Anti-Mycobacterial Drugs (Anti-TB, Anti-Leprosy) MCQs

Pharmacology · 82 free questions with answers & explanations.

1. A patient on anti-TB therapy (RHEZ regimen) develops orange discoloration of urine and tears. Which drug is responsible, and why is this finding clinically important to counsel the patient about?
2. In multibacillary leprosy, clofazimine contributes to the MDT regimen. Its anti-mycobacterial mechanism and a significant adverse effect are:
3. Bedaquiline, approved for MDR-TB, has a unique mechanism of action. Which target does it inhibit?
4. A patient on isoniazid develops peripheral neuropathy. The pharmacogenomic basis and the specific metabolic pathway involved are:
5. Pyrazinamide is uniquely active against semi-dormant intracellular bacilli in acidic environments. Its mechanism of action requires bacterial pyrazinamidase (PZase). In drug-resistant TB, PZase-encoding gene mutations most frequently occur in:
6. Bedaquiline, a first-in-class drug for MDR-TB, acts by a mechanism distinct from all older anti-TB drugs. Its target is:
7. Bedaquiline is used in MDR-TB regimens. Its unique mechanism targets which bacterial component?
8. In a patient on rifampicin for TB who is also taking combined OCP for contraception, failure of contraception can occur. The molecular mechanism is:
9. Bedaquiline, approved for multidrug-resistant tuberculosis, exerts bactericidal activity through a unique target. Which molecular target does it inhibit?
10. Isoniazid resistance in M. tuberculosis most commonly arises from mutations in which gene, and what is the consequence of this mutation?
11. Clofazimine's bactericidal effect against M. leprae involves generation of reactive oxygen species. The mechanism involves which electron transfer pathway?
12. Bedaquiline is the first new anti-TB drug in 40 years and is used in multidrug-resistant TB (MDR-TB). Its mechanism differs from all existing first- and second-line drugs. It inhibits:
13. A patient on rifampicin for TB develops sub-therapeutic levels of oral contraceptive pills and becomes pregnant. The mechanism of this drug interaction is:
14. A patient with MDR-TB is started on pretomanid (Pa) as part of the BPaL regimen. Pretomanid's mechanism of action against M. tuberculosis involves:
15. Isoniazid resistance in M. tuberculosis most commonly results from mutation in katG (catalase-peroxidase). This means INH resistance arises because:
16. Pretomanid, used in the BPaL regimen for XDR-TB, has a novel mechanism. Which statement best describes its mechanism and why it is effective against non-replicating (dormant) mycobacteria?
17. A patient with drug-resistant leprosy is found to have a mutation in the folP1 gene of M. leprae. Which anti-leprosy drug does this resistance affect, and what is the mechanism?
18. Bedaquiline is a diarylquinoline approved for drug-resistant TB. Its novel mechanism targets which mycobacterial component, and what is the key black-box warning that mandates ECG monitoring?
19. The mechanism of pyrazinamide (PZA) resistance in Mycobacterium tuberculosis most commonly involves mutations in which gene, and why does PZA have NO activity at neutral pH in vitro?
20. Bedaquiline is active against drug-resistant TB because its target is unique among anti-TB drugs. It inhibits:
21. Pyrazinamide has activity exclusively against Mycobacterium tuberculosis and not against other mycobacteria because of a species-specific mechanism. Resistance occurs when:
22. Bedaquiline (BDQ) is used in drug-resistant TB. Its mechanism of action is unique among anti-TB drugs because it:
23. A patient completes 6 months of RHEZ therapy for drug-sensitive TB. Monitoring for adverse effects at month 2 reveals asymptomatic elevated ALT (3× ULN). The correct management is:
24. Bedaquiline, a WHO Group B drug for MDR-TB, has a novel mechanism of action. Which statement correctly describes it?
25. In leprosy, the mechanism of dapsone resistance involves mutations that lead to overproduction of which enzyme, allowing competitive displacement of dapsone?
26. Bedaquiline is a novel anti-TB drug effective against MDR-TB. Its target is distinct from all traditional anti-TB drugs. What is its mechanism?
27. Delamanid, another novel anti-TB drug for MDR-TB, inhibits methoxy-mycolic acid and keto-mycolic acid synthesis. What is the activated intermediate responsible for its bactericidal effect?
28. A patient on anti-TB therapy develops peripheral neuropathy. The biochemical mechanism of isoniazid-induced neuropathy is:
29. Rifampicin resistance in M. tuberculosis most commonly results from a point mutation in the gene encoding:
30. Bedaquiline, a newer anti-TB drug used in MDR-TB, acts by inhibiting:
31. Pretomanid, used in the BPaL regimen for extensively drug-resistant TB, is a nitroimidazole that acts by a mechanism involving:
32. In a patient with pulmonary TB, the sputum smear converts to negative after 2 months of HRZE therapy. This early bactericidal activity (EBA) is primarily attributable to which drug's activity against the rapidly dividing bacilli population?
33. Bedaquiline, approved for MDR-TB, exerts its bactericidal activity by inhibiting:
34. A leprosy patient on dapsone monotherapy develops haemolytic anaemia and methaemoglobinaemia more severely than expected. The most likely explanation is:
35. Isoniazid prophylaxis (IPT) is given to a child who is a close contact of an active TB case. The child has a positive Mantoux test (>10 mm) but a normal chest X-ray. After 6 months of isoniazid, the mechanism by which latent TB infection is prevented from progressing is:
36. Isoniazid (INH) causes peripheral neuropathy as a dose-related adverse effect. The mechanism is:
37. Dapsone is used in multi-drug therapy for leprosy. Its mechanism of action is similar to which antibiotic class?
38. Bedaquiline is a new anti-TB drug used for MDR-TB. Its mechanism of action is unique because it targets:
39. In a tuberculosis patient treated with rifampicin, the plasma levels of warfarin fall dramatically within a week of starting anti-TB treatment. What is the mechanism?
40. Isoniazid (INH) requires activation by the mycobacterial enzyme KatG (catalase-peroxidase). The active intermediate then inhibits which mycobacterial enzyme?
41. Pyrazinamide (PZA) is uniquely active against tubercle bacilli in which microenvironment, explaining its irreplaceable role in the intensive phase of TB therapy?
42. Rifampicin causes a harmless red-orange discolouration of urine, tears, and saliva. More importantly, it is a potent enzyme inducer. Which enzyme system does it primarily induce, and what is the clinical consequence for oral contraceptive users?
43. In multi-bacillary leprosy, dapsone is used as part of WHO-MDT regimen. The mechanism of action of dapsone is:
44. Pyrazinamide (PZA) is a key sterilising drug in TB treatment but is only active in an acidic environment. This is because:
45. Dapsone is used in multibacillary leprosy and as prophylaxis in Pneumocystis jirovecii pneumonia. Its mechanism of action is:
46. Bedaquiline is a novel anti-TB drug approved for MDR-TB. Its mechanism, unique among anti-TB drugs, is:
47. Pyrazinamide is only active at acidic pH (pH 5.0–5.5) and is particularly effective against dormant intracellular mycobacteria. The reason for pH dependence is:
48. Dapsone is used in leprosy and also in Pneumocystis jirovecii pneumonia (PCP) prophylaxis. The common mechanism for both indications is:
49. A patient on rifampicin-based anti-TB therapy is also on warfarin for a prosthetic heart valve. After two weeks of starting rifampicin, his INR drops from 2.8 to 1.3 despite unchanged warfarin dose. The mechanism is:
50. A leprosy patient develops erythema nodosum leprosum (ENL, Type 2 lepra reaction). The drug of choice for managing severe ENL is thalidomide. Its mechanism in ENL involves:
51. Bedaquiline, a newer anti-TB drug for MDR-TB, has a unique mechanism of action compared to all traditional anti-TB agents. It targets:
52. Clofazimine, used in multidrug regimens for leprosy and MDR-TB, exerts its antimycobacterial effect through which primary mechanism?
53. Pyrazinamide is a crucial component of the short-course anti-TB regimen. Its activity is unique because it:
54. A leprosy patient on WHO multidrug therapy develops acute haemolytic anaemia and methaemoglobinaemia. The drug most likely responsible is:
55. Bedaquiline (Sirturo) is a novel anti-TB drug used in MDR/XDR-TB. Its unique mechanism of action targets:
56. Isoniazid (INH) requires activation by mycobacterial catalase-peroxidase (KatG). The final toxic intracellular target and mechanism of bactericidal action of activated INH is:
57. A patient on multidrug therapy for leprosy (WHO MDT) develops sudden onset acute inflammation in old leprosy lesions with fever and nerve pain. This is a Type 1 (reversal) reaction. The appropriate pharmacological management is:
58. A 30-year-old man develops peripheral neuropathy on isoniazid therapy. The MECHANISM of this toxicity and its prevention:
59. A patient with rifampicin-resistant tuberculosis is started on a regimen containing bedaquiline. The mechanism of bedaquiline is:
60. A patient with multibacillary leprosy is started on WHO MDT. Which drug in the regimen is responsible for the lepromatous reaction known as Lucio phenomenon?
61. Pyrazinamide is a first-line anti-TB drug that is particularly active against which mycobacterial population and under which condition?
62. In multi-bacillary leprosy (MB), dapsone is combined with rifampicin and clofazimine in the WHO MDT regimen. Which unique mechanism does clofazimine employ to exert its anti-mycobacterial effect?
63. Pyrazinamide is uniquely active in killing dormant, semi-dormant bacilli in acidic environments (e.g., within macrophages). Its mechanism requires:
64. A patient with leprosy develops reversal reaction (Type 1 lepra reaction) during multidrug therapy. The correct management is:
65. Bedaquiline, approved for MDR-TB, is a novel agent that acts by:
66. Pyrazinamide is most active at acidic pH and kills intracellular mycobacteria. Its mechanism of action after conversion to pyrazinoic acid involves inhibition of which target?
67. A patient with multibacillary leprosy is started on WHO-recommended multidrug therapy. Which statement about the role of clofazimine in this regimen is CORRECT?
68. Pyrazinamide (PZA) is uniquely active against intracellular, 'dormant' mycobacteria in acidic macrophage phagolysosomes but inactive at neutral pH. This is because:
69. In multibacillary leprosy, clofazimine exerts its antimycobacterial and anti-inflammatory effects by:
70. A patient on standard anti-TB therapy (HRZE) develops optic neuritis with loss of red-green colour discrimination. The drug responsible and the mechanism of toxicity is:
71. Clofazimine, used in multibacillary leprosy and MDR-TB regimens, has an additional anti-inflammatory mechanism relevant to type 2 lepra reactions. This mechanism is:
72. Rifampicin resistance in M. tuberculosis results from mutations in the rpoB gene. Rifampicin binds to the beta subunit of RNA polymerase. Which statement correctly explains how the specific rpoB mutation at codon 531 (Ser531Leu) confers resistance without impairing mycobacterial fitness?
73. Bedaquiline is a novel anti-TB drug used for MDR-TB and XDR-TB. It has a unique mechanism unlike any existing anti-TB agent. What is this mechanism?
74. Bedaquiline (Sirturo) is approved for MDR-TB and XDR-TB. Its novel mechanism of action, distinct from all existing anti-TB drugs, is:
75. Pyrazinamide is uniquely active in acidic environments (within macrophage phagolysosomes). Its mechanism depends on conversion to pyrazinoic acid by pyrazinamidase (PncA enzyme). Resistance is most commonly caused by:
76. Isoniazid (INH) is a prodrug requiring mycobacterial activation. Which enzyme activates INH and what is the primary target of the activated form?
77. Bedaquiline, approved for drug-resistant tuberculosis, is unique because it targets:
78. Rifampicin is a potent enzyme inducer. Which of the following drug interactions is MOST clinically critical in TB/HIV co-infection?
79. Bedaquiline is used in extensively drug-resistant TB. Its mechanism of action is:
80. A patient on rifampicin-based anti-TB therapy is started on an oral contraceptive. The pharmacokinetic interaction most likely to occur is:
81. Rifampicin resistance in Mycobacterium tuberculosis is clinically used as a proxy marker for MDR-TB. The molecular basis for rifampicin resistance is:
82. Clofazimine, used in multibacillary leprosy and MDR-TB regimens, exerts its antimycobacterial effect through which mechanism?