Toxicological Emergencies: Acute Intoxications
Emergency · Clinical Specialties
How it begins
Toxicology in the emergency department requires a deep understanding of toxicokinetics (what the body does to the xenobiotic under supraphysiological doses) and toxicodynamics (the molecular pathophysiological impact of the xenobiotic on target systems). When an overdose occurs, conventional first-order kinetic laws often become saturated, transitioning toward zero-order kinetics…
What it covers
- Pharmacokinetic Alterations in Acute Intoxication
- Zero Order Kinetics vs. Order One
- Biotransformation Pathways and Generation of Toxic Metabolites
- Airway with a Toxicological Approach
- Ventilation (Breathing)
- Circulation
- Neurological Status (Disability) and the "Coma Cocktail"
- Activated Charcoal (Single Dose and Multiple Dose)
- · Single Dose Activated Carbon Protocol (CADU)
- · Multiple Dose Activated Carbon (CADM) and "Gastrointestinal Dialysis"
- Gastric Lavage (Current Status and Restrictions)
- Total Intestinal Irrigation (IIT)
- Appropriateness Criteria for Hemodialysis (HD)
- Intravenous Lipid Emulsion Therapy (ILE / Lipid Rescue)
- · Proposed Action Mechanisms
- Pathophysiology and Clinical Semiotics
- Urinary Retention and Ileus
- Management and Use of Physostigmine
- Peripheral Muscarinic Pathophysiology (Mnemonic: DUMBELS)
- Peripheral Nicotinic Effects (Mnemonic: MTWTF — Days of the Week in English)
- Central Manifestations
- Adrenergic Pathophysiology
- Thermoregulation and Rhabdomyolysis
- Physiopathological Differences: Benzodiazepines vs. Barbiturates
- Risks of Flumazenil
- Classic Triad of Opioid Intoxication
- Cardiovascular and Pulmonary Complications
- Pathophysiology of Cell Damage and Metabolism
- Clinical Phases of Intoxication
- The Rumack-Matthew Nomogram
- N-Acetylcysteine (NAC): Mechanisms and Administration Protocol
- · NAC Action Mechanisms
- · Classic 21-hour Intravenous Protocol (3-Stage Protocol)
- NAC-induced Anaphylactoid Reactions
- Pathophysiology of Complex Acid-Base Disorder
- Cellular Neuroglycopenia and pH-Dependency
- Urinary Alkalinization: The Principle of "Ionic Trapping"
- Pathophysiology of Cardiotoxicity and Neurotoxicity
- Electrocardiographic Criteria for Risk of Death
- The Use of Sodium Bicarbonate as a Physiological Antidote
- Cellular Pathophysiology
- Serum Potassium as a Prognostic Factor
- Clinical and Electrocardiographic Manifestations
- Physiopathological Differentiation
- High Dose Insulin-Euglycemia Therapy (HDI)
- · Mechanism of Action
- The Use of Glucagon in Beta-Blocker Overdose
- The Alcohol Dehydrogenase (ADH) Pathway
- Isopropanol (Rubbing Alcohol): The Exception without Acidosis
- Gap Diagnosis (Anion Gap and Osmolal Gap)
- ADH inhibition: Fomepizole vs. Ethanol
- Cardiovascular Complications from Cocaine
- Ecstasy (MDMA), Dilutional Hyponatremia and Cerebral Edema
- Cellular Pathophysiology
- Late Neurological Syndrome (TLS)
- Treatment: Normobaric Oxygen Therapy vs. Hyperbaric (HBO)
- Pathophysiology of Cellular Respiratory Blockade
- Clinical Presentation and the Diagnostic Key "Cherry Red"
- Specific Antidote Treatment
- Molecular Mechanism of Action
- Atropinization and the Role of Oximes (Pralidoxime, Obidoxime)
- Intermediate Syndrome
- Acute and Chronic Saturnism (Lead)
- Mercury and Arsenic
- Chelating Agents: Molecular Pharmacology
- Analysis of the Electrocardiogram as a Toxicological Tool
- Analytical Limitations of Urine Drug Screening (Screeing)
- Consideration of Closure and Clinical Safety
The complete study guide is in the app
This page summarizes the outline. The full interactive study guide —with high-yield diagrams, clinical tables, and board review cases— can be read inside Epistemis, completely offline and ad-free.
- Subject
- Emergency
- Category
- Clinical Specialties
- Type
- Study Guide
- Sections
- 68
- Reviewed
- 2026-08-02