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a brief description about antidotes

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  2. 2. ANTIDOTES • According to WHO “Antidote was defined as a therapeutic substance used to counteract the toxic action(s) of a specified xenobiotic.” • Antidotes reduce the overall burden of health service in managing of poisoning cases Supportive therapy Correct antidote Patient survival
  3. 3. ANTIDOTES Classification of antidote- • According to mode of action • According to site of action
  4. 4. ANTIDOTES Classification of antidote- According to mode of action 1. Physical 2. Chemical 3. Physiological/ Pharmacological
  5. 5. ANTIDOTES Classification of antidote- According to site of action 1. Interacts with the poison to form a non toxic complex that can be excreted Chelators 2. Accelerates the detoxification of the poison N-acetylcystine, thiosulfate 3. Decrease the rate of conversion of poison into toxic metabolite Ethanol, fomepizole 4. Compete the poison for certain receptors Naloxone 5. Block the receptor through which the toxic effect of the poison is mediated Atropine 6. Bypass the effect of poison Oxygen in the treatment of CO and cyanide toxicity 7. Antibodies to the poison : digibind and antivenins
  6. 6. PHYSICAL ANTIDOTE: Agent use to interfere with poison through physical properties, not change their nature a) Adsorbing: Adsorption is the adhesion of atoms, ions, or molecules from a gas, liquid, or dissolved solid to a surface. This process creates a film of the adsorbate on the surface of the adsorbent. The main example is activated charcoal b) Coating: A mixture of egg & milk make a coat over the mucosa. c) Dissolving: 10% alcohol or glycine for carbolic acid ANTIDOTES
  7. 7. CHARCOL: (UNIVERSAL ANTIDOTE) • Produced by heating pulverized carbonaceous substances sawdust, peat, or coconut shells • Activation: hot air to erode the internal surfaces of the product and thereby increase its adsorptive surface area. • Adsorption results from weak intermolecular (van der Waals) forces • AC can prevent systemic absorption of drugs when given within 1- 2 h of ingestion • the optimal dose is probably a 40:1 ratio (by weight) of charcoal to drug • Contraindicated for iron, lithium, potassium, and ethanol overdose
  8. 8. CHEMICAL ANTIDOTE: • Interact specifically with a toxicant, or neutralize the toxicant. E.G. Metal chelators combine with metals to form complexes that can then be eliminated by the kidneys Mainly act by two mechanisms: Complex formation: Antidote make complex with the toxicant making it unavailable to cross the membrane or to interact with receptors DMSA (dimercaprol and dimercaptosuccinic acid are sulfohydral compounds that bind metal such as arsenic acid ,lead.
  9. 9. Sp. Binding agents like EDTA, defroxamine and d-pencillamine act by chelation of metal forming more water soluble complex Antivenins and antibodies against digitoxin are immunologicaly genrated agents that bind specifically to the toxin or venom Metabolic conversion: Detoxification to less toxic product Nitrite interact with hemoglobin and cyanide to form cyanomethamoglobin , which is less toxic than cyanide and interfere with the cyanide access to cytochrome oxidase system.
  10. 10. PHYSIOLOGICAL ANTIDOTE: • They act by producing opposite effect to that of poison. • Sodium nitrite converts hemoglobin into methemoglobin in order to bind cyanide.
  11. 11. PHARMACOLOGICAL ANTIDOTE: • Counteract the effects of a poison by producing the opposite pharmacological effects, e.g. ACHE inhibitors atropine • Pharmacologic antidotes may neutralize or antagonize the effects of a toxicant. • This type of antidote may act by following 5 mechanism-
  12. 12. 1. Preventing the formation of toxic metabolites: More effective when given immediately before toxic metabolic activation Example: Ethanol and 4-methylpyrazole(4-mp) which compete with the alcohol dehydrogenase which prevent the formation of toxic intermediate from ethylene glycol. 2. By facilitation of more rapid or complete elimination of A toxicant : Change the physiochemical nature of toxin, allowing better glomerular filtration and prohibit tubular reabsorption. e.g. Molybdenum and sulfate for copper toxicity by making water soluble complex,
  13. 13. 3. By competing with the toxicant’s action at a receptor site: a) Antagonism: Competitive antagonism: Naloxone/naltrexone: opioid dependence, longer action and affinity for mu receptor. Flumenazil: antagonist for benzodiazepine Atropine: organophosphate, carbamate and other parasympathomimetic antidote. It is also used to correct bradycardia caused by morphine, digitalis, beta blockers
  14. 14. non competitive antagonism: calcium gluconate: used for calcium channel blocker especially verapamil black widow spider bite lead colic oxalic acid paralidoxime : CHE activator act by breaking alkyl phosphate che bond. it is used in organophosphate toxicity. diacetyl monoxyime(dam): action same as pam but with more bbb penetration.
  15. 15. 4. By blocking receptors responsible for the toxic effect : The physiologic effect induced by a toxin is prevented by an antidote, although the toxicant is unchanged and may still be active. Example: Atropine blocks the physiologic effect of acetylcholine at cholinergic synapse and neuromuscular junction in organophosphate toxicity
  16. 16. 5. By aiding in the restoration of normal function: The antidote promotes return to normal function by repairing a defect or enhancing a function that correct the effect of poison. Example: Methylene blue: In nitrite poisoning, methylene blue interact with reduced NADPH to reduce the ferric iron of methemoglobin back to ferrous ion in hemoglobin, which can again transport oxygen Acetylcysteine : Acetylcysteine supplies the precursor amino acids for glutathione, which serves as biologic antioxidant against acetaminophen toxicities