Toxidromes Part I Flashcards

1
Q

Describe the mechanism of action of cocaine and the signs and symptoms associated with its administration.

A

It is a sympathomimetic leading to tachycardia, increased alertness, hypertension, etc.

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2
Q

What is the least reliable route of absorption of cocaine?

A

PO –> oral ingestion of cocaine is only lethal in very large amounts

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3
Q

What is the most reliable route of absorption of cocaine?

A

Smoking cocaine easily crosses the alveoli and the blood-brain barrier

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4
Q

What are some common emergent sequelae of cocaine toxicity?

A
Stroke, including intracerebral or subarachnoid hemorrhage
Decreased seizure threshold
Chest pain associated with MI
Rhabdomyolysis
Anxiety and psychosis
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5
Q

What medications and interventions (7) are used to manage complications associated with cocaine toxicity?

A

Benzos - anxiety and to stop seizures
Phenytoin - to prevent seizures
Haloperidol - anxiety
Ca Channel Blockers - HTN
Bicarb - rhabdomyolysis (alkalinizes the urine)
IV fluids - rhabdomyolysis
CT scan and supportive care - HA or stroke

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6
Q

Why are beta blockers avoided in cocaine toxicity?

A

Resultant unopposed alpha-1 stimulation may result in further HTN

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7
Q

List 2 reasons CO toxicity is on the decline in recent years.

A

Increased use of CO detectors

Decreased CO emissions from automobiles

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8
Q

What is the mechanism of action that causes CO toxicity?

A

CO binds to Hgb with 250x more affinity than O2. The resultant anaerobic metabolism leads to metabolic acidosis which causes the body’s enzymes (which are proteins) to denature

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9
Q

Where is someone likely to be exposed to CO?

A

In a fire - especially in closed spaces

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10
Q

How is a diagnosis of CO toxicity made and what drives treatment?

A

Dx based on serum carboxyhemoglobin. Often times the patient cannot wait for this lab to return for treatment to start. So treatment is driven by presenting S/S.

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11
Q

What is the treatment for CO toxicity?

A

High flow O2 for all patients.

Hyperbaric oxygen for severe cases with decreased consciousness.

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12
Q

T/F: TCAs account for a small amount of overdoses and deaths.

A

False: TCAs are involved in 12% of intentional ODs and 36% of deaths.

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13
Q

What three things are a major part of the clinical presentation of a TCA overdose?

A

Tonic-clonic seizures
Cardiac arrhythmias
Anticholinergic affects (C-DUST)

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14
Q

How does a potential TCA overdose affect administration of the classic drug cocktail for an unresponsive patient?

A

Flumazenil (a benzo antagonist) is part of the drug cocktail. If the patient OD’d on TCAs and flumazenil is administered, they are more likely to have a seizure that is difficult to stop.

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15
Q

What ECG finding is most consistent with TCA toxicity?

A

Wide QRS

  • QRS of 0.10 - 0.15 = increased risk of seizure
  • QRS > 0.16 = increased risk of seizure and arrhythmia
  • QRS < 0.10 does not rule out toxicity
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16
Q

What is the treatment of TCA toxicity and why is it effective?

A

Sodium bicarbonate for 2 reasons.

  • increases plasma protein binding of the drug
  • stabilization of fast Na channels
17
Q

What two drugs that are not TCAs but when in toxicity are treated the same as TCA toxicity?

A

Cyclobenzaprine and Carbamazepine

18
Q

What is the classic triad of S/S associated with opioid toxicity?

A

Miosis (pinpoint pupils)
Decreased level of consciousness
Respiratory depression

19
Q

What is the antidote for opioid toxicity used to reverse respiratory depression?

A

Naloxone –> 2mg IV

20
Q

If IV access is unavailable, what other route of administration is the antidote for opioid toxicity given?

A

ET Tube (intubation)

21
Q

For what opioids are a large amount of naloxone required for reversal?

A

Pentazocine, codeine, methadone

22
Q

What is important in the management of opioid toxicity after the initial dose of naloxone is given?

A

All opioids have a longer half life than naloxone. Continuous naloxone infusion is administered at an hourly rate at 2/3 the amount in mg that was needed to reverse the respiratory depression.

23
Q

Differentiate naltrexone from methylnaltrexone from naloxone.

A

Naltrexone is an opiod antagonist with a longer half life than naloxone. It can be used to ween SUD patients off of narcotics. But naltrexone cannot be used in toxicity.
Methylnaltrexone is used to counter opioid induced constipation