DHA Mental Health & Psychiatry Flashcards

A patient stabilized on phenelzine for treatment-resistant depression is prescribed tramadol by an orthopedic surgeon without consulting psychiatry. He arrives at the ER with hyperthermia (39.8°C), diaphoresis, myoclonus, and brisk hyperreflexia. A colleague suggests neuroleptic malignant syndrome. Which clinical feature BEST differentiates the correct diagnosis from NMS?

Answer: Hyperreflexia and myoclonus rather than lead-pipe rigidity

This is serotonin syndrome triggered by the MAOI + tramadol combination (tramadol has serotonergic properties). The key differentiator is neuromuscular activity: serotonin syndrome produces hyperreflexia, clonus, and myoclonus, while NMS presents with lead-pipe rigidity and hyporeflexia. Both conditions share hyperthermia, elevated CK, and altered mental status, making those findings non-discriminating. Rapid onset (hours) also favors serotonin syndrome over NMS, which typically evolves over days.

A patient with treatment-resistant schizophrenia on clozapine 350 mg/day has his routine CBC checked. His absolute neutrophil count (ANC) is 1,250 cells/mm³ — the first time it has dropped below 1,500. He is asymptomatic. What is the correct next step according to clozapine monitoring guidelines?

Answer: Continue clozapine and increase CBC monitoring to three times per week

An ANC of 1,000–1,499 cells/mm³ constitutes mild (Grade 1) neutropenia per REMS clozapine guidelines. The recommended action is to CONTINUE clozapine while increasing monitoring frequency to three times per week until the ANC recovers to ≥1,500. Permanent discontinuation is reserved for severe neutropenia (ANC < 500). Dose reduction has no established role in managing neutropenia. Interruption with rechallenge applies to moderate neutropenia (ANC 500–999).

A 52-year-old woman with bipolar I disorder has been stable on lithium carbonate (serum level 0.8 mEq/L) for three years. Her PCP prescribes ibuprofen 600 mg TID for osteoarthritic knee pain. Two weeks later she presents with coarse tremor, ataxia, and confusion; her lithium level is now 2.3 mEq/L. What is the PRIMARY pharmacokinetic mechanism responsible?

Answer: NSAIDs reduce renal prostaglandin synthesis, decreasing lithium excretion by the kidney

Lithium is entirely eliminated by the kidneys and is not hepatically metabolized or protein-bound. NSAIDs inhibit cyclooxygenase, reducing renal prostaglandin synthesis. Prostaglandins normally oppose the action of angiotensin II and aldosterone in the kidney; when they are depleted, sodium (and lithium, which is handled similarly by tubular cells) is reabsorbed more avidly, reducing lithium clearance and causing toxic accumulation. This interaction is clinically significant and can be life-threatening.

A 27-year-old woman presents with a two-year history of intense mood swings, impulsivity, and recurrent suicidal gestures. She reports her mood can plummet from baseline to severe despair within 1–2 hours, invariably in the context of a real or perceived rejection. She denies sustained periods of elevated mood lasting longer than a few hours. Childhood adversity is noted. Which finding MOST specifically supports Borderline Personality Disorder over Bipolar II Disorder as the primary diagnosis?

Answer: Mood shifts of hours duration consistently triggered by interpersonal rejection or perceived abandonment

While chronic emptiness (DSM-5 BPD criterion 7) is also relatively specific to BPD, the most diagnostically discriminating feature between BPD and Bipolar II is the temporal relationship of mood episodes to interpersonal triggers. In BPD, affective instability is due to marked reactivity of mood — shifts are driven by relational stressors and last hours, not days. In Bipolar II, hypomanic episodes are not precipitated by rejection and must last ≥4 days by DSM-5 criteria. Childhood trauma and impulsivity are shared features that do not reliably distinguish the two diagnoses.

A 34-year-old man with a diagnosis of Major Depressive Disorder has failed two adequate SSRI trials (each at therapeutic doses for ≥8 weeks). He is currently on escitalopram 20 mg for 10 weeks with minimal response (PHQ-9 remains 18). According to current evidence-based guidelines for treatment-resistant depression, which augmentation strategy carries the strongest Level A evidence and regulatory approval?

Answer: Add an atypical antipsychotic such as aripiprazole or quetiapine

Atypical antipsychotic augmentation (aripiprazole, quetiapine XR, brexpiprazole, olanzapine/fluoxetine) carries the highest level of evidence for adjunctive treatment of MDD and multiple FDA approvals specifically for this indication. Lithium augmentation has historical evidence but is less commonly used as first-line augmentation today given the monitoring burden and narrower therapeutic window. Buspirone augmentation has weak and inconsistent evidence. Psychostimulants may be used adjunctively but lack robust randomized controlled trial evidence for augmentation in MDD.

A 70-year-old man with severe psychotic depression has stopped eating and lost 8 kg over three weeks. He has failed trials of sertraline + risperidone and venlafaxine + olanzapine, each at adequate doses and duration. He is medically frail with mild renal impairment. His family asks about electroconvulsive therapy (ECT). Which statement about ECT is MOST accurate in this clinical context?

Answer: ECT is a guideline-supported, potentially life-saving intervention and represents an appropriate next step given the severity and treatment resistance

There is no absolute age cutoff for ECT. Advanced age with medical comorbidity increases anesthetic risk, which requires careful pre-ECT evaluation, but is not a contraindication. ECT is specifically indicated for severe, psychotic, or life-threatening depression — particularly when rapid response is required (as in nutritional compromise). ECT has superior response rates (60–80%) for psychotic depression compared to pharmacotherapy. MAOI trials are not required before ECT, and many guidelines consider ECT a first-line option in life-threatening presentations. Bilateral placement has more cognitive side effects but is not absolutely contraindicated; it may actually be preferred for faster efficacy in severe presentations.