Toxins and Acute Poisoning – Key Vocabulary

A comprehensive set of vocabulary flashcards covering key terms, toxins, mechanisms, doses, symptoms, diagnostic clues, and treatments discussed in the lecture on acute poisoning.

Acute toxicity

Adverse effects produced by a single or short-term exposure to a substance.

Chronic toxicity

Harmful effects resulting from repeated or continuous exposure to a substance over an extended period.

Routes of exposure

The ways a toxin enters the body: ingestion, inhalation, or transdermal absorption.

Passive diffusion (GIT)

Primary mechanism by which toxins are absorbed from the gastrointestinal tract.

Ethanol

A sedative–hypnotic alcohol rapidly absorbed from the GIT and metabolized in the liver by alcohol dehydrogenase.

Fatal dose of ethanol

Approximately 300–400 mL of pure ethanol consumed in less than one hour.

Alcohol dehydrogenase (ADH)

Liver enzyme that oxidizes ethanol to acetaldehyde while converting NAD⁺ to NADH.

Blood Alcohol Concentration (BAC)

Amount of ethanol in blood; levels above 0.45 g/100 mL are usually lethal.

Enzymatic ethanol assay

Laboratory method measuring NADH absorbance at 340 nm to quantify serum ethanol.

Methanol

Toxic alcohol found in methylated spirits; metabolized to formaldehyde and formic acid causing ocular damage and metabolic acidosis.

Toxic dose of methanol

Ingestion of roughly 60–250 mL can be lethal; toxic serum level ≈ 50 mg/dL.

Formic acid

End-product of methanol metabolism responsible for optic-nerve toxicity and acidosis.

Ocular toxicity (methanol)

Blurred vision or blindness resulting from formic-acid damage to the optic nerve.

Ethylene glycol

Antifreeze ingredient (1,2-ethanediol) metabolized to glycolic and oxalic acids causing renal failure.

Glycolic acid

Major ethylene-glycol metabolite that correlates with symptom severity and mortality.

Fatal dose of ethylene glycol

About 100 g in adults.

Ethanol therapy (EG poisoning)

Competitive substrate treatment used to block ethylene-glycol metabolism.

Isopropyl alcohol

Rubbing alcohol; metabolized to acetone, causing CNS depression and hyperosmolarity without acidosis.

Acetonuria

Presence of acetone in urine, a key clue to isopropanol poisoning.

Carbon monoxide (CO)

Colorless, odorless gas that binds hemoglobin to form carboxyhemoglobin, producing tissue hypoxia.

Carboxyhemoglobin (COHb)

Complex of CO with hemoglobin that impairs oxygen transport; yields cherry-red skin color.

Cyanide (CN⁻)

Rapid-acting poison that binds ferric iron, forming cyanoferric complexes and inhibiting cytochrome oxidase.

Cyanide mechanism

Inhibition of electron-transport chain, preventing cellular respiration and causing hypoxia.

Cyanide antidote protocol

Methemoglobin formation with nitrites followed by IV sodium thiosulfate to produce thiocyanate.

Arsenic

Metalloid in rodenticides; binds sulfhydryl groups disrupting enzymes, leading to severe GI symptoms.

Arsenic treatment

Gastric lavage, dimercaprol (BAL), and possible hemodialysis.

Iron toxicity

Common pediatric poisoning; > 30 mg/kg causes vomiting, GI bleeding, shock, and hepatic injury.

Deferoxamine

Chelation agent of choice for severe iron poisoning.

Mercury forms

Elemental (inhalation), inorganic salts (mercurous/mercuric), and organic (alkyl) species.

Mercury antidotes

Dimercaprol or succimer after gastric decontamination.

Lead poisoning

Toxicity from inorganic or organic lead affecting CNS, PNS, and hematopoiesis; half-life in bone ≈ 32 years.

Basophilic stippling

RBC inclusion characteristic of lead poisoning due to disturbed heme synthesis.

Lead chelators

Dimercaprol, calcium disodium EDTA, and succimer.

Organophosphates

Phosphate ester insecticides that irreversibly inhibit acetylcholinesterase.

Acetylcholinesterase inhibition

Prevents acetylcholine breakdown, leading to cholinergic overstimulation (SLUD symptoms).

Organophosphate antidotes

Atropine for muscarinic symptoms and pralidoxime to reactivate acetylcholinesterase.

Benzopyrene

Polycyclic aromatic hydrocarbon from cigarette smoke and engine exhaust linked to lung cancer.

Aflatoxin

Fungal toxin (Aspergillus) contaminating grains and nuts; causes hepatocellular carcinoma.

Vinyl chloride

Plastic monomer associated with hepatic angiosarcoma.

Asbestos

Fibrous silicate mineral causing lung cancer and mesothelioma upon inhalation.