MCQ Quiz: Personalized Medicine and Antidepressants

Welcome to an engaging MCQ quiz focused on the cutting-edge intersection of personalized medicine and antidepressant therapy. The University of Florida’s PharmD curriculum emphasizes how pharmacogenetics contributes to variability in drug metabolism and transport, preparing students to use evidence-based information to advance patient care. This quiz, drawing from concepts taught in courses like Principles of Drug Therapy Individualization and Patient Care VII, will test your ability to apply pharmacogenomic principles to optimize antidepressant selection and dosing

1. The field of pharmacogenomics (PGx) primarily studies how:

• A. A person’s diet affects drug absorption.
• B. An individual’s genetic makeup influences their response to drugs.
• C. Age and gender affect drug clearance.
• D. All drugs are metabolized by the same enzyme.

Answer: B. An individual’s genetic makeup influences their response to drugs.

2. In pharmacogenetics, what is a “phenotype”?

• A. The specific genetic sequence of a patient.
• B. The observable clinical or metabolic trait resulting from a genotype, such as being a “poor metabolizer”.
• C. A type of antidepressant medication.
• D. The structure of a CYP450 enzyme.

Answer: B. The observable clinical or metabolic trait resulting from a genotype, such as being a “poor metabolizer”.

3. Which two cytochrome P450 enzymes are most frequently implicated in the metabolism of SSRIs and TCAs, making them common targets for PGx testing?

• A. CYP1A2 and CYP3A4
• B. CYP2D6 and CYP2C19
• C. CYP2E1 and CYP2A6
• D. CYP2C9 and CYP2B6

Answer: B. CYP2D6 and CYP2C19

4. A patient’s PGx test result shows they are a CYP2D6 Poor Metabolizer (PM). If they are prescribed a standard dose of paroxetine, a CYP2D6 substrate, what is the likely outcome?

• A. Subtherapeutic drug levels and lack of efficacy.
• B. Increased drug levels and a higher risk of adverse effects.
• C. Rapid clearance of the drug.
• D. No effect on drug levels or side effects.

Answer: B. Increased drug levels and a higher risk of adverse effects.

5. The Clinical Pharmacogenetics Implementation Consortium (CPIC) provides guidelines for what purpose?

• A. To mandate which drugs a pharmacist can dispense.
• B. To provide peer-reviewed, evidence-based recommendations on how to use genetic test results to guide prescribing.
• C. To set the price of pharmacogenomic tests.
• D. To regulate the manufacturing of antidepressants.

Answer: B. To provide peer-reviewed, evidence-based recommendations on how to use genetic test results to guide prescribing.

6. A patient is found to be a CYP2C19 Ultrarapid Metabolizer (UM). According to CPIC guidelines, which antidepressant should be avoided due to a high likelihood of therapeutic failure?

• A. Bupropion
• B. Mirtazapine
• C. Citalopram
• D. Venlafaxine

Answer: C. Citalopram

7. “Star allele” nomenclature (e.g., CYP2D6*4) is used in pharmacogenomics to describe:

• A. A drug’s brand name.
• A specific haplotype or variant allele of a gene.
• C. The number of side effects a drug has.
• D. The clinical trial phase of a new medication.

Answer: B. A specific haplotype or variant allele of a gene.

8. Tricyclic antidepressants (TCAs) have a narrow therapeutic index. PGx testing for CYP2D6 is particularly important because being a Poor Metabolizer can lead to:

• A. Rapid symptom relief.
• B. A significantly increased risk of toxicity, including cardiotoxicity.
• C. The need for a much higher dose than normal.
• D. A switch in the drug’s mechanism of action.

Answer: B. A significantly increased risk of toxicity, including cardiotoxicity.

9. The lecture “Personalized Medicine and Antidepressants” is a component of which Patient Care course, indicating its relevance to clinical practice?

• A. Patient Care II: Infectious Disease and Oncology
• B. Patient Care VI: Skin and Musculoskeletal Disorders
• C. Patient Care VII: Brain and Behavior
• D. Patient Care VIII: Complex Patients

Answer: C. Patient Care VII: Brain and Behavior

10. A “drug-drug-gene interaction” refers to a situation where:

• A. Two drugs interact, but genetics are not involved.
• B. A patient’s genetic makeup alters their response to two different drugs.
• C. A drug’s effect is altered by a patient’s genetics, and this is further modified by a second co-administered drug that inhibits or induces the relevant enzyme.
• D. A patient’s genes cause two drugs to have the exact same effect.

Answer: C. A drug’s effect is altered by a patient’s genetics, and this is further modified by a second co-administered drug that inhibits or induces the relevant enzyme.

11. Beyond metabolizing enzymes, genetic variations in which of the following could also theoretically contribute to variability in antidepressant response?

• A. Drug transporters (e.g., ABCB1)
• B. Drug targets (e.g., serotonin transporter gene, SLC6A4)
• C. Genes involved in immune response
• D. All of the above

Answer: D. All of the above

12. If a patient is a CYP2C19 Poor Metabolizer (PM), the CPIC guideline for citalopram recommends:

• A. Using the standard starting dose.
• B. Considering a 50% dose reduction or selecting an alternative drug not metabolized by CYP2C19.
• C. Doubling the standard starting dose.
• D. Switching to escitalopram, as it is not metabolized by CYP2C19.

Answer: B. Considering a 50% dose reduction or selecting an alternative drug not metabolized by CYP2C19.

13. A key goal of using personalized medicine in antidepressant therapy is to:

• A. Make treatment more expensive.
• B. Reduce the trial-and-error process of finding an effective and well-tolerated medication.
• C. Prove that genetics is the only factor in drug response.
• D. Eliminate the need for patient counseling.

Answer: B. Reduce the trial-and-error process of finding an effective and well-tolerated medication.

14. What does the term “genotype” refer to?

• A. The observable characteristics of an individual.
• B. The specific set of alleles (genes) inherited by an individual.
• C. The patient’s response to a medication.
• D. The environmental factors affecting a patient.

Answer: B. The specific set of alleles (genes) inherited by an individual.

15. A patient who is a CYP2D6 Ultrarapid Metabolizer (UM) is prescribed nortriptyline (a TCA). What is the likely clinical outcome?

• A. High risk of toxicity due to elevated drug levels.
• B. Therapeutic failure due to rapid metabolism and subtherapeutic drug levels.
• C. A predictable and effective response at standard doses.
• D. A severe allergic reaction.

Answer: B. Therapeutic failure due to rapid metabolism and subtherapeutic drug levels.

16. One of the core principles of drug therapy individualization is understanding that variability in patient response is common. Pharmacogenomics helps explain the __________ component of this variability.

• A. Environmental
• B. Dietary
• C. Genetic
• D. Adherence-related

Answer: C. Genetic

17. Before applying a CPIC guideline, what is the most important piece of information the clinician must have?

• A. The patient’s diet.
• B. The patient’s PGx test result (genotype).
• C. The cost of the medication.
• D. The patient’s favorite color.

Answer: B. The patient’s PGx test result (genotype).

18. The curriculum objective to “Discuss how pharmacogenetics contributes to variability in drug metabolism and transport” is a key part of which foundational course?

• A. Principles of Law & Ethics
• B. Principles of Drug Therapy Individualization
• C. Principles of Patient-Centered Care
• D. Pathophysiology and Patient Assessment

Answer: B. Principles of Drug Therapy Individualization

19. A patient is a known CYP2D6 Intermediate Metabolizer (IM). This means their enzyme activity is:

• A. Absent.
• B. Decreased compared to a Normal Metabolizer.
• C. Increased compared to a Normal Metabolizer.
• D. The same as a Poor Metabolizer.

Answer: B. Decreased compared to a Normal Metabolizer.

20. While PGx testing provides valuable information, what other factors must a pharmacist consider when personalizing antidepressant therapy?

• A. Co-administered medications (potential for drug-drug interactions)
• B. Patient comorbidities (e.g., renal or hepatic impairment)
• C. Patient preferences and cost
• D. All of the above

Answer: D. All of the above

21. Fluvoxamine is a potent inhibitor of CYP1A2 and a moderate inhibitor of CYP2C19 and CYP3A4. This information is crucial for personalizing therapy because it highlights the risk of:

• A. Pharmacogenomic interactions.
• B. Pharmacokinetic drug-drug interactions regardless of patient genotype.
• C. Only pharmacodynamic interactions.
• D. Auto-induction.

Answer: B. Pharmacokinetic drug-drug interactions regardless of patient genotype.

22. The use of PGx testing is an example of which “transcending concept” in the Patient Care course series?

• A. Social/Health Disparities
• B. Quality Assessment
• C. Personalized Medicine
• D. Self-Care

Answer: C. Personalized Medicine

23. If a PGx test for a specific drug-gene pair is not available or not yet recommended by CPIC, how should a clinician personalize therapy?

• A. By refusing to prescribe any medication.
• B. By using clinical factors (age, organ function), monitoring for response and adverse effects, and managing drug interactions.
• C. By guessing the patient’s genotype.
• D. By prescribing the highest possible dose of the medication.

Answer: B. By using clinical factors (age, organ function), monitoring for response and adverse effects, and managing drug interactions.

24. The enzyme CYP2C19 metabolizes the proton-pump inhibitor omeprazole. A patient who is a CYP2C19 PM taking citalopram is then prescribed omeprazole. What is a potential concern?

• A. A drug-drug-gene interaction, where both the genetic defect and the inhibiting drug could increase citalopram levels.
• B. The omeprazole will not work.
• C. The citalopram will be metabolized too quickly.
• D. There is no potential for an interaction.

Answer: A. A drug-drug-gene interaction, where both the genetic defect and the inhibiting drug could increase citalopram levels.

25. Some PGx panels test for the SLC6A4 gene, which codes for the serotonin transporter (SERT). The clinical utility of this gene for guiding antidepressant therapy is currently:

• A. Well-established with strong CPIC guidelines for dosing.
• B. Still under investigation and not yet recommended for clinical use by CPIC due to conflicting evidence.
• C. Only useful for predicting side effects of TCAs.
• D. A replacement for CYP2D6 testing.

Answer: B. Still under investigation and not yet recommended for clinical use by CPIC due to conflicting evidence.

26. The goal of using pharmacogenomics to personalize antidepressant therapy is to increase the probability of selecting a drug that will be:

• A. The most expensive.
• B. The newest one on the market.
• C. Both effective and well-tolerated for that specific patient.
• D. A medication that requires no monitoring.

Answer: C. Both effective and well-tolerated for that specific patient.

27. Which of the following describes a normal metabolizer (NM) or extensive metabolizer (EM) phenotype?

• A. Greatly increased metabolic activity.
• B. Fully functional metabolic activity, representing the reference or “normal” group.
• C. Greatly reduced or absent metabolic activity.
• D. Intermediate metabolic activity.

Answer: B. Fully functional metabolic activity, representing the reference or “normal” group.

28. A patient has a gene duplication for CYP2D6. This genotype is most likely to result in which phenotype?

• A. Poor Metabolizer (PM)
• B. Intermediate Metabolizer (IM)
• C. Normal Metabolizer (NM)
• D. Ultrarapid Metabolizer (UM)

Answer: D. Ultrarapid Metabolizer (UM)

29. The concept of “phenoconversion” describes a situation where:

• A. A patient’s genotype changes over time.
• B. A patient with a normal metabolizer genotype exhibits a poor metabolizer phenotype due to a co-administered inhibiting drug.
• C. A PGx test result is incorrect.
• D. A drug changes a patient’s physical appearance.

Answer: B. A patient with a normal metabolizer genotype exhibits a poor metabolizer phenotype due to a co-administered inhibiting drug.

30. The “Principles of Genetic Medicine” are covered in the

PHA5132 course to provide a foundation for understanding pharmacogenomics. This includes concepts like:

• A. Drug delivery systems.
• B. How genetic variations (polymorphisms) arise and are inherited.
• C. Pharmaceutical calculations.
• D. The laws governing pharmacy practice.

Answer: B. How genetic variations (polymorphisms) arise and are inherited.

31. For which antidepressant is PGx testing for CYP2C19 most strongly recommended by CPIC before initiation?

• A. Bupropion
• B. Mirtazapine
• C. Sertraline
• D. Citalopram and Escitalopram

Answer: D. Citalopram and Escitalopram

32. Personalized medicine extends beyond genomics. Which of the following patient-specific factors is also critical for personalizing antidepressant therapy?

• A. Patient preference and past experience with medications.
• B. Comorbid health conditions.
• C. Concomitant medications.
• D. All of the above.

Answer: D. All of the above.

33. What is the most significant limitation of current pharmacogenomic testing for antidepressants?

• A. The tests are 100% predictive of a patient’s response.
• B. The tests can predict efficacy with certainty, but not side effects.
• C. The tests primarily predict pharmacokinetic variability, not pharmacodynamic effects, and do not account for all factors influencing drug response.
• D. The tests are not regulated by any government agency.

Answer: C. The tests primarily predict pharmacokinetic variability, not pharmacodynamic effects, and do not account for all factors influencing drug response.

34. A patient brings you a direct-to-consumer genetic test report. As a pharmacist, the most appropriate first step is to:

• A. Use the report to immediately change their medication regimen.
• B. Advise the patient that such reports may not be clinical grade and recommend they discuss the results with their prescriber to consider confirmatory, clinical-grade testing if appropriate.
• C. Disregard the report completely as it is medically useless.
• D. Tell the patient to stop all of their medications.

Answer: B. Advise the patient that such reports may not be clinical grade and recommend they discuss the results with their prescriber to consider confirmatory, clinical-grade testing if appropriate.

35. The

PHA5132 syllabus lists “Database Tools for Pharmacogenomics” as a lecture topic. Which of the following is the leading online knowledge base for pharmacogenomics?

• A. PubMed
• B. UpToDate
• C. PharmGKB (Pharmacogenomics Knowledge Base)
• D. Google

Answer: C. PharmGKB (Pharmacogenomics Knowledge Base)

36. A patient who is a CYP2D6 PM is taking amitriptyline. They are at increased risk for which side effects?

• A. Insomnia and agitation.
• B. Anticholinergic effects (dry mouth, constipation) and sedation.
• C. Weight loss.
• D. Nausea and diarrhea.

Answer: B. Anticholinergic effects (dry mouth, constipation) and sedation.

37. The FDA label for which SSRI contains information about the influence of CYP2C19 genotype on exposure and recommends dose limitations?

• A. Fluoxetine
• B. Paroxetine
• C. Citalopram
• D. Sertraline

Answer: C. Citalopram

38. The implementation of personalized medicine requires an interprofessional approach. The pharmacist’s role is to:

• A. Make unilateral decisions about drug therapy.
• B. Interpret PGx results and provide recommendations to the prescriber and patient.
• C. Order the genetic tests for the patient.
• D. Only dispense the medication as written.

Answer: B. Interpret PGx results and provide recommendations to the prescriber and patient.

39. If a PGx test result is not available, which clinical clue might suggest a patient is a poor metabolizer of a certain drug?

• A. The patient reports the drug works perfectly at a standard dose.
• B. The patient has a history of tolerating very high doses of the drug.
• C. The patient reports experiencing significant side effects at a very low dose of the drug.
• D. The patient reports the drug has no side effects at all.

Answer: C. The patient reports experiencing significant side effects at a very low dose of the drug.

40. The ultimate goal of personalized antidepressant therapy is to move from a “one-size-fits-all” approach to a:

• A. “One-drug-fits-all” approach.
• B. “Right drug, right dose, right patient” approach.
• C. “Genetics-only” approach.
• D. “Trial-and-error-only” approach.

Answer: B. “Right drug, right dose, right patient” approach.

41. The

PHA5878C syllabus mentions the CPIC guideline for CYP2C19 and clopidogrel. This shows that the curriculum teaches students to apply guidelines for:

• A. Only antidepressants.
• B. Only cardiovascular drugs.
• C. Multiple therapeutic areas, demonstrating a consistent, evidence-based approach to PGx.
• D. Only oncology drugs.

Answer: C. Multiple therapeutic areas, demonstrating a consistent, evidence-based approach to PGx.

42. A patient is a CYP2C19 UM. If they take escitalopram, they will likely have _________ serum levels of the drug.

• A. Higher
• B. Lower
• C. Unchanged
• D. Toxic

Answer: B. Lower

43. A patient’s “genotype” is determined by _______, while their “phenotype” can be influenced by their genotype and ________.

• A. Their diet; their genetics
• B. The drugs they take; their age
• C. Their DNA sequence; other drugs and environmental factors
• D. Their clinical symptoms; their DNA sequence

Answer: C. Their DNA sequence; other drugs and environmental factors

44. Which of the following is NOT a CPIC-defined phenotype?

• A. Poor Metabolizer
• B. Intermediate Metabolizer
• C. Super-Fast Metabolizer
• D. Ultrarapid Metabolizer

Answer: C. Super-Fast Metabolizer

45. Why is PGx for TCAs particularly important from a safety perspective?

• A. They have no side effects.
• B. They have a wide therapeutic index.
• C. They have a narrow therapeutic index and risk of severe toxicity (e.g., cardiotoxicity) at high concentrations.
• D. They are not metabolized by CYP enzymes.

Answer: C. They have a narrow therapeutic index and risk of severe toxicity (e.g., cardiotoxicity) at high concentrations.

46. The PHA5132 course objective to “explain the nomenclature that is used to describe genotype and phenotype” is foundational for a pharmacist to be able to:

• A. Calculate drug dosages.
• B. Read and interpret a pharmacogenomic test report.
• C. Compound a sterile preparation.
• D. Understand pharmacy law.

Answer: B. Read and interpret a pharmacogenomic test report.

47. A patient is taking paroxetine (a CYP2D6 substrate) and is also a CYP2D6 Poor Metabolizer. They are then prescribed bupropion, which is a CYP2D6 inhibitor. This situation represents a:

• A. Low-risk combination.
• B. High risk for therapeutic failure of paroxetine.
• C. High risk for paroxetine toxicity due to two factors reducing its clearance.
• D. High risk for bupropion toxicity.

Answer: C. High risk for paroxetine toxicity due to two factors reducing its clearance.

48. In personalizing medicine, a patient’s report of “this drug has never worked for any of my family members” is:

• A. Irrelevant information that should be ignored.
• B. A potential clue to a shared genetic trait affecting drug response that warrants consideration.
• C. Proof that the patient will not respond to the drug.
• D. A sign of medication-seeking behavior.

Answer: B. A potential clue to a shared genetic trait affecting drug response that warrants consideration.

49. The

PHA5789C syllabus has a dedicated lecture on “Personalized Medicine and Antidepressants”, separate from the main management lecture. This implies that personalized medicine is considered:

• A. A minor, unimportant topic.
• B. A key, advanced concept in modern psychiatric pharmacotherapy.
• C. A topic for researchers only.
• D. The same as standard treatment.

Answer: B. A key, advanced concept in modern psychiatric pharmacotherapy.

50. The future of personalized medicine in depression treatment aims to integrate pharmacogenomics with other biomarkers to:

• A. Replace the need for pharmacists.
• B. Create more predictive models to guide therapy from the outset.
• C. Make treatment more complicated.
• D. Focus only on a patient’s genetics.

Answer: B. Create more predictive models to guide therapy from the outset.