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:
ATASHIA
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:
ATASHIA
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:
