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Poisons/Antidotes

Overdosed DrugSymptoms/Diagnostic methodsAntidote(s)MoA of AntidoteSpecial ConsiderationsTreatment Approach
acetaminophen nausea/vomiting clinical signs of liver failure levels can be measured in the blood N-acetylcysteine (NAC) replenishes glutathione antidote loses effectiveness 8 hours after OD, but should still administer past that point toxicokinetic-based: enhancement of metabolism (detoxification)
toxic alcohols (methanol & ethylene glycol) methanol active metabolites can cause anion-gap metabolic acidosis and ocular toxicity ethylene glycol metabolites can crystalize in microvasculature; common in renal toxicity Ethanol or Fomepizole inhibition of alcohol dehydrogenase (ADH) Fomepizole is a stronger and safer ADH inhibitor with fewer ADRs than ethanol toxicokinetic-based: inhibition of toxication (bioactivation)
benzodiazepines CNS depression with relatively normal vitals levels can be measured in the blood Flumazenil competitive antagonist of benzodiazepine receptor can cause withdrawal symptoms in a benzo-dependent patient pharmacological treatment: receptor antagonist
beta blockers hypotension, bradycardia, altered mental status, respiratory depression Atropine, Calcium, Glucagon, HIET, Vasopressors, IFE Atropine increases HR Calcium tries to drive Ca2+ into cardiac cells Glucagon increases cardiac cellular cAMP to increase HR HIET: mechanisms not understood Vasopressors: increase BP IV20%FE acts as lipid sink if drug is lipophilic enough beta blocker OD may have altered mental status, CCBs do not pharmacological treatments: receptor antagonist
calcium channel blockers hypotension, bradycardia, but often alert Atropine, Calcium, Glucagon, HIET, Vasopressors, IFE Atropine increases HR Calcium tries to drive Ca2+ into cardiac cells Glucagon increases cardiac cellular cAMP to increase HR HIET: mechanisms not understood Vasopressors: increase BP IV20%FE acts as lipid sink if drug is lipophilic enough pharmacological treatments: receptor antagonist
digoxin bradycardia, arrythmias, elevated serum K+, nausea/vomiting levels can be measured in the blood Digoxin Specific Antibody Fragments (Fab) binds digoxin and will be renally eliminated checking serum digoxin levels after giving antidote is not helpful because total concentration (free + bound) will be increased can't be used as a measurement to calculate more Fab doses inactvation of poisions: antivenoms/antibody binding
tricyclic antidepressants tachycardia, dilated pupils, dry mouth, agitation, seizures, sometimes vasodilation, elongated QRS interval, reduced cardiac contractility IV fluids, Dopamine or Norepinephrine, Sodium Bicarbonate for elongated QRS mostly supportive care, trying to maintain BP Sodium bicarb counteracts inhibition of Na+ cardiac channels
opioids somnolence, coma, decreased HR and RR, constricted pupiles Nalxonone competitive antagonist of opioid receptors can trigger withdrawal pharmacological treatment: receptor antagonist
salicylates (aspirin) hyperventilation and respiratory alkalosis, then metabolic acidosis, hyperthermia, confusion and seizures Supportive care, IV Sodium bicarbonate renal ion trapping to enhance elimination toxicokinetic-based: enhancement of elimination
sulfonylureas & miglitinide hypoglycemia Octreotide inhibits insulin release from the pancreas toxicokinetic-based: inhibition of toxication (bioactivation)
iron vomiting/abdominal pain, and diarrhea within 1-6 hrs lethargy, coma, seizures, bloody vomiting, bloody diarrhea, and shock within 6-24 hrs hypotension and tachycardia within 6-24 hrs liver dysfunction and fsailure possible in 2-5 days Deferoxamine chelates the circulating ferric iron inactivation of poisons: heavy metal chelator
Created by: user-1963003
 



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