Depression

Intranasal esketamine has been approvable as monotherapy since 2025 — but her payer's criteria still require a concurrent oral antidepressant, and the only dose she can tolerate may not be doing anything at all.

Tricyclics remain among the most effective drugs available for treatment-resistant depression — and among the most lethal in overdose. Two patients with the same failed history put that tradeoff on opposite ends of the same decision.

The oldest comparative trials in depression pharmacology still favor MAOIs for atypical features — the barrier to using one here isn't efficacy, it's a five-week washout and a diet most patients aren't warned is this strict.

Bupropion's eating-disorder contraindication is absolute on the label — but the seizure signal behind it came from actively purging patients with electrolyte disturbance, not from a diagnosis sitting a decade in the past.

A combinatorial pharmacogenomic panel came back with a clean answer for why two drugs failed on side effects — the harder question is how far that same result should reach into which drug gets tried next.

Aripiprazole, lithium, T3, and switching to a new agent are all reasonable next steps after two failed antidepressant trials — none has ever shown clear superiority over the others in a real head-to-head comparison.

ECT still has the strongest response data of anything available for severe treatment-resistant depression — but this patient has already refused it, and that refusal has to shape the sequence, not just be noted and overridden.

She's eight months into remission from a first depressive episode — inside the guideline window for continuing treatment, but close enough to the edge that stopping now isn't clearly wrong either.

Sertraline has kept his depression in remission for a year — the erectile and ejaculatory side effects it caused are now straining his marriage enough that stopping the drug is genuinely on the table.

She stopped her antidepressant the day the pregnancy test came back positive — the relapse risk that decision carries turns out to be the bigger question than the medication ever was.

Fluoxetine is the only antidepressant that has ever put her depression into full remission — it's also the one lactation pharmacology has the most specific reservations about.

SSRIs act fast enough in PMDD to be dosed only in the luteal phase — a real option for a patient with predictable cycles, and a much harder one for a patient whose cycles won't reliably tell her when the luteal phase begins.

A GnRH agonist can shut down the ovarian cycle driving her PMDD entirely — the progestin needed to protect her uterus from unopposed estrogen is the same class of hormone her PMDD may already be sensitive to.

Zuranolone can lift postpartum depression within days through an entirely different mechanism than an SSRI — the obstacle isn't whether it would work, it's a payer criterion built around a drug that takes weeks.

One trial suggested prophylactic fluoxetine after stroke improves motor recovery; a much larger one found no benefit and a real fracture-risk signal. Which reading should govern depends heavily on who is actually at risk for depression in the first place.

Her TSH is high enough to warrant thyroid treatment on its own — but subclinical hypothyroidism's actual link to depression is contested enough that treating the thyroid alone is a real gamble on a four-month, functionally disabling episode.

High-dose prednisone is the most likely cause of her new depression, and it's also the only thing currently holding a kidney-threatening flare of lupus nephritis in check — tapering it isn't an option, so the depression has to be treated around it.

His selegiline makes a standard SSRI a real serotonin-syndrome consideration — a dopamine agonist could treat his mood and his motor symptoms with one drug, at the cost of a very different risk profile.

Isotretinoin's depression signal has never been cleanly separated from the psychological weight of severe acne itself — and the regulatory program everyone assumes is watching for it is watching for something else entirely.

The old teaching that beta-blockers cause depression traces to decades-old case reports that modern meta-analyses haven't replicated — but it's exactly what's making a post-MI patient hesitate to take a drug proven to reduce his mortality.

The FDA removed varenicline's neuropsychiatric black box warning in 2016 after a trial specifically designed to test it in patients with her exact diagnosis — the outdated caution has outlived the evidence behind it.

Nothing about her symptoms has ever looked severe enough to seem urgent at a single visit — six years of that same low-grade weight is exactly what makes the case for treating it now.

A short benzodiazepine bridge could cover the weeks before his SSRI takes effect on severe anxious distress — his father's alcohol use disorder is exactly the kind of family history that makes that bridge a genuine dependence risk, not just a convenience.

Psilocybin isn't FDA-approved for depression yet, and the pathways to access it outside a clinical trial come with real gaps in medical oversight — including a real interaction with the SSRI keeping him stable enough to consider it at all.

She needs an antidepressant, a chronic NSAID for a bad knee, and an anticoagulant for her heart rhythm — three separately reasonable medications that stack on the exact same bleeding risk.