in
HIT. IgA anti-platelet antibodies are seen in immune thrombocytopenia, not HIT.
9. A patient on long-term phenytoin therapy develops nystagmus, ataxia, and slurred
speech. Which intervention should the nurse anticipate?
A. Increase the phenytoin dose to achieve therapeutic levels
B. Administer folic acid supplementation to correct deficiency
C. Hold the next dose and obtain a serum phenytoin level
D. Switch to a different anticonvulsant without phenytoin
Answer: C
Rationale: These symptoms indicate phenytoin toxicity. The nurse should hold the dose and check
serum levels to confirm. Increasing the dose would worsen toxicity. Folic acid is given for
long-term deficiency but does not treat acute toxicity. Switching anticonvulsants may be
considered after stabilization, but the immediate action is to hold the dose.
10. A patient with severe hypertension is started on nitroprusside infusion. Which adverse
effect requires immediate monitoring?
A. Metabolic alkalosis due to bicarbonate retention
B. Cyanide toxicity due to metabolism of nitroprusside
Page 3
, C. Hyperkalemia due to renal impairment
D. Hyperglycemia due to catecholamine release
Answer: B
Rationale: Nitroprusside is metabolized to cyanide, which can accumulate and cause toxicity,
especially with prolonged infusion or renal impairment. Metabolic alkalosis is not typical; it
may cause metabolic acidosis from cyanide. Hyperkalemia and hyperglycemia are not direct
effects. Therefore, cyanide levels and acid-base status must be monitored.
11. A patient receiving vancomycin develops red man syndrome. Which intervention is
most appropriate?
A. Administer diphenhydramine and slow the infusion rate
B. Discontinue the infusion immediately and administer epinephrine
C. Increase the infusion rate to shorten exposure
D. Switch to oral vancomycin therapy
Answer: A
Rationale: Red man syndrome is a histamine-mediated reaction to rapid vancomycin infusion.
Slowing the rate and pre-treating with antihistamines like diphenhydramine is standard.
Epinephrine is for anaphylaxis, not this reaction. Oral vancomycin has minimal systemic
absorption and does not cause this reaction.
12. Which drug class requires monitoring of serum potassium levels to prevent
life-threatening arrhythmias when used with digoxin?
A. Loop diuretics
B. Thiazide diuretics
C. Potassium-sparing diuretics
D. Beta blockers
Answer: B
Rationale: Thiazide diuretics cause hypokalemia, which increases digoxin toxicity risk and
arrhythmias. Loop diuretics also cause hypokalemia but are less commonly used chronically
with digoxin. Potassium-sparing diuretics raise potassium, not relevant. Beta blockers do not
significantly affect potassium.
13. A patient on warfarin has an INR of 5.2 with no bleeding. What is the appropriate
management?
A. Administer vitamin K 10 mg orally
B. Hold warfarin and administer fresh frozen plasma
C. Administer vitamin K 1-2.5 mg orally
D. Administer prothrombin complex concentrate
Answer: C
Rationale: For INR 4.5-10 without bleeding, guidelines recommend withholding warfarin and
giving low-dose oral vitamin K (1-2.5 mg). Higher doses (10 mg) can cause warfarin resistance.
Page 4
Questions & Answers
1. A patient with a history of chronic alcoholism is prescribed a high dose of
acetaminophen for acute pain. Which pathophysiological change most significantly
increases the risk of hepatotoxicity?
A. Induction of CYP2E1 leading to increased production of NAPQI
B. Decreased glucuronidation capacity due to liver enzyme inhibition
C. Reduced renal clearance of acetaminophen and its metabolites
D. Increased activity of glutathione S-transferase depleting glutathione
Answer: A
Rationale: Chronic alcohol consumption induces CYP2E1, which metabolizes acetaminophen to
the toxic metabolite NAPQI. With glutathione stores depleted, NAPQI accumulates, causing
hepatotoxicity. Option B is incorrect because glucuronidation is impaired in severe liver
disease, not typically induced by alcohol. Option C is incorrect as renal clearance is minor.
Option D is incorrect because glutathione S-transferase is not induced and glutathione depletion
results from NAPQI binding.
2. A patient on warfarin develops a subtherapeutic INR after starting a new medication.
Which drug most likely caused this interaction by inducing CYP450 enzymes?
A. Fluconazole
B. Carbamazepine
C. Amiodarone
D. Cimetidine
Answer: B
Rationale: Carbamazepine is a potent CYP450 inducer, increasing warfarin metabolism and
reducing its anticoagulant effect, leading to subtherapeutic INR. Fluconazole, amiodarone, and
cimetidine are CYP450 inhibitors that would potentiate warfarin and increase INR. Thus, only
carbamazepine causes the described interaction.
3. A patient receiving intravenous vancomycin develops redness and flushing of the face,
neck, and upper torso shortly after infusion. What intervention should the nurse prioritize?
A. Administer diphenhydramine and decrease the infusion rate
B. Discontinue the infusion immediately and obtain a serum vancomycin trough
C. Apply cool compresses and monitor vital signs every 5 minutes
D. Increase the infusion rate to complete the dose faster
Page 1
,Answer: A
Rationale: This describes vancomycin flushing reaction (red man syndrome) due to histamine
release. Slowing the infusion rate and administering antihistamines like diphenhydramine is the
appropriate intervention. Discontinuation is not necessary unless severe. Increasing rate would
worsen symptoms. Cool compresses are supportive but not the priority.
4. A patient on digoxin develops nausea, vomiting, and visual disturbances. Lab results
show potassium 3.1 mEq/L. How does hypokalemia contribute to digoxin toxicity?
A. Increases digoxin absorption from the gastrointestinal tract
B. Reduces competition between potassium and digoxin at the Na+/K+ ATPase pump
C. Enhances renal excretion of digoxin leading to electrolyte imbalance
D. Increases protein binding of digoxin, raising free drug concentration
Answer: B
Rationale: Hypokalemia reduces the competition between potassium and digoxin for binding to
the Na+/K+ ATPase pump, allowing more digoxin to bind and increasing its toxic effects. It does
not affect absorption or protein binding significantly, and renal excretion is not enhanced but
rather may be decreased due to hypokalemia-induced renal effects.
5. A patient with type 2 diabetes is prescribed metformin. Which laboratory value should
be monitored to assess the risk of lactic acidosis?
A. Hemoglobin A1c
B. Serum creatinine
C. Fasting blood glucose
D. Liver function tests
Answer: B
Rationale: Metformin is contraindicated in patients with renal impairment because it
accumulates and can cause lactic acidosis. Serum creatinine is used to estimate renal function.
Hemoglobin A1c and fasting glucose monitor glycemic control but not risk of lactic acidosis.
Liver function tests are not directly related.
6. A patient on a selective serotonin reuptake inhibitor (SSRI) is prescribed linezolid for a
bacterial infection. What is the primary concern with this combination?
A. Increased risk of serotonin syndrome due to MAO inhibition by linezolid
B. Reduced antibacterial efficacy of linezolid due to hepatic enzyme induction
C. Additive QT prolongation leading to cardiac arrhythmias
D. Decreased SSRI effectiveness due to competitive protein binding
Answer: A
Rationale: Linezolid is a reversible non-selective MAO inhibitor, which can precipitate serotonin
syndrome when combined with SSRIs that increase serotonin levels. Option B is incorrect
because linezolid is not a CYP inducer. Option C is less specific and not the primary concern;
linezolid has minimal QT effect. Option D is not clinically significant.
Page 2
,7. A patient with a history of opioid use disorder is started on buprenorphine/naloxone.
What is the rationale for including naloxone in the formulation?
A. To enhance the analgesic effect of buprenorphine through synergy
B. To prevent diversion by causing withdrawal symptoms if injected
C. To increase the half-life of buprenorphine by inhibiting its metabolism
D. To reduce the risk of respiratory depression by antagonizing mu receptors
Answer: B
Rationale: Naloxone has poor oral bioavailability but is active when injected. In the combination
tablet, naloxone is included to deter misuse by injection; if crushed and injected, naloxone
precipitates withdrawal. It does not enhance analgesia, alter buprenorphine metabolism, or
significantly reduce respiratory depression when taken sublingually as directed.
8. A patient receiving IV heparin develops a platelet count drop from 250,000 to 90,000
over 4 days. Which antibody is most likely responsible?
A. IgG anti-heparin-PF4 complex antibody
B. IgM anti-heparin antibody
C. IgE anti-heparin antibody
D. IgA anti-platelet antibody
Answer: A
Rationale: This presentation suggests heparin-induced thrombocytopenia (HIT), caused by IgG
antibodies against the heparin-platelet factor 4 (PF4) complex. These antibodies activate
platelets, leading to thrombocytopenia and thrombosis risk. IgM and IgE are not implicated in
HIT. IgA anti-platelet antibodies are seen in immune thrombocytopenia, not HIT.
9. A patient on long-term phenytoin therapy develops nystagmus, ataxia, and slurred
speech. Which intervention should the nurse anticipate?
A. Increase the phenytoin dose to achieve therapeutic levels
B. Administer folic acid supplementation to correct deficiency
C. Hold the next dose and obtain a serum phenytoin level
D. Switch to a different anticonvulsant without phenytoin
Answer: C
Rationale: These symptoms indicate phenytoin toxicity. The nurse should hold the dose and check
serum levels to confirm. Increasing the dose would worsen toxicity. Folic acid is given for
long-term deficiency but does not treat acute toxicity. Switching anticonvulsants may be
considered after stabilization, but the immediate action is to hold the dose.
10. A patient with severe hypertension is started on nitroprusside infusion. Which adverse
effect requires immediate monitoring?
A. Metabolic alkalosis due to bicarbonate retention
B. Cyanide toxicity due to metabolism of nitroprusside
Page 3
, C. Hyperkalemia due to renal impairment
D. Hyperglycemia due to catecholamine release
Answer: B
Rationale: Nitroprusside is metabolized to cyanide, which can accumulate and cause toxicity,
especially with prolonged infusion or renal impairment. Metabolic alkalosis is not typical; it
may cause metabolic acidosis from cyanide. Hyperkalemia and hyperglycemia are not direct
effects. Therefore, cyanide levels and acid-base status must be monitored.
11. A patient receiving vancomycin develops red man syndrome. Which intervention is
most appropriate?
A. Administer diphenhydramine and slow the infusion rate
B. Discontinue the infusion immediately and administer epinephrine
C. Increase the infusion rate to shorten exposure
D. Switch to oral vancomycin therapy
Answer: A
Rationale: Red man syndrome is a histamine-mediated reaction to rapid vancomycin infusion.
Slowing the rate and pre-treating with antihistamines like diphenhydramine is standard.
Epinephrine is for anaphylaxis, not this reaction. Oral vancomycin has minimal systemic
absorption and does not cause this reaction.
12. Which drug class requires monitoring of serum potassium levels to prevent
life-threatening arrhythmias when used with digoxin?
A. Loop diuretics
B. Thiazide diuretics
C. Potassium-sparing diuretics
D. Beta blockers
Answer: B
Rationale: Thiazide diuretics cause hypokalemia, which increases digoxin toxicity risk and
arrhythmias. Loop diuretics also cause hypokalemia but are less commonly used chronically
with digoxin. Potassium-sparing diuretics raise potassium, not relevant. Beta blockers do not
significantly affect potassium.
13. A patient on warfarin has an INR of 5.2 with no bleeding. What is the appropriate
management?
A. Administer vitamin K 10 mg orally
B. Hold warfarin and administer fresh frozen plasma
C. Administer vitamin K 1-2.5 mg orally
D. Administer prothrombin complex concentrate
Answer: C
Rationale: For INR 4.5-10 without bleeding, guidelines recommend withholding warfarin and
giving low-dose oral vitamin K (1-2.5 mg). Higher doses (10 mg) can cause warfarin resistance.
Page 4
