NURS 5334 QUIZ 6: ANTIMYCOBACTERIAL THERAPEUTICS
(TUBERCULOSIS & LEPROSY) QUESTIONS AND CORRECT
ANSWERS PLUS RATIONALE NEW UPDATE 2026-2027 UTA
48 QUESTIONS
TABLE OF CONTENTS
# TOPIC
1 Differentiate first-line and second-line antitubercular agents by mechanism, activation requirements, and
resistance pathways
2 Construct and adjust multidrug regimens for drug-susceptible, drug-resistant, and latent tuberculosis
using current guidelines
3 Apply therapeutic drug monitoring and pharmacogenomic principles to optimize antimycobacterial efficacy
and minimize toxicity
4 Evaluate and manage clinically significant drug-drug interactions involving rifamycins and other
antimycobacterials
5 Distinguish leprosy treatment regimens and recognize and manage leprosy reactions and drug-specific
adverse effects
6 NURS 5334 Quiz 6
7 Antimycobacterial Therapeutics
8 Tuberculosis & Leprosy
9 Questions and Correct Answers plus Rationale New Update 2026
10 2027 UTA
11 Foundations of Antimycobacterial Therapeutics - Tuberculosis and Leprosy
12 Applied Antimycobacterial Therapeutics - Tuberculosis and Leprosy
13 Advanced Antimycobacterial Therapeutics - Tuberculosis and Leprosy
14 Antimycobacterial Therapeutics - Tuberculosis and Leprosy Review
ABSTRACT
Page 1
,This study document brings together 48 carefully worded exam questions drawn from NURS 5334
Quiz 6: Antimycobacterial Therapeutics (Tuberculosis & Leprosy) Questions and Correct Answers
plus Rationale New Update 2026-2027 UTA, with the strongest emphasis placed on Differentiate
first-line and second-line antitubercular agents by mechanism, activation requirements, and
resistance pathways, Construct and adjust multidrug regimens for drug-susceptible, drug-resistant,
and latent tuberculosis using current guidelines and Apply therapeutic drug monitoring and
pharmacogenomic principles to optimize antimycobacterial efficacy and minimize toxicity. Every
item follows the wording style and level of reasoning you meet in the real paper, and each one is
paired with a clear rationale so the correct choice is never a guess. Work through the set at your
own pace, mark the questions that slow you down, then come back to them until the reasoning
feels automatic. Learners who revise this way walk into the exam room recognising the pattern
behind the questions instead of meeting them for the first time. Keep going - steady, honest
practice is what turns a difficult paper into a comfortable pass.
Q1 DIFFERENTIATE FIRST-LINE AND SECOND-LINE ANTITUBERCULAR AGENTS BY
MECHANISM, ACTIVATION REQUIREMENTS, AND RESISTANCE PATHWAYS
A patient with HIV and latent tuberculosis is being started on a two-drug
short-course regimen. Which statement best explains why the regimen achieves
efficacy comparable to longer isoniazid monotherapy despite a shorter duration?
A. Rifapentine's long half-life permits weekly dosing that maintains bactericidal concentrations
sufficient to sterilize dormant bacilli.
B. Isoniazid and rifapentine are both prodrugs activated by mycobacterial catalase-peroxidase,
producing synergistic killing of persisters.
C. Rifapentine is a rifamycin that inhibits RNA polymerase, and its combination with isoniazid
targets both actively replicating and intermittent-metabolism bacilli. CORRECT
D. The combination induces efflux pump inhibition, preventing emergence of isoniazid
monoresistance.
RATIONALE: The 3HP regimen (isoniazid plus rifapentine weekly) is effective because
rifapentine's RNA polymerase inhibition complements isoniazid's inhibition of mycolic acid
synthesis, targeting both actively replicating and intermittently metabolizing bacilli. Option A is
incorrect because rifapentine's long half-life alone does not fully explain sterilization of dormant
organisms. Option B is wrong because rifapentine is not a prodrug. Option D describes a
mechanism not responsible for the regimen's efficacy.
Page 2
, Q2 DIFFERENTIATE FIRST-LINE AND SECOND-LINE ANTITUBERCULAR AGENTS BY
MECHANISM, ACTIVATION REQUIREMENTS, AND RESISTANCE PATHWAYS
A patient with multidrug-resistant tuberculosis is prescribed bedaquiline. Which
ECG finding would most strongly warrant discontinuation or modification of
therapy?
A. QTc prolongation to 480 ms with a prior history of syncope CORRECT
B. QTc prolongation to 450 ms without symptoms
C. New-onset atrial fibrillation with rapid ventricular response
D. Sinus bradycardia with heart rate of 52 beats/min
RATIONALE: Bedaquiline prolongs the QT interval, and a QTc exceeding 480 ms (or 500 ms in
some guidelines) with a history of syncope or arrhythmia significantly increases the risk of
torsades de pointes, warranting discontinuation or regimen change. Option B is less concerning
as 450 ms is below the threshold for high risk. Options C and D are not the primary ECG toxicity
associated with bedaquiline.
Q3 DIFFERENTIATE FIRST-LINE AND SECOND-LINE ANTITUBERCULAR AGENTS BY
MECHANISM, ACTIVATION REQUIREMENTS, AND RESISTANCE PATHWAYS
A patient on rifampin for tuberculosis develops reduced efficacy of their
antiretroviral therapy. Which mechanism best explains this interaction?
A. Rifampin inhibits CYP3A4, increasing antiretroviral levels and toxicity.
B. Rifampin induces CYP3A4 and P-glycoprotein, accelerating metabolism and efflux of protease
inhibitors and some integrase inhibitors. CORRECT
C. Rifampin chelates antiretrovirals in the gut, reducing absorption.
D. Rifampin displaces antiretrovirals from plasma protein binding sites, increasing clearance.
RATIONALE: Rifampin is a potent inducer of CYP3A4 and P-glycoprotein, which increases the
metabolism and efflux of many antiretrovirals (e.g., protease inhibitors, some integrase
inhibitors), reducing their plasma concentrations and efficacy. Option A is incorrect because
rifampin induces, not inhibits, CYP3A4. Option C is not a recognized mechanism. Option D is not
the primary mechanism for this interaction.
Page 3
(TUBERCULOSIS & LEPROSY) QUESTIONS AND CORRECT
ANSWERS PLUS RATIONALE NEW UPDATE 2026-2027 UTA
48 QUESTIONS
TABLE OF CONTENTS
# TOPIC
1 Differentiate first-line and second-line antitubercular agents by mechanism, activation requirements, and
resistance pathways
2 Construct and adjust multidrug regimens for drug-susceptible, drug-resistant, and latent tuberculosis
using current guidelines
3 Apply therapeutic drug monitoring and pharmacogenomic principles to optimize antimycobacterial efficacy
and minimize toxicity
4 Evaluate and manage clinically significant drug-drug interactions involving rifamycins and other
antimycobacterials
5 Distinguish leprosy treatment regimens and recognize and manage leprosy reactions and drug-specific
adverse effects
6 NURS 5334 Quiz 6
7 Antimycobacterial Therapeutics
8 Tuberculosis & Leprosy
9 Questions and Correct Answers plus Rationale New Update 2026
10 2027 UTA
11 Foundations of Antimycobacterial Therapeutics - Tuberculosis and Leprosy
12 Applied Antimycobacterial Therapeutics - Tuberculosis and Leprosy
13 Advanced Antimycobacterial Therapeutics - Tuberculosis and Leprosy
14 Antimycobacterial Therapeutics - Tuberculosis and Leprosy Review
ABSTRACT
Page 1
,This study document brings together 48 carefully worded exam questions drawn from NURS 5334
Quiz 6: Antimycobacterial Therapeutics (Tuberculosis & Leprosy) Questions and Correct Answers
plus Rationale New Update 2026-2027 UTA, with the strongest emphasis placed on Differentiate
first-line and second-line antitubercular agents by mechanism, activation requirements, and
resistance pathways, Construct and adjust multidrug regimens for drug-susceptible, drug-resistant,
and latent tuberculosis using current guidelines and Apply therapeutic drug monitoring and
pharmacogenomic principles to optimize antimycobacterial efficacy and minimize toxicity. Every
item follows the wording style and level of reasoning you meet in the real paper, and each one is
paired with a clear rationale so the correct choice is never a guess. Work through the set at your
own pace, mark the questions that slow you down, then come back to them until the reasoning
feels automatic. Learners who revise this way walk into the exam room recognising the pattern
behind the questions instead of meeting them for the first time. Keep going - steady, honest
practice is what turns a difficult paper into a comfortable pass.
Q1 DIFFERENTIATE FIRST-LINE AND SECOND-LINE ANTITUBERCULAR AGENTS BY
MECHANISM, ACTIVATION REQUIREMENTS, AND RESISTANCE PATHWAYS
A patient with HIV and latent tuberculosis is being started on a two-drug
short-course regimen. Which statement best explains why the regimen achieves
efficacy comparable to longer isoniazid monotherapy despite a shorter duration?
A. Rifapentine's long half-life permits weekly dosing that maintains bactericidal concentrations
sufficient to sterilize dormant bacilli.
B. Isoniazid and rifapentine are both prodrugs activated by mycobacterial catalase-peroxidase,
producing synergistic killing of persisters.
C. Rifapentine is a rifamycin that inhibits RNA polymerase, and its combination with isoniazid
targets both actively replicating and intermittent-metabolism bacilli. CORRECT
D. The combination induces efflux pump inhibition, preventing emergence of isoniazid
monoresistance.
RATIONALE: The 3HP regimen (isoniazid plus rifapentine weekly) is effective because
rifapentine's RNA polymerase inhibition complements isoniazid's inhibition of mycolic acid
synthesis, targeting both actively replicating and intermittently metabolizing bacilli. Option A is
incorrect because rifapentine's long half-life alone does not fully explain sterilization of dormant
organisms. Option B is wrong because rifapentine is not a prodrug. Option D describes a
mechanism not responsible for the regimen's efficacy.
Page 2
, Q2 DIFFERENTIATE FIRST-LINE AND SECOND-LINE ANTITUBERCULAR AGENTS BY
MECHANISM, ACTIVATION REQUIREMENTS, AND RESISTANCE PATHWAYS
A patient with multidrug-resistant tuberculosis is prescribed bedaquiline. Which
ECG finding would most strongly warrant discontinuation or modification of
therapy?
A. QTc prolongation to 480 ms with a prior history of syncope CORRECT
B. QTc prolongation to 450 ms without symptoms
C. New-onset atrial fibrillation with rapid ventricular response
D. Sinus bradycardia with heart rate of 52 beats/min
RATIONALE: Bedaquiline prolongs the QT interval, and a QTc exceeding 480 ms (or 500 ms in
some guidelines) with a history of syncope or arrhythmia significantly increases the risk of
torsades de pointes, warranting discontinuation or regimen change. Option B is less concerning
as 450 ms is below the threshold for high risk. Options C and D are not the primary ECG toxicity
associated with bedaquiline.
Q3 DIFFERENTIATE FIRST-LINE AND SECOND-LINE ANTITUBERCULAR AGENTS BY
MECHANISM, ACTIVATION REQUIREMENTS, AND RESISTANCE PATHWAYS
A patient on rifampin for tuberculosis develops reduced efficacy of their
antiretroviral therapy. Which mechanism best explains this interaction?
A. Rifampin inhibits CYP3A4, increasing antiretroviral levels and toxicity.
B. Rifampin induces CYP3A4 and P-glycoprotein, accelerating metabolism and efflux of protease
inhibitors and some integrase inhibitors. CORRECT
C. Rifampin chelates antiretrovirals in the gut, reducing absorption.
D. Rifampin displaces antiretrovirals from plasma protein binding sites, increasing clearance.
RATIONALE: Rifampin is a potent inducer of CYP3A4 and P-glycoprotein, which increases the
metabolism and efflux of many antiretrovirals (e.g., protease inhibitors, some integrase
inhibitors), reducing their plasma concentrations and efficacy. Option A is incorrect because
rifampin induces, not inhibits, CYP3A4. Option C is not a recognized mechanism. Option D is not
the primary mechanism for this interaction.
Page 3
