Stage 11: Special Populations & Combinations
Concept 7 of 10
R11.7

Drug-Drug Interactions Framework

CYP inhibition/induction, P-glycoprotein, serotonin syndrome, additive QTc — the major interaction categories.

CYP interactions: inhibitors (fluoxetine 2D6, fluvoxamine 1A2, paroxetine 2D6, bupropion 2D6) raise substrate levels — toxicity risk. Inducers (carbamazepine 3A4, smoking 1A2) lower substrate levels — efficacy loss.

Drug-drug interactions are one of the most common sources of preventable adverse events in psychiatric prescribing. A clinically useful framework distinguishes pharmacokinetic interactions (one drug changes the levels of another) from pharmacodynamic interactions (two drugs combine their effects at the receptor or system level). Both matter.

Drug card
Class
Drug interaction framework
Mechanism
Major interaction categories: (1) CYP inhibition (raises substrate levels — fluoxetine, paroxetine, fluvoxamine, bupropion are inhibitors); (2) CYP induction (lowers substrate levels — carbamazepine, smoking induces 1A2); (3) Pharmacodynamic (additive serotonergic → serotonin syndrome; additive QTc; additive CNS depression); (4) Transporter (P-glycoprotein)
FDA indications
All prescribing scenarios — pre-prescription screening, post-prescription monitoring

Key interactions: SSRI/SNRI + MAOI (serotonin syndrome — never combine, requires washout); SSRI + tramadol (serotonin syndrome); fluoxetine/paroxetine 2D6 inhibition raising other psychotropic levels; carbamazepine induction lowering many drugs including oral contraceptives, warfarin; QTc-prolonging combinations (multiple antipsychotics + methadone + ondansetron). Always screen at prescription.

CYP enzyme interactions are the most common pharmacokinetic concern. Inhibitors slow metabolism and raise substrate levels: fluoxetine and paroxetine are potent CYP2D6 inhibitors (raising levels of 2D6 substrates like other psychotropics, tamoxifen, codeine). Fluvoxamine is a potent 1A2 inhibitor. Bupropion is a 2D6 inhibitor (the basis of Auvelity's design). Inducers speed metabolism and lower substrate levels: carbamazepine induces 3A4 (reducing oral contraceptive efficacy, anticoagulant levels, many psychotropics). Smoking induces 1A2 (smokers need higher clozapine doses than non-smokers).

Mechanism in practice

The drug-drug interaction framework in psychiatry rests on two mechanisms — pharmacokinetic (one drug changing another's levels) and pharmacodynamic (additive effects at a shared target).

Mechanism
CYP enzyme inhibition (one drug raises another's levels)
Effect
Increased exposure and toxicity of the affected drug
Clinical applications
Fluoxetine, paroxetine, bupropion (2D6); fluvoxamine (1A2/2C19); know your strong inhibitors — they raise levels of co-prescribed substrates.
Mechanism
CYP enzyme induction (one drug lowers another's levels)
Effect
Reduced exposure and apparent treatment failure
Clinical applications
Carbamazepine and other inducers lower levels of many co-medications, including oral contraceptives — anticipate the loss of efficacy.
Mechanism
Pharmacodynamic additivity at a shared receptor/system
Effect
Amplified effect — therapeutic or toxic
Clinical applications
Serotonergic agents → serotonin syndrome; CNS depressants → respiratory depression; QT-prolonging agents → torsades. Additive risk at a shared target.
Mechanism
Transporter and protein-binding interactions
Effect
Altered drug distribution and effective concentration
Clinical applications
Less common but relevant — e.g., displacement interactions; check when a highly protein-bound drug behaves unexpectedly.

Mechanism note: Interactions are either pharmacokinetic (CYP inhibition/induction changing levels) or pharmacodynamic (additive effect at a shared target) — the framework lets you anticipate, rather than discover, the clinically dangerous combinations.

Serotonin syndrome is the most dangerous pharmacodynamic interaction in psychiatry. Combining serotonergic drugs can produce excessive serotonergic signaling — hyperreflexia, clonus (especially lower extremity), tremor, hyperthermia, GI symptoms, autonomic instability, altered mental status. The combinations to avoid: SSRI plus MAOI (never; mandatory washout). SSRI plus tramadol, dextromethorphan, linezolid, St. John's Wort, triptans. MAOI plus meperidine. Each strongly serotonergic combination raises the risk.

Serotonin syndrome from drug combinations: SSRI/SNRI + MAOI (most dangerous — never combine), SSRI + tramadol, SSRI + dextromethorphan, SSRI + linezolid (an MAOI antibiotic). Recognition: hyperreflexia, clonus, hyperthermia, autonomic instability.

Additive QTc prolongation is the cardiac interaction. The patient on methadone plus citalopram plus ondansetron plus ziprasidone may accumulate enough QTc effect to risk torsades. ECG screening when multiple QTc-prolonging agents combined. Identify and address electrolyte risk factors (K, Mg).

Additive QTc prolongation: methadone + ziprasidone + ondansetron + citalopram in a single patient → torsades risk. ECG monitoring when multiple QTc-prolonging agents combined.

Additive CNS depression with combined sedatives, benzodiazepines plus opioids being the most consequential (the black-box on both classes). Respiratory depression from combined CNS depressants is responsible for many preventable overdose deaths.

Screen at every prescription. Use interaction checkers. Pay particular attention when adding new drugs, when symptoms emerge that could be interaction-related, and when the patient's medication list grows complex.

The anchor

Drug interactions occur via CYP inhibition (raises substrate levels), CYP induction (lowers substrate levels), pharmacodynamic additive effects (serotonin syndrome, QTc, sedation), and transporters. Screen at every prescription and major change.

Prove it

A patient on fluoxetine 40 mg starts taking dextromethorphan-containing cold medicine. Two days later, family brings them in with confusion, tremor, hyperthermia, and rapid clonus. What is the diagnosis?

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