peds74 Flashcards
(32 cards)
antidote for acetominophen poisoning
n-acetylcysteine (NAC); a glutathione precursor; given orally as loading dose and followed every 4 hours for 17 doses; can also use IV NAC; hepatoprotective if given within 8 hrs of ingestion. Still helpful up to 72 hours
salicylates found in what?
pepto-bismol, ben-gay, and oil of wintergreen
pathophys of salicylate poisoning
directly stimulate respiratory centers; causes hypervent that may overcompensate for metabolic acidosis produced by salicylate, resulting in resp alkalosis
how do salicylate poisonings work
uncouple ox-phos, producing lactic acidosis and enhancing ketosis
lab findings with salicylic acid poisoning
resp alkalosis with an anion gap metabolic acidosis is the most common; hyperglycemia then hypoglycema; hypokalemia
mangement of salicylate poisoning
gastric lavage; activated charcoal; obtain serum salicylate; alkalinization or urine with sodium bicarb; fluids to enhance renal excretion; dialysis may be required
stages of acetominophen toxicity
30 mins-24 hours asymptomatic or vom/diarrhea; 24-72 hours GI sx resolve; 72-96 hour hepatic necrosis; 4 days to 2 weeks resolution of sx
most common sources of accidental iron poisoning
adult stregnth ferrous sulfate tabs and iron in prenatal vitamins
pathophys of iron poisoning
direct damage to GI tract; hepatic injury and necrosis; third spacing and pooling of blood in the vasculature leading to hypotension; interference with oxphos
management of iron poisoning
gastric lavage; activated charcoal does NOT bind to iron; hypovolemia should be anticipated and tx; whole bowel irrig; IV deferoxamine
determining use of IV deferoxamine in iron poisoning
if serum iron over 500 or if less than 300 and acidosis, hyperglycemia or leuocytosis; severe GI sx; more than 100 mg/kg iron ingested
before serum iron level is known, how much deferoxamine do you give?
test dose may be administered; if patients urine turns red or pink, the challenge is considered positive, indicating clinically signif iron ingestion. IV def should be continued
clinical features of lead poisoning
abdominal complaints, CNS complaints, peripheral blood smear shows microcytic anemia, basophilic stippling, and RBC precursors; radioopacities on abdom xra
dense metaphyseal bands on radiographs of knees and wrists
lead lines due to lead poisoning
diagnosis of lead poisoning
elevated lead level or elevated erythrocyte protoporphyrin
management of lead poisoning
dimercaprol, british anti-lewisits, or calcium disodium EDTA
how does acid ingestion hurt your body
coagulation necrosis that produces superficial damage to the mouth, esoph, and stomach
how do alkalis cause damage to the body if ingested?
liquefaction necrosis that produces deep and penetrating damage, most commonly to the mouth and esoph
example of acid that is ingested
toilet bowl cleaner
example of bases that can be ingested
oven and drain cleaners, bleach, laundry detergent
clinical features of ingesting either acidic or basic caustic agent
immediate burning with intense dysphagia, salivation, retrosternal pain, and vomiting; obstructive airway edema; gastric perforation and peritonitis; esoph perforation with mediastinitis
management of ingestion of caustic substances
no attempt to neutralize the reaction; ipecac, gastric lavage, and activated charcoal are all contraindic; endoscopy is performed; household bleach requires no tx
carbon monoxide poisoning
odorless, tasteless, colorless gas; interferes with oxygen deliv;
how does CO interfere with oxygen delivery?
CO displaces oxygen from hgb and binds much stronger than ox; ox-hgb dissociation curve is shifted to the left (tighter binding of ox and impaired release of ox)
