Free CSPI Practice Questions

Correct answer: C - Refer immediately to the nearest emergency department

Amlodipine is a calcium channel blocker and a well-established 'one-pill-killer' - a single adult-dose tablet can be fatal in a small child. At 10 mg ÷ 11 kg = 0.91 mg/kg, this dose far exceeds the toxic threshold for a toddler. Critically, amlodipine has a very long half-life (30-50 hours) and an extended time-to-peak effect, meaning a child who is completely asymptomatic at the time of the call can deteriorate hours later with life-threatening bradycardia and cardiovascular collapse. Home observation is never acceptable for calcium channel blocker ingestion in a toddler regardless of current symptoms. Activated charcoal should not be given at home by an untrained caregiver, and home management with follow-up calls is insufficient given the potential for sudden hemodynamic deterioration.

Correct answer: C - Diaphoresis

Diaphoresis (sweating) is the key distinguishing feature. Both sympathomimetic and anticholinergic toxidromes share mydriasis, tachycardia, hypertension, hyperthermia, and agitation - making those four findings useless for differentiation when seen alone. The critical distinction is skin moisture: sympathomimetic toxidrome produces diaphoresis (wet, sweaty skin) because sweat glands remain active under adrenergic stimulation, whereas anticholinergic toxidrome produces anhidrosis (dry, flushed skin) because muscarinic blockade eliminates sweating. This wet/dry distinction is the most reliable bedside differentiator and directly drives management - sympathomimetic toxidrome is treated with benzodiazepines, not physostigmine.

Correct answer: B - Physostigmine may precipitate seizures or asystole in TCA overdose

Physostigmine is an acetylcholinesterase inhibitor that reverses pure anticholinergic toxidrome effectively - but in TCA overdose, it is a potentially lethal choice. TCAs block fast sodium channels, causing QRS widening (seen here at 134 ms). Physostigmine's cholinergic effect can precipitate bradycardia, heart block, and asystole in the setting of sodium-channel blockade - and can also lower the seizure threshold. The correct treatment for this patient is sodium bicarbonate (1-2 mEq/kg IV bolus) targeting serum pH 7.45-7.55, which narrows the QRS by increasing sodium gradient and directly binding the TCA-channel complex. The QRS width itself - not the anticholinergic features - is the priority finding here.

Correct answer: B - Admit for observation and serial liver function tests

The timing of symptom onset is the critical diagnostic key: GI symptoms beginning 6 or more hours after ingestion must be presumed to represent amatoxin poisoning (cyclopeptide group - Amanita phalloides, A. virosa, A. bisporigera) until proven otherwise. The classical amatoxin course is biphasic: Phase 1 (6-24 hours): severe GI illness; Phase 2 (12-24 hours): apparent improvement as GI symptoms subside - exactly what this patient is experiencing; Phase 3 (2-4 days): fulminant hepatic failure (and often renal failure), which can be fatal. Currently normal LFTs are entirely consistent with this early phase - hepatic injury has not yet peaked. Discharging this patient during apparent improvement is a critical error. Activated charcoal has minimal benefit at 14 hours post-ingestion. Mushroom identification alone is never sufficient to exclude amatoxin toxicity.

Correct answer: D - Administer antivenom immediately, before any neurologic symptoms develop

Red-on-yellow pattern in North America identifies the Eastern coral snake (Micrurus fulvius), an elapid whose venom contains post-synaptic neurotoxins that block acetylcholine receptors at the neuromuscular junction. The critical and counterintuitive clinical feature of coral snake envenomation is the prolonged latency before neurologic symptoms: ptosis, diplopia, dysarthria, dysphagia, and ultimately respiratory failure may not appear for 12-24 hours after the bite. The danger of a 'watch and wait' approach is that by the time respiratory failure becomes apparent, antivenom may be unable to reverse established neuromuscular blockade - the toxin-receptor bond is effectively irreversible once symptomatic. Antivenom (North American Coral Snake Antivenom, NACSA) must be administered prophylactically in any confirmed or highly suspected coral snake bite, before neurologic signs appear. Absence of local tissue destruction or pain is expected - coral snake venom is not cytotoxic and causes minimal local reaction, which falsely reassures both patients and providers.

Correct answer: C - Begin N-acetylcysteine therapy immediately

The Rumack-Matthew treatment line begins at 150 mcg/mL at exactly 4 hours post-ingestion. A level of 160 mcg/mL at 4 hours plots ABOVE the treatment line, making NAC initiation mandatory regardless of the patient's asymptomatic status or currently normal LFTs. LFTs are typically normal in Stage I (0-24 hours); hepatic injury does not peak until 72-96 hours. Repeating the level introduces dangerous delay - the nomogram provides a definitive answer at 4 hours and waiting is not indicated. Activated charcoal alone, without NAC, is insufficient at this time point and the level is already known.

Correct answer: B - Administer oxygen at the lowest flow rate necessary to maintain SpO2 above 85-90%

Paraquat causes toxicity through redox cycling - it accepts electrons to form a radical cation, then donates them to molecular oxygen (O2) to regenerate superoxide (O2•−) and ultimately hydroxyl radicals via Fenton chemistry. This process causes progressive lipid peroxidation of pulmonary alveolar cells (type I and II pneumocytes). Supplemental oxygen increases the availability of O2 as a substrate for this radical-generating cycle, directly accelerating lung injury. The established management principle is to use the lowest FiO2 that maintains acceptable (not normal) oxygenation - most guidelines accept SpO2 ≥85-90% rather than correcting toward 95-100%. High-flow oxygen is contraindicated and can accelerate an already fatal pulmonary fibrosis. Hyperbaric oxygen would dramatically worsen paraquat toxicity. This is one of the few toxicologic scenarios where withholding supplemental oxygen is the correct intervention.

Correct answer: A - Osmolal gap elevation with ketosis, no metabolic acidosis

This is the classic isopropanol (isopropyl alcohol) presentation. The osmolal gap is elevated: 338 − 298 = 40 mOsm/kg (normal <10), confirming a significant unmeasured osmole. However, the anion gap is normal (24 mEq/L bicarbonate, normal pH 7.38) - there is NO metabolic acidosis. This is the defining feature of isopropanol toxicity: it is metabolized by alcohol dehydrogenase (ADH) to acetone, not to an organic acid. Acetone produces ketonemia and ketonuria (explaining the positive urine dipstick) but does NOT generate protons, so no acidosis develops. This distinguishes isopropanol sharply from methanol (→ formate → severe anion-gap acidosis + optic neuropathy) and ethylene glycol (→ oxalate → anion-gap acidosis + calcium oxalate crystals + renal failure). Fomepizole (ADH blocker) is NOT indicated for isopropanol - the acetone metabolite is not acutely dangerous, and blocking ADH would only prolong isopropanol exposure.

Correct answer: C - Continue atropine and titrate to drying of secretions

The therapeutic endpoint for atropine in organophosphate poisoning is the drying of secretions - specifically bronchorrhea, salivation, and lacrimation - and the resolution of bronchospasm. Heart rate is NOT a valid endpoint. Patients with organophosphate poisoning often have baseline tachycardia from the nicotinic effects of acetylcholine excess; conversely, severe poisoning may cause bradycardia. In either case, targeting a specific heart rate will result in either undertreating (if HR is already elevated) or massively overtreating (if HR is used as the only endpoint). A heart rate increase from 58 to 82 bpm after 2 mg of atropine simply reflects partial muscarinic blockade at the sinoatrial node - the fact that the patient still has copious secretions and bronchospasm means atropine dosing is still grossly inadequate. In severe OP poisoning, cumulative atropine doses of 10-100 mg may be required. Pralidoxime is an adjunct that reactivates acetylcholinesterase (addressing nicotinic effects) and should be started concurrently - it does not replace atropine.

Correct answer: B - Pulse oximetry cannot reliably detect CO poisoning; co-oximetry must be obtained

Pulse oximetry (SpO2) is fundamentally unreliable in carbon monoxide poisoning - this is one of the most important and frequently tested diagnostic traps in clinical toxicology. Standard pulse oximeters use two wavelengths of light and cannot distinguish oxyhemoglobin (HbO2) from carboxyhemoglobin (COHb). Both absorb light similarly at the red wavelength used, so the device reads COHb as oxyhemoglobin and reports a falsely normal or near-normal SpO2 regardless of the actual COHb level. A patient with 40% COHb may display a pulse oximetry reading of 95-99%. Diagnosis requires co-oximetry (multi-wavelength spectrophotometry on an arterial or venous blood gas), which directly measures COHb percentage. In a patient with smoke inhalation and an altered level of consciousness, CO poisoning must be assumed and co-oximetry obtained immediately - a normal SpO2 provides no reassurance whatsoever.