Practice questions written for this chapter. These are not past NMC papers.
π About these questions: These are practice questions written to test the reasoning in this chapter. They are NOT reproduced from any past Nepal Medical Council examination, and no verified past NMC questions were supplied for this chapter.
Level 1β2 β recall and understanding
Q1. Which antituberculous drug causes optic neuritis?
A. Rifampicin B. Isoniazid
C. Pyrazinamide D. Ethambutol
ANSWER: D β Ethambutol.
Why: it causes dose-related optic neuritis affecting acuity
and colour discrimination. "E for Eyes."
A: orange body fluids and hepatitis.
B: peripheral neuropathy.
C: hyperuricaemia and hepatitis.
LEARNING POINT: each first-line drug has one defining
toxicity; know which nerve or organ each targets.
Q2. Why is pyridoxine given alongside isoniazid?
A. To improve absorption
B. To prevent peripheral neuropathy
C. To prevent optic neuritis
D. To reduce hepatotoxicity
ANSWER: B β to prevent peripheral neuropathy.
Why: isoniazid interferes with pyridoxine (vitamin B6)
metabolism, and the resulting deficiency causes peripheral
neuropathy. Supplementation prevents it.
C: that is ethambutol's toxicity, and pyridoxine does not
prevent it.
LEARNING POINT: routine in malnutrition, pregnancy, alcohol
dependence, diabetes, HIV and CKD.
Level 3β4 β application and clinical reasoning
Q3. An asymptomatic 28-year-old has a positive IGRA on
pre-employment screening. Chest X-ray is normal.
The correct management is:
A. Full RIPE therapy for 6 months
B. Exclude active disease, then offer preventive therapy
C. No action β the test is a false positive
D. Repeat the IGRA in one year
ANSWER: B.
Why: a positive IGRA indicates infection. With no symptoms
and a normal film, this is LATENT TB, treated with preventive
therapy rather than a full multi-drug regimen.
A: over-treatment for latent infection.
C: BCG does not cause a false positive IGRA.
LEARNING POINT: the test proves infection, not disease.
Q4. A patient with HIV starts antiretrovirals three weeks
into TB treatment. Two weeks later fever and
lymphadenopathy worsen, but TB cultures show a good
response. The most likely explanation is:
A. Treatment failure
B. MDR-TB
C. Immune reconstitution inflammatory syndrome
D. Drug-induced fever from rifampicin
ANSWER: C β IRIS.
Why: as antiretrovirals restore immune function, the
recovering immune system reacts vigorously to residual
mycobacterial antigen, producing paradoxical worsening
despite genuine microbiological improvement.
A, B: contradicted by the good culture response.
LEARNING POINT: IRIS signals immunity returning. Continue
both treatments; do not stop.
Q5. A patient with a three-week cough, night sweats and
weight loss has a NEGATIVE sputum smear. The correct
next step is:
A. Exclude TB and treat as pneumonia
B. Send for molecular testing and culture, and treat on
clinical suspicion if indicated
C. Repeat the smear in three months
D. Start RIPE only if a second smear is positive
ANSWER: B.
Why: smear microscopy has limited sensitivity and requires a
high bacillary load, so a negative result cannot exclude TB
in a clinically compatible case. Molecular testing gives a
rapid answer including rifampicin resistance.
A: the dangerous conclusion this question targets.
LEARNING POINT: a negative smear never excludes TB.
Level 5 β exception-based
Q6. A woman on the combined oral contraceptive pill starts
TB treatment. The most important counselling point is:
A. The pill will work normally
B. Rifampicin induces CYP450 and reduces contraceptive
efficacy β use an alternative method
C. Isoniazid inactivates the pill
D. She should stop the pill permanently
ANSWER: B β rifampicin is an enzyme INDUCER.
Why: it accelerates metabolism of oestrogen and progestogen,
so contraceptive efficacy falls and pregnancy can occur.
Alternative or additional contraception is needed.
C: isoniazid is an enzyme INHIBITOR, not an inducer, and
is not the issue here.
LEARNING POINT: rifampicin interacts with a long list of
drugs β always check what else the patient takes.
Q7. Why is tuberculosis treated with four drugs
simultaneously rather than one?
A. Four drugs kill faster than one
B. To prevent selection of spontaneously resistant
mutants
C. Because each drug treats a different organ
D. To shorten treatment to two weeks
ANSWER: B β to prevent resistance.
Why: mutations conferring resistance to any single drug arise
naturally in a large bacillary population. Monotherapy simply
selects for them. Simultaneous resistance to four unrelated
drugs is vanishingly rare.
A: potency is not the primary reason.
D: treatment still takes months.
LEARNING POINT: combination therapy denies resistance a
foothold β and interrupted treatment reopens that door,
which is how MDR-TB arises.
Syllabus points
Recall and understanding questions
Application and clinical reasoning questions
Exception-based questions
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