PHARMACOTHERAPEUTICS FOR ADVANCED PRACTICE NURSE PRESCRIBERS,QUESTIONS &
ANSWERS FULLY ANALYSED EDITION EXAM 100% CORRECTLY/VERIFIED ANSWERS WITH
SATISFACTION GUARANTEED SUCCESS LATEST UPDATE 2023/2024 5TH EDITION WOO ROBINSON
TEST BANK GRADED A+
ANATASHIA
Chapter 1.
An Introduction to Pharmacogenetics
Multiple Choice
Identify the choice that best completes the statement or answers the question.
1. Genetic polymorphisms account for differences in metabolism, including:
1. Poor metabolizers, who lack a working enzyme
2. Intermediate metabolizers, who have one working, wild-type allele and one mutant
3. Extensive metabolizers, with two normally functioning alleles
4. All of the above
2. Up to 21% of Asians are ultra-rapid 2D6 metabolizers, leading to:
1. A need to monitor drugs metabolized by 2D6 for toxicity
2. Increased dosages needed of drugs metabolized by 2D6, such as the
selective serotoreuptake inhibitors
3. Decreased conversion of codeine to morphine by CYP 2D6
4. The need for lowered dosages of drugs, such as beta blockers
3. Rifampin is a nonspecific CYP450 inducer that may:
1. Lead to toxic levels of rifampin and must be monitored closely
2. Cause toxic levels of drugs, such as oral contraceptives, when coadministered
3. Induce the metabolism of drugs, such as oral contraceptives, leading to therapeutic
4. Cause nonspecific changes in drug metabolism
4. Inhibition of P-glycoprotein by a drug such as quinidine may lead to:
1. Decreased therapeutic levels of quinidine
2. Increased therapeutic levels of quinidine
3. Decreased levels of a coadministered drug, such as digoxin, that
requires P-glycoprabsorption and elimination
4. Increased levels of a coadministered drug, such as digoxin, that
requires P-glycoproabsorption and elimination
5. Warfarin resistance may be seen in patients with VCORC1 mutation, leading to:
1. Toxic levels of warfarin building up
, 2. Decreased response to warfarin
3. Increased risk for significant drug interactions with warfarin
4. Less risk of drug interactions with warfarin
6. Genetic testing for VCORC1 mutation to assess potential warfarin
resistance is requiredprior to prescribing warfarin.
1. True
2. False
7. Pharmacogenetic testing is required by the U.S. Food and Drug
Administration prior toprescribing:
1. Erythromycin
2. Digoxin
3. Cetuximab
, 4. Rifampin
8. Carbamazepine has a Black Box Warning recommending testing for the
HLA-B*1502 allelein patients with Asian ancestry prior to starting
therapy due to:
ANATASHIA
1. Decreased effectiveness of carbamazepine in treating seizures in Asian patients wit
HLA-B*1502 allele
2. Increased risk for drug interactions in Asian patients with the HLA-B*1502 allele
3. Increased risk for Stevens-Johnson syndrome in Asian patients with HLA-B*1502 a
4. Patients who have the HLA-B*1502 allele being more likely to
have a resistance tocarbamazepine
9. A genetic variation in how the metabolite of the cancer drug
irinotecan SN-38 isinactivated by the body may lead to:
1. Decreased effectiveness of irinotecan in the treatment of cancer
2. Increased adverse drug reactions, such as neutropenia
3. Delayed metabolism of the prodrug irinotecan into the active metabolite SN-38
4. Increased concerns for irinotecan being carcinogenic
10. Patients who have a poor metabolism phenotype will have:
1. Slowed metabolism of a prodrug into an active drug, leading to accumulation of pr
2. Accumulation of inactive metabolites of drugs
3. A need for increased dosages of medications
4. Increased elimination of an active drug
11. Ultra-rapid metabolizers of drugs may have:
1. To have dosages of drugs adjusted downward to prevent drug accumulation
2. Active drug rapidly metabolized into inactive metabolites, leading
to potential therafailure
3. Increased elimination of active, nonmetabolized drug
4. Slowed metabolism of a prodrug into an active drug, leading to an accumulation of
12. A provider may consider testing for CYP2D6 variants prior to
starting tamoxifen forbreast cancer to:
1. Ensure the patient will not have increased adverse drug reactions to the tamoxifen
2. Identify potential drug-drug interactions that may occur with tamoxifen
3. Reduce the likelihood of therapeutic failure with tamoxifen treatment
4. Identify poor metabolizers of tamoxifen
, Chapter 1. An Introduction to
PharmacogeneticsAnswer Section
MULTIPLE CHOICE
1. ANS: 4 PTS: 1
2. ANS: 2 PTS: 1
3. ANS: 3 PTS: 1
4. ANS: 4 PTS: 1
5. ANS: 2 PTS: 1
6. ANS: 2 PTS: 1
7. ANS: 3 PTS: 1
8. ANS: 3 PTS: 1
9. ANS: 2 PTS: 1
10. 1 PTS: 1
ANS:
11. 2 PTS: 1
ANS:
12. 3 PTS: 1
ANS:
ANSWERS FULLY ANALYSED EDITION EXAM 100% CORRECTLY/VERIFIED ANSWERS WITH
SATISFACTION GUARANTEED SUCCESS LATEST UPDATE 2023/2024 5TH EDITION WOO ROBINSON
TEST BANK GRADED A+
ANATASHIA
Chapter 1.
An Introduction to Pharmacogenetics
Multiple Choice
Identify the choice that best completes the statement or answers the question.
1. Genetic polymorphisms account for differences in metabolism, including:
1. Poor metabolizers, who lack a working enzyme
2. Intermediate metabolizers, who have one working, wild-type allele and one mutant
3. Extensive metabolizers, with two normally functioning alleles
4. All of the above
2. Up to 21% of Asians are ultra-rapid 2D6 metabolizers, leading to:
1. A need to monitor drugs metabolized by 2D6 for toxicity
2. Increased dosages needed of drugs metabolized by 2D6, such as the
selective serotoreuptake inhibitors
3. Decreased conversion of codeine to morphine by CYP 2D6
4. The need for lowered dosages of drugs, such as beta blockers
3. Rifampin is a nonspecific CYP450 inducer that may:
1. Lead to toxic levels of rifampin and must be monitored closely
2. Cause toxic levels of drugs, such as oral contraceptives, when coadministered
3. Induce the metabolism of drugs, such as oral contraceptives, leading to therapeutic
4. Cause nonspecific changes in drug metabolism
4. Inhibition of P-glycoprotein by a drug such as quinidine may lead to:
1. Decreased therapeutic levels of quinidine
2. Increased therapeutic levels of quinidine
3. Decreased levels of a coadministered drug, such as digoxin, that
requires P-glycoprabsorption and elimination
4. Increased levels of a coadministered drug, such as digoxin, that
requires P-glycoproabsorption and elimination
5. Warfarin resistance may be seen in patients with VCORC1 mutation, leading to:
1. Toxic levels of warfarin building up
, 2. Decreased response to warfarin
3. Increased risk for significant drug interactions with warfarin
4. Less risk of drug interactions with warfarin
6. Genetic testing for VCORC1 mutation to assess potential warfarin
resistance is requiredprior to prescribing warfarin.
1. True
2. False
7. Pharmacogenetic testing is required by the U.S. Food and Drug
Administration prior toprescribing:
1. Erythromycin
2. Digoxin
3. Cetuximab
, 4. Rifampin
8. Carbamazepine has a Black Box Warning recommending testing for the
HLA-B*1502 allelein patients with Asian ancestry prior to starting
therapy due to:
ANATASHIA
1. Decreased effectiveness of carbamazepine in treating seizures in Asian patients wit
HLA-B*1502 allele
2. Increased risk for drug interactions in Asian patients with the HLA-B*1502 allele
3. Increased risk for Stevens-Johnson syndrome in Asian patients with HLA-B*1502 a
4. Patients who have the HLA-B*1502 allele being more likely to
have a resistance tocarbamazepine
9. A genetic variation in how the metabolite of the cancer drug
irinotecan SN-38 isinactivated by the body may lead to:
1. Decreased effectiveness of irinotecan in the treatment of cancer
2. Increased adverse drug reactions, such as neutropenia
3. Delayed metabolism of the prodrug irinotecan into the active metabolite SN-38
4. Increased concerns for irinotecan being carcinogenic
10. Patients who have a poor metabolism phenotype will have:
1. Slowed metabolism of a prodrug into an active drug, leading to accumulation of pr
2. Accumulation of inactive metabolites of drugs
3. A need for increased dosages of medications
4. Increased elimination of an active drug
11. Ultra-rapid metabolizers of drugs may have:
1. To have dosages of drugs adjusted downward to prevent drug accumulation
2. Active drug rapidly metabolized into inactive metabolites, leading
to potential therafailure
3. Increased elimination of active, nonmetabolized drug
4. Slowed metabolism of a prodrug into an active drug, leading to an accumulation of
12. A provider may consider testing for CYP2D6 variants prior to
starting tamoxifen forbreast cancer to:
1. Ensure the patient will not have increased adverse drug reactions to the tamoxifen
2. Identify potential drug-drug interactions that may occur with tamoxifen
3. Reduce the likelihood of therapeutic failure with tamoxifen treatment
4. Identify poor metabolizers of tamoxifen
, Chapter 1. An Introduction to
PharmacogeneticsAnswer Section
MULTIPLE CHOICE
1. ANS: 4 PTS: 1
2. ANS: 2 PTS: 1
3. ANS: 3 PTS: 1
4. ANS: 4 PTS: 1
5. ANS: 2 PTS: 1
6. ANS: 2 PTS: 1
7. ANS: 3 PTS: 1
8. ANS: 3 PTS: 1
9. ANS: 2 PTS: 1
10. 1 PTS: 1
ANS:
11. 2 PTS: 1
ANS:
12. 3 PTS: 1
ANS:
