Instructions: Read each vignette carefully, select the single best answer (AβE). Target: 90 seconds per question. Answers and explanations lock after each click; scores appear in the Score Report tab.
A 19-year-old woman presents to the ED 6 hours after ingesting "a whole bottle" of extra-strength acetaminophen in a suicide attempt. She is asymptomatic. Labs: AST 22, ALT 18, INR 1.0. The attending orders N-acetylcysteine. By what mechanism does NAC prevent hepatotoxicity in this patient?
ACompetitive inhibition of cytochrome P450 2E1
BChelation of unabsorbed acetaminophen in the gut
CReplenishes hepatic glutathione stores allowing conjugation of NAPQI
DInhibits bacterial deconjugation in the enterohepatic circulation
EInduces glucuronidation and sulfation pathways
Answer: C. At therapeutic doses, APAP is cleared by glucuronidation (~60%) + sulfation (~30%); ~5% is oxidized by CYP2E1 to the toxic electrophile NAPQI, which is rapidly detoxified by conjugation with glutathione (GSH). In overdose, the sulfation/glucuronidation pathways saturate, more APAP is shunted to CYP2E1, and GSH is depleted (>70% depletion causes hepatocyte necrosis). NAC is metabolized to cysteine β glutathione, replenishing stores and allowing safe conjugation of NAPQI. Maximal benefit when given within 8β10 h of ingestion. Use the Rumack-Matthew nomogram (4-hr level) to decide on NAC.
Question 2 Β· Salicylate Toxicity β AcidβBase
A 42-year-old woman with chronic low back pain is brought to the ED confused, hyperventilating, and complaining of tinnitus. Temperature 38.9Β°C, RR 32. ABG: pH 7.44, PaCOβ 18 mmHg, HCOββ» 12 mEq/L. Serum Na 140, Cl 100, glucose 48 mg/dL. Which acidβbase disturbance is MOST consistent with her presentation?
EMS brings a 23-year-old man found unresponsive in a parking lot. Vitals: BP 110/70, HR 52, RR 4, Oβ sat 78% on RA. On exam the pupils are 2 mm and symmetric; needle tracks are visible on both antecubital fossae. Bag-mask ventilation improves saturation. What is the MOST appropriate next pharmacologic step?
AIV flumazenil 0.2 mg
BIV/IM/IN naloxone 0.04β0.4 mg, titrated to respiratory rate
CIV physostigmine 2 mg
DIV glucagon 5 mg
EIV dextrose 25 g + thiamine 100 mg
Answer: B. Classic opioid toxidrome: CNS depression + miosis (pinpoint pupils) + respiratory depression (the lethal feature). Naloxone is a competitive ΞΌ-opioid antagonist. Start with a LOW dose (0.04β0.4 mg IV) titrated to adequate respirations β large bolus doses in opioid-dependent patients precipitate severe withdrawal, vomiting β aspiration, and pulmonary edema. Repeat doses often needed due to short half-life (~30β80 min) versus long-acting opioids (methadone, SR oxycodone). Flumazenil is wrong (benzo antagonist β and dangerous if TCA/seizure risk); physostigmine = anticholinergic; glucagon = Ξ²-blocker/CCB. Meperidine and tramadol can cause opioid toxicity WITHOUT miosis.
Question 4 Β· Carbon Monoxide β Pulse Oximetry
A family of four β mother, father, and two children β presents to the ED during a winter blackout after the whole family spent the night with a kerosene heater running in a closed room. All report headache, dizziness, and nausea. The 6-year-old is somnolent. Vitals are normal; pulse oximetry reads SpOβ 99% on room air, yet an arterial blood gas co-oximeter shows PaOβ 105 mmHg and carboxyhemoglobin 32%. Which intervention is MOST appropriate for the 6-year-old?
ARoom air observation; SpOβ is normal
BNasal cannula at 2 L/min
CIV hydroxocobalamin 5 g
D100% Oβ via non-rebreather; consider hyperbaric Oβ
EMethylene blue 1β2 mg/kg IV
Answer: D.Carbon monoxide poisoning: CO has ~240Γ affinity for hemoglobin vs Oβ β reduces Oβ-carrying capacity, left-shifts the curve, and inhibits cytochrome c oxidase. Standard pulse oximeters cannot distinguish HbOβ from HbCO (same wavelength absorbance) β the saturation gap (normal SpOβ with hypoxic symptoms). Diagnosis requires co-oximetry. Treatment: 100% Oβ via non-rebreather drops CO half-life from ~300 min (room air) to ~90 min. Hyperbaric Oβ (reduces tΒ½ to ~20 min) is indicated for: COHb >25% (>20% in pregnancy), any neuro symptoms (LOC, syncope, seizure), pregnancy with any symptoms, end-organ ischemia (ECG changes, troponinβ), persistent deficits after initial Oβ. Hydroxocobalamin = cyanide; methylene blue = methemoglobinemia.
Question 5 Β· TCA Overdose β ECG + NaHCOβ
A 28-year-old man with major depression is brought in by his roommate, who found him with an empty bottle of amitriptyline. He is drowsy, tachycardic (HR 128), with dilated pupils and dry mucous membranes. Initial ECG shows QRS 140 ms with a prominent terminal R wave in aVR. BP 92/54. Fifteen minutes later, he has a generalized tonicβclonic seizure. Which intervention will MOST directly reverse both the cardiac and CNS toxicity?
AIV lidocaine infusion
BIV procainamide
CIV sodium bicarbonate bolus (1β2 mEq/kg)
DIV physostigmine 2 mg
EIV flumazenil 0.2 mg
Answer: C.TCA toxicity β the "3 C's": Cardiotoxicity, Convulsions, Coma, plus anticholinergic features (dry, dilated, tachy, hot). The lethal feature is NaβΊ-channel blockade in myocardium β QRS widening >100 ms, R in aVR >3 mm, R/S ratio in aVR >0.7 β all predict arrhythmia and seizures. IV NaHCOβ works by: (1) raising extracellular NaβΊ (overcomes channel block), (2) alkalinization (pH 7.50β7.55) favors non-ionized TCA that dissociates from the channel. Indications: QRS >100 ms, VT, hypotension. Physostigmine is contraindicated in TCA overdose (precipitates asystole). Class IA/IC antiarrhythmics worsen NaβΊ blockade. Flumazenil can precipitate seizures in co-ingestion. Lipid emulsion is 2nd-line rescue for TCA-induced arrest.
Instructions: Read each vignette carefully, select the single best answer (AβE). Target: 90 seconds per question.
Question 6 Β· Anticholinergic Toxidrome
A 17-year-old is brought to the ED by friends after ingesting an unknown plant at a party. On exam: T 39.3Β°C, HR 138, BP 148/92, skin flushed, dry, and warm, pupils 8 mm and nonreactive, bowel sounds absent, bladder distended on palpation. He is agitated, mumbling incoherently, and picking at the air. Which of the following BEST characterizes the toxidrome and explains his hyperthermia?
Answer: B. Classic "Hot as a hare, Dry as a bone, Red as a beet, Mad as a hatter, Blind as a bat" = anticholinergic syndrome. Likely culprits: Jimsonweed (Datura), diphenhydramine, TCAs, antipsychotics, antispasmodics, scopolamine. Hyperthermia arises from loss of muscarinic-driven eccrine sweating (sweat glands are sympathetic-cholinergic β the exception to sympathetic-adrenergic rule). Key distinction from sympathomimetics: anticholinergic patients are DRY; sympathomimetics (cocaine, meth) are DIAPHORETIC with normal bowel sounds. Antidote: physostigmine (crosses BBB), reserved for severe agitation/delirium β contraindicated in TCA OD (QRS widening / asystole).
A 48-year-old farmer is brought in from a pesticide-spraying accident 90 minutes ago. He is diaphoretic with pinpoint pupils, salivating, vomiting, urinary incontinence, and diffuse wheezing. Atropine 2 mg IV has been given twice with modest improvement in secretions. Which adjunct is MOST critical to give NOW to prevent permanent enzyme inactivation?
APhysostigmine 2 mg IV
BGlycopyrrolate 0.2 mg IV
CPralidoxime (2-PAM) 30 mg/kg IV
DDiazepam 10 mg IV
EHydroxocobalamin 5 g IV
Answer: C. Classic SLUDGE / DUMBELS cholinergic toxidrome from organophosphate (AChE inhibitor) exposure. Pathophysiology: OP covalently binds AChE β initially reversible, but over hours the OPβenzyme complex undergoes "aging" (loss of an alkyl group) β becomes irreversibly bound. Atropine blocks MUSCARINIC effects (wheezing, secretions, bradycardia) β titrate until secretions dry up. Pralidoxime (2-PAM) physically removes the OP from AChE before aging and is essential for reversing NICOTINIC effects (muscle weakness, paralysis, respiratory failure) β must give EARLY (aging takes minutes to hours depending on agent). Benzos for seizures (sarin/soman). Physostigmine would worsen cholinergic excess.
Question 8 Β· Sympathomimetic vs Anticholinergic
Two patients arrive simultaneously. Patient A (age 24) was found agitated and combative at a rave β T 40.2, HR 150, BP 188/110, pupils 7 mm reactive, skin soaked in sweat, hyperactive bowel sounds. Patient B (age 76) has dementia; her daughter increased her diphenhydramine β T 39.5, HR 125, BP 155/95, pupils 6 mm minimally reactive, skin dry and flushed, absent bowel sounds, urinary retention. Which single physical-exam finding BEST distinguishes Patient A's toxidrome from Patient B's?
AMydriasis
BTachycardia
CHyperthermia
DDiaphoresis and preserved bowel sounds
EHypertension
Answer: D. Both toxidromes share mydriasis, tachycardia, hypertension, hyperthermia, agitation. The distinguishing features are sweat glands and gut motility: β’ Sympathomimetic (cocaine, meth, MDMA, amphetamine) β DIAPHORETIC, normal/hyperactive bowel sounds (sweat glands are sympathetic cholinergic β activated; sympathetic does NOT shut down gut directly in OD context). β’ Anticholinergic (diphenhydramine, atropine, TCA, jimsonweed) β DRY skin (no sweating), absent bowel sounds, urinary retention. Treatment diverges too: sympathomimetics respond to benzodiazepines + active cooling (avoid Ξ²-blockers alone β unopposed Ξ±); anticholinergics with severe delirium may respond to physostigmine.
Question 9 Β· Cyanide β Smoke Inhalation Victim
A 38-year-old firefighter is pulled from a house fire. At the scene: GCS 8, HR 52, BP 78/40, breath with a faint bitter almond odor, skin flushed. ABG: pH 6.95, lactate 14 mmol/L, venous Oβ saturation 90%. Carboxyhemoglobin is 8%. Which antidote is MOST appropriate?
AN-acetylcysteine
BIV hydroxocobalamin 5 g (or sodium thiosulfate + nitrites)
CMethylene blue 1β2 mg/kg IV
DDeferoxamine 15 mg/kg/hr IV
EAtropine 2 mg IV + pralidoxime
Answer: B.Cyanide poisoning from smoke inhalation (combustion of wool, polyurethane, plastics). Mechanism: CNβ» binds cytochrome c oxidase (complex IV), halting oxidative phosphorylation β cells cannot extract Oβ β elevated venous Oβ sat (>90% β cells can't use it), severe anion-gap lactic acidosis, and the classic bitter almond breath (not everyone can smell it). Hydroxocobalamin (Cyanokit) binds CNβ» to form cyanocobalamin (vitamin B12) β preferred in smoke-inhalation victims because it does NOT worsen CO toxicity. Alternative: nitrites (induce methemoglobin to scavenge CNβ») + sodium thiosulfate (substrate for rhodanese β thiocyanate) β but nitrites are contraindicated if co-existing CO because methemoglobinemia further reduces Oβ delivery. CO alone would not explain venous sat 90% or the almond odor.
Question 10 Β· Methemoglobinemia β Saturation Gap
A 3-year-old boy is brought in for evaluation of "turning blue around the lips" after his pediatrician sprayed benzocaine on his gums for teething pain. Vitals: HR 132, RR 30, SpOβ 85% on 100% NRB. ABG reveals PaOβ 455 mmHg, calculated SaOβ 99%, and chocolate-brown arterial blood. Which intervention is MOST appropriate?
AHyperbaric oxygen therapy
BIV methylene blue 1β2 mg/kg (after confirming G6PD status)
CPacked RBC transfusion 10 mL/kg
DIV deferoxamine
EIV N-acetylcysteine
Answer: B. Classic methemoglobinemia: oxidant drug (benzocaine, dapsone, nitrates, nitrites, sulfonamides, aniline dyes) oxidizes hemoglobin FeΒ²βΊ β FeΒ³βΊ, which cannot bind Oβ and left-shifts the curve (worsening tissue hypoxia). Key clues: saturation gap (pulse ox reads ~85% regardless of supplemental Oβ, but PaOβ is normal), chocolate-brown blood, cyanosis unresponsive to Oβ. Co-oximetry confirms MetHb. Methylene blue is reduced by NADPH-methemoglobin reductase to leucomethylene blue, which reduces FeΒ³βΊ β FeΒ²βΊ. Caution in G6PD deficiency β lack of NADPH means MB cannot be reduced AND MB itself is an oxidant β hemolysis. Alternatives for G6PD patients: ascorbic acid, exchange transfusion, HBO. Benzocaine teething sprays have been restricted by FDA for infants due to this complication.
Instructions: Read each vignette carefully, select the single best answer (AβE). Target: 90 seconds per question.
Question 11 Β· Methanol β "Snowstorm" Vision
A 52-year-old homeless man is brought to the ED with headache, nausea, and "snowstorm" vision described as a blurred, whited-out visual field. He is known to drink whatever alcohol he can find. Vitals: HR 110, BP 132/80, RR 28 (Kussmaul). Labs: pH 7.11, HCOββ» 8, anion gap 32, osmolar gap 42, creatinine 1.0. Urine has no oxalate crystals. Which intervention MOST specifically blocks further production of the toxic metabolite?
AIV pyridoxine 5 g
BIV fomepizole (4-methylpyrazole) + hemodialysis
CIV thiamine 500 mg + dextrose
DActivated charcoal 1 g/kg PO
EIV calcium gluconate 2 g
Answer: B.Methanol poisoning: alcohol dehydrogenase (ADH) converts methanol β formaldehyde β formic acid, which causes severe AG metabolic acidosis + characteristic optic nerve injury (snowstorm blindness, disc edema). Lack of oxalate crystals rules out ethylene glycol (oxalate β Ca-oxalate crystalluria, renal failure, tetany). Diagnosis: large osmolar gap (>10) + AG acidosis. Fomepizole competitively inhibits ADH (Ki ~8,000Γ greater affinity than ethanol) β the first-line antidote. Hemodialysis removes both parent alcohol and metabolites (indicated for severe acidosis, visual symptoms, level >50 mg/dL, renal failure). Ethanol is 2nd-line (dose difficult to titrate). Charcoal does NOT bind alcohols. Add folate for methanol (helps metabolize formate); thiamine + pyridoxine for ethylene glycol.
Question 12 Β· Pediatric Iron Overdose
A 2-year-old girl is rushed to the ED 1 hour after ingesting an unknown number of her pregnant mother's prenatal iron tablets. She has had two episodes of bloody vomiting and one dark tarry stool. Vitals: HR 160, BP 74/40, cap refill 4 sec. Labs: glucose 48, WBC 18k, pH 7.20, lactate 6. KUB shows multiple radiopaque tablets in the stomach. Which is the MOST appropriate decontamination + antidote strategy?
AActivated charcoal 1 g/kg PO + IV N-acetylcysteine
BSyrup of ipecac to induce emesis
CWhole-bowel irrigation (polyethylene glycol) + IV deferoxamine
DGastric lavage + IV succimer
EObservation; iron is not a dangerous pediatric ingestion
A 3-year-old boy living in a 1920s row house undergoes a routine screening lead level of 72 ΞΌg/dL. On exam he has pallor and mild irritability. CBC shows microcytic anemia with basophilic stippling. Abdominal X-ray shows a metallic-opaque object in the stomach. He is admitted, and soon begins vomiting and having seizures. Which chelation regimen is MOST appropriate NOW?
AOral succimer (DMSA) monotherapy
BOral D-penicillamine monotherapy
CIV calcium-disodium EDTA + IM dimercaprol (BAL)
DIV deferoxamine
EIV N-acetylcysteine
Answer: C.Lead encephalopathy β lead inhibits Ξ΄-ALA dehydratase and ferrochelatase in heme synthesis (β microcytic anemia, basophilic stippling), and crosses the BBB causing encephalopathy (seizure, coma, cerebral edema) when levels are extreme. Treatment thresholds (CDC 2022 reference value 3.5 ΞΌg/dL): β₯45 ΞΌg/dL (asymptomatic) β oral succimer (DMSA); β₯70 ΞΌg/dL OR encephalopathy β dimercaprol (BAL) IM + EDTA IV. Give BAL FIRST, then EDTA (EDTA alone can redistribute lead into the CNS β worsening encephalopathy). Environmental remediation + identify source (paint chips, contaminated soil, imported remedies/cosmetics like azarcΓ³n, greta). Deferoxamine = iron; NAC = APAP; D-penicillamine is used in Wilson disease and occasionally lead (2nd line).
Question 14 Β· INH Overdose β Pyridoxine
A 19-year-old woman recently diagnosed with latent TB is started on isoniazid. Her 3-year-old brother ingests an unknown number of her tablets. Within 90 minutes he develops repeated generalized tonicβclonic seizures refractory to two doses of IV lorazepam. Labs: pH 7.14, AG 22, lactate 8. Which antidote is MOST appropriate?
Answer: C.INH toxicity β the "3 C's": Coma, Convulsions (refractory), metabolic aCidosis. Mechanism: INH depletes pyridoxine (vitamin B6), which is a cofactor for glutamate decarboxylase β β GABA synthesis β seizures resistant to benzodiazepines (the benzo substrate, GABA, is missing). Pyridoxine (vitamin B6) gram-for-gram of INH ingested (max 5 g empiric if amount unknown) is the specific antidote, typically terminates seizures within minutes. Mushroom (Gyromitra) poisoning causes similar GABA depletion seizures and also responds to pyridoxine. Flumazenil is dangerous (can precipitate INH seizures). Glucagon = Ξ²-blocker/CCB. DigiFab = digoxin.
Question 15 Β· Digoxin Toxicity + Hyperkalemia
A 78-year-old woman with atrial fibrillation, CKD III, and heart failure takes digoxin 0.25 mg daily. After a week of "stomach flu" with poor PO intake she presents with nausea, yellow-green halos around lights, and confusion. Vitals: HR 44, BP 98/62. ECG: junctional bradycardia with frequent PVCs + downsloping ST depressions. Labs: KβΊ 6.4 mEq/L, creatinine 2.2, dig level 4.8 ng/mL. Which intervention is MOST appropriate?
AIV calcium chloride 1 g to stabilize the myocardium
BIV digoxin-specific Fab fragments (DigiFab)
CEmergent hemodialysis
DIV sodium bicarbonate 100 mEq
EIV magnesium sulfate 2 g
Answer: B.Digoxin toxicity β classic: visual changes (yellow-green halos, "scooped" ST depressions on ECG β "Salvador DalΓ's mustache"), bradyarrhythmias, junctional rhythms, GI symptoms. Risk factors: renal failure (digoxin renally cleared), hypoKALEMIA in chronic dosing (β dig binding to Na/K-ATPase), and drug interactions (amiodarone, verapamil). In ACUTE toxicity, hyperkalemia is an independent marker of mortality (Na/K-ATPase inhibition β KβΊ cannot enter cells). Indications for DigiFab: life-threatening arrhythmia, KβΊ >5, level >10 acute or >4 chronic with symptoms, ingestion >10 mg adult / 4 mg child. DigiFab binds free digoxin β reverses both hemodynamic toxicity AND hyperkalemia within minutes (very large Vd means Fab is unusually effective). IV calcium is traditionally avoided in dig toxicity β "stone heart" risk (though newer data are softening this). Digoxin's very large Vd makes it NOT dialyzable. Chronic toxicity KβΊ tends normal or low; DigiFab still reverses.
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Total Score
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Block 1 Β· Core Tox
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Block 2 Β· Toxidromes
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Block 3 Β· Specific Agents
Question-by-Question Breakdown
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