SAEM Poisoning Written Study Solution Question Fully Solved.

When is gastric lavage contraindicated? - correct answer hydrocarbon and caustic ingestion due to high risk of aspiration w/ hydrocarbons and further injury w/ caustic ingestions 23 y/o F dropped off to ED by boyfriend after unknown OD. Her pupils are very large and she is sweating profusely. Respiratory rate, BP, and HR are elevated. What agent most likely caused her sx? - correct answer cocaine sympathomimetic How can you differentiate OD of sympathomimetic vs anticholinergics? - correct answer presence of sweating sympathomimetics (eg, cocaine) cause sweating anticholinergics make you "dry as a cracker" both can cause delirium and mydriasis Belladona poisoning: s/s - correct answer belladonna is an anticholinergic: hot as Hades blind as a bat dry as a bone red as a beet mad as a hatter ==> flushed skin, warm, psychotic, mydriatic, dry; hypoactive bowel sounds When is activated charcoal therapy most appropriate? - correct answer acetaminophen overdose (w/in 1-2 hrs of ingestion) When is activated charcoal therapy not indicated/contraindicated? - correct answer heavy metal poisoning (lithium, lead, and iron) - they don't bind to charcoal in pts w/ unprotected airways due to risk of aspiration caustic ingestion - black color of charcoal interferes w/ endoscopic evaluation that often follows caustic ingestion (also, caustic ingestion causes direct damage, not damage by absorption) Indicator of severe amitryptyline toxicity? - correct answer prolonged QRS interval sodium channel blockade is one of the major means by which TCAs exert their toxicity --> responsible for the prolongation of phase 0 action potential --> PR & QRS prolongation other pharm actions of TCAs: GABA-a antagonism inhibition of amine (NE, 5HT) reuptake alpha-adrenergic blockade anti-muscarinic/anti-histaminic effects EKG findings in TCA OD? - correct answer sinus tachycardia (antimuscarinic activity) prolongation of any of the EKG intervals (via Na and K channel blockade) ventricular dysrhythmias (Na channel blockade) R axis deviation of the terminal 40 ms of the QRS complex (Na channel blockade) What is the best treatment 8 h s/p large lithium OD? - correct answer hemodialysis Common precipitants of lithium toxicity? - correct answer dehydration over-diuresis drug-drug interaction (esp NSAIDs) Best tx for 26 y/o presenting with agitation, chest pain, and HR of 142 w/p intranasal cocaine use? EKG normal except for sinus tachycardia. - correct answer lorazepam (benzo) benzos are mainstay of tx for cocaine tox don't give beta blockers - due to potential for unopposed a-adrenergic stimulation & resultant HTN What ocular finding would you expect in a pt who has taken PCP? - correct answer nystagmus (multidirectional) non-ocular manifestations: HTN, bizarre behavior ABG in pt who took a bottle of aspirin ~3 hours PTA? - correct answer pH normal (metabolic acidosis + respiratory alkalosis) pCO2 down (resp alk) pO2 up/normal HCO3 down (met acid) ASA OD = metabolic acidosis + respiratory alkalosis eg: pH 7.45, pCO2 21, pO2 124, HCO3 14 MOA of toxicity in acetaminophen OD? - correct answer NAPQI builds up when glutathione stores deplete --> cause hepatotoxicity What is considered a toxic acetaminophen dose? - correct answer about 140 mg/kg (eg: in "standard" 70 kg person = 9800 mg = 9.8 g) Decision to use N-acetylcysteine in acute acetaminophen OD is dictated by the ___ - correct answer Rumack-Matthew nomogram How does N-acetylcystine tx acetaminophen OD? - correct answer prevents toxicity by inhibiting binding of NAPQI to hepatocytes A teenager presents one hour after ingesting a "handful" of acetaminophen tablets. Which of the following statements is TRUE? A. Serial liver function tests are indicated in all acetaminophen ingestions. B. Renal sequelae are expected. C. An acetaminophen level drawn at hour four dictates need for antidotal therapy. D. The intravenous formulation of N-acetylcysteine is safer than oral N-acetylcysteine. - correct answer C acetaminophen level drawn at 4-20 hours can be plotted on the Rumack-Matthew nomogram to guide therapy based on potential for hepatic toxicity What route of administration (PO vs I