ABEM Medical Tox cheat sheet

Volume of distribution (Vd) = dose / plasma concentration; a Vd greater than 1 L/kg indicates extensive tissue distribution and poor removal by hemodialysis.

First-order elimination: t½ = 0.693 × Vd / clearance; steady state is reached after approximately 5 half-lives.

Clearance = elimination rate / plasma concentration; for high-extraction drugs, hepatic clearance approaches liver blood flow.

Hemodialysis removes toxins best when Vd is low (<1 L/kg), protein binding is low, molecular mass is small, and the compound is water soluble.

Activated charcoal 1 g/kg (maximum 50 g) is most effective within 1 hour; contraindicated with an unprotected airway, caustic ingestion, GI obstruction, and high-aspiration-risk hydrocarbons.

Whole bowel irrigation with polyethylene glycol 1-2 L/h in adults is used for sustained-release products, iron, lithium, and body packing.

Urine alkalinization to pH 7.5-8.5 enhances elimination of weak acids such as salicylate and phenobarbital.

Reference dose = NOAEL / uncertainty factors; hazard quotient = exposure / reference dose, and a quotient greater than 1 prompts further risk evaluation.

Anion gap = Na − (Cl + HCO3), normal 8-12 mEq/L; osmolar gap = measured − calculated osmolality, and a gap above 10 suggests an unmeasured osmole.

Acetaminophen is oxidized by CYP2E1 to NAPQI; N-acetylcysteine restores glutathione, and the Rumack-Matthew nomogram is applied from 4 hours post-ingestion.

Salicylate poisoning produces mixed respiratory alkalosis and metabolic acidosis; bicarbonate alkalinizes urine, and hemodialysis is used for severe toxicity.

Calcium channel blocker overdose: IV calcium, high-dose insulin with dextrose, vasopressors, and intravenous lipid emulsion for refractory shock.

Beta blocker overdose: glucagon 3-10 mg IV and high-dose insulin euglycemia are used for refractory bradycardia and hypotension.

Tricyclic antidepressant toxicity: sodium bicarbonate for QRS >100 ms; flumazenil and class IA or IC antiarrhythmics are contraindicated.

Digoxin toxicity: Fab fragments for life-threatening arrhythmia or hyperkalemia; calcium is traditionally avoided.

Iron poisoning: deferoxamine for shock, acidosis, or serum iron >500 µg/dL with symptoms; abdominal radiograph may show radiopaque tablets.

Lithium: hemodialysis for level >4 mEq/L, or >2.5 mEq/L with symptoms or renal failure; activated charcoal does not bind lithium.

Sulfonylurea-induced hypoglycemia: octreotide suppresses insulin secretion and reduces recurrent hypoglycemia.

Ethanol is oxidized by alcohol dehydrogenase and, at high concentrations, by CYP2E1; fomepizole inhibits alcohol dehydrogenase in methanol and ethylene glycol poisoning.

Methanol → formaldehyde → formic acid: anion gap metabolic acidosis, visual loss, and putaminal necrosis; treat with fomepizole, folinic acid, bicarbonate, and hemodialysis.

Ethylene glycol → glycolic and oxalic acid: anion gap acidosis, hypocalcemia, calcium oxalate crystalluria, and renal failure; treat with fomepizole, thiamine, pyridoxine, and hemodialysis.

Isopropanol → acetone: ketosis without metabolic acidosis, hemorrhagic gastritis, and CNS depression; supportive care is usually sufficient.

The osmolar gap rises early in toxic alcohol ingestion and falls as metabolites accumulate and the anion gap rises.

Cocaine toxicity: benzodiazepines first; sodium bicarbonate for QRS widening; avoid pure beta blockade because of unopposed alpha effects.

Opioid overdose: miosis, respiratory depression, and CNS depression; naloxone reverses effects but may precipitate withdrawal.

Alcohol withdrawal: symptom-triggered benzodiazepines using CIWA scoring; give thiamine before glucose to prevent Wernicke encephalopathy.

GHB intoxication: rapid-onset deep coma with preserved reflexes and bradycardia; recovery usually occurs within hours and no antidote exists.

Lead inhibits ALA dehydratase and ferrochelatase, producing microcytic anemia with basophilic stippling; chelation options include succimer, EDTA, and dimercaprol.

Dimercaprol is contraindicated in methylmercury poisoning because it redistributes mercury into the brain; DMPS or DMSA may be considered.

Arsenic: DMPS or DMSA chelation, with dimercaprol for acute severe cases; sources include contaminated groundwater and rice.

Cadmium: inhalation pneumonitis and emphysema, renal tubular proteinuria, and osteomalacia; no chelator has proven benefit.

Carbon monoxide half-life is 4-6 hours in room air and about 1 hour on 100% oxygen; hyperbaric oxygen is considered for neurologic deficits, cardiac ischemia, or pregnancy.

Cyanide poisoning: cellular hypoxia with high lactate and normal PaO2; hydroxocobalamin or sodium thiosulfate are antidotes.

Methemoglobinemia: cyanosis unresponsive to oxygen, chocolate-brown blood, and a saturation gap; methylene blue 1-2 mg/kg is avoided in G6PD deficiency.

Organophosphate poisoning: bradycardia, bronchorrhea, miosis, and fasciculations; atropine is titrated to secretions and pralidoxime given early.

Silica and asbestos cause pneumoconiosis and malignancy; beryllium causes chronic beryllium disease with granulomas and sensitization.

Nerve agents (sarin, soman, VX) irreversibly inhibit acetylcholinesterase; treat with atropine, pralidoxime, and benzodiazepines for seizures.

Succinylcholine should be avoided in nerve agent poisoning because prolonged paralysis results from inhibited plasma cholinesterase.

Sulfur mustard is an alkylating vesicant with a latent period before erythema, blisters, and airway injury; no antidote exists.

Lewisite is an arsenical vesicant; dimercaprol is the chelating antidote.

Phosgene and chlorine cause delayed noncardiogenic pulmonary edema; treatment is removal from exposure, oxygen, and observation.

Ricin is a ribosome-inactivating protein from castor beans; inhalation causes delayed pulmonary edema and there is no antidote.

Botulism causes descending flaccid paralysis with cranial nerve findings; equine antitoxin and ventilatory support are treatment.

Anthrax: post-exposure prophylaxis with ciprofloxacin or doxycycline; cutaneous disease produces a painless black eschar.

Hazmat PPE: Level A is fully encapsulating with SCBA; Level B uses SCBA with chemical-resistant clothing; Levels C and D offer progressively less protection.

Immunoassay is used for screening and GC-MS or LC-MS/MS for confirmation; a screening result alone is not forensic proof.

Amphetamine immunoassays can be falsely positive with pseudoephedrine, bupropion, and ranitidine; opioid assays with poppy seeds; PCP assays with ketamine and dextromethorphan.

Ethanol: the Widmark equation estimates BAC from dose, body weight, and distribution factor; elimination averages 15-20 mg/dL/h.

Postmortem drug concentrations are affected by redistribution; femoral blood and vitreous humor are preferred specimens.

CO-oximetry measures carboxyhemoglobin and methemoglobin; standard pulse oximetry cannot distinguish these from oxyhemoglobin.

Antidote pairs: acetaminophen–NAC, methanol or ethylene glycol–fomepizole, opioids–naloxone, benzodiazepines–flumazenil (with caution), iron–deferoxamine, digoxin–Fab.

Physostigmine can reverse anticholinergic delirium but is avoided in wide QRS or suspected tricyclic overdose.

Chain of custody documents specimen handling from collection to court; a break in the chain can invalidate forensic results.

Delta-delta ratio = (measured anion gap − normal anion gap) / (normal HCO3 − measured HCO3); it helps detect mixed metabolic disorders.