Flashcards in Drug Tox Deck (35):
altered mental status. Decreased respiratory rate. decreased heart rate, blood pressure, and temperature. pinpoint pupils. decreased bowel sounds. "sleeping" vital signs
competitive mu, delta, and kappa opioid receptor antagonist. depressed respiratory rate best predicts response. higher doses needed for synthetic opioids. can precipitate withdrawal. lasts 45 minutes
nalmefene and naltrexone
similar action to naloxone, but differ in pharmacokinetics. doesnt change patient observation time, and may prolong it. may produce a prolonged withdrawal state: N/V, pilorection/yawning
naloxone associated opioid withdrawal symptoms
flu-like. N/V, diarrhea. piloerection. yawning, irritability. NORMAL MENTAL STATUS. lasts 15-30 minutes
depressed mental status. NORMAL VITAL SIGNS. sedative hypnotics can cause this toxidrome.
treatment for benzo overdose
ABCs, supportive care. consider flumazenil.
competitive non-selective benzodiazepine receptor antagonist. only works for benzos! doesnt work for barbitol ODs
side effects of flumazenil
can precipitate acute withdrawal. seizures reported in mixed OD. not uniform in reversal of respiratory depression.
acetaminophen toxicity stages
1: asymptomatic, mild GI irritation. 0.5-25 hrs.
2: LFT and renal function abnormalities, sometimes RUQ pain. 24-72 hrs.
3: Hepatic necrosis, sometimes renal failure. 72-96 hrs.
4: resolution of organ function. 4 days - 2 weeks.
what happens biochemically when you take too much acetominophen
run out of glutathione so you can't get rid of the toxic substrates from the acetaminophen. leads to central lobular toxicity
antidote for acetominophen OD?
N-acetylcysteine. best if given within 8 hrs of overdose. effective for all stages of poisoning
resupplis glutathione stores!
tells you if the patient is in danger from their OD on acetominophen.
late acetominophen hepatotoxicity signs
known as Kings Criteria.
prothrombin time > 200s. Serum creatinine > 3.3 mg/dl. Hepatic encephalopathy III-IV. blood pH 30
what two tests got added to kings criteria and made the sensitivity better
serum lactate and serum phosphate
tricyclic antidepressant toxidrome
anticholinergic. catechol reuptake inhibitor. alpha adrenergic blocker (hypotension). GABA antagonist (seizures). Sodium channel blocker (This is lethal)
if your QRS is over 100ms or over 160ms, what are you at risk for?
>100ms, at risk for seizures. >160ms, at risk for dysrhythmias.
antidote for tricyclic overdose?
sodium bicarbonate mechanism
provides sodium to fight the sodium channel blockade, and alkalinization to reduce TCA affinity to its receptor in the myocardium.
mydriasis, dry flushed face, decreased bowel sounds, urinary retention, increased temperature, altered mental status. increased sympathetic nervous system signs
what is the antidote for anticholinergic overdose?
physostigmine! can also use sedative hypnotics instead of physostigmine when unsure of indications
anticholinesterase. prevents breakdown of ACh.
opposite of anticholinergic. miosis, salivation, lacrimation, urination, defecation. CNS excitation, bronchorrhea/spasm, fasciculations
what is antidote for cholinergic overdose?
atropine or pralidoxime
enzyme regenerator. decreases atropine requirement. can take the toxin off the acetocholinesterase
ethylene glycol or methanol overdose treatment
treat with ethanol or fomepizole. fomepizole blocks further metabolism by using up ADH. ethanol competes with toxic things for the enzymes
when is hemodialysis indicated in ethylene glycol/methanol ODs?
methanol or ethylene glycol level > 25-50 mg/dL. metabolic acidosis. coma. hemodynamic instability.
pathophysiology of calcium channel blocker OD
blocks the slow inward calcium current, causing decreased ventricular contractility. sinus node depression leads to bradycardia. AV node depression leads to various blocks. vasodilation leads to hypotension.
clinical effects of calcium channel blocker OD
vital signs: pulse and BP decreased. Temp and RR normal. Shock: CNS depression and lactic acidosis
management of calcium channel OD
decrease absorption, increase elimination. specific treatment/antidotes
antidotes for Calcium channel blocker OD
calcium salts. glucagon. High dose insulin. pacing. amrinone. vasopressors. intraeortic baloon pump. lipid emulsion
Cocaine / Amphetamines Toxicity
CNS stimulation, agitation, hallucinations, seizures. increased muscke activity. can lead to increased temperature and kidney injury, even heart attacks.
PCP / Ketamine toxicity
low: euphoria. medium: agitation, anesthesia, increased strength. high: CNS anesthesia