Psychiatry Flashcards

A 34-year-old woman with treatment-resistant bipolar I disorder is started on clozapine. After 6 weeks, her absolute neutrophil count (ANC) drops to 1,400/μL. She is currently asymptomatic and has no signs of infection. What is the most appropriate next step?

Answer: Continue clozapine and recheck ANC in 3 days

An ANC of 1,000–1,499/μL (mild neutropenia) requires increased monitoring (3× weekly) but not discontinuation. An ANC of 1,400/μL falls into the 'mild neutropenia' range per REMS guidelines — continue clozapine and recheck in 3 days. Discontinuation is mandated only when ANC falls below 1,000/μL (severe neutropenia/agranulocytosis). Dose reduction is not a recognized protocol step for neutropenia management.

A 28-year-old man presents with 3 months of auditory hallucinations, social withdrawal, and flat affect. His symptoms began insidiously and have never fully remitted. He has no prior psychiatric history and denies substance use. Urine toxicology is negative. MRI brain is unremarkable. Which finding on neuropsychological testing would MOST strongly support a diagnosis of schizophrenia over a primary mood disorder with psychotic features?

Answer: Deficits in sustained attention and working memory that predate psychosis onset

Schizophrenia is associated with neurocognitive deficits — particularly in working memory, attention, and processing speed — that predate the full onset of psychosis and are considered trait markers rather than state markers. The premorbid cognitive deficits, especially in sustained attention and working memory, distinguish schizophrenia from mood disorders with psychotic features, where cognitive impairment is typically state-dependent (occurring during episodes). Verbal memory deficits and affective recognition deficits can occur in both conditions.

A 52-year-old man with a 20-year history of alcohol use disorder undergoes medically supervised detoxification. On day 3, he develops confusion, nystagmus, and ataxia. He is given thiamine 100 mg IV and admitted. On day 5, despite thiamine repletion, he is still confused but the ocular findings have resolved. His family reports he can hold a conversation but cannot recall what he had for breakfast. He confabulates when asked about recent events. Which neuroanatomical structures are MOST likely damaged?

Answer: Dorsomedial thalamus and mammillary bodies

This presentation describes the transition from Wernicke encephalopathy (confusion, nystagmus, ataxia — the classic triad) to Korsakoff syndrome (anterograde amnesia with confabulation, relative preservation of procedural memory and consciousness). Korsakoff syndrome results specifically from thiamine-deficiency damage to the dorsomedial thalamus and mammillary bodies. The hippocampus is primarily involved in other amnestic syndromes (e.g., herpes encephalitis, anoxia). The cerebellum/CN VI are affected in Wernicke's acute phase but do not account for the amnestic syndrome.

A psychiatrist is treating a 45-year-old woman with OCD. She has failed two adequate SSRI trials (each at maximum dose for 12 weeks). She is currently on fluvoxamine 300 mg/day with partial response. Which augmentation strategy has the STRONGEST evidence base for treatment-resistant OCD?

Answer: Adding risperidone 0.5–2 mg/day

For SSRI-refractory OCD, augmentation with low-dose antipsychotics — particularly risperidone and haloperidol — has the strongest evidence from randomized controlled trials. Risperidone (0.5–2 mg/day) augmentation of an SSRI is a first-line recommendation for treatment-resistant OCD per IOCDF and APA guidelines. Buspirone augmentation has inconsistent evidence and is not recommended as a first choice. Venlafaxine (SNRI) switching is considered but has weaker evidence than antipsychotic augmentation. Benzodiazepines do not address the core OCD pathology.

A 19-year-old college student is brought to the ED after being found unresponsive at a party. He is bradycardic (HR 48), bradypneic (RR 8), and has pinpoint pupils. He is given naloxone 0.4 mg IV with partial improvement in respiratory rate to 12 and some arousal, but he remains sedated. A second dose of naloxone is given with no further improvement. Toxicology returns positive for fentanyl and another opioid. Which co-ingested substance MOST likely explains the incomplete response to naloxone?

Answer: Methadone

Methadone has an extremely long half-life (24–60 hours) and can cause prolonged respiratory depression that outlasts standard naloxone dosing. Partial response to naloxone followed by re-sedation (or incomplete reversal requiring a naloxone infusion) is classic for methadone toxicity. Buprenorphine's high mu-receptor affinity can cause partial naloxone resistance, but in overdose it causes a 'ceiling effect' on respiratory depression and rarely causes life-threatening bradypnea in isolation. Tramadol overdose can cause seizures (serotonin syndrome component) in addition to opioid effects. Loperamide in toxic doses can cause opioid effects but is less likely at a party context.

A 67-year-old man is referred for psychiatric evaluation after his wife notices he has been emotionally detached, makes socially inappropriate comments at dinner parties, and has developed a new interest in collecting rubber bands obsessively. Neuropsychological testing reveals relative preservation of memory and visuospatial skills but significant deficits in executive function and social cognition. Which of the following CSF biomarker profiles is MOST consistent with the MOST likely underlying diagnosis?

Answer: Elevated total tau, normal phospho-tau, normal Aβ42

This clinical picture — insidious personality change, disinhibition, stereotyped/repetitive behaviors (collecting rubber bands), preserved memory early on, and executive/social cognition deficits — is characteristic of behavioral variant frontotemporal dementia (bvFTD). The most common underlying pathology in bvFTD is TDP-43 or tau (Pick's disease/FTLD-tau). The CSF biomarker profile in FTLD typically shows elevated total tau with normal or near-normal phospho-tau and normal Aβ42 — distinguishing it from Alzheimer's disease (which shows elevated phospho-tau AND decreased Aβ42). Elevated 14-3-3 with rapidly elevated tau suggests prion disease (CJD). A completely normal profile would argue against a neurodegenerative cause.