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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)


clinical features of CO poisoning

low levels nonspec sx; high levels are visual and aud changes, confusion


classic physical exam findings on phys exam of CO poisoning

cherry red skin (venous blood carries more ox than normal); retinal hemorrhages; tachycardia and tachypnea may be present


Co poisoning and little kids

kids less than 8 yo have more sx at lower CO levels; little kids are also more likely to have GI sx than neuro sx


delayed permanent neuropsych syndrome

can occur in people with CO poisoning 4 weeks after exposure


lab findings in CO poisoning

anion gap met acidosis , low ox sat (even though PaO2 may be normal), and evidence of myocardial ischemia


management of CO poisoning

100 percent oxygen; if available, hyperbaric oxygen; hospitalization indic for CO-Hb greater than 25 percent or other things


typical animal bite victim

boy during the summer


young kids are typically bitten where?

head and neck, whereas older kids on the extremites