10 free EMT practice questions: Toxicology & Substance Use Emergencies

Acute alcohol intoxication with a declining level of consciousness: Heavy daily alcohol use makes intoxication the reflex pick, but the last drink was about 40 hours ago with no alcohol odor on the breath, so the blood alcohol has already cleared and this is withdrawal, not intoxication.

Wernicke encephalopathy from chronic thiamine deficiency: Chronic drinkers do face real risk for Wernicke encephalopathy from thiamine deficiency, but that condition presents with confusion, ataxic gait, and abnormal eye movements like nystagmus, none of which appear here.

Delirium tremens, which begins within 6 hours of the last drink: Delirium tremens shares the tremor, tachycardia, hypertension, and diaphoresis seen here, so it's an easy reach. It requires disorientation and severe global confusion on top of the autonomic storm, and it classically begins 48 to 96 hours after the last drink. At 40 hours out, oriented enough to describe the hallucination, this is withdrawal with hallucinosis, not delirium tremens yet.

The ingestion occurred too recently for charcoal to be effective: Timing does matter for charcoal, but the direction is backwards here: with the ingestion only about 20 minutes old, most of the drug is likely still in the stomach, which is exactly when charcoal works best. This reasoning would fit an ingestion many hours old, not this one.

The patient took an over-the-counter rather than a prescription medication: Whether a drug is over the counter or prescription tells you nothing about whether charcoal binds it; that depends on the substance itself, and OTC pain relievers are commonly appropriate for charcoal. This sorts by where the drug was purchased instead of by a clinical variable, and it ignores the mental status change entirely.

Activated charcoal is only effective for ingested corrosive substances: Corrosive or caustic ingestions are a real, classic contraindication to charcoal, since charcoal binds them poorly and obscures the endoscopy view they need, so this option has the rule exactly backwards by calling corrosives the one thing charcoal treats. It also does not describe this patient, who swallowed an over-the-counter pain reliever, not a corrosive.

Administer naloxone by the intramuscular route: Intramuscular naloxone is a real route, and the paramedic meeting you will likely use it. It is not yours to give. At the EMT level epinephrine is the only medication you administer intramuscularly, so drawing up IM naloxone puts you outside your scope on a patient who is already being ventilated adequately. The key gets the same drug to the patient by calling the person licensed to give it, and keeps you doing the intervention that is already working.

Place naloxone under the tongue to be absorbed through the oral mucosa: Sublingual is a real route, and nitroglycerin is the one you know, because that drug is formulated to absorb through oral mucosa. Naloxone is not manufactured or approved for sublingual use, so absorption is unreliable. This patient is also unresponsive and cannot protect their own airway, so putting anything in the mouth to dissolve invites aspiration on top of the overdose. The key never asks an unprotected airway to hold a dissolving dose.

Delay transport until naloxone can be given by an available route: Delaying is reasonable when the treatment can safely wait. Four breaths a minute cannot, and a nosebleed from a facial injury may not stop in the field at all, so this ties the patient's care to an event that may never happen. Ventilation and transport both continue regardless of whether naloxone is ever given, because the ventilation is the treatment.

Nausea and occasional vomiting without other symptoms: exactly what activated charcoal itself commonly produces, since the slurry is unpleasant to swallow and irritates the stomach. Vomiting after a dose calls for repeating or slowing the dose, not withholding it, so this finding treats an expected side effect as if it were a reason to stop treatment.

Passage of black, tarry stools without other symptoms: Passage of black, tarry stools looks like melena from an upper GI bleed, a condition that does present with dark, tarry stool along with hematemesis, tachycardia, and hypotension from blood loss. Here the stool is described "without other symptoms," meaning none of those bleeding signs are present, and black stool by itself is simply the expected color change charcoal produces as it passes through the gut.

Chronic constipation with no associated abdominal pain: describes a known side effect of activated charcoal, which slows GI transit, not a bowel obstruction or ileus; a true obstruction would present with pain and distension, which this option specifically excludes.

Dilated pupils: associated with sympathomimetic or anticholinergic overdose, not opioids.

Hypertension: seen with sympathomimetic or anticholinergic toxicity, whereas opioids typically cause hypotension.

Hyperthermia: associated with sympathomimetic or anticholinergic overdose, not opioid overdose.

Anticholinergic toxidrome (dry mouth, dilated pupils, agitation, rapid heart rate): Anticholinergic toxidrome shows dry mouth, flushed dry skin, dilated pupils, agitation, and a rapid heart rate, the classic antihistamine or belladonna alkaloid picture. This couple has the opposite findings, excessive salivation and pinpoint pupils instead of dryness and dilation, because anticholinergic and cholinergic effects sit at opposite ends of the same receptor system and can't both describe one patient.

Sympathomimetic toxidrome (dilated pupils, tachycardia, hypertension, agitation): Sympathomimetic toxidrome brings dilated pupils, tachycardia, hypertension, and agitation, typical of cocaine or amphetamine toxicity. Here the pupils are pinpoint, the patients are confused rather than agitated, and the diarrhea and salivation point to parasympathetic overload, so this answers a stimulant-overdose question, not the organophosphate exposure in front of you.

Sedative-hypnotic toxidrome (lethargy, respiratory depression, hypotension): Sedative-hypnotic toxidrome causes lethargy, respiratory depression, and hypotension from a CNS depressant like a benzodiazepine or barbiturate. It gives no explanation for the salivation, muscle twitching, or diarrhea here, findings that reflect autonomic overstimulation rather than depression.

Administer high-flow oxygen by NRB to slow the rapid heart rate and reduce the patient's agitation: High-flow oxygen by NRB treats hypoxia or respiratory distress, not agitation. The stem gives no low SpO2 or breathing complaint, only stimulant-driven tachycardia, so oxygen doesn't touch the catecholamine surge causing this presentation.

Apply physical restraints immediately to prevent the patient from causing harm to themselves or to the crew: Restraints fit a patient who is combative and an immediate danger to self or crew, and the agitation and hostility here make that call tempting. The stem states the patient is not an immediate danger, only verbally hostile, so force isn't justified. Restraining a hyperadrenergic patient drives catecholamines higher, raising the risk of sudden cardiac arrest.

Administer a dose of intranasal naloxone to reverse the effects of the powdered substance the patient used: Naloxone reverses opioid toxidrome: bradycardia, hypotension, respiratory depression, pinpoint pupils. This patient has tachycardia, hypertension, and fever, the stimulant pattern, not opioid, so naloxone has no target here.

The naloxone has completely reversed the opioid effect, and the patient may now safely refuse further evaluation and transport: The patient aroused and the respiratory rate rose to 16 after the naloxone, looking like full reversal. The drowsiness returning minutes later shows the opioid effect is still active, just outlasting the antagonist. A patient who was unresponsive with opioid induced respiratory depression cannot give a valid refusal, and this recurrence proves the crisis isn't over.

The patient is now experiencing acute opioid withdrawal, which shows the overdose has resolved and the crisis has passed: Acute opioid withdrawal produces agitation, tachycardia, sweating, and gastrointestinal distress, not sedation, so it doesn't match this patient's renewed drowsiness. The recurring sedation reflects ongoing opioid toxicity as naloxone wears off, not withdrawal, and the crisis is not resolved.

The recurring drowsiness indicates the naloxone dose was ineffective and a different medication is needed to reverse the substance: The initial response, arousal and a respiratory rate up to 16, shows the dose worked. The later drowsiness reflects naloxone's shorter duration compared to the opioid, not treatment failure, and no alternative reversal agent exists at the EMT level.

Withhold ventilatory support until naloxone takes effect: Waiting to see whether a drug works before adding support is reasonable when the patient is holding their own in the meantime: someone breathing adequately while a nitroglycerin dose takes effect. This patient is breathing 6 times a minute at 82% on room air, which is not holding anything; brain tissue is hypoxic for every second of that wait. The key beats it because ventilation and naloxone are not competing choices here, and ventilating is what keeps the patient alive during the minutes the naloxone needs.

Administer oral glucose: Oral glucose is the right answer for an altered patient with a low blood glucose who can still protect their own airway. Nothing points there: pinpoint pupils are an opioid finding, not a hypoglycemia finding, and an unresponsive patient breathing 6 times a minute cannot safely take anything by mouth. The key beats it because the findings name opioids specifically, and giving glucose would delay the ventilation this patient needs immediately.

Apply a tourniquet to the affected extremity: A tourniquet is the correct immediate action for life-threatening external hemorrhage from an extremity, where direct pressure cannot control the bleeding. This question describes no injury, no bleeding, and no trauma at all. The key beats it because there is nothing for a tourniquet to control, and the actual life threat on this call is a respiratory rate of 6.

Approach and administer intranasal naloxone: Pinpoint pupils and slow breathing look like an opioid overdose, and naloxone is right for that patient. But the chemical odor and sprayer point to a pesticide exposure instead. Naloxone has no effect on cholinergic toxicity.

Begin positive pressure ventilations without protective equipment: Supporting this patient's breathing is genuinely the next step. But the order matters. The same chemical soaking the coveralls can transfer onto an EMT who makes contact without protection first. So decontamination comes before hands-on ventilation.

Perform a rapid trauma assessment for open wounds: Any patient found down can pull you toward a head-to-toe trauma survey out of habit. But nothing on this call describes a fall, a crash, or any other mechanism of injury. A trauma survey is also hands-on contact with a worker who is still covered in a chemical, so it answers neither the contamination nor the failing breathing.