USMLE Step 2 CK psychiatry questions

Major depressive disorder requires at least 5 of 9 characteristic symptoms (depressed mood, anhedonia, sleep change, appetite/weight change, fatigue, poor concentration, feelings of worthlessness, psychomotor change, suicidal ideation) present nearly every day for at least 2 weeks, with at least one being depressed mood or anhedonia. This patient has depressed mood, insomnia, decreased appetite/weight loss, poor concentration, feelings of worthlessness, and anhedonia for 3 weeks, meeting full criteria. Her symptoms are not tied to a specific identifiable stressor severity threshold and have persisted beyond the minimum duration. A normal thyroid-stimulating hormone excludes hypothyroidism as a contributing medical cause.

• B. Persistent depressive disorder requires depressed mood for at least 2 years, not 3 weeks.
• C. A normal bereavement reaction would be expected only after a significant loss and typically does not include pervasive worthlessness or meet full symptom criteria.
• D. Cyclothymic disorder involves fluctuating hypomanic and depressive symptoms for at least 2 years without meeting full episode criteria.
• E. Adjustment disorder requires symptoms disproportionate to an identifiable stressor but not meeting full criteria for a major depressive episode.

Selective serotonin reuptake inhibitors such as sertraline are recommended as first-line pharmacotherapy for major depressive disorder because of their comparable efficacy to older antidepressants with a more favorable side-effect and safety profile. SSRIs inhibit presynaptic serotonin reuptake, increasing synaptic serotonin availability, and have a wide therapeutic index with low lethality in overdose compared with tricyclic antidepressants and monoamine oxidase inhibitors. Tricyclics and MAOIs are generally reserved for treatment-resistant depression because of anticholinergic, cardiac, and dietary/drug interaction risks. Benzodiazepines and lithium are not indicated as first-line monotherapy for an uncomplicated major depressive episode.

• A. Phenelzine is a monoamine oxidase inhibitor requiring dietary tyramine restriction and carrying risk of hypertensive crisis, reserved for refractory cases.
• B. Amitriptyline is a tricyclic antidepressant with significant anticholinergic effects and cardiotoxicity in overdose, making it a second-line agent.
• C. Lorazepam is a benzodiazepine that may help anxiety symptoms but does not treat the core features of depression and carries dependence risk.
• E. Lithium is used for bipolar disorder and as an augmentation agent in resistant depression, not as first-line monotherapy for unipolar MDD.

Serotonin syndrome results from excess serotonergic activity, classically from combining an SSRI with another serotonergic agent such as a triptan or a monoamine oxidase inhibitor, and presents with the triad of autonomic instability (hyperthermia, tachycardia, hypertension, diaphoresis), neuromuscular abnormalities (hyperreflexia, clonus, tremor, more pronounced in the lower extremities), and altered mental status (agitation). The rapid onset within hours of adding a second serotonergic drug and the presence of clonus and hyperreflexia distinguish it from neuroleptic malignant syndrome, which typically develops over days with lead-pipe rigidity and hyporeflexia. Management includes discontinuing serotonergic agents, supportive care, and cyproheptadine for moderate to severe cases.

• A. An anxiety exacerbation would not explain the fever, clonus, hyperreflexia, or autonomic instability present in this patient.
• B. Malignant hyperthermia occurs with volatile anesthetics or succinylcholine exposure, not antidepressant-triptan combinations.
• D. Neuroleptic malignant syndrome occurs with antipsychotic use, develops over days, and presents with rigidity and hyporeflexia rather than clonus and hyperreflexia.
• E. Anticholinergic toxicity causes dry skin and absent bowel sounds rather than diaphoresis, diarrhea, and clonus.

Venlafaxine, a serotonin-norepinephrine reuptake inhibitor, can cause dose-dependent increases in blood pressure due to increased noradrenergic tone from norepinephrine reuptake inhibition, an effect most prominent at higher doses. The temporal relationship between the dose increase and the new-onset elevated blood pressure, in a patient without other risk factors or secondary causes suggested by history, supports this as a medication adverse effect. Blood pressure should be monitored periodically in patients on venlafaxine, especially after dose increases, and the dose may need to be reduced or the drug switched if hypertension persists. This is a recognized class effect more common with SNRIs than SSRIs.

• A. Primary hyperaldosteronism typically presents with hypertension and hypokalemia and would not correlate acutely with a venlafaxine dose increase.
• B. Essential hypertension would not typically have such an abrupt onset tightly linked temporally to a medication dose increase.
• C. Renal artery stenosis typically presents with resistant hypertension and would not have this acute temporal correlation with a medication change.
• D. White coat hypertension would not explain a sustained, newly elevated reading following a specific pharmacologic change and should be confirmed with out-of-office readings, but the clear temporal link to the dose increase points to a drug effect.

Mirtazapine is an antidepressant that antagonizes central presynaptic alpha-2 adrenergic receptors and postsynaptic serotonin 5-HT2 and 5-HT3 receptors, and its antihistaminergic (H1) activity produces sedation and increased appetite as common side effects. These side effects become therapeutic advantages in depressed patients with insomnia and poor appetite or weight loss, such as this older adult. It is typically dosed at night given its sedating effect, and weight gain is more common at lower doses due to proportionally greater antihistaminergic activity. This makes mirtazapine a rational pharmacologic choice when both insomnia and appetite stimulation are desired treatment goals.

• A. Fluoxetine is more activating and can cause insomnia and appetite suppression, which would worsen this patient's symptoms.
• B. Bupropion is activating, suppresses appetite, and can cause insomnia, making it unsuitable here.
• C. Modafinil is a wakefulness-promoting agent used for narcolepsy or shift-work disorder and would worsen insomnia and is not an antidepressant.
• D. Varenicline is a smoking cessation aid and is not indicated for depression.

Bupropion lowers the seizure threshold and is contraindicated in patients with a current or prior eating disorder involving purging behaviors (bulimia nervosa or anorexia nervosa with purging), because the resulting electrolyte disturbances (such as hypokalemia and hypochloremia from repeated vomiting) further increase seizure risk. It is also contraindicated in patients with seizure disorders for the same reason. This patient's recurrent self-induced vomiting places her at elevated risk for electrolyte abnormalities, making bupropion an unsafe choice despite its otherwise favorable weight and sexual side-effect profile. An SSRI such as fluoxetine, which is FDA-approved for bulimia nervosa, would be a more appropriate choice.

• A. Bupropion is not a major cause of hepatotoxicity.
• B. Bupropion does not cause hyperprolactinemia; this is more associated with antipsychotics.
• C. Bupropion has minimal serotonergic activity and is not strongly associated with serotonin syndrome.
• E. Bupropion is not associated with significant QT prolongation.

Persistent depressive disorder (dysthymia) is characterized by a chronically depressed mood lasting at least 2 years in adults, along with at least 2 additional symptoms such as poor appetite, low self-esteem, poor concentration, or low energy, without ever meeting full criteria for a major depressive episode or without the symptom-free period exceeding 2 months. This patient's chronic, low-grade symptoms lasting 2.5 years without a discrete 2-week period of major depressive episode severity fit this pattern. Major depressive disorder requires discrete episodes of at least 5 symptoms for 2 weeks, which is not described here. The key differentiator is chronicity and lower severity in persistent depressive disorder versus episodic, more severe presentation in MDD.

• B. A single episode of major depressive disorder requires a discrete 2-week period meeting full symptom criteria, which this patient does not describe.
• C. Recurrent major depressive disorder requires at least two discrete major depressive episodes, which are not present here.
• D. Adjustment disorder requires a specific identifiable stressor and symptoms typically resolving within 6 months after the stressor or its consequences end, inconsistent with this chronic 2.5-year course.
• E. Cyclothymic disorder requires alternating periods of hypomanic and depressive symptoms over at least 2 years, and this patient has no history of hypomania.

This patient has an abnormally elevated, expansive mood with decreased need for sleep, increased talkativeness, flight of ideas, and excessive involvement in risky activities (spending savings) lasting at least 1 week with marked impairment in functioning, meeting DSM-5-TR criteria for a manic episode. A manic episode with significant functional impairment, regardless of the presence of psychotic features, establishes a diagnosis of bipolar I disorder. A negative toxicology screen helps exclude a substance-induced cause. No psychotic symptoms are present, so schizoaffective disorder is not indicated.

• A. Cyclothymic disorder involves chronic, fluctuating hypomanic and depressive symptoms for at least 2 years, not a single acute manic episode.
• C. Hypomania lasts at least 4 days without marked impairment in functioning, whereas this episode caused severe impairment (financial, social) and lasted a week, meeting criteria for full mania.
• D. A negative urine toxicology screen argues against a substance-induced etiology.
• E. Schizoaffective disorder requires psychotic symptoms for at least 2 weeks in the absence of mood symptoms, which is not described here.

Cyclothymic disorder is characterized by numerous periods of hypomanic symptoms and numerous periods of depressive symptoms that do not meet full criteria for a hypomanic, manic, or major depressive episode, present for at least 2 years in adults, with no symptom-free period longer than 2 months. This patient's chronic, fluctuating subthreshold mood symptoms over 3 years without a full major depressive or manic episode fit this pattern. Bipolar II disorder requires at least one full hypomanic episode and one full major depressive episode, which are absent here.

• A. Bipolar I disorder requires at least one full manic episode, which has not occurred.
• B. Borderline personality disorder involves pervasive instability in relationships, self-image, and affect typically tied to interpersonal triggers, rather than sustained discrete mood periods as described.
• C. Bipolar II disorder requires at least one documented hypomanic episode and one major depressive episode meeting full criteria, neither of which has occurred in this patient.
• D. Persistent depressive disorder involves chronic low mood without the hypomanic-like periods described here.

Postpartum depression presents with persistent depressive symptoms (low mood, sleep disturbance beyond infant care demands, feelings of worthlessness, difficulty bonding) lasting more than 2 weeks and extending beyond the first 2 weeks postpartum, distinguishing it from postpartum blues. Postpartum blues is a self-limited condition with mild mood lability and tearfulness that peaks around day 3-5 and resolves within 2 weeks without treatment, which matches her initial first week but not her current persistent symptoms. The absence of hallucinations, delusions, or disorganized behavior rules out postpartum psychosis, which is a psychiatric emergency requiring immediate intervention.

• A. Adjustment disorder requires an identifiable stressor with symptoms disproportionate to it but not meeting criteria for a major depressive episode; her presentation is most consistent with full postpartum depression.
• B. Postpartum psychosis presents with hallucinations, delusions, or grossly disorganized behavior, none of which this patient has.
• C. Her symptoms center on depressed mood and worthlessness rather than predominant excessive worry, making generalized anxiety disorder less fitting.
• D. Postpartum blues is transient, resolving within 2 weeks, whereas this patient's symptoms have persisted and progressed beyond that window.

This patient has catatonia (waxy flexibility, mutism, immobility) in the setting of severe major depression, with only partial response to a benzodiazepine trial, which is the first-line treatment for catatonia. When catatonia is refractory to benzodiazepines or when depression is severe with psychotic features or poses an urgent risk (such as from poor food and fluid intake), electroconvulsive therapy is the most appropriate and effective next step. ECT works rapidly and has a high response rate in catatonia and severe refractory depression, making it preferable to waiting weeks for a medication trial to take effect in this acutely ill patient.

• A. Switching antidepressant classes does not address catatonia directly and takes weeks to show effect, which is unsafe in this acute presentation.
• B. Antipsychotics alone, particularly without addressing catatonia first, are not first-line and can occasionally worsen catatonia or precipitate neuroleptic malignant syndrome in vulnerable patients.
• C. Continuing to wait on an SSRI trial is inappropriate given the severity of her catatonic symptoms and poor oral intake, which require urgent intervention.
• E. Transcranial magnetic stimulation is used for treatment-resistant depression without catatonia or psychotic features, and its onset of benefit is too slow for this acute, severe presentation.

Generalized anxiety disorder requires excessive, difficult-to-control worry about multiple life domains for at least 6 months, accompanied by at least three associated symptoms such as muscle tension, restlessness, fatigue, poor concentration, irritability, or sleep disturbance. This patient's worry spans multiple domains (work, family, finances), has lasted 8 months, and is accompanied by muscle tension and sleep disturbance, meeting diagnostic criteria. Medical causes such as hyperthyroidism have been excluded with normal thyroid function tests. The chronic, pervasive, multi-domain nature of the worry distinguishes it from the other anxiety-spectrum conditions listed.

• A. There is no mention of depressed mood, anhedonia, or other core depressive symptoms.
• B. Adjustment disorder requires an identifiable stressor within the preceding 3 months and resolves within 6 months of the stressor ending, not described here.
• C. Illness anxiety disorder centers on preoccupation with having a serious illness, not diffuse worry about multiple life domains.
• D. Panic disorder involves recurrent discrete panic attacks, not chronic pervasive worry.

Panic disorder is characterized by recurrent, unexpected panic attacks (abrupt surges of fear peaking within minutes with symptoms such as palpitations, dyspnea, sweating, and fear of dying), followed by persistent worry about additional attacks or behavioral changes such as avoidance. This patient has had three discrete attacks with subsequent avoidance behavior, and cardiac and thyroid causes have been excluded with normal ECG, troponin, and TSH. The diagnosis of panic disorder is clinical and requires ruling out medical mimics before attributing symptoms to a primary anxiety disorder. The combination of recurrent attacks plus anticipatory anxiety/avoidance confirms the diagnosis.

• A. Generalized anxiety disorder involves chronic diffuse worry rather than discrete, abrupt panic attacks.
• B. Hyperthyroidism is excluded by a normal TSH.
• C. Pulmonary embolism is excluded by the normal findings and lack of risk factors such as hypoxia or tachycardia with hypoxemia.
• E. Stable angina is exertional and relieved by rest or nitrates, and would show ischemic changes or risk factors, not isolated discrete attacks with normal ECG and troponin.

A short-acting benzodiazepine such as lorazepam provides rapid relief of an acute panic attack because SSRIs/SNRIs take several weeks to achieve full anxiolytic effect, and she is only 3 days into sertraline therapy. Benzodiazepines are appropriate for short-term symptomatic control during the lag period before SSRIs become effective, while the SSRI is continued as maintenance therapy. Long-term benzodiazepine use is avoided due to dependence risk, but a single acute dose during an attack is reasonable here. Her ECG and vital signs do not suggest a cardiac emergency, supporting symptomatic anxiolytic treatment.

• B. Switching SSRIs is premature after only 3 days and does not address the acute attack.
• C. Buspirone has a slow onset and is primarily used for generalized anxiety disorder, not acute panic attacks.
• D. Increasing the sertraline dose this early will not provide acute relief and should wait until an adequate trial period has passed.
• E. Propranolol is used for performance-type anxiety with autonomic symptoms, not as first-line abortive therapy for a panic attack.

Social anxiety disorder is characterized by marked fear or anxiety about social situations in which the person may be scrutinized or negatively evaluated by others, such as public speaking or eating in front of others, persisting for at least 6 months and leading to avoidance. This patient's fear centers specifically on being judged by others across multiple social contexts (presentations, eating in front of peers), which is the hallmark of social anxiety disorder rather than fear of a single discrete object or situation. Specific phobia involves fear of a particular object or situation unrelated to social evaluation. The broad pattern of fear tied to social scrutiny, not isolated triggers, establishes the diagnosis.

• A. Generalized anxiety disorder involves diffuse worry about multiple life domains, not focused fear of social scrutiny.
• B. Agoraphobia involves fear of situations where escape might be difficult or help unavailable, such as crowds or open spaces, not fear of social judgment.
• C. Avoidant personality disorder is a pervasive lifelong pattern of social inhibition and feelings of inadequacy beginning in early adulthood, broader than situation-specific social fear.
• D. Specific phobia involves fear of a discrete object or situation (e.g., heights, flying) rather than fear of social evaluation across multiple contexts.

Posttraumatic stress disorder requires exposure to a traumatic event followed by symptoms from four clusters—intrusion (nightmares, intrusive memories), avoidance, negative alterations in cognition or mood (persistent negative beliefs, emotional numbing), and hyperarousal (exaggerated startle)—lasting more than 1 month. This patient has symptoms from all four clusters persisting for several months after the trauma, meeting full PTSD criteria. Acute stress disorder is limited to the first month after trauma, which has already passed here. The combination of duration beyond 1 month and representation across all four symptom clusters confirms PTSD.

• A. Acute stress disorder is diagnosed only within the first month after trauma; this patient's symptoms have persisted well beyond that window.
• B. Adjustment disorder does not require re-experiencing, hyperarousal, and avoidance clusters tied specifically to a traumatic, life-threatening event.
• C. Generalized anxiety disorder lacks the trauma-specific intrusion and avoidance symptoms described.
• E. While emotional numbing can mimic depression, the intrusive memories, trauma-specific avoidance, and hyperarousal point to PTSD rather than major depressive disorder.

Sertraline and paroxetine are the only medications FDA-approved for PTSD and are recommended as first-line pharmacotherapy along with other SSRIs (fluoxetine) and the SNRI venlafaxine. These agents reduce symptoms across intrusion, avoidance, and hyperarousal clusters and have the strongest evidence base and most favorable safety profile for long-term use. Benzodiazepines are avoided in PTSD because they do not improve core symptoms, carry dependence risk, and may worsen outcomes. Trazodone is sometimes added for sleep disturbance but is not used as monotherapy for the full disorder.

• A. Propranolol lacks robust evidence for PTSD treatment and is not a guideline-recommended first-line agent.
• B. Trazodone alone is used adjunctively for sleep but is not adequate monotherapy for the broader disorder.
• C. Quetiapine is sometimes used as an augmenting agent in refractory cases but is not first-line initial therapy.
• D. Benzodiazepines are not recommended for PTSD; they fail to improve core symptoms and carry risk of dependence and potential symptom worsening.

Acute stress disorder is diagnosed when trauma-related symptoms—intrusion, negative mood, dissociation, avoidance, and arousal—occur between 3 days and 1 month after exposure to a traumatic event. This patient's symptoms began after a life-threatening traumatic event and have been present for only 2 weeks, fitting within this window. If symptoms persist beyond 1 month, the diagnosis would be reclassified as PTSD. The presence of dissociative symptoms (feeling detached) alongside intrusion and hyperarousal within the acute timeframe is characteristic of acute stress disorder rather than the other conditions listed.

• A. PTSD requires symptoms lasting more than 1 month; this patient is only 2 weeks out from the event.
• B. Adjustment disorder is used for stressors that are not necessarily life-threatening or traumatic in the DSM sense, and does not require the specific symptom clusters seen here.
• C. There is no evidence of hallucinations or delusions, only dissociative and anxiety symptoms.
• E. Generalized anxiety disorder involves chronic diffuse worry unrelated to a specific trauma, not an acute trauma-linked presentation.

Tardive dyskinesia is a delayed complication of chronic dopamine receptor blockade, classically presenting with orobuccolingual movements (lip puckering, tongue protrusion) and choreoathetoid finger movements after months to years of antipsychotic exposure. It results from dopamine receptor upregulation and supersensitivity in the nigrostriatal pathway. Management includes switching to a lower-potency or second-generation agent, dose reduction if possible, and considering a VMAT2 inhibitor such as valbenazine or deutetrabenazine. Unlike acute dystonia, which occurs within days of starting or increasing an antipsychotic, tardive dyskinesia develops after prolonged use.

• A. Acute dystonia causes sustained muscle contractions (e.g., torticollis, oculogyric crisis) within days of starting antipsychotics, not after years.
• B. Huntington disease causes chorea but would present with cognitive decline and family history, and would not be temporally linked to antipsychotic duration.
• C. Akathisia is subjective inner restlessness with an urge to move, not orobuccolingual dyskinesia.
• D. Essential tremor is a postural/action tremor, not orofacial choreoathetoid movements, and is unrelated to antipsychotic use.

Neuroleptic malignant syndrome is a life-threatening reaction to dopamine antagonists characterized by fever, generalized rigidity, autonomic instability, and markedly elevated creatine kinase from muscle breakdown, which can lead to acute kidney injury. The first step is immediate discontinuation of the offending antipsychotic, followed by aggressive intravenous hydration to prevent renal failure and supportive cooling. Dantrolene, a skeletal muscle relaxant, is used for severe rigidity and hyperthermia, and bromocriptine may be added as a dopamine agonist once the antipsychotic is stopped. Mortality is reduced primarily by early recognition and prompt drug cessation.

• A. Continuing the causative antipsychotic worsens NMS; lorazepam alone does not address the underlying cause.
• B. Bromocriptine can be used but only after stopping the offending agent, not while continuing it.
• D. ECT is a treatment option for refractory NMS but is not the initial next step before drug discontinuation and supportive care.
• E. Switching to another antipsychotic, even clozapine, still provides dopamine blockade and will not resolve NMS.

Delusional disorder is characterized by one or more fixed, non-bizarre delusions lasting at least 1 month, in the absence of prominent hallucinations, disorganized speech, or significant functional impairment outside the delusion's direct impact. This patient's persecutory belief about poisoning fits the persecutory subtype, and his preserved occupational and social functioning distinguishes it from schizophrenia, which requires broader functional decline and other psychotic features. The diagnosis requires ruling out mood disorders and substance use, both of which are absent here. Treatment often involves antipsychotics, though insight is typically limited and treatment engagement can be difficult.

• A. Brief psychotic disorder lasts less than 1 month, whereas this patient's delusion has persisted for 7 months.
• B. Schizophrenia requires at least 6 months of symptoms with significant functional decline and often other features like hallucinations or disorganized speech, none of which are present.
• C. Schizoaffective disorder requires a concurrent major mood episode, which this patient does not have.
• D. Schizotypal personality disorder involves odd beliefs and eccentric behavior without a fixed, false belief held with full conviction.

Alcohol withdrawal typically begins 6–24 hours after the last drink with autonomic hyperactivity, tremor, and anxiety, as seen in this patient with a CIWA-Ar score of 16 indicating moderate withdrawal. Symptom-triggered benzodiazepine dosing, using a validated scale like CIWA-Ar, is the standard of care because it allows medication to be titrated to symptom severity, reducing total benzodiazepine exposure and length of treatment compared to fixed dosing. Lorazepam is often preferred in patients with significant hepatic impairment because of its direct glucuronidation without active metabolites requiring oxidative metabolism. Benzodiazepines prevent progression to more severe withdrawal, including seizures and delirium tremens.

• A. A CIWA-Ar score of 16 indicates moderate withdrawal requiring pharmacologic treatment, not observation alone.
• B. Phenobarbital loading is reserved for severe or benzodiazepine-refractory withdrawal, not first-line moderate withdrawal.
• C. Haloperidol does not treat the underlying GABA-ergic withdrawal state and does not prevent seizures or delirium tremens.
• D. Disulfiram is used for relapse prevention after detoxification, not for treating acute withdrawal symptoms.

Delirium tremens is a severe, life-threatening form of alcohol withdrawal that typically develops 48–96 hours after the last drink, presenting with confusion, visual hallucinations, severe autonomic instability (tachycardia, hypertension, fever, diaphoresis), and disorientation. High-dose intravenous benzodiazepines, such as diazepam or lorazepam, are the treatment of choice, titrated aggressively to control agitation and prevent complications like seizures, cardiovascular collapse, or death. Frequent reassessment using a withdrawal severity scale guides further dosing, and untreated delirium tremens carries significant mortality. Intensive care monitoring is often required given the severity of autonomic dysregulation.

• A. Empiric antibiotics are not indicated without evidence of infection; this presentation is explained by alcohol withdrawal.
• B. Acamprosate helps maintain abstinence after withdrawal but has no role in treating acute delirium tremens.
• C. Restraints without pharmacologic treatment do not address the underlying withdrawal physiology and risk harm.
• D. Naltrexone is used for relapse prevention after detoxification, not for treating acute delirium tremens.

This patient has the classic triad of Wernicke encephalopathy: confusion, ataxia, and ophthalmoplegia (nystagmus with gaze limitation), caused by thiamine (vitamin B1) deficiency, commonly seen in chronic alcohol use with poor nutrition. Thiamine must be administered before or simultaneously with glucose because dextrose administration in a thiamine-deficient patient can precipitate or worsen Wernicke encephalopathy by increasing metabolic demand for thiamine as a cofactor in carbohydrate metabolism. In practice, thiamine should be given immediately, and glucose should not be withheld for hypoglycemia, but thiamine must not be delayed or omitted. This is a clinical diagnosis requiring immediate empiric treatment rather than imaging confirmation.

• A. While giving both is acceptable, the key teaching point is that thiamine must not be delayed relative to glucose; simultaneous dosing through two lines is not the standard emphasized practice and overcomplicates management.
• B. Giving dextrose first can precipitate or worsen Wernicke encephalopathy by depleting remaining thiamine stores.
• D. There is no indication of opioid intoxication; naloxone is not relevant to this presentation.
• E. Wernicke encephalopathy is a clinical diagnosis requiring immediate empiric thiamine; imaging should never delay treatment.

This patient has the classic opioid overdose triad of respiratory depression, miosis (pinpoint pupils), and decreased consciousness, likely from intravenous drug use given the found syringe. Naloxone, a competitive opioid receptor antagonist, is the immediate treatment of choice because it rapidly reverses respiratory depression and can be given intravenously, intramuscularly, or intranasally, making it suitable for prehospital and emergency use. Ventilatory support should accompany naloxone administration if the patient does not respond quickly, but reversal should not be delayed for diagnostic testing. Repeat dosing may be needed because naloxone's duration of action is shorter than that of many opioids.

• A. Treatment for respiratory failure should not be delayed for laboratory testing in a patient with evident hypoxia and respiratory depression.
• B. Flumazenil reverses benzodiazepine toxicity, not opioid toxicity, and does not match this clinical picture.
• C. Intubation may ultimately be needed if naloxone fails, but reversal with naloxone should be attempted first given its rapid onset and low risk.
• D. Naltrexone is a long-acting oral or injectable antagonist used for relapse prevention, not for acute overdose reversal.

This patient has classic opioid withdrawal symptoms, including rhinorrhea, lacrimation, piloerection, yawning, gastrointestinal distress, and autonomic hyperactivity, which typically begin 6–24 hours after last use of short-acting opioids like heroin. Buprenorphine, a partial mu-opioid agonist, is first-line for both withdrawal management and long-term maintenance therapy because it reduces withdrawal symptoms and cravings while having a ceiling effect that lowers overdose risk; it should be started only once withdrawal symptoms are clearly established (to avoid precipitating withdrawal in the presence of residual full agonist). The naloxone component deters intravenous misuse. Methadone is an alternative but requires administration through a certified opioid treatment program and careful dose titration rather than a single high outpatient dose.

• A. Disulfiram is used for alcohol use disorder, not opioid use disorder.
• B. A full agonist taper is not standard outpatient management and does not provide the long-term maintenance the patient is requesting.
• C. Naloxone is an antagonist that would precipitate or worsen withdrawal symptoms, not relieve them.
• D. A single high-dose methadone administration outside a certified opioid treatment program risks overdose and is not standard induction practice.

Buprenorphine is a partial mu-opioid agonist with high receptor affinity; if administered before withdrawal is established, it can precipitate acute withdrawal by displacing full agonists from the receptor while providing only partial activation. It is approved for office-based, take-home induction once the patient is in mild-to-moderate withdrawal (confirmed by a Clinical Opiate Withdrawal Scale score), unlike methadone, which requires daily dosing at a federally regulated opioid treatment program. This combination of home induction and the precipitated-withdrawal risk makes buprenorphine the correct choice here.

• A. Naltrexone requires full detoxification (7-10 days opioid-free) before starting, or it will precipitate severe withdrawal immediately.
• C. Clonidine only treats autonomic withdrawal symptoms and is not a maintenance therapy for opioid use disorder.
• D. Loperamide treats diarrhea symptomatically but has no role in opioid use disorder maintenance treatment.
• E. Methadone is effective but must be dispensed daily through a certified opioid treatment program, not taken home independently at the start of treatment.

Abrupt cessation of long-term, high-dose benzodiazepine use causes a withdrawal syndrome with autonomic instability, tremor, agitation, and risk of generalized tonic-clonic seizures, typically emerging 1-3 days after the last dose for short-acting agents like alprazolam. This is why benzodiazepines must always be tapered gradually rather than stopped abruptly, especially in hospitalized patients whose home medications are often inadvertently omitted. The temporal correlation with discontinuation of her long-term alprazolam and the classic withdrawal features (autonomic hyperactivity plus seizure) point to this diagnosis. Seizures from benzodiazepine withdrawal can occur even without a prior seizure disorder.

• B. Opioid analgesics typically cause sedation or delirium but are not a common cause of generalized tonic-clonic seizures.
• C. The clear temporal link to benzodiazepine discontinuation makes withdrawal far more likely than an undiagnosed seizure disorder.
• D. There is no history given of alcohol use, and her symptom pattern directly follows discontinuation of her home benzodiazepine.
• E. There is no mention of serotonergic drug use or classic serotonin syndrome findings such as clonus and hyperreflexia.

Phencyclidine (PCP) intoxication classically produces vertical or horizontal nystagmus, dissociative behavior with violent or bizarre agitation, analgesia or decreased pain sensation, and muscle rigidity, along with hypertension, tachycardia, and hyperthermia. Nystagmus, especially vertical, is a distinguishing clue not typically seen with other stimulant or hallucinogen intoxications. The combination of dissociation, analgesia, and nystagmus is the key pattern that differentiates PCP from other drugs of abuse. Management is supportive, with benzodiazepines for agitation and a quiet, low-stimulation environment.

• B. GHB intoxication usually presents with sedation and respiratory depression rather than agitation, rigidity, and nystagmus.
• C. Methamphetamine causes sympathomimetic toxicity with agitation and tachycardia but does not typically cause nystagmus or profound analgesia.
• D. Synthetic cannabinoids can cause agitation and tachycardia but are not classically associated with vertical nystagmus and pain insensitivity.
• E. LSD intoxication typically causes visual hallucinations and perceptual distortions without the prominent nystagmus and analgesia seen with PCP.

Cannabinoid hyperemesis syndrome occurs in long-term, heavy cannabis users and presents with recurrent episodes of severe nausea and vomiting, often with compulsive hot showers or baths that transiently relieve symptoms, a distinguishing clinical clue. It is a diagnosis of exclusion once other causes of recurrent vomiting (pancreatitis, bowel obstruction, cyclic vomiting syndrome) are ruled out, and symptoms typically resolve with sustained cannabis cessation. Unlike acute intoxication, which occurs during use and is not predominantly characterized by vomiting cycles, this syndrome occurs in chronic, frequent users regardless of timing relative to the most recent use. The hot-shower relief behavior is a highly specific feature for this diagnosis on USMLE-style vignettes.

• A. Cannabis withdrawal presents with irritability, insomnia, and decreased appetite rather than recurrent vomiting relieved by hot showers.
• C. Acute cannabis intoxication causes euphoria, conjunctival injection, and increased appetite, not recurrent cyclic vomiting with hot-shower relief.
• D. Normal lipase and the lack of significant epigastric pain make acute pancreatitis unlikely.
• E. Cyclic vomiting syndrome is a consideration but lacks the specific association with chronic heavy cannabis use and hot-shower relief described here.

Schizoid personality disorder is characterized by a pervasive pattern of detachment from social relationships and a restricted range of emotional expression, with the individual genuinely preferring solitude rather than avoiding others out of fear or distrust. This patient's indifference to social isolation, lack of desire for closeness, and emotional flatness without odd beliefs or perceptual disturbances fit schizoid personality disorder rather than schizotypal disorder, which requires eccentric beliefs or magical thinking, or paranoid disorder, which requires pervasive distrust and suspicion of others' motives.

• B. Schizotypal personality disorder requires odd beliefs, magical thinking, or perceptual distortions, none of which this patient has.
• C. Autism spectrum disorder requires childhood-onset deficits in social communication and restricted, repetitive behaviors, which are not described in this adult-onset personality pattern.
• D. Avoidant personality disorder involves social withdrawal driven by fear of rejection and low self-esteem, whereas this patient is indifferent to, not fearful of, social contact.
• E. Paranoid personality disorder requires pervasive suspiciousness and distrust of others' motives, which is not described here.

This patient's pattern of unstable relationships, identity disturbance, chronic emptiness, fear of abandonment, affective instability, and impulsivity with recurrent self-harm meets criteria for borderline personality disorder. Dialectical behavior therapy, which combines individual therapy and group skills training focused on emotion regulation, distress tolerance, and interpersonal effectiveness, is the first-line, evidence-based treatment and has been shown to reduce self-harm and hospitalization. Pharmacotherapy may be used adjunctively for specific symptom clusters (such as mood lability or impulsivity), but no medication is considered first-line or curative for the underlying personality disorder.

• A. Lithium is used for bipolar disorder, not as first-line therapy for borderline personality disorder.
• C. SSRIs like fluoxetine may help with comorbid mood or anxiety symptoms but are not first-line treatment for the core features of borderline personality disorder.
• D. Quetiapine may be used adjunctively for severe affective symptoms but is not the first-line treatment for borderline personality disorder.
• E. Routine psychiatric hospitalization is not indicated for chronic personality pathology without acute, immediate safety concerns and can reinforce maladaptive coping.

Histrionic personality disorder is characterized by excessive emotionality, attention-seeking behavior, theatrical and exaggerated expression of emotions, use of physical appearance to draw attention, and discomfort when not the center of attention. This patient's dramatic gestures, need for reassurance about her attractiveness, and distress at perceived inattention are classic features. Narcissistic personality disorder instead centers on grandiosity, entitlement, and need for admiration of one's superiority rather than physical attractiveness or dramatic emotional display. The key distinguishing feature is that histrionic patients seek attention and approval, while narcissistic patients seek admiration for perceived greatness.

• A. Somatic symptom disorder requires distressing physical symptoms with excessive health-related anxiety, which is not the primary feature here.
• B. Narcissistic personality disorder involves grandiosity and entitlement, not primarily theatrical attention-seeking about appearance.
• D. Borderline personality disorder features identity disturbance, chronic emptiness, and fear of abandonment with impulsivity, not primarily theatrical emotionality.
• E. Dependent personality disorder involves submissiveness and fear of separation, not dramatic, attention-seeking behavior.

Malingering is the intentional production or exaggeration of symptoms motivated by an external incentive, such as financial compensation from a lawsuit, avoiding work, or obtaining medication, as seen in this patient who explicitly admits the pain is not genuinely severe. Factitious disorder also involves intentional symptom fabrication, but the motivation is an internal psychological need to assume the sick role, not external gain such as money. This patient's inconsistent examination findings (normal movement when distracted) and admitted motivation for financial gain are classic for malingering rather than a true somatoform or factitious process.

• A. Somatic symptom disorder requires genuine distress from a real symptom, not conscious fabrication for external reward.
• C. Conversion disorder involves genuine, unintentionally produced neurological symptoms incompatible with recognized disease, not intentional deception for gain.
• D. Illness anxiety disorder involves genuine fear of having a disease, not deliberate symptom exaggeration for financial benefit.
• E. Factitious disorder involves fabricating illness for internal psychological gain (assuming the sick role), not external incentives like lawsuit money.

Conversion disorder (functional neurological symptom disorder) presents with neurologic deficits, such as weakness, that are incompatible with known neuroanatomic patterns and demonstrate inconsistency on examination, such as a positive Hoover sign in which the weak leg involuntarily presses down when the patient uses the contralateral leg against resistance. Symptoms typically follow a psychologically stressful event and are not intentionally produced, distinguishing this from malingering and factitious disorder. Normal reflexes, absence of atrophy, and normal imaging support a functional rather than structural neurologic cause.

• A. Guillain-Barré syndrome causes ascending symmetric weakness with areflexia, inconsistent with this patient's normal reflexes and positive Hoover sign.
• B. Malingering involves conscious symptom fabrication for external gain, which is not suggested here and there is no secondary gain identified.
• C. Factitious disorder requires intentional symptom production for internal psychological gain, which is not indicated by the unconscious, stress-triggered presentation.
• D. Multiple sclerosis would show demyelinating lesions on MRI and a pattern of deficits consistent with specific neuroanatomic pathways, not seen here.

Anorexia nervosa is diagnosed by restriction of energy intake leading to significantly low body weight, intense fear of weight gain or persistent behavior interfering with weight gain, and a disturbance in body image (believing oneself to be fat despite being underweight). This patient's low BMI, caloric restriction, body image distortion, and associated medical complications of starvation, including bradycardia, hypotension, amenorrhea, and lanugo hair, are classic findings. Bulimia nervosa involves binge eating with compensatory behaviors in patients who are typically normal weight or overweight, which does not fit this low-BMI presentation.

• A. Bulimia nervosa involves recurrent binge-purge cycles typically in patients of normal or above-normal weight, not the significantly low BMI seen here.
• B. Major depressive disorder can cause weight loss but does not explain the specific fear of weight gain and body image distortion described.
• C. Avoidant/restrictive food intake disorder involves food avoidance without body image disturbance or fear of weight gain, which is present in this patient.
• D. Body dysmorphic disorder involves preoccupation with a perceived physical defect, not a global fear of fatness driving starvation behavior.

This patient has developed refeeding syndrome, characterized by hypophosphatemia, hypokalemia, and hypomagnesemia that occur when carbohydrate-driven insulin release causes a shift of phosphate, potassium, and magnesium into cells in a previously starved patient. The most appropriate management is to slow the rate of caloric advancement and aggressively replete phosphorus, potassium, and magnesium, since severe hypophosphatemia can cause cardiac arrhythmias, respiratory failure, and rhabdomyolysis. Serum electrolytes, particularly phosphorus, should be monitored closely during the first week of refeeding in malnourished patients. Continuing or increasing caloric intake without addressing the electrolyte derangements would worsen the syndrome and risk cardiac decompensation.

• A. Water restriction does not address the critical electrolyte abnormalities driving this patient's symptoms.
• C. Furosemide would further lower potassium and magnesium and does not address the underlying cause of the edema, which relates to sodium and fluid shifts during refeeding.
• D. Higher-rate parenteral nutrition would exacerbate the electrolyte shifts responsible for refeeding syndrome.
• E. Increasing caloric intake further would worsen the insulin-driven intracellular electrolyte shifts and risk cardiac arrhythmia.

Bulimia nervosa is characterized by recurrent episodes of binge eating with a sense of loss of control, followed by compensatory behaviors such as self-induced vomiting, occurring at least once weekly for 3 months, in a patient who maintains a normal or near-normal body weight. The dental enamel erosion (perimylolysis) and knuckle calluses (Russell sign) from repeated self-induced vomiting, along with hypochloremic, hypokalemic metabolic alkalosis from loss of gastric acid, are classic findings. Anorexia nervosa, binge-eating/purging type requires a significantly low body weight, which this patient does not have with a BMI of 22 kg/m².

• A. Pica involves persistent eating of nonnutritive substances, unrelated to this presentation.
• B. Binge-eating disorder involves binge eating without recurrent compensatory purging behaviors, which does not fit this patient's vomiting and metabolic alkalosis.
• D. Anorexia nervosa requires significantly low body weight, which is absent given this patient's BMI of 22 kg/m².
• E. Rumination disorder involves repeated effortless regurgitation of recently eaten food without the binge-purge cycle or weight concerns described here.

Binge eating disorder is characterized by recurrent episodes of eating an objectively large amount of food with a sense of loss of control, occurring at least once a week for 3 months, in the absence of regular compensatory behaviors such as vomiting, laxative use, or excessive exercise. The marked distress and guilt after binges, without weight-control behaviors, distinguish it from bulimia nervosa, where recurrent compensatory behavior is required for diagnosis. Patients with binge eating disorder are often overweight or obese, as seen here. First-line treatment includes cognitive behavioral therapy, and lisdexamfetamine is FDA-approved pharmacotherapy.

• A. Night eating syndrome involves recurrent nocturnal awakenings with eating or excessive eating after the evening meal, not discrete uncontrolled binges.
• B. There is no mention of depressed mood, anhedonia, or other core features of depression; the binge pattern itself defines the disorder.
• C. Bulimia nervosa requires recurrent inappropriate compensatory behavior (e.g., vomiting, laxatives), which this patient does not exhibit.
• E. Avoidant/restrictive food intake disorder involves inadequate food intake and nutritional deficiency, the opposite of this patient's presentation.

Cognitive behavioral therapy for insomnia (CBT-I) is the recommended first-line treatment for chronic insomnia disorder according to the American Academy of Sleep Medicine. CBT-I includes sleep restriction, stimulus control, cognitive restructuring, and sleep hygiene education, and produces durable improvement without the dependence or tolerance risks of hypnotic medications. Pharmacotherapy (e.g., zolpidem, suvorexant) is reserved for patients who do not respond to or cannot access CBT-I, and is generally used short-term. Polysomnography is not indicated unless there is suspicion of a comorbid sleep disorder such as obstructive sleep apnea, which this patient does not have.

• A. Zolpidem is effective but is not first-line; it carries risks of dependence and should follow a trial of CBT-I.
• B. Polysomnography is unnecessary here because there are no features suggesting sleep apnea, narcolepsy, or a parasomnia.
• D. Diphenhydramine has anticholinergic side effects and anticipatory tolerance, making it a poor and non-preferred choice.
• E. Trazodone is sometimes used off-label for insomnia but is not recommended as initial therapy over CBT-I.

The diagnosis of narcolepsy is confirmed by overnight polysomnography to exclude other causes of sleep disruption, followed the next day by a multiple sleep latency test (MSLT). A mean sleep latency of 8 minutes or less and two or more sleep-onset REM periods on the MSLT support the diagnosis, especially when combined with the history of cataplexy, hypnagogic hallucinations, and sleep paralysis seen in this patient. Cataplexy, triggered by strong emotions such as laughter, is a hallmark feature caused by orexin (hypocretin) deficiency and is highly specific for narcolepsy type 1. Low cerebrospinal fluid orexin-A level is an alternative confirmatory test when available.

• B. EEG during wakefulness does not capture the abnormal REM sleep intrusion characteristic of narcolepsy.
• C. Actigraphy measures rest-activity patterns and is used for circadian rhythm disorders, not to diagnose narcolepsy.
• D. Brain MRI is not part of the diagnostic workup for narcolepsy unless a secondary cause is suspected.
• E. Hypothyroidism can cause fatigue but does not explain cataplexy or REM-related phenomena.

This child meets DSM-5-TR criteria for attention-deficit/hyperactivity disorder, combined presentation, with symptoms of inattention and hyperactivity-impulsivity present before age 12, across multiple settings, and causing functional impairment. Stimulants such as methylphenidate or amphetamine salts are first-line pharmacotherapy for ADHD in school-age children, working by increasing synaptic dopamine and norepinephrine to improve attention and impulse control. Before starting a stimulant, baseline cardiac history and vital signs should be assessed, which are unremarkable here. Non-stimulants such as atomoxetine or guanfacine are second-line options for children with contraindications to stimulants or comorbid tics.

• A. Risperidone is an antipsychotic used for irritability in autism or severe aggression, not for core ADHD symptoms.
• B. Clonazepam is a benzodiazepine with no role in ADHD treatment and risks sedation and dependence in children.
• D. Fluoxetine is an SSRI used for depression and anxiety, not indicated for ADHD.
• E. Bupropion is sometimes used off-label for ADHD in adults but is not first-line therapy in children.

Autism spectrum disorder is diagnosed by persistent deficits in social communication and interaction (poor eye contact, lack of joint attention, not responding to name) together with restricted, repetitive patterns of behavior (insistence on sameness, rigid food preferences, hand flapping, repetitive object use), with onset in early childhood. This child demonstrates both required symptom domains, which distinguishes autism from isolated language delay. Hearing loss has been excluded as a cause of the lack of response to name. Early intensive behavioral intervention, such as applied behavior analysis, improves outcomes and should begin as soon as the diagnosis is suspected.

• A. Reactive attachment disorder results from grossly inadequate caregiving and presents with inhibited or disinhibited social behavior, not this symptom pattern.
• B. Social (pragmatic) communication disorder involves social communication deficits without the restricted, repetitive behaviors seen in this child.
• C. Specific language impairment involves delayed language without the social deficits or repetitive behaviors described here.
• E. Intellectual disability involves global deficits in intellectual and adaptive functioning, not specifically the social and repetitive behavior pattern described.

Oppositional defiant disorder is characterized by a pattern of angry or irritable mood, argumentative or defiant behavior, and vindictiveness lasting at least 6 months, without the serious violation of others' rights or societal norms (aggression toward people or animals, property destruction, deceitfulness, theft) that defines conduct disorder. This child's behavior is limited to defiance, irritability, and blame-shifting, fitting ODD rather than conduct disorder. Distinguishing the two is important because conduct disorder carries a higher risk of progression to antisocial personality disorder in adulthood and may warrant more intensive intervention.

• B. Intermittent explosive disorder involves discrete episodes of impulsive aggressive outbursts grossly out of proportion to the situation, not a pattern of defiance.
• C. Conduct disorder requires repetitive violation of rights of others or norms, such as aggression, destruction of property, or theft, which are absent here.
• D. Disruptive mood dysregulation disorder requires severe recurrent temper outbursts plus a persistently irritable or angry mood most of the day, nearly every day, which is not described.
• E. Antisocial personality disorder cannot be diagnosed before age 18 and requires a history consistent with conduct disorder before age 15.

Separation anxiety disorder is characterized by developmentally inappropriate and excessive fear or anxiety about separation from attachment figures, lasting at least 4 weeks in children, manifested by distress upon separation, worry about harm befalling caregivers, reluctance to be away from home or sleep away from the attachment figure, and physical symptoms such as stomachaches when separation is anticipated. This child's symptoms are specifically tied to separation from her mother and resolve when her mother is present, which is the defining feature distinguishing this disorder from other anxiety disorders. First-line treatment is cognitive behavioral therapy, with SSRIs considered for more severe or refractory cases.

• A. Panic disorder involves recurrent unexpected panic attacks with persistent worry about future attacks, not a pattern tied to separation.
• B. Specific phobia involves fear of a particular object or situation, not a pervasive fear centered on separation from attachment figures.
• D. Generalized anxiety disorder involves excessive worry about multiple areas of life, not specifically centered on separation from a caregiver.
• E. Social anxiety disorder involves fear of social or performance situations due to scrutiny by others, not fear of separation itself.

Delirium is distinguished from dementia primarily by its acute onset (hours to days), fluctuating course over the day, and prominent impairment of attention and arousal, typically triggered by an underlying medical condition such as infection, here suggested by fever, tachycardia, and a urinalysis consistent with urinary tract infection. Dementia, in contrast, has an insidious onset and a slowly progressive, generally stable course without the marked fluctuation or primary attentional deficit seen in delirium. While hallucinations can occur in both conditions and advanced age is a risk factor for each, these features do not reliably differentiate the two. Identifying and treating the underlying cause, such as infection, is essential in managing delirium.

• A. Visual hallucinations can occur in both delirium and some dementias (e.g., Lewy body dementia), so they do not reliably distinguish the two.
• B. Advanced age increases risk for both delirium and dementia and does not help differentiate between them.
• D. Abnormal vital signs point to an underlying cause but are not themselves a core diagnostic feature distinguishing delirium from dementia.
• E. Progressive memory loss over months to years is characteristic of dementia, not the acute presentation described in this patient.

A patient who expresses active suicidal ideation with a specific plan and means, combined with a prior attempt, is at high imminent risk of self-harm and lacks the capacity to make a safe decision about her own care in this context. When a patient with acute suicidal ideation and intent refuses voluntary treatment, the appropriate action is an involuntary psychiatric hold (civil commitment) to ensure safety, as permitted under state law, followed by inpatient admission for stabilization. Confidentiality and autonomy are overridden when there is an imminent danger to self. This is a medical and legal emergency that takes priority over the patient's refusal.

• A. A liability waiver does not address the clinical emergency and does not override the physician's duty to prevent imminent harm.
• B. Forced medication is not indicated here; the issue is safety and the need for containment, not treatment refusal requiring a separate judicial process for medication.
• C. Outpatient follow-up is inadequate given active suicidal intent, a specific plan, and access to means; this risks an imminent completed suicide.
• E. Relying on a family member to remove means at home is insufficient when the patient has expressed active intent and a specific plan requiring inpatient-level safety and treatment.

Decision-making capacity requires that a patient understand the relevant information, appreciate the situation and its consequences, reason through the options, and clearly communicate a consistent choice. This patient demonstrates all four elements: he understands his diagnosis and prognosis, appreciates the risks and benefits of treatment versus no treatment, reasons based on his own values regarding quality of life, and communicates a stable, consistent decision. A capacitated patient has the right to refuse any medical treatment, even life-sustaining therapy, and this right supersedes the wishes of a healthcare proxy, which only becomes activated once the patient loses capacity.

• A. There is no indication of depression impairing his reasoning; routine psychiatric consultation is not required when capacity is clearly demonstrated through standard clinical assessment.
• B. A healthcare power of attorney only has authority to make decisions once the patient loses decision-making capacity; it does not apply while the patient remains capacitated.
• D. A court order is unnecessary and inappropriate because the patient has intact capacity and is legally entitled to refuse treatment.
• E. Administering chemotherapy against the wishes of a capacitated patient who has refused treatment constitutes battery and violates patient autonomy.