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level: Level 6

Questions and Answers List

level questions: Level 6

Question	Answer
→ This therapeutic agent counteracts the toxic action of drugs or toxins. → Modify the kinetic of toxic substances or interfere with the effect on the receptor site. As a result, prevents the absorption, binding and neutralization. ● Prevention of absorption, binding, and neutralizing the poison directly ● Antagonize the poison end-organ effect ● Inhibit the metabolic activation	Antidote
1 Toxic agent – classify to 2 group 2 → Main variable that impacts the harmful effect of the toxin in the body:	1) 1 Specific treatment exists 2 No specific therapy 2) 1. Dose 2. Duration of exposure
DIRECT ACTION OF THE TOXIN 1 → Chelation (heavy metals) → immunotherapy (digoxin) → Bio scavenger therapy (Organophosphorus compound) 2 → Activated charcoal → Intra-lipid (lipophilic Local Anesthetics and nonLA drugs) → Enhanced elimination → Hemadsorption: resin/charcoal based urinary alkalinization (salicylates, phenobarbital)	. 1 Binding ● Specific 2 Binding ● Non specific
ACTION ON THE TOXIN BINDING SITE 1 → Blocking the site of action. → Achieve by __ 2 → they Competitively inhibit enzyme 3 → Competitive block of receptor	. 1 competitive inhibition of enzymes. 2 → Ethanol (methanol, ethylene glycol, fomepizole (methanol, ethylene glycol) 3 → Naloxone (opioids) → Flumazenil (benzodiazepine)
1 Antidote to cyanide 2 Antidote to Organophosphorus	1 Sodium thiosulphate 2 atropine
Direct antagonism of toxin action – used for reversing the toxicity Examples of this	1 Vitamin K - antidote for warfarin overdose 2 Pyridoxine - antidote for isoniazid toxicity 3 Folinic acid - antidote for methotrexate
How does an Antidote Work?	1. DECREASE IN TOXIN LEVEL 2. ACTION ON THE TOXIN-BINDING SITE 3. DECREASING TOXIC METABOLITES
(DECREASE IN TOXIN LEVEL) 1 → Beneficial to administer up to 4 hours, after large ingestion and for ingestion with substances with anticholinergic and opioid properties that decrease intestinal motility. → It should not be administered routinely in poison patient	. 1 Single-dose activated charcoal (SDAC): <1–12 years: 0.5–1.0 g/kg (max 50 g) adults: 25–100g
(DECREASE IN TOXIN LEVEL) 1 → Given for carbamazepine, dapsone, quinine, phenobarbitone, theophylline poison. → Benefit in anti-epileptic overdose.	. 1 Multidose activated charcoal (MDAC): 50 g Q4H
(DECREASE IN TOXIN LEVEL) “both SDAC (Single-dose activated charcoal ) and MDAC (Multidose activated charcoal) cannot be used in __ → “activated charcoal in intralipid are nonspecific binders”	organophosphate poisoning, acid, alkali and alcohol, metals like iron, lithium, potassium, lead and silver.”
(DECREASE IN TOXIN LEVEL) → chelating agent. They act by binding in toxic chelation by structure of sulfhydryl group. combined with heavy metals will form a relatively non- stable, non-toxic chelate that is easily excreted in urine. DECREASES EFFECT IF URINE IS ACIDIC or the patient is acidic. → More effective, soon after exposure with gold induce thrombocytopenia, symptomatic or asymptomatic mercury poisoning with mercury whole blood	Dimercaprol → Combination with EDTA, you should give first Dimercaprol before EDTA to prevent the distribution of the lead to the brain. Disadvantage - if metal itself is metabolize to liver, dimercaprol is not effective. It is also short half life and readily excreted to urine.
1→ used for severe arsenic gold poisoning. → Severe arsenic or gold poisoning: 3.5–5 mg/kg Q4H for six doses, then Q6H for four doses, Q8H for three doses, followed Q12H for two doses and then OD for 10 days → Mercury: 5 mg/kg initially Q4H for 1–2 days, followed by 2.5 mg/kg 1–2 times/day for 10 days → Lead: 4 mg/kg Q4H for 3 days, begin chelation with EDTA with second dose, followed by 2.5 mg/kg for 1–4 days	1 Ethylene diamine tetraacetic acid (EDTA)
→ immunotherapy used for digoxin therapy → By binding it facilitates dissociation of digoxin from sodium potassium aTPase. combines free digoxin then the digoxin is easily excreted through renal secretion. → Effective acute or severe chronic digitoxicity, life-threatening tachyarrhythmia or bradyarrhythmia, patient with hyperkalemia with potassium level less than 6 mmol/L, renal failure, hemodynamic instability with digoxin concentration of more than 2 mcg/L. → Acute ingestion of digoxin. → Adult more than 10 mg → children more than 4 mg → 1 vial binds 0.5 mg of digoxin. If unknown ingestion, administer 10 vials for adults and 5 vials for children	Digi-Fab (digoxin-specific antibody fragments) → Fab - free digoxin= digoxin-immune fragment complexes
→ causes sinking of lipid by expanding the lipid compartment within the intravascular space therefore, sequestering the lipid soluble drug from tissue. → Intralipid efficacy is Related to metabolic effect in myocardium, specifically, ability to enhance fatty acid intracellular transport in myocardial cells → Used for treatment of poisoning by lipid poisoning drugs like Bupivacaine, propranolol, verapamil.	Intralipid - bupivacaine, propranolol, verapamil
→ enhances elimination by increasing the ionized form of the toxin therefore, less absorption from renal tubules. → Useful for acid overdose, tricyclic antidepressant, or ECG abnormalities, salicylate overdose more than 300 mg/kg. → Bolus 1–2 mEq/kg followed by infusion diluted in 5% dextrose	Urinary alkalinization
→ Work by enhancing elimination in which blood passes through columns named by AC or synthetic iron resin. → Like dialysis, blood is passed by resin or AC exchange resins. Therefore, protein bound substances bind to the resin and therefore, remove in the circulation	Hemoperfusion - charcoal, resin base