A physician-validated, board-style question from the Active Transport QBank. Try it, then check the reasoning for every option.
A 31-year-old man with untreated HIV infection is admitted to the hospital because of a 3-day history of blurred vision and flashing lights in his left eye. Indirect ophthalmoscopy shows retinal hemorrhages of the left eye. Treatment with a drug that directly inhibits viral DNA polymerases by binding to pyrophosphate-binding sites is initiated. Two days later, the patient has a generalized tonic-clonic seizure. This patient's seizure was most likely caused by which of the following?
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A
DemyelinationIncorrect. Demyelination (PML from JC virus) causes progressive focal deficits over weeks — not a seizure 2 days after a new drug is started.
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B
HypocalcemiaCorrect. Foscarnet chelates divalent cations and causes hypocalcemia, which precipitates seizures, paresthesias, and QT prolongation.
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C
HypoglycemiaIncorrect. Hypoglycemia is not a foscarnet adverse effect; it would also typically present with autonomic prodromal symptoms before seizure.
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D
Lactic acidosisIncorrect. Lactic acidosis is a chronic adverse effect of NRTIs (didanosine, stavudine), not foscarnet, and would have a metabolic rather than electrolyte signature.
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E
PancreatitisIncorrect. Pancreatitis is the classic adverse effect of didanosine; foscarnet's metabolic profile is dominated by nephrotoxicity and electrolyte derangements rather than pancreatic injury.
↑ Tap an answer to reveal the reasoning
Answer: B. An HIV-positive patient with CMV retinitis (blurred vision, flashing lights, retinal hemorrhages on ophthalmoscopy) is being treated with foscarnet — a pyrophosphate analog that directly inhibits viral DNA polymerase by binding the pyrophosphate-binding site. Foscarnet does not require viral thymidine kinase, making it useful for ganciclovir-resistant CMV and acyclovir-resistant HSV.
Foscarnet chelates divalent cations and causes electrolyte derangements: hypocalcemia, hypomagnesemia, hypokalemia, and hypophosphatemia (or sometimes hyperphosphatemia). Symptomatic hypocalcemia can precipitate tetany, perioral paresthesias, prolonged QT, and seizures — exactly what occurred two days into therapy. Foscarnet is also significantly nephrotoxic.
Distinguishing the differential for HIV-related seizure: demyelination (PML from JC virus) typically presents with focal neurologic deficits over weeks, not abrupt seizure two days into a drug. Hypoglycemia would have other markers (sweating, hunger, low fingerstick). Lactic acidosis from NRTIs (especially didanosine, stavudine) is dose-related and chronic, not acute after foscarnet initiation. Clinical pearl: always check ionized calcium, magnesium, and phosphate before and during foscarnet — and replete aggressively.
**Why each option:**
**A.** Demyelination (PML from JC virus) causes progressive focal deficits over weeks — not a seizure 2 days after a new drug is started.
**B.** Correct. Foscarnet chelates divalent cations and causes hypocalcemia, which precipitates seizures, paresthesias, and QT prolongation.
**C.** Hypoglycemia is not a foscarnet adverse effect; it would also typically present with autonomic prodromal symptoms before seizure.
**D.** Lactic acidosis is a chronic adverse effect of NRTIs (didanosine, stavudine), not foscarnet, and would have a metabolic rather than electrolyte signature.