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PH9.1-7 | Miscellaneous Therapeutics — Practice Quiz
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A renal transplant recipient on cyclosporine develops oropharyngeal candidiasis and is started on fluconazole. Which pharmacokinetic consequence is MOST expected?
Correct. Fluconazole inhibits CYP3A4, slowing cyclosporine metabolism and raising its blood level — a clinically significant interaction requiring dose adjustment and TDM.
Cyclosporine is a narrow-therapeutic-index CYP3A4 substrate. Fluconazole is a potent CYP3A4/CYP2C19 inhibitor. Co-administration raises cyclosporine levels, risking nephrotoxicity. Close TDM and dose reduction are required.
Incorrect. Fluconazole is a CYP3A4 inhibitor (not inducer), and cyclosporine IS metabolised by CYP3A4. The net effect is increased cyclosporine exposure.
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A 28-year-old farmer presents with profuse sweating, miosis, bradycardia, muscle fasciculations, and copious bronchial secretions after spraying pesticide. The FIRST priority antidote is:
Correct. Atropine is the life-saving first step — it competes at muscarinic receptors to dry secretions and prevent bronchospasm. Pralidoxime follows to reactivate the enzyme. The common error is stopping atropine when heart rate rises rather than when secretions dry.
Organophosphate poisoning produces a cholinergic toxidrome. Atropine (antimuscarinic) rapidly dries secretions and prevents death from bronchospasm/secretions. Pralidoxime reactivates acetylcholinesterase but must be given early (before irreversible ageing). Atropine endpoint: drying of secretions, NOT heart rate.
Incorrect. This is organophosphate poisoning (SLUDGE + fasciculations). Atropine must come first to control the life-threatening muscarinic effects; NAC treats paracetamol toxicity; naloxone reverses opioids.
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A child is brought with acute iron poisoning (ingested iron tablets). After gastric decontamination, chelation is indicated. The drug of choice for acute iron poisoning is:
Correct. Deferoxamine is the only approved chelator for acute iron poisoning. It forms a stable complex (ferrioxamine) excreted in urine, which turns characteristic vin rosé in significant poisoning.
Iron-specific chelation: deferoxamine chelates free iron via hydroxamate groups, forming ferrioxamine which is renally excreted (urine turns vin rosé — a useful clinical sign). BAL is contraindicated in iron poisoning (worsens toxicity). DMSA and D-penicillamine are used for lead and copper respectively.
Incorrect. Deferoxamine is the drug of choice for iron poisoning. BAL is actually contraindicated in iron toxicity.
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A patient with lead encephalopathy needs chelation. Which is the CORRECT sequence?
Correct. This is the established protocol for lead encephalopathy. BAL penetrates the CNS, lowers brain lead, then EDTA is started 4 hours later to enhance systemic excretion without the risk of EDTA-induced CSF lead surge.
The '4-hour BAL-before-EDTA' rule: In lead encephalopathy, CaNa₂EDTA alone mobilises lead into the CSF and can worsen encephalopathy. BAL (which is lipid-soluble and CNS-penetrant) is given first to lower brain lead burden; EDTA is added 4 hours later for systemic chelation. DMSA is not used for encephalopathy.
Incorrect. Starting EDTA alone or skipping BAL in encephalopathy can worsen the neurological picture by mobilising lead into the CSF.
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For pre-operative hand antisepsis, which agent provides the BEST persistent (residual) antimicrobial activity after a single application?
Correct. Chlorhexidine's covalent binding to skin proteins gives it prolonged residual activity (up to 6 hours), making it the gold standard for surgical hand antisepsis and central-line care.
Chlorhexidine binds covalently to skin proteins and keratinocytes, providing 6-hour residual (persistent) bacteriostatic activity. Alcohol is rapidly bactericidal but has NO residual activity (evaporates). Povidone-iodine has minimal residual activity. Chlorhexidine is therefore preferred for surgical hand antisepsis and catheter care.
Incorrect. Chlorhexidine is distinctive for its persistent (residual) activity due to protein binding. Alcohols have no residual effect.
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A 17-year-old male with severe nodulocystic acne is started on isotretinoin. Which MANDATORY monitoring/counselling point applies SPECIFICALLY to isotretinoin (not other acne drugs)?
Correct. Teratogenicity is the defining safety concern with isotretinoin — it causes severe craniofacial, cardiac, and CNS malformations. Strict pregnancy prevention protocols are mandatory worldwide.
Isotretinoin is a potent teratogen (Category X). In countries following iPLEDGE-equivalent protocols, pregnancy must be excluded before starting and monthly during treatment; two contraception methods are mandatory for childbearing-age patients. It also causes dyslipidaemia (monitor LFT/lipids), mucocutaneous dryness, and rarely pseudotumour cerebri. CBC monitoring is not specifically required. It does not cause photosensitisation (doxycycline does). The dose is 0.5–1 mg/kg/day until cumulative dose 120–150 mg/kg.
Incorrect. The hallmark isotretinoin-specific concern is teratogenicity. Mandatory pregnancy exclusion and dual contraception are non-negotiable.
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Methotrexate is prescribed for a 45-year-old woman with plaque psoriasis. The CORRECT dosing frequency is:
Correct. Once-weekly dosing is non-negotiable for methotrexate in psoriasis. Daily dosing has caused patient deaths from bone marrow suppression. This 'clinical pearl' from the SDL must be remembered and communicated to every patient.
Methotrexate for psoriasis (and rheumatoid arthritis) is ALWAYS dosed ONCE A WEEK (7.5–25 mg orally or SC). Daily dosing causes fatal bone marrow suppression and mucositis — this is the most dangerous dosing error in dermatology and rheumatology. The once-weekly dose allows normal cells to recover between doses while affecting rapidly dividing keratinocytes. Leucovorin rescue is used if overdose occurs.
Incorrect. Methotrexate for inflammatory indications (psoriasis, RA) is ALWAYS once weekly. Daily dosing causes life-threatening haematological and mucosal toxicity.
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A 62-year-old man presents with gradual loss of peripheral vision. Slit-lamp examination reveals increased intraocular pressure (IOP). He is started on latanoprost eye drops. What is the mechanism?
Correct. Latanoprost is a prostaglandin F₂α analogue (FP receptor agonist) that enhances uveoscleral outflow — the non-trabecular pathway. It is the first-line choice for open-angle glaucoma given its potency and once-daily dosing.
Prostaglandin analogues (latanoprost, bimatoprost, travoprost) are the most potent single-agent IOP-lowering drugs (25–35% reduction). They act on FP receptors in the ciliary body to remodel the extracellular matrix, increasing uveoscleral (unconventional) outflow. They are given once daily in the evening and do NOT reduce aqueous production. Main ADRs: iris hyperpigmentation, eyelash elongation, periorbital fat atrophy.
Incorrect. Latanoprost is a prostaglandin analogue that INCREASES outflow (uveoscleral route), not reduces production. CAIs reduce production; beta-blockers reduce production; alpha-2 agonists primarily reduce production.
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A child presents for vaccination. The paediatrician wants to give BCG vaccine. Which statement about BCG is CORRECT?
Correct. BCG is a live attenuated vaccine. Administering a live vaccine to a severely immunocompromised patient risks disseminated BCG disease (BCGosis). WHO advises withholding BCG in HIV-positive infants with symptomatic disease or CD4 <25%.
BCG (Bacille Calmette-Guérin) is a live attenuated mycobacterial vaccine. Like all live vaccines, it is contraindicated in severe immunocompromise (HIV with CD4 <200, primary immunodeficiency, on immunosuppressants). BCG does not prevent primary TB infection but reduces severe forms (miliary TB, TB meningitis) in children by 70–80%. Route: intradermal (NOT SC/IM) at the left deltoid region.
Incorrect. BCG is a live attenuated vaccine (not inactivated). Live vaccines carry risk of disease in immunocompromised patients.
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A patient receiving N-acetylcysteine (NAC) for paracetamol poisoning should ideally receive it within what timeframe from ingestion for maximum hepatoprotection?
Correct. NAC within 8–10 hours prevents hepatotoxicity almost completely. Referral and treatment should not be delayed — the nomogram is used to guide threshold decisions.
NAC is most effective when given within 8–10 hours of paracetamol ingestion (before NAPQI overwhelms remaining glutathione). It works by replenishing glutathione stores, allowing conjugation and detoxification of NAPQI. The Rumack-Matthew nomogram guides treatment decisions. After 10 hours, NAC is still beneficial but hepatoprotection decreases. After 24 hours, it may still reduce fulminant hepatic failure risk but cannot fully prevent established hepatocellular injury.
Incorrect. The critical window for NAC efficacy is within 8–10 hours. Within 2 hours, gastric decontamination (activated charcoal) may still be useful, but NAC's peak hepatoprotection window is 8–10 hours post-ingestion.
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