Skip to main content
Sign in Create a free account
Varsity Tutors
Sign in

Overdose And Exposure Management - NAPLEX

  1. A 28-year-old female (weight 62 kg) is brought to the emergency department for severe drowsiness after taking "a handful" of her prescribed alprazolam about 1 hour ago with alcohol. Current medications: alprazolam 1 mg by mouth three times daily as needed, sertraline 100 mg by mouth daily, ethinyl estradiol/levonorgestrel 1 tablet daily. Medical history: panic disorder. Allergies: penicillin (rash). Vitals: blood pressure 108/66 mmHg, heart rate 92 bpm, respiratory rate 8/min, oxygen saturation 90% on room air; pupils mid-size and reactive. Labs: serum creatinine 0.8 mg/dL, aspartate aminotransferase 22 U/L, alanine aminotransferase 18 U/L, ethanol level 180 mg/dL, urine toxicology positive for benzodiazepines only. Which antidote is most appropriate for this overdose?
    Answer: Flumazenil 0.2 mg intravenous, may repeat in 0.2 mg increments to a maximum of 1 mg This question tests the appropriate antidote selection for benzodiazepine overdose with concurrent alcohol intoxication. The patient presents with severe drowsiness, respiratory depression (RR 8/min, O2 sat 90%), and positive urine toxicology for benzodiazepines after alprazolam overdose with alcohol. Flumazenil (B) is the specific benzodiazepine receptor antagonist that competitively reverses benzodiazepine effects, making it the correct choice for this patient with respiratory depression. Naloxone (A) is incorrect as it reverses opioid effects, not benzodiazepines, and the patient has no evidence of opioid exposure. N-acetylcysteine (C) is the antidote for acetaminophen overdose, and fomepizole (D) treats toxic alcohol ingestions, neither of which apply here. When using flumazenil, monitor for seizures, especially in chronic benzodiazepine users or those with seizure history, and be aware that its shorter half-life compared to most benzodiazepines may require repeated dosing.
  2. A 52-year-old male (86 kg) with chronic pain is brought in with lethargy and slow respirations after applying multiple fentanyl patches. Current medications: fentanyl transdermal 50 mcg/hour every 72 hours, diazepam 5 mg by mouth three times daily, duloxetine 60 mg by mouth daily. Labs: serum creatinine 1.0 mg/dL; aspartate aminotransferase 34 units/L; alanine aminotransferase 30 units/L. Allergies: none. History: caregiver reports he applied "three patches" today due to pain. What is the pharmacist's best recommendation for follow-up care?
    Answer: Remove all fentanyl patches, provide naloxone and observe for recurrent respiratory depression due to long duration of fentanyl This question tests follow-up care in transdermal fentanyl overdose, emphasizing prolonged effects. The key patient-specific factor is the multiple patches applied, causing lethargy and respiratory depression from sustained release. Removing patches, giving naloxone, and observing for recurrence are best due to fentanyl's long duration and depot effect. Flumazenil is for benzos and inappropriate here; N-acetylcysteine irrelevant; single naloxone insufficient without monitoring. A pearl is that transdermal fentanyl can cause delayed toxicity lasting 24+ hours post-removal. Continuous naloxone infusion may be needed for persistent symptoms.
  3. A 64-year-old male (80 kg) is brought in for altered mental status and shallow breathing after taking "extra" oxycodone for back pain; respiratory rate is 6/min, oxygen saturation 86% on room air, pupils are pinpoint. Current medications: oxycodone immediate-release 10 mg by mouth every 6 hours as needed, gabapentin 300 mg by mouth three times daily, lisinopril 20 mg by mouth daily. Labs: serum creatinine 1.0 mg/dL; aspartate aminotransferase 30 units/L; alanine aminotransferase 26 units/L. Toxicology: urine positive for opioids; negative for benzodiazepines. Allergies: none. History: chronic low back pain, hypertension. Which antidote is most appropriate for this overdose?
    Answer: Naloxone 0.04 mg intravenous, titrate every 2–3 minutes to adequate ventilation This question tests the management of opioid overdose, emphasizing reversal of respiratory depression. The key patient-specific factor is the altered mental status, shallow breathing, pinpoint pupils, and positive urine opioid screen consistent with oxycodone excess. Naloxone is the best choice as it competitively antagonizes mu-opioid receptors, rapidly restoring ventilation when titrated carefully to avoid withdrawal. Flumazenil is incorrect without benzodiazepine involvement; N-acetylcysteine is not indicated absent acetaminophen toxicity; atropine is suboptimal as bradycardia is not the primary issue here. A clinical pearl is to monitor for recurrent respiratory depression due to opioids' longer half-life compared to naloxone. Use lower initial doses in chronic users to minimize precipitation of severe withdrawal.
  4. A 45-year-old male (weight 90 kg) presents to the emergency department for nausea and tinnitus after taking "a lot" of aspirin for back pain over the last 24 hours. Current medications: aspirin 325 mg tablets as needed (self-directed), lisinopril 20 mg by mouth daily. Medical history: hypertension, chronic low back pain. Allergies: none known. Vitals: blood pressure 128/74 mmHg, heart rate 110 bpm, respiratory rate 30/min, oxygen saturation 99% on room air; patient is diaphoretic and hyperventilating. Labs: sodium 140 mEq/L, potassium 3.2 mEq/L (low), bicarbonate 16 mEq/L (low), serum creatinine 1.1 mg/dL, salicylate level 52 mg/dL (elevated), arterial pH 7.48, partial pressure of carbon dioxide 22 mmHg. Which monitoring parameter should be assessed following this overdose?
    Answer: Serial serum salicylate concentrations and acid–base status (arterial or venous blood gas, bicarbonate) This question tests appropriate monitoring parameters for salicylate toxicity. The patient presents with classic salicylate toxicity symptoms: tinnitus, hyperventilation (RR 30/min), and mixed respiratory alkalosis with metabolic acidosis (pH 7.48, low bicarbonate, low PCO2). Serial serum salicylate concentrations and acid-base status (B) are essential for monitoring salicylate toxicity because levels can continue to rise, and acid-base disturbances guide treatment decisions including alkalinization and hemodialysis. Acetaminophen concentration at 4 hours (A) is irrelevant as the patient took aspirin, not acetaminophen. INR monitoring (C) would be appropriate for warfarin overdose, not salicylate toxicity. Serum digoxin concentration (D) is unnecessary without digoxin exposure. In salicylate toxicity, monitor levels every 2-4 hours until declining, along with frequent acid-base assessment, as tissue distribution increases with acidemia. Remember that clinical severity doesn't always correlate with serum levels, especially in chronic toxicity.
  5. A 28-year-old female (62 kg) presents to the emergency department 45 minutes after ingesting an unknown quantity of acetaminophen 500 mg tablets in a suicide attempt; she is nauseated but alert. Current medications: sertraline 50 mg by mouth daily; ethinyl estradiol/levonorgestrel 1 tablet daily. Labs: serum creatinine 0.8 mg/dL; aspartate aminotransferase 32 units/L; alanine aminotransferase 28 units/L; international normalized ratio (INR) 1.0; 4-hour acetaminophen concentration is pending. Allergies: penicillin (rash). Past history: major depressive disorder; no chronic liver disease; reports no alcohol use. Which antidote is most appropriate for this overdose?
    Answer: N-acetylcysteine (NAC) per acetaminophen overdose protocol (intravenous or oral regimen) This question tests the management of acetaminophen overdose, focusing on timely antidote administration to prevent hepatotoxicity. The key patient-specific factor is the recent ingestion (45 minutes ago) of an unknown quantity, with pending 4-hour acetaminophen concentration and no evidence of other substances. N-acetylcysteine (NAC) is the best choice as it replenishes glutathione stores and detoxifies the toxic metabolite NAPQI, ideally started within 8 hours for optimal efficacy. Flumazenil is incorrect as there is no benzodiazepine involvement; naloxone is suboptimal without opioid symptoms like respiratory depression; fomepizole is not indicated absent toxic alcohol exposure. A transferable clinical pearl is to use the Rumack-Matthew nomogram for risk stratification once the 4-hour level is available. Always consider co-ingestants in suicide attempts, but prioritize NAC if acetaminophen overdose is suspected.
  6. A 26-year-old female (58 kg) presents with severe nausea and vomiting after taking an entire bottle of extended-release bupropion 150 mg tablets (estimated 30 tablets) 2 hours ago. Current medications: bupropion XL 150 mg by mouth daily (recent), combined oral contraceptive 1 tablet daily. Labs: serum creatinine 0.7 mg/dL; aspartate aminotransferase 26 units/L; alanine aminotransferase 22 units/L; electrocardiogram shows QTc 470 ms. Allergies: none. History: depression; no seizure history. Which symptom indicates severe toxicity in this patient?
    Answer: Seizures (including delayed-onset seizures) and significant cardiac dysrhythmias This question tests recognition of severe bupropion toxicity, focusing on neurologic and cardiac effects. The key patient-specific factor is the large ingestion of extended-release bupropion with prolonged QTc indicating high risk. Seizures and cardiac dysrhythmias indicate severe toxicity due to sodium channel blockade and lowered seizure threshold. Mild headache is common but not severe; increased appetite atypical; runny nose irrelevant. A pearl is that seizures can be delayed up to 24 hours with XL formulations. Treat wide QRS with sodium bicarbonate and use benzodiazepines for seizure prophylaxis.
  7. A 6-year-old female (weight 20 kg) is brought to the emergency department after ingesting an unknown quantity of her grandfather's ferrous sulfate 325 mg tablets approximately 45 minutes ago; the family estimates up to 10 tablets were accessible. Current medications: none. Medical history: none. Allergies: none known. Vitals: blood pressure 92/54 mmHg, heart rate 128 bpm, respiratory rate 22/min, oxygen saturation 98% on room air; she has abdominal pain and repeated vomiting. Labs: serum iron 520 micrograms/dL (very high), anion gap metabolic acidosis with bicarbonate 14 mEq/L (low), serum creatinine 0.4 mg/dL, aspartate aminotransferase 60 U/L (high), alanine aminotransferase 55 U/L (high). What is the pharmacist's best recommendation for follow-up care?
    Answer: Initiate deferoxamine chelation and recommend admission for monitoring of acidosis, hepatic injury, and shock This question tests management recommendations for severe pediatric iron overdose. The child has ingested potentially 10 ferrous sulfate tablets (65 mg elemental iron each = 650 mg total or 32.5 mg/kg), with severely elevated serum iron (520 mcg/dL), metabolic acidosis, and early hepatotoxicity signs. Initiating deferoxamine chelation and recommending admission (B) is correct because serum iron >500 mcg/dL with systemic toxicity (acidosis, hypotension, repeated vomiting) requires immediate chelation therapy and intensive monitoring for the five stages of iron toxicity. Discharge home (A) is dangerous as iron toxicity has multiple phases including a deceptive latent period. Oral activated charcoal (C) doesn't bind iron and home management is inappropriate for severe toxicity. Vitamin K (D) treats warfarin toxicity, not iron poisoning. Iron toxicity progresses through GI, latent, shock/acidosis, hepatotoxicity, and GI scarring phases. Deferoxamine creates vin rosé colored urine and should continue until iron levels normalize and systemic toxicity resolves.
  8. A 58-year-old female (72 kg) presents with confusion, vomiting, and tinnitus after taking "a lot" of aspirin for knee pain over the last 24 hours; respiratory rate is 28/min. Current medications: aspirin 325 mg by mouth as needed (self-directed), hydrochlorothiazide 25 mg by mouth daily. Labs: serum creatinine 1.3 mg/dL; arterial blood gas shows pH 7.49, PaCO2 25 mmHg, HCO3− 18 mEq/L; salicylate concentration 78 mg/dL (therapeutic 10–30). Allergies: none. History: osteoarthritis, hypertension. Which monitoring parameter should be assessed following this overdose?
    Answer: Serial serum salicylate concentrations and acid–base status (arterial/venous blood gas and electrolytes) This question tests monitoring in salicylate overdose, focusing on serial assessments for toxicity progression. The key patient-specific factor is the elevated salicylate level (78 mg/dL), respiratory alkalosis, and symptoms like tinnitus indicating significant exposure. Serial salicylate concentrations and acid-base status are best as they guide alkalinization, dialysis decisions, and detect evolving metabolic acidosis. INR monitoring is incorrect as coagulopathy is not primary in acute salicylate toxicity; digoxin levels are irrelevant; neutrophil count is suboptimal without infection risk. A pearl is that salicylate toxicity causes uncoupled oxidative phosphorylation, leading to mixed acid-base disturbances. Enhanced elimination via urinary alkalinization is key when levels exceed 40 mg/dL with symptoms.
  9. A 46-year-old male (88 kg) with type 2 diabetes is brought in for confusion and diaphoresis; fingerstick glucose is 34 mg/dL. Current medications: glyburide 10 mg by mouth daily, metformin 1,000 mg by mouth twice daily, atorvastatin 40 mg by mouth nightly. Labs: serum creatinine 1.0 mg/dL; aspartate aminotransferase 28 units/L; alanine aminotransferase 24 units/L. Allergies: none. History: skipped dinner but took glyburide; symptoms started 2 hours later. Which monitoring parameter should be assessed following this overdose/exposure?
    Answer: Frequent blood glucose monitoring for recurrent hypoglycemia and need for dextrose infusion This question tests monitoring in sulfonylurea overdose, focusing on prolonged hypoglycemia risk. The key patient-specific factor is the low glucose (34 mg/dL) after taking glyburide without food, indicating insulin release stimulation. Frequent blood glucose monitoring is best to detect and treat recurrent hypoglycemia, often requiring dextrose infusion. INR is incorrect without coagulopathy; acetaminophen level is irrelevant; lithium level is not applicable. A pearl is that long-acting sulfonylureas like glyburide can cause hypoglycemia lasting 24-72 hours. Octreotide may be used as an antidote to suppress insulin release in refractory cases.
  10. A 5-year-old male (20 kg) is brought in after accidentally ingesting his grandmother's clonidine 0.1 mg tablets; estimated ingestion is 6 tablets about 1 hour ago. He is somnolent with bradycardia (heart rate 52/min) and hypotension (82/46 mmHg). Current medications: none. Labs: serum creatinine 0.4 mg/dL; aspartate aminotransferase 28 units/L; alanine aminotransferase 20 units/L; glucose 92 mg/dL. Allergies: none. History: otherwise healthy. Which antidote is most appropriate for this overdose?
    Answer: Naloxone intravenous (higher doses may be required) as part of supportive care for clonidine toxicity This question tests management of clonidine overdose in pediatrics, using opioid reversal for central effects. The key patient-specific factor is the somnolence, bradycardia, and hypotension post-ingestion mimicking opioid toxidrome. Naloxone is best as it can reverse clonidine's alpha-2 agonism, improving hemodynamics, often requiring higher doses. Flumazenil for benzos; vitamin K for coagulopathy; deferoxamine for iron. A pearl is that clonidine toxicity responds variably to naloxone, with atropine as alternative for bradycardia. Supportive care includes fluids and monitoring for rebound hypertension upon recovery.
  11. A 2-year-old female (12 kg) is brought to the emergency department after drinking an unknown amount of a household bleach solution; she is crying but has no respiratory distress and is drooling slightly. Current medications: none. Labs: serum creatinine 0.2 mg/dL; aspartate aminotransferase 30 units/L; alanine aminotransferase 18 units/L. Allergies: none. History: accidental ingestion 20 minutes ago; caregiver attempted to make her vomit at home. What is the most important initial action for this exposure?
    Answer: Do not induce vomiting; assess airway and give small amounts of water or milk if able to swallow, and contact poison control This question tests initial management of caustic ingestion in pediatrics, prioritizing avoidance of further injury. The key patient-specific factor is the bleach ingestion with drooling but no respiratory distress in a child. Not inducing vomiting, assessing airway, giving water/milk, and contacting poison control are best to prevent aspiration or perforation. Activated charcoal is ineffective for caustics; gastric lavage risks injury; ipecac is contraindicated. A pearl is that endoscopy within 24 hours assesses damage in symptomatic cases. Diluents like milk neutralize without causing exothermic reactions in alkali ingestions.
  12. A 31-year-old female (60 kg) presents with flushing, sweating, lacrimation, wheezing, and muscle fasciculations after using an insecticide in a poorly ventilated apartment; she is drooling and has pinpoint pupils. Current medications: albuterol inhaler 2 puffs every 4 hours as needed. Labs: serum creatinine 0.7 mg/dL; aspartate aminotransferase 24 units/L; alanine aminotransferase 20 units/L. Allergies: none. History: asthma; exposure was 30 minutes ago. Which antidote is most appropriate for this exposure?
    Answer: Atropine intravenous with repeated dosing until bronchial secretions and bronchospasm improve, plus pralidoxime as indicated This question tests the management of organophosphate poisoning, emphasizing anticholinergic and reactivator therapy. The key patient-specific factor is the cholinergic toxidrome (wheezing, pinpoint pupils, fasciculations) post-insecticide exposure. Atropine with pralidoxime is best as atropine dries secretions and counters muscarinic effects, while pralidoxime regenerates acetylcholinesterase. N-acetylcysteine is incorrect without acetaminophen; naloxone is for opioids; deferoxamine is for iron. A pearl is to titrate atropine to resolution of bronchial secretions, not heart rate. Early decontamination and airway protection are critical in severe cases to prevent aspiration.
  13. A 4-year-old male (18 kg) is in the emergency department after his caregiver found him with an open bottle of iron tablets (ferrous sulfate 325 mg; 65 mg elemental iron per tablet); the caregiver estimates up to 10 tablets may be missing. The child is vomiting and has abdominal pain. Current medications: none. Labs: serum creatinine 0.3 mg/dL; aspartate aminotransferase 40 units/L; alanine aminotransferase 35 units/L; serum iron concentration 520 mcg/dL (normal 50–170). Allergies: none. History: healthy child; accidental ingestion 2 hours ago. Which antidote is most appropriate for this overdose?
    Answer: Deferoxamine intravenous, start based on severe symptoms and markedly elevated serum iron This question tests the management of iron overdose in pediatrics, focusing on chelation for severe toxicity. The key patient-specific factor is the child's vomiting, abdominal pain, and markedly elevated serum iron (520 mcg/dL) indicating significant absorption. Deferoxamine is the best choice as it chelates free iron, forming ferrioxamine excreted in urine, and is indicated for severe symptoms or iron >500 mcg/dL. N-acetylcysteine is incorrect without acetaminophen involvement; naloxone is not relevant absent opioid signs; physostigmine is suboptimal for anticholinergic issues not present here. A transferable pearl is to obtain serum iron levels 4-6 hours post-ingestion for peak assessment. Whole bowel irrigation may be considered for sustained-release formulations to enhance elimination.
  14. A 33-year-old male (74 kg) is found somnolent with slurred speech after taking an unknown number of alprazolam tablets; respiratory rate is 14/min, oxygen saturation 97% on room air, blood pressure 108/64 mmHg. Current medications: alprazolam 1 mg by mouth three times daily as needed, buprenorphine/naloxone 8 mg/2 mg sublingual twice daily, bupropion XL 300 mg by mouth daily. Labs: serum creatinine 0.9 mg/dL; aspartate aminotransferase 29 units/L; alanine aminotransferase 25 units/L. Allergies: none. History: opioid use disorder and seizure history (remote). Which antidote is most appropriate for this overdose?
    Answer: Naloxone intravenous titrated to adequate ventilation if opioid co-ingestion is suspected and respiratory depression develops This question tests antidote selection in benzodiazepine overdose with complicating factors. The key patient-specific factor is the somnolence from alprazolam, opioid maintenance therapy, and seizure history increasing risks. Naloxone is best if opioid co-ingestion is suspected and respiratory depression develops, as it safely reverses opioids without seizure risk. Flumazenil is contraindicated due to seizure history and potential opioid interaction; N-acetylcysteine irrelevant; fomepizole for alcohols. A pearl is to avoid flumazenil in mixed overdoses or chronic benzo users to prevent withdrawal seizures. Supportive care with ventilation is preferred for pure benzo toxicity.
  15. A 49-year-old male (95 kg) presents with severe muscle rigidity, hyperthermia (40.2°C), and altered mental status after taking multiple doses of his antidepressants. Current medications: phenelzine 15 mg by mouth three times daily, sertraline 100 mg by mouth daily (recently restarted on his own), sumatriptan 50 mg by mouth as needed for migraines. Labs: serum creatinine 1.2 mg/dL; creatine kinase 6,500 units/L; aspartate aminotransferase 110 units/L; alanine aminotransferase 90 units/L. Allergies: none. History: depression; symptoms began today. Which symptom indicates severe toxicity in this patient?
    Answer: Hyperthermia with neuromuscular rigidity and rapidly rising creatine kinase This question tests recognition of severe serotonin syndrome from drug interactions. The key patient-specific factor is the hyperthermia, rigidity, elevated CK, and combination of MAOI, SSRI, and triptan precipitating excess serotonin. Hyperthermia with neuromuscular rigidity and rising CK indicate severe toxicity risking rhabdomyolysis and multiorgan failure. Mild nausea is common but not severe; yawning/insomnia are withdrawal; bradycardia/hypothermia are atypical. A pearl is to avoid serotonergic agents in MAOI users for 2 weeks post-discontinuation. Cyproheptadine may be used as an antidote in moderate-severe cases after benzodiazepines.
  16. A 67-year-old female (weight 70 kg) presents with confusion and vomiting after her family reports she accidentally took an extra day's worth of her medications, including metformin and glipizide, about 3 hours ago. Current medications: metformin 1000 mg by mouth twice daily, glipizide 10 mg by mouth daily, atorvastatin 40 mg by mouth nightly, amlodipine 10 mg by mouth daily. Medical history: type 2 diabetes, hypertension, hyperlipidemia. Allergies: sulfonamide antibiotics (hives). Vitals: blood pressure 136/78 mmHg, heart rate 88 bpm, respiratory rate 18/min, oxygen saturation 97% on room air. Labs: point-of-care glucose 38 mg/dL (critically low), serum creatinine 1.0 mg/dL, aspartate aminotransferase 24 U/L, alanine aminotransferase 20 U/L. Which antidote is most appropriate for this overdose?
    Answer: Octreotide 50 micrograms subcutaneous (or intravenous) and repeat every 6 hours as needed with dextrose support This question tests antidote selection for sulfonylurea-induced hypoglycemia. The patient has critically low glucose (38 mg/dL) after taking extra glipizide, presenting with confusion and vomiting typical of severe hypoglycemia. Octreotide (A) is the correct antidote as it inhibits insulin secretion from pancreatic beta cells, counteracting sulfonylurea's mechanism and preventing recurrent hypoglycemia that often occurs with dextrose alone. Protamine sulfate (B) reverses heparin anticoagulation, not hypoglycemia. Vitamin K (C) reverses warfarin anticoagulation, which is unrelated to this case. Leucovorin (D) provides folate rescue for methotrexate toxicity, not sulfonylurea overdose. For sulfonylurea overdose, octreotide prevents the hyperinsulinemic response to dextrose administration, reducing the risk of rebound hypoglycemia. The typical dose is 50-100 micrograms subcutaneously every 6-12 hours, with concurrent dextrose support and frequent glucose monitoring.
  17. A 63-year-old female (68 kg) is admitted with pneumonia and develops acute kidney injury and hearing changes after 5 days of gentamicin. Current medications: gentamicin 7 mg/kg intravenous every 24 hours, piperacillin-tazobactam 4.5 g intravenous every 6 hours, furosemide 40 mg by mouth daily. Labs: serum creatinine increased from 0.9 to 2.0 mg/dL; gentamicin trough 3.2 mg/L (goal <1 mg/L for extended-interval dosing); aspartate aminotransferase 25 units/L; alanine aminotransferase 22 units/L. Allergies: none. History: heart failure. Which monitoring parameter should be assessed following this toxicity?
    Answer: Aminoglycoside concentrations (especially trough) and renal function (serum creatinine/urine output) This question tests monitoring for aminoglycoside toxicity, focusing on nephrotoxicity and ototoxicity. The key patient-specific factor is the rising creatinine and high gentamicin trough after prolonged therapy, indicating accumulation. Aminoglycoside concentrations and renal function are best to guide dosing adjustments and discontinuation. INR irrelevant; acetaminophen level not applicable; lithium incorrect. A pearl is to target trough <1 mg/L for extended-interval gentamicin to minimize toxicity. Monitor audiometry in long courses for early ototoxicity detection.
  18. A 22-year-old male (70 kg) presents with agitation, tremor, diaphoresis, and tachycardia after a party where he used "ecstasy"; temperature is 39.4°C and blood pressure is 168/96 mmHg. Current medications: none. Labs: serum creatinine 1.1 mg/dL; creatine kinase 2,800 units/L (normal 30–200); sodium 128 mEq/L (normal 135–145); aspartate aminotransferase 55 units/L. Toxicology: urine positive for amphetamines. Allergies: none. History: no chronic conditions; last use about 3 hours ago. What is the most important initial action for this exposure?
    Answer: Initiate rapid external cooling and give benzodiazepines for agitation/hyperthermia management This question tests the initial management of MDMA (ecstasy) toxicity, emphasizing supportive care for hyperthermia and agitation. The key patient-specific factor is the hyperthermia (39.4°C), hyponatremia, elevated CK, and positive amphetamine screen indicating severe sympathomimetic effects. Rapid cooling and benzodiazepines are the best choice to reduce heat generation, control agitation, and prevent rhabdomyolysis complications. Activated charcoal is suboptimal as adsorption is poor for amphetamines post-ingestion; flumazenil is incorrect without benzodiazepine toxicity; N-acetylcysteine is not indicated absent hepatic injury. A clinical pearl is to monitor for serotonin syndrome in MDMA use due to its serotonergic properties. Aggressive fluid management is crucial for hyponatremia, avoiding hypotonic fluids to prevent cerebral edema.
  19. A 52-year-old male (weight 84 kg) is evaluated after a workplace exposure in which he inhaled fumes from a methylene chloride–based paint stripper in a poorly ventilated room for approximately 20 minutes. Current medications: none. Medical history: coronary artery disease with prior stent, gastroesophageal reflux disease. Allergies: none known. Vitals: blood pressure 142/86 mmHg, heart rate 104 bpm, respiratory rate 22/min, oxygen saturation 100% on room air; he reports headache and dizziness. Labs: carboxyhemoglobin 18% (elevated), serum creatinine 0.9 mg/dL, aspartate aminotransferase 30 U/L, alanine aminotransferase 26 U/L. What is the most important initial action for this exposure?
    Answer: Administer 100% oxygen via nonrebreather mask and remove the patient from the exposure source This question tests initial management of methylene chloride exposure with carbon monoxide formation. The patient has elevated carboxyhemoglobin (18%) from methylene chloride metabolism to carbon monoxide, presenting with headache and dizziness after paint stripper inhalation. Administering 100% oxygen via nonrebreather mask and removing from exposure (A) is the most important initial action, as high-flow oxygen accelerates carbon monoxide elimination and prevents further exposure. Flumazenil (B) is inappropriate as this is an inhalation exposure producing carbon monoxide, not sedative overdose. Activated charcoal (C) doesn't bind inhaled toxins and is useless for gas exposures. Deferoxamine (D) chelates iron, not carbon monoxide. Methylene chloride uniquely continues producing carbon monoxide through hepatic metabolism even after exposure ends, potentially causing delayed or prolonged toxicity. Monitor carboxyhemoglobin levels serially and consider hyperbaric oxygen for severe poisoning, especially with the patient's cardiac history.
  20. A 36-year-old male (90 kg) presents after being found in a garage with a running car; he has headache, dizziness, and nausea. Current medications: none. Labs: carboxyhemoglobin 24% (normal <2% nonsmoker), serum creatinine 0.9 mg/dL, aspartate aminotransferase 22 units/L, alanine aminotransferase 20 units/L. Allergies: none. History: no chronic illness; exposure occurred about 1 hour ago. What is the most important initial action for this exposure?
    Answer: Administer 100% oxygen via non-rebreather mask immediately and monitor neurologic status This question tests the initial management of carbon monoxide poisoning, prioritizing oxygen therapy to displace CO from hemoglobin. The key patient-specific factor is the elevated carboxyhemoglobin (24%) with symptoms like headache and nausea confirming significant exposure. Administering 100% oxygen via non-rebreather is best as it reduces CO half-life from 4-6 hours on room air to about 1 hour, improving tissue oxygenation. Naloxone is incorrect without opioid involvement; N-acetylcysteine is not indicated; inducing emesis is contraindicated for inhalation exposures. A clinical pearl is to consider hyperbaric oxygen for severe cases with neurologic deficits or carboxyhemoglobin >25%. Always screen for co-exposures like cyanide in fire-related incidents.

Start this quiz