Chamberlain University
9 TINU • 355 NM
★ ★
C College of Nursing & Public Health
J O U R N E Y T O E X T R A O R D I N A R Y CO M PA S S I O N AT E C A R E
EST. 1889
MN 553 — Unit 9: Pharmacogenomics, Herbal Therapies &
OTC Drugs
A D VA N C E D P H A R M A CO LO G Y
INSTITUTION Chamberlain University COURSE CODE MN 553
PROGRAM Master of Science in Nursing (MSN / FNP) ACADEMIC YEAR
UNIT Unit 9 — Pharmacogenomics & OTC TOTAL QUESTIONS 20 Questions
Medications
COURSE TITLE Advanced Pharmacology FORMAT Multiple Choice — Select the Single Best
Answer
EXAMINATION INSTRUCTIONS
▸ Select the single best answer for each multiple-choice question.
▸ This Unit 9 assessment covers pharmacogenomics (CYP450 polymorphisms, HLA testing, VKORC1), herb-drug interactions,
traditional Chinese medicine, Ayurvedic medicine, melatonin use, and OTC drug regulation.
▸ Correct answers and detailed rationales appear below each question.
▸ All content is aligned with Chamberlain University MN 553 Unit 9 course competencies.
PHARMACOGENOMICS, HERB-DRUG INTERACTIONS & OTC Questions 1 –
REGULATION 20
1. Up to 21% of Asians are ultra-rapid CYP2D6 metabolizers. This leads to:
A. A need to monitor drugs metabolized by 2D6 for toxicity
B. Increased dosages needed of drugs metabolized by 2D6, such as SSRIs
C. Decreased conversion of codeine to morphine by CYP2D6
D. The need for lowered dosages of drugs, such as beta blockers
CORRECT ANSWER B — Increased dosages needed of drugs metabolized by 2D6, such as SSRIs
RATIONALE Ultra-rapid CYP2D6 metabolizers have multiple copies of the CYP2D6 gene, resulting in significantly faster
drug metabolism. Higher doses of drugs metabolized by CYP2D6 (SSRIs, tricyclic antidepressants, some beta
blockers) are needed to achieve therapeutic levels. Codeine-to-morphine conversion (C) is increased, not
decreased, in ultra-rapid metabolizers.
, 2. Rifampin is a nonspecific CYP450 inducer. Its clinical implication is that it may:
A. Lead to toxic levels of rifampin requiring close monitoring
B. Cause toxic levels of drugs such as oral contraceptives when coadministered
C. Induce the metabolism of drugs such as oral contraceptives, leading to therapeutic failure
D. Cause nonspecific changes in drug metabolism without clinical significance
CORRECT ANSWER C — Induce the metabolism of drugs such as oral contraceptives, leading to therapeutic failure
RATIONALE Rifampin is a potent CYP450 enzyme inducer that accelerates the metabolism of many coadministered drugs.
This can cause therapeutic failure of oral contraceptives, warfarin, antiretrovirals, and other CYP450
substrates. Inducers decrease, not increase (B), drug concentrations by enhancing clearance.
3. Inhibition of P-glycoprotein by quinidine may lead to:
A. Decreased therapeutic levels of quinidine
B. Increased therapeutic levels of quinidine
C. Decreased levels of a coadministered drug, such as digoxin, that requires P-glycoprotein for absorption and
elimination
D. Increased levels of a coadministered drug, such as digoxin, that requires P-glycoprotein for absorption and
elimination
CORRECT ANSWER D — Increased levels of a coadministered drug, such as digoxin, that requires P-glycoprotein for
absorption and elimination
RATIONALE P-glycoprotein (P-gp) is an efflux transporter that pumps drugs out of cells. Quinidine inhibits P-gp, reducing
digoxin efflux from intestinal cells and renal tubules, thereby increasing digoxin serum concentrations and
toxicity risk. This is a classic drug-drug interaction mediated by transport protein inhibition.
4. Warfarin resistance may be seen in patients with VKORC1 mutation, leading to:
A. Toxic levels of warfarin building up
B. Decreased response to warfarin
C. Increased risk for significant drug interactions with warfarin
D. Less risk of drug interactions with warfarin
CORRECT ANSWER B — Decreased response to warfarin
RATIONALE VKORC1 encodes vitamin K epoxide reductase, the enzyme inhibited by warfarin. Certain VKORC1
polymorphisms reduce warfarin sensitivity, requiring significantly higher doses to achieve therapeutic
anticoagulation. This pharmacogenomic variation, along with CYP2C9 variants, guides warfarin dosing.
5. Pharmacogenetic testing is required by the FDA prior to prescribing:
A. Erythromycin
B. Digoxin
C. Cetuximab
D. Rifampin
CORRECT ANSWER C — Cetuximab
RATIONALE The FDA requires KRAS mutation testing before prescribing cetuximab (a monoclonal antibody targeting
EGFR) for metastatic colorectal cancer. Cetuximab is ineffective in patients with KRAS mutations. This is one of
the few FDA-mandated pharmacogenetic tests. The other drugs do not have FDA-required genetic testing.
9 TINU • 355 NM
★ ★
C College of Nursing & Public Health
J O U R N E Y T O E X T R A O R D I N A R Y CO M PA S S I O N AT E C A R E
EST. 1889
MN 553 — Unit 9: Pharmacogenomics, Herbal Therapies &
OTC Drugs
A D VA N C E D P H A R M A CO LO G Y
INSTITUTION Chamberlain University COURSE CODE MN 553
PROGRAM Master of Science in Nursing (MSN / FNP) ACADEMIC YEAR
UNIT Unit 9 — Pharmacogenomics & OTC TOTAL QUESTIONS 20 Questions
Medications
COURSE TITLE Advanced Pharmacology FORMAT Multiple Choice — Select the Single Best
Answer
EXAMINATION INSTRUCTIONS
▸ Select the single best answer for each multiple-choice question.
▸ This Unit 9 assessment covers pharmacogenomics (CYP450 polymorphisms, HLA testing, VKORC1), herb-drug interactions,
traditional Chinese medicine, Ayurvedic medicine, melatonin use, and OTC drug regulation.
▸ Correct answers and detailed rationales appear below each question.
▸ All content is aligned with Chamberlain University MN 553 Unit 9 course competencies.
PHARMACOGENOMICS, HERB-DRUG INTERACTIONS & OTC Questions 1 –
REGULATION 20
1. Up to 21% of Asians are ultra-rapid CYP2D6 metabolizers. This leads to:
A. A need to monitor drugs metabolized by 2D6 for toxicity
B. Increased dosages needed of drugs metabolized by 2D6, such as SSRIs
C. Decreased conversion of codeine to morphine by CYP2D6
D. The need for lowered dosages of drugs, such as beta blockers
CORRECT ANSWER B — Increased dosages needed of drugs metabolized by 2D6, such as SSRIs
RATIONALE Ultra-rapid CYP2D6 metabolizers have multiple copies of the CYP2D6 gene, resulting in significantly faster
drug metabolism. Higher doses of drugs metabolized by CYP2D6 (SSRIs, tricyclic antidepressants, some beta
blockers) are needed to achieve therapeutic levels. Codeine-to-morphine conversion (C) is increased, not
decreased, in ultra-rapid metabolizers.
, 2. Rifampin is a nonspecific CYP450 inducer. Its clinical implication is that it may:
A. Lead to toxic levels of rifampin requiring close monitoring
B. Cause toxic levels of drugs such as oral contraceptives when coadministered
C. Induce the metabolism of drugs such as oral contraceptives, leading to therapeutic failure
D. Cause nonspecific changes in drug metabolism without clinical significance
CORRECT ANSWER C — Induce the metabolism of drugs such as oral contraceptives, leading to therapeutic failure
RATIONALE Rifampin is a potent CYP450 enzyme inducer that accelerates the metabolism of many coadministered drugs.
This can cause therapeutic failure of oral contraceptives, warfarin, antiretrovirals, and other CYP450
substrates. Inducers decrease, not increase (B), drug concentrations by enhancing clearance.
3. Inhibition of P-glycoprotein by quinidine may lead to:
A. Decreased therapeutic levels of quinidine
B. Increased therapeutic levels of quinidine
C. Decreased levels of a coadministered drug, such as digoxin, that requires P-glycoprotein for absorption and
elimination
D. Increased levels of a coadministered drug, such as digoxin, that requires P-glycoprotein for absorption and
elimination
CORRECT ANSWER D — Increased levels of a coadministered drug, such as digoxin, that requires P-glycoprotein for
absorption and elimination
RATIONALE P-glycoprotein (P-gp) is an efflux transporter that pumps drugs out of cells. Quinidine inhibits P-gp, reducing
digoxin efflux from intestinal cells and renal tubules, thereby increasing digoxin serum concentrations and
toxicity risk. This is a classic drug-drug interaction mediated by transport protein inhibition.
4. Warfarin resistance may be seen in patients with VKORC1 mutation, leading to:
A. Toxic levels of warfarin building up
B. Decreased response to warfarin
C. Increased risk for significant drug interactions with warfarin
D. Less risk of drug interactions with warfarin
CORRECT ANSWER B — Decreased response to warfarin
RATIONALE VKORC1 encodes vitamin K epoxide reductase, the enzyme inhibited by warfarin. Certain VKORC1
polymorphisms reduce warfarin sensitivity, requiring significantly higher doses to achieve therapeutic
anticoagulation. This pharmacogenomic variation, along with CYP2C9 variants, guides warfarin dosing.
5. Pharmacogenetic testing is required by the FDA prior to prescribing:
A. Erythromycin
B. Digoxin
C. Cetuximab
D. Rifampin
CORRECT ANSWER C — Cetuximab
RATIONALE The FDA requires KRAS mutation testing before prescribing cetuximab (a monoclonal antibody targeting
EGFR) for metastatic colorectal cancer. Cetuximab is ineffective in patients with KRAS mutations. This is one of
the few FDA-mandated pharmacogenetic tests. The other drugs do not have FDA-required genetic testing.
