MCCQE Part I psychiatry questions

Valproate is associated with a high risk of neural tube defects, congenital malformations, and long-term neurodevelopmental impairment (lower IQ, autism spectrum features) when taken during pregnancy, with risk highest in the first trimester, often before pregnancy is recognized. Preconception counseling should address switching to an alternative agent with a better reproductive safety profile, such as lamotrigine or certain second-generation antipsychotics, ideally before contraception is stopped. Folic acid supplementation does not eliminate valproate's teratogenic risk. Abrupt discontinuation of mood stabilizers risks relapse, so any change should be planned and gradual under psychiatric guidance.

• A. Folic acid reduces neural tube defect risk generally but does not offset valproate's teratogenic potential, including other malformations and cognitive effects.
• B. Continuing valproate unchanged exposes the fetus to major malformation risk from the earliest weeks of pregnancy, before most women realize they are pregnant.
• C. Abrupt discontinuation of all psychiatric medication risks relapse of bipolar disorder, which itself carries maternal and fetal risks.
• D. Waiting until pregnancy is confirmed means the fetus has already been exposed during the critical first trimester period of organogenesis.

Cyclothymic disorder is characterized by at least 2 years (1 year in adolescents) of 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, with symptoms present more than half the time and no symptom-free period longer than 2 months. This patient's chronic subthreshold mood fluctuations without ever meeting full episode criteria fit this pattern. Bipolar II requires at least one major depressive episode and one hypomanic episode meeting full duration and symptom criteria. Bipolar I requires a full manic episode. Her presentation does not meet threshold for major depressive disorder since her depressive periods are subsyndromal.

• A. Bipolar I disorder requires at least one full manic episode, which this patient has never had.
• B. Borderline personality disorder involves pervasive instability in relationships, self-image, and affect with impulsivity, not primarily sustained mood cycling of this chronicity.
• C. Her depressive periods never meet full criteria for a major depressive episode, so recurrent major depressive disorder is not met.
• E. Bipolar II disorder requires at least one full hypomanic episode and one full major depressive episode, neither of which this patient has had.

This presentation, persistent depressive symptoms beyond 2 weeks postpartum without psychotic features, is consistent with postpartum depression rather than postpartum blues (which peaks around day 3-5 and resolves within 2 weeks) or postpartum psychosis (which involves hallucinations, delusions, or grossly disorganized behaviour, usually within the first 2 weeks). Treatment with an SSRI such as sertraline, which has a favourable profile in lactation, along with psychotherapy, is first-line management. Involuntary admission is not indicated in the absence of safety concerns or psychosis. Breastfeeding does not need to be stopped, as several antidepressants are considered compatible with breastfeeding.

• A. Symptoms lasting beyond 2 weeks and causing functional impairment exceed what is expected for postpartum blues and warrant treatment.
• B. There are no psychotic symptoms described, so an antipsychotic is not indicated, and her presentation does not require urgent psychiatric referral.
• D. Involuntary admission requires evidence of risk to self or others or inability to care for herself; this patient has none of these features.
• E. Breastfeeding does not need to be discontinued, as SSRIs such as sertraline are considered compatible with lactation.

Electroconvulsive therapy is indicated for severe major depressive episodes with psychotic features (as seen here with his nihilistic delusion about his organs), catatonia, or situations where rapid response is needed due to medical instability from poor oral intake, as well as treatment resistance to multiple adequate antidepressant trials. ECT has the highest response rates for psychotic depression, often superior to antidepressant-antipsychotic combinations, and acts faster than oral pharmacotherapy. Given his dehydration and inability to sustain adequate intake, waiting weeks for another medication trial poses significant medical risk. Psychotherapy alone and benzodiazepines are not adequate for severe psychotic depression.

• A. Trialing another antidepressant would take weeks to show effect and delays treatment in a medically unstable patient with psychotic depression.
• B. Psychotherapy alone is inadequate for severe depression with psychotic features and would not address his acute medical risk.
• C. A benzodiazepine does not treat the underlying psychotic depression and simple observation is inappropriate given his deteriorating medical status.
• D. Lithium augmentation may help in treatment-resistant depression but is not the fastest or most effective option for severe psychotic depression with medical instability.

This patient's history of recurrent depressive episodes with a regular seasonal onset in fall/winter and remission in spring/summer over several years is consistent with major depressive disorder with a seasonal pattern (seasonal affective disorder). First-line treatment for mild to moderate seasonal affective disorder is bright light therapy, typically 10,000 lux administered in the morning for about 30 minutes, which helps correct circadian phase shifts. SSRIs are also first-line and can be combined with light therapy, but among these options light therapy is the standard initial step for this presentation. Melatonin has a more limited evidence base for this indication, and ECT and lithium prophylaxis are reserved for severe, refractory, or psychotic presentations, not initial management of SAD.

• A. Clozapine is reserved for treatment-resistant schizophrenia and has no role in seasonal affective disorder.
• C. Melatonin has weaker evidence than bright light therapy for seasonal affective disorder and is not first-line.
• D. ECT is reserved for severe, psychotic, or treatment-refractory depression, not initial management of seasonal affective disorder.
• E. Lithium prophylaxis is used for bipolar disorder maintenance, not as first-line therapy for unipolar seasonal affective disorder.

This patient has multiple high-risk features: a planned, potentially lethal overdose, a prior attempt, ongoing expressed intent (regret at being found), and a stated wish to have died, all indicating high acute suicide risk requiring hospitalization. In addition, acetaminophen overdose of this quantity requires urgent medical workup including serum acetaminophen level, liver enzymes, and INR, with N-acetylcysteine therapy if indicated per nomogram, since untreated overdose can cause fulminant hepatic failure. He requires admission with continuous safety observation (e.g., 1:1 observation or a safe room) until formal psychiatric assessment and stabilization. Discharge in any form is inappropriate given his expressed ongoing suicidal intent and medical risk from the overdose itself.

• A. Normal vital signs do not exclude acetaminophen hepatotoxicity, which may be delayed, and outpatient counselling does not address his acute risk or medical needs.
• B. Discharge is inappropriate given his expressed regret at being found and high lethality overdose; family supervision cannot substitute for inpatient safety monitoring and medical treatment.
• C. A safety plan alone is insufficient given his ongoing expressed suicidal intent and the need for medical management of a potentially hepatotoxic overdose.
• D. Even if he denies ongoing suicidal ideation at this moment, the recency of intent, lethality of the attempt, and need for acetaminophen levels and possible N-acetylcysteine mandate admission rather than discharge.

Provincial mental health legislation across Canada (e.g., Ontario's Mental Health Act, similar statutes elsewhere) permits involuntary psychiatric admission when a physician determines the person has a mental disorder that is likely to result in serious harm to themselves or others, or serious physical impairment, and the person is unable to fully appreciate the need for treatment. This patient has psychotic symptoms (persecutory delusions), is refusing to eat due to delusional beliefs leading to physical deterioration, and has voiced intent to react violently, meeting criteria for certification without requiring a prior attempt or a court order for the emergency admission itself. Substitute decision-makers are relevant to consent for specific treatments once admitted, not to the initial certification decision, which is made by the examining physician based on statutory criteria.

• B. Provincial mental health legislation does not require a completed suicide attempt or actual harm to another person; risk of serious harm is sufficient.
• C. The right to refuse treatment is not absolute when a mental disorder impairs the person's ability to recognize the need for treatment and creates serious risk of harm.
• D. Emergency involuntary admission under provincial mental health legislation does not require a prior court order; it is based on physician assessment against statutory criteria, with subsequent rights review available.
• E. Substitute decision-maker consent is relevant to consenting to specific treatments after admission, not to the physician's authority to certify involuntary admission based on statutory risk criteria.

Canadian case law (notably Smith v. Jones) establishes that the duty to protect overrides confidentiality when there is a clear, serious, and imminent risk of harm to an identifiable person or group. The three criteria are: a clear risk to an identifiable person or group, a risk of serious bodily harm or death, and imminence of the danger. This patient's threat meets all three criteria, an identified victim, lethal means, and a specific imminent timeframe, obligating the psychiatrist to take protective action, which includes warning the potential victim and/or notifying police. Waiting for the next appointment, referring without action, or requiring patient consent would leave an identifiable person at imminent risk of serious harm.

• B. Confidentiality must be breached when there is a clear, serious, and imminent risk of harm to an identifiable person, which is present here.
• C. Patient consent is not required to breach confidentiality when the legal duty to protect a third party from imminent serious harm applies.
• D. Waiting 2 weeks ignores the stated imminent timeframe of the threat and leaves the intended victim unprotected.
• E. Simply referring the patient elsewhere does not fulfill the duty to protect the identified victim from imminent serious harm.

Delusional disorder is characterized by one or more non-bizarre, encapsulated delusions lasting at least one month, in the absence of prominent hallucinations, disorganized speech, or negative symptoms, with largely preserved functioning outside the area affected by the delusion. This patient's persecutory belief is circumscribed, his occupational and social functioning remain intact, and there is no evidence of the broader symptom profile required for schizophrenia. Schizophrenia requires significant functional decline and typically involves hallucinations, disorganization, or negative symptoms alongside delusions. The preservation of overall functioning and the isolated nature of the delusion are the key distinguishing features.

• A. Paranoid schizophrenia requires additional psychotic features and marked functional decline, neither of which is present here.
• B. Schizotypal personality disorder involves odd beliefs and eccentricity without a fixed, well-organized delusion of this intensity.
• D. Brief psychotic disorder lasts less than 1 month and typically follows a stressor, inconsistent with this 8-month course.
• E. Schizophreniform disorder requires schizophrenia-like symptoms lasting 1 to 6 months with associated functional impairment, which is not seen here.

Generalized anxiety disorder is diagnosed when excessive, difficult-to-control worry about multiple life domains persists for at least 6 months and is accompanied by associated symptoms such as restlessness, fatigue, muscle tension, or sleep disturbance, causing significant distress or impairment. Selective serotonin reuptake inhibitors such as sertraline are first-line pharmacotherapy for GAD because of their established efficacy, favourable side-effect profile, and low abuse potential, consistent with Canadian treatment guidelines. Benzodiazepines may provide rapid symptomatic relief but are reserved for short-term use because of tolerance and dependence risk. Response to SSRIs typically takes several weeks, and patients should be counselled about this delayed onset.

• A. Benzodiazepines are effective short-term but are not recommended as first-line therapy because of dependence and tolerance risk.
• B. Propranolol targets autonomic symptoms of acute anxiety but does not address the core features of chronic GAD.
• D. Bupropion is not established as first-line therapy for GAD and may worsen anxiety symptoms in some patients.
• E. Quetiapine is not first-line for GAD and carries metabolic risks that outweigh its benefit in this context.

In a young patient with recurrent, abrupt panic-like episodes and situational avoidance suggestive of panic disorder, a focused but thorough work-up in the emergency department should first exclude an acute cardiac cause with a 12-lead ECG, given the overlapping presentation of chest pain, palpitations, and dyspnea. A normal ECG, combined with reassuring vital signs and a classic symptom pattern, supports a diagnosis of panic disorder without the need for more invasive or resource-intensive cardiac testing. Further cardiac investigations such as stress testing, CT angiography, or echocardiography are reserved for patients with risk factors, abnormal initial findings, or atypical presentations. Over-investigation in low-risk patients can reinforce illness anxiety and delay appropriate psychiatric treatment.

• A. Exercise stress testing is not indicated as an initial test in a young patient without cardiac risk factors or exertional symptoms.
• B. Prolonged ambulatory monitoring is not the first step before a baseline ECG has been obtained and reviewed.
• C. Echocardiography is not warranted as an initial test without evidence of structural heart disease on exam or ECG.
• E. Coronary CT angiography is unnecessary in a young, low-risk patient with a normal initial evaluation and typical panic symptoms.

Social anxiety disorder involves marked fear or anxiety about specific social or performance situations in which the person may be scrutinized or judged negatively, with avoidance limited largely to those triggering contexts while broader interpersonal and occupational functioning remains intact. This man's fear is circumscribed to public speaking and eating in front of others, and he otherwise maintains close relationships and professional competence, arguing against a pervasive personality disorder. Avoidant personality disorder, in contrast, involves a lifelong, pervasive pattern of social inhibition, feelings of inadequacy, and hypersensitivity to criticism across virtually all interpersonal contexts, not situation-specific triggers. The preserved global functioning and situation-specific nature of his anxiety point to an anxiety disorder rather than a personality disorder.

• A. Generalized anxiety disorder involves diffuse worry about multiple life domains, not fear limited to specific performance situations.
• B. Panic disorder involves recurrent unexpected panic attacks and fear of future attacks, not situation-specific social fear.
• C. Avoidant personality disorder requires pervasive social inhibition and feelings of inadequacy across most relationships, which this patient does not show.
• D. Schizoid personality disorder is characterized by a lack of desire for close relationships, inconsistent with this patient's active social and dating life.

Benzodiazepines such as lorazepam can provide rapid relief of acute anxiety and panic symptoms and are sometimes used short-term as a bridge while waiting for an SSRI to reach therapeutic effect, which typically takes several weeks. However, because of the risk of tolerance, physical dependence, and withdrawal with continued use, benzodiazepines should be prescribed at the lowest effective dose for the shortest duration necessary and tapered once the SSRI becomes effective. Long-term benzodiazepine use is discouraged as primary or maintenance therapy for panic disorder because SSRIs and psychotherapy offer durable benefit without the same dependence liability. Patients should be counselled about this planned taper at the time the benzodiazepine is initiated.

• A. SSRIs, not benzodiazepines, are the appropriate long-term maintenance treatment for panic disorder.
• B. Escalating the dose over time reflects developing tolerance and is a sign that the medication should be tapered, not increased.
• C. Lorazepam does have an evidence-based short-term bridging role in acute panic symptom control.
• D. Indefinite combination therapy increases dependence risk without added long-term benefit once the SSRI is effective.

Obsessive-compulsive disorder (OCD) is characterized by obsessions and/or compulsions that the person recognizes as excessive, intrusive, or senseless (ego-dystonic), causing marked distress or functional impairment. In contrast, obsessive-compulsive personality disorder (OCPD) involves a pervasive, lifelong pattern of rigidity, perfectionism, and need for control that the person views as appropriate and justified (ego-syntonic), without discrete obsessions or compulsions. Insight that the behaviour is irrational and a specific target symptom (checking) rather than a global personality style points to OCD. The other options describe trait features of OCPD from DSM-5 criteria.

• A. Excessive devotion to work/productivity is a defining OCPD trait.
• B. Preoccupation with orderliness/control is a core OCPD trait, not specific to OCD.
• C. Difficulty discarding objects (hoarding tendency) is a classic OCPD trait.
• E. Reluctance to delegate is a classic OCPD trait reflecting need for control.

Exposure and response prevention (ERP), a specific form of cognitive-behavioural therapy, is first-line treatment for obsessive-compulsive disorder and is as effective as medication for many patients, with durable benefit after treatment ends. It works by having the patient confront feared stimuli (e.g., contamination) while refraining from the compulsive response, leading to extinction of the anxiety response over repeated exposures. For patients who prefer to avoid pharmacotherapy and have mild-to-moderate OCD, ERP alone is an appropriate first step; an SSRI would be added if CBT is unavailable, ineffective, or the patient prefers medication. Benzodiazepines, antipsychotics, and beta-blockers are not first-line OCD treatments.

• A. Non-directive supportive therapy lacks evidence for OCD compared with ERP-based CBT.
• C. Antipsychotics are reserved as augmentation in treatment-resistant OCD, not monotherapy.
• D. Beta-blockers address autonomic symptoms of anxiety but do not treat OCD's core psychopathology.
• E. Benzodiazepines are not effective for OCD and carry dependence risk; not first-line.

Posttraumatic stress disorder requires exposure to actual or threatened death, serious injury, or sexual violence, followed by symptoms from four clusters: intrusion (nightmares, intrusive memories), avoidance (of reminders), negative alterations in cognition/mood (numbing, anhedonia), and hyperarousal (exaggerated startle, irritability, poor sleep), persisting more than 1 month and causing functional impairment. This patient meets all four clusters with duration well beyond 1 month, consistent with PTSD. Acute stress disorder is excluded because symptoms have lasted longer than 1 month; the other diagnoses do not account for the specific trauma-linked intrusion and avoidance symptoms.

• A. Adjustment disorder lacks the specific intrusion, avoidance, and hyperarousal symptom clusters tied to a traumatic stressor meeting PTSD's Criterion A.
• B. Generalized anxiety disorder involves pervasive worry unrelated to a specific trauma, not intrusion/avoidance symptoms.
• C. Acute stress disorder is diagnosed only within the first month after trauma; this presentation is at 7 months.
• D. Major depressive disorder does not explain the trauma-specific intrusive memories, avoidance, and hyperarousal.

Acute stress disorder shares the same symptom clusters as PTSD (intrusion, avoidance, negative mood, hyperarousal, and dissociative symptoms such as depersonalization or dissociative amnesia) but is diagnosed when symptoms occur between 3 days and 1 month after trauma exposure. This patient's symptoms began after a clear Criterion A traumatic event and have lasted only 10 days, placing her within the acute stress disorder window; if symptoms persist beyond 1 month, the diagnosis would be reclassified as PTSD. Dissociative symptoms (depersonalization, amnesia for the event) are more characteristic of acute stress disorder than PTSD.

• A. Panic disorder involves recurrent unexpected panic attacks, not trauma-specific intrusion and avoidance symptoms.
• B. Specific phobia involves fear of a discrete object or situation without the full trauma symptom cluster described.
• D. PTSD cannot be diagnosed until symptoms have been present for at least 1 month; only 10 days have elapsed.
• E. Brief psychotic disorder requires delusions, hallucinations, or disorganized speech/behaviour, which are absent here.

Adjustment disorder is diagnosed when emotional or behavioural symptoms develop within 3 months of an identifiable psychosocial stressor (here, job loss), cause marked distress or impairment, and do not meet full criteria for another specific disorder such as major depression or generalized anxiety disorder. Symptoms typically resolve within 6 months after the stressor or its consequences end. This patient's presentation began within weeks of a clear stressor and falls short of full diagnostic thresholds for depression or anxiety disorders, fitting adjustment disorder. Job loss, while stressful, does not meet PTSD's Criterion A threshold of actual or threatened death, serious injury, or sexual violence.

• B. Persistent depressive disorder requires depressed mood for at least 2 years, far longer than this presentation.
• C. He does not meet full criteria for generalized anxiety disorder, which is explicitly stated.
• D. Job loss is not a Criterion A traumatic stressor (threatened death, serious injury, or sexual violence) required for PTSD.
• E. He does not meet full symptom criteria for major depressive disorder, which is explicitly stated.

Alcohol withdrawal typically begins 6-24 hours after the last drink, with autonomic hyperactivity (tachycardia, hypertension, tremor, diaphoresis) peaking around 24-72 hours; symptom-triggered benzodiazepine dosing guided by the CIWA-Ar scale is the standard of care, giving medication only when the score exceeds a threshold (commonly ≥8-10) to reduce symptoms and prevent progression to seizures or delirium tremens. Lorazepam is often preferred in patients with significant hepatic impairment because it does not require hepatic oxidation, though diazepam or chlordiazepoxide are also used. Symptom-triggered dosing reduces total benzodiazepine exposure and length of stay compared with fixed-schedule dosing. Antipsychotics, anticonvulsants, and imaging are not first-line for uncomplicated withdrawal, and dextrose should not be given before thiamine in at-risk patients.

• A. Phenytoin is not indicated for alcohol withdrawal seizures, which are better prevented and treated with benzodiazepines.
• C. There are no focal neurologic findings or signs of head injury to warrant urgent CT imaging.
• D. Haloperidol does not prevent seizures or delirium tremens and is not first-line for withdrawal; it may be used adjunctively for severe agitation only.
• E. Dextrose should be preceded by thiamine administration in at-risk patients to avoid precipitating Wernicke encephalopathy, and there is no indication of hypoglycemia here.

In patients with chronic alcohol use or malnutrition who are at risk of thiamine deficiency, administering glucose before thiamine can precipitate or worsen Wernicke encephalopathy by accelerating thiamine-dependent metabolic pathways and depleting remaining stores, potentially causing irreversible damage to mammillary bodies and periaqueductal grey matter. Current guidelines recommend giving intravenous thiamine before or simultaneously with glucose in any at-risk patient, especially one with signs suggestive of Wernicke encephalopathy such as gait ataxia. This is a simple, low-risk intervention that prevents a serious and largely irreversible neurologic complication. Folate, oral multivitamins, imaging, and magnesium do not address the immediate risk of precipitating Wernicke encephalopathy.

• A. Folate deficiency can contribute to anemia but does not prevent Wernicke encephalopathy, which is specifically due to thiamine deficiency.
• B. CT imaging is not the immediate priority and would not reverse or prevent evolving thiamine deficiency-related injury.
• C. Oral multivitamins are absorbed too slowly and unreliably to provide urgent thiamine repletion in this acute setting.
• E. Magnesium deficiency can impair thiamine utilization but magnesium repletion does not substitute for giving thiamine itself first.

This patient has delirium tremens, a medical emergency characterized by autonomic instability (tachycardia, hypertension, fever, diaphoresis), confusion, and hallucinations typically occurring 48-96 hours after the last drink, with a mortality risk if untreated. Management requires aggressive intravenous benzodiazepine dosing (e.g., diazepam or lorazepam) titrated to effect, ideally in a closely monitored setting such as an intensive care or step-down unit, along with correction of fluid, electrolyte, and glucose abnormalities and treatment of precipitating illness. Benzodiazepines potentiate GABA-A receptor activity, counteracting the unopposed excitatory state from chronic alcohol-induced glutamate upregulation and GABA downregulation. Oral therapy, fluids alone, or restraint without pharmacologic treatment do not adequately address the underlying withdrawal physiology and risk of seizure, arrhythmia, or death.

• A. Physical restraints without pharmacologic treatment do not treat the underlying pathophysiology and increase risk of injury; discharge during active DTs is unsafe.
• B. Delirium tremens requires inpatient, often ICU-level, aggressive IV dosing, not a slow fixed outpatient taper, given the risk of seizures and death.
• C. Fluids alone do not address the withdrawal neurochemistry and would not control autonomic instability or prevent seizures.
• D. Antipsychotics alone do not prevent seizures or correct the GABAergic deficit driving delirium tremens and are not first-line monotherapy.

Naloxone is a competitive opioid receptor antagonist that rapidly reverses respiratory depression from opioid overdose and should be given immediately by any available route (intranasal, intramuscular, or intravenous) while supporting ventilation. Take-home naloxone programs across Canada allow bystanders and patients to administer it before paramedics arrive, reducing overdose mortality. Repeat dosing may be needed because naloxone's duration of action is shorter than that of many opioids, particularly fentanyl. Airway and breathing support should accompany naloxone but should not delay its administration.

• B. An ECG does not address the immediate airway and breathing emergency.
• C. IV fluids do not address the life-threatening respiratory depression.
• D. Flumazenil reverses benzodiazepines, not opioids, and is not indicated here.
• E. Intubation may be needed if naloxone fails to restore adequate ventilation, but it is not the first step.

Buprenorphine-naloxone is recommended as first-line agonist therapy for opioid use disorder in Canada due to its favourable safety profile, lower overdose risk, and feasibility for outpatient induction. Buprenorphine is a partial mu-opioid agonist with very high receptor affinity; if administered while full agonist opioids still occupy receptors, it displaces them and can precipitate acute withdrawal. For this reason, induction is timed to begin after objective withdrawal signs appear, confirmed using tools such as the Clinical Opiate Withdrawal Scale. Methadone, a full agonist, does not carry this same precipitated withdrawal risk.

• A. Buprenorphine does not significantly inhibit CYP enzymes relevant to opioid metabolism.
• B. Buprenorphine is a partial agonist, not a full agonist, and this is why precipitated withdrawal is a concern.
• C. Methadone, not buprenorphine, carries a notable QT prolongation risk requiring ECG monitoring.
• E. Naloxone in the combination product is poorly absorbed sublingually and primarily deters injection misuse rather than acting as the main pharmacologic effect.

The CAGE questionnaire is a brief, validated screening tool for at-risk alcohol use in primary care, consisting of four questions on Cutting down, Annoyance, Guilt, and Eye-openers. A score of two or more affirmative answers is considered a positive screen and has good sensitivity and specificity for identifying problem drinking, warranting further clinical assessment using criteria such as DSM-5 for alcohol use disorder. It is a screening tool, not diagnostic, so a positive result should trigger a more detailed history rather than an automatic diagnosis. Its brevity makes it practical for routine use in busy primary care settings as recommended by Canadian preventive care guidance.

• A. Relying on one item alone ignores the validated cumulative scoring method of the tool.
• C. CAGE does not use quantity of consumption; it is based on qualitative impact questions.
• D. Four affirmative answers is an overly stringent threshold that would miss many at-risk patients.
• E. A single affirmative answer has lower specificity and is not the validated cutoff for a positive screen.

Benzodiazepines such as lorazepam are first-line for cocaine intoxication because they reduce central sympathetic outflow, controlling agitation, tachycardia, and hypertension simultaneously. Beta-blockers are avoided in acute cocaine toxicity due to the theoretical risk of unopposed alpha-adrenergic stimulation leading to worsened vasospasm and hypertension. Antipsychotics may lower seizure threshold and can worsen hyperthermia by impairing heat dissipation, so they are not first-line. If chest pain persists after sedation, nitrates or calcium channel blockers can be used for cocaine-associated vasospasm, but the initial step is benzodiazepine administration to address the sympathetic surge.

• A. Antipsychotics may lower seizure threshold and worsen hyperthermia, making them a second-line option at best.
• C. Nitroglycerin may be used for persistent chest pain only after sedation has been attempted, not as the initial agent.
• D. Diphenhydramine has anticholinergic effects that could worsen hyperthermia and does not address the sympathetic surge.
• E. Beta-blockade can cause unopposed alpha stimulation, worsening hypertension and coronary vasospasm.

Canadian guidance supports routine, confidential screening of adolescents for substance use using validated brief tools (such as the CRAFFT or similar instruments) that assess frequency, context, and functional impact rather than relying on urine testing or assumptions. Confidentiality should generally be maintained unless there is a safety risk, since trust encourages honest disclosure and future help-seeking. A structured screen helps distinguish experimental use from use associated with harm, guiding whether brief counselling or specialist referral is warranted. Routine urine drug screening is not recommended as a primary screening method due to limited correlation with functional impairment and ethical concerns about testing without clear clinical indication.

• A. Urine drug screening is not the recommended first step for screening and raises consent and ethical issues.
• B. Dismissing the use without assessment misses an opportunity to screen for risk factors and provide appropriate counselling.
• D. Specialist referral is reserved for cases where screening indicates significant use disorder or risk, not as an automatic first step.
• E. Confidentiality should be maintained in adolescent care unless there is a significant safety concern, not disclosed automatically.

Borderline personality disorder is characterized by a pervasive pattern of instability in relationships, self-image, and affect, along with marked impulsivity, including recurrent self-harm and fears of abandonment, typically beginning by early adulthood. The rapid mood shifts lasting hours in reaction to interpersonal stress, rather than sustained mood episodes, help distinguish it from a primary mood disorder. Chronic emptiness and identity disturbance are core features that further support this diagnosis over other personality disorders. Recognizing this pattern is important because treatment such as dialectical behaviour therapy has strong evidence for reducing self-harm and improving functioning.

• A. Histrionic personality disorder features excessive emotionality and attention-seeking but lacks the chronic emptiness and self-harm pattern described.
• B. Antisocial personality disorder involves disregard for others' rights and lawbreaking, not the relational instability and self-harm described.
• D. The mood shifts last hours and are reactive to interpersonal stress, not sustained episodes, making bipolar II disorder less likely.
• E. Dependent personality disorder involves excessive need to be cared for and submissiveness, not the identity disturbance and mood lability seen here.

This presentation describes obsessive-compulsive personality disorder, characterized by preoccupation with orderliness, perfectionism, and control, which falls under Cluster C, the anxious or fearful cluster, alongside avoidant and dependent personality disorders. Cluster A disorders (paranoid, schizoid, schizotypal) feature odd or eccentric thinking and social detachment, which are absent here. Cluster B disorders (antisocial, borderline, histrionic, narcissistic) feature dramatic, emotional, or erratic behaviour, which also does not match this rigid, perfectionistic pattern. Recognizing cluster groupings helps organize the differential diagnosis among personality disorders sharing similar core features.

• A. The presentation fits a single cluster, not a combination of two unrelated clusters.
• B. There is no dramatic, impulsive, or emotionally erratic behaviour to suggest a Cluster B disorder.
• D. There is no odd belief, perceptual disturbance, or social detachment to suggest a Cluster A disorder.
• E. Personality disorders in DSM-5 are organized into three clusters, and this pattern fits clearly within one of them.

Malingering is the intentional production of false or exaggerated symptoms motivated by an external incentive, such as avoiding incarceration or obtaining a specific controlled substance. Clues include inconsistency between observed and unobserved behaviour, a clear secondary gain, and a specific drug request rather than relief of symptoms by any effective means. Unlike factitious disorder, where the motivation is primarily to assume the sick role itself, malingering is goal-directed toward a tangible external benefit. Malingering is not a psychiatric diagnosis but a behaviour that should be documented objectively without accusatory language in the chart.

• A. Borderline personality disorder is characterized by instability in relationships, identity, and affect, not goal-directed symptom fabrication.
• B. Somatic symptom disorder involves genuine distress and preoccupation with symptoms, not conscious fabrication for a specific external reward.
• C. Conversion disorder produces genuine, involuntary neurological symptoms incompatible with recognized disease, not deliberate exaggeration for gain.
• E. Factitious disorder involves assuming the sick role as an internal psychological need, without an identifiable external incentive like avoiding jail.

Conversion disorder (functional neurological symptom disorder) is diagnosed clinically through positive signs of incompatibility, such as Hoover's sign, which demonstrate that the neurological pathways are intact despite subjective weakness. Management begins with a clear, non-judgmental explanation that frames the diagnosis in positive terms, using the physical findings to show the nervous system is not sending the right signals, which improves acceptance and outcomes. This is followed by multidisciplinary treatment including physiotherapy and psychological therapy such as cognitive behavioural therapy. Normal tone, reflexes, and imaging support a functional rather than structural cause and further invasive investigation is not indicated once the diagnosis is secure.

• A. Normal imaging and positive signs of functional weakness do not warrant neurosurgical referral.
• B. Dismissing symptoms as not real is invalidating, damages the therapeutic relationship, and is inconsistent with evidence-based communication of this diagnosis.
• D. Electromyography and nerve conduction studies are not needed when clinical signs already confirm a functional neurological disorder and would delay appropriate treatment.
• E. Benzodiazepines are not first-line treatment for conversion disorder and do not address the underlying psychological process.

Attention-deficit/hyperactivity disorder requires symptoms of inattention and/or hyperactivity-impulsivity present in two or more settings (here, both school and home), causing functional impairment, with onset before age 12. Once the diagnosis is confirmed through comprehensive assessment, stimulant medications such as methylphenidate or amphetamine-based agents are first-line pharmacotherapy according to Canadian ADHD guidelines, given their strong efficacy and well-established safety profile in children. Non-stimulant agents such as atomoxetine or alpha-2 agonists are reserved for cases with contraindications to stimulants, significant side effects, or comorbid conditions such as tics or substance use concerns.

• A. Clonidine is a second-line alpha-2 agonist typically used when stimulants are contraindicated or poorly tolerated, or for comorbid tics.
• B. Fluoxetine is an SSRI indicated for depression and anxiety disorders, not a first-line ADHD treatment.
• C. Risperidone is an atypical antipsychotic used for severe aggression or irritability, not first-line for uncomplicated ADHD.
• D. Bupropion is sometimes used off-label as a second-line agent but is not first-line therapy for pediatric ADHD.

The child demonstrates several red flags for autism spectrum disorder, including lack of response to name, absence of joint attention behaviours such as pointing to show, restricted repetitive play, language delay, and reduced eye contact. Canadian guidelines recommend that children with such concerns undergo a validated screening tool, such as the Modified Checklist for Autism in Toddlers, Revised (M-CHAT-R), followed by referral for a comprehensive developmental and diagnostic assessment if screening is positive. Early identification allows for timely access to early intervention services, which improves developmental outcomes. Watchful waiting is not appropriate when multiple red flags are present at 18 months.

• A. Delaying assessment to age 4 ignores established red flags and forfeits the benefit of early intervention during a critical developmental window.
• C. Brain MRI is not part of routine autism spectrum disorder screening and is reserved for cases with specific neurological findings such as regression or focal signs.
• D. Behavioural therapy should follow a formal diagnostic assessment to confirm the diagnosis and guide an individualized treatment plan.
• E. Genetic testing for fragile X may be considered as part of the diagnostic workup after autism is suspected, but it is not the appropriate first step at this point.

Oppositional defiant disorder is characterized by a pattern of angry or irritable mood, argumentative or defiant behaviour, and vindictiveness lasting at least 6 months, without the serious violation of societal norms or the rights of others that defines conduct disorder. This child's behaviours, temper outbursts, defiance, and blaming others, fit the ODD pattern, while the absence of aggression toward people or animals, property destruction, deceitfulness, or serious rule violations excludes conduct disorder. The preserved ability to behave well with grandparents is also typical of ODD, which often shows situational variability. Antisocial personality disorder cannot be diagnosed before age 18.

• A. Antisocial personality disorder requires the individual to be at least 18 years old and show a pervasive pattern of disregard for others' rights since age 15.
• C. Conduct disorder requires repetitive violation of the rights of others or societal norms, such as aggression, property destruction, deceit, or theft, none of which are present here.
• D. Intermittent explosive disorder involves discrete episodes of impulsive aggression grossly out of proportion to provocation, not a pervasive pattern of defiance and argumentativeness.
• E. Disruptive mood dysregulation disorder requires severe recurrent temper outbursts with persistently irritable mood between outbursts most of the day, nearly every day, which is not described here.

This patient meets multiple criteria for medical instability requiring hospital admission, including severe bradycardia (heart rate 38/min), hypotension, hypothermia, and a prolonged corrected QT interval, all of which indicate significant cardiovascular compromise from severe malnutrition. Canadian and international guidelines recommend inpatient admission for medical stabilization when vital sign abnormalities such as bradycardia below 50/min, systolic blood pressure below 90 mmHg, or temperature below 36°C are present, as these patients are at risk of arrhythmia and sudden cardiac death. Outpatient management, regardless of modality, is unsafe until the patient is medically stabilized.

• A. Medication management does not address the immediate life-threatening cardiovascular compromise requiring hospital-level monitoring.
• B. Nutritional rehabilitation in this medically unstable patient must occur in a monitored inpatient setting, not through outpatient dietary referral alone.
• C. Family-based therapy is an evidence-based treatment for adolescent anorexia nervosa but is not appropriate until the patient is medically stabilized as an inpatient.
• D. Outpatient psychotherapy is inappropriate given the severe bradycardia, hypotension, and QT prolongation indicating acute medical instability.

This patient has developed refeeding syndrome, characterized by severe hypophosphatemia, hypokalemia, and hypomagnesemia triggered by the intracellular shift of electrolytes when carbohydrate-driven insulin release resumes after prolonged starvation. The priority is to slow or temporarily reduce the rate of caloric advancement while aggressively replacing phosphate, potassium, and magnesium, as untreated hypophosphatemia can lead to cardiac arrhythmia, respiratory failure, and death. Close electrolyte monitoring, typically at least daily during the high-risk first week, is essential in any patient with significant malnutrition undergoing nutritional rehabilitation. Thiamine supplementation should also be given but is not sufficient on its own to address the electrolyte derangements.

• A. Increasing caloric intake would worsen the electrolyte shifts and risk precipitating life-threatening cardiac and neurologic complications.
• B. Discontinuing feeding is not necessary; the feeding rate should be adjusted while electrolytes are corrected, as nutritional rehabilitation must continue.
• D. Thiamine alone does not correct the dangerous hypophosphatemia, hypokalemia, and hypomagnesemia driving this presentation.
• E. The clinical and laboratory picture reflects phosphate, potassium, and magnesium depletion from refeeding syndrome, not primarily hypoglycemia.

Bulimia nervosa is characterized by recurrent episodes of binge eating with a sense of loss of control, followed by compensatory behaviours such as self-induced vomiting, at a frequency of at least once weekly for 3 months, occurring in a patient who maintains a normal or above-normal body weight. The parotid gland enlargement, Russell's sign (calluses on the knuckles from inducing vomiting), dental erosion, and hypokalemia from recurrent vomiting are classic physical findings. Anorexia nervosa is excluded because the patient's BMI is normal and she is not restricting to maintain a significantly low body weight. The distinguishing feature from binge-eating disorder is the presence of compensatory purging behaviour.

• A. Atypical depression does not explain the binge-purge cycle, Russell's sign, or dental erosion.
• B. Binge-eating disorder lacks the recurrent compensatory behaviours (purging) seen in this patient.
• C. This disorder involves avoidance or restriction of food intake without concern about body shape or weight, which does not fit this presentation.
• E. Anorexia nervosa requires a significantly low body weight for age, height, and sex, which this patient does not have.

Delirium is distinguished from dementia primarily by its acute onset, fluctuating course, and impaired attention with altered level of consciousness (ranging from hyperalert to drowsy), reflecting an underlying acute medical cause such as infection. Dementia typically has an insidious onset with a gradually progressive course, and attention is relatively preserved until late stages. This patient's acute confusional state with fluctuating attention and arousal, in the setting of a febrile infection, is characteristic of delirium superimposed on possible mild cognitive impairment. Memory impairment, word-finding difficulty, disorientation, and functional decline can occur in both conditions and are not distinguishing features.

• A. Word-finding difficulty can occur in both delirium and dementia and is not the key distinguishing feature.
• B. Impaired ADLs occur in both conditions and do not differentiate delirium from dementia.
• C. Gradual progression over months is characteristic of dementia, not the acute presentation described here.
• D. Disorientation can be present in both delirium and dementia and does not distinguish between them.

Initial workup for new cognitive decline should screen for common reversible or contributing metabolic causes, including hypothyroidism, vitamin B12 deficiency, anemia, and electrolyte disturbances, as recommended by Canadian consensus guidelines on dementia. These blood tests are inexpensive, low-risk, and can identify treatable contributors to cognitive impairment before more invasive or costly investigations are pursued. Neuroimaging (CT or MRI) is also recommended in the initial workup to look for structural causes but is not the single best first step when basic bloodwork has not yet been obtained. Lumbar puncture, EEG, and genetic testing are reserved for atypical presentations and are not part of routine initial dementia workup.

• A. Genetic testing for APOE is not recommended for routine dementia diagnosis due to limited predictive value and ethical concerns.
• B. Neuroimaging is appropriate but should be paired with basic bloodwork, which is the lowest-risk and most universally recommended first step to exclude reversible metabolic causes.
• C. EEG is used when seizures or a specific encephalopathy are suspected, not as a routine screening test for cognitive decline.
• E. Lumbar puncture is reserved for atypical presentations such as suspected rapidly progressive dementia or CNS infection, not routine workup.

Dementia with Lewy bodies is characterized by the core clinical features of fluctuating cognition, recurrent visual hallucinations, spontaneous parkinsonism, and marked sensitivity to antipsychotic medications, which can precipitate severe neuroleptic sensitivity reactions with worsened rigidity and confusion. Parkinsonian motor features typically develop around the same time as or shortly after the cognitive decline, distinguishing it from Parkinson disease dementia, where motor symptoms precede cognitive decline by a year or more. Alzheimer disease classically presents with insidious progressive memory loss without prominent early hallucinations or parkinsonism. Vascular dementia presents with stepwise decline and focal neurologic signs correlating with vascular events, and frontotemporal dementia presents with early personality and behavioural change rather than hallucinations and parkinsonism.

• A. Vascular dementia presents with stepwise decline and focal neurologic deficits correlating with cerebrovascular events, not prominent hallucinations and neuroleptic sensitivity.
• B. Frontotemporal dementia presents with early personality change, disinhibition, or language difficulty rather than hallucinations and parkinsonism.
• C. Alzheimer disease typically presents with progressive memory impairment rather than early visual hallucinations, fluctuating cognition, and antipsychotic sensitivity.
• E. In Parkinson disease dementia, motor symptoms of parkinsonism typically precede cognitive decline by at least a year, unlike the near-simultaneous onset described here.

Current Canadian and international guidelines recommend non-pharmacologic interventions as first-line management for behavioural and psychological symptoms of dementia once reversible medical causes (infection, pain, medication effects) have been excluded, as in this patient. Strategies such as consistent caregivers, simplified and unhurried care routines, and reducing environmental overstimulation address identifiable triggers and carry no risk of adverse drug effects. Antipsychotics such as risperidone or quetiapine are reserved for severe agitation or psychosis posing risk of harm that is unresponsive to non-pharmacologic measures, given their association with increased stroke and mortality risk in elderly dementia patients. Physical restraints and benzodiazepines are inappropriate and carry high risk of harm, including falls, paradoxical agitation, and loss of dignity.

• B. Physical restraints increase agitation, injury risk, and are inconsistent with patient-centred dementia care.
• C. Benzodiazepines increase fall risk and can cause paradoxical agitation and sedation in elderly patients with dementia.
• D. Antipsychotics carry a boxed warning for increased mortality and stroke risk in dementia and should be reserved for severe symptoms unresponsive to non-pharmacologic measures.
• E. Quetiapine carries the same risks as risperidone and is not first-line before non-pharmacologic strategies have been tried.

Capacity to consent to treatment is decision-specific and is assessed using the functional criteria of whether the patient can understand the information relevant to the decision and appreciate the reasonably foreseeable consequences of the decision or lack of decision, as established in Canadian common law and provincial consent legislation. A diagnosis of dementia does not automatically render a patient incapable; capacity must be assessed for the specific decision at hand, and this patient's delusional belief impairing his appreciation of the consequences of refusing surgery suggests incapacity for this decision. If found incapable, a substitute decision-maker would then be consulted, but capacity must be assessed first rather than assumed based on diagnosis or a screening cognitive test score.

• B. The right to refuse treatment applies only to capable patients; this patient's capacity for this specific decision has not yet been established.
• C. A diagnosis of dementia alone does not establish incapacity; capacity must be formally assessed for the specific decision before invoking a substitute decision-maker.
• D. A court order is not the first step; capacity assessment and, if needed, substitute decision-making processes should be used before judicial intervention.
• E. A cognitive screening score like the MoCA assesses general cognition but does not by itself determine legal capacity for a specific treatment decision.

In most Canadian provinces, physicians have a statutory or regulatory duty to report patients with medical conditions that may make driving dangerous, including uncontrolled seizure disorders, to the provincial transportation authority (such as the Ministry of Transportation), which constitutes a legally recognized exception to confidentiality. The physician should first inform the patient of this obligation, as transparency preserves the therapeutic relationship where possible, but the report must be made regardless of the patient's consent given the direct risk to public safety. Confidentiality is not absolute and yields to specific statutory duties, including this one and mandatory reporting of suspected child abuse. Informing the employer directly would breach confidentiality beyond what is legally required and is not the appropriate channel.

• A. Physician responsibility extends beyond advising the patient; there is a legal duty to report to the transportation authority when the patient continues to drive unsafely.
• B. Confidentiality has defined legal exceptions, including mandatory reporting of medical conditions affecting fitness to drive, which overrides privilege in this situation.
• D. The legal duty is to report to the provincial transportation authority, not to the employer, which would be an unauthorized disclosure.
• E. Documentation alone is insufficient; the physician has an active duty to report an unsafe driver to the transportation authority given the direct public safety risk.

When clinical findings raise suspicion of intimate partner violence (IPV), such as a bruising pattern inconsistent with the stated mechanism, the physician should ask directly, privately, and non-judgmentally about abuse once the patient is separated from the suspected abuser. Direct questioning in a safe, confidential setting increases disclosure rates and allows the physician to assess safety, offer support, and provide information about resources without pressuring the patient to act immediately. Unlike child abuse, there is no legal mandate in Canada to report suspected IPV involving a competent adult without her consent, so reporting to police without consent is inappropriate unless she is in immediate danger or there are mandatory reporting triggers (e.g., a weapon involved, in some jurisdictions). Routine universal screening for IPV in asymptomatic patients is not recommended by the Canadian Task Force on Preventive Health Care, but case-finding based on clinical suspicion is appropriate.

• A. There is no indication of acute risk to self or others that would justify involuntary admission; her anxiety is better explained by the abuse history.
• B. Involving the partner compromises patient safety and confidentiality and may escalate violence at home.
• D. Reporting to police without the patient's consent breaches confidentiality and autonomy when she is a competent adult not in immediate danger.
• E. Ignoring a suspicious injury pattern misses an opportunity to identify and support a patient experiencing abuse.

Schizophrenia is diagnosed when signs of disturbance are present continuously for at least 6 months, including at least 1 month of active-phase symptoms (delusions, hallucinations, disorganized speech, grossly disorganized or catatonic behaviour, or negative symptoms), with the remainder being prodromal or residual periods. This patient's combined 7-month course with 2 months of active psychotic symptoms meets this duration criterion. Mood episodes must be excluded or brief relative to the psychotic phase, and substance or another medical condition must be ruled out. Catatonia and an identifiable stressor are not required features.

• A. Catatonic features may occur in schizophrenia but are not a required criterion.
• C. Manic episodes preceding psychosis would suggest a mood disorder with psychotic features, not schizophrenia.
• D. An identifiable stressor is not a diagnostic requirement for schizophrenia.
• E. Symptoms resolving within 1 month describes brief psychotic disorder, not schizophrenia.

Brief psychotic disorder is characterized by the sudden onset of one or more psychotic symptoms lasting at least 1 day but less than 1 month, with eventual full return to premorbid functioning, often precipitated by severe stress. This patient's 3-week course with complete resolution fits this pattern. Schizophreniform disorder requires symptoms lasting 1 to 6 months, and schizophrenia requires at least 6 months of continuous illness. Delusional disorder involves fixed, non-bizarre delusions without prominent hallucinations or disorganization for at least 1 month, and schizoaffective disorder requires a concurrent major mood episode.

• A. Delusional disorder presents with isolated non-bizarre delusions, not disorganized speech, and lacks the sudden brief course described.
• B. Schizophrenia requires at least 6 months of continuous disturbance.
• D. There is no evidence of a concurrent major depressive or manic episode.
• E. Schizophreniform disorder requires a duration of 1 to 6 months, longer than this patient's 3-week course.

In first-episode psychosis, initial workup should rule out common organic and substance-related causes before attributing symptoms to a primary psychiatric disorder. A urine toxicology screen identifies substance-induced psychosis (e.g., stimulants, cannabis), and basic bloodwork (electrolytes, glucose, renal and thyroid function, complete blood count) screens for metabolic, endocrine, and infectious causes. Neuroimaging, lumbar puncture, EEG, and genetic testing are reserved for cases with atypical features, focal neurological signs, abnormal vital signs, or an atypical age of onset, not as routine first-line tests.

• A. EEG is indicated only if seizure activity or an organic brain syndrome is specifically suspected.
• B. Lumbar puncture is reserved for suspected central nervous system infection or autoimmune encephalitis, not routine first-episode workup.
• D. Neuroimaging is reserved for atypical presentations, focal neurologic findings, or abnormal vital signs, not routine screening.
• E. Genetic testing is not part of standard initial evaluation unless specific syndromic features are present.

Clozapine is indicated for treatment-resistant schizophrenia, defined as failure to respond to adequate trials of at least two different antipsychotics, including at least one second-generation agent, at optimized doses for sufficient duration with confirmed adherence. Because of the risk of agranulocytosis, clozapine requires mandatory baseline and regular ongoing absolute neutrophil count monitoring through a registered monitoring program before each dispensation. Antipsychotic polypharmacy and above-maximum dosing lack strong evidence and increase side-effect burden without proven added benefit. Electroconvulsive therapy is reserved for specific scenarios such as catatonia or when clozapine is ineffective or not tolerated.

• A. Increasing a dose beyond the recommended maximum increases toxicity risk without established additional benefit.
• B. Electroconvulsive therapy is not first-line for treatment-resistant schizophrenia without clozapine failure or catatonic features.
• C. Switching formulation within the same drug class without changing medication does not address true treatment resistance.
• E. Combining two full-dose antipsychotics lacks strong evidence of benefit and increases adverse effects; clozapine is the guideline-recommended next step.

Clozapine monitoring protocols require weekly absolute neutrophil and white blood cell counts for the first 6 months of treatment, when the risk of agranulocytosis is highest, followed by every 2 weeks for the next 6 months, and then every 4 weeks thereafter if counts remain normal. This patient is still within the highest-risk period, so weekly monitoring is required regardless of symptoms, since agranulocytosis can develop silently before symptoms appear. Monitoring only when symptomatic would miss asymptomatic neutropenia, and widely spaced or one-time testing is insufficient during the early high-risk phase.

• B. Agranulocytosis can occur without symptoms, so monitoring must occur on a fixed schedule rather than only when symptomatic.
• C. This interval applies only after a full year of stable counts, not during the first months of treatment.
• D. This interval is far too infrequent during the high-risk period of the first 6 months.
• E. A single baseline count does not detect agranulocytosis developing after treatment initiation.

Akathisia is a subjective sense of inner restlessness with an compelling urge to move, often manifesting as pacing or an inability to remain still, typically occurring within days to weeks of starting or increasing an antipsychotic. It is managed by reducing the antipsychotic dose if feasible, or adding a beta-blocker such as propranolol or a benzodiazepine. Acute dystonia presents with sudden, painful, sustained muscle contractions (e.g., torticollis, oculogyric crisis), tardive dyskinesia develops after months to years of treatment with repetitive involuntary movements (e.g., lip-smacking, tongue protrusion), and parkinsonism presents with bradykinesia, rigidity, and tremor rather than restlessness.

• A. Tardive dyskinesia typically develops after months to years of antipsychotic exposure and presents with involuntary orofacial or limb movements, not restlessness.
• B. Acute dystonia involves sustained, painful muscle contractions or abnormal posturing, not a subjective urge to move without muscle spasm.
• C. Neuroleptic malignant syndrome presents with fever, rigidity, and autonomic instability, which are absent here.
• D. Parkinsonism presents with bradykinesia, rigidity, and tremor rather than an internal urge to move.