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NU 518 QUIZ 5 2026/2027 | ADVANCED
PHARMACOLOGY | 50 VERIFIED Q&A |
DETAILED RATIONALES | NGN-ALIGNED |
PASS GUARANTEED – A+ GRADED
SECTION 1: PHARMACOGENOMICS AND PERSONALIZED MEDICINE - Questions 1-10
Q1: HLA-B*1502 and Carbamazepine
The student is reviewing pharmacogenomics. Which serious adverse effect is associated with
carbamazepine in patients carrying the HLA-B*1502 allele?
A. Stevens-Johnson syndrome and toxic epidermal necrolysis
B. Aplastic anemia
C. Nephrotoxicity
D. Hepatotoxicity
Correct Answer: A
Rationale: The HLA-B*1502 allele is strongly associated with an increased risk of Stevens-Johnson
syndrome (SJS) and toxic epidermal necrolysis (TEN) in patients taking carbamazepine, especially in
individuals of Asian descent. Genetic screening is recommended before initiating carbamazepine in
high-risk populations. [100% CORRECT]
Q2: CYP2C9 and Phenytoin
The student is reviewing pharmacogenomics. A patient is a CYP2C9 poor metabolizer. Which drug's
dose should be reduced to avoid toxicity?
A. Phenytoin
B. Clopidogrel
C. Codeine
D. Omeprazole
Correct Answer: A
Rationale: Phenytoin is metabolized primarily by CYP2C9. Poor metabolizers have reduced enzyme
activity, leading to increased phenytoin levels and a higher risk of toxicity (nystagmus, ataxia,
confusion). Dose reduction and therapeutic drug monitoring are recommended. [100% CORRECT]
Q3: DPYD and Fluorouracil
The student is reviewing pharmacogenomics. Which enzyme deficiency increases the risk of severe
toxicity from fluorouracil?
,2
A. Dihydropyrimidine dehydrogenase (DPD)
B. Thiopurine methyltransferase (TPMT)
C. Glucose-6-phosphate dehydrogenase (G6PD)
D. N-acetyltransferase 2 (NAT2)
Correct Answer: A
Rationale: Dihydropyrimidine dehydrogenase (DPD) deficiency, encoded by the DPYD gene, impairs
the metabolism of fluorouracil, leading to severe and potentially fatal toxicity (myelosuppression,
mucositis, neurotoxicity). DPYD testing is recommended before initiating fluorouracil or
capecitabine. [100% CORRECT]
Q4: G6PD Deficiency and Rasburicase
The student is reviewing pharmacogenomics. Which medication is contraindicated in patients with
G6PD deficiency?
A. Rasburicase
B. Allopurinol
C. Colchicine
D. Probenecid
Correct Answer: A
Rationale: Rasburicase is a urate oxidase enzyme that generates hydrogen peroxide, which can
cause severe hemolysis in patients with G6PD deficiency. It is contraindicated in these patients.
Allopurinol, colchicine, and probenecid are not contraindicated. [100% CORRECT]
Q5: CYP2D6 and Tamoxifen
The student is reviewing pharmacogenomics. A patient is a CYP2D6 poor metabolizer. Which drug's
efficacy may be reduced?
A. Tamoxifen
B. Warfarin
C. Metoprolol
D. Omeprazole
Correct Answer: A
Rationale: Tamoxifen is a prodrug that is metabolized by CYP2D6 to its active metabolite, endoxifen.
Poor metabolizers have reduced conversion and may have decreased efficacy in breast cancer
treatment. Alternative therapy may be considered. [100% CORRECT]
Q6: UGT1A1 and Irinotecan
The student is reviewing pharmacogenomics. Which genetic polymorphism increases the risk of
severe diarrhea and neutropenia from irinotecan?
, 3
A. UGT1A1*28
B. CYP2D6*4
C. CYP2C19*2
D. VKORC1 -1639G>A
Correct Answer: A
Rationale: The UGT1A1*28 allele reduces glucuronidation of SN-38, the active metabolite of
irinotecan, leading to increased levels and severe toxicity (diarrhea, neutropenia). Dose reduction is
recommended for homozygous carriers. [100% CORRECT]
Q7: CYP2C19 and Voriconazole
The student is reviewing pharmacogenomics. A patient is a CYP2C19 ultra-rapid metabolizer. Which
drug's levels may be subtherapeutic?
A. Voriconazole
B. Warfarin
C. Clopidogrel
D. Phenytoin
Correct Answer: A
Rationale: Voriconazole is metabolized by CYP2C19. Ultra-rapid metabolizers clear the drug rapidly,
leading to subtherapeutic levels and potential treatment failure. Therapeutic drug monitoring and
alternative therapy may be needed. [100% CORRECT]
Q8: TPMT and Azathioprine
The student is reviewing pharmacogenomics. Which enzyme deficiency increases the risk of severe
myelosuppression from azathioprine?
A. Thiopurine methyltransferase (TPMT)
B. Dihydropyrimidine dehydrogenase (DPD)
C. Glucose-6-phosphate dehydrogenase (G6PD)
D. N-acetyltransferase 2 (NAT2)
Correct Answer: A
Rationale: TPMT deficiency leads to accumulation of thioguanine nucleotides, causing severe
myelosuppression from azathioprine and 6-mercaptopurine. TPMT testing is recommended before
initiating therapy. [100% CORRECT]
Q9: CYP3A5 and Tacrolimus
The student is reviewing pharmacogenomics. A patient is a CYP3A5 expresser. Which drug's dose
may need to be increased?
A. Tacrolimus
B. Cyclosporine
NU 518 QUIZ 5 2026/2027 | ADVANCED
PHARMACOLOGY | 50 VERIFIED Q&A |
DETAILED RATIONALES | NGN-ALIGNED |
PASS GUARANTEED – A+ GRADED
SECTION 1: PHARMACOGENOMICS AND PERSONALIZED MEDICINE - Questions 1-10
Q1: HLA-B*1502 and Carbamazepine
The student is reviewing pharmacogenomics. Which serious adverse effect is associated with
carbamazepine in patients carrying the HLA-B*1502 allele?
A. Stevens-Johnson syndrome and toxic epidermal necrolysis
B. Aplastic anemia
C. Nephrotoxicity
D. Hepatotoxicity
Correct Answer: A
Rationale: The HLA-B*1502 allele is strongly associated with an increased risk of Stevens-Johnson
syndrome (SJS) and toxic epidermal necrolysis (TEN) in patients taking carbamazepine, especially in
individuals of Asian descent. Genetic screening is recommended before initiating carbamazepine in
high-risk populations. [100% CORRECT]
Q2: CYP2C9 and Phenytoin
The student is reviewing pharmacogenomics. A patient is a CYP2C9 poor metabolizer. Which drug's
dose should be reduced to avoid toxicity?
A. Phenytoin
B. Clopidogrel
C. Codeine
D. Omeprazole
Correct Answer: A
Rationale: Phenytoin is metabolized primarily by CYP2C9. Poor metabolizers have reduced enzyme
activity, leading to increased phenytoin levels and a higher risk of toxicity (nystagmus, ataxia,
confusion). Dose reduction and therapeutic drug monitoring are recommended. [100% CORRECT]
Q3: DPYD and Fluorouracil
The student is reviewing pharmacogenomics. Which enzyme deficiency increases the risk of severe
toxicity from fluorouracil?
,2
A. Dihydropyrimidine dehydrogenase (DPD)
B. Thiopurine methyltransferase (TPMT)
C. Glucose-6-phosphate dehydrogenase (G6PD)
D. N-acetyltransferase 2 (NAT2)
Correct Answer: A
Rationale: Dihydropyrimidine dehydrogenase (DPD) deficiency, encoded by the DPYD gene, impairs
the metabolism of fluorouracil, leading to severe and potentially fatal toxicity (myelosuppression,
mucositis, neurotoxicity). DPYD testing is recommended before initiating fluorouracil or
capecitabine. [100% CORRECT]
Q4: G6PD Deficiency and Rasburicase
The student is reviewing pharmacogenomics. Which medication is contraindicated in patients with
G6PD deficiency?
A. Rasburicase
B. Allopurinol
C. Colchicine
D. Probenecid
Correct Answer: A
Rationale: Rasburicase is a urate oxidase enzyme that generates hydrogen peroxide, which can
cause severe hemolysis in patients with G6PD deficiency. It is contraindicated in these patients.
Allopurinol, colchicine, and probenecid are not contraindicated. [100% CORRECT]
Q5: CYP2D6 and Tamoxifen
The student is reviewing pharmacogenomics. A patient is a CYP2D6 poor metabolizer. Which drug's
efficacy may be reduced?
A. Tamoxifen
B. Warfarin
C. Metoprolol
D. Omeprazole
Correct Answer: A
Rationale: Tamoxifen is a prodrug that is metabolized by CYP2D6 to its active metabolite, endoxifen.
Poor metabolizers have reduced conversion and may have decreased efficacy in breast cancer
treatment. Alternative therapy may be considered. [100% CORRECT]
Q6: UGT1A1 and Irinotecan
The student is reviewing pharmacogenomics. Which genetic polymorphism increases the risk of
severe diarrhea and neutropenia from irinotecan?
, 3
A. UGT1A1*28
B. CYP2D6*4
C. CYP2C19*2
D. VKORC1 -1639G>A
Correct Answer: A
Rationale: The UGT1A1*28 allele reduces glucuronidation of SN-38, the active metabolite of
irinotecan, leading to increased levels and severe toxicity (diarrhea, neutropenia). Dose reduction is
recommended for homozygous carriers. [100% CORRECT]
Q7: CYP2C19 and Voriconazole
The student is reviewing pharmacogenomics. A patient is a CYP2C19 ultra-rapid metabolizer. Which
drug's levels may be subtherapeutic?
A. Voriconazole
B. Warfarin
C. Clopidogrel
D. Phenytoin
Correct Answer: A
Rationale: Voriconazole is metabolized by CYP2C19. Ultra-rapid metabolizers clear the drug rapidly,
leading to subtherapeutic levels and potential treatment failure. Therapeutic drug monitoring and
alternative therapy may be needed. [100% CORRECT]
Q8: TPMT and Azathioprine
The student is reviewing pharmacogenomics. Which enzyme deficiency increases the risk of severe
myelosuppression from azathioprine?
A. Thiopurine methyltransferase (TPMT)
B. Dihydropyrimidine dehydrogenase (DPD)
C. Glucose-6-phosphate dehydrogenase (G6PD)
D. N-acetyltransferase 2 (NAT2)
Correct Answer: A
Rationale: TPMT deficiency leads to accumulation of thioguanine nucleotides, causing severe
myelosuppression from azathioprine and 6-mercaptopurine. TPMT testing is recommended before
initiating therapy. [100% CORRECT]
Q9: CYP3A5 and Tacrolimus
The student is reviewing pharmacogenomics. A patient is a CYP3A5 expresser. Which drug's dose
may need to be increased?
A. Tacrolimus
B. Cyclosporine
