Toxicology high yield terms

Modes of Toxic Action

Includes consideration of events at organ, cell, and molecular levels that lead to toxicity via uptake, distribution, metabolism, mode of action, and excretion

Modes of Toxic Action

Describes important molecular events in the cascade of toxicity, such as inhibition of acetylcholinesterase in organophosphorus and carbamate pesticide toxicity

Biochemical and molecular toxicology

Considers events at biochemical and molecular levels, including enzymes that metabolize xenobiotics, reaction of intermediates with macromolecules, and gene expression changes

Behavioral toxicology

Studies effects of toxicants on animal and human behavior, affecting nervous function and central nervous systems, along with endocrine effects

Nutritional toxicology

Deals with dietary effects on the expression and mechanisms of toxicity

Carcinogenesis

Includes chemical, biochemical, and molecular events leading to cancer

Teratogenesis

Includes chemical, biochemical, and molecular events leading to developmental defects

Mutagenesis

Studies effects of toxicants on genetic material and inheritance of those effects

Organ toxicology

Considers effects at organ level (neurotoxicity, hepatotoxicity, nephrotoxicity, etc.)

Measurement of Toxicants and Toxicity

Uses analytical chemistry, bioassay, and applied mathematics to answer questions on substance toxicity

Analytical toxicology

Branch of chemistry for identifying and assaying toxic chemicals and metabolites in biological and environmental materials

Toxicity testing

Uses living systems to estimate toxicity, from short-term genetic tests to long-term animal studies

Toxicological pathology

Examines toxic effects on subcellular, cellular, tissue, and organ levels

Structure-activity studies

Examines relationships between chemical structure and toxicity, aiding predictions

Biomath and statistics

Helps in significance determination and formulation of risk estimates

Epidemiology

Studies the relationship between chemical exposure and disease in human populations

Applied Toxicology

Focuses on applying toxicology for methodology development and toxicity assessment in real-world scenarios

Clinical toxicology

Diagnosing and treating human poisoning

Veterinary toxicology

Diagnosing and treating poisoning in animals, including livestock and companion animals

Forensic toxicology

Detecting and interpreting poisons in medico-legal cases

Environmental toxicology

Studying chemicals in the environment, including movement and effects

Industrial toxicology

Studying workplace toxic exposures and industrial hygiene

Acetaminophen

Causes nausea, vomiting, delayed jaundice, and hepatic and renal failure.

Acetaminophen

Toxicity results from liver damage due to excessive metabolite accumulation.

Salicylates

Causes metabolic acidosis, respiratory alkalosis, dehydration, and hyperthermia.

Salicylates

Toxicity results from excessive aspirin ingestion, leading to acid-base imbalances.

Carbon monoxide

Binds to hemoglobin, reducing oxygen transport and leading to hypoxia.

Carbon monoxide

Symptoms include headache, dizziness, nausea, and potential death.

Ethylene glycol

Causes metabolic acidosis, renal failure, and CNS depression.

Ethylene glycol

Toxicity results from ingestion of antifreeze, forming toxic metabolites.

Iron

Causes hepatotoxicity, metabolic acidosis, and gastrointestinal irritation.

Iron

Toxic in large amounts, leading to organ damage and systemic toxicity.

Lead

Causes cognitive impairment, anemia, neuropathy, and kidney damage.

Lead

Toxicity results from chronic exposure, especially in children and industrial workers.

Isopropyl alcohol

Causes CNS depression, gastritis, and metabolic acidosis.

Isopropyl alcohol

More toxic than ethanol, leading to severe intoxication effects.

Mercury

Causes neurological impairment, renal dysfunction, and tremors.

Mercury

Toxicity depends on the form—elemental, inorganic, or organic mercury.

Methanol

Causes metabolic acidosis, blindness, and CNS depression.

Methanol

Toxicity results from metabolism into formic acid, leading to optic nerve damage.

Mushrooms (Amanita phalloides-type)

Causes severe hepatotoxicity, leading to liver failure.

Mushrooms (Amanita phalloides-type)

Toxicity results from ingestion of amatoxins, inhibiting RNA polymerase.

Phenylcyclidine (PCP)

Causes nystagmus, hallucinations, and vertical eye movements.

Phenylcyclidine (PCP)

Toxicity results from NMDA receptor antagonism, leading to dissociative symptoms.

Acetaminophen

Antidote → N-acetylcysteine (NAC)

Acetaminophen

Best given within 8–10 hours of overdose to prevent liver failure.

Anticholinesterase (Organophosphates)

Antidote → Atropine + Pralidoxime (2-PAM)

Anticholinesterase (Organophosphates)

Atropine blocks muscarinic effects, while pralidoxime regenerates acetylcholinesterase.

Benzodiazepines

Antidote → Flumazenil

Benzodiazepines

Flumazenil is a competitive GABA receptor antagonist.

Beta-blockers

Antidote → Glucagon

Beta-blockers

Glucagon increases heart rate and contractility by bypassing beta-receptor blockade.

Carbon monoxide

Antidote → 100% Oxygen or Hyperbaric Oxygen Therapy

Carbon monoxide

Displaces CO from hemoglobin, restoring oxygen transport.

Copper, Arsenic, Gold

Antidote → Penicillamine

Copper, Arsenic, Gold

Penicillamine is a chelating agent that binds heavy metals.

Cyanide

Antidote → Hydroxocobalamin or Sodium thiosulfate

Cyanide

Hydroxocobalamin binds cyanide to form nontoxic cyanocobalamin.

Digoxin

Antidote → Digoxin-specific antibody fragments (Digibind)

Digoxin

Digibind binds free digoxin, reversing its effects.

Ethylene glycol, Methanol

Antidote → Fomepizole or Ethanol

Ethylene glycol, Methanol

Fomepizole inhibits alcohol dehydrogenase, preventing toxic metabolite formation.

Heparin

Antidote → Protamine sulfate

Heparin

Protamine binds heparin, reversing anticoagulation effects.

Iron

Antidote → Deferoxamine

Iron

Deferoxamine is a chelator that binds excess iron.

Lead

Antidote → EDTA, Dimercaprol, Succimer, or Penicillamine

Lead

These chelating agents remove lead from the body.

Methanol, Ethylene glycol

Antidote → Fomepizole or Ethanol

Methanol, Ethylene glycol

Prevents formation of toxic metabolites like formic acid.

Methemoglobin

Antidote → Methylene blue

Methemoglobin

Reduces methemoglobin back to hemoglobin, restoring oxygen transport.

Opioids

Antidote → Naloxone or Naltrexone

Opioids

These are opioid receptor antagonists that reverse respiratory depression.

Salicylates (Aspirin toxicity)

Antidote → Sodium bicarbonate

Salicylates (Aspirin toxicity)

Alkalinizes urine to enhance excretion.

Tricyclic antidepressants (TCAs)

Antidote → Sodium bicarbonate

Tricyclic antidepressants (TCAs)

Increases serum pH to reduce TCA cardiotoxicity.