Psychiatry Practice Questions — USMLE Step 2 CK — Page 26

Which psychiatric diagnosis or behavioral characterization best corresponds to each of the following patient scenarios?

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Answer

The scenarios represent Somatic symptom disorder, Illness anxiety disorder, Factitious disorder imposed on self, and Malingering, respectively.

Correct matching distinguishes the somatic spectrum by evaluating the prominence of physical symptoms (Somatic symptom vs. Illness anxiety) and the motivation for deceptive behaviors (primary gain in Factitious disorder vs. secondary gain in Malingering).

Step-by-Step Solution

1

Evaluate symptom severity and health-related behaviors for unconscious disorders.

The paralegal has prominent somatic symptoms and excessive thoughts about them (Somatic symptom disorder), whereas the accountant has minimal symptoms but extreme anxiety about acquiring a disease (Illness anxiety disorder).

Differentiates between Somatic symptom disorder and Illness anxiety disorder based on the physical symptom burden.

2

Assess for evidence of deception or intentional symptom fabrication.

Both the phlebotomist and the warehouse worker exhibit clear signs of feigned or self-induced illness, ruling out unconscious disorders like conversion disorder.

Identifies intentionality as the key driver of the clinical presentation.

3

Determine the underlying motivation for deceptive behavior.

The phlebotomist seeks the sick role (primary gain), indicating Factitious disorder, while the warehouse worker seeks financial compensation (secondary gain), indicating Malingering.

Differentiates between Factitious disorder and Malingering based on the presence of external rewards.

Key Concept

Differential diagnosis of somatic symptom and related disorders based on symptom severity, symptom intentionality, and underlying motivation.

Question 502Question →

Match each of the following distinct clinical presentations to the most likely psychiatric medication-induced emergency or movement disorder.

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Answer

Match the specific clinical features and timeline of symptom onset to their respective psychiatric medication-induced emergencies and adverse effects.

Each clinical scenario contains pathognomonic features for a specific medication-induced adverse effect. Acute dystonia involves sudden sustained muscle contractions. NMS presents with lead-pipe rigidity and hyperthermia. Serotonin syndrome features hyperreflexia and clonus. Tardive dyskinesia involves delayed-onset choreoathetoid movements. Akathisia is characterized by severe restlessness.

Step-by-Step Solution

1

Analyze the onset timeframe and specific neuromuscular findings in each clinical scenario.

Identified the hallmarks: sudden muscle contraction (acute dystonia), 'lead-pipe' rigidity and hyperthermia (NMS), hyperreflexia and clonus (Serotonin syndrome), late-onset choreoathetoid movements (Tardive dyskinesia), and subjective/objective restlessness (Akathisia).

Differentiating these emergencies relies primarily on the physical exam findings and the symptom timeline relative to medication exposure.

2

Differentiate between the two major life-threatening toxidromes (NMS and Serotonin Syndrome).

Confirmed that the presentation with lead-pipe rigidity matches NMS, whereas the presentation with hyperreflexia and clonus matches Serotonin Syndrome.

These two syndromes are frequently confused due to shared features of hyperthermia and autonomic instability, but their neuromuscular manifestations are opposite.

Key Concept

Distinguishing characteristics of psychiatric medication-induced emergencies and movement disorders

Question 503Question →

Match each pediatric neurodevelopmental and behavioral clinical vignette with the primary neuropharmacological mechanism of action of the most appropriate targeted pharmacotherapy.

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Answer

The vignettes correctly map to alpha-2 agonism for the patient with tics, selective norepinephrine reuptake inhibition for the patient with substance use risk, partial D2 agonism for the patient with autism and irritability, and DAT/NET blockade for the patient with uncomplicated ADHD.

Each vignette requires a highly specific medication based on comorbidities: tics warrant an alpha-2 agonist, substance use history necessitates a selective norepinephrine reuptake inhibitor, autism with irritability and a desire for lower prolactin risk points to a partial D2 agonist, and uncomplicated severe ADHD requires a stimulant (reuptake blocker of dopamine and norepinephrine).

Step-by-Step Solution

1

Evaluate each patient's comorbidities and side effect sensitivities to determine the most appropriate drug class.

The patient with tics needs an alpha-2 agonist; the patient with substance use needs atomoxetine; the patient with autism needs an atypical antipsychotic like aripiprazole; the uncomplicated ADHD patient needs a stimulant.

Clinical guidelines dictate specific pharmacological choices based on a patient's unique clinical profile and risk factors.

2

Map the identified drug classes to their primary neuropharmacological mechanisms of action.

Alpha-2 agonists match central alpha-2 adrenergic receptor agonism; atomoxetine matches selective presynaptic norepinephrine transporter inhibition; aripiprazole matches partial D2 and 5-HT1A agonism; stimulants match presynaptic dopamine and norepinephrine reuptake blockade.

This confirms the correct scientific rationale for the selected treatments.

Key Concept

The selection of psychopharmacotherapy in pediatric neurodevelopmental disorders relies on matching specific drug mechanisms (e.g., alpha-2 agonism, specific transporter blockade) to the patient's symptom profile and comorbid conditions.

Question 504Question →

Accompanied by her roommate, a 22-year-old female university student is evaluated at the student health center for progressive social withdrawal over the past month. The patient reports pervasive sadness, sleeping up to 14 hours daily, and an inability to concentrate on her coursework. The roommate mentions that two years prior, the patient had a distinct two-week period where she painted her entire apartment overnight, slept only 2 hours a night without feeling tired, and exhibited pressured speech, which culminated in an emergency department visit. Currently, the patient's vital signs are within normal limits. Physical examination shows no abnormalities. Mental status examination reveals a tearful young woman with psychomotor retardation and a restricted affect. She denies active suicidal ideation, homicidal ideation, or psychotic symptoms. She explicitly requests that her parents not be contacted regarding her evaluation. Laboratory results, including a comprehensive metabolic panel and thyroid-stimulating hormone levels, are normal. Which of the following is the most appropriate next step in management?

Initiate sertraline

Notify the patient's parents and arrange involuntary admission

Initiate quetiapine

Initiate fluoxetine and phenelzine

Initiate venlafaxine

Show answer & explanation

Answer: Initiate quetiapine

Answer

The most appropriate next step in management is to initiate quetiapine.

The patient's current presentation of pervasive sadness, hypersomnia, and psychomotor retardation is consistent with a major depressive episode. However, her history of a distinct two-week period characterized by a decreased need for sleep, increased goal-directed activity, and pressured speech indicates a prior manic episode. Therefore, her correct diagnosis is bipolar I disorder, currently in a depressed episode. The most appropriate next step in management is the initiation of an atypical antipsychotic with proven efficacy for acute bipolar depression. Quetiapine is an FDA-approved, first-line pharmacological treatment for this condition.

Step-by-Step Solution

1

Analyze the patient's current symptoms and past psychiatric history.

The patient is experiencing a major depressive episode but has a clear history of a manic episode (decreased need for sleep, impulsivity, pressured speech).

Accurate identification of both current and past affective episodes is required to differentiate unipolar depression from bipolar disorder.

2

Formulate a diagnosis based on the clinical presentation.

The presence of a manic episode combined with the current depressive symptoms confirms a diagnosis of bipolar I disorder, currently in a depressed episode.

The diagnosis dictates the appropriate pharmacological class and highlights treatments that are contraindicated.

3

Determine the most appropriate pharmacological treatment for the current episode.

First-line treatment for acute bipolar depression includes agents like quetiapine, lurasidone, or lithium.

These medications effectively target depressive symptoms without significantly increasing the risk of a manic switch.

4

Evaluate the ethical constraints regarding the patient's request.

Since the patient is a competent adult without active suicidal or homicidal ideation, her confidentiality must be maintained.

Physicians must respect adult patients' autonomy and confidentiality unless there is an imminent threat of severe harm to the patient or a third party.

Key Concept

Treatment of acute bipolar depression requires mood stabilizers or specific second-generation antipsychotics (e.g., quetiapine, lurasidone); antidepressant monotherapy is contraindicated due to the risk of inducing a manic switch. Additionally, adult patient confidentiality must be maintained in the absence of imminent danger.

Estimated Time:1m 30s

Question 505Question →

A 76-year-old retired architect is brought to the clinic by his son. Over the past $8$ months, the patient has experienced a progressive decline in his cognitive abilities. His son notes that the patient's alertness fluctuates significantly from day to day; he sometimes stares blankly for several minutes during conversations. The patient also frequently reports seeing unfamiliar children playing in his living room, though he is not distressed by their presence. His medical history includes major depressive disorder, for which he has taken fluoxetine for $5$ years. Vital signs are within normal limits. Neurological examination reveals a resting tremor in the left hand, symmetric rigidity, and a slow, shuffling gait. The Montreal Cognitive Assessment (MoCA) score is $19/30$ . Laboratory studies show:

Thyroid-stimulating hormone (TSH): $2.4 \text{ \mu U/mL}$ (normal: $0.4-4.0 \text{ \mu U/mL}$ )
Free thyroxine (T4): $1.3 \text{ ng/dL}$ (normal: $0.9-2.4 \text{ ng/dL}$ )

The son is overwhelmed by the recent changes and demands that his father be admitted to a locked psychiatric facility immediately. However, the patient's previously executed advance directive designates his wife as the healthcare proxy and expresses a clear preference for home-based care.

Which of the following is the most appropriate next step in the management of this patient?

Initiate rivastigmine therapy

Add selegiline to the current medication regimen

Authorize psychiatric admission at the son's request

Initiate levothyroxine supplementation

Initiate haloperidol for schizophreniform disorder

Show answer & explanation

Answer: Initiate rivastigmine therapy

Answer

The most appropriate next step is to initiate rivastigmine therapy.

This patient's clinical presentation—progressive cognitive decline, marked fluctuations in alertness, well-formed visual hallucinations, and spontaneous parkinsonism—is highly characteristic of major neurocognitive disorder with Lewy bodies (LBD). Cholinesterase inhibitors, such as rivastigmine, donepezil, or galantamine, are the first-line pharmacological treatment to manage the cognitive and behavioral symptoms of LBD. They effectively improve hallucinations, stabilize fluctuating cognition, and carry a lower risk of exacerbating motor symptoms compared to antipsychotics.

Step-by-Step Solution

1

Analyze the clinical presentation and timeline.

The patient has an 8-month history of progressive cognitive decline, marked fluctuations in alertness, well-formed visual hallucinations, and spontaneous parkinsonism (resting tremor, rigidity, shuffling gait).

Identifying the classic clinical triad establishes the diagnosis of Major Neurocognitive Disorder with Lewy bodies (LBD).

2

Evaluate the laboratory results and ethical context.

TSH and free T4 are within normal limits, ruling out primary hypothyroidism. The patient has a valid advance directive naming his wife as proxy and preferring home care, superseding the son's demands.

Ruling out reversible causes (like thyroid dysfunction) and respecting ethical guidelines are mandatory before initiating new therapies.

3

Determine the optimal pharmacological management for the confirmed diagnosis.

Rivastigmine, a central acetylcholinesterase inhibitor, is selected.

Cholinesterase inhibitors are the first-line evidence-based treatment for the cognitive and behavioral symptoms (including hallucinations) of LBD. Antipsychotics must be avoided due to severe neuroleptic sensitivity.

Key Concept

Major neurocognitive disorder with Lewy bodies (LBD) presents with fluctuating cognition, visual hallucinations, and parkinsonism; cholinesterase inhibitors are the preferred initial treatment for cognitive and neuropsychiatric symptoms.

Estimated Time:1m 30s

Question 506Question →

Match each patient's clinical presentation to the primary pathophysiological mechanism responsible for their psychiatric emergency or drug-induced toxicity.

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Answer

The clinical presentations match their pathophysiological mechanisms as follows: NMS is caused by D2 blockade; Serotonin Syndrome by 5-HT overactivation; Acute Dystonia by nigrostriatal cholinergic excess; TCA toxicity by sodium channel blockade and muscarinic antagonism; and Lithium toxicity by enhanced proximal tubule reabsorption.

Each psychiatric emergency requires matching the distinct clinical toxidrome to its underlying receptor or pharmacokinetic etiology. Neuroleptic Malignant Syndrome (characterized by lead-pipe rigidity and extreme hyperthermia) is driven by profound dopamine D2 receptor blockade. Serotonin Syndrome (presenting with hyperreflexia and ankle clonus) is caused by excess 5-HT receptor activation. Acute dystonia (manifesting as sustained muscle contractions like torticollis) results from a relative cholinergic excess in the nigrostriatal tract following D2 blockade. TCA toxicity (presenting with a widened QRS and severe anticholinergic signs) is characterized by fast sodium channel blockade in the myocardium. Finally, Lithium toxicity (presenting with coarse tremor and ataxia) is frequently precipitated by thiazide diuretics, which induce volume depletion and trigger a compensatory proximal tubule reabsorption of both sodium and lithium.

Step-by-Step Solution

1

Analyze each clinical vignette to diagnose the specific psychiatric emergency or drug-induced toxidrome.

Identified the following diagnoses: Patient 1 has Neuroleptic Malignant Syndrome (NMS), Patient 2 has Serotonin Syndrome, Patient 3 has Acute Dystonia, Patient 4 has Tricyclic Antidepressant (TCA) toxicity, and Patient 5 has Lithium toxicity.

Accurate pattern recognition of vital sign abnormalities, neuromuscular findings, and medication history is the first step in psychiatric emergency triage.

2

Differentiate between hyperthermic syndromes with overlapping features (NMS vs. Serotonin Syndrome).

Patient 1 exhibits lead-pipe rigidity pointing to NMS (dopamine-driven), whereas Patient 2 exhibits hyperreflexia and clonus pointing to Serotonin Syndrome (serotonin-driven).

Neuromuscular examination findings are the most reliable clinical way to distinguish between these two life-threatening medication-induced toxidromes.

3

Correlate the identified toxidromes with their underlying cellular, receptor-level, or pharmacokinetic mechanisms.

Matched NMS to D2 blockade, Serotonin Syndrome to 5-HT activation, Dystonia to cholinergic excess, TCA toxicity to sodium channel blockade, and Lithium toxicity to proximal tubule reabsorption.

Understanding the definitive pathophysiological mechanism is required to choose the correct targeted pharmacological reversal agents (e.g., bromocriptine for NMS, sodium bicarbonate for TCA overdose).

Key Concept

Psychiatric Emergencies and Toxidromes: Pathophysiology and Presentation

Question 507Question →

Match each psychological therapy modality with its core clinical focus and primary indicated psychiatric condition.

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Answer

Dialectical behavioral therapy pairs with distress tolerance for borderline personality disorder. Exposure and response prevention pairs with graduated contact for obsessive-compulsive disorder. Motivational interviewing pairs with resolving ambivalence for substance use disorders. Interpersonal psychotherapy pairs with resolving role transitions for major depressive disorder.

Each psychological therapy has specific, evidence-based indications based on its underlying mechanism. Dialectical behavioral therapy targets the emotional dysregulation of borderline personality disorder. Exposure and response prevention breaks the cycle of obsessive-compulsive disorder. Motivational interviewing addresses the ambivalence common in substance use disorders. Interpersonal psychotherapy targets the relational stressors often underlying major depressive disorder.

Step-by-Step Solution

1

Evaluate the clinical focus of Dialectical behavioral therapy.

Identified as focusing on mindfulness and emotional regulation for borderline personality disorder.

This matches the core curriculum developed specifically for the volatile emotional states seen in borderline personality disorder.

2

Evaluate the clinical focus of Exposure and response prevention.

Identified as involving contact with feared stimuli while withholding rituals for obsessive-compulsive disorder.

This is the definitive mechanism by which the obsessive-compulsive cycle is broken.

3

Evaluate the clinical focus of Motivational interviewing.

Identified as a client-centered approach to resolving ambivalence for substance use disorders.

Patients with addictions often struggle with readiness to change, which this therapy directly targets.

4

Evaluate the clinical focus of Interpersonal psychotherapy.

Identified as resolving role transitions and grief for major depressive disorder.

This therapy conceptualizes depressive episodes as deeply intertwined with interpersonal stressors and transitions.

Key Concept

Indications and core mechanisms of evidence-based psychological therapies.

Question 508Question →

A 29-year-old woman presents to the psychiatric clinic for evaluation of severe, pervasive anxiety, muscle tension, and sleep disturbance that have been present for the past 8 months. She constantly worries about her finances, her family's health, and her job security, which has severely impaired her daily functioning. Her past psychiatric history is significant for a depressive episode at age 22. At that time, she was prescribed fluoxetine, but within two weeks of starting the medication, she developed a markedly elevated mood, decreased need for sleep, and grandiosity, leading to hospitalization. Her symptoms resolved shortly after fluoxetine was discontinued. She is currently taking phenelzine for her anxiety, but she reports it is ineffective and she struggles with the dietary restrictions.

Recent laboratory tests, ordered by her primary care physician to investigate her fatigue, reveal the following:

Test	Result	Reference Range
Thyroid-stimulating hormone (TSH)	$0.1 \text{ mU/L}$	$0.5 - 5.0 \text{ mU/L}$
Free thyroxine (T4)	$0.4 \text{ ng/dL}$	$0.9 - 1.7 \text{ ng/dL}$

She requests a new medication for her anxiety and asks what her laboratory results mean.

Which of the following are appropriate next steps in the management of this patient? (Select all that apply)

Select all that apply

Initiate cognitive-behavioral therapy focused on worry exposure and relaxation techniques

Refer the patient for a pituitary MRI and comprehensive endocrinologic evaluation

Initiate citalopram monotherapy to manage her generalized anxiety symptoms

Discontinue phenelzine and immediately start sertraline to avoid a gap in anxiety treatment

Diagnose primary hypothyroidism based on the low free T4 and recommend initiating levothyroxine

Show answer & explanation

Answer: Initiate cognitive-behavioral therapy focused on worry exposure and relaxation techniques; Refer the patient for a pituitary MRI and comprehensive endocrinologic evaluation

Answer

The correct steps are to initiate cognitive-behavioral therapy and to refer the patient for a pituitary MRI and endocrinologic evaluation.

The patient's presentation of excessive worry, muscle tension, and sleep disturbance over 8 months is consistent with Generalized Anxiety Disorder (GAD). Because she has a history of antidepressant-induced mania, she is on the bipolar spectrum. Cognitive-behavioral therapy (CBT) is an excellent, safe, first-line treatment for GAD that does not carry the risk of inducing a manic episode. Additionally, her laboratory results (low TSH and low free T4) indicate central (secondary) hypothyroidism. The appropriate next step for this endocrine abnormality is further evaluation of the pituitary-hypothalamic axis, typically including a pituitary MRI and checking other anterior pituitary hormones, before initiating levothyroxine. Initiating levothyroxine blindly in central hypothyroidism can precipitate an adrenal crisis if concurrent secondary adrenal insufficiency is present.

Step-by-Step Solution

1

Analyze the psychiatric presentation and history.

The patient has symptoms of Generalized Anxiety Disorder (GAD). However, her history of fluoxetine-induced mania indicates underlying Bipolar I disorder.

Identifying the bipolar diathesis is critical to avoid prescribing antidepressant monotherapy, which can trigger mania.

2

Evaluate the current psychiatric medications and potential interactions.

The patient is taking phenelzine, an MAOI. Any switch to a serotonergic medication (like an SSRI) requires a strict 14-day washout period.

Concurrent use or insufficient washout between MAOIs and SSRIs can precipitate severe, potentially fatal serotonin syndrome.

3

Interpret the laboratory findings.

The patient has both a low TSH and a low free T4.

This pattern indicates central (secondary) hypothyroidism, implying a pituitary or hypothalamic issue, rather than primary hypothyroidism (which would have elevated TSH).

4

Select the appropriate management steps based on the findings.

CBT is a safe and effective first-line treatment for GAD in bipolar disorder. An endocrinologic evaluation and pituitary MRI are required to investigate the central hypothyroidism.

These steps address both her psychiatric and medical needs safely without risking mania or dangerous drug interactions.

Key Concept

Management of Generalized Anxiety Disorder in patients with bipolar disorder, MAOI pharmacological safety, and interpretation of central hypothyroidism labs.

Question 509Question →

Parents bring their $16$ -year-old son to the acute care clinic due to the sudden onset of profound lower extremity weakness. The patient states that his legs feel "like jelly" and he is unable to stand independently. Over the past several months, his parents have noted a significant decline in his academic performance, increased irritability, and a tendency to isolate himself in the family's poorly ventilated detached garage for hours. Vital signs are within normal limits. Physical examination reveals flaccid paralysis of the bilateral lower extremities with absent deep tendon reflexes. A well-demarcated, erythematous, scaling dermatitis is noted surrounding his mouth and nares. His breath emits a faint, sweet, chemical odor. Laboratory studies are obtained and reveal the following:

Laboratory test	Result	Reference range
Sodium	$138 \text{ mEq/L}$	$136-145 \text{ mEq/L}$
Potassium	$1.8 \text{ mEq/L}$	$3.5-5.0 \text{ mEq/L}$
Chloride	$115 \text{ mEq/L}$	$95-105 \text{ mEq/L}$
Bicarbonate	$12 \text{ mEq/L}$	$22-28 \text{ mEq/L}$
Blood urea nitrogen	$14 \text{ mg/dL}$	$7-18 \text{ mg/dL}$
Creatinine	$0.9 \text{ mg/dL}$	$0.6-1.2 \text{ mg/dL}$

Which of the following is the most likely primary mechanism underlying this patient's clinical presentation and laboratory findings?

Impaired hydrogen ion excretion in the distal renal tubule

Accumulation of unmeasured acidic metabolic byproducts

Defective reabsorption of filtered bicarbonate in the proximal renal tubule

Excessive gastrointestinal elimination of potassium and bicarbonate

Noncompetitive antagonism of N-methyl-D-aspartate receptors

Show answer & explanation

Answer: Impaired hydrogen ion excretion in the distal renal tubule

Answer

Impaired hydrogen ion excretion in the distal renal tubule

The correct answer is impaired hydrogen ion excretion in the distal renal tubule. This patient's presentation of perioral dermatitis ('glue sniffer's rash'), sweet chemical odor, behavioral changes, and garage isolation is highly characteristic of inhalant abuse, specifically toluene. Toluene toxicity famously causes a Type

1

(distal) renal tubular acidosis (RTA) by impairing hydrogen ion excretion in the distal renal tubule. This primary defect leads to a normal anion gap metabolic acidosis (NAGMA) and severe urinary potassium wasting. The resulting profound hypokalemia manifests clinically as flaccid paralysis, areflexia, and severe muscle weakness.

Step-by-Step Solution

1

Calculate the serum anion gap to classify the metabolic acidosis.

Anion gap = Na - (Cl + HCO3) = 138 - (115 + 12) = 11 mEq/L.

Determining if the acidosis is a normal or high anion gap narrows the differential diagnosis for toxic ingestions and metabolic disturbances.

2

Identify the clinical syndrome based on the metabolic profile and physical exam findings.

The patient has a normal anion gap metabolic acidosis (NAGMA) with severe hypokalemia, flaccid paralysis, and a classic perioral "glue sniffer's rash".

Synthesizing the lab data (hypokalemia + NAGMA) with the unique dermatologic and behavioral clues points to a specific toxic etiology.

3

Determine the pathophysiologic mechanism of the suspected toxicity.

Toluene inhalation causes Type 1 renal tubular acidosis by impairing distal tubule hydrogen ion excretion.

Matching the toxin (toluene) to its physiological effect on the kidneys confirms the correct underlying mechanism.

Key Concept

Toluene inhalation (inhalant abuse) causes a Type 1 (distal) renal tubular acidosis, characterized by a normal anion gap metabolic acidosis and severe hypokalemia that can present with rapidly progressive flaccid paralysis.

Question 510Question →

A 33-year-old woman is brought to the outpatient psychiatry clinic by her wife. The patient reports a 3-week history of profound sadness, overwhelming fatigue, increased appetite, and sleeping up to 14 hours a day. She states she has been unable to go to work because she "cannot concentrate on anything." Her medical history is significant for primary hypothyroidism diagnosed 5 years ago, for which she is prescribed levothyroxine. Laboratory tests obtained this morning show a thyroid-stimulating hormone (TSH) level of $1.5 \text{ mIU/L}$ (normal: $0.4-4.0 \text{ mIU/L}$ ) and a free thyroxine (T4) level of $1.2 \text{ ng/dL}$ (normal: $0.8-1.8 \text{ ng/dL}$ ).

Further psychiatric interview reveals that two years ago, the patient experienced a 10-day episode where she felt "on top of the world," required only 2 hours of sleep per night, started multiple simultaneous home renovation projects, and spoke so rapidly it was difficult to interrupt her. She was prescribed a medication at that time but discontinued it after a month. She currently takes no psychiatric medications.

Which of the following are appropriate pharmacological interventions for this patient's current episode? (Select all that apply)

Select all that apply

Initiate quetiapine

Initiate lurasidone

Initiate fluoxetine monotherapy

Increase the levothyroxine dose

Initiate venlafaxine monotherapy

Show answer & explanation

Answer: Initiate quetiapine; Initiate lurasidone

Answer

The appropriate interventions are to initiate quetiapine and initiate lurasidone.

The patient's history of a manic episode (decreased need for sleep, grandiosity, pressured speech lasting over a week) paired with her current severe depressive episode confirms a diagnosis of Bipolar I Disorder, current episode depressed. The first-line pharmacological treatment for acute bipolar depression includes specific second-generation antipsychotics, notably quetiapine and lurasidone, which are highly effective and FDA-approved for this indication. These agents manage the depression without risking a manic switch.

Step-by-Step Solution

1

Diagnose the current psychiatric episode based on presenting symptoms.

The patient has 3 weeks of depressed mood, hypersomnia, fatigue, hyperphagia, and poor concentration, which meets the criteria for a major depressive episode.

Establishing the current affective state is necessary to guide acute pharmacological treatment.

2

Assess past psychiatric history to differentiate unipolar from bipolar depression.

The patient had a prior 10-day episode of grandiosity, decreased need for sleep, hyper-productivity, and pressured speech. This meets the criteria for a manic episode, establishing a diagnosis of Bipolar I Disorder.

The treatment for bipolar depression differs drastically from unipolar major depressive disorder, primarily regarding the use of antidepressants.

3

Evaluate laboratory results to rule out secondary causes of depressive symptoms.

The TSH and free T4 levels are normal, confirming that the depressive symptoms are psychiatric in origin and not due to undertreated hypothyroidism.

Medical mimics, such as hypothyroidism, must be ruled out before initiating psychotropic medications.

4

Select appropriate pharmacological therapies for Bipolar I depression.

First-line agents include specific atypical antipsychotics (quetiapine, lurasidone, cariprazine) or mood stabilizers (lithium, lamotrigine).

Antidepressant monotherapy must be strictly avoided in bipolar disorder due to the high risk of inducing mania.

Key Concept

Treatment of Acute Bipolar Depression

Estimated Time:1m 30s

Question 511Question →

A 24-year-old woman is brought to the emergency department by her older sister due to increasingly erratic behavior. The patient has a history of major depressive disorder, for which she currently takes no medications. For the past two weeks, she has been sleeping only 2 hours a night, exhibiting pressured speech, and endorsing grand delusions that she is a highly-trained secret agent. Today, she told her sister, "I have to jump off the hospital roof tonight to prove my immortality to the agency." In the emergency department, the patient is highly agitated, pacing the room, and attempting to elope. She adamantly refuses voluntary admission and any medical treatment. The patient has a valid advance directive from a previous depressive episode that explicitly names her sister as her healthcare proxy. However, the patient's father arrives at the emergency department, states that psychiatric care is a "hoax," and demands to take his daughter home immediately. Which of the following is the most appropriate next step in management?

Place the patient on an involuntary psychiatric hold

Discharge the patient to the custody of her father

Initiate escitalopram monotherapy to treat the underlying depression

Notify local authorities to warn the patient's employer about her delusions

Diagnose schizophreniform disorder and coordinate intensive outpatient therapy

Show answer & explanation

Answer: Place the patient on an involuntary psychiatric hold

Answer

The most appropriate next step is to place the patient on an involuntary psychiatric hold to ensure her safety.

The correct action is to place the patient on an involuntary psychiatric hold. This patient is experiencing a severe manic episode with psychotic features (bipolar I disorder) and has expressed a clear, lethal plan to harm herself ("jump off the hospital roof... to prove my immortality"). Because she lacks decision-making capacity due to her psychosis and poses an imminent threat to her own life, she meets the universal criteria for involuntary psychiatric commitment. When a patient is an acute danger to themselves, emergency safety protocols and state laws supersede the wishes of family members, even legally appointed healthcare proxies. Therefore, the physician must legally and ethically detain the patient to provide life-saving psychiatric stabilization.

Step-by-Step Solution

1

Assess the patient's clinical presentation and risk of imminent harm.

The patient exhibits classic signs of acute mania with psychotic features and has a specific, lethal plan for self-harm (jumping off the roof).

Determining the safety risk is the absolute first priority in any acute psychiatric emergency.

2

Evaluate the patient's capacity and willingness to accept psychiatric treatment.

The patient lacks insight into her illness and adamantly refuses voluntary admission or treatment.

When a patient lacks capacity and refuses life-saving care, legal frameworks for involuntary treatment must be considered.

3

Determine the appropriate legal and ethical intervention regarding surrogate decision-makers.

Because the patient is an imminent danger to herself, state involuntary hold laws supersede all surrogate or family preferences.

Even though a healthcare proxy exists, emergency involuntary commitment is mandated when the threshold for self-harm is met, making discharge to any family member inappropriate.

Key Concept

Criteria for involuntary psychiatric holds and management of acute mania with safety risks

Estimated Time:1m 15s

Question 512Question →

A 25-year-old female fashion model is evaluated in the emergency department for severe muscle cramps, dizziness, and palpitations. She says her symptoms began this morning and have progressively worsened. The patient is under immense pressure from her agency to meet strict body measurement requirements for an upcoming international campaign. Vital signs show a temperature of $36.8^\circ$ C ( $98.2^\circ$ F), heart rate of $115$ /min, respiratory rate of $20$ /min, and blood pressure of $102/62$ mm Hg. BMI is $19.5$ kg/m $^2$ . Physical examination reveals dry mucous membranes and hyperactive bowel sounds. There is no parotid gland enlargement, and the dorsal surfaces of her hands are unremarkable.

Laboratory results are as follows:

Test	Result
Serum sodium	$140$ mEq/L
Serum potassium	$2.4$ mEq/L
Serum chloride	$116$ mEq/L
Serum bicarbonate	$14$ mEq/L
Blood urea nitrogen	$32$ mg/dL
Serum creatinine	$1.2$ mg/dL

Arterial blood gas (room air):

Parameter	Result
pH	$7.28$
pCO $_2$	$29$ mm Hg
pO $_2$	$95$ mm Hg

Which of the following is the most likely cause of this patient's current presentation?

Frequent self-administration of bisacodyl

Self-induced vomiting with concomitant respiratory failure

Severe caloric restriction leading to starvation ketosis

Surreptitious ingestion of excessive levothyroxine

Co-ingestion of fluoxetine and phenelzine

Show answer & explanation

Answer: Frequent self-administration of bisacodyl

Answer

The correct answer is frequent self-administration of bisacodyl, which is a stimulant laxative.

The correct answer describes surreptitious laxative abuse. This patient has a primary metabolic acidosis (pH

7.28

, low

\text{HCO}_3^-

). Her anion gap is calculated as

140 - (116 + 14) = 10

, which indicates a normal anion gap metabolic acidosis (NAGMA). The

\text{pCO}_2

of

29

mm Hg reflects appropriate respiratory compensation according to Winter's formula (Expected

\text{pCO}_2 = 1.5 \times 14 + 8 = 29

). In a young woman with immense professional pressure to maintain a low body weight, a hypokalemic NAGMA combined with signs of volume depletion (BUN:Cr ratio

> 20

) and hyperactive bowel sounds strongly indicates surreptitious laxative abuse. Laxatives stimulate rapid colonic transit, leading to profound gastrointestinal loss of both potassium and bicarbonate.

Step-by-Step Solution

1

Analyze the primary acid-base disturbance using the arterial blood gas.

The patient has a low pH (

7.28

) and low bicarbonate (

14

mEq/L), indicating a primary metabolic acidosis.

Establishing the primary disorder is the mandatory first step in evaluating any electrolyte/acid-base derangement.

2

Calculate the serum anion gap to narrow the differential diagnosis.

Anion Gap =

\text{Na}^+ - (\text{Cl}^- + \text{HCO}_3^-) = 140 - (116 + 14) = 10

mEq/L. This falls within the normal range (

8-12

mEq/L).

Differentiating between High Anion Gap (HAGMA) and Normal Anion Gap (NAGMA) completely changes the underlying physiological etiology.

3

Determine if the respiratory compensation is appropriate using Winter's formula.

Expected

\text{pCO}_2 = 1.5 \times [\text{HCO}_3^-] + 8 \pm 2 = 1.5 \times 14 + 8 \pm 2 = 29 \pm 2

mm Hg. The actual

\text{pCO}_2

is

29

mm Hg, indicating perfect respiratory compensation.

This rules out any concomitant primary respiratory acidosis or alkalosis (e.g., respiratory failure or primary hyperventilation).

4

Synthesize the lab findings (hypokalemic NAGMA, high BUN/Cr ratio > 20) with the clinical vignette (young woman under pressure to be thin, hyperactive bowel sounds).

The combined picture of gastrointestinal bicarbonate and potassium loss, resulting in a volume-depleted NAGMA, strongly points to surreptitious laxative abuse.

Eating disorder patients often use different purging methods. Differentiating them relies heavily on specific lab patterns: vomiting causes alkalosis, laxatives cause acidosis.

Key Concept

Surreptitious laxative abuse in eating disorders presents clinically with volume depletion, severe hypokalemia, and a normal anion gap metabolic acidosis (NAGMA) due to massive gastrointestinal bicarbonate loss.

Question 513Question →

A 32-year-old man with a recent diagnosis of schizophrenia is admitted to the inpatient psychiatric unit due to worsening paranoia and command auditory hallucinations. Due to severe agitation, he is treated with multiple doses of intramuscular haloperidol over a 48-hour period. On hospital day 3, the patient develops profound "lead-pipe" muscle rigidity, a temperature of 39.4°C (102.9°F), profuse diaphoresis, and mutism. His blood pressure fluctuates between 160/100 mmHg and 90/60 mmHg, and his pulse is 122/min. Laboratory testing reveals a serum creatine kinase level of 4,500 U/L.

Arrange the following steps in the most appropriate chronological order for the acute management and subsequent follow-up of this patient's condition.

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Show answer & explanation

Answer

The correct sequence for managing neuroleptic malignant syndrome (NMS) is: 1) Discontinue the offending agent, 2) Initiate supportive care, 3) Administer targeted pharmacotherapy, 4) Consider ECT for refractory cases, and 5) Wait at least two weeks before cautiously re-challenging with an alternative antipsychotic.

The algorithm for managing Neuroleptic Malignant Syndrome (NMS) requires a strict stepwise approach to minimize mortality and morbidity. The very first step is to remove the offending cause by discontinuing all dopamine antagonists. Because NMS can cause severe dehydration, hyperthermia, and rhabdomyolysis leading to acute renal failure, aggressive supportive care (IV fluids, cooling blankets) is the immediate next priority. If the patient does not respond adequately to these foundational steps, specific medical therapies that reverse dopamine blockade (e.g., bromocriptine, amantadine) or act as direct muscle relaxants (e.g., dantrolene) are administered. In the most severe, treatment-refractory cases, or those presenting with profound catatonia, electroconvulsive therapy (ECT) is highly effective. Finally, for the long-term management of the patient's underlying schizophrenia, it is critical to wait at least two weeks after complete resolution of NMS symptoms before cautiously re-challenging with a different, usually lower-potency, antipsychotic to prevent a recurrence.

Step-by-Step Solution

1

Identify the clinical presentation as Neuroleptic Malignant Syndrome (NMS).

The patient's classic tetrad of altered mental status, autonomic instability, hyperthermia, and "lead-pipe" muscle rigidity, combined with recent high-dose haloperidol use and elevated creatine kinase, confirms the diagnosis of NMS.

Accurate diagnosis is required to initiate the specific, stepwise, life-saving management protocol.

2

Determine the first and most critical acute intervention.

The immediate discontinuation of all dopamine receptor antagonists (in this case, haloperidol) is the paramount first step.

Continued exposure to the offending agent will worsen the dopamine blockade driving the syndrome, rendering other treatments ineffective.

3

Sequence the subsequent acute stabilization interventions.

Aggressive supportive care (IV fluids, cooling) must be instituted next. If this fails, targeted pharmacotherapy (bromocriptine, dantrolene, amantadine) is added. If the patient remains refractory and severely ill, ECT is the definitive acute treatment.

Treatment escalates from least invasive/fundamental (supportive care) to targeted medical therapy, and finally to highly invasive procedures (ECT) based on clinical response.

4

Establish the long-term management strategy for the underlying psychosis.

After full recovery from NMS, a washout period of at least two weeks is mandatory before cautiously re-challenging the patient with a different antipsychotic (typically an atypical, lower-potency agent like quetiapine or clozapine).

Premature re-introduction of antipsychotics carries an unacceptably high risk of NMS recurrence.

Key Concept

Neuroleptic Malignant Syndrome (NMS) Stepwise Management Algorithm

Estimated Time:1m 30s

Question 514Question →

An 80-year-old man, a former university professor, visits his outpatient provider accompanied by his daughter. She expresses concern that over the past 18 months, he has been repeatedly misplacing important documents, forgetting appointments, and struggling to manage his finances. Last week, he was found wandering several blocks from his house, unable to remember the route back. Vital signs are stable, and the neurological examination shows no focal deficits. The provider plans a comprehensive evaluation and anticipates a long-term management strategy for presumed Alzheimer disease.

Arrange the following clinical steps in the appropriate chronological sequence for the standard diagnostic evaluation and progressive longitudinal management of this patient's condition.

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Answer

The correct sequence begins with the objective quantification of the cognitive deficit, followed by ruling out secondary causes via labs and imaging, initiating first-line monotherapy for mild-to-moderate disease, escalating to combination therapy as the disease reaches the moderate-to-severe stage, and finally focusing on palliative and skilled care in the terminal stages.

The standard of care for evaluating and managing progressive memory loss follows a strict chronological pathway. First, the physician must objectively confirm the impairment using validated cognitive scales. Second, neuroimaging and laboratory tests must be obtained to exclude reversible causes such as hypothyroidism, neurosyphilis, B12 deficiency, or structural intracranial lesions. Only after a clinical diagnosis of major neurocognitive disorder (likely Alzheimer disease) is established should first-line pharmacotherapy with an acetylcholinesterase inhibitor (donepezil) be started. As the disease naturally progresses over years to a moderate-to-severe stage, the addition of an NMDA receptor antagonist (memantine) is indicated. Finally, in the late/terminal stages of the disease, when the patient is fully dependent and medications offer little to no functional benefit, the focus appropriately shifts toward skilled nursing and palliative care.

Step-by-Step Solution

1

Administer a cognitive screening tool (e.g., MoCA or MMSE).

Establishes the presence and severity of objective cognitive decline.

It is necessary to confirm that the patient's cognitive deficits are genuine and measurable before proceeding with an extensive medical workup.

2

Order screening labs (TSH, B12, CMP, CBC) and a noncontrast Head CT or Brain MRI.

Excludes potentially reversible causes of dementia.

Guidelines mandate ruling out metabolic disturbances, nutritional deficiencies, and structural lesions before diagnosing Alzheimer disease.

3

Start an acetylcholinesterase inhibitor (AChEI).

Provides symptomatic benefit for mild-to-moderate Alzheimer disease.

AChEIs (donepezil, rivastigmine, galantamine) are the standard first-line pharmacotherapy following a formal diagnosis.

4

Add memantine.

Augments therapy for advancing disease.

Memantine, an NMDA receptor antagonist, is indicated only when the patient's condition progresses from mild to moderate-to-severe Alzheimer disease.

5

Implement palliative care and skilled nursing transition.

Ensures safety and comfort in end-stage dementia.

When patients completely lose the ability to perform basic activities of daily living (ADLs) and require 24/7 care, the clinical focus shifts to custodial and palliative care.

Key Concept

Diagnostic algorithm and progressive pharmacological management of Alzheimer disease

Question 515Question →

Match the following clinical vignettes to the most likely underlying neurocognitive disorder etiology.

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Answer

Vignette 1 maps to Vascular dementia, Vignette 2 maps to Frontotemporal dementia, Vignette 3 maps to Dementia with Lewy bodies, Vignette 4 maps to Alzheimer disease, and Vignette 5 maps to Normal pressure hydrocephalus.

Each neurocognitive disorder has a distinct initial clinical presentation. Alzheimer disease presents with insidious memory loss. Frontotemporal dementia presents with early personality and behavioral changes. Lewy body dementia is characterized by visual hallucinations, parkinsonism, and fluctuating cognition. Vascular dementia shows a step-wise decline with focal neurological deficits. Normal pressure hydrocephalus presents with the classic triad of gait apraxia, urinary incontinence, and dementia.

Step-by-Step Solution

1

Analyze the first vignette for the pattern of decline and presence of neurologic signs.

Identified a step-wise progression and focal neurologic deficits.

These are hallmark features of a vascular etiology due to sequential ischemic events.

2

Evaluate the second vignette for predominant early symptoms.

Identified prominent behavioral changes and hyperorality overshadowing memory loss.

Behavioral disinhibition is the core diagnostic criterion for frontotemporal lobar degeneration.

3

Review the third vignette for characteristic symptom triads.

Recognized the combination of visual hallucinations, parkinsonism, and REM sleep behavior disorder.

This combination is highly specific for an alpha-synucleinopathy with Lewy bodies.

4

Assess the fourth vignette for onset speed and the domain of impairment.

Noted an insidious onset of purely episodic memory and visuospatial deficits.

This represents the typical amnestic presentation of Alzheimer disease.

5

Examine the fifth vignette for a classic symptom triad.

Identified the 'wobbly, wet, and wacky' triad.

This constellation is pathognomonic for idiopathic normal pressure hydrocephalus.

Key Concept

Differentiation of major neurocognitive disorders based on core clinical features and initial presentation.

Estimated Time:1m 30s

Question 516Question →

A 32-year-old elementary school teacher schedules a telehealth appointment with a psychiatrist, reporting overwhelming distress that is threatening her career. Over the last 5 months, she has experienced relentless, horrific mental images of herself physically striking her students. She describes these images as 'sickening' and completely contrary to her morals. To neutralize her anxiety, she spends up to 3 hours each day securing any heavy or sharp objects in her classroom and repeatedly reviewing her actions at the end of the day. She tearfully states she would never actually hurt a child and has absolutely no desire to do so, but the thoughts will not stop. She has no prior psychiatric history and takes no medications.

Which of the following are appropriate clinical actions for the physician to take? (Select all that apply)

Select all that apply

Referral for exposure and response prevention therapy

Initiation of fluoxetine pharmacotherapy

Notification of the school administration regarding a potential safety threat

Filing a mandatory report with local child protective services

Disclosure of the patient's clinical presentation to local law enforcement

Show answer & explanation

Answer: Referral for exposure and response prevention therapy; Initiation of fluoxetine pharmacotherapy

Answer

The appropriate clinical actions are referral for exposure and response prevention therapy and initiation of fluoxetine pharmacotherapy.

The correct actions involve initiating evidence-based treatments for obsessive-compulsive disorder (OCD). This patient is presenting with classic ego-dystonic harm obsessions—intrusive, unwanted thoughts of causing harm that are highly distressing and contrary to her actual desires. Her behavior of securing objects and engaging in mental review represent compulsions performed to alleviate the intense anxiety caused by these thoughts. Because she has no intent or desire to act on these thoughts, she does not pose a danger to her students. First-line treatment for OCD consists of a specialized form of cognitive-behavioral therapy known as exposure and response prevention (ERP), as well as pharmacotherapy with selective serotonin reuptake inhibitors (SSRIs) like fluoxetine, which are typically utilized at higher doses than those required for depression.

Step-by-Step Solution

1

Diagnose the patient's underlying psychiatric condition based on her clinical presentation.

The patient is suffering from obsessive-compulsive disorder (OCD), characterized by ego-dystonic harm obsessions (intrusive thoughts of striking students) and neutralizing compulsions (securing objects, mental reviewing).

Accurate diagnosis is strictly required to differentiate the symptoms of OCD from true homicidal ideation or psychosis.

2

Assess the patient's risk of violence and evaluate the ethical duty to report.

The patient finds the thoughts sickening, has no intent to act, and actively uses compulsions to prevent harm. She poses no imminent threat, meaning confidentiality must be strictly maintained.

Breaching confidentiality is only legally and ethically permissible when there is a specific, imminent threat to a third party or suspected active abuse.

3

Select first-line, evidence-based treatments for the diagnosed condition.

First-line treatments for OCD include exposure and response prevention (ERP) therapy and SSRI pharmacotherapy (e.g., fluoxetine).

These two modalities have the strongest evidence base for effectively reducing obsessive-compulsive symptoms.

Key Concept

Harm obsessions in obsessive-compulsive disorder are ego-dystonic and do not indicate true homicidal intent; therefore, they do not warrant a breach of confidentiality. First-line management involves exposure and response prevention (ERP) and SSRI pharmacotherapy.

Estimated Time:1m 0s

Question 517Question →

Match each of the following distinct clinical scenarios to the most appropriate legal or ethical course of action.

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Answer

Scenario 1 matches to seeking surrogate consent; Scenario 2 matches to overriding the advance directive; Scenario 3 matches to providing confidential care without parental notification; Scenario 4 matches to initiating an involuntary hold and breaching confidentiality to warn the victim.

Each scenario tests a nuanced boundary of psychiatric law and ethics. Scenario 1 requires distinguishing psychiatric holds from global medical incapacity. Scenario 2 tests the emergency safety exception to advance directives. Scenario 3 applies the emancipated/specific-condition consent rules for minors regarding substance abuse. Scenario 4 requires applying the duty to protect in the setting of a voluntary psychiatric admission.

Step-by-Step Solution

1

Analyze Scenario 1 (Psych hold + medical refusal).

Identify that the patient's refusal is based on a delusion, meaning he lacks capacity for this decision. Recognize that psych holds do not cover non-psychiatric medical care.

Determines that surrogate consent is legally required for non-emergent medical procedures when a psychiatric patient lacks capacity.

2

Analyze Scenario 2 (Advance directive + violence).

Identify that the patient is an imminent danger to staff.

Establishes that the emergency exception applies, allowing physicians to override psychiatric advance directives to administer chemical restraints for immediate safety.

3

Analyze Scenario 3 (Minor + SUD treatment).

Identify that the 16-year-old is seeking substance use disorder treatment and wishes to keep it confidential from parents.

Applies the legal exception allowing minors to consent to specific treatments (SUD, STI, contraception) without parental involvement.

4

Analyze Scenario 4 (Specific threat + voluntary patient).

Identify a specific, credible threat against a named individual by a patient planning imminent discharge.

Triggers the Tarasoff duty to protect, requiring the physician to breach confidentiality to warn the victim/police and to hold the patient involuntarily.

Key Concept

Complex intersections of medical jurisprudence in psychiatry: capacity vs. involuntary holds, emergency overrides of advance directives, minor consent exceptions, and the duty to protect.

Estimated Time:2m 0s

Question 518Question →

A 21-year-old woman is evaluated in the emergency department after fainting during a ballet rehearsal. Over the past month, she has experienced profound fatigue, recurrent dizziness, and muscle cramps. The patient states she feels immense pressure to maintain a thin physique for her upcoming dance performance. Her mother, who accompanied her, mentions finding several empty packages of bisacodyl in the patient's bathroom. The patient exercises for three hours daily and rigidly restricts her caloric intake, although she admits to occasionally consuming large quantities of food before feeling intensely guilty.

Vital signs show a temperature of $36.4^\circ\text{C}$ ( $97.5^\circ\text{F}$ ), blood pressure of 92/58 mm Hg, and pulse of 114/min. Her current body mass index (BMI) is $17.0 \text{ kg/m}^2$ .

Physical examination reveals poor skin turgor and hyperactive bowel sounds.

Laboratory results are as follows:
Serum sodium: 139 mEq/L
Serum potassium: 2.4 mEq/L
Serum chloride: 115 mEq/L
Serum bicarbonate: 14 mEq/L
Blood urea nitrogen: 26 mg/dL
Serum creatinine: 1.1 mg/dL

Arterial blood gas analysis on room air:
pH: 7.27
$PaCO_2$ : 30 mm Hg
$PaO_2$ : 96 mm Hg

Which of the following represents the most accurate psychiatric diagnosis and the correct interpretation of this patient's acid-base status?

Anorexia nervosa, binge-eating/purging subtype; normal anion gap metabolic acidosis with appropriate respiratory compensation

Anorexia nervosa, binge-eating/purging subtype; normal anion gap metabolic acidosis with a superimposed primary respiratory alkalosis

Bulimia nervosa; normal anion gap metabolic acidosis with appropriate respiratory compensation

Anorexia nervosa, restricting subtype; high anion gap metabolic acidosis with appropriate respiratory compensation

Bulimia nervosa; high anion gap metabolic acidosis with a superimposed primary respiratory alkalosis

Show answer & explanation

Answer: Anorexia nervosa, binge-eating/purging subtype; normal anion gap metabolic acidosis with appropriate respiratory compensation

Answer

Anorexia nervosa, binge-eating/purging subtype; normal anion gap metabolic acidosis with appropriate respiratory compensation

The correct answer accurately identifies both the psychiatric condition and the acid-base disturbance. The patient's significantly low body weight (BMI of 17.0 kg/m^2) combined with an intense fear of weight gain confirms anorexia nervosa, while her objective binges and laxative abuse specify the binge-eating/purging subtype. Laxative abuse causes significant gastrointestinal loss of potassium and bicarbonate, resulting in a normal anion gap metabolic acidosis. The anion gap is calculated as 139 - (115 + 14) = 10 mEq/L, which is within the normal range of 8-12 mEq/L. To evaluate for appropriate respiratory compensation, Winter's formula is applied: expected PaCO2 = 1.5 * (14) + 8 +/- 2 = 29 +/- 2 mm Hg. The patient's measured PaCO2 of 30 mm Hg falls exactly within this expected compensatory range.

Step-by-Step Solution

1

Identify the primary psychiatric diagnosis based on physical measurements and behavior.

The patient's BMI is 17.0 kg/m^2 (below the 18.5 kg/m^2 threshold), establishing anorexia nervosa. Her episodes of eating large quantities of food and using bisacodyl confirm the binge-eating/purging subtype.

Differentiating anorexia nervosa from bulimia nervosa relies heavily on the BMI threshold; diagnosing the subtype relies on the presence of binge/purge behaviors versus pure restriction.

2

Determine the primary acid-base disorder from the ABG and basic metabolic panel.

The pH of 7.27 indicates acidemia, and the low serum bicarbonate of 14 mEq/L confirms a primary metabolic acidosis, commonly caused by laxative-induced bicarbonate loss in the stool.

Identifying the primary disturbance is the first step in acid-base interpretation.

3

Calculate the anion gap to classify the metabolic acidosis.

Anion Gap = Na+ - (Cl- + HCO3-) = 139 - (115 + 14) = 139 - 129 = 10 mEq/L. This falls in the normal range (8-12 mEq/L).

Calculating the anion gap distinguishes between hyperchloremic acidosis (diarrhea/laxatives) and high anion gap acidosis (starvation ketoacidosis).

4

Apply Winter's formula to determine if respiratory compensation is appropriate.

Expected PaCO2 = 1.5 * (14) + 8 = 29 (+/- 2). The expected range is 27-31 mm Hg. Since the patient's measured PaCO2 is 30 mm Hg, the respiratory compensation is appropriate.

Winter's formula determines if there is a mixed acid-base disorder. If the measured PaCO2 falls within the expected range, no superimposed respiratory disorder is present.

Key Concept

Patients with anorexia nervosa, binge-eating/purging subtype due to laxative abuse present with a BMI < 18.5 kg/m^2 and typically develop a normal anion gap (hyperchloremic) metabolic acidosis with appropriate respiratory compensation.

Estimated Time:2m 0s

Question 519Question →

Match each clinical scenario describing a patient with a substance use disorder to the most appropriate pharmacologic intervention for their long-term management.

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Answer

The clinical scenarios correctly match with Acamprosate for the patient with decompensated cirrhosis, Naltrexone for the patient with dual alcohol and opioid use disorders, Buprenorphine for the pregnant patient seeking office-based treatment, and Disulfiram for the patient seeking aversion therapy.

Each clinical scenario presents a unique medical constraint or requirement that dictates the specific pharmacotherapy for substance use disorder management. The correct matches perfectly align the patient's medical comorbidities, dual diagnoses, prescribing setting restrictions, and personal preferences with the distinct pharmacokinetic and pharmacodynamic profiles of acamprosate, naltrexone, buprenorphine, and disulfiram.

Step-by-Step Solution

1

Analyze the first patient's comorbidities (decompensated cirrhosis) and indication (alcohol use disorder).

The patient requires a medication that is not metabolized by the liver.

Medications like naltrexone and disulfiram carry risks of hepatotoxicity. Acamprosate is renally excreted and therefore safe in severe liver disease.

2

Analyze the second patient's diagnoses (alcohol and opioid use disorders) and period of abstinence (18 days).

The patient needs a dual-efficacy medication and has safely passed the required washout window.

Naltrexone effectively treats both disorders but will precipitate severe withdrawal if given to a patient who has used opioids within the past 7 to 14 days.

3

Analyze the third patient's condition (pregnancy) and preferred treatment setting (office-based outpatient clinic).

The patient requires medication-assisted treatment that can be legally prescribed outside of a federal methadone program.

Buprenorphine is safe during pregnancy and can be prescribed by waivered physicians in a standard clinic, offering greater flexibility than methadone.

4

Analyze the fourth patient's specific request (noxious physical reaction to alcohol) and high motivation level.

The patient is explicitly asking for aversion therapy.

Disulfiram inhibits aldehyde dehydrogenase, leading to toxic acetaldehyde accumulation and severe physical symptoms if alcohol is ingested.

Key Concept

Pharmacotherapy selection for substance use disorders must be individualized based on medical comorbidities, specific patient needs, and regulatory treatment settings.

Question 520Question →

A 9-year-old boy is brought to the clinic by his parents due to academic difficulties and new behavioral habits. Over the past 14 months, his parents have noticed him frequently and forcefully blinking his eyes, shrugging his shoulders, and clearing his throat. The parents initially attributed the throat clearing to seasonal allergies, but a two-month trial of daily cetirizine provided no relief. His teacher reports that he frequently leaves his seat during class, interrupts others, and struggles to sustain focus on assignments, which is severely impacting his grades. He has no history of sudden behavioral changes following infections. The physician diagnoses a neurodevelopmental disorder and recommends starting a medication that can simultaneously address both his movement symptoms and his behavioral difficulties. Which of the following describes the mechanism of action of the most appropriate initial pharmacotherapy for this patient?

Agonism at central alpha-2 adrenergic receptors

Inhibition of presynaptic dopamine and norepinephrine reuptake

Selective inhibition of presynaptic norepinephrine reuptake

Antagonism at postsynaptic dopamine D2 and serotonin 5-HT2A receptors

Selective inhibition of presynaptic serotonin reuptake

Show answer & explanation

Answer: Agonism at central alpha-2 adrenergic receptors

Answer

Agonism at central alpha-2 adrenergic receptors

The patient's clinical presentation of multiple motor tics (eye blinking, shoulder shrugging) and at least one vocal tic (throat clearing) persisting for over a year is diagnostic of Tourette syndrome. Concurrently, his inattention, hyperactivity, and impulsivity causing academic impairment are diagnostic of comorbid Attention-Deficit/Hyperactivity Disorder (ADHD). When Tourette syndrome and ADHD co-occur, central alpha-2 adrenergic agonists (such as guanfacine and clonidine) are the most appropriate initial pharmacological choice because they demonstrate efficacy in simultaneously reducing the severity of tics and improving ADHD symptoms. Their mechanism of action is agonism at central alpha-2 adrenergic receptors, which enhances prefrontal cortical regulation of attention and impulse control.

Step-by-Step Solution

1

Analyze the patient's movement and vocal symptoms.

The patient has multiple motor tics (eye blinking, shoulder shrugging) and a vocal tic (throat clearing) lasting more than 1 year (14 months).

To establish the diagnosis of Tourette syndrome and rule out transient tic disorder or allergies.

2

Analyze the patient's behavioral and academic symptoms.

The patient exhibits hyperactivity (leaving seat), impulsivity (interrupting), and inattention (struggles to sustain focus) causing severe academic impairment.

To establish the comorbid diagnosis of Attention-Deficit/Hyperactivity Disorder (ADHD).

3

Determine the optimal pharmacological management for the combined diagnoses.

Alpha-2 adrenergic agonists (guanfacine or clonidine) are indicated.

They uniquely provide dual efficacy, reducing both tic severity and ADHD symptoms, making them the preferred initial monotherapy for this specific comorbidity.

4

Identify the mechanism of action of the chosen medication.

Guanfacine and clonidine act via agonism at central alpha-2 adrenergic receptors.

To answer the specific question asked in the stem regarding the neuropharmacology of the optimal drug.

Key Concept

Patients with comorbid Tourette syndrome and Attention-Deficit/Hyperactivity Disorder (ADHD) are typically best managed initially with central alpha-2 adrenergic agonists (e.g., guanfacine, clonidine), which effectively target both symptom clusters.

Psychiatry

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