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ANATASHIA
Chapter 1.
An Introduction to Pharmacogenetics
Multiple Choice
Identify the choice tha bes completes the statemen or answers the question. J J J
1. Genetic polymorphisms account for differences in metabolism, including: J J J J J J
1. Poor metabolizers, wholacka working enzyme
J J J J J J
2. Intermediate metabolizers, who have one working, wild-type allele and one mutant J J J J J J J J J J
3. Extensive metabolizers, withtwo normally functioning alleles J J J J J J
4. All of the above
J J J
J 2. Up to 21% of Asians are ultra-rapid 2D6 metabolizers, leading to:
J J J J J J J J J J J
1. A need to monitor drugs metabolized by 2D6 for toxicity
J J J J J J J J J
2. Increased dosages needed of drugs metabolized by 2D6, suchas the J J J J J J J J J J JJ
selective serotoreuptake inhibitors J J
3. Decreased conversion of codeine tomorphine by CYP 2D6 J J J J J J J J
4. The need for lowered dosages of drugs, suchas beta blockers
J J J J J J J J J J
J 3. Rifampin is a nonspecific CYP450 inducer that may:
J J J J J J J J
1. Lead to toxic levels of rifampin and must be monitored closely
J J J J J J J J J J
2. Cause toxic levels of drugs, suchas oral contraceptives, whencoadministered
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3. Induce the metabolism of drugs, suchas oral contraceptives, leading totherapeutic
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4. Cause nonspecific changes indrug metabolism
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J 4. Inhibition of P-glycoprotein by a drug such as quinidine may lead to:
J J J J J J J J J J J J
1. Decreasedtherapeutic levels of quinidine J J J J
2. Increased therapeutic levels of quinidine J J J J
3. Decreased levels of a coadministered drug, suchas digoxin, that J J J J J J J J J J
requires P-glycoprabsorption and elimination J J J
4. Increased levels of a coadministered drug, such as digoxin, that J J J J J J J J J JJ
requires P-glycoproabsorption and elimination J J J
J 5. Warfarin resistance may be seen in patients with VCORC1 mutation, leading to:
J J J J J J J J J J J J
1. Toxic levels of warfarinbuilding up
J J J J J
, 2. Decreased response to warfarin J J J
3. Increased riskfor significant drug interactions with warfarin
J J J J J J J
4. Less riskof drug interactions with warfarin
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J 6. Genetic testing for VCORC1 mutation to assess potential warfarin
J J J J J J J J J J
resistance is requiredprior to prescribing warfarin.
J J J J J
1. True
2. False
J 7. Pharmacogenetic testing is required by the U.S. Food and Drug
J J J J J J J J J J J
Administration prior toprescribing: J J
1. Erythromycin
2. Digoxin
3. Cetuximab
4. Rifampin
J 8. Carbamazepine has a BlackBoxWarning recommending testing for the
J J J J J J J J J J J
HLA-B*1502 allelein patients with Asian ancestry prior to starting
J J J J J J J J J
therapy due to:
ATASHIA
J J
1. Decreased effectiveness of carbamazepine intreating seizures in Asian patients wit
J J J J J J J J J J J
HLA-B*1502 allele J
2. Increased riskfor drug interactions in Asian patients with the HLA-B*1502 allele
J J J J J J J J J J J
3. Increased riskfor Stevens-Johnson syndrome in Asianpatients with HLA-B*1502 a
J J J J J J J J J J
4. Patients who have the HLA-B*1502 allele being more likely to
J J J J J J J J J J
have a resistance tocarbamazepine
J J J
J 9. Agenetic variationin how the metabolite of the cancer drug
J J J J J J J J J J J J
irinotecan SN-38 isinactivated by the body may lead to:
J J J J J J J J
1. Decreased effectiveness of irinotecanin the treatment of cancer J J J J J J J J
2. Increased adverse drug reactions, suchas neutropenia J J J J J J
3. Delayed metabolism of the prodrug irinotecanintothe active metabolite SN-38
J J J J J J J J J J
4. Increasedconcerns for irinotecanbeing carcinogenic J J J J J
10. Patients who have a poor metabolism phenotype will have:
J J J J J J J J J J
1. Slowed metabolism of a prodrug intoan active drug, leading toaccumulation of pr
J J J J J J J J J J J J J
2. Accumulation of inactive metabolites of drugs J J J J J
3. A needfor increased dosages of medications
J J J J J J
4. Increased elimination of anactive drug J J J J J
11. Ultra-rapid metabolizers of drugs may have:
J J J J J J J
, 1. To have dosages of drugs adjusted downward toprevent drug accumulation
J J J J J J J J J J
2. Active drug rapidly metabolized intoinactive metabolites, leading to
J J J J J J J JJ J
potential therafailure J
3. Increasedelimination of active, nonmetabolized drug
J J J J J
4. Slowed metabolism of a prodrug into anactive drug, leading to anaccumulation of
J J J J J J J J J J J J J
12. A provider may consider testing for CYP2D6 variants prior to
J J J J J J J J J J J J
starting tamoxifen forbreast cancer to:
J J J J
1. Ensure the patient will not have increased adverse drug reactions to the tamoxifen
J J J J J J J J J J J J
2. Identify potential drug-drug interactions that may occur withtamoxifen
J J J J J J J J
3. Reduce the likelihood of therapeutic failure with tamoxifentreatment
J J J J J J J J
4. Identify poor metabolizers of tamoxifen
J J J J
, Chapter 1. An Introduction to
J J J J J
PharmacogeneticsAnswerSection
J
MULTIPLECHOICE J
1. ANS:
J 4 PTS: 1
2. ANS:
J 2 PTS: 1
3. ANS:
J 3 PTS: 1
4. ANS:
J 4 PTS: 1
5. ANS:
J 2 PTS: 1
6. ANS:
J 2 PTS: 1
7. ANS:
J 3 PTS: 1
8. ANS:
J 3 PTS: 1
9. ANS:
J 2 PTS: 1
10. 1 PTS: 1
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11. 2 PTS: 1
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12. 3 PTS: 1
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