Toxidromes Flashcards
Opioid overdose - classic symptoms
Pinpoint pupils
decreased bowel sounds
depressed respiratory rate
Opioids (examples)
- Codeine
- hydrocodone
- meperidine
- oxycodone
- propoxyphene
- methadone
- buprinorphine
Pretty much all derivates of morphine
Opioid overdose - cause of death
respiratory arrest due to respriatory depression
Opioid overdose - antidote?
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)
Naloxone
- 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)
Other opioid receptor antagonists (2)
- Nalmefene
- 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)
Opioid overdose - withdrawal symptoms
N&V
piloerection/yawning
Benzodiazepine toxidrome
Normal vitals
Depressed mental status (probably the only thing you will see on exam)
Does NOT depress respiratory drive unless given IV
Benzodiazepine toxidrome - antidote
Flumazenil - competitive non-selective benzodiazepine receptor antagonist
ONLY works for benzodiazepines. Will not work for phenobarbital
Flumazenil
a competitive non-selective benzodiazepine receptor antagonist
antidote for Benzodiazepine toxidrome
Flumazenil - dangers
- 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)
Largest cause of liver failure in the United States
Acetaminophen toxicity
Acetaminophen toxicity (4 stages)
- Stage 1 (0-24 Hours)
- asymptomatic, mild GI irritation
- Stage 2 (24-72 hours)
- LFT(liver function test) and renal function abnormalities + RUQ pain
- Stage 3 (72-96 hours)
- hepatic necrosis +/- renal failure
- Stage 4 (4days - 2 weeks)
- resolution of organ function
Acetaminophen toxicity - antidote
N-acetylcysteine (NAC)
Effective for all stages of poisoning
- Best if given within 8 hours of overdose (almost 100% chance of preventing hepatotoxicity)
N-acetylcysteine (NAC) - mechanism and uses
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
Antimuscarinic toxidrome symptoms
- Pupills dilated
- Dry mucous membranes
- dry flushed skin
- no bowel sounds
How to differentiate between anti-muscarinic and tri-cyclic antidepressant overdose?
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)
Tricyclic antidepressant toxidrome
- Anti-cholinergic
- Catechol reuptake inhibitor
- Alpha adrenergic blocker (hypotension)
- GABA antagonist (seizures)
- Sodium channel blocker (this kills!) – widening of the QRS complex
Widened QRS complex in tricyclic antidepressants
What is the chance of having a seizure?
if QRS:
- >0.1 seconds (seizures)
- >0.16 seconds (dysrhythmias)
tricyclic antidepressants - sodium bicarbonate
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)
Anti-cholinergic toxidrome
- Mydriasis
- dry, flushed skin
- decreased bowel sounds
- urinary retention
- increased temperature (b/c can’t sweat)
- altered mental status – confusion, hallucinations, seizures
Anti-cholinergics (examples)
- Atropine
- diphenhydramine (Benadryl)
- scopolamine
- meclizine
Many agents have anticholinergic side-effects (ie tricyclics)
Anti-cholingeric toxidrome - antidote
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
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
Physostigmine - when is it contraindicated?
after TCA exposure – can cause asystole after administration (muscarinic and nicotinic excess)
Cholinergic toxidrome
Opposite of anticholinergic
- miosis, salivation, lacrimation, urination, defecation
- CNS excitation, bronchorrhea/spasm, fasciculations
Cholinergic agents
Anticholinesterases
- nerve gases, organophosphates, carbamates
- physostigmine, neostigmine
Cholinomimetics
- bethanechol
cholinergic toxidrome - antidote
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
Alcohol toxidrome - antidote
- (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)
Fomepizole
inhibits the activity of alcohol dehydrogenase
Hemodialysis
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
Hemodialysis - indications
- 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
Phencyclidine (PCP)/ Ketamine/ DM
dissociative anesthetic – varying degrees of effect according to dose
- low – euphoria
- medium – agitation, anesthesia, increased strength
- high – CNS anesthesia
When you administer an anti-hypertensive, what is the expected response?
Hypotension followed by a reflex tachycardia
If a patient suffers from hypotension AND hypotension, what are possible causes?
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
Calcium blocker overdose - pathophysiology
- decreased ventricular contractility
- negative ionotrope
- sinus node depression leads to bradycardia
- negative chronotrope
- atrioventricular node depression leads to various blocks
- hypotension
- vasodilation –> hypotension
