Tricyclic and Other Cyclic Antidepressants

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Question-and-answer flashcards covering indications, pharmacodynamics, toxicity, diagnosis, and management of tricyclic and other cyclic antidepressant use and overdose.

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22 Terms

1
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What are the primary clinical uses of cyclic antidepressants (CAs)?

Depression, neuropathic pain, migraine prophylaxis, obsessive-compulsive disorder, ADHD, and enuresis.

2
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According to the monoamine hypothesis, how do CAs exert antidepressant effects?

By inhibiting the reuptake of norepinephrine, serotonin, and dopamine at CNS nerve terminals.

3
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Which neurotransmitter channel do CAs inhibit that may contribute to seizures?

The γ-aminobutyric acid (GABA) chloride channel.

4
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Name three receptor types blocked by CAs.

Muscarinic cholinergic, histaminic (H1), and α1-adrenergic receptors.

5
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How does sodium channel blockade by CAs relate to their therapeutic use?

It contributes to their efficacy in treating neuropathic pain.

6
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List the classic toxic symptoms seen in severe CA overdose.

Hypotension, dysrhythmias, coma, seizures, and hyperthermia.

7
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What are the primary mechanisms behind CA-induced cardiovascular toxicity?

Effects on the cardiac action potential, negative inotropy, altered vascular tone, and autonomic nervous system effects.

8
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Why are seizures a major concern in CA overdose?

Because CNS toxicity from cholinergic and GABA interference plus sodium channel blockade lowers the seizure threshold.

9
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What neurologic presentation characterized by agitation, disorientation, and delusions is associated with CA anticholinergic effects?

Delirium.

10
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Within what time frame do most deaths from CA overdose occur after hospital arrival?

Within the first 24 hours, often the first few hours.

11
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Which ECG finding is the most useful predictor of serious CA toxicity?

QRS interval prolongation.

12
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A QRS width of ≥100 msec on ECG in a CA overdose indicates what?

Significant sodium channel blockade and need for aggressive treatment such as sodium bicarbonate.

13
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What qualitative laboratory methods can detect CAs in urine?

Thin-layer chromatography or liquid chromatography.

14
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At what serum CA concentration does life-threatening toxicity usually begin?

Above 100 ng/mL.

15
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Describe the initial supportive measures for a suspected CA overdose patient.

Establish IV access, continuous cardiac monitoring, and frequent vital sign checks including temperature.

16
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When should early endotracheal intubation be considered in CA overdose?

In patients with extreme lethargy, agitation, seizures, or dysrhythmias.

17
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What decontamination step is recommended if CA ingestion occurred within 1 hour?

Prompt administration of activated charcoal.

18
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Why is airway protection essential before giving charcoal to a drowsy CA-overdose patient?

To prevent aspiration of charcoal and resulting pulmonary complications.

19
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How does intravenous sodium bicarbonate (NaHCO3) help in CA cardiotoxicity?

Alkalinizes serum, decreasing free CA binding in cardiac cells and provides sodium to overcome Na+ channel blockade.

20
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List standard indications for starting NaHCO3 therapy in CA overdose.

Serum pH

21
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When can a symptomatic CA-overdose patient be discharged from monitoring?

After being symptom-free for at least 24 hours.

22
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In immediate-release CA overdose, what observation period is sufficient for an asymptomatic patient?

6 hours of monitoring (longer if sustained-release formulation involved).