Drug Tox

Question 1

opioid toxidrome

Answer 1

altered mental status. Decreased respiratory rate. decreased heart rate, blood pressure, and temperature. pinpoint pupils. decreased bowel sounds. “sleeping” vital signs

Question 2

naloxone

Answer 2

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

Question 3

nalmefene and naltrexone

Answer 3

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

Question 4

naloxone associated opioid withdrawal symptoms

Answer 4

flu-like. N/V, diarrhea. piloerection. yawning, irritability. NORMAL MENTAL STATUS. lasts 15-30 minutes

Question 5

benzodiazepine toxidrome

Answer 5

depressed mental status. NORMAL VITAL SIGNS. sedative hypnotics can cause this toxidrome.

Question 6

treatment for benzo overdose

Answer 6

ABCs, supportive care. consider flumazenil.

Question 7

flumazenil

Answer 7

competitive non-selective benzodiazepine receptor antagonist. only works for benzos! doesnt work for barbitol ODs

Question 8

side effects of flumazenil

Answer 8

can precipitate acute withdrawal. seizures reported in mixed OD. not uniform in reversal of respiratory depression.

Question 9

acetaminophen toxicity stages

Answer 9

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.

Question 10

what happens biochemically when you take too much acetominophen

Answer 10

run out of glutathione so you can’t get rid of the toxic substrates from the acetaminophen. leads to central lobular toxicity

Question 11

antidote for acetominophen OD?

Answer 11

N-acetylcysteine. best if given within 8 hrs of overdose. effective for all stages of poisoning

Question 12

N-acetylcysteine mechanism

Answer 12

resupplis glutathione stores!

Question 13

rumack-matthew nomogram

Answer 13

tells you if the patient is in danger from their OD on acetominophen.

Question 14

late acetominophen hepatotoxicity signs

Answer 14

known as Kings Criteria.

prothrombin time > 200s. Serum creatinine > 3.3 mg/dl. Hepatic encephalopathy III-IV. blood pH 30

Question 15

what two tests got added to kings criteria and made the sensitivity better

Answer 15

serum lactate and serum phosphate

Question 16

tricyclic antidepressant toxidrome

Answer 16

anticholinergic. catechol reuptake inhibitor. alpha adrenergic blocker (hypotension). GABA antagonist (seizures). Sodium channel blocker (This is lethal)

Question 17

if your QRS is over 100ms or over 160ms, what are you at risk for?

Answer 17

> 100ms, at risk for seizures. >160ms, at risk for dysrhythmias.

Question 18

antidote for tricyclic overdose?

Answer 18

sodium bicarb!

Question 19

sodium bicarbonate mechanism

Answer 19

provides sodium to fight the sodium channel blockade, and alkalinization to reduce TCA affinity to its receptor in the myocardium.

Question 20

anticholinergic toxidrome

Answer 20

mydriasis, dry flushed face, decreased bowel sounds, urinary retention, increased temperature, altered mental status. increased sympathetic nervous system signs

Question 21

what is the antidote for anticholinergic overdose?

Answer 21

physostigmine! can also use sedative hypnotics instead of physostigmine when unsure of indications

Question 22

physostigmine mechanism

Answer 22

anticholinesterase. prevents breakdown of ACh.

Question 23

cholinergic toxidrome

Answer 23

opposite of anticholinergic. miosis, salivation, lacrimation, urination, defecation. CNS excitation, bronchorrhea/spasm, fasciculations

Question 24

what is antidote for cholinergic overdose?

Answer 24

atropine or pralidoxime

Question 25

atropine mechanism

Answer 25

anticholinergic

Question 26

pralidoxime mechanism

Answer 26

enzyme regenerator. decreases atropine requirement. can take the toxin off the acetocholinesterase

Question 27

ethylene glycol or methanol overdose treatment

Answer 27

treat with ethanol or fomepizole. fomepizole blocks further metabolism by using up ADH. ethanol competes with toxic things for the enzymes

Question 28

when is hemodialysis indicated in ethylene glycol/methanol ODs?

Answer 28

methanol or ethylene glycol level > 25-50 mg/dL. metabolic acidosis. coma. hemodynamic instability.

Question 29

pathophysiology of calcium channel blocker OD

Answer 29

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.

Question 30

clinical effects of calcium channel blocker OD

Answer 30

vital signs: pulse and BP decreased. Temp and RR normal. Shock: CNS depression and lactic acidosis

Question 31

management of calcium channel OD

Answer 31

decrease absorption, increase elimination. specific treatment/antidotes

Question 32

antidotes for Calcium channel blocker OD

Answer 32

calcium salts. glucagon. High dose insulin. pacing. amrinone. vasopressors. intraeortic baloon pump. lipid emulsion

Question 33

Cocaine / Amphetamines Toxicity

Answer 33

CNS stimulation, agitation, hallucinations, seizures. increased muscke activity. can lead to increased temperature and kidney injury, even heart attacks.

Question 34

PCP / Ketamine toxicity

Answer 34

low: euphoria. medium: agitation, anesthesia, increased strength. high: CNS anesthesia

Question 35

LSD/psilocybin toxicity

Answer 35

produces alterations in perceptions and hallucinations. adverse effects are related to the experience. no inherent toxicity.