Flashcards in Toxicology Deck (70)
What substances are used in the general management of poisoning?
dextrose, O2, naloxone, thiamine
What is the role of dextrose in the management of poisoning?
increases blood sugar, b/c hypoglycemia can cause coma or stupor = empirical treatment
What is the role of oxygen in the management of poisoning?
continuously assess airway since ongoing absorption of poison can disrupt consciousness
pulse ox not accurate if CO poisoning or methemoglobinemia - use cooximetry
What is the role of naloxone in the management of poisoning?
give just enough to reverse resp dep (.2 mg intervals)
may limit to pts w RR less than 12, mitotic pupils, and circumstantial evidence of opioid abuse
beware of withdrawal
What is the role of thiamine in the management of poisoning?
100 mg IVP for anyone w altered mental status with signs of Wernicke's, malnourishment, hx of alcoholism, prolonged vomiting, chronically ill
IV thiamine is safe - only 1% with AEs
What is ipecac?
syrup for decontamination - proven to be ineffective
AE of lethargy can be confused w poison's effects, complicating dx
may delay or reduce effectiveness of other treatments
acts locally by irritating gastric mucosa and centrally to stimulate medullary chemoreceptor trigger zone - but vomiting doesn't guarantee removal of poison
What is the role of gastric lavage in decontamination?
current lit suggests not a lot or only w/i one hour but research is flawed
truth: consider for anyone w massive ingestions, early presentation, severely ill w/o antecedent vomiting, substances not bound to charcoal, if pts ingested substance that delays gastric emptying or forms bezoar
What are substances not bound to charcoal?
mnemonic is CHARCOAL
rapid onset/absorption (CN, liquids)
others (insoluble in tablet form or bezoar)
What are toxins that form bezoars?
mnemonic = BIGMESS
enteric coated tablets
sustained release products
What are the pros and cons of giving activated charcoal for decontamination?
pros: superior to ipecac-induced emesis and gastric lavage at preventing absorption in volunteer studies
cons: some drugs not bound to it, severe complications inc aspiration
uncertainties: many overdose cases involve inaccurate hx
What are the recommendations for giving activated charcoal for decontamination?
give to most oral drug overdoses
exceptions = drug not bound to AC, child ingestion of small amount and known entity, known benign ingestion, risk of aspiration, drug already absorbed (greater than 2 hrs for most)
What is multiple dose activated charcoal?
select group w enteroenteric or enterohepatic re-circulation - phenobarbitol, cbzp, theophylline, ASA, dapsone and quinine
caution: aspiration, ileus, obstipation, and electrolyte abnormalities from multiple dose sorbitol admin
What is the role of whole bowel irrigation in decontamination?
admin of 2L/hr in adults, 0.5 L/hr in child of PEG-ELS solution via NGT to flush out GI tract
given to body packers: pts who ingested sustained release preps (theophylline, verapamil, bupropion)
pts who ingested substances that form bezoars (iron, lead, large amts ASA)
What are toxidromes?
collection of symptoms characteristic for specific agent groups
management of any toxidrome is same regardless of agent
What are the different toxidromes?
sympathomimetic, anticholinergic, cholinergic, opioid, sedative-hypnotic
What are the symptoms of anticholinergic and sympathomimetic toxidromes and how can you tell the difference between them?
both have increased HR and BP and pupil size, agitated mental status, hyperthermia
anticholinergic only has hypoactive bowel sounds and possible increased bladder size
anticholinergic has dry skin, sympathomimetic has wet
What is the opioid toxidrome?
depressed mental status, miosis, decreased respirations
What is the cholinergic toxidrome?
muscarinic = DUMBELS = diarrhea, urination, miosis, bronchorrhea, emesis, lacrimation, salivation
nicotinic = days of the week = mydriasis, tremor, weak, HTN, fasciculations
What is the sedative hypnotic toxidrome?
mental status depression
rarely bradypnea, hypotension, ataxia, hyporeflexia
What is the salicylates toxidrome?
SOB, increased breathing, N/V, tinnitus/hearing changes, diaphoresis, dizzy, respiratory alkalosis w metabolic acidosis
What are the principles of absorption in toxicology?
usually first order kinetics = concentration dependent
decreased by charcoal, gastric emptying, catharsis, WBI
faster if liquid form, non-ionized, small molecular size
What is the antidote for acetaminophen poisoning and how is it delivered?
orally! - want first pass to concentrate it in the liver
What are factors affecting drug distribution?
protein binding, size, lipophilicity
What are examples of small and large volume of distributions?
small is less than 1 L/kg (water, stays in IV space and interstitium)
large is greater than 3-4 L/kg (lipids, enter cells), not in plasma and not amenable to being removed by hemodialysis
Where are most drugs metabolized?
Wat are the different metabolism kinetics?
first order: steady fraction removed per unit time, enzymes not saturated, complete after 5 half lives
zero order: steady absolute amt removed per unit time, enzyme saturated
michaelis-menton: rate of elimination varies w drug concentration, high concentrations saturates enzyme and causes zero order, opposite at lower concentrations
What is important about the metabolism of acetaminophen?
small amt metabolized to NAPQ1 = hepatotoxic
glutathione = sulfur donor key to elimination of this
NAC is a sulfur donor = antidote
Where are most drugs eliminated?
What is clearance?
removal of drug from plasma per unit time
blood flow important to clearance rate