MCQ Quiz: Personalized Medicine for Epilepsy

The era of personalized medicine is transforming epilepsy management, moving beyond a one-size-fits-all approach to a more precise, evidence-based strategy tailored to the individual patient. The PharmD curriculum, through dedicated lectures like “Precision Medicine for Epilepsy” in the Patient Care VII course and foundational principles in Principles of Drug Therapy Individualization, equips future pharmacists to use pharmacogenomic data to optimize outcomes. This quiz will test your knowledge on applying these principles to prevent severe adverse reactions, guide dosing, and truly personalize the care of patients with epilepsy.

1. The “Personalized Medicine for Epilepsy” lecture is a key component of which Patient Care course module?

• A. Module 5: Anxiety and Sleep-Wake Disorders
• B. Module 6: Epilepsy
• C. Module 4: Mood Disorders
• D. Module 2: Neurodegenerative Disorders

Answer: B. Module 6: Epilepsy

2. Pharmacogenomic testing for the HLA-B*1502 allele is strongly recommended before initiating carbamazepine in patients of which ancestry due to a high risk of Stevens-Johnson Syndrome (SJS)?

• A. Northern European
• B. African
• C. Asian
• D. South American

Answer: C. Asian

3. The field of pharmacogenomics is a core component of “Personalized Medicine.” What does it study?

• A. How diet and lifestyle affect drug response.
• B. How an individual’s genetic makeup influences their response to medications.
• C. The cost-effectiveness of different drugs.
• D. The manufacturing process of medications.

Answer: B. How an individual’s genetic makeup influences their response to medications.

4. A patient’s PGx test reveals they are a CYP2C9 poor metabolizer (PM). If this patient is prescribed a standard dose of phenytoin, which is metabolized by CYP2C9, what is the most likely outcome?

• A. Therapeutic failure due to rapid drug clearance.
• B. Increased risk of toxicity due to elevated drug levels.
• C. No change in drug levels or response.
• D. A severe skin rash.

Answer: B. Increased risk of toxicity due to elevated drug levels.

5. The Clinical Pharmacogenetics Implementation Consortium (CPIC) provides what type of guidance for clinicians?

• A. Legally binding prescribing mandates.
• B. Peer-reviewed, evidence-based guidelines on how to use genetic test results to optimize drug therapy.
• C. Pricing information for genetic tests.
• D. A list of all available drugs for a condition.

Answer: B. Peer-reviewed, evidence-based guidelines on how to use genetic test results to optimize drug therapy.

6. The “Principles of Genetic Medicine” are a foundational topic in the PHA5132 course. What does a patient’s “genotype” refer to?

• A. Their observable traits, like hair color.
• B. Their specific genetic makeup at a particular location.
• C. Their response to a medication.
• D. A list of their medications.

Answer: B. Their specific genetic makeup at a particular location.

7. A patient’s observable metabolic capacity (e.g., poor metabolizer, normal metabolizer) is referred to as their:

• A. Genotype
• B. Haplotype
• C. Phenotype
• D. Karyotype

Answer: C. Phenotype

8. Besides carbamazepine, the CPIC guideline for HLA-B*1502 also applies to which other aromatic anti-seizure medication?

• A. Levetiracetam
• B. Valproic acid
• C. Oxcarbazepine
• D. Gabapentin

Answer: C. Oxcarbazepine

9. A patient is a known CYP2C9 intermediate metabolizer (IM). According to CPIC guidelines, their starting maintenance dose for phenytoin should be:

• A. Higher than the standard dose.
• B. The standard recommended dose.
• C. Approximately 25% lower than the standard dose.
• D. A weight-based loading dose only.

Answer: C. Approximately 25% lower than the standard dose.

10. What is the primary goal of using personalized medicine in epilepsy management?

• A. To increase the use of older, less effective drugs.
• B. To select an anti-seizure medication and dose that maximizes efficacy and minimizes the risk of adverse effects for that individual.
• C. To make treatment decisions more complicated.
• D. To eliminate the need for patient counseling.

Answer: B. To select an anti-seizure medication and dose that maximizes efficacy and minimizes the risk of adverse effects for that individual.

11. Star allele nomenclature (e.g., CYP2C9*3) is used to describe:

• A. A drug’s brand name.
• B. A specific variant or allele of a pharmacogene.
• C. The severity of a patient’s epilepsy.
• D. The number of side effects.

Answer: B. A specific variant or allele of a pharmacogene.

12. While HLA-B*1502 is a major risk factor for carbamazepine-induced SJS in Asian populations, which other allele is associated with hypersensitivity reactions in other populations?

• A. HLA-A*31:01
• B. HLA-B*57:01
• C. HLA-DRB1*07:01
• D. There are no other known alleles.

Answer: A. HLA-A*31:01

13. A patient fails therapy with an ASM metabolized by CYP2C19. PGx testing reveals they are an ultrarapid metabolizer (UM) for this enzyme. This provides a potential ___________ explanation for the treatment failure.

• A. pharmacodynamic
• B. pharmacokinetic
• C. ethical
• D. social

Answer: B. pharmacokinetic

14. The “Principles of Drug Therapy Individualization” course is essential for understanding personalized medicine because it covers:

• A. How genetic variations contribute to variability in drug metabolism and transport.
• B. Only the laws related to pharmacy practice.
• C. Only the pathophysiology of disease.
• D. Only drug compounding techniques.

Answer: A. How genetic variations contribute to variability in drug metabolism and transport.

15. A patient’s PGx test result should be used as:

• A. The sole factor in determining their treatment.
• B. A piece of clinical information to be integrated with other patient factors like age, comorbidities, and concomitant medications.
• C. A reason to refuse treatment.
• D. A replacement for therapeutic drug monitoring.

Answer: B. A piece of clinical information to be integrated with other patient factors like age, comorbidities, and concomitant medications.

16. A patient who has two no-function alleles for the CYP2C9 gene would be classified as which phenotype?

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

Answer: D. Poor Metabolizer (PM).

17. The pharmacist’s role in personalized medicine for epilepsy includes:

• A. Ordering the genetic test for the patient.
• B. Interpreting the PGx results and providing recommendations to the prescriber.
• C. Making a definitive diagnosis of epilepsy.
• D. Administering the anti-seizure medication.

Answer: B. Interpreting the PGx results and providing recommendations to the prescriber.

18. Phenytoin exhibits non-linear kinetics due to saturation of CYP2C9/2C19. A patient who is a CYP2C9 PM will experience this saturation at:

• A. Much higher doses than a normal metabolizer.
• B. Much lower doses than a normal metabolizer.
• C. The same dose as a normal metabolizer.
• D. Phenytoin does not exhibit saturable kinetics.

Answer: B. Much lower doses than a normal metabolizer.

19. Where can a pharmacist find reliable, evidence-based information on how to act on a pharmacogenomic test result?

• A. A general internet search.
• B. The drug’s package insert.
• C. A peer-reviewed resource like the CPIC guidelines.
• D. The patient’s social media page.

Answer: C. A peer-reviewed resource like the CPIC guidelines.

20. The implementation of “precision medicine” in epilepsy care is an example of which course-level objective?

• A. Using evidence-based information to advance patient care.
• B. Performing administrative operations of a pharmacy.
• C. Identifying populations at risk for prevalent diseases.
• D. Fulfilling a medication order.

Answer: A. Using evidence-based information to advance patient care.

21. A patient of Japanese descent is prescribed carbamazepine. The pharmacist should recommend screening for:

• A. HLA-B*1502
• B. CYP2C9
• C. HLA-A*31:01
• D. Both A and C may be considered.

Answer: D. Both A and C may be considered.

22. If PGx testing is not available, what clinical information might suggest a patient is a poor metabolizer of phenytoin?

• A. The patient requires very high doses to achieve a therapeutic level.
• B. The patient experiences signs of toxicity at a low or standard dose.
• C. The patient reports no side effects.
• D. The patient has a history of excellent response to the drug.

Answer: B. The patient experiences signs of toxicity at a low or standard dose.

23. The term “phenoconversion” describes when a genotypic normal metabolizer behaves like a poor metabolizer. This can be caused by:

• A. A change in their DNA sequence.
• B. Co-administration of a potent enzyme-inhibiting drug.
• C. A high-fat diet.
• D. The patient’s age.

Answer: B. Co-administration of a potent enzyme-inhibiting drug.

24. The relationship between the HLA-B*1502 allele and carbamazepine-induced SJS is an example of a pharmacogenomic effect related to:

• A. Drug metabolism.
• B. Drug transport.
• C. An immune system response.
• D. The drug’s primary therapeutic target.

Answer: C. An immune system response.

25. A key benefit of preemptive PGx testing before starting a drug like carbamazepine is:

• A. To increase the cost of care.
• B. To delay the start of therapy.
• C. To prevent a predictable, severe, and potentially fatal adverse drug reaction.
• D. To ensure the drug will be 100% effective.

Answer: C. To prevent a predictable, severe, and potentially fatal adverse drug reaction.

26. The PHA5132 syllabus objective, “demonstrate how to use available pharmacogenomics databases,” refers to resources like:

• A. PubMed and Google Scholar.
• B. UpToDate and Lexicomp.
• C. PharmGKB and the CPIC website.
• D. The pharmacy’s dispensing software.

Answer: C. PharmGKB and the CPIC website.

27. The association between HLA-B*1502 and SJS/TEN is strongest for which anti-seizure medication?

• A. Levetiracetam
• B. Topiramate
• C. Carbamazepine
• D. Valproic acid

Answer: C. Carbamazepine

28. If a patient who is a CYP2C9 poor metabolizer takes phenytoin, their calculated half-life for the drug would be:

• A. Shorter than a normal metabolizer.
• B. The same as a normal metabolizer.
• C. Longer than a normal metabolizer.
• D. Unpredictable.

Answer: C. Longer than a normal metabolizer.

29. The ultimate goal of personalized medicine is to:

• A. Treat the genotype, not the patient.
• B. Use genetic information as one tool among many to optimize individual patient care.
• C. Replace clinical judgment with genetic test results.
• D. Only use drugs for which there is a genetic test.

Answer: B. Use genetic information as one tool among many to optimize individual patient care.

30. The “Assess” step of the PPCP for a patient with a known pharmacogenomic variant would involve:

• A. Ignoring the genetic information.
• B. Evaluating how the genetic information impacts the appropriateness, effectiveness, and safety of the current medication regimen.
• C. Telling the patient their genes are “bad.”
• D. Only checking their vital signs.

Answer: B. Evaluating how the genetic information impacts the appropriateness, effectiveness, and safety of the current medication regimen.

31. The concept of “drug-drug-gene interactions” is taught in the PHA5132 course. An example would be a CYP2C9 PM taking phenytoin who is also given:

• A. A drug that induces CYP2C9.
• B. A drug that inhibits CYP2C9, further reducing clearance.
• C. A drug that is not metabolized.
• D. An herbal supplement.

Answer: B. A drug that inhibits CYP2C9, further reducing clearance.

32. While not a primary ASM, the metabolism of the TCA amitriptyline is highly dependent on CYP2D6. A patient who is a CYP2D6 PM would be at risk for:

• A. Subtherapeutic levels of amitriptyline.
• B. Increased toxicity from amitriptyline.
• C. No change in drug effect.
• D. Faster clearance of the drug.

Answer: B. Increased toxicity from amitriptyline.

33. The FDA-approved label for carbamazepine contains a black box warning regarding:

• A. The risk of hepatotoxicity.
• B. The risk of pancreatitis.
• C. Serious dermatologic reactions and the HLA-B*1502 allele.
• D. The risk of weight gain.

Answer: C. Serious dermatologic reactions and the HLA-B*1502 allele.

34. A patient’s phenotype as a “normal metabolizer” (NM) is also sometimes referred to as a(n):

• A. Poor Metabolizer (PM)
• B. Ultrarapid Metabolizer (UM)
• C. Extensive Metabolizer (EM).
• D. Slow Metabolizer (SM)

Answer: C. Extensive Metabolizer (EM).

35. Applying personalized medicine principles to epilepsy demonstrates the pharmacist’s ability to:

• A. Perform administrative duties.
• B. Contribute patient-specific medication-related expertise as part of an interprofessional care team.
• C. Only fulfill a medication order.
• D. Manage pharmacy operations.

Answer: B. Contribute patient-specific medication-related expertise as part of an interprofessional care team.

36. A patient has one normal-function allele and one no-function allele for CYP2C9. Their predicted phenotype is:

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

Answer: B. Intermediate Metabolizer (IM)

37. The CPIC recommendation for a CYP2C9 poor metabolizer starting phenytoin is to:

• A. Use the standard dose.
• B. Increase the standard dose by 25%.
• C. Decrease the standard dose by 50% and monitor levels closely.
• D. Avoid phenytoin entirely.

Answer: C. Decrease the standard dose by 50% and monitor levels closely.

38. The evidence supporting the use of PGx in epilepsy management comes from which type of studies?

• A. Case reports and case series.
• B. Cohort and case-control studies associating genotypes with outcomes.
• C. Animal studies only.
• D. Marketing surveys.

Answer: B. Cohort and case-control studies associating genotypes with outcomes.

39. Personalized medicine aims to minimize which type of medication-related problem?

• A. The need for prior authorization.
• B. The cost of the medication.
• C. Adverse drug reactions.
• D. The availability of the medication.

Answer: C. Adverse drug reactions.

40. A patient asks if their genetic test means they can never take carbamazepine. If they are positive for HLA-B*1502, the most appropriate response is:

• A. “Yes, you can never take it.”
• B. “The test is probably wrong, so you can take it.”
• C. “This result indicates a very high risk of a severe rash, and the drug should be avoided per guidelines.”
• D. “You can take it, but you have to take a lower dose.”

Answer: C. “This result indicates a very high risk of a severe rash, and the drug should be avoided per guidelines.”

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

• A. Compound a medication.
• B. Read and understand a pharmacogenomic test report.
• C. Interpret a patient’s vital signs.
• D. Manage pharmacy inventory.

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

42. The “Plan” step of the PPCP, when incorporating a new PGx result, would involve:

• A. Collecting the patient’s medication history.
• B. Developing a new, genetically-guided therapeutic plan in collaboration with the prescriber.
• C. Assessing the patient’s current problems.
• D. Dispensing the medication.

Answer: B. Developing a new, genetically-guided therapeutic plan in collaboration with the prescriber.

43. A patient with a gene duplication of CYP2C19 would be considered a(n) ________ for drugs metabolized by this enzyme.

• A. Poor Metabolizer
• B. Intermediate Metabolizer
• C. Normal Metabolizer
• D. Ultrarapid Metabolizer

Answer: D. Ultrarapid Metabolizer

44. The personalization of epilepsy treatment should always consider:

• A. Only genetic factors.
• B. A combination of genetic factors, clinical factors, and patient preferences.
• C. Only patient preferences.
• D. Only the cost of the medication.

Answer: B. A combination of genetic factors, clinical factors, and patient preferences.

45. Which of the following best describes the current state of personalized medicine for epilepsy?

• A. It is a futuristic concept with no current clinical applications.
• B. There are specific, actionable gene-drug pairs (like HLA-B*1502-carbamazepine) that are standard of care, with more research ongoing.
• C. It is used to guide therapy for every single anti-seizure medication.
• D. It has been proven to be not useful.

Answer: B. There are specific, actionable gene-drug pairs (like HLA-B*1502-carbamazepine) that are standard of care, with more research ongoing.

46. A pharmacist’s ability to apply PGx knowledge to minimize adverse drug events is a key component of which Entrustable Professional Activity?

• A. Minimize adverse drug events and medication errors.
• B. Fulfill a medication order.
• C. Perform administrative operations.
• D. Identify at-risk populations.

Answer: A. Minimize adverse drug events and medication errors.

47. If a patient is a CYP2C9 poor metabolizer, they have less functional enzyme. This leads to _________ of a drug that is a CYP2C9 substrate.

• A. increased clearance
• B. decreased clearance
• C. no change in clearance
• D. faster clearance

Answer: B. decreased clearance

48. The ultimate goal of integrating pharmacogenomics into epilepsy care is to:

• A. Increase the complexity of treatment.
• B. Improve patient safety and treatment outcomes.
• C. Order more lab tests.
• D. Lengthen the time to find an effective medication.

Answer: B. Improve patient safety and treatment outcomes.

49. The PHA5132 curriculum includes “Drug-Drug-Gene Interactions,” a concept where:

• A. A patient’s genetics are the only factor to consider.
• B. A drug interaction is modified by a patient’s underlying genotype.
• C. Two genes interact with each other.
• D. A drug changes a patient’s DNA.

Answer: B. A drug interaction is modified by a patient’s underlying genotype.

50. Personalized medicine is a prime example of how pharmacists:

• A. Are becoming obsolete.
• B. Use evidence-based information to advance and individualize patient care.
• C. Only follow orders from physicians.
• D. Focus solely on the dispensing process.

Answer: B. Use evidence-based information to advance and individualize patient care. Sources