All practice questions

8270 questions

Question 121Question →

A 55-year-old boy is brought to the clinic by his parents due to rapid growth, facial acne, and the development of pubic hair over the past 66 months. The parents also report that he has recently developed adult-type body odor. His height is at the 9999 th percentile for his age, whereas it was at the 5050 th percentile one year ago. His weight is at the 9090 th percentile. Vital signs are within normal limits. Physical examination reveals coarse, dark pubic hair (Tanner stage III) and facial acne. Genitourinary examination shows a stretched penile length of 66 cm and bilaterally enlarged, symmetric testes with a volume of 88 mL each. Neurologic examination is unremarkable.

Laboratory studies show:
Testosterone: 180180 ng/dL (Normal prepubertal: <30<30 ng/dL)
Basal luteinizing hormone (LH): 0.10.1 mIU/mL (Normal prepubertal: <0.3<0.3 mIU/mL)
Thyroid-stimulating hormone (TSH): 1.81.8 μ\mu U/mL

A radiograph of the left hand and wrist reveals a bone age of 88 years.

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

Show answer & explanation

Answer: Administration of exogenous leuprolide and measurement of subsequent luteinizing hormone levels

Answer

Administration of exogenous leuprolide and measurement of subsequent luteinizing hormone levels
The correct next step is a GnRH stimulation test (leuprolide administration). This patient presents with precocious puberty (advanced bone age, rapid growth, virilization). His bilaterally enlarged testes (88 mL) strongly suggest gonadotropin-dependent (central) precocious puberty (CPP). However, his basal LH is prepubertal (0.10.1 mIU/mL). Because LH is secreted in a pulsatile manner, a single basal LH measurement can be falsely reassuring in early CPP. Therefore, standard algorithms mandate a GnRH stimulation test to differentiate CPP (which will show a robust LH surge) from peripheral precocious puberty (which will show a suppressed LH response).

Step-by-Step Solution

1
Analyze the patient's physical examination and growth parameters.
The patient has advanced bone age, linear growth acceleration, virilization, and bilateral testicular enlargement (88 mL).
Testicular volume >4>4 mL indicates activation of the hypothalamic-pituitary-gonadal (HPG) axis, pointing toward Central Precocious Puberty (CPP) or a rare peripheral disorder like testotoxicosis.
2
Evaluate the laboratory results in the context of the physical exam.
Testosterone is high, confirming precocious puberty. However, the basal LH is 0.10.1 mIU/mL, which is in the prepubertal range (<0.3<0.3 mIU/mL).
Because LH secretion is pulsatile, a single basal LH level may be low even in early CPP.
3
Determine the algorithmic next step for advanced bone age and low basal LH.
A GnRH stimulation test (using a GnRH agonist like leuprolide) must be performed.
If the stimulated LH rises to pubertal levels, it confirms CPP, and a brain MRI is the subsequent step. If the stimulated LH remains suppressed, it confirms peripheral precocious puberty (e.g., testotoxicosis), necessitating targeted imaging of the testes or adrenal glands.

Key Concept

In the evaluation of precocious puberty, bilateral testicular enlargement suggests central precocious puberty, but a GnRH stimulation test is required to biochemically confirm HPG axis activation if the basal LH is in the prepubertal range.
Question 122Question →

A 66-month-old boy is brought to the clinic by his parents due to abnormal movements. Over the past 22 weeks, he has had multiple episodes daily where he suddenly bends his head and trunk forward while stiffening his arms. These episodes occur in clusters, most often just after waking up from a nap. The parents are also highly concerned about his development because he has not yet begun to crawl or pull himself to a stand, though he rolls over in both directions and babbles. Vital signs are within normal limits. Neurologic examination shows a slightly hypotonic infant. Skin examination reveals three 2-cm2\text{-cm}, elliptical, hypopigmented macules on his trunk that are accentuated under a Wood lamp. Laboratory studies show a thyroid-stimulating hormone (TSH) level of 2.5 μU/mL2.5\ \mu\text{U/mL} and a free T4 of 1.2 ng/dL1.2\ \text{ng/dL}. An electroencephalogram demonstrates a high-voltage, chaotic, slow-wave background with multifocal spikes. Which of the following is the most appropriate next step in management?

Show answer & explanation

Answer: Initiation of vigabatrin

Answer

The most appropriate next step in management is the initiation of vigabatrin.
This patient presents with classic infantile spasms (clusters of symmetric spasms upon awakening, hypsarrhythmia on electroencephalogram) and ash-leaf spots (elliptical, hypopigmented macules that fluoresce under a Wood lamp). This combination is highly suggestive of Tuberous Sclerosis Complex. Vigabatrin is an irreversible inhibitor of GABA transaminase and is the specific first-line treatment of choice for infantile spasms in patients with Tuberous Sclerosis Complex.

Step-by-Step Solution

1
Identify the clinical syndrome based on the seizure semiology and electroencephalogram findings.
The patient has infantile spasms (West syndrome), characterized by clusters of flexion/extension spasms and hypsarrhythmia on electroencephalogram.
Establishing the primary neurologic presentation is required before determining the underlying etiology.
2
Correlate the neurologic presentation with the dermatologic findings.
The presence of infantile spasms alongside ash-leaf spots (hypopigmented macules that fluoresce) confirms a diagnosis of Tuberous Sclerosis Complex.
The underlying etiology dictates the specific targeted pharmacotherapy for the seizures.
3
Select the most appropriate first-line medication for this specific condition.
Vigabatrin is indicated.
While adrenocorticotropic hormone (ACTH) is first-line for idiopathic infantile spasms, vigabatrin is the specific drug of choice for infantile spasms associated with Tuberous Sclerosis Complex.

Key Concept

Vigabatrin is the first-line treatment for infantile spasms associated with Tuberous Sclerosis Complex.
Estimated Time:1m 15s
Question 123Question →

Correlate each of the following clinical encounters or professional scenarios with the legally or ethically mandated next step regarding disclosure.

Click a left item, then click its matching right item

Items

A toddler displaying symmetric lower extremity scald injuries that the guardian attributes to an accidental slip into a hot shower.
An octogenarian whose live-in relative refuses to allow private clinical interviews and is actively diverting the patient's retirement funds.
An attending interventionalist who smells strongly of ethanol and exhibits motor tremors immediately prior to a scheduled angiogram.
A married, competent young adult requesting an elective medical pregnancy termination while demanding absolute secrecy from their spouse.
A sexually active adult whose nucleic acid amplification test confirms an active infection with Neisseria gonorrhoeae.

Matches

Show answer & explanation

Answer

The toddler with burns maps to Child Protective Services. The exploited octogenarian maps to Adult Protective Services. The impaired interventionalist maps to the Physician Health Program. The abortion request maps to maintaining confidentiality. The Neisseria gonorrhoeae infection maps to the Department of Public Health.
Each scenario represents a distinct legal or ethical pillar of medical practice. Child Protective Services and Adult Protective Services are designated for vulnerable populations suffering abuse. The Physician Health Program manages professional impairment to protect the public. The Department of Public Health handles communicable diseases. Conversely, a competent adult seeking an abortion does not fall under any reporting exception, making confidentiality the only correct action.

Step-by-Step Solution

1
Analyze the pediatric scenario (toddler with burns).
Identify suspicion of child abuse due to an incompatible mechanism of injury.
Stocking-glove pattern immersion burns require immediate mandatory reporting to CPS.
2
Analyze the geriatric scenario (diverted funds).
Identify financial and potential emotional elder abuse.
Vulnerable adults and elders require mandated reporting to APS when exploitation is suspected.
3
Analyze the professional scenario (intoxicated attending).
Identify a medically impaired colleague posing imminent patient harm.
Ethical and legal guidelines mandate reporting impaired colleagues to supervisory clinical entities or a state-approved PHP.
4
Analyze the reproductive health scenario (abortion request).
Recognize a competent adult exercising medical autonomy.
There is no mandatory reporting to spouses; breaking HIPAA here is a legal violation.
5
Analyze the infectious disease scenario (gonorrhea).
Identify a reportable sexually transmitted disease.
Public health law requires clinicians to report specific communicable diseases to the DPH.

Key Concept

Physicians must balance standard patient confidentiality with specific statutory mandates requiring the disclosure of suspected child or elder abuse, certain communicable diseases, and impaired colleagues.
Question 124Question →

An internal medicine rapid response team is activated for a 6868-year-old hospitalized male who developed profound lower extremity weakness and lethargy. The patient was admitted two days ago for a diabetic foot infection and is receiving intravenous piperacillin-tazobactam. His home medications, including lisinopril and spironolactone for heart failure with reduced ejection fraction, were continued on admission. Over the past 1212 hours, his urine output has dropped significantly to 150150 mL. Vital signs demonstrate a heart rate of 4242/min and a blood pressure of 98/6098/60 mmHg. A point-of-care basic metabolic panel reveals a serum potassium of 7.87.8 mEq/L and a serum creatinine of 3.23.2 mg/dL (baseline 1.41.4 mg/dL). A stat 1212-lead electrocardiogram demonstrates widened QRS complexes, absent P waves, and peaked T waves.

Arrange the following management steps in the most appropriate chronological sequence for this patient's acute presentation, from the most immediate intervention to subsequent actions.

Drag items to arrange them in the correct order

Show answer & explanation

Answer

The correct sequence is: 1) Administer intravenous calcium gluconate, 2) Infuse intravenous regular insulin with dextrose, 3) Administer an enteral potassium-binding resin, 4) Discontinue lisinopril and spironolactone, 5) Prepare for urgent hemodialysis.
The algorithm for severe hyperkalemia dictates that life-saving membrane stabilization with intravenous calcium (onset 1-3 minutes) must occur first. This is immediately followed by agents that shift potassium into cells (insulin/dextrose, onset 15-30 minutes) to buy time. Next, definitive elimination therapies like gastrointestinal binders (onset 2-6 hours) are given, alongside stopping offending agents (ACE inhibitors/MRAs) to prevent recurrence. Finally, if conservative measures fail or the patient remains anuric, hemodialysis serves as the ultimate rescue therapy.

Step-by-Step Solution

1
Recognize severe, symptomatic hyperkalemia with cardiotoxicity.
Identification of a life-threatening emergency requiring immediate membrane stabilization.
The patient's potassium is critically high (7.87.8 mEq/L) with corresponding bradycardia and widened QRS complexes, indicating imminent risk of cardiac arrest.
2
Prioritize rapid-acting pharmacological interventions based on time to onset.
Intravenous calcium gluconate is administered first (onset 1-3 minutes), followed by insulin and dextrose (onset 15-30 minutes).
Myocardial stabilization must occur before shifting agents take effect to prevent fatal arrhythmias during the interim.
3
Implement measures for total body potassium reduction and secondary prevention.
Gastrointestinal binders are administered (onset in hours), and offending medications are halted.
Intracellular shifting is only temporary. True elimination of potassium is required for definitive resolution.
4
Establish a rescue plan for refractory hyperkalemia.
Preparation for hemodialysis is initiated.
The patient has severe acute kidney injury with oliguria, making pharmacological elimination unreliable.

Key Concept

The algorithmic pharmacological management of severe hyperkalemia follows a strict physiological hierarchy based on time-to-onset: membrane stabilization, followed by intracellular shifting, and finally, total body elimination.
Estimated Time:1m 30s
Question 125Question →

An 18-month-old boy is brought to the pediatric pulmonology clinic due to persistent respiratory difficulties. Three months ago, he was hospitalized in the pediatric intensive care unit for a severe lower respiratory tract infection caused by *Adenovirus*, which required mechanical ventilation for seven days. Since discharge, he has exhibited continuous tachypnea, a daily wet cough, and audible wheezing. The patient has had no recent fever or rhinorrhea. Two separate five-day courses of oral prednisolone and regular administration of nebulized albuterol have provided no symptomatic relief. On physical examination, his temperature is 37.1∘C37.1^\circ\text{C} (98.8∘F98.8^\circ\text{F}), heart rate is 130/min130/\text{min}, respiratory rate is 52/min52/\text{min}, and oxygen saturation is 91%91\% on room air. Pulmonary auscultation reveals diffuse, bilateral expiratory wheezes and coarse crackles. A chest radiograph demonstrates bilateral hyperinflation without focal consolidation. Which of the following is the most appropriate next step in the evaluation or management of this patient?

Show answer & explanation

Answer: High-resolution computed tomography of the chest

Answer

High-resolution computed tomography of the chest
The correct answer is high-resolution computed tomography of the chest. This patient's clinical presentation—persistent tachypnea, wheezing, and hypoxemia that are unresponsive to bronchodilators and systemic corticosteroids following a severe lower respiratory tract infection—is classic for post-infectious constrictive bronchiolitis (bronchiolitis obliterans). Adenovirus is a notorious trigger for this condition, causing severe necrotizing damage to the respiratory epithelium that heals with submucosal fibrosis and fixed narrowing of the bronchioles. Because the obstruction is fibrotic and fixed, it does not respond to asthma therapies. The diagnostic test of choice is a high-resolution CT scan of the chest, which typically demonstrates a mosaic pattern of attenuation (patchy areas of varied lung density) due to regional air trapping and secondary hypoxic vasoconstriction.

Step-by-Step Solution

1
Analyze the patient's history and prior interventions.
The patient has a history of severe adenovirus infection followed by 3 months of continuous respiratory distress that is completely unresponsive to bronchodilators and systemic corticosteroids.
Identifying the lack of response to asthma medications rules out reversible airway disease and points toward a fixed structural or fibrotic airway obstruction.
2
Correlate the clinical presentation with the preceding viral illness.
Severe adenovirus pneumonia in infancy is classically associated with the development of post-infectious constrictive bronchiolitis (bronchiolitis obliterans).
Adenovirus can cause severe necrotizing damage to the terminal bronchioles, leading to submucosal fibrosis and fixed airway narrowing.
3
Determine the optimal diagnostic modality for the suspected condition.
High-resolution computed tomography (HRCT) of the chest is selected to identify the classic mosaic attenuation and air trapping seen in bronchiolitis obliterans.
Standard chest radiographs often show only non-specific hyperinflation. HRCT is the non-invasive gold standard before considering a lung biopsy.

Key Concept

Diagnosis of post-infectious bronchiolitis obliterans following severe adenovirus infection.
Estimated Time:1m 30s
Question 126Question →

A 16-year-old girl, who recently immigrated from a region with limited access to pediatric healthcare, is brought to the clinic for evaluation of primary amenorrhea and severe, progressive facial hair growth. Her mother notes that she has had a deep voice and experienced a rapid growth spurt during early childhood. Her blood pressure is 162/100 mm Hg, and her pulse is 78/min. Physical examination reveals severe nodulocystic acne, temporal hair thinning, and Tanner stage 5 pubic hair development, but Tanner stage 1 breast development. Pelvic examination demonstrates significant clitoromegaly and partial fusion of the labioscrotal folds. A transabdominal pelvic ultrasound confirms the presence of a uterus and bilateral ovaries. Laboratory testing shows a serum sodium of 146 mEq/L and a serum potassium of 2.8 mEq/L. Which of the following serum laboratory profiles (17-hydroxyprogesterone, 11-deoxycorticosterone, and plasma renin activity) is most likely present in this patient?

Show answer & explanation

Answer: 17-hydroxyprogesterone: Elevated; 11-deoxycorticosterone: Elevated; Plasma renin activity: Decreased

Answer

17-hydroxyprogesterone: Elevated; 11-deoxycorticosterone: Elevated; Plasma renin activity: Decreased
The correct answer identifies the laboratory profile of 11-beta-hydroxylase deficiency. This patient's presentation of severe virilization, primary amenorrhea, and ambiguous genitalia (partial fusion of the labioscrotal folds) in the presence of a uterus indicates profound prenatal and postnatal androgen excess. The concurrent finding of hypertension and hypokalemia points to excess mineralocorticoid activity. In the adrenal steroidogenesis pathway, 11-beta-hydroxylase converts 11-deoxycorticosterone (DOC) to corticosterone and 11-deoxycortisol to cortisol. A deficiency in this enzyme leads to decreased cortisol, which removes negative feedback on the pituitary, causing increased ACTH secretion. This drives the overproduction of precursors proximal to the block. Consequently, 17-hydroxyprogesterone (17-OHP) is significantly elevated and shunted into the androgen synthesis pathway, causing virilization. Simultaneously, the direct precursor DOC is markedly elevated. DOC possesses intrinsic mineralocorticoid activity, leading to sodium retention, potassium wasting, and hypertension. This resulting volume expansion suppresses the juxtaglomerular apparatus, leading to decreased plasma renin activity.

Step-by-Step Solution

1
Analyze the patient's clinical presentation and vital signs.
The patient has severe virilization (deep voice, clitoromegaly, labioscrotal fusion), primary amenorrhea with a uterus present, hypertension (162/100 mm Hg), and hypokalemia (2.8 mEq/L).
Identifying the combination of prenatal/postnatal androgen excess and mineralocorticoid excess is crucial for narrowing down the differential diagnosis of congenital adrenal hyperplasia (CAH) variants.
2
Determine the specific enzymatic defect responsible for this presentation.
The clinical picture strongly indicates 11-beta-hydroxylase deficiency.
21-hydroxylase deficiency causes androgen excess but salt-wasting (hypotension). 17-alpha-hydroxylase deficiency causes mineralocorticoid excess (hypertension) but lack of androgens (no virilization). 11-beta-hydroxylase deficiency is the only CAH variant causing both severe virilization and hypertension.
3
Deduce the laboratory profile by tracing the interrupted steroidogenesis pathway.
17-hydroxyprogesterone is elevated, 11-deoxycorticosterone (DOC) is elevated, and plasma renin activity is decreased.
The enzyme block prevents the conversion of DOC to corticosterone, causing DOC to accumulate and act as a weak mineralocorticoid, which suppresses renin. Upstream precursors like 17-OHP also accumulate and are subsequently shunted into the active androgen synthesis pathway.

Key Concept

11-beta-hydroxylase deficiency causes congenital adrenal hyperplasia characterized by virilization (due to androgen excess) and hypertension with hypokalemia (due to the accumulation of 11-deoxycorticosterone, a weak mineralocorticoid that suppresses renin).
Question 127Question →

In early February, the parents of an 18-month-old girl bring her to the emergency department because she has been breathing rapidly and feeding poorly for the past 24 hours. The parents note that her symptoms began four days ago with a runny nose, mild nasal congestion, and a "tight" cough. She has a past medical history of atopic dermatitis managed with emollients. Her immunizations are up to date. Her temperature is 37.9°C (100.2°F), pulse is 158/min, respirations are 58/min, and oxygen saturation is 89% on room air. Physical examination reveals an irritable but consolable toddler with prominent nasal flaring and subcostal retractions. Lung auscultation demonstrates a prolonged expiratory phase, diffuse polyphonic wheezing, and bilateral coarse crackles. A chest radiograph displays bilateral hyperinflation, flattened hemidiaphragms, and a focal, wedge-shaped area of increased opacity in the right middle lobe. Which of the following is the most appropriate next step in management?

Show answer & explanation

Answer: Supplemental oxygen and nasal suctioning

Answer

Supplemental oxygen and nasal suctioning
This patient's clinical presentation—an infant in the winter months with a viral prodrome followed by respiratory distress, diffuse polyphonic wheezing, and crackles—is highly characteristic of acute bronchiolitis, most commonly caused by Respiratory Syncytial Virus (RSV). The primary indications for intervention are hypoxia (oxygen saturation <90%) and severe increased work of breathing (retractions, nasal flaring). The standard of care for bronchiolitis is purely supportive, prioritizing supplemental oxygen to correct hypoxia and nasal suctioning to clear thick upper airway secretions. The focal, wedge-shaped opacity seen on the chest radiograph is a classic presentation of atelectasis due to mucus plugging, which is extremely common in severe bronchiolitis and does not independently indicate a superimposed bacterial infection.

Step-by-Step Solution

1
Analyze the patient's clinical presentation and demographics.
The patient is an 18-month-old with a viral prodrome followed by acute respiratory distress, wheezing, and crackles during the winter season.
Identifying the classic age group and symptom progression is essential for distinguishing bronchiolitis from asthma or typical bacterial pneumonia.
2
Evaluate the objective findings, including vital signs and chest radiograph.
The patient has hypoxia (SpO2 89%), severe tachypnea, and increased work of breathing. The chest radiograph shows hyperinflation and atelectasis.
Recognizing that focal opacities in this context represent mucus plugging (atelectasis) rather than lobar consolidation prevents inappropriate antibiotic administration.
3
Determine the most appropriate management based on the diagnosis and severity.
Given the diagnosis of severe bronchiolitis with hypoxia, supportive care with supplemental oxygen and airway clearance is the indicated treatment.
Evidence-based guidelines for bronchiolitis strongly recommend against bronchodilators, corticosteroids, and antibiotics, focusing entirely on supportive care.

Key Concept

The management of acute bronchiolitis relies on supportive care, specifically supplemental oxygen for hypoxia and nasal suctioning, while avoiding bronchodilators, corticosteroids, and unnecessary antibiotics even when atelectasis is present on imaging.
Estimated Time:1m 30s
Question 128Question →

A 12-year-old boy is brought to the clinic for a 4-week history of right-sided knee pain and a progressive limp. The pain is characterized as a dull ache that is exacerbated by walking and participating in sports. He has no history of trauma, falls, or fever. His medical history is significant for growth hormone deficiency, for which he has been receiving somatropin injections for the past 6 months. His body mass index is at the 60th percentile for his age. His temperature is 37.1°C (98.8°F), blood pressure is 110/70 mm Hg, and pulse is 78/min. On physical examination, there is no swelling, erythema, or localized tenderness over the right knee, and ligamentous testing is stable. Range of motion of the right knee is full and painless. When the patient walks, he exhibits an antalgic gait with the right foot pointing outward. During examination of the hips, passive flexion of the right hip results in obligate external rotation of the thigh. Internal rotation of the right hip is limited compared to the left. Which of the following is the most appropriate next step in management?

Show answer & explanation

Answer: Obtain bilateral anteroposterior and frog-leg lateral pelvic radiographs

Answer

Obtain bilateral anteroposterior and frog-leg lateral pelvic radiographs
The correct answer is to obtain bilateral anteroposterior and frog-leg lateral pelvic radiographs. This patient's clinical presentation is highly suspicious for Slipped Capital Femoral Epiphysis (SCFE). While the classic demographic for SCFE is an obese adolescent boy, it frequently occurs in children with underlying endocrinopathies, such as hypothyroidism or those receiving growth hormone therapy, which weakens the physeal plate. A classic diagnostic pitfall in SCFE is referred pain to the anterior thigh or knee via the sensory branches of the obturator nerve, causing the patient to complain primarily of knee pain. However, physical examination will reveal a normal knee but an abnormal hip, characteristically demonstrating obligate external rotation of the thigh during passive hip flexion and loss of internal rotation. When SCFE is suspected, the most appropriate next step is to obtain bilateral AP and frog-leg lateral radiographs of the pelvis. Bilateral imaging is crucial because contralateral asymptomatic slippage occurs in up to 40% of patients. Once the diagnosis is confirmed, patients must be strictly non-weight-bearing to prevent further slippage and urgently referred for surgical pinning in situ.

Step-by-Step Solution

1
Analyze the patient's clinical presentation and underlying risk factors.
The patient is a 12-year-old boy presenting with insidious-onset right knee pain, an antalgic gait, and obligate external rotation of the hip upon passive flexion. He is receiving growth hormone therapy and has a normal BMI.
Identifying these key demographic and clinical features is necessary to recognize atypical presentations of common pediatric orthopedic conditions.
2
Localize the source of the pain based on physical examination findings.
Despite the complaint of knee pain, the knee examination is entirely normal. Conversely, the hip examination reveals limited internal rotation and obligate external rotation during flexion, indicating the true pathology is in the hip.
Referred knee pain via the sensory branches of the obturator nerve is a classic diagnostic pitfall in pediatric hip disorders.
3
Synthesize the findings to formulate the most likely diagnosis.
The combination of hip pathology in an adolescent exacerbated by growth hormone therapy strongly points to Slipped Capital Femoral Epiphysis (SCFE).
Growth hormone therapy causes rapid bone growth, which alters the biomechanics of the physis and is a known risk factor for SCFE, even in non-obese children.
4
Determine the most appropriate initial diagnostic test for the suspected condition.
The diagnostic modality of choice for SCFE is bilateral anteroposterior and frog-leg lateral radiographs of the pelvis.
Bilateral imaging is required to identify the physeal displacement and to check for asymptomatic contralateral slippage, which is common in these patients.

Key Concept

Patients with Slipped Capital Femoral Epiphysis (SCFE) often present with referred thigh or knee pain and a normal knee examination. The physical exam finding of obligate external rotation with passive hip flexion is characteristic. Diagnosis requires bilateral anteroposterior and frog-leg lateral pelvic radiographs.
Estimated Time:1m 30s
Question 129Question →

A 7272-year-old woman is brought to the emergency department for sudden-onset severe shortness of breath, lightheadedness, and right-sided chest pain. She recently returned from a 1212-hour international flight two days ago. Her medical history includes moderate chronic obstructive pulmonary disease (COPD) and hypertension.

On arrival, she is somnolent but arousable. Temperature is 37.0∘C37.0^\circ\text{C} (98.6∘F98.6^\circ\text{F}), blood pressure is 82/50 mm Hg82/50\text{ mm Hg}, pulse is 118/min118/\text{min}, and respirations are 28/min28/\text{min}. Oxygen saturation is 85%85\% on room air.

Physical examination reveals elevated jugular venous pressure. Lung auscultation is clear bilaterally.

Bedside transthoracic echocardiography demonstrates a severely enlarged right ventricle with hypokinesis of the free wall and normal apical contraction. The left ventricle is small and hyperdynamic.

An arterial blood gas on room air shows:
pH: 7.297.29
PaCO2\text{PaCO}_2: 26 mm Hg26\text{ mm Hg}
PaO2\text{PaO}_2: 54 mm Hg54\text{ mm Hg}
HCO3−\text{HCO}_3^-: 12 mEq/L12\text{ mEq/L}

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

Show answer & explanation

Answer: Administration of systemic alteplase

Answer

Administration of systemic alteplase
The correct answer is the administration of systemic alteplase. This patient presents with classic signs of a massive (high-risk) pulmonary embolism (PE): sudden-onset dyspnea, hypoxia, and hemodynamic instability (hypotension) following a major risk factor (prolonged travel). In patients with suspected massive PE who are too unstable to safely undergo definitive imaging (CT pulmonary angiography), bedside transthoracic echocardiography is the diagnostic test of choice. The presence of right ventricular dilation and free wall hypokinesis with apical sparing (McConnell's sign) provides sufficient evidence of acute right heart strain to justify immediate intervention. The treatment of choice for massive PE in the absence of absolute contraindications is systemic thrombolysis (e.g., alteplase). Thrombolytics rapidly lyse the clot, reducing pulmonary vascular resistance, alleviating right ventricular strain, and improving cardiac output.

Step-by-Step Solution

1
Identify the primary clinical syndrome.
The patient presents with sudden-onset dyspnea, hypoxia, right-sided chest pain, and profound hypotension (82/5082/50 mm Hg) following a period of prolonged immobilization.
Establishing the severity and likely etiology (massive pulmonary embolism causing cardiogenic shock).
2
Interpret the diagnostic data.
Bedside echocardiography shows right ventricular dilation and hypokinesis with apical sparing (McConnell's sign), confirming acute right heart strain. The ABG shows a primary metabolic acidosis (lactic acidosis from shock) with appropriate respiratory compensation.
To confirm the diagnosis of massive PE and safely rule out other causes of shock or acute respiratory failure.
3
Determine the most appropriate next step in management.
In a hemodynamically unstable patient with high clinical suspicion for PE and bedside echo evidence of RV strain, systemic thrombolysis (alteplase) is indicated immediately without waiting for definitive CT imaging.
To rapidly dissolve the thrombus, reduce right ventricular afterload, and restore cardiac output.

Key Concept

Massive (high-risk) pulmonary embolism is defined by hemodynamic instability (systolic BP <90< 90 mm Hg) and should be managed with systemic thrombolytics if bedside echocardiography shows right heart strain, as these patients are often too unstable for CT pulmonary angiography.

Alternative Method

In advanced centers, catheter-directed thrombolysis or surgical pulmonary embolectomy may be considered as alternative emergent treatments for massive PE, particularly if systemic thrombolysis has failed or is absolutely contraindicated.
Estimated Time:1m 30s
Question 130Question →

A 32-year-old woman is brought to the emergency department by her partner due to 5 days of severe, voluminous diarrhea and abdominal cramping. She has a history of ulcerative colitis and panic disorder. In the waiting room, she experienced a severe panic attack and was noted to have visibly rapid, deep breathing. Physical examination reveals dry mucous membranes, decreased skin turgor, a heart rate of 115/min115/\text{min}, a respiratory rate of 28/min28/\text{min}, and a blood pressure of 105/65 mm Hg105/65\text{ mm Hg}.

Laboratory results are as follows:

Laboratory TestResultReference Range
Sodium136 mEq/L136 \text{ mEq/L}136−145 mEq/L136-145 \text{ mEq/L}
Potassium3.2 mEq/L3.2 \text{ mEq/L}3.5−5.0 mEq/L3.5-5.0 \text{ mEq/L}
Chloride115 mEq/L115 \text{ mEq/L}95−105 mEq/L95-105 \text{ mEq/L}
Bicarbonate12 mEq/L12 \text{ mEq/L}22−28 mEq/L22-28 \text{ mEq/L}
Blood urea nitrogen34 mg/dL34 \text{ mg/dL}7−18 mg/dL7-18 \text{ mg/dL}
Creatinine1.2 mg/dL1.2 \text{ mg/dL}0.6−1.2 mg/dL0.6-1.2 \text{ mg/dL}

Arterial blood gas (room air):

Arterial Blood GasResultReference Range
pH7.407.407.35−7.457.35-7.45
pCO2\text{pCO}_220 mm Hg20 \text{ mm Hg}35−45 mm Hg35-45 \text{ mm Hg}
pO2\text{pO}_298 mm Hg98 \text{ mm Hg}80−100 mm Hg80-100 \text{ mm Hg}

Which of the following best describes this patient's acid-base status?

Show answer & explanation

Answer: Mixed normal anion gap metabolic acidosis and respiratory alkalosis

Answer

Mixed normal anion gap metabolic acidosis and respiratory alkalosis
The patient's initial insult is severe diarrhea, which causes profound gastrointestinal loss of bicarbonate, resulting in a normal anion gap metabolic acidosis (NAGMA). This is confirmed by an anion gap of 9 mEq/L9 \text{ mEq/L} (136−115−12=9136 - 115 - 12 = 9). To evaluate if respiratory compensation is appropriate, Winter's formula is applied: Expected pCO2=(1.5×12)+8±2=26±2 mm Hg\text{Expected pCO}_2 = (1.5 \times 12) + 8 \pm 2 = 26 \pm 2 \text{ mm Hg}. Because the patient's actual pCO2\text{pCO}_2 (20 mm Hg20 \text{ mm Hg}) is significantly lower than the expected range (24−28 mm Hg24-28 \text{ mm Hg}), she is 'blowing off' more CO2\text{CO}_2 than expected. This indicates a coexisting primary respiratory alkalosis, clinically correlating with her panic attack and hyperventilation in the waiting room. The two opposing disorders (acidosis and alkalosis) offset each other, resulting in a seemingly normal pH of 7.407.40.

Step-by-Step Solution

1
Calculate the anion gap to identify the primary metabolic disturbance.
Anion Gap=Na+−(Cl−+HCO3−)=136−(115+12)=9 mEq/L\text{Anion Gap} = \text{Na}^+ - (\text{Cl}^- + \text{HCO}_3^-) = 136 - (115 + 12) = 9 \text{ mEq/L}.
Since the anion gap is within the normal range (8−12 mEq/L8-12 \text{ mEq/L}), the patient has a normal anion gap metabolic acidosis (NAGMA), consistent with bicarbonate loss from severe diarrhea.
2
Apply Winter's formula to determine the expected respiratory compensation.
Expected pCO2=1.5×[HCO3−]+8±2=(1.5×12)+8±2=26±2 mm Hg\text{Expected pCO}_2 = 1.5 \times [\text{HCO}_3^-] + 8 \pm 2 = (1.5 \times 12) + 8 \pm 2 = 26 \pm 2 \text{ mm Hg}. The expected range is 24−28 mm Hg24-28 \text{ mm Hg}.
Winter's formula determines if the lungs are appropriately compensating for a metabolic acidosis by decreasing pCO2\text{pCO}_2.
3
Compare the actual measured pCO2\text{pCO}_2 with the expected pCO2\text{pCO}_2 range.
The patient's actual pCO2\text{pCO}_2 is 20 mm Hg20 \text{ mm Hg}, which is lower than the expected range of 24−28 mm Hg24-28 \text{ mm Hg}.
Because the pCO2\text{pCO}_2 is lower than what pure metabolic compensation would dictate, there is an additional process driving CO2 down—a primary respiratory alkalosis (due to hyperventilation from her panic attack).

Key Concept

In patients with metabolic acidosis, Winter's formula (1.5×[HCO3−]+8±21.5 \times [\text{HCO}_3^-] + 8 \pm 2) must be used to calculate expected pCO2\text{pCO}_2. An actual pCO2\text{pCO}_2 lower than the expected range indicates a superimposed primary respiratory alkalosis.
Question 131Question →

Match each post-bariatric surgery clinical presentation with its most appropriate diagnostic or therapeutic next step.

Click a left item, then click its matching right item

Items

A 42-year-old woman experiences crampy abdominal pain, diaphoresis, and palpitations 30 minutes after eating, 6 months following a Roux-en-Y gastric bypass.
A 35-year-old man presents with severe, colicky abdominal pain and nausea 2 years after a Roux-en-Y gastric bypass; CT abdomen shows a mesenteric swirl sign.
A 48-year-old woman who recently resumed smoking reports burning epigastric pain that worsens with fasting, 1 year after a Roux-en-Y gastric bypass.
A 39-year-old man develops sustained tachycardia of 130/min, fever, and left shoulder pain on postoperative day 2 following a Roux-en-Y gastric bypass.

Matches

Show answer & explanation

Answer

Dumping syndrome requires dietary modification; internal hernias require prompt surgical exploration; marginal ulcers require endoscopy and proton pump inhibitors; and anastomotic leaks require urgent water-soluble contrast imaging or reoperation.
Bariatric surgery, specifically Roux-en-Y gastric bypass, alters normal gastrointestinal anatomy and physiology, leading to unique complications that mandate specific interventions. Early complications like anastomotic leaks manifest primarily as unexplained tachycardia and peritonitis, requiring urgent imaging or exploration. Late complications include dumping syndrome (managed conservatively with diet), marginal ulcers (managed medically after endoscopic confirmation), and internal hernias (requiring definitive surgical closure to prevent ischemia). Aligning the pathophysiology with the correct intervention is critical for surgical triage.

Step-by-Step Solution

1
Analyze the timing and nature of symptoms for the first presentation.
Postprandial vasomotor and gastrointestinal symptoms at 6 months indicate early dumping syndrome.
Rapid transit of hyperosmolar food boluses draws fluid into the intestine and triggers autonomic reflexes; this is best managed with dietary changes.
2
Evaluate the radiographic findings and timeline for the second presentation.
A mesenteric swirl sign on CT years after surgery points to an internal hernia.
Roux-en-Y gastric bypass creates mesenteric defects that allow bowel herniation and strangulation, requiring prompt surgical intervention.
3
Identify the risk factors and symptom pattern in the third presentation.
A smoker experiencing fasting epigastric pain at 1 year is highly suspicious for a marginal ulcer.
The gastrojejunal anastomosis is vulnerable to ulceration from poor mucosal perfusion, NSAIDs, or smoking, warranting endoscopic evaluation and acid suppression.
4
Assess the acute vital sign abnormalities in the fourth presentation.
Unexplained early postoperative tachycardia and signs of peritonitis suggest an anastomotic leak.
Leaks are life-threatening early complications that demand immediate identification with water-soluble contrast or urgent surgical exploration.

Key Concept

Diagnosis and management of common early and late complications of Roux-en-Y gastric bypass.
Question 132Question →

A 58-year-old man collapses in the hospital lobby. A nearby physician confirms he is unresponsive, apneic, and lacks a palpable carotid pulse. A resuscitation team arrives immediately with a crash cart, and the initial cardiac monitor displays coarse ventricular fibrillation. Arrange the following interventions in the correct chronological sequence according to standard Advanced Cardiac Life Support (ACLS) guidelines for adult cardiac arrest.

Drag items to arrange them in the correct order

Show answer & explanation

Answer

The correct sequence for managing ventricular fibrillation is to first initiate CPR and attach the defibrillator, then deliver an immediate shock, followed immediately by 2 minutes of CPR while obtaining IV/IO access, and finally performing a rhythm check with subsequent epinephrine administration if the rhythm remains shockable.
The Advanced Cardiac Life Support algorithm dictates a strict sequence to maximize survival in shockable cardiac arrests (ventricular fibrillation and pulseless ventricular tachycardia). The sequence must begin with high-quality CPR and defibrillator attachment. Once a shockable rhythm is confirmed, the immediate next step is a single unsynchronized shock. Following the shock, providers must immediately resume CPR for 2 minutes without pausing for a rhythm check, during which time intravenous or intraosseous access should be established. Only after these 2 minutes of CPR is another rhythm check performed; if the rhythm remains shockable, another shock is delivered, followed by the administration of 1 mg of epinephrine.

Step-by-Step Solution

1
Recognize cardiac arrest and prepare for intervention.
CPR is initiated and the monitor is attached to identify the rhythm.
Minimizing time without perfusion is critical. The defibrillator must be attached to determine if the rhythm is shockable.
2
Treat the primary shockable rhythm.
An unsynchronized shock is delivered.
Ventricular fibrillation requires immediate electrical therapy to depolarize the myocardium and allow a normal pacemaker to resume.
3
Provide post-shock perfusion and prepare for medical therapy.
High-quality compressions are resumed for 2 minutes while IV or IO access is secured.
Compressions immediately after a shock are necessary because the heart rarely generates effective perfusion immediately after defibrillation. Pausing for a pulse check is contraindicated.
4
Evaluate rhythm and escalate therapy.
A rhythm check is performed, a second shock is delivered if appropriate, and epinephrine is given.
Epinephrine is indicated after the initial shock and subsequent 2-minute CPR cycle if the rhythm remains in ventricular fibrillation or pulseless ventricular tachycardia.

Key Concept

Advanced Cardiac Life Support (ACLS) Ventricular Fibrillation Algorithm
Estimated Time:1m 0s
Question 133Question →

A 3131-year-old woman, G 11 P 00 at 3434 weeks gestation, is brought to the emergency department after being involved in a high-speed motor vehicle collision. She complains of anterior chest pain and severe shortness of breath. Her blood pressure is 78/4878/48 mm Hg, heart rate is 135135 bpm, and respiratory rate is 2626/min. Pulse oximetry shows 93%93\% on room air. Physical examination reveals distended jugular veins and distant, muffled heart sounds. Breath sounds are equal bilaterally, but faint scattered wheezes are auscultated. The trachea is midline. Bedside focused assessment with sonography for trauma (FAST) demonstrates a large anechoic space surrounding the heart with right ventricular free wall inversion during diastole. There is no evidence of intraperitoneal fluid. Continuous fetal heart rate monitoring shows a baseline of 140140 bpm with moderate variability and no decelerations. Which of the following is the most appropriate next step in management for this patient?

Show answer & explanation

Answer: Immediate echocardiography-guided pericardiocentesis

Answer

Immediate echocardiography-guided pericardiocentesis
The correct option is immediate pericardiocentesis because the patient presents with classic signs of cardiac tamponade (Beck's triad) leading to obstructive shock following blunt chest trauma. The FAST exam confirms a large pericardial effusion with right ventricular diastolic collapse. In a hemodynamically unstable patient, the immediate life-saving intervention is bedside pericardiocentesis to relieve intrapericardial pressure, allowing the right ventricle to fill during diastole and restoring cardiac output. Pregnancy does not change the fundamental algorithm for treating life-threatening obstructive shock.

Step-by-Step Solution

1
Identify the primary diagnosis based on the clinical presentation and ultrasound findings.
The patient has Beck's triad (hypotension, jugular venous distension, muffled heart sounds) and sonographic evidence of right ventricular diastolic collapse, confirming cardiac tamponade.
Accurate diagnosis is required before choosing an intervention in a trauma patient.
2
Assess the patient's hemodynamic status.
The patient is severely hypotensive and tachycardic, indicating obstructive shock.
Hemodynamic instability dictates the urgency of the management plan.
3
Determine the most appropriate immediate management.
Emergent pericardiocentesis is required.
Removing the pericardial fluid relieves the pressure on the heart, restoring venous return and cardiac output, regardless of pregnancy status.

Key Concept

Cardiac tamponade causes obstructive shock by impairing right ventricular filling; hemodynamically unstable patients require immediate pericardiocentesis to relieve intrapericardial pressure.
Estimated Time:1m 30s
Question 134Question →

An established clinic patient, who is 68 years old, presents for evaluation of bilateral leg swelling that has gradually worsened over the past 3 months. He additionally notes new-onset abdominal fullness and becoming breathless after walking short distances. The patient is oxygen-dependent due to a long-standing history of severe chronic obstructive pulmonary disease (COPD) and has previously smoked heavily for four decades. His temperature is 37.0°C (98.6°F), blood pressure is 135/85 mm Hg, and pulse is 88/min. Physical examination reveals markedly distended jugular veins, a palpable parasternal heave, and 3+ pitting edema of the lower extremities bilaterally. Cardiac auscultation reveals a holosystolic murmur at the left lower sternal border that increases in intensity with inspiration. Breath sounds are decreased bilaterally with a prolonged expiratory phase, but no crackles are heard. Which of the following is the most likely primary mechanism for this patient's current presentation?

Show answer & explanation

Answer: Elevated pulmonary arterial pressure

Answer

Elevated pulmonary arterial pressure
This patient's presentation is classic for cor pulmonale, which is defined as right ventricular hypertrophy and eventually right heart failure due to primary pulmonary disease. In patients with severe COPD, chronic alveolar hypoxia triggers hypoxic pulmonary vasoconstriction. Over time, this diffuse vasoconstriction leads to structural remodeling of the pulmonary vasculature and elevated pulmonary arterial pressure (pulmonary hypertension). The right ventricle must pump against this increased afterload, leading to right ventricular hypertrophy (evidenced by the palpable parasternal heave) and eventual right ventricular failure. This failure causes systemic venous congestion, manifesting as jugular venous distention, hepatic congestion (abdominal fullness), and significant peripheral edema. The dilation of the right ventricle also stretches the tricuspid valve annulus, causing functional tricuspid regurgitation (a holosystolic murmur at the left lower sternal border that increases in intensity during inspiration).

Step-by-Step Solution

1
Analyze the patient's history and risk factors.
The patient has severe, oxygen-dependent COPD.
Identifying the underlying chronic disease helps point toward its systemic complications.
2
Interpret the physical examination findings.
JVD, parasternal heave, lower extremity edema, and a murmur of tricuspid regurgitation (increases with inspiration) are present without pulmonary crackles.
These findings specifically indicate isolated right ventricular hypertrophy and right-sided heart failure.
3
Synthesize history and exam to determine the mechanism.
The combination of severe lung disease and right heart failure is diagnostic of cor pulmonale, which is driven by pulmonary hypertension.
Chronic hypoxia induces pulmonary vasoconstriction, leading to elevated pulmonary arterial pressure that overwhelms the right ventricle.

Key Concept

Cor Pulmonale
Estimated Time:1m 0s
Question 135Question →

Match each clinical presentation and characteristic physical examination finding with the most likely underlying valvular pathology.

Click a left item, then click its matching right item

Items

A 24-year-old woman with a mid-systolic click followed by a late systolic murmur that becomes longer and louder with the Valsalva maneuver.
A 68-year-old man with syncope, a delayed carotid upstroke, and a harsh crescendo-decrescendo systolic murmur at the right upper sternal border.
A 45-year-old man with a bounding pulse, head bobbing, and a high-pitched, blowing early diastolic decrescendo murmur at the left sternal border.
A 32-year-old woman with hemoptysis, a loud first heart sound (S1), and a low-pitched mid-diastolic rumbling murmur at the cardiac apex.

Matches

Show answer & explanation

Answer

The mid-systolic click with Valsalva accentuation matches mitral valve prolapse; the delayed carotid upstroke with a harsh systolic murmur matches aortic valve stenosis; the bounding pulse with an early diastolic murmur matches aortic valve regurgitation; and the loud S1 with a mid-diastolic rumble matches mitral valve stenosis.
Each clinical vignette presents a pathognomonic set of physical exam findings for a specific valvular lesion. A mid-systolic click with a late systolic murmur that worsens with decreased preload points to mitral valve prolapse. A delayed carotid upstroke with a harsh right-sided systolic murmur indicates aortic valve stenosis. Bounding pulses with an early diastolic murmur reveal aortic valve regurgitation. A loud S1 with a mid-diastolic rumbling murmur is characteristic of mitral valve stenosis.

Step-by-Step Solution

1
Analyze the young woman's presentation of a click and late systolic murmur.
Identified the murmur as mitral valve prolapse.
Valsalva decreases preload, which worsens the prolapse of redundant mitral valve leaflets, causing the murmur to appear earlier and become louder.
2
Analyze the elderly man's presentation of syncope and delayed carotid upstroke.
Identified the murmur as aortic valve stenosis.
The classic triad of symptoms (syncope, angina, dyspnea) along with pulsus parvus et tardus indicates fixed left ventricular outflow tract obstruction.
3
Analyze the middle-aged man's presentation of bounding pulses and head bobbing.
Identified the murmur as aortic valve regurgitation.
These peripheral signs indicate a hyperdynamic circulation and widened pulse pressure resulting from the rapid runoff of blood back into the left ventricle during diastole.
4
Analyze the young woman's presentation of hemoptysis and a diastolic rumble.
Identified the murmur as mitral valve stenosis.
This auscultatory profile, combined with signs of elevated pulmonary venous pressure (hemoptysis), strongly points to an obstructed mitral orifice, often rheumatic in origin.

Key Concept

Valvular Heart Disease Physical Examination Findings
Question 136Question →

A 72-year-old woman is brought to the emergency department at 3:00 AM due to the sudden onset of severe shortness of breath and wheezing that awoke her from sleep. She has a history of essential hypertension, type 2 diabetes mellitus, and a 35-pack-year smoking history. Current medications include amlodipine and metformin. Her blood pressure is 170/95 mm Hg, pulse is 92/min, and respirations are 24/min. Pulse oximetry shows 90% on room air. Physical examination reveals diffuse bilateral expiratory wheezing and a prolonged expiratory phase. Jugular venous pulsation is estimated at 9 cm H₂O. Cardiac auscultation reveals a regular rate and rhythm with a prominent S4 gallop; no murmurs are appreciated. Trace bilateral lower extremity edema is present. An electrocardiogram shows normal sinus rhythm with voltage criteria for left ventricular hypertrophy. A chest radiograph reveals a slightly enlarged cardiac silhouette but no focal consolidation or pleural effusion. The patient is administered continuous nebulized albuterol and intravenous methylprednisolone for a presumed chronic obstructive pulmonary disease exacerbation. One hour later, her dyspnea acutely worsens. Repeat vital signs show a blood pressure of 120/70 mm Hg and a pulse of 128/min. Repeat lung auscultation now reveals prominent bibasilar crackles extending to the mid-lung fields. Which of the following pathophysiologic mechanisms best explains this patient's acute clinical deterioration?

Show answer & explanation

Answer: Decreased duration of ventricular diastole impairing myocardial filling

Answer

Decreased duration of ventricular diastole impairing myocardial filling
The patient initially presented with cardiac asthma (bronchospasm secondary to interstitial pulmonary congestion) due to heart failure with preserved ejection fraction (HFpEF). This underlying diagnosis is evidenced by her paroxysmal nocturnal dyspnea, S4 gallop, left ventricular hypertrophy, and elevated JVP. She was misdiagnosed with a COPD exacerbation and treated with albuterol. Albuterol, a beta-agonist, induced significant tachycardia (pulse rose to 128/min). In a patient with a stiff, hypertrophied ventricle, filling is heavily dependent on the duration of diastole. Tachycardia drastically shortens diastolic filling time, leading to a rapid rise in left atrial pressure. This backward pressure causes acute hydrostatic alveolar edema, manifesting as new bibasilar crackles, while the impaired forward stroke volume causes a drop in blood pressure.

Step-by-Step Solution

1
Analyze the initial presentation and recognize the misdiagnosis.
The patient presented with wheezing waking her from sleep (paroxysmal nocturnal dyspnea), elevated JVP, LVH, and an S4 gallop, which strongly indicates 'cardiac asthma' due to acute decompensated heart failure with preserved ejection fraction (HFpEF), not a primary COPD exacerbation.
Differentiating cardiac asthma from a true COPD exacerbation is critical, as therapies for one can be detrimental to the other.
2
Evaluate the physiologic effect of the administered intervention.
The patient was given high-dose nebulized albuterol, a beta-agonist that commonly causes reflex tachycardia or direct chronotropic effects due to beta-1 cross-reactivity, raising her heart rate from 92/min to 128/min.
Understanding the systemic side effects of respiratory medications is necessary to explain the clinical change.
3
Synthesize the hemodynamic consequences of the altered vital signs on the underlying pathology.
In a patient with a stiff, non-compliant left ventricle (S4 gallop, LVH), cardiac output and pulmonary pressures are highly dependent on adequate diastolic filling time.
Diastolic dysfunction requires longer filling times. Tachycardia drastically shortens diastole.
4
Connect the pathophysiology to the new physical exam findings.
The shortened diastole leads to a rapid backward accumulation of pressure into the left atrium and pulmonary veins, precipitating acute hydrostatic pulmonary edema, which manifests clinically as a drop in stroke volume (hypotension) and new bibasilar crackles.
This fully explains both the drop in blood pressure and the transition from wheezing (interstitial edema) to crackles (alveolar edema).

Key Concept

Patients with heart failure with preserved ejection fraction (HFpEF) are highly dependent on adequate diastolic filling time; tachycardia (e.g., from inappropriate albuterol use) shortens diastole, leading to acute left atrial hypertension and flash pulmonary edema.
Estimated Time:2m 0s
Question 137Question →

Match each patient's clinical presentation and laboratory profile to the most likely underlying pathophysiologic mechanism.

Click a left item, then click its matching right item

Items

A 68-year-old man with a long smoking history presents with confusion and a central lung mass. Laboratory studies show serum calcium 13.5 mg/dL, phosphorus 2.1 mg/dL, and intact PTH 9 pg/mL (normal 15-65 pg/mL).
A 45-year-old woman is evaluated for a history of recurrent renal colic. Laboratory studies show serum calcium 11.2 mg/dL, phosphorus 2.4 mg/dL, and intact PTH 88 pg/mL.
A 24-year-old man is found to have asymptomatic hypercalcemia on routine insurance screening. Laboratory studies show serum calcium 11.4 mg/dL, intact PTH 42 pg/mL, and 24-hour urine calcium of 35 mg/day.
A 32-year-old African American woman presents with persistent dry cough, erythema nodosum, and bilateral facial nerve palsy. Laboratory studies show serum calcium 11.9 mg/dL, phosphorus 4.4 mg/dL, and intact PTH 12 pg/mL.
A 60-year-old housebound woman presents with diffuse, dull bone pain and proximal muscle weakness. Laboratory studies show serum calcium 7.8 mg/dL, phosphorus 2.2 mg/dL, intact PTH 145 pg/mL, and elevated alkaline phosphatase.

Matches

Show answer & explanation

Answer

The clinical vignettes represent distinct mechanisms of calcium and phosphorus dysregulation: Humoral hypercalcemia of malignancy (PTHrP), Primary hyperparathyroidism (PTH overproduction), Familial hypocalciuric hypercalcemia (calcium-sensing receptor mutation), Sarcoidosis (ectopic 1-alpha-hydroxylase), and Osteomalacia (Vitamin D deficiency).
Correct matching requires evaluating serum calcium alongside serum phosphorus, intact PTH levels, and key clinical contextual clues to determine whether the metabolic abnormality is PTH-driven, PTH-independent, or a result of a defective receptor set-point.

Step-by-Step Solution

1
Analyze patient 1's profile
High calcium, low phosphorus, low PTH, central lung mass.
Identifies PTH-independent hypercalcemia due to malignancy (PTHrP secretion mimicking PTH effects).
2
Analyze patient 2's profile
High calcium, low phosphorus, high PTH, kidney stones.
Identifies PTH-dependent hypercalcemia caused by primary hyperparathyroidism.
3
Analyze patient 3's profile
High calcium, normal PTH, highly restricted urine calcium.
Identifies an altered calcium sensing set point indicative of Familial Hypocalciuric Hypercalcemia (FHH).
4
Analyze patient 4's profile
High calcium, high-normal phosphorus, low PTH, signs of sarcoidosis.
Identifies 1,25-dihydroxyvitamin D-mediated hypercalcemia from granulomatous macrophage activity.
5
Analyze patient 5's profile
Low calcium, low phosphorus, very high PTH, high alkaline phosphatase.
Identifies secondary hyperparathyroidism in response to severe Vitamin D deficiency causing osteomalacia.

Key Concept

Differential diagnosis of calcium and bone metabolism disorders using paired serum calcium, phosphorus, and parathyroid hormone levels.
Question 138Question →

A 58-year-old individual undergoing maintenance hemodialysis is admitted to the hospital due to progressive shortness of breath, orthopnea, and generalized fatigue over the past month. The patient has a history of type 2 diabetes mellitus and underwent creation of a left brachiocephalic arteriovenous fistula six months ago. Current medications include sevelamer, amlodipine, and erythropoietin. Vital signs reveal a blood pressure of 165/55165/55 mmHg, a pulse of 110110/min with bounding peripheral pulses, and a respiratory rate of 2222/min. Oxygen saturation is 93%93\% on ambient air. Physical examination demonstrates distended jugular veins up to 99 cm H2OH_2O. Auscultation of the lungs reveals bilateral basilar crackles and scattered expiratory wheezes. Cardiac examination shows a hyperdynamic precordium, a soft systolic ejection murmur at the left upper sternal border, and an audible S3 gallop. The left arm exhibits a very prominent thrill and a continuous bruit over the access site. Echocardiography demonstrates a left ventricular ejection fraction of 68%68\%, biatrial enlargement, and a dilated left ventricle. Which of the following best describes the primary underlying hemodynamic derangement responsible for this patient's current symptoms?

Show answer & explanation

Answer: Bypass of capillary beds resulting in decreased systemic vascular resistance

Answer

The condition is driven by the bypass of capillary beds resulting in decreased systemic vascular resistance.
The correct answer accurately describes the pathophysiology of high-output heart failure caused by a surgically created arteriovenous (AV) fistula. An AV fistula creates a direct connection between the high-pressure arterial system and the low-pressure venous system. This large shunt completely bypasses the systemic capillary beds, which normally provide the bulk of systemic vascular resistance (SVR). The sudden and sustained drop in SVR leads to a massive increase in venous return to the right heart. To maintain adequate perfusion pressure, the heart must dramatically increase its cardiac output by increasing both stroke volume (leading to a wide pulse pressure and bounding pulses) and heart rate. Over time, the chronic volume overload causes the ventricles to dilate, ultimately leading to decompensation and symptomatic high-output heart failure, presenting with pulmonary edema (crackles, 'cardiac asthma' wheezing) and elevated filling pressures (JVD, S3 gallop).

Step-by-Step Solution

1
Analyze the physical exam findings and vital signs.
The patient exhibits signs of volume overload and left heart failure (crackles, orthopnea, S3 gallop, JVD) alongside signs of a hyperdynamic state (bounding pulses, wide pulse pressure, tachycardia).
Identifying both the heart failure syndrome and the hyperdynamic circulation narrows the differential to high-output states.
2
Evaluate the echocardiogram data.
The ejection fraction is normal to high (68%68\%), ruling out standard left ventricular systolic dysfunction (HFrEF).
This confirms that the heart is contracting well and pumping a large volume of blood, rather than failing to eject.
3
Connect the clinical picture to the patient's medical history.
The patient has a large left brachiocephalic arteriovenous (AV) fistula with a very prominent thrill.
A large AV fistula acts as a massive left-to-right shunt, bypassing the high-resistance systemic arterioles. This drastically drops systemic vascular resistance, leading to increased venous return, which forces the heart to increase its stroke volume and heart rate, eventually resulting in high-output heart failure.

Key Concept

High-Output Heart Failure secondary to Arteriovenous Fistula
Question 139Question →

A 68-year-old man presents to the urgent care clinic with a 2-day history of progressively worsening shortness of breath and cough. He states that he is having to work much harder to breathe than usual. His past medical history is significant for a myocardial infarction 3 years ago and chronic obstructive pulmonary disease (COPD) managed with an inhaled long-acting bronchodilator. He has a 40-pack-year smoking history. Temperature is 37.0°C (98.6°F), blood pressure is 152/90 mmHg, pulse is 108/min, and respiratory rate is 26/min. Oxygen saturation is 89% on room air. Lung auscultation reveals diffuse expiratory wheezes and scattered basilar crackles. Cardiac examination is difficult to hear clearly due to loud breath sounds, and the neck veins are not easily visible due to his body habitus. Which of the following is the most appropriate next diagnostic test to determine whether his symptoms are primarily due to acute decompensated heart failure rather than a COPD exacerbation?

Show answer & explanation

Answer: Serum B-type natriuretic peptide

Answer

Serum B-type natriuretic peptide
The correct answer is serum B-type natriuretic peptide (BNP). This patient presents with acute dyspnea and wheezing in the setting of both a smoking history (COPD) and coronary artery disease (prior myocardial infarction). Wheezing can be a classic sign of a COPD exacerbation, but it can also occur in acute decompensated heart failure ('cardiac asthma') due to peribronchial fluid accumulation. Because his physical exam is non-diagnostic for volume overload (obscured JVP, no clear S3), a serum BNP level is the most useful next step. BNP is released from ventricular myocytes in response to increased wall tension. A normal BNP has a very high negative predictive value for ruling out heart failure, whereas a significantly elevated level supports a cardiac etiology for the dyspnea.

Step-by-Step Solution

1
Identify the patient's overlapping clinical features and risk factors.
The patient has dyspnea, wheezing, and hypoxemia with a history of both structural heart disease (prior myocardial infarction) and chronic lung disease (COPD).
Recognizing that 'cardiac asthma' (wheezing due to heart failure) mimics a COPD exacerbation is essential for determining the diagnostic approach.
2
Determine the limitation of the physical examination.
The physical exam cannot definitively confirm fluid overload (JVP is obscured) or rule out heart failure due to loud respiratory sounds.
When clinical signs are ambiguous, an objective biomarker is needed to differentiate the two conditions.
3
Select the most specific diagnostic test to distinguish heart failure from pulmonary disease.
Serum B-type natriuretic peptide (BNP) is selected.
BNP is released by ventricular myocytes under stretch; normal levels highly rule out acute decompensated heart failure, pointing toward COPD, while significantly elevated levels point toward heart failure.

Key Concept

B-type natriuretic peptide (BNP) is the most helpful laboratory test for differentiating between acute decompensated heart failure and a COPD exacerbation in patients presenting with undifferentiated dyspnea and wheezing.
Estimated Time:1m 0s
Question 140Question →

A 24-year-old woman with type 1 diabetes mellitus presents to the emergency department with abdominal pain, nausea, vomiting, and deep, rapid breathing. Vital signs show a heart rate of 118 /min118\text{ /min} and blood pressure of 90/60 mmHg90/60\text{ mmHg}. Laboratory studies show a blood glucose of 480 mg/dL480 \text{ mg/dL}, an arterial pH of 7.15, positive serum ketones, and a serum potassium of 4.8 mEq/L4.8 \text{ mEq/L}. Arrange the following management steps in the most appropriate chronological sequence for this patient.

Drag items to arrange them in the correct order

Show answer & explanation

Answer

The correct sequence is: 1) Administer an initial bolus of 0.9% normal saline, 2) Initiate continuous intravenous regular insulin infusion, 3) Add 5% dextrose to the intravenous maintenance fluids, 4) Transition to subcutaneous basal and bolus insulin.
The standard protocol for Diabetic Ketoacidosis (DKA) management requires a strict sequence of interventions based on patient safety and pathophysiology. The absolute first priority is intravascular volume repletion with 0.9% normal saline because patients are severely dehydrated from osmotic diuresis. Once volume expansion has begun and serum potassium is confirmed to be safely elevated (> 3.3 mEq/L), an intravenous regular insulin infusion is started to stop lipolysis and ketogenesis. As the insulin works, blood glucose typically drops faster than the ketoacidosis resolves. To prevent hypoglycemia while continuing the insulin necessary to close the anion gap, 5% dextrose is added to the IV fluids once the blood glucose reaches approximately 200 to 250 mg/dL. Finally, after the anion gap is closed, the acidosis has resolved, and the patient can eat, they are safely transitioned to a subcutaneous insulin regimen.

Step-by-Step Solution

1
Recognize the diagnosis of diabetic ketoacidosis (DKA) and the immediate need for volume expansion.
Identify 0.9% normal saline bolus as the priority first step.
Patients with DKA are profoundly dehydrated due to osmotic diuresis, and restoring intravascular volume takes precedence over all other interventions.
2
Evaluate the serum potassium level to determine the safety of insulin therapy.
Identify that since potassium is 4.8 mEq/L, an intravenous insulin infusion can be started safely.
Insulin drives potassium into cells. Starting insulin without checking potassium (or if K+ < 3.3 mEq/L) can cause fatal hypokalemia. With a normal level, insulin is the immediate next step.
3
Determine the management approach for when blood glucose improves but the anion gap remains open.
Identify adding 5% dextrose to IV fluids as the subsequent step.
Glucose usually normalizes faster than the anion gap closes. Dextrose prevents hypoglycemia while allowing the insulin infusion to continue suppressing ketogenesis.
4
Identify the criteria for transitioning off the insulin infusion.
Select transitioning to subcutaneous insulin as the final step.
Once the anion gap closes (DKA resolved) and the patient can eat, they are transitioned to a standard subcutaneous insulin regimen.

Key Concept

The standard sequence of treatment for Diabetic Ketoacidosis (DKA) prioritizes aggressive volume resuscitation, followed by intravenous insulin (dependent on safe potassium levels), adding dextrose when glucose reaches 200 mg/dL, and finally transitioning to subcutaneous insulin upon resolution.
Estimated Time:1m 0s
PreviousPage 7 / 414Next
All practice questions — USMLE Step 2 CK | Examkin