1. ANTIDOTES
AASHISH PARIHAR
NURSING TUTOR
AIIMS, JODHPUR

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. ANTIDOTES
Classification of antidote-
• According to mode of action
• According to site of action

4. ANTIDOTES
Classification of antidote- According to mode of action
1. Physical
2. Chemical
3. Physiological/ Pharmacological

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. 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. 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. 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. 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. PHYSIOLOGICAL ANTIDOTE:
• They act by producing opposite effect
to that of poison.
• Sodium nitrite converts hemoglobin into
methemoglobin in order to bind
cyanide.

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. 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. 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. 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. 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. 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