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Unit 6 > Toxidromes > Flashcards

Toxidromes Flashcards

1
Q

Opioid overdose - classic symptoms

A

Pinpoint pupils

decreased bowel sounds

depressed respiratory rate

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2
Q

Opioids (examples)

A
  • Codeine
  • hydrocodone
  • meperidine
  • oxycodone
  • propoxyphene
  • methadone
  • buprinorphine

Pretty much all derivates of morphine

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3
Q

Opioid overdose - cause of death

A

respiratory arrest due to respriatory depression

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4
Q

Opioid overdose - antidote?

A

Naloxone - competitive mu, delta and kappa opioid receptor antagonist

Higher doses required for synthetic opioids (they have higher affinity)

Can cause withdrawal

Lasts ~45 mins (half life = 15 mins)

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5
Q

Naloxone

A
  • competitive mu, delta and kappa opioid receptor antagonist used for opioid overdoses
  • Higher doses required for synthetic opioids (they have higher affinity)
  • Can cause withdrawal
  • Lasts ~45 mins (half life = 15 mins)
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6
Q

Other opioid receptor antagonists (2)

A
  1. Nalmefene
  2. Naltrexone

Same mechanism as Naloxone, but differ in pharmacokinetics

Does not change patient observation time (may acutally prolong it because of increased withdrawal symptoms)

May produce prolonged withdrawal (due to lasting longer or stronger affinity)

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7
Q

Opioid overdose - withdrawal symptoms

A

N&V

piloerection/yawning

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8
Q

Benzodiazepine toxidrome

A

Normal vitals

Depressed mental status (probably the only thing you will see on exam)

Does NOT depress respiratory drive unless given IV

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9
Q

Benzodiazepine toxidrome - antidote

A

Flumazenil - competitive non-selective benzodiazepine receptor antagonist

ONLY works for benzodiazepines. Will not work for phenobarbital

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10
Q

Flumazenil

A

a competitive non-selective benzodiazepine receptor antagonist

antidote for Benzodiazepine toxidrome

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11
Q

Flumazenil - dangers

A
  • Can precipitate acute withdrawal
  • seizures reported in mixed overdoses
  • not uniform in refversal of respiratory depression (should use naloxone for respiratory depression, remember benzodiazepine really doesn’t give respiratory depression unless given IV)
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12
Q

Largest cause of liver failure in the United States

A

Acetaminophen toxicity

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13
Q

Acetaminophen toxicity (4 stages)

A
  1. Stage 1 (0-24 Hours)
    • asymptomatic, mild GI irritation
  2. Stage 2 (24-72 hours)
    • LFT(liver function test) and renal function abnormalities + RUQ pain
  3. Stage 3 (72-96 hours)
    • hepatic necrosis +/- renal failure
  4. Stage 4 (4days - 2 weeks)
    • resolution of organ function
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14
Q

Acetaminophen toxicity - antidote

A

N-acetylcysteine (NAC)

Effective for all stages of poisoning

  • Best if given within 8 hours of overdose (almost 100% chance of preventing hepatotoxicity)
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15
Q

N-acetylcysteine (NAC) - mechanism and uses

A

Used in acetaminophen toxicity as well as many other situations

Mechanism: replenishes glutathione storages

Additionally it:

  • supplies sulfhydryl groups
  • antioxidant
  • improves microcirculation
  • anti-inflammatory properties
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16
Q

Antimuscarinic toxidrome symptoms

A
  • Pupills dilated
  • Dry mucous membranes
  • dry flushed skin
  • no bowel sounds
17
Q

How to differentiate between anti-muscarinic and tri-cyclic antidepressant overdose?

A

Classic symptoms

  • Pupills dilated
  • Dry mucous membranes
  • dry flushed skin
  • no bowel sounds

Tri-cyclics in additionally will have tachycardia (this is why differentiates it from other anti-depressants)

18
Q

Tricyclic antidepressant toxidrome

A
  • Anti-cholinergic
  • Catechol reuptake inhibitor
  • Alpha adrenergic blocker (hypotension)
  • GABA antagonist (seizures)
  • Sodium channel blocker (this kills!) – widening of the QRS complex
19
Q

Widened QRS complex in tricyclic antidepressants

What is the chance of having a seizure?

A

if QRS:

  • >0.1 seconds (seizures)
  • >0.16 seconds (dysrhythmias)
20
Q

tricyclic antidepressants - sodium bicarbonate

A

Sodium bicarbonate

  • provides sodium to partially relieve the sodium channel blockade
  • alkalinization of serum –> tricyclics are weak bases so alkalinization will change it to un-ionized (thereby reducing its affinity to its receptor)
21
Q

Anti-cholinergic toxidrome

A
  • Mydriasis
  • dry, flushed skin
  • decreased bowel sounds
  • urinary retention
  • increased temperature (b/c can’t sweat)
  • altered mental status – confusion, hallucinations, seizures
22
Q

Anti-cholinergics (examples)

A
  • Atropine
  • diphenhydramine (Benadryl)
  • scopolamine
  • meclizine

Many agents have anticholinergic side-effects (ie tricyclics)

23
Q

Anti-cholingeric toxidrome - antidote

A

Physostigmine – anticholinesterase (inhibits breakdown of AChE – increased competition for receptor)

  • can cause cholinergic excess if you are wrong about the cause
  • contraindicated after TCA exposure –> causes asystole
24
Q

Physostigmine

A

anticholinesterase (inhibits breakdown of AChE – increased competition for receptor)

  • can cause cholinergic excess if you are wrong about the cause
  • contraindicated after TCA exposure –> causes asystole
25
Q

Physostigmine - when is it contraindicated?

A

after TCA exposure – can cause asystole after administration (muscarinic and nicotinic excess)

26
Q

Cholinergic toxidrome

A

Opposite of anticholinergic

  • miosis, salivation, lacrimation, urination, defecation
  • CNS excitation, bronchorrhea/spasm, fasciculations
27
Q

Cholinergic agents

A

Anticholinesterases

  • nerve gases, organophosphates, carbamates
  • physostigmine, neostigmine

Cholinomimetics

  • bethanechol
28
Q

cholinergic toxidrome - antidote

A

Muscarinic agent: atropine

  • dose to effect: very high doses may be needed in cases like organophosphates
  • works for muscarinic only

Can also use: Pralidoxime (enzyme regenerator – takes the drug off the AChE so it can properly function)

  • decreases atropine requirement
  • works for both nicotinic AND muscarinic
29
Q

Alcohol toxidrome - antidote

A
  • (old school) alcohol
  • (modernized) Fomepizole

Overall goal is to block the function of alcohol dehydrogenase (so it doesn’t degrade the methanol or ethylene glycol ingested into its toxic metabolites)

30
Q

Fomepizole

A

inhibits the activity of alcohol dehydrogenase

31
Q

Hemodialysis

A

removes toxin and metabolites

indication

  • methanol or ethylene glycol level > 25-50 mg/dl
  • metabolic acidosis (means that there are some byproducts already which can be harmful)
  • coma
  • hemodynamic instability
32
Q

Hemodialysis - indications

A
  • methanol or ethylene glycol level > 25-50 mg/dl
  • metabolic acidosis (means that there are some byproducts already which can be harmful)
  • coma
  • hemodynamic instability
33
Q

Phencyclidine (PCP)/ Ketamine/ DM

A

dissociative anesthetic – varying degrees of effect according to dose

  • low – euphoria
  • medium – agitation, anesthesia, increased strength
  • high – CNS anesthesia
34
Q

When you administer an anti-hypertensive, what is the expected response?

A

Hypotension followed by a reflex tachycardia

35
Q

If a patient suffers from hypotension AND hypotension, what are possible causes?

A

Remember, hypotension is typically associated with a reflex tachy. Only drugs that can cause both is:

  • beta blockers
  • calcium channel blockers
  • alpha-2 agonist (clonidine quanfacine, imidazolines)
  • digoxin
36
Q

Calcium blocker overdose - pathophysiology

A
  • decreased ventricular contractility
    • negative ionotrope
  • sinus node depression leads to bradycardia
    • negative chronotrope
  • atrioventricular node depression leads to various blocks
    • hypotension
  • vasodilation –> hypotension

Unit 6 (10 decks)

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