70 - Toxicology II Flashcards

1
Q

What are the receptor competitor therapies?

A
  • Warfarin
  • Opioids
  • Competitive receptor antagonists (naloxone, naltrexone)
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2
Q

What is warfarin?

A

Anticoagulant that interferes with synthesis of vitamin K-dependent coagulation factors

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3
Q

What are the adverse symptoms of warfarin?

A

Adverse symptoms include hemoptysis, excessive bruising, bleeding from nose or gums, or blood in urine or stool

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4
Q

How do you treat bleeding and high INR due to warfarin?

A

Requires reversal by injection of vitamin K (phytonadione), or (in case of severe bleeding) prothrombin complex or fresh frozen plasma infusion to replace coagulation proteins

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5
Q

What are the opioids that are receptor competitors?

A

Heroin, morphine, meperidine, codeine, etc.

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6
Q

Describe the action of naloxone

A

Naloxone (Narcan®, Nalone®, and Narcanti®)

  • Acts at µ, κ, and δ receptors to competitively block/reverse the effects of opiates
  • Duration of action: ~45 minutes
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7
Q

Describe how naltrexone is different than naloxone

A

Naltrexone (Revia®)

  • Same action as naloxone
  • Longer duration of action (24-72 hrs) than naloxone
  • Can also be used in withdrawal treatment

First use naloxone to save their life within minutes, then give naltrexone for maintenance to treat poisoning so the effects of the opioids don’t come back

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8
Q

What is methemoglobinemia?

A
  • State in which the heme iron is in the Fe+3 state (ferric), and not Fe+2 (ferrous) of normal hemoglobin
  • Methemoglobin, is unable to transport oxygen ***
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9
Q

What causes methemoglobinemia?

A

Caused by exposure to various chemicals (nitrites, sulfa drugs, many others)

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10
Q

What is the anecdote used to treat methemoglobinemia?

A

Methylene blue

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11
Q

How does methylene blue work?

A

Mechanism of Action: causes a direct chemical reduction of methemoglobin back to hemoglobin

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12
Q

What are toxidromes?

A

Toxidromes are common, and often well-characterized, clinical syndromes that provide a symptomatic fingerprint allowing for the successful recognition of patterns of poisoning associated with specific intoxicants

This means that in the ER, you see a certain set of symptoms, and you can match the toxidrome to the presenting patient in order to determine the cause of poison

Not “bullet proof” or 100%, but it gives you a good idea

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13
Q

What are the most prevalent clinical toxidromes?

A
  • sympathomimetics
  • sedative hypnotics
  • opioids
  • anticholinergics
  • cholinergics
  • tricyclic antidepressants (TCAs)
  • salicylates
  • acetaminophen
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14
Q

Describe the symptoms and cause of a sympathomimetic toxidrome

A

Cause = CNS stimulant (cocaine, amphetamines, PCP)

Pupils = mydriasis

Other = hypertension, tremor, hyperthermia

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15
Q

Describe the symptoms and cause of a sedative/hypnotic toxidrome

A

Cause = CNS depressants (alcohol, barbiturates, benzodiazepines)

CNS = coma

Respiration = decreased

Pupils = miosis or mydriasis

Other = hypotension

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16
Q

Describe the symptoms and cause of a opioid/opiate toxidrome

A

Cause = opiates, morphine, codeine, propoxyphene, oxycodone, hydrocodone

CNS = coma (decreased consciousness)

Respiration = depression

Pupils = “pinpoint” miosis

Other = hypothermia, hypotension, “opiate triad”, histamine release

17
Q

Describe the symptoms and cause of a anticholinergic toxidrome

A

Cause = anticholinergics, antidepressants

CNS = agitation

Pupils = mydriasis

Other = fever, dry skin, flushing, urinary retention [hot, dry, mad, red, blind] ***

18
Q

Describe the symptoms and cause of a cholinergic toxidrome

A

Cause = organophosphates/carbamates and other insecticides, nicotine

Pupils = “pinpoint” pupils (PPP)

Other = SLUDE - everything is wet

19
Q

Describe the symptoms and cause of a tricyclic antidepressant toxidrome

A

Cause = TCAs (amitriptyline; imipramine; desipramine)

CNS = coma, agitation

Pupils = mydriasis

Other = dysrhythmia, convulsions, hypotension (due to alpha blockade)

20
Q

Describe the symptoms and cause of a salicylate toxidrome

A

Cause = ASA, aspirin, other salicylates

Respiration = can increase or normal

Other = diaphoresis, tinnitis, agitation, alkalosis (early), acidosis (late), hyperpyrexia

A little less defined than some of the others

21
Q

What are some of the other frequently encountered toxicants?

A
  • Acidic substances (cleaners)
  • Alkaline substances (cleaners)

In general, monitor ABCs and dilute with water to neutralize

22
Q

How do you treat benzodiazepine poisoning?

A

Rarely fatal unless taken with ETOH or other CNS depressant due to synergistic CNS depression

Receptor antagonist: flumazenil

23
Q

How do you treat acetaminophen poisoning?

A

Acetaminophen poisoning occurs after the depletion of glutathione - can result in hepatic necrosis, death due to hepatic failure

N-acetylcysteine (Mucomyst®) to restore glutathione

24
Q

How do you treat cocaine overdose?

A

Cocaine overdose leads to cardiac dysrhythmias leading to cardiac arrest

Treat the dysrhythmia with lidocaine and monitor ABCs

25
Q

How do you treat opiate overdose?

A

Main signs are bilateral miosis (PPP) and HR/respiratory depression and arrest

Treat with naloxone

26
Q

How do you treat a meperidine overdose (an opioid)?

A

You will see dilated pupils due to antimuscarininc effects and increased HR

Treat with naloxone

27
Q

What is the last “interesting toxicant”?

A

Dioxin

Prime minister of Ukraine was poisoned this way