List an antidote  (one (1) drug specific to the agent) in the event of an overdose with each of the agents listed below in the table.

Agent

Antidote

Benzodiazepines

 

Beta blockers

 

Bupivacaine

 

Cyanide

 

Digoxin

 

Ethylene glycol

 

Isoniazid

 

Methanol,

 

Methemoglobinemia

 

Organophosphate

 

Opiates

 

Lead

 

Valproate

 
 

[Click here to toggle visibility of the answers]

College Answer

List an antidote  (one (1) drug specific to the agent) in the event of an overdose with each of the agents listed below in the table.

Agent

Antidote

Benzodiazepines

Flumazenil

Beta blockers

Glucagon

Bupivacaine

Intralipid

Cyanide

Cyanocbalamin/ Sodium thiosulphate

Digoxin

Fab

Ethylene glycol

Ethanol, Fomepizole

Isoniazid

Pyridoxine

Methanol,

Ethyl alcohol

Methemoglobinemia

Methylene blue

Organophosphate

Atropine

Opiates

Naloxone

Lead

Dimercaprol, BAL

Valproate

Carnitine

Discussion

This question does not warrant an especially extensive discussion.

Instead, I will link to intersting articles.

In the list provided by the college, there are standard drugs which everyone would know the antidotes for, and non-standard ones which may not be totally familiar to people without a toxicology background.

Pyridoxine is the antidote for isoniazid

Pyridoxine is a co-factor in the synthesis of GABA; isoniazid interferes with this synthesis, and causes seizures in overdose. The supplementation of pyridoxine seems to prevent the worst of isoniazid toxicity (it seems the inhibition of lactate metabolism is not such a big deal).

Carnitine is the antidote for valproate

Or so it is thought. The most disturbing aspects of valproate toxicity are valroate-induced hyperammonaemic encephalopathy and hepatotoxicity. Carnitine deficiency is implicated in both, and seems to be caused by chronic valproate administration more so than acute. The reason for the efficacy of carnitine in valproate overdose seems to stem from its central role in beta-oxidation of long chain fatty acids (which is the metabolic pathway taken by valproate). It appears to hasten the resolution of coma, and it seems to protect the liver from necrosis; the mechanism is thought to be the prevention of accumulation of toxic metabolites of valproate.

(Incidentally, carnitine is also being considered as a rescue therapy for propofol infusion syndrome)

Dimercaprol is the antidote for lead poisoning

And mercury, antimony, gold, chrome, cobalt and nickel poisoning. First developed to treat arsenic poisoning during the Second World War, dimercaprol (or British Anti-Lewisite, BAL) is a chelating agent which competes for heavy metal ions with the thiol groups of enzymes, thus preventing the inactivation of those enzymes. The metal-dimercaprol complex is then renally excreted.

Dimercaprol itself is horribly toxic, and its use in heavy metal poisoning is limited to situations where heavy metal levels are high, toxicity is already severe, and water-soluble analogues of dimercaprol (eg. DMPS and DMSA) are not available.

References

Murakami, K., et al. "Effect of L‐Carnitine Supplementation on Acute Valproate Intoxication." Epilepsia 37.7 (1996): 687-688.

Lheureux, Philippe ER, et al. "Science review: Carnitine in the treatment of valproic acid-induced toxicity–what is the evidence?." Critical care 9.5 (2005): 431.

Kam, P. C. A., and D. Cardone. "Propofol infusion syndrome." Anaesthesia 62.7 (2007): 690-701.

Peters, Rudolph A., Lloyd A. Stocken, and R. H. S. Thompson. "British anti-lewisite (BAL)." Nature 156.Nov. 24 (1945): 616.

There is an indepth entry on dimercaprol in www.inchem.org.