Psychopharmacology and Somatic Treatments: Mechanisms, Monitoring, and Risk
Expect questions on mechanism, indication, adverse-effect profile, monitoring, and interactions. For antidepressants, know that SSRIs act on the serotonin transporter, that onset is delayed weeks, and that activation, sexual dysfunction, hyponatremia, and bleeding risk are common concerns. For antipsychotics, separate high-potency (EPS, hyperprolactinemia) from low-potency (sedation, anticholinergic, orthostasis) profiles, and know metabolic monitoring for second-generation agents. For mood stabilizers, lithium requires renal and thyroid monitoring and has a narrow therapeutic index; valproate carries hepatotoxicity, pancreatitis, and teratogenicity; lamotrigine risks Stevens-Johnson syndrome with rapid titration.
Traps
- Serotonin syndrome (clonus, hyperreflexia, hyperthermia) versus neuroleptic malignant syndrome (rigidity, lead-pipe, autonomic instability, elevated CK).
- Tyramine interaction with MAOIs and hypertensive crisis.
- QT prolongation with certain antipsychotics and antidepressants.
- Discontinuation syndromes mistaken for relapse.
- Somatic treatments: ECT indications (catatonia, severe depression with psychosis or refusal of food), TMS, and ketamine/esketamine.
Rule of thumb
For any psychotropic question, run the sequence: mechanism, indication, common adverse effect, dangerous adverse effect, monitoring parameter, and key interaction. A worked example: a patient on lithium develops tremor and vomiting with a rising creatinine-suspect toxicity, check a level, and consider interacting drugs such as NSAIDs or thiazides.