All practice questions

8270 questions

Question 3341Question →

A 74-year-old man with a 9-year history of Parkinson disease and emerging cognitive decline is brought to the emergency department by his daughter due to acute-onset, severe agitation and frightening visual hallucinations over the past 48 hours. He states that strangers are hiding in his room. His current medication regimen includes carbidopa-levodopa, pramipexole, and trihexyphenidyl. Arrange the following steps in the correct clinical escalation sequence for the evaluation and management of this patient's acute neuropsychiatric presentation, moving from initial assessment to therapies for refractory symptoms.

Drag items to arrange them in the correct order

Show answer & explanation

Answer

The correct sequence for managing acute psychosis and agitation in a patient with Parkinson disease or Lewy body dementia is: (1) medical evaluation for secondary causes, (2) discontinuation of anticholinergics, (3) discontinuation of dopamine agonists, (4) addition of a safe atypical antipsychotic like quetiapine, and finally (5) clozapine for refractory cases.
The management of acute behavioral changes and psychosis in patients with Parkinson disease or Lewy body dementia follows a strict, stepwise algorithm designed to balance psychiatric symptom control with the preservation of motor function. The essential first step is always to rule out an acute delirium secondary to a systemic illness. Once a systemic etiology is excluded, the existing medication regimen must be systematically simplified to eliminate medications that contribute most heavily to psychosis while providing the least critical motor benefit. Anticholinergic drugs (like trihexyphenidyl) are notoriously deliriogenic and are stopped first. Next, dopamine agonists (like pramipexole) are tapered off. Carbidopa-levodopa is maintained at the lowest effective dose because it is the most critical agent for motor function. If hallucinations persist despite this optimization, targeted pharmacotherapy is indicated. Only atypical antipsychotics with very low affinity for the dopamine D2 receptor (specifically quetiapine, pimavanserin, or clozapine) should be used, as other antipsychotics will induce severe parkinsonian rigidity. Quetiapine or pimavanserin are first-line choices. Clozapine is highly effective but is reserved for refractory cases due to the risk of agranulocytosis and the logistical burden of mandatory neutrophil monitoring.

Step-by-Step Solution

1
Evaluate for Delirium
Identifies or excludes systemic triggers
Acute behavioral changes in neurocognitive disorders are frequently driven by underlying infections or metabolic issues that require immediate medical treatment.
2
Optimize existing medications by withdrawing the most deliriogenic agents
Discontinues trihexyphenidyl
Anticholinergics provide minimal motor benefit in advanced disease but carry a massive risk for delirium and visual hallucinations.
3
Further simplify the dopaminergic regimen
Discontinues pramipexole
Dopamine agonists are the next most likely culprits for psychosis. Levodopa is spared as long as possible to preserve motor function.
4
Introduce targeted psychiatric symptom control
Initiates quetiapine or pimavanserin
Standard antipsychotics will severely worsen parkinsonism. Low D2-affinity agents are required to treat hallucinations safely.
5
Escalate to the treatment of last resort
Initiates clozapine
Used only when other safe antipsychotics fail, due to the burdensome requirement for absolute neutrophil count monitoring to prevent agranulocytosis.

Key Concept

Management algorithm for psychosis and delirium in Major Neurocognitive Disorder due to Parkinson Disease
Question 3342Question →

A 35-year-old male architect is brought to the outpatient psychiatry clinic by his brother due to worsening depression. For the past 5 weeks, the patient has exhibited profound sadness, anhedonia, and severe fatigue. He struggles to concentrate at work and is sleeping up to 14 hours a day. The brother reports that 3 years ago, the patient had a 3-week period where he slept only 2 hours a night, spoke extremely rapidly, and believed he was receiving direct telepathic messages from aliens instructing him to redesign the city's infrastructure. During that time, he drained his personal savings to fund the project before his symptoms gradually subsided without formal medical treatment. The patient has no other medical conditions and takes no medications. Vital signs are within normal limits. Mental status examination reveals a depressed affect, psychomotor retardation, and tearfulness, but no current suicidal ideation or psychotic symptoms. Which of the following is the most appropriate next step in management?

Show answer & explanation

Answer: Initiate lurasidone

Answer

Initiate lurasidone
This patient is currently experiencing a major depressive episode, but his history of a 3-week episode characterized by decreased sleep, pressured speech, and grandiose delusions confirms a diagnosis of Bipolar I Disorder. First-line pharmacotherapy for acute bipolar depression includes certain second-generation antipsychotics (e.g., lurasidone, quetiapine, cariprazine) or mood stabilizers (e.g., lithium). Lurasidone is highly effective for bipolar depression and has a favorable metabolic profile.

Step-by-Step Solution

1
Analyze the patient's past psychiatric history.
The patient had a 3-week episode of decreased sleep, pressured speech, severe impulsivity (draining savings), and grandiose delusions.
Identifying past episodes is crucial to differentiating unipolar major depressive disorder from bipolar disorder. The prior episode meets full criteria for a Manic Episode with psychotic features.
2
Assess the current clinical presentation.
The patient is currently experiencing a major depressive episode (depressed mood, anhedonia, hypersomnia, fatigue, psychomotor retardation for 5 weeks).
Combining the past manic episode with the current depressive episode establishes a diagnosis of Bipolar I Disorder, currently in a depressed phase.
3
Evaluate treatment options for acute bipolar depression while ruling out contraindications.
Antidepressant monotherapy must be avoided. An agent approved for bipolar depression, such as lurasidone, is required.
Using traditional antidepressants without a mood stabilizer in Bipolar I disorder can precipitate a manic switch. First-line treatments for acute bipolar depression include lurasidone, quetiapine, cariprazine, or the olanzapine-fluoxetine combination.

Key Concept

Patients presenting with depressive episodes must be screened for past manic episodes to accurately diagnose Bipolar I Disorder and avoid the administration of antidepressant monotherapy, which can trigger a manic switch.
Estimated Time:1m 30s
Question 3343Question →

A 34-year-old male distance runner is brought to the hospital by his partner due to profound weakness and near-syncope. His body mass index is 13.5 kg/m213.5 \text{ kg/m}^2, heart rate is 38/min38/\text{min}, and blood pressure is 82/50 mm Hg82/50 \text{ mm Hg}. He reports eating fewer than 500 kcal500 \text{ kcal} daily for the past three months to 'improve race times'. He is admitted to the medical intensive care unit for severe anorexia nervosa. Arrange the following steps in the optimal sequence for managing this patient's acute and long-term care to minimize the risk of potentially fatal complications.

Drag items to arrange them in the correct order

Show answer & explanation

Answer

The correct sequence requires establishing a metabolic baseline, proactively correcting electrolyte deficits, initiating feeding at a low caloric threshold, slowly advancing calories with close monitoring, and finally initiating formal psychotherapy once the patient is medically and cognitively stable.
The management of severe anorexia nervosa requires a highly orchestrated sequence to prevent refeeding syndrome. Prolonged starvation leads to a total body depletion of phosphorus, potassium, and magnesium, despite potentially normal serum levels due to metabolic adaptation. When carbohydrates are reintroduced, the sudden surge in insulin drives glucose and these electrolytes into the cells. If feeding is started before assessing and repleting these electrolytes, the serum levels crash catastrophically, causing arrhythmias, heart failure, and seizures. Therefore, baseline labs and ECG must be obtained first, followed immediately by fluid and electrolyte repletion. Only after baseline stability is achieved should low-calorie feeding begin (10−15 kcal/kg/day10-15 \text{ kcal/kg/day}). Calories are then cautiously advanced while continuously monitoring for electrolyte shifts and fluid overload. Finally, intensive psychotherapy (CBT) should be delayed until the patient is medically stable and the brain is sufficiently nourished to engage in complex cognitive tasks.

Step-by-Step Solution

1
Obtain baseline electrocardiogram and electrolytes.
Identifies pre-existing hypophosphatemia, hypokalemia, hypomagnesemia, or prolonged QTc.
Establishing a baseline is critical before any intervention that could trigger fluid shifts or insulin release.
2
Replete electrolytes prior to caloric loading.
Normalizes serum levels of critical intracellular ions.
Introducing carbohydrates causes a surge of insulin, which drives phosphorus, potassium, and magnesium into cells. Pre-repletion prevents fatal depletion.
3
Initiate feeding at 10−15 kcal/kg10-15 \text{ kcal/kg} per day.
Safely reintroduces glucose to a starved metabolic system.
Starting at a low caloric rate minimizes the magnitude of the insulin spike, serving as a primary defense against refeeding syndrome.
4
Gradually advance caloric intake with continuous monitoring.
Achieves nutritional restoration while mitigating risk.
The risk of refeeding syndrome persists for up to two weeks; careful titration and daily monitoring allow for early detection and treatment of electrolyte shifts.
5
Initiate cognitive-behavioral therapy (CBT-E).
Addresses the underlying psychiatric pathology.
Severely malnourished brains lack the cognitive flexibility required for CBT. Psychotherapy is only effective once baseline medical stability and partial weight restoration are achieved.

Key Concept

Refeeding syndrome pathophysiology and sequential management in severe Anorexia Nervosa.
Question 3344Question →

A 7575-year-old man is brought to the clinic by his daughter due to a progressive decline in his mobility and memory over the past 88 months. The daughter reports that he has become increasingly forgetful and struggles to manage his finances. Additionally, his walking has become remarkably slow and unsteady; he walks with his feet spread apart and appears as if his shoes are 'stuck to the floor.' In the past month, he has had several episodes of urinary incontinence, which he seems largely unconcerned about. His medical history includes hypertension and osteoarthritis. Neurological examination reveals a wide-based, magnetic gait with short steps. Muscle strength and deep tendon reflexes are normal, and there is no resting tremor or cogwheel rigidity. Montreal Cognitive Assessment score is 21/3021/30. Which of the following is the most appropriate next step in the diagnostic workup?

Show answer & explanation

Answer: Magnetic resonance imaging of the brain

Answer

Magnetic resonance imaging of the brain
The correct answer is magnetic resonance imaging of the brain. This patient's presentation of cognitive impairment, a wide-based 'magnetic' gait, and urinary incontinence constitutes the classic triad of normal pressure hydrocephalus (NPH). The initial diagnostic step for suspected NPH is always structural neuroimaging (MRI or CT of the brain). This is essential to document ventriculomegaly out of proportion to cerebral atrophy and to rule out other structural etiologies before any invasive testing is attempted.

Step-by-Step Solution

1
Analyze the patient's clinical presentation.
The patient exhibits a progressive triad of cognitive impairment, wide-based magnetic gait, and urinary incontinence.
Identifying symptom clusters is essential for accurate syndromic diagnosis in geriatrics.
2
Formulate a primary differential diagnosis based on the triad.
The combination of 'wacky, wobbly, and wet' is the classic presentation of normal pressure hydrocephalus (NPH).
This specific combination distinguishes NPH from other dementias like Alzheimer disease or vascular dementia.
3
Determine the safest and most appropriate initial diagnostic step.
Structural neuroimaging must be performed first.
Imaging confirms ventriculomegaly and rules out structural lesions, which is a prerequisite before performing invasive testing like a high-volume lumbar puncture.

Key Concept

Diagnostic evaluation algorithm for Normal Pressure Hydrocephalus
Question 3345Question →

A forensic psychiatrist is reviewing the medical file of a female inmate being evaluated for transfer to a long-term psychiatric facility. Comprehensive longitudinal medical records indicate that her psychiatric illness began exactly 10 years ago with the insidious onset of auditory hallucinations, persecutory delusions, and severe avolition. Over this entire 10-year period, these psychotic symptoms have been continuously present on a daily basis without any periods of remission. The records also reveal that 8 years ago, she suffered a distinct 6-month period of profound anhedonia, hypersomnia, and feelings of worthlessness. Four years ago, she had a 3-month episode characterized by pressured speech, grandiosity, and a decreased need for sleep. There are no other documented mood episodes throughout her lifespan. Toxicology screens and medical evaluations have been consistently unremarkable throughout her incarceration and previous hospitalizations. Based on the patient's longitudinal history, which of the following is the most appropriate DSM-5 diagnosis?

Show answer & explanation

Answer: Schizophrenia

Answer

Schizophrenia
The correct diagnosis is schizophrenia. This patient has a 10-year (120-month) history of continuous psychotic symptoms, satisfying the core criteria for schizophrenia. While she has a history of both a major depressive episode and a manic episode, the cumulative duration of these mood episodes is only 9 months. According to DSM-5 criteria, a diagnosis of schizoaffective disorder requires that symptoms meeting the criteria for a major mood episode be present for the *majority* (greater than 50%) of the total duration of the active and residual portions of the illness. Because 9 months is a small minority (7.5%) of her 10-year illness, the criteria for schizoaffective disorder are not met, and the diagnosis remains schizophrenia.

Step-by-Step Solution

1
Analyze the duration and continuity of psychotic symptoms.
The patient has experienced hallucinations, delusions, and avolition continuously for 10 years (120 months).
This establishes that Criterion A for a schizophrenia spectrum disorder is met and confirms an active psychotic illness.
2
Calculate the total duration of all major mood episodes.
The patient had one depressive episode (6 months) and one manic episode (3 months), totaling 9 months of active mood symptoms.
Tracking mood episode duration is required to differentiate schizophrenia from schizoaffective disorder.
3
Compare the duration of mood episodes to the total duration of the psychotic illness.
The 9 months of mood symptoms constitute 7.5% of the 120-month total illness duration.
DSM-5 Criterion C for schizoaffective disorder dictates that mood episodes must be present for the majority (>50%) of the total active and residual portions of the illness.
4
Synthesize findings to confirm the final diagnosis.
Because mood symptoms do not account for the majority of the illness, the diagnosis defaults to schizophrenia rather than schizoaffective disorder.
Applying the strict longitudinal timeline rules eliminates other differential diagnoses.

Key Concept

To diagnose schizoaffective disorder, mood episodes must be present for the majority (>50%) of the total duration of the active and residual portions of the illness; if they are not, the diagnosis is schizophrenia.
Question 3346Question →

Match each patient's comprehensive clinical vignette to the most accurate psychiatric diagnosis.

Click a left item, then click its matching right item

Items

A 19-year-old college freshman reports feeling tearful and having difficulty sleeping for the past 2 months since moving away from home. She feels overwhelmed by classes but denies anhedonia, guilt, or suicidal ideation. She is able to attend classes and feels her mood improve significantly when visiting her family.
A 28-year-old man presents with a 4-week history of severe anhedonia, hypersomnia, and feelings of worthlessness. Upon detailed screening, he reports a distinct 6-day period last year where he felt uncharacteristically energetic, slept only 3 hours a night without feeling tired, and impulsively bought a sports car he could not afford.
A 45-year-old woman develops severe depressed mood, emotional lability, and profound insomnia. These symptoms began two weeks after she was prescribed high-dose oral prednisone to manage a severe systemic lupus erythematosus flare. Prior to this, she had no history of psychiatric illness.
A 35-year-old woman presents with a 6-week history of pervasive sadness, inability to enjoy her usual hobbies, early morning awakenings, a 5-kg (11-lb) weight loss, and difficulty concentrating at work. She reports feeling guilty over minor past mistakes and states her performance at work has severely declined.

Matches

Show answer & explanation

Answer

The college student with homesickness has an adjustment disorder. The man with current depression and past hypomania has bipolar disorder. The woman on prednisone has a medication-induced depressive disorder. The woman with 6 weeks of pervasive anhedonia and somatic symptoms has major depressive disorder.
Correct diagnosis in depressive disorders relies on precise pattern recognition: distinguishing the sub-threshold, stressor-related presentation of adjustment disorder; identifying past hypomanic episodes that define bipolar disorder; recognizing temporal associations with offending agents like glucocorticoids; and confirming the full symptom cluster required for major depressive disorder.

Step-by-Step Solution

1
Analyze the timeline, symptom severity, and functional impairment of each clinical vignette.
Identified that the 19-year-old does not meet full MDD criteria and has a clear stressor. The 35-year-old fully meets MDD criteria with marked functional impairment.
Differentiating major depressive disorder from adjustment disorder requires evaluating symptom count (at least 5 for MDD) and severity of functional impairment.
2
Screen for history of elevated mood or external triggers (medications/substances).
The 28-year-old has a history of a 6-day hypomanic episode. The 45-year-old's symptoms clearly align with the initiation of high-dose corticosteroids.
Failing to identify past hypomania/mania leads to inappropriate unipolar MDD treatment, and failing to recognize medication triggers leads to unnecessary primary psychiatric diagnoses.

Key Concept

Discrimination between unipolar major depressive disorder, bipolar depression, adjustment disorder, and substance/medication-induced depressive disorder based on clinical history and timeline.
Question 3347Question →

Match each clinical presentation with the most appropriate psychiatric diagnosis.

Click a left item, then click its matching right item

Items

Sudden onset of unilateral blindness with completely normal ophthalmologic and neurologic exams after witnessing a traumatic accident.
Excessive preoccupation with having pancreatic cancer for 8 months despite negative workups, with no active physical symptoms.
Persistent, distressing abdominal pain and fatigue for over a year with excessive, disproportionate anxiety and time devoted to these symptoms despite negative medical evaluations.
Surreptitious self-injection of insulin resulting in recurrent hypoglycemia (high insulin, low C-peptide), done to assume the sick role without obvious external reward.

Matches

Show answer & explanation

Answer

The presentations match as follows: unilateral blindness with normal exams corresponds to Conversion disorder; preoccupation with pancreatic cancer without symptoms corresponds to Illness anxiety disorder; chronic abdominal pain and fatigue with excessive worry corresponds to Somatic symptom disorder; and surreptitious insulin injection to assume the sick role corresponds to Factitious disorder imposed on self.
Each clinical presentation uniquely aligns with the core diagnostic criteria of a specific disorder within the somatic symptom and related disorders spectrum. Correct identification relies on evaluating the presence and nature of somatic symptoms, whether symptoms are intentionally produced, and the underlying motivation (primary vs. secondary gain).

Step-by-Step Solution

1
Analyze the first presentation regarding sudden blindness.
Identified as a neurological symptom inconsistent with known medical disease, pointing to conversion disorder.
Conversion disorder involves altered voluntary motor or sensory deficits without underlying neurological pathology, often following acute stress.
2
Evaluate the second presentation involving cancer preoccupation.
Recognized as illness anxiety disorder.
The patient has no significant somatic symptoms but exhibits high anxiety and preoccupation about acquiring a severe illness.
3
Assess the third presentation with abdominal pain and fatigue.
Matched with somatic symptom disorder.
The patient has actual distressing somatic symptoms paired with excessive, disproportionate thoughts, feelings, and behaviors regarding them.
4
Examine the fourth presentation involving surreptitious insulin use.
Classified as factitious disorder.
The hypoglycemia is intentionally produced to assume the sick role (primary gain), rather than for external incentives like avoiding work or obtaining compensation (secondary gain).

Key Concept

Differentiation of somatic symptom and related disorders based on symptom presence, intentionality, and underlying motivation.
Question 3348Question →

A 54-year-old man with a severe alcohol use disorder is brought to the emergency department by emergency medical services due to confusion and unsteadiness. He was found wandering in the street. His last alcoholic drink was approximately 24 hours ago. On presentation, he is diaphoretic, tachycardic (heart rate 118/min), and visibly tremulous. Neurologic examination reveals bilateral horizontal nystagmus, a wide-based ataxic gait, and profound global confusion. Point-of-care blood glucose testing shows 58 mg/dL (3.2 mmol/L). The patient is admitted to the hospital.

Arrange the following management steps in the most appropriate chronological sequence for this patient, from immediate acute stabilization to pre-discharge planning.

Drag items to arrange them in the correct order

Show answer & explanation

Answer

The correct chronological sequence is to first administer intravenous thiamine, followed by intravenous dextrose, then initiate symptom-triggered intravenous lorazepam, perform a comprehensive psychosocial evaluation, and finally initiate oral naltrexone as maintenance pharmacotherapy.
The management of severe alcohol use disorder requires a structured, chronological approach that prioritizes immediate, life-threatening conditions before addressing long-term recovery. This patient presents with the classic triad of Wernicke encephalopathy (confusion, ataxia, nystagmus) and concurrent hypoglycemia. Because thiamine is an essential cofactor for glucose metabolism, administering glucose without thiamine can precipitate severe, irreversible neurologic damage. Therefore, intravenous thiamine is the absolute first step. Immediately following thiamine, intravenous dextrose is given to correct the hypoglycemia. Once these acute metabolic derangements are addressed, the focus shifts to treating his acute alcohol withdrawal (manifested by tremor, tachycardia, and diaphoresis) using symptom-triggered benzodiazepines such as lorazepam to prevent seizures and delirium tremens. After the patient is medically cleared, sober, and free of acute withdrawal symptoms, a comprehensive psychosocial evaluation is performed to gauge his readiness for behavioral change. Finally, as part of discharge planning, maintenance pharmacotherapy such as naltrexone is initiated to reduce cravings and prevent long-term relapse.

Step-by-Step Solution

1
Identify the immediate metabolic threats: Wernicke encephalopathy and hypoglycemia.
Recognize that thiamine must precede glucose administration.
Glucose metabolism rapidly utilizes thiamine as a cofactor. Administering glucose without thiamine to a malnourished patient can severely deplete remaining stores, worsening Wernicke encephalopathy.
2
Address the life-threatening hypoglycemia.
Administer intravenous dextrose.
A blood glucose level of 58 mg/dL contributes to global confusion and must be corrected immediately after thiamine is provided.
3
Manage the acute alcohol withdrawal syndrome.
Initiate symptom-triggered intravenous lorazepam.
The patient is diaphoretic, tachycardic, and tremulous approximately 24 hours after his last drink, indicating acute withdrawal. Benzodiazepines are required to prevent progression to withdrawal seizures or delirium tremens.
4
Transition to post-acute care and recovery planning.
Perform a comprehensive psychosocial evaluation.
Medical stabilization must be fully achieved before a meaningful assessment of the patient's support system, psychiatric comorbidities, and readiness to change can be conducted.
5
Initiate relapse prevention therapy.
Prescribe oral naltrexone.
Once the patient is detoxified, oriented, and assessed, long-term pharmacotherapy is initiated prior to discharge to reduce cravings and decrease the risk of relapse.

Key Concept

Sequential management of severe alcohol use disorder requires immediate metabolic stabilization (thiamine before dextrose), followed by acute withdrawal management (benzodiazepines), and finally post-acute rehabilitation (psychosocial evaluation and maintenance pharmacotherapy).
Question 3349Question →

A 33-year-old woman, currently 14 weeks pregnant, presents to her obstetrician to evaluate a new lump in her right breast. She detected the nodule two weeks ago while bathing. The patient denies any associated pain, fever, or nipple discharge. Her family history is notable for a maternal grandmother diagnosed with breast cancer at age 70. On physical examination, a 3.0-cm, firm, mobile, non-tender mass is palpated in the upper outer quadrant of the right breast. The overlying skin is intact without dimpling, retraction, or erythema. There is no palpable axillary or supraclavicular lymphadenopathy. Which of the following is the most appropriate initial step in the evaluation of this finding?

Show answer & explanation

Answer: Sonographic evaluation of the palpable mass

Answer

The most appropriate initial step is to perform a targeted ultrasound of the palpable breast mass.
In pregnant or lactating women, any new discrete, palpable breast mass requires thorough evaluation to rule out malignancy, regardless of the patient's age. Pregnancy and lactation stimulate significant glandular hyperplasia, which dramatically increases breast tissue density. This elevated density substantially reduces the sensitivity and diagnostic utility of mammography. Consequently, targeted ultrasonography is the initial diagnostic imaging modality of choice. Ultrasound is highly sensitive for distinguishing between solid and cystic masses, is not hindered by dense glandular tissue, and involves no ionizing radiation. If the ultrasound reveals suspicious features, further evaluation with a mammogram (with appropriate fetal shielding) and/or tissue biopsy would then be indicated.

Step-by-Step Solution

1
Identify the patient's demographic and clinical status.
The patient is a 33-year-old woman presenting with a new, discrete palpable breast mass during the first trimester of pregnancy.
Age and pregnancy status dictate the diagnostic algorithm for breast masses.
2
Recall the standard diagnostic algorithm for breast masses based on age.
In nonpregnant women, targeted ultrasound is used first for those under 30, while diagnostic mammography (usually with ultrasound) is used first for those 30 and older.
This establishes the baseline protocol before applying physiological exceptions.
3
Apply the modifications required for pregnant and lactating patients.
Pregnancy causes marked glandular hyperplasia, increasing breast density and lowering the sensitivity of mammography. Therefore, ultrasound becomes the initial imaging modality of choice regardless of age.
Ultrasound avoids fetal radiation exposure and effectively differentiates solid from cystic lesions in dense breasts.

Key Concept

Evaluation of palpable breast masses during pregnancy and lactation.
Estimated Time:1m 0s
Question 3350Question →

A 21-year-old female university student presents to the student health center accompanied by a residence hall advisor. The patient is visibly distraught, weeping uncontrollably, and stating that her life is 'completely empty' after a three-week romantic relationship ended abruptly the previous night. Physical examination reveals several superficial, linear scratches on her left volar forearm. She admits to making these marks with a safety pin, stating, 'I just needed to feel something.' The advisor mentions that the patient has a history of intense, unstable friendships, often idolizing peers before suddenly turning against them. The patient's medical history includes a diagnosis of 'atypical depression,' for which she currently takes phenelzine. During the interview, she mentions that last night she briefly suspected the campus security was tracking her phone, but she now realizes this was an irrational thought. She denies any current suicidal ideation or plan. Which of the following are appropriate next steps in the ongoing management of this patient? (Select all that apply.)

Select all that apply

Show answer & explanation

Answer: Provide a referral for dialectical behavior therapy; Establish clear, firm boundaries regarding the parameters of future clinical interactions

Answer

The most appropriate management steps for this patient include referring her for dialectical behavior therapy (DBT) and establishing clear, consistent clinical boundaries.
This patient's presentation—characterized by an intense fear of abandonment, unstable relationships, emotional lability, chronic feelings of emptiness, superficial self-injury, and transient stress-related paranoia—is highly consistent with borderline personality disorder (BPD). The primary, evidence-based treatment for BPD is dialectical behavior therapy (DBT), which focuses on emotional regulation, distress tolerance, and mindfulness. Additionally, patients with BPD often test limits and engage in splitting (idealizing and then devaluing providers). Therefore, establishing clear, consistent, and firm boundaries regarding communication and clinical availability is an essential component of management to ensure a stable therapeutic framework.

Step-by-Step Solution

1
Analyze the patient's clinical presentation and history.
The patient displays emotional lability, chronic feelings of emptiness, superficial non-suicidal self-injury, intense unstable relationships, and transient stress-related paranoia.
Identifying the core pattern of symptoms is necessary to establish the primary psychiatric diagnosis of borderline personality disorder (BPD).
2
Determine the appropriate psychotherapeutic and interpersonal interventions for BPD.
Dialectical behavior therapy (DBT) is the evidence-based treatment of choice, and setting firm clinical boundaries prevents splitting and excessive dependency.
Psychotherapy is the mainstay of treatment for BPD, and clear boundaries protect both the patient and the therapeutic relationship.
3
Evaluate the proposed pharmacological and ethical interventions in the distractors.
Adding fluoxetine to phenelzine causes serotonin syndrome. Transient paranoia does not meet the timeline for schizophreniform disorder. Superficial self-harm does not justify breaching an adult's confidentiality.
To rule out contraindicated or inappropriate clinical actions based on patient safety and diagnostic criteria.

Key Concept

Management of borderline personality disorder (BPD)
Question 3351Question →

A 62-year-old woman undergoes a routine screening mammogram that reveals a new, highly suspicious 1.5-cm spiculated density with clustered microcalcifications in her left breast. She has no palpable masses or axillary lymphadenopathy on physical examination. Arrange the following interventions in the most appropriate chronological sequence for the evaluation and initial management of this patient's findings.

Drag items to arrange them in the correct order

Show answer & explanation

Answer

The correct sequence is: Targeted breast ultrasound and diagnostic mammography, followed by Image-guided core needle biopsy of the lesion, followed by Breast-conserving surgery with sentinel lymph node evaluation, and finally Adjuvant whole-breast radiation therapy.
The standard management pathway for an abnormal screening mammogram begins with diagnostic imaging (diagnostic mammography and ultrasound) to fully characterize the lesion and evaluate the rest of the breast and axilla. Once fully evaluated radiographically, an image-guided core needle biopsy is performed to establish a histological diagnosis and determine receptor status. Following the confirmation of an early-stage breast cancer, surgical resection (e.g., lumpectomy with sentinel node evaluation) is the primary treatment modality. Finally, patients who undergo breast-conserving surgery subsequently require adjuvant radiation therapy to ensure optimal local disease control.

Step-by-Step Solution

1
Identify the initial presentation
An asymptomatic postmenopausal woman with a highly suspicious finding on a screening mammogram.
This establishes that the patient has a screen-detected abnormality requiring further characterization before any intervention.
2
Determine the initial workup
Targeted breast ultrasound and diagnostic mammography.
Screening mammography only provides standard views. Diagnostic imaging is required to fully visualize the lesion, assess for additional ipsilateral or contralateral lesions, and evaluate the axilla.
3
Establish a definitive diagnosis
Image-guided core needle biopsy.
Once imaging confirms a suspicious lesion (e.g., BI-RADS 4 or 5), a tissue sample must be obtained to confirm the histological diagnosis and test for hormone receptors and HER2 amplification.
4
Plan the primary definitive treatment
Breast-conserving surgery with sentinel lymph node evaluation.
For an early-stage, localized breast malignancy, primary surgical resection is indicated for local tumor control and accurate nodal staging.
5
Determine appropriate postoperative management
Adjuvant whole-breast radiation therapy.
Patients who undergo breast-conserving surgery require adjuvant radiation therapy to eliminate residual microscopic disease and minimize local recurrence risk.

Key Concept

The standard diagnostic and therapeutic sequence for screen-detected suspicious breast lesions begins with diagnostic imaging, followed by tissue biopsy, primary surgical resection, and finally adjuvant therapies such as radiation.
Question 3352Question →

A 1919-year-old man is brought to the emergency department by his friends due to severe agitation, confusion, and muscle twitching. The friends report they were at an electronic music festival where the patient consumed an unknown pill approximately 44 hours ago. His medical history is significant for major depressive disorder, for which he has been taking sertraline for the past 66 months.

Temperature is 39.6∘C39.6^\circ\text{C} (103.3∘F103.3^\circ\text{F}), blood pressure is 168/102 mm Hg168/102 \text{ mm Hg}, pulse is 132/min132/\text{min}, and respirations are 24/min24/\text{min}.

On examination, the patient is disoriented, markedly diaphoretic, and has mydriasis. Neurologic examination reveals shivering, hyperreflexia in the lower extremities, and sustained bilateral ankle clonus.

Laboratory studies reveal:

Laboratory ParameterResultReference Range
Sodium122 mEq/L122 \text{ mEq/L}136−145 mEq/L136-145 \text{ mEq/L}
Potassium4.0 mEq/L4.0 \text{ mEq/L}3.5−5.0 mEq/L3.5-5.0 \text{ mEq/L}
Bicarbonate24 mEq/L24 \text{ mEq/L}22−28 mEq/L22-28 \text{ mEq/L}
Blood urea nitrogen10 mg/dL10 \text{ mg/dL}7−18 mg/dL7-18 \text{ mg/dL}
Creatinine0.8 mg/dL0.8 \text{ mg/dL}0.6−1.2 mg/dL0.6-1.2 \text{ mg/dL}
Thyroid-stimulating hormone (TSH)2.1 μU/mL2.1 \ \mu\text{U/mL}0.5−5.0 μU/mL0.5-5.0 \ \mu\text{U/mL}

Urine toxicology screen is positive for amphetamines.

Which of the following is the most likely underlying mechanism for this patient's acute presentation?

Show answer & explanation

Answer: Synergistic elevation of intrasynaptic serotonin levels

Answer

Synergistic elevation of intrasynaptic serotonin levels
The correct answer identifies the pathogenesis of Serotonin Syndrome. This patient's triad of altered mental status, autonomic instability (hyperthermia, tachycardia, diaphoresis), and neuromuscular excitability (hyperreflexia, clonus) is classic for Serotonin Syndrome. He ingested an unknown pill at a music festival, which, given the clinical picture and positive amphetamine screen, is highly likely to be MDMA (ecstasy). MDMA is a synthetic amphetamine derivative that promotes the massive presynaptic release of serotonin, dopamine, and norepinephrine. His home medication, sertraline, is a selective serotonin reuptake inhibitor (SSRI). The combination of a serotonin-releasing agent (MDMA) and a reuptake inhibitor (sertraline) causes a massive synergistic accumulation of serotonin in the synaptic cleft, precipitating this crisis. Furthermore, MDMA frequently causes profound hyponatremia (as seen with this patient's sodium of 122 mEq/L122 \text{ mEq/L}) via drug-induced inappropriate antidiuretic hormone secretion (SIADH) and increased free water intake, which confirms the diagnosis.

Step-by-Step Solution

1
Evaluate the clinical presentation and vital signs.
The patient exhibits hyperthermia, tachycardia, diaphoresis, and altered mental status.
These signs indicate an acute hypermetabolic toxidrome, narrowing the differential to serotonergic, sympathomimetic, or anticholinergic toxicity.
2
Analyze the specific neurologic findings.
The presence of shivering, hyperreflexia, and sustained bilateral ankle clonus is noted.
Clonus and hyperreflexia are the hallmark distinguishing features of Serotonin Syndrome, separating it from neuroleptic malignant syndrome (which presents with 'lead-pipe' rigidity) and pure sympathomimetic toxicity.
3
Correlate the toxidrome with the patient's history and lab findings.
The patient took an unknown pill (MDMA/ecstasy) while on home sertraline, and labs show severe hyponatremia without an acid-base disturbance.
MDMA promotes massive serotonin release and uniquely causes SIADH-like hyponatremia. Combining MDMA with an SSRI (sertraline) prevents serotonin clearance, leading to a life-threatening synergistic serotonergic crisis.

Key Concept

MDMA (ecstasy) intoxication combined with selective serotonin reuptake inhibitors (SSRIs) can precipitate severe serotonin syndrome. Additionally, MDMA is unique among common drugs of abuse for causing profound hyponatremia.
Question 3353Question →

A 1919-year-old male collegiate wrestler is brought to the student health center due to profound fatigue, dizziness, and muscle cramps over the past two weeks. He has been intensely focused on "making weight" for the upcoming wrestling season. His BMI is 21.5 kg/m221.5 \text{ kg/m}^2. Vital signs show temperature 37.0∘C37.0^\circ\text{C} (98.6∘F98.6^\circ\text{F}), pulse 112112/min, respirations 1212/min, and blood pressure 96/60 mm Hg96/60 \text{ mm Hg}. Physical examination reveals dry mucous membranes, bilateral parotid gland swelling, and calluses on the dorsum of his right hand. The lungs are clear to auscultation, and the heart has a regular rhythm with no murmurs.

Laboratory studies show:
Sodium: 138 mEq/L138 \text{ mEq/L}
Potassium: 2.6 mEq/L2.6 \text{ mEq/L}
Chloride: 86 mEq/L86 \text{ mEq/L}
Bicarbonate: 36 mEq/L36 \text{ mEq/L}
Thyroid-stimulating hormone (TSH): 1.2 μU/mL1.2 \text{ }\mu\text{U/mL} (normal 0.40.4-4.04.0)
Free T4: 0.7 ng/dL0.7 \text{ ng/dL} (normal 0.90.9-2.42.4)

An arterial blood gas on room air shows pH 7.527.52 and PaCO2 48 mm Hg48 \text{ mm Hg}. An ECG reveals sinus tachycardia with flattened T waves and prominent U waves.

Which of the following is the most accurate statement regarding this patient's condition?

Show answer & explanation

Answer: The arterial carbon dioxide level reflects appropriate physiological compensation.

Answer

The arterial carbon dioxide level reflects appropriate physiological compensation.
The correct answer accurately interprets the patient's acid-base status. The patient's self-induced vomiting (suggested by parotid swelling and Russell sign) has caused a hypokalemic, hypochloremic metabolic alkalosis. In metabolic alkalosis, the expected respiratory compensation (hypoventilation) is calculated as: Expected PaCO2 = 40+[0.7×(HCO3−−24)]±240 + [0.7 \times (\text{HCO}_3^- - 24)] \pm 2. For this patient, Expected PaCO2 = 40+0.7(12)=48.4±2 mm Hg40 + 0.7(12) = 48.4 \pm 2 \text{ mm Hg}. The patient's measured PaCO2 of 48 mm Hg48 \text{ mm Hg} falls perfectly within this range, indicating appropriate respiratory compensation without a superimposed respiratory acid-base disorder.

Step-by-Step Solution

1
Identify the primary psychiatric and medical diagnosis.
The patient has Bulimia Nervosa, evidenced by normal BMI, purging signs (Russell sign, parotid swelling), and volume depletion.
Recognizing the eating disorder contextualizes the electrolyte abnormalities, specifically vomiting-induced hypokalemia and metabolic alkalosis.
2
Analyze the primary acid-base disturbance.
The arterial blood gas shows alkalemia (pH 7.527.52) with a high bicarbonate (36 mEq/L36 \text{ mEq/L}), confirming a primary metabolic alkalosis.
Vomiting causes loss of gastric acid (HCl) and volume depletion, driving aldosterone-mediated bicarbonate retention and potassium wasting.
3
Calculate the expected respiratory compensation for the metabolic alkalosis.
Expected PaCO2 = 40+[0.7×(36−24)]=40+8.4=48.4 mm Hg±240 + [0.7 \times (36 - 24)] = 40 + 8.4 = 48.4 \text{ mm Hg} \pm 2.
To determine if there is a mixed acid-base disorder, the measured PaCO2 (48 mm Hg48 \text{ mm Hg}) must be compared to the expected PaCO2 (46.4−50.4 mm Hg46.4 - 50.4 \text{ mm Hg}). Since it falls within the range, compensation is appropriate.

Key Concept

Metabolic complications of purging behavior and acid-base compensation calculations

Alternative Method

When evaluating complex patients, group the findings by organ system. The calluses and parotid swelling quickly isolate the psychiatric diagnosis (Bulimia Nervosa). The labs isolate the nephrology diagnosis (metabolic alkalosis). Evaluating the answers sequentially against these isolated domains saves time.
Estimated Time:1m 30s
Question 3354Question →

An outpatient psychiatric consultation is requested for a 42-year-old female patient experiencing debilitating, multi-domain worry. Over the last 7 months, she has been unable to control her persistent apprehension regarding her career stability, household finances, and the well-being of her children. These pervasive concerns are accompanied by chronic cervical muscle tension, poor concentration, and prominent fatigue. She denies any prior manic or hypomanic episodes.

Four weeks ago, the patient began taking phenelzine for refractory atypical depression. While her mood has significantly brightened, her anxiety symptoms have remained unchanged. At age 20, she experienced a discrete 14-day period characterized by intense auditory hallucinations and paranoid delusions, which resolved entirely without long-term sequelae.

Midway through the consultation, the clinic's front desk forwards a phone call from the patient's supervisor. The supervisor wishes to verify that the patient is receiving medical care so that her paid leave can be formally approved. The patient has not completed any release of information forms.

Recent laboratory investigations reveal:
Thyroid-stimulating hormone (TSH): 2.4 µU/mL (normal: 0.5-5.0 µU/mL)
Free thyroxine (T4): 0.5 ng/dL (normal: 0.9-1.7 ng/dL)

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

Show answer & explanation

Answer: Recommend structured psychotherapy aimed at cognitive restructuring

Answer

Recommend structured psychotherapy aimed at cognitive restructuring
The correct answer recommends structured psychotherapy aimed at cognitive restructuring (Cognitive-Behavioral Therapy, CBT). This patient meets the DSM-5 criteria for Generalized Anxiety Disorder (GAD), characterized by excessive worry across multiple domains for at least 6 months, accompanied by somatic symptoms such as muscle tension and fatigue. Both CBT and selective serotonin reuptake inhibitors (SSRIs) are first-line treatments for GAD. However, this patient was recently started on phenelzine, a monoamine oxidase inhibitor (MAOI). The concomitant use of an MAOI and a serotonergic agent (like an SSRI) is absolutely contraindicated due to the high risk of precipitating potentially fatal serotonin syndrome. Therefore, initiating a non-pharmacologic first-line therapy like CBT is the safest and most appropriate next step.

Step-by-Step Solution

1
Analyze the patient's primary psychiatric symptoms.
The patient presents with 7 months of excessive, multi-domain worry, fatigue, and muscle tension.
These symptoms fulfill the DSM-5 diagnostic criteria for Generalized Anxiety Disorder (GAD).
2
Identify contraindications in the current medication regimen.
The patient is taking phenelzine, a monoamine oxidase inhibitor (MAOI).
MAOIs can cause life-threatening serotonin syndrome if combined with serotonergic medications like SSRIs or SNRIs, ruling out first-line pharmacotherapy for GAD.
3
Evaluate laboratory results to rule out medical mimics.
TSH is normal and Free T4 is low.
This pattern indicates central (secondary) hypothyroidism, not primary hypothyroidism (which presents with elevated TSH). Additionally, hypothyroidism causes fatigue rather than the excessive worry typical of GAD.
4
Determine the safest and most effective management step while maintaining ethical boundaries.
Recommend structured psychotherapy (CBT).
CBT is a first-line treatment for GAD, avoids the fatal risk of serotonin syndrome, and properly addresses her primary complaint without violating patient confidentiality.

Key Concept

First-line management of Generalized Anxiety Disorder (GAD) involves CBT or SSRI/SNRIs; however, CBT is the safest and most appropriate choice when pharmacotherapy is absolutely contraindicated (e.g., concurrent MAOI use).
Estimated Time:1m 30s
Question 3355Question →

An emergency medical team brings a 35-year-old woman to the hospital due to the acute onset of confusion, severe agitation, and muscle twitching. The patient's husband reports that she has a long-standing history of treatment-resistant depression that has been managed with phenelzine for the past year. Four days ago, she consulted a different clinician for persistent low mood and was started on an additional psychiatric medication. Her vital signs show a temperature of 39.4°C (102.9°F), pulse of 124/min, respirations of 20/min, and blood pressure of 165/95 mm Hg. Physical examination reveals profuse diaphoresis, dilated pupils, a bilateral resting tremor, and pronounced hyperreflexia with spontaneous clonus in the lower extremities. The addition of which of the following medications most likely precipitated this patient's current condition?

Show answer & explanation

Answer: Citalopram

Answer

Citalopram
The correct answer is citalopram. This patient is experiencing serotonin syndrome, a potentially life-threatening condition characterized by the classic triad of altered mental status (confusion, agitation), autonomic instability (hyperthermia, tachycardia, diaphoresis), and neuromuscular hyperactivity (hyperreflexia, spontaneous clonus, tremor). This syndrome is most often precipitated by the concurrent use of two or more highly serotonergic medications. Phenelzine is an irreversible monoamine oxidase inhibitor (MAOI) that prevents the enzymatic breakdown of serotonin. Adding a selective serotonin reuptake inhibitor (SSRI) such as citalopram leads to a massive and rapid accumulation of synaptic serotonin, triggering this dangerous interaction. In clinical practice, MAOIs must be discontinued for at least 14 days before initiating an SSRI (and wait 5 weeks if switching from fluoxetine to an MAOI).

Step-by-Step Solution

1
Identify the clinical syndrome based on the physical examination and vital signs.
The patient exhibits fever, tachycardia, hypertension, altered mental status, diaphoresis, and severe neuromuscular hyperactivity (hyperreflexia and spontaneous clonus), which is the classic triad of Serotonin Syndrome.
Recognizing the distinct neuromuscular signs (clonus/hyperreflexia) helps differentiate Serotonin Syndrome from Neuroleptic Malignant Syndrome (which presents with rigidity).
2
Review the patient's baseline medication list to identify predisposing factors.
The patient takes phenelzine, which is a monoamine oxidase inhibitor (MAOI) that strongly inhibits the breakdown of serotonin in the central nervous system.
MAOIs carry a severe risk of drug-drug interactions, particularly with other serotonergic agents.
3
Determine which newly added psychiatric medication could trigger this syndrome when combined with an MAOI.
Citalopram, a selective serotonin reuptake inhibitor (SSRI), blocks serotonin reuptake. Combining it with an MAOI leads to massive serotonin accumulation.
A minimum 14-day washout period is required when switching between SSRIs and MAOIs to prevent this exact complication.

Key Concept

Serotonin syndrome resulting from the combination of a monoamine oxidase inhibitor (MAOI) and a selective serotonin reuptake inhibitor (SSRI).
Question 3356Question →

During a routine home-visit evaluation, a geriatric psychiatrist examines a 73-year-old man whose daughter reports a 9-month history of progressive cognitive decline and unusual behaviors. The daughter emphasizes that his mental clarity fluctuates dramatically; he can be highly alert in the morning but profoundly lethargic and disorganized by the afternoon. Over the past 3 months, he has started seeing "strangers sitting on the living room couch," which causes him significant distress and agitation. For the past 4 years, he has exhibited violent thrashing and shouting movements during sleep. His medical history is significant for major depressive disorder, for which he has taken fluoxetine continuously for the last 5 years. Vital signs are within normal limits. Neurologic examination demonstrates bilateral cogwheel rigidity and a mild resting tremor in the left upper extremity. His Montreal Cognitive Assessment score is 20/30, featuring prominent deficits in visuospatial construction. The physician discusses management options with the daughter to address the patient's distressing visual hallucinations. Which of the following is the most appropriate next step in the pharmacologic management of this patient's condition?

Show answer & explanation

Answer: Initiate a central acetylcholinesterase inhibitor

Answer

The correct answer is to initiate a central acetylcholinesterase inhibitor.
The correct answer involves initiating a central acetylcholinesterase inhibitor (such as rivastigmine or donepezil). This patient's presentation of progressive cognitive decline, prominent fluctuations in alertness, recurrent well-formed visual hallucinations, parkinsonism (rigidity, resting tremor), and REM sleep behavior disorder is the classic clinical triad/tetrad for Major Neurocognitive Disorder with Lewy Bodies (DLB). In patients with DLB, acetylcholinesterase inhibitors are considered the first-line pharmacotherapy. They effectively reduce the frequency and severity of visual hallucinations and improve cognitive fluctuations. Importantly, they achieve this without carrying the severe morbidity and mortality risks associated with antipsychotic medications in this specific patient population.

Step-by-Step Solution

1
Identify the primary underlying syndrome based on the clinical presentation.
The combination of fluctuating cognition, well-formed visual hallucinations, parkinsonism (rigidity, resting tremor), and REM sleep behavior disorder establishes a diagnosis of Major Neurocognitive Disorder with Lewy Bodies (DLB).
Accurate diagnosis is required because DLB has unique pharmacological sensitivities compared to other neurocognitive disorders.
2
Determine the primary goal of the requested intervention.
The patient requires management for distressing visual hallucinations and agitation.
Treatment should target the specific symptom causing the most distress while avoiding harm to the patient.
3
Select the safest and most effective initial pharmacotherapy for DLB.
Central acetylcholinesterase inhibitors (e.g., rivastigmine, donepezil) are the treatment of choice.
These medications safely improve both cognitive and neuropsychiatric symptoms (including hallucinations) in DLB without the severe risks associated with antipsychotics.
4
Evaluate the remaining options for dangerous drug interactions or contraindications.
Haloperidol is ruled out due to the risk of severe neuroleptic sensitivity in DLB; selegiline is ruled out due to the risk of Serotonin Syndrome when combined with the patient's current fluoxetine prescription.
Ruling out dangerous psychopharmacological interactions confirms the safety and necessity of the correct choice.

Key Concept

Major Neurocognitive Disorder with Lewy Bodies presents with fluctuating cognition, visual hallucinations, parkinsonism, and REM sleep behavior disorder; initial pharmacotherapy for cognitive and behavioral symptoms should utilize acetylcholinesterase inhibitors while strictly avoiding typical antipsychotics.
Question 3357Question →

Match each clinical vignette with the most appropriate psychiatric diagnosis from the somatic symptom and related disorders spectrum.

Click a left item, then click its matching right item

Items

A 28-year-old female medical resident is admitted for profound hypoglycemia (glucose 32 mg/dL). Labs show elevated insulin and low C-peptide. She denies medication use, tearfully demands a pancreatectomy for 'suspected insulinoma,' and has no external incentives.
A 45-year-old man involved in litigation following a minor car accident claims severe neck pain and cognitive disability. On formal neuropsychological testing, his performance is markedly worse than patients with severe brain injuries, showing inconsistent effort.
A 42-year-old man with occasional, mild caffeine-induced muscle twitches visits the clinic weekly, terrified he has Huntington disease. He spends hours daily researching the disease and checking his gait, despite consistently normal neurological exams.
A 38-year-old woman with a 3-year history of non-cardiac chest pain and fatigue has had multiple negative cardiac catheterizations. She states the pain is constantly on her mind and quit her job to rest, fearing an imminent heart attack.
A 25-year-old man develops sudden-onset right arm weakness after a marital argument. Examination reveals weakness during active elbow flexion but simultaneous palpable contraction of the triceps. He exhibits 'la belle indifférence' toward his deficit.

Matches

Show answer & explanation

Answer

Vignette 1 maps to Factitious disorder; Vignette 2 to Malingering; Vignette 3 to Illness anxiety disorder; Vignette 4 to Somatic symptom disorder; Vignette 5 to Functional neurological symptom disorder.
Each vignette provides pathognomonic clues to differentiate the psychiatric diagnoses. Intentional production with no external gain is factitious disorder; intentional production for external gain is malingering. Unconscious production with minimal symptoms but high disease fear is illness anxiety disorder; unconscious production with prominent physical symptoms is somatic symptom disorder; and incompatible neurologic findings indicate conversion disorder.

Step-by-Step Solution

1
Determine if the symptoms are intentionally produced or unconsciously experienced.
Vignettes 1 and 2 feature conscious deception; Vignettes 3, 4, and 5 involve unconscious symptom generation.
Establishing intent is the first critical branch point in evaluating somatic and factitious presentations.
2
Evaluate the motivation for the intentionally produced symptoms.
Vignette 1 involves primary gain (assuming the sick role) indicating Factitious disorder. Vignette 2 involves secondary gain (financial compensation) indicating Malingering.
The distinction between factitious disorder and malingering relies entirely on the presence or absence of an external incentive.
3
Analyze the focus of anxiety and symptom burden for the unconsciously produced symptoms.
Vignette 3 focuses on disease fear with minimal symptoms (Illness anxiety disorder). Vignette 4 focuses on prominent physical symptoms (Somatic symptom disorder). Vignette 5 presents with an anatomically incompatible neurological deficit (Functional neurological symptom disorder).
DSM-5 criteria differentiate these disorders based on symptom severity, chronicity, and specific neurologic incompatibility.

Key Concept

Differentiation of somatic symptom and related disorders based on intent, motivation, and symptom focus.
Question 3358Question →

An accompanying friend brings a 2323-year-old female ballet dancer to the emergency department after the patient experienced an episode of syncope during a rehearsal. The friend notes that the patient has been increasingly obsessed with her weight, often skipping meals and expressing intense fear of becoming overweight despite appearing remarkably thin. Her current body mass index is 17.1 kg/m217.1 \text{ kg/m}^2.

On physical examination, blood pressure is 86/52 mmHg86/52 \text{ mmHg} and heart rate is 114/min114/\text{min}. Tapping over the facial nerve elicits a twitch of the nose and lips.

Initial laboratory studies reveal:

Laboratory TestResultReference Range
Sodium133 mEq/L133 \text{ mEq/L}136−145 mEq/L136-145 \text{ mEq/L}
Potassium2.2 mEq/L2.2 \text{ mEq/L}3.5−5.0 mEq/L3.5-5.0 \text{ mEq/L}
Chloride80 mEq/L80 \text{ mEq/L}95−105 mEq/L95-105 \text{ mEq/L}
Bicarbonate39 mEq/L39 \text{ mEq/L}22−28 mEq/L22-28 \text{ mEq/L}
Blood urea nitrogen42 mg/dL42 \text{ mg/dL}7−18 mg/dL7-18 \text{ mg/dL}
Creatinine1.5 mg/dL1.5 \text{ mg/dL}0.6−1.2 mg/dL0.6-1.2 \text{ mg/dL}
Ionized calcium3.6 mg/dL3.6 \text{ mg/dL}4.5−5.6 mg/dL4.5-5.6 \text{ mg/dL}
Magnesium1.0 mg/dL1.0 \text{ mg/dL}1.7−2.2 mg/dL1.7-2.2 \text{ mg/dL}

Arterial blood gas (room air):

ParameterResult
pH7.557.55
pCO2_249 mmHg49 \text{ mmHg}
pO2_294 mmHg94 \text{ mmHg}

Random urine studies:

TestResult
Urine chloride55 mEq/L55 \text{ mEq/L}

Which of the following is the most likely etiology of this patient's laboratory abnormalities?

Show answer & explanation

Answer: Pharmacological inhibition of the thick ascending limb sodium-potassium-chloride cotransporter

Answer

The correct etiology is the pharmacological inhibition of the thick ascending limb sodium-potassium-chloride cotransporter (covert loop diuretic abuse).
The correct answer describes the mechanism of action of loop diuretics, which inhibit the Na +^+-K +^+-22 Cl −^- cotransporter in the thick ascending limb of the loop of Henle. This patient, an elite dancer with body image distortion and a remarkably low BMI, suffers from an eating disorder. Her presentation of hypokalemia, hypochloremia, and profound metabolic alkalosis points to a purging mechanism. The critical distinguishing factor is her elevated random urine chloride (55 mEq/L55 \text{ mEq/L}). While vomiting (another common purging method) causes metabolic alkalosis, it is associated with a low urine chloride (<20 mEq/L<20 \text{ mEq/L}) because the functioning kidneys avidly reabsorb sodium and chloride to restore intravascular volume. In contrast, active diuretic use blocks chloride reabsorption, leading to high urine chloride despite systemic hypovolemia (evidenced by her elevated BUN/creatinine ratio). Furthermore, loop diuretics increase calcium excretion, explaining her hypocalcemia and resulting tetany (Chvostek sign), whereas thiazides would typically cause hypercalcemia.

Step-by-Step Solution

1
Analyze the arterial blood gas and serum electrolyte values.
The patient has a primary metabolic alkalosis (pH 7.557.55, HCO 3−_3^- 39 mEq/L39 \text{ mEq/L}) with appropriate respiratory compensation (pCO 2_2 49 mmHg49 \text{ mmHg}).
Establishing the primary acid-base disorder is the crucial first step in narrowing the differential diagnosis.
2
Evaluate the urine chloride concentration.
The urine chloride is elevated (55 mEq/L55 \text{ mEq/L}), indicating a saline-unresponsive etiology.
Urine chloride helps distinguish between volume-depleted states where the kidney reabsorbs chloride (e.g., vomiting, <20 mEq/L<20 \text{ mEq/L}) and states where chloride reabsorption is blocked (e.g., diuretic use, >20 mEq/L>20 \text{ mEq/L}).
3
Correlate physical findings and remaining electrolytes with the suspected etiology.
The hypocalcemia (3.6 mg/dL3.6 \text{ mg/dL}) causing Chvostek sign, along with hypomagnesemia, confirms the use of loop diuretics rather than thiazides.
Loop diuretics increase urinary calcium excretion, leading to hypocalcemia, whereas thiazide diuretics decrease urinary calcium excretion.

Key Concept

In patients with eating disorders, identifying the specific purging behavior relies on acid-base and electrolyte patterns. Loop diuretic abuse uniquely presents with hypokalemic, hypochloremic metabolic alkalosis, elevated urine chloride (>20 mEq/L>20 \text{ mEq/L}), and hypocalcemia.
Question 3359Question →

Emergency medical responders transport a 48-year-old male to the trauma bay after he was found obtunded in his apartment. According to his live-in girlfriend, the patient has a history of treatment-resistant depression managed with phenelzine. She notes that over the past two days, he consumed multiple bottles of over-the-counter dextromethorphan for an upper respiratory infection. Vital signs upon arrival include a temperature of 39.9∘C39.9^\circ\text{C} (103.8∘F103.8^\circ\text{F}), heart rate of 132/min132/\text{min}, blood pressure of 170/105 mm Hg170/105\text{ mm Hg}, and respiratory rate of 24/min24/\text{min}. Physical examination is remarkable for profuse diaphoresis, hyperactive bowel sounds, and pronounced hyperreflexia with bilateral ankle clonus. The patient is stuporous and unable to communicate. A review of the electronic medical record reveals a legally executed advance directive designating the patient's sister as his sole healthcare proxy. Reached by telephone, the sister unequivocally requests that all life-sustaining and necessary medical treatments be provided. However, the girlfriend, who is present at the bedside, demands that no interventions be initiated, claiming the patient recently expressed a desire to 'die naturally without medical interference.' Which of the following is the most appropriate next step in the management of this patient?

Show answer & explanation

Answer: Initiate cyproheptadine and supportive care in accordance with the sister's directive.

Answer

Initiate cyproheptadine and supportive care in accordance with the sister's directive.
The correct answer accurately combines the medical management of serotonin syndrome with appropriate ethical decision-making. The patient's presentation of autonomic instability, altered mental status, and marked neuromuscular hyperactivity (hyperreflexia, clonus) in the setting of phenelzine and dextromethorphan ingestion is classic for serotonin syndrome. The primary treatment includes supportive care and the serotonin antagonist cyproheptadine. Ethically, because the patient lacks capacity, the physician must rely on the legally appointed healthcare proxy—in this case, the sister—whose decisions override the informal requests of the live-in girlfriend.

Step-by-Step Solution

1
Diagnose the underlying acute medical emergency based on history and physical exam.
The combination of an MAOI (phenelzine), dextromethorphan, hyperthermia, autonomic instability, hyperactive bowel sounds, and hyperreflexia with clonus firmly points to Serotonin Syndrome.
Accurate identification of the toxidrome dictates the need for specific antidotal therapy (cyproheptadine) over contraindicated medications.
2
Assess the patient's decision-making capacity.
The patient is stuporous and unable to communicate, meaning he lacks the capacity to make his own medical decisions.
When a patient lacks capacity, a surrogate decision-maker must be identified to guide care.
3
Determine the legal surrogate decision-maker.
The electronic medical record explicitly names the sister as the designated healthcare proxy via a legally executed advance directive.
A legally designated proxy supersedes informal caregivers, partners, or next-of-kin who are not named in the directive.
4
Execute the management plan.
Proceed with the administration of cyproheptadine and aggressive supportive care (e.g., cooling, intravenous fluids, benzodiazepines) as authorized by the sister.
This aligns with both the correct medical protocol for serotonin syndrome and the legal/ethical framework of surrogate decision-making.

Key Concept

Management of Serotonin Syndrome and proper identification of the legal healthcare proxy in incapacitated patients.
Question 3360Question →

During morning rounds on the surgical ward, a 62-year-old woman complains of new-onset pain around her incision and burning with urination. She is currently on postoperative day 6 following a total abdominal hysterectomy for symptomatic uterine fibroids. Her indwelling urinary catheter was removed 48 hours ago. Her temperature is 38.6°C (101.5°F), blood pressure is 122/78 mmHg, heart rate is 94/min, and respiratory rate is 16/min. Examination of the abdomen reveals significant erythema, induration, and a small amount of purulent drainage at the surgical incision site. Auscultation of the lungs reveals clear breath sounds bilaterally. Which of the following are the most appropriate next steps in the management of this patient? (Select all that apply)

Select all that apply

Show answer & explanation

Answer: Open the surgical incision to allow for adequate drainage; Perform a microscopic urinalysis and send a urine sample for culture

Answer

The correct steps are to open the surgical incision to allow for adequate drainage AND perform a microscopic urinalysis while sending a urine sample for culture.
This patient presents with a fever on postoperative day 6 along with two distinct sources of infection: a surgical site infection (SSI) and a likely urinary tract infection (UTI). The definitive initial management for a superficial SSI with purulent drainage is to open the wound to allow for proper drainage and healing by secondary intention. Simultaneously, her dysuria following Foley catheter removal warrants a urinalysis and urine culture to confirm a UTI and guide specific antibiotic therapy.

Step-by-Step Solution

1
Analyze the timing of the fever and physical exam findings.
The patient has a fever on postoperative day 6 with a purulent abdominal wound and dysuria.
Postoperative fever etiologies correlate strongly with the timeline. POD 6 fevers are classically associated with wound infections or deep space infections, while the recent catheter removal and dysuria point to a urinary tract infection.
2
Determine the appropriate management for the wound finding.
The presence of purulence and induration indicates a surgical site infection. The primary treatment is source control.
Superficial surgical site infections are primarily managed by opening the incision, draining the purulent material, and packing the wound. Systemic antibiotics are often unnecessary unless there is overlying cellulitis or systemic toxicity.
3
Determine the appropriate diagnostic step for the urinary symptoms.
A urinalysis and urine culture must be obtained.
Catheter-associated urinary tract infections are a common cause of postoperative fever, and targeted antibiotic therapy requires identification of the offending organism via culture.

Key Concept

Diagnosis and management of common postoperative complications based on the timeline, specifically surgical site infections (POD 5-7) and urinary tract infections (POD 3-5).
PreviousPage 168 / 414Next