GPAT, Pharmacist & Drug Inspector Exclusive = Poison & Antidotes With Their Mechanism of Action

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Poison: Any substance that can cause severe organ damage or death if ingested, breathed in, injected into the body or absorbed through the skin. The fields of medicine (particularly veterinary) and zoology often distinguish a poison from a toxin, and from a venom. Toxins are poisons produced by organisms in nature, and venoms are toxins injected by a bite or sting (this is exclusive to animals). The difference between venom and other poisons is the delivery method.
Industry, agriculture, and other sectors employ poisonous substances for reasons other than their toxicity. Most poisonous industrial compounds have associated material safety data sheets and are classed as hazardous substances. Hazardous substances are subject to extensive regulation on production, procurement and use in overlapping domains of occupational safety and health, public health, drinking water quality standards, air pollution and environmental protection. Due to the mechanics of molecular diffusion, many poisonous compounds rapidly diffuse into biological tissues, air, water, or soil on a molecular scale. By the principle of entropy, chemical contamination is typically costly or infeasible to reverse, unless specific chelating agents or micro-filtration processes are available. Chelating agents are often broader in scope than the acute target, and therefore their ingestion necessitates careful medical or veterinarian supervision.
Antidotes are agents that negate the effect of a poison or toxin. Antidotes mediate its effect either by preventing the absorption of the toxin, by binding and neutralizing the poison, antagonizing its end-organ effect or by inhibition of the conversion of the toxin to more toxic metabolites. Antidote administration may not only result in the reduction of free or active toxin level, but also in the mitigation of end-organ effects of the toxin by mechanisms that include competitive inhibition, receptor blockade or direct antagonism of the toxin.
Reduction in free toxin level can be achieved by specific and non-specific agents that bind to the toxin. The most commonly used non-specific binding agent is activated charcoal. Specific binders include chelating agents, scavenger therapy and immunotherapy. In some situations, enhanced elimination can be achieved by urinary alkalization or hemadsorption. Competitive inhibition of enzymes (e.g. ethanol for methanol poisoning), enhancement of enzyme function (e.g. oximes for organophosphorus poisoning) and competitive receptor blockade (e.g. naloxone, flumazenil) are other mechanisms by which antidotes act. Drugs such as N-acetyl cysteine and sodium thiocyanate reduce the formation of toxic metabolites in paracetamol and cyanide poisoning respectively. Drugs such as atropine and magnesium are used to counteract the end-organ effects in organophosphorus poisoning. Vitamins such as vitamin K, folic acid and pyridoxine are used to antagonise the effects of warfarin, methotrexate and INH respectively in the setting of toxicity or overdose. This review provides an overview of the role of antidotes in poisoning.
Common Example-
(1) Acetylcysteine for acetaminophen poisoning
(2) Activated charcoal for most poisons
(3) Atropine for organophosphates and carbamates
(4) Digoxin immune fab for digoxin toxicity
(5) Dimercaprol for arsenic, gold, or inorganic mercury poisoning
(6) Flumazenil for benzodiazepine overdose
(7)Methylene blue for drug-induced methemoglobinemia
Naloxone for opioid overdose
Pralidoxime for poisoning by anti-cholinesterase nerve agents.
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