Drug interactions – pharmacodynamic MCQs With Answer

Introduction

Drug interactions — pharmacodynamic MCQs With Answer offers B. Pharm students a focused review of how drugs interact at targets to modify response. This short, analytical guide emphasizes core concepts: receptor antagonism, competitive versus noncompetitive blockade, partial and inverse agonism, synergism versus additive effects, potentiation, physiological and chemical antagonism, spare receptors, tachyphylaxis, and clinical consequences such as altered efficacy and safety. Keywords for revision include drug interactions, pharmacodynamic mechanisms, receptor theory, dose–response shifts, therapeutic index, and clinical significance. Clear examples and reasoning prepare students for exams and practice. Now let’s test your knowledge with 30 MCQs on this topic.

Q1. What best defines a pharmacodynamic drug interaction?

• An interaction that changes drug absorption and plasma concentration
• An interaction at the site of drug action altering pharmacological effect without changing concentration
• An interaction that only affects drug metabolism in the liver
• An interaction that modifies renal excretion rates

Correct Answer: An interaction at the site of drug action altering pharmacological effect without changing concentration

Q2. A competitive antagonist produces which characteristic effect on an agonist dose–response curve?

• Leftward shift and increased Emax
• Rightward shift with no change in maximal effect
• Decrease in Emax regardless of agonist concentration
• Complete reversal of agonist potency and efficacy

Correct Answer: Rightward shift with no change in maximal effect

Q3. How does a noncompetitive antagonist affect maximal response (Emax)?

• Increases Emax
• Does not change Emax but alters potency
• Decreases Emax even if agonist concentration increases
• Only affects potency at low agonist concentrations

Correct Answer: Decreases Emax even if agonist concentration increases

Q4. Which statement describes a partial agonist?

• Has full intrinsic activity and cannot be displaced
• Produces maximal effect greater than a full agonist
• Acts as agonist with submaximal efficacy and can antagonize a full agonist
• Always behaves as a pure antagonist in all systems

Correct Answer: Acts as agonist with submaximal efficacy and can antagonize a full agonist

Q5. What is the pharmacodynamic action of an inverse agonist?

• Enhances constitutive receptor activity
• Blocks agonist but does not alter basal activity
• Reduces constitutive receptor activity producing opposite effect to agonist
• Irreversibly binds and activates the receptor

Correct Answer: Reduces constitutive receptor activity producing opposite effect to agonist

Q6. How does synergism differ from an additive effect?

• Synergism equals the sum of individual drug effects
• Synergism is less than the sum of individual effects
• Synergism produces an effect greater than the sum of individual effects
• Synergism always indicates a pharmacokinetic interaction

Correct Answer: Synergism produces an effect greater than the sum of individual effects

Q7. On an isobologram, what does a point below the line of additivity indicate?

• Antagonism between drugs
• Additive interaction
• Synergism between drugs
• No interaction

Correct Answer: Synergism between drugs

Q8. What is the effect of spare receptors on drug potency and maximal response?

• Spares receptors reduce potency and lower Emax
• Spare receptors increase apparent potency while Emax remains achievable
• Spare receptors abolish drug response completely
• Spare receptors only affect drug metabolism

Correct Answer: Spare receptors increase apparent potency while Emax remains achievable

Q9. Tachyphylaxis refers to which phenomenon?

• Gradual hypersensitivity developing over months
• Rapid decrease in response to a drug after repeated administration
• Permanent receptor upregulation after a single dose
• Increased drug clearance due to enzyme induction

Correct Answer: Rapid decrease in response to a drug after repeated administration

Q10. Which is an example of chemical antagonism?

• Protamine neutralizing heparin by forming an inactive complex
• Beta-blocker reducing response to a beta-agonist
• Glucagon opposing insulin’s effect via different receptors
• Epinephrine reversing histamine bronchoconstriction physiologically

Correct Answer: Protamine neutralizing heparin by forming an inactive complex

Q11. Which scenario exemplifies physiological antagonism?

• Naloxone binding opioid receptors to displace morphine
• Epinephrine causing bronchodilation that opposes histamine-induced bronchoconstriction
• Protamine binding and inactivating heparin
• A noncompetitive antagonist reducing Emax of an agonist

Correct Answer: Epinephrine causing bronchodilation that opposes histamine-induced bronchoconstriction

Q12. Co-administration of benzodiazepines and opioids primarily risks which pharmacodynamic interaction?

• Reduced analgesia only
• Enhanced respiratory depression due to synergistic CNS depression
• Increased renal clearance of both drugs
• Mutual inactivation through chemical binding

Correct Answer: Enhanced respiratory depression due to synergistic CNS depression

Q13. How does a beta-blocker interact with a beta-agonist at the receptor level?

• Enhances beta-agonist efficacy
• Blocks the receptor and reduces agonist response
• Increases receptor expression leading to potentiation
• Forms a chemical complex in plasma

Correct Answer: Blocks the receptor and reduces agonist response

Q14. Flumazenil is used to reverse benzodiazepine overdose. Its mechanism is best described as:

• Irreversible agonist at GABA-A
• Competitive antagonist at the benzodiazepine binding site on GABA-A
• Allosteric agonist enhancing benzodiazepine effects
• Enzyme inducer increasing benzodiazepine metabolism

Correct Answer: Competitive antagonist at the benzodiazepine binding site on GABA-A

Q15. Naloxone reverses opioid effects by which pharmacodynamic mechanism?

• Positive allosteric modulation of opioid receptors
• Competitive antagonism at opioid receptors
• Irreversible inactivation of opioid peptides
• Enhancement of opioid receptor signaling

Correct Answer: Competitive antagonism at opioid receptors

Q16. What defines an allosteric modulator?

• Binds the orthosteric site to block the agonist physically
• Alters receptor response by binding to a different site than the agonist
• Always produces the same effect as the agonist
• Only affects drug metabolism, not receptor function

Correct Answer: Alters receptor response by binding to a different site than the agonist

Q17. Why does combining warfarin and aspirin increase bleeding risk as a pharmacodynamic interaction?

• Aspirin accelerates warfarin metabolism
• Both agents reduce hemostasis by additive anticoagulant and antiplatelet effects
• Aspirin chemically binds and inactivates warfarin
• Warfarin increases aspirin renal excretion

Correct Answer: Both agents reduce hemostasis by additive anticoagulant and antiplatelet effects

Q18. Chronic exposure to an agonist causing receptor downregulation leads to which outcome?

• Increased drug sensitivity over time
• Tachyphylaxis or tolerance with decreased responsiveness
• Immediate enhancement of agonist potency
• Permanent irreversible receptor activation

Correct Answer: Tachyphylaxis or tolerance with decreased responsiveness

Q19. Which statement about noncompetitive antagonists is true?

• They are always reversible by increasing agonist concentration
• They may bind irreversibly or allosterically and reduce maximal effect
• They increase potency without affecting efficacy
• They act only on intracellular enzymes, not receptors

Correct Answer: They may bind irreversibly or allosterically and reduce maximal effect

Q20. Intrinsic activity of a drug refers to:

• The drug’s concentration in plasma
• The drug’s ability to produce a maximal effect after binding
• The rate of drug elimination
• The drug’s molecular weight

Correct Answer: The drug’s ability to produce a maximal effect after binding

Q21. NSAIDs can attenuate the antihypertensive effect of some drugs by which pharmacodynamic mechanism?

• Inducing hepatic enzymes to fasten metabolism of antihypertensives
• Opposing prostaglandin-mediated vasodilation, reducing antihypertensive efficacy
• Binding directly to ACE inhibitors in plasma
• Increasing renal excretion of antihypertensive drugs

Correct Answer: Opposing prostaglandin-mediated vasodilation, reducing antihypertensive efficacy

Q22. A hallmark of surmountable (competitive) antagonism is:

• Inability to restore effect by increasing agonist concentration
• Decrease in maximal response that cannot be overcome
• Restoration of effect by sufficiently increasing agonist concentration
• Permanent receptor inactivation

Correct Answer: Restoration of effect by sufficiently increasing agonist concentration

Q23. If two drugs produce a combined effect greater than their separate summed effects, this is called:

• Additive interaction
• Synergistic interaction
• Antagonistic interaction
• Pharmacokinetic interaction

Correct Answer: Synergistic interaction

Q24. Which drug is an example of a partial agonist used clinically?

• Morphine (full μ-opioid agonist)
• Buprenorphine (partial μ-opioid agonist)
• Naloxone (pure opioid antagonist)
• Propranolol (β-blocker)

Correct Answer: Buprenorphine (partial μ-opioid agonist)

Q25. Which description fits an inverse agonist at a constitutively active receptor?

• Blocks agonists but has no effect on basal activity
• Stabilizes the receptor in an inactive conformation reducing basal signalling
• Enhances constitutive activity above basal levels
• Only acts when the orthosteric ligand is present

Correct Answer: Stabilizes the receptor in an inactive conformation reducing basal signalling

Q26. How can pharmacodynamic interactions affect a drug’s therapeutic index?

• They never influence therapeutic index
• They can narrow or widen the therapeutic window by altering effect or toxicity
• They only change drug absorption, not safety
• They only produce new metabolites with no clinical relevance

Correct Answer: They can narrow or widen the therapeutic window by altering effect or toxicity

Q27. Receptor occupancy theory helps explain which pharmacodynamic concept?

• How plasma protein binding always determines effect
• The relationship between fraction of receptors occupied and magnitude of response
• Why metabolism is unaffected by receptor number
• How renal clearance dictates receptor activation

Correct Answer: The relationship between fraction of receptors occupied and magnitude of response

Q28. A negative allosteric modulator will most likely:

• Increase agonist affinity and efficacy
• Decrease agonist-induced receptor activation by binding at a distinct site
• Directly activate the orthosteric site producing full agonism
• Enhance drug absorption in the gut

Correct Answer: Decrease agonist-induced receptor activation by binding at a distinct site

Q29. Combining benzodiazepines with barbiturates illustrates which pharmacodynamic principle?

• Chemical antagonism through drug binding
• Synergistic CNS depression via additive effects on GABAergic transmission
• Mutual reduction of efficacy due to competitive binding
• Pharmacokinetic inhibition of barbiturate metabolism only

Correct Answer: Synergistic CNS depression via additive effects on GABAergic transmission

Q30. On an isobologram, a point above the line of additivity indicates what type of interaction?

• Synergy
• Additivity
• Antagonism
• No interaction

Correct Answer: Antagonism

G S Sachin

I am a Registered Pharmacist under the Pharmacy Act, 1948, and the founder of PharmacyFreak.com. I hold a Bachelor of Pharmacy degree from Rungta College of Pharmaceutical Science and Research. With a strong academic foundation and practical knowledge, I am committed to providing accurate, easy-to-understand content to support pharmacy students and professionals. My aim is to make complex pharmaceutical concepts accessible and useful for real-world application.

Mail- Sachin@pharmacyfreak.com