Clinical Toxicology: Overdose & Poisoning

Learning Goal: This curriculum aims to equip medical professionals, emergency responders, and advanced healthcare students with the clinical reasoning and practical protocols needed to accurately diagnose and safely manage acute poisonings, common drug overdoses, and toxicological emergencies.

• Prerequisites: Basic biology and general chemistry.
• Estimated Total Study Time: 18 Hours

Module 1: Foundations of Pharmacology and Physiology

Before diagnosing complex toxic states, you must master how substances interact with human systems. This module establishes the core principles of pharmacokinetics (how the body processes a substance) and pharmacodynamics (how the substance alters physiology), with a deep dive into the autonomic nervous system—the clinical target for many classic toxidromes.

Recommended Videos

Introduction to Pharmacology

@ProfessorDaveExplains07:37424,396

Introduction to Pharmacology

Pharmacology is the branch of medicine concerned with the uses, effects, and mechanisms of action of drugs, which are substances that produce physiological effects in the body beyond nutritional value; understanding pharmacology requires foundational knowledge in chemistry, biochemistry, biology, anatomy, physiology, and microbiology to comprehend how drugs interact with molecular targets like enzymes and signaling molecules to treat diseases.

@ProfessorDaveExplains · 07:37

• Why this video: This video provides a structured entry point into pharmacology, clarifying the difference between exogenous drugs and endogenous molecules, and laying out the basic taxonomy of drug actions. It establishes the vocabulary required for all subsequent clinical lectures.
• Knowledge Checkpoint:
  • Define the primary difference between a drug's therapeutic effect and its toxicological profile.
  • Explain how molecular structure dictates a drug's target binding affinity.

Pharmacokinetics vs Pharmacodynamics Explained | Intro to Pharmacology

@advancedeclinicaltraining03:437,903

Pharmacokinetics vs Pharmacodynamics Explained | Intro to Pharmacology

Pharmacokinetics describes how the body processes a drug through absorption, distribution, metabolism, and excretion (ADME), while pharmacodynamics explains how the drug affects the body through receptor binding and biochemical mechanisms; together they determine drug concentration-effect relationships and guide optimal dosing within the therapeutic window to ensure safe and effective therapy.

@advancedeclinicaltraining · 03:43

• Why this video: Mastering the ADME framework (Absorption, Distribution, Metabolism, and Excretion) is crucial to predicting how long a toxin will persist in a poisoned patient. This video clearly contrasts ADME with receptor-mediated pharmacodynamics, which is vital for understanding why certain antidotes work at the receptor level.
• Knowledge Checkpoint:
  • Sketch out the ADME pathway and identify how hepatic first-pass metabolism alters bioavailability.
  • Describe the difference between agonist and antagonist actions at the cellular level.

Pharmacology - AUTONOMIC NERVOUS SYSTEM (MADE EASY)

@SpeedPharmacology08:151,827,590

Pharmacology - AUTONOMIC NERVOUS SYSTEM (MADE EASY)

The autonomic nervous system regulates involuntary body functions through two opposing divisions: the sympathetic division (fight-or-flight response) arising from thoracic and lumbar spinal cord regions, which uses preganglionic cholinergic neurons and postganglionic adrenergic neurons to produce effects like pupil dilation, increased heart rate, and inhibited digestion; and the parasympathetic division (rest-and-digest response) arising from cranial nerves III, VII, IX, X and sacral regions S2-

@SpeedPharmacology · 08:15

• Why this video: The autonomic nervous system (ANS) controls the involuntary functions commonly disrupted in acute poisonings (pupil size, heart rate, sweating). This video clarifies the anatomical divisions, neurotransmitters (acetylcholine and norepinephrine), and receptors (muscarinic, nicotinic, alpha, and beta) that dictate toxidrome presentation.
• Knowledge Checkpoint:
  • Differentiate between the sympathetic (thoracolumbar) and parasympathetic (craniosacral) pathways.
  • List the primary receptors targeted by norepinephrine and acetylcholine, along with their physiological responses in target organs.

Module 2: Introduction to Toxicology and Toxidromes

This module transitions from basic pharmacology to active emergency triage. You will learn to recognize "toxidromes"—constellations of clinical signs that point to specific drug classes—and master the foundational triage priorities of clinical toxicology.

Recommended Videos

What is toxicology?

@riskbites03:0657,651

What is toxicology?

Toxicology is the scientific study of how substances interact with living organisms, examining where chemicals go in the body, what they do, and how they leave, with the goal of understanding and preventing harm from chemical exposure while recognizing that our bodies require certain chemicals to function properly but can be disrupted by excessive or insufficient amounts of harmful substances.

@riskbites · 03:06

• Why this video: This video introduces the core toxicological tenet: "the dose makes the poison." It frames how acute exposure profiles shape systemic cellular damage, helping you build a conceptual foundation before studying clinical presentations.
• Knowledge Checkpoint:
  • Explain how exposure duration (acute vs. chronic) alters toxicity presentation.
  • Describe how individual patient biological variation shifts the toxic threshold curve.

The Ohio EMS Conference 2012-05-21 Brad Raetzke Drugs on the Streets Where We Live

@ohiohealthems35:31152

The Ohio EMS Conference 2012-05-21 Brad Raetzke Drugs on the Streets Where We Live

Emergency physicians must approach overdose patients using the ABCs (Airway, Breathing, Circulation) with most treatment being supportive care. Initial assessment includes mental status, breathing patterns, heart rate, and temperature. Intoxicated patients require trauma considerations as altered mental status can mask injuries. The five common toxidromes are: sympathetic (cocaine, amphetamines) with fight-or-flight response, hypertension, tachycardia, and dilated pupils; severe cases develop ex

@ohiohealthems · 35:31

• Why this video: To address the need for a practical emergency department framework, this video details how to clinically approach a poisoned patient. It stresses prioritizing the airway, breathing, and circulation (ABCs) and emphasizes that most toxicology management centers on high-quality supportive care.
• Knowledge Checkpoint:
  • Explain the sequential steps of the ABC assessment during initial emergency resuscitation of an overdose patient.
  • State why empiric supportive care often takes priority over chasing a definitive toxicology screen.

Toxidrome Crash Course: Symptoms & Mnemonics 🧪

@lecturiomedical07:354,148

Toxidrome Crash Course: Symptoms & Mnemonics 🧪

Toxidromes are characteristic clinical syndromes caused by specific drug classes that can be differentiated by their autonomic effects: sympathomimetic toxidrome causes tachycardia, hypertension, hyperthermia, and mydriasis with normal secretions; anticholinergic toxidrome presents similarly but with dry skin and secretions (remembered by 'Mad as a Hatter, Blind as a Bat, Red as a Beet, Hot as a Hare, Dry as a Bone'); cholinergic toxidrome shows bradycardia, hypotension, miosis, and copious secr

@lecturiomedical · 07:35

• Why this video: This high-yield clinical lecture uses mnemonics and clear physiological groupings to break down major toxidromes (anticholinergic, cholinergic, sympathomimetic, and opioid). It helps you quickly identify toxidromes using key vital signs and physical exam findings like pupil diameter and skin moisture.
• Knowledge Checkpoint:
  • Contrast the clinical presentation of a sympathomimetic toxidrome with an anticholinergic toxidrome based on diaphoresis (sweating).
  • List the classic symptoms of cholinergic toxicity using the SLUDGE or DUMBBELS mnemonic.

Module 3: Managing Common Analgesic and Opioid Overdoses

Analgesics (acetaminophen, aspirin) and opioids represent the most common and dangerous intentional and accidental toxic exposures. This module covers the complex pathophysiology, diagnostic timelines, and life-saving antidotal therapies for these overdoses.

Recommended Videos

Paracetamol Overdose | Administering NAC | Details

@DetailsMedical07:43133,276

Paracetamol Overdose | Administering NAC | Details

Paracetamol overdose causes severe hepatic necrosis by overwhelming the body's reduced glutathione supply, which normally binds the toxic metabolite NAPQI; N-acetylcysteine (NAC) acts as an antidote by providing cysteine for glutathione synthesis and directly binding NAPQI. The therapeutic dose is 4g in 24 hours, with overdose defined as >4g in <1 hour (single) or >1 hour (staggered). Management requires calculating ingested mg/kg (using 500mg/tablet), checking paracetamol levels at 4 hours, and

@DetailsMedical · 07:43

• Why this video: Acetaminophen (paracetamol) is highly hepatotoxic in overdose due to the depletion of glutathione and the accumulation of the reactive metabolite NAPQI. This clinical video provides an in-depth breakdown of paracetamol metabolism and details the exact administration protocol for the antidote, N-acetylcysteine (NAC).
• Knowledge Checkpoint:
  • Draw the pathway of acetaminophen metabolism, noting the roles of glutathione and the toxic metabolite NAPQI.
  • Explain how to use the Rumack-Matthew nomogram to guide the timing and administration of NAC.

Aspirin (ASA) Toxicity: "EM in 5"

@EMin506:4243,548

Aspirin (ASA) Toxicity: "EM in 5"

Acute salicylate toxicity presents with a characteristic triad of metabolic acidosis, respiratory alkalosis, and metabolic alkalosis, with treatment focusing on aggressive fluid resuscitation, urinary alkalinization to achieve a urine pH of 7.5, and hemodialysis for serum levels exceeding 100 mg/dL or severe symptoms; key diagnostic thresholds include ingestion of >150 mg/kg or serum levels >30 mg/dL indicating toxicity, with hemodialysis indicated for levels >100 mg/dL or significant clinical m

@EMin5 · 06:42

• Why this video: Salicylate (aspirin) toxicity is uniquely dangerous, presenting with a mixed acid-base disorder (respiratory alkalosis and metabolic acidosis). This rapid, high-yield guide explains the complex physiology of aspirin overdose and covers key management strategies, including urinary alkalinization and indications for emergent hemodialysis.
• Knowledge Checkpoint:
  • Explain why salicylate toxicity causes both hyperventilation (respiratory alkalosis) and a widened anion gap metabolic acidosis.
  • Describe the physiological mechanism behind urinary alkalinization with sodium bicarbonate to promote salicylate excretion.

Teaching Friends & Family How to Reverse a Drug Overdose: Project Hope

@NationwideChildrens03:24106,983

Teaching Friends & Family How to Reverse a Drug Overdose: Project Hope

Naloxone (Narcan) is a medication that reverses opioid overdoses by displacing opioids from brain receptors, enabling breathing to resume; it is administered via nasal spray with half the dose going into each nostril, and if the person doesn't respond within 2-3 minutes, a second dose should be given while placing the victim in a recovery position on their side to prevent choking on vomit.

@NationwideChildrens · 03:24

• Why this video: Opioid overdose primarily kills by depressing the respiratory drive in the brainstem. This clinical training video demonstrates how to recognize severe opioid toxicity and safely administer naloxone (Narcan) via the nasal route to restore respiration.
• Knowledge Checkpoint:
  • Identify the clinical triad of acute opioid overdose.
  • Describe how naloxone acts at the receptor level to reverse respiratory depression and state the parameters for administering repeat doses.

Module 4: Cardiovascular, Psychotropic, and Stimulant Toxicity

This module addresses some of the most hemodynamically unstable patients in toxicology. You will study how to recognize and treat toxicities from key cardiovascular medications (beta-blockers and calcium channel blockers), cyclic antidepressants, and acute sympathomimetic stimulant use.

Recommended Videos

Treating beta blocker and calcium channel blocker toxicity

@MedMastery03:438,857

Treating beta blocker and calcium channel blocker toxicity

Beta blocker and calcium channel blocker toxicity causes bradycardia and hypotension by blocking calcium influx into cardiac myocytes; treatment follows the ABC roadmap with intravenous calcium salts (directly increasing calcium availability) and glucagon (indirectly activating calcium channels through beta-receptor stimulation), supported by atropine for heart rate, epinephrine for systemic support, and hyperinsulinemia-euglycemia for metabolic support, with magnesium added specifically for sot

@MedMastery · 03:43

• Why this video: Beta-blocker and calcium channel blocker overdoses cause profound, life-threatening bradycardia and shock. This video explains the physiological mechanisms of these overdoses and outlines step-by-step critical therapies, including the use of intravenous calcium and high-dose insulin euglycemia therapy (HIET).
• Knowledge Checkpoint:
  • Contrast how beta-blockers and calcium channel blockers impair intracellular calcium availability in cardiac myocytes.
  • Explain the therapeutic rationale for using high-dose insulin therapy in severe calcium channel blocker toxicity.

TCA Toxicity

@EMin505:0541,718

TCA Toxicity

Tricyclic antidepressant (TCA) toxicity presents with varied symptoms due to multiple mechanisms including anticholinergic effects (confusion, dilated pupils, flushed skin, dryness), seizures, hypotension, and sodium channel blockade causing cardiac toxicity. Key diagnostic features include EKG findings of widened QRS complex and dominant R wave in AVR >3mm, which correlate with severity (QRS >100ms indicates increased seizure risk, >160ms indicates risk of VTAC). Management involves sodium bica

@EMin5 · 05:05

• Why this video: Tricyclic antidepressant (TCA) toxicity causes rapid clinical deterioration through three main pathways: cardiotoxicity, seizures, and severe anticholinergic effects. This guide demonstrates how to detect TCA cardiotoxicity on an ECG and outlines the critical, immediate use of sodium bicarbonate to prevent lethal ventricular arrhythmias.
• Knowledge Checkpoint:
  • State the "three Cs" of TCA toxicity.
  • Identify the classic ECG signs of TCA toxicity, focusing on QRS duration and the terminal R wave in lead aVR.
  • Describe how sodium bicarbonate therapy reverses TCA-induced sodium channel blockade.

Serotonin Syndrome vs. Neuroleptic Malignant Syndrome | Similarities & Differences

@jjmedicine06:2993,503

Serotonin Syndrome vs. Neuroleptic Malignant Syndrome | Similarities & Differences

Serotonin Syndrome and Neuroleptic Malignant Syndrome are both life-threatening conditions with overlapping symptoms but distinct underlying mechanisms; Serotonin Syndrome involves overactivation of the serotonergic system from SSRIs, MAOIs, or TCAs and presents with the MAN triad (mental status changes, autonomic hyperactivity, neuromuscular abnormalities) plus clonus and diarrhea, while Neuroleptic Malignant Syndrome results from dopamine receptor antagonism from antipsychotics or abrupt dopam

@jjmedicine · 06:29

• Why this video: Serotonin Syndrome and Neuroleptic Malignant Syndrome (NMS) are life-threatening psychiatric emergencies that present with overlapping symptoms like hyperthermia and altered mental status. This clinical video contrasts their different pathophysiologies, physical exam signs, and distinct medical management.
• Knowledge Checkpoint:
  • Differentiate Serotonin Syndrome from NMS using neuromuscular physical exam findings (e.g., clonus vs. "lead-pipe" rigidity).
  • List the primary causative agents for both syndromes and their respective targeted antidotal treatments.

Exam Recall Series (NEET-PG '24) - Forensic

@marrowmed07:4947,829

Exam Recall Series (NEET-PG '24) - Forensic

This segment covers toxicology of common poisons. Cocaine poisoning presents with sympathetic toxidrome: tachycardia, tachypnea, diaphoresis, dilated pupils. Treatment is benzodiazepines. Chronic cocaine abuse triad: septal perforation, tongue ulceration, peripheral gangrene. Cocaine bugs (formication) are tactile hallucinations. Ethylene glycol (antifreeze) metabolism: glycolic acid (high anion gap metabolic acidosis) and oxalic acid (hypocalcemia from calcium oxalate crystals). Treatment: fome

@marrowmed · 07:49

• Why this video: This medical review details acute cocaine and stimulant toxicity. It highlights how sympathomimetic overdoses present, notes the risk of severe coronary vasospasm, and reviews why benzodiazepines are the first-line treatment for managing these hyperadrenergic states.
• Knowledge Checkpoint:
  • Describe the physiological mechanism of cocaine-induced sympathomimetic crisis.
  • Explain why beta-blockers must be avoided or used with extreme caution in acute cocaine toxicity due to "unopposed alpha-stimulation."

Module 5: Environmental Toxins, Alcohols, and Antidotes

This module covers complex, biochemically-driven toxicology, focusing on toxic alcohols (methanol and ethylene glycol), metabolic cellular poisons (cyanide), and the practical procedures of gastrointestinal decontamination in the acute setting.

Recommended Videos

Alcohol Metabolism, Methanol Poisoning, Fatty Change Alcoholic Hypoglycemia Fomepazole

@stomponstep198913:4857,707

Alcohol Metabolism, Methanol Poisoning, Fatty Change Alcoholic Hypoglycemia Fomepazole

Ethanol is metabolized by alcohol dehydrogenase to acetaldehyde, then by acetaldehyde dehydrogenase to acetate; this process generates NADH which disrupts normal metabolism by decreasing gluconeogenesis and fat oxidation while increasing anaerobic glycolysis, leading to hypoglycemia, lactic acidosis, and fatty liver changes. Methanol poisoning is treated with fomepizole (which inhibits alcohol dehydrogenase) or ethanol (which competitively inhibits the same enzyme), preventing the toxic conversi

@stomponstep1989 · 13:48

• Why this video: This clinical lecture covers the cellular biochemistry of alcohol metabolism. It explains why methanol and ethylene glycol are relatively non-toxic until they are metabolized by alcohol dehydrogenase into formic acid and glycolic/oxalic acids, and details how the antidote fomepizole stops this toxic transformation.
• Knowledge Checkpoint:
  • Diagram the metabolism of methanol and ethylene glycol, naming the toxic intermediate acids that cause metabolic acidosis.
  • Explain how fomepizole works at the molecular level to treat toxic alcohol poisonings.

A Dad Mistakenly Drank A Snowglobe. This Is What Happened To His Kidneys.

@chubbyemu14:452,197,282

A Dad Mistakenly Drank A Snowglobe. This Is What Happened To His Kidneys.

Ethylene glycol, commonly found in antifreeze, is metabolized in the liver into toxic compounds including glycolic acid, glyoxylic acid, and oxalic acid, which are negatively charged anions that cause high anion gap metabolic acidosis; these metabolites bind with calcium to form insoluble calcium oxalate crystals that accumulate in kidney tubules, causing severe kidney damage and potentially requiring dialysis, especially when treatment is delayed beyond 2 days.

@chubbyemu · 14:45

• Why this video: This clinical case study presents a clear, narrative breakdown of ethylene glycol toxicity. It traces how antifreeze ingestion leads to profound anion-gap metabolic acidosis, calcium oxalate crystal deposition in renal tubules, and acute kidney injury, emphasizing how quickly clinical parameters can deteriorate.
• Knowledge Checkpoint:
  • Describe the classic urinary microscopy finding associated with ethylene glycol poisoning.
  • Explain why hypocalcemia occurs in ethylene glycol ingestion and how it relates to oxalate precipitation.

Cyanide Poisoning

@klossandbruce389707:5771,370

Cyanide Poisoning

Cyanide poisoning occurs when cyanide molecules bind to cytochrome oxidase, blocking the electron transport chain and causing cellular hypoxia; clinical manifestations include headache, nausea, vomiting, altered mental status, and respiratory distress, progressing to cardiac collapse; diagnosis relies on detecting extreme lactic acidosis (often >10 mEq/L) with metabolic acidosis; treatment involves administering hydroxocobalamin (the preferred antidote), sodium thiosulfate, and avoiding amyl/nit

@klossandbruce3897 · 07:57

• Why this video: Cyanide is a highly lethal metabolic poison that shuts down cellular respiration. This clinical presentation details how cyanide binds to the mitochondrial electron transport chain and reviews the standard antidotal options (hydroxocobalamin and the sodium thiosulfate/nitrite regimen) used in emergency treatment.
• Knowledge Checkpoint:
  • Identify which specific mitochondrial enzyme complex cyanide inhibits, and explain how this causes severe lactic acidosis.
  • Contrast how hydroxocobalamin and sodium thiosulfate work differently as antidotes for cyanide poisoning.

Gastric Lavage Demo

@sammygold426300:42286,772

Gastric Lavage Demo

Before performing gastric lavage, administer 50 grams of activated charcoal through the blue port of the lavage system. This initial dose helps absorb any toxin that may have moved into the duodenum during the procedure. Close the blue port after administration, then proceed with the lavage by opening the inbag (blue side) and using both plungers simultaneously to instill and remove fluid.

@sammygold4263 · 00:42

• Why this video: This video provides a quick demonstration of gastric lavage and highlights the critical timing of clinical gastrointestinal decontamination. It shows how administering activated charcoal alongside lavage can absorb remaining toxins before they pass into the duodenum.
• Knowledge Checkpoint:
  • State the primary contraindications for gastric lavage (e.g., airway protection status, corrosive ingestions).
  • Explain the optimal time window post-ingestion for administering activated charcoal to a patient in the emergency department.

Independent Study Alert (GI Decontamination Guidelines): The video pool lacks a comprehensive clinical lecture on whole-bowel irrigation (WBI) protocols. To master this topic, independently search for the AACT/EAPCCT Position Statements on Gastrointestinal Decontamination. Be sure to learn the specific indications for WBI, such as ingestions of heavy metals (lead, iron), lithium, or enteric-coated/sustained-release medications.

Course Map

This map outlines the recommended progression through the curriculum. Modules build on each other, moving from fundamental physiological principles to clinical toxidromes, and finally to specific drug classes and toxicological interventions.

Key People Index

The following clinicians, emergency educators, and toxicologists are highlighted for their high-yield contributions to the lectures in this curriculum:

• Dr. Brad Raetzke, MD (Ohio EMS Conference): An emergency physician specializing in clinical triage protocols and pre-hospital management of street drugs and acute toxidrome presentations.
• Dr. Rodrigo Cavallazzi, MD (UofL Medicine): A critical care specialist who provides clear teaching on toxic inhalation, cyanide poisoning, and mechanical ventilation strategies for poisoned patients.
• Dr. Tom Rogers, MD (Performance Medicine): A preventive medicine specialist and clinical educator who reviews clinical protocols for administering N-acetylcysteine (NAC) in acute hepatic injury.
• Chubbyemu (Dr. Bernard Hsu, PharmD): A clinical pharmacist and medical educator who uses detailed case studies to explain metabolic biochemistry, toxin pathophysiology, and multi-system organ failure.

Final Self-Assessment

Complete this comprehensive self-assessment to verify your clinical mastery of the curriculum material.

• M1: Explain how a drug's volume of distribution ($V_d$) impacts its clearance rate and dictates whether it can be removed via emergency hemodialysis.
• M1: Map out the physiological changes that occur during a sympathomimetic surge, noting changes in heart rate, blood pressure, pupillary response, and sweating.
• M2: Correctly classify a patient presenting with hyperthermia, dry skin, urinary retention, delirium, and dilated pupils into their correct toxidrome.
• M2: State the sequential steps of the initial "resus" assessment (ABCs) for an unresponsive patient suspected of ingestion.
• M3: Determine if a patient requires N-acetylcysteine (NAC) therapy by plotting a timed 4-hour serum paracetamol concentration on the Rumack-Matthew nomogram.
• M3: Explain the physiological mechanisms behind respiratory alkalosis and metabolic acidosis in salicylate toxicity, and detail how to safely alkalinize urine.
• M3: State the proper clinical indications, dosing, and administration routes for naloxone (Narcan) in an acute opioid overdose emergency.
• M4: Explain why high-dose insulin is used as an inotropic support agent in severe calcium channel blocker overdoses.
• M4: Identify a wide QRS complex on an ECG in the context of an antidepressant overdose, and explain how to treat it with sodium bicarbonate.
• M4: Contrast the neuromotor presentations of Serotonin Syndrome and Neuroleptic Malignant Syndrome (NMS), and state the target therapies for each.
• M5: Explain the biochemical mechanism of fomepizole in treating methanol or ethylene glycol poisoning.
• M5: Describe how cyanide impairs mitochondrial cellular ATP production, and outline the emergency management protocol for cyanide toxicity.
• M5: Identify the key contraindications and time windows for gastrointestinal decontamination techniques, including activated charcoal and gastric lavage.