Antidepressant/Lithium/BZD Toxicity Flashcards

1
Q

TCA is not really used for depression anymore. Why?

A

Due to high risk of toxicity, and safer alternatives

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2
Q

T or F: Srs TCA toxicity can appear to be trivial.

A

T (which is why TCA’s are particularly dangerous)

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3
Q

How well are TCAs absorbed?

A

Well absorbed

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4
Q

TCA tmax?

A

up to 12h (OD dosing)

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5
Q

What kind of effect do TCAs have on gastric emptying?

A

Delays it due to anticholinergic effects

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6
Q

How extensive is plasma protein binding of TCAs?

A

V. extensive 85-98%

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7
Q

TCAs are…

  1. lipophilic
  2. hydrophilic
  3. amphipathic
A
  1. lipophilic (highly)
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8
Q

normal t1/2 of TCA? t1/2 in toxicity?

A

6-24h (up to 72h in toxicity)

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9
Q

Why is TCA toxicity variable in the pop?

A

bc it’s metabolized by enzymes that are subject to genetic polymorphisms

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10
Q

What is the main enzyme that metabolizes TCA?

A

2D6

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11
Q

T or F: If the pt ingested a little TCA, then no need to worry too much

A

F

Dose ingested is a poor predictor of outcome

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12
Q

CV signs/sx’s of TCA tox

A

Hypotn, cardiac dysrhythmias

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13
Q

How do TCAs cause hypotn?

A

by antagonizing peripheral alpha-1 receptors on blood vessels

by causing dysrhythmias

by directly suppressing myocardial activity (binds Na channels)

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14
Q

What’s important to do early on during TCA tox?

A

Take early ECG track heart’s electrical activity

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15
Q

CNS signs/sx’s of TCA overdose?

A

agitation
seizures
coma (can be rapid)

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16
Q

T or F: serum TCA levels are essential for TCA overdose dx

A

F

17
Q

Single most important diagnostic tool during TCA overdose

A

ECG

18
Q

TCA overdose: what does a QRS < 100ms tell us?

A

no seizure or ventricular arrhythmia

19
Q

TCA overdose: what does a QRS > 100ms tell us?

A

26% risk of seizure

20
Q

TCA overdose: what does a QRS > 160 ms tell us?

A

50% risk of ventricular arrhythmia

21
Q

What’s used to tx the hypotn assoc w/ TCA tox?

A

fluid boluses

22
Q

What’s used to tx dysrhythmias assoc w/ TCA tox?

A

NaHCO3

23
Q

How does NaHCO3 help with dysrhythmias?

A

The Na helps overcome the Na channel blockade induced by TCAs

AND

blood alkalinization > reducing TCA binding to myocardial Na channels

24
Q

T or F: NaHCO3 is used to enhance elimination of TCA faster from the body, much like it enhances elimination of salicylates

A

F

-NaHCO3 does NOT enhance elimination of the TCAs > we’re just treating sx’s and hoping for elimination of toxicity (this is unlike salicylates, which IS eliminated faster with NaHCO3)

25
Q

When would we give lidocaine to a pt suffering from TCA-induced ventricular fib or ventricular tachycardia?

A

If they’re unresponsive to NaHCO3

26
Q

If NaHCO3 isn’t helping w/ dysrhythmias assoc w/ TCA tox, what can we use?

A

lidocaine, hypertonic saline, magnesium sulfate

27
Q

What do we AVOID in TCA-induced dysrhythmias?

A

BBs, class IA and IC antiarrhytmics (may worsen cardiac depression/hypotn)

28
Q

What can we give for additional hypotn management during TCA toxicity (if NaHCO3 isn’t enough)?

A

Vasopressors (NE is the best one), DA (not as effective)

29
Q

During TCA tox, what would make a pt’s hypotn worse?

A

B-agonists (B2, specifically)

30
Q

During TCA tox, if a seizure arises, what should we give?

A

BZDs (diazepam)

31
Q

What is recommended for decontamination of TCAs?

A

Single dose activated charcoal

32
Q

Gastric lavage for TCA tox is reasonable in a certain situation.

A

Adults w/ intentional ODs

33
Q

Is hemodialysis useful for TCA tox? Why?

A

No > TCAs have extensive plasma protein binding, are lipophilic, and hence also distribute widely in tissues

34
Q

Antidote for TCA?

A

IV lipid emulsion (don’t use if not life-threatening)

-Based on case reports only

35
Q

What must be tx’ed right away during an MAOI-induced toxicity?

A

Hyperthermia

36
Q

Decontamination strats for MAOI-induced toxicity

A

SDAC, gastric lavage

37
Q

Elimination strats MAOI-induced toxicity

A

?MDAC

hemodialysis = not effective