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Pharmacology · Toxicology: paraquat
Sample itemA 20-year-old man swallowed a herbicide. He has oral mucosal ulceration and then renal failure, and 10 days later progressive breathlessness with hypoxaemia and fibrosis on imaging. Which mechanism explains the lung injury?
Original practice item, not a recalled exam question. Nothing here is recorded.
The answer and the reasoning
A. Redox cycling that generates reactive oxygen species in alveolar type II cells
Paraquat is actively taken up by alveolar type I and II cells and undergoes cyclic reduction and re-oxidation, producing superoxide radicals and depleting NADPH, which causes lipid peroxidation and progressive pulmonary fibrosis. High oxygen concentrations increase the injury, so oxygen is withheld unless hypoxia is severe. There is no specific antidote, and early gut decontamination is vital.
Option by option
A. Redox cycling that generates reactive oxygen species in alveolar type II cells (correct)
Redox cycling generates free radicals that damage pneumocytes and cause fibrosis.
B. Binding to haemoglobin to form carboxyhaemoglobin
Carboxyhaemoglobin forms in carbon monoxide poisoning.
C. Release of cyanide in the lung
Cyanide release is not part of paraquat toxicity.
D. Inhibition of acetylcholinesterase in the lung
Cholinesterase inhibition causes bronchorrhoea and not fibrosis.
Source note: Original NextPrep sample item — pending expert review. This item is original practice material awaiting independent expert review, so confirm important facts in a standard textbook.
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