Internal Medicine

3151 questions

All types3,151 Multiple choice1,611 Multiple select73 Numeric81 Matching714 Ordering672

A 24-year-old man is admitted to the hospital with newly diagnosed Burkitt lymphoma. He has a massive abdominal mass and significant cervical lymphadenopathy. Temperature is 37.2°C (99.0°F), blood pressure is 120/78 mmHg, heart rate is 88/min, and respiratory rate is 16/min. Initial laboratory studies show:

Laboratory Parameter	Result
Leukocyte count	12,500/mm³
Hemoglobin	13.2 g/dL
Platelet count	210,000/mm³
Serum creatinine	0.9 mg/dL
Serum uric acid	7.8 mg/dL
Serum potassium	4.2 mEq/L
Serum phosphorus	3.8 mg/dL
Serum calcium	9.2 mg/dL

The patient is scheduled to receive intensive, multi-agent cytotoxic induction chemotherapy. Arrange the following interventions in the most appropriate chronological sequence for the prophylaxis and subsequent step-wise management of tumor lysis syndrome in this patient.

Drag items to arrange them in the correct order

Show answer & explanation

Answer

The correct chronological sequence is: 1. Initiate hydration and allopurinol, 2. Administer chemotherapy, 3. Perform intensive laboratory monitoring, 4. Administer rasburicase for rising uric acid, 5. Initiate hemodialysis for refractory renal failure.

The correct sequence for managing a patient at high risk for tumor lysis syndrome (TLS) begins with absolute prevention. Aggressive intravenous hydration and allopurinol must be initiated prior to chemotherapy to establish high urine flow and prevent initial uric acid formation. Once this prophylaxis is firmly established, the inciting cytotoxic chemotherapy can be safely administered. Following chemotherapy, intensive laboratory monitoring (every 4-6 hours) is crucial to rapidly detect early signs of TLS. If uric acid levels rise significantly despite initial prophylaxis, escalating medical management with rasburicase is administered to rapidly clear existing uric acid. Finally, if life-threatening electrolyte abnormalities like refractory hyperkalemia or acute renal failure occur despite all medical management, emergent hemodialysis is required as the definitive rescue therapy.

Step-by-Step Solution

Identify the patient's condition and risk profile.

The patient has Burkitt lymphoma with a high tumor burden, placing him at very high risk for tumor lysis syndrome (TLS) upon starting chemotherapy.

Burkitt lymphoma is a rapidly dividing tumor that is highly responsive to chemotherapy, predictably leading to massive cell breakdown.

Determine the first required preventive intervention.

Select the initiation of aggressive intravenous hydration and allopurinol.

Pre-hydration ensures adequate urine flow to flush metabolites, and allopurinol blocks the synthesis of new uric acid. This must occur before any tumor breakdown begins.

Identify the inciting event that triggers cell lysis.

Select the administration of the scheduled cytotoxic chemotherapy.

Chemotherapy is the trigger for lysis and must only be given after prophylaxis is fully established.

Determine the immediate post-treatment management strategy.

Select intensive laboratory monitoring of electrolytes and renal function every 4-6 hours.

Close surveillance is necessary to catch the early development of TLS despite prophylaxis.

Identify the escalating medical intervention for developing TLS.

Select rasburicase administration for rapidly rising uric acid levels.

If uric acid rises despite allopurinol, rasburicase is needed to actively degrade the existing uric acid burden.

Determine the final rescue therapy for severe, refractory complications.

Select the initiation of emergent hemodialysis.

Indicated when medical management fails and life-threatening hyperkalemia or anuric acute kidney injury occurs.

Key Concept

The management of Tumor Lysis Syndrome (TLS) follows a strict chronological protocol: prophylaxis (hydration and allopurinol), inciting event (chemotherapy), intensive surveillance, escalating medical management (rasburicase), and finally rescue therapy (hemodialysis).

Estimated Time:1m 30s

Question 1062Question →

A 64-year-old woman with a 10-year history of severe, erosive rheumatoid arthritis comes to the emergency department due to a 2-week history of worsening shortness of breath, orthopnea, and a persistent dry cough. Four months ago, her rheumatologist added a new biologic disease-modifying antirheumatic drug (DMARD) to her regimen of methotrexate and folic acid due to inadequate joint symptom control. She also has a history of mild asthma and diet-controlled type 2 diabetes mellitus.

Vital signs are temperature 37.1°C (98.8°F), blood pressure 110/70 mm Hg, pulse 108/min, and respirations 22/min. Oxygen saturation is 92% on room air.

Physical examination reveals jugular venous distention to 10 cm H2O. Pulmonary auscultation reveals bibasilar crackles without wheezing. Cardiac examination shows a regular tachycardia with a prominent S3 gallop. There is 2+ pitting edema in the bilateral lower extremities.

Laboratory Study	Result	Reference Range
Sodium	135 mEq/L	136–145 mEq/L
Potassium	4.2 mEq/L	3.5–5.0 mEq/L
Chloride	101 mEq/L	95–105 mEq/L
Bicarbonate	18 mEq/L	22–28 mEq/L
Blood urea nitrogen	32 mg/dL	7–18 mg/dL
Creatinine	1.6 mg/dL	0.6–1.2 mg/dL
Thyroid-stimulating hormone (TSH)	5.8 µU/mL	0.4–4.0 µU/mL
Free thyroxine (T4)	1.1 ng/dL	0.9–1.7 ng/dL

Arterial Blood Gas (Room Air)	Result	Reference Range
pH	7.34	7.35–7.45
PaO2	68 mm Hg	75–105 mm Hg
PaCO2	35 mm Hg	33–45 mm Hg

Chest radiograph reveals bilateral interstitial markings, prominent pulmonary vasculature, and cardiomegaly.

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

Discontinue the recently added biologic agent and administer intravenous furosemide

Administer nebulized bronchodilators and oral prednisone

Administer intravenous sodium bicarbonate

Initiate oral levothyroxine therapy

Start empiric intravenous piperacillin-tazobactam

Show answer & explanation

Answer: Discontinue the recently added biologic agent and administer intravenous furosemide

Answer

Discontinue the recently added biologic agent and administer intravenous furosemide

This patient is presenting with classic signs of acute decompensated heart failure (ADHF), including orthopnea, jugular venous distention, an S3 gallop, and pulmonary edema (crackles, bilateral interstitial markings). In a patient with severe rheumatoid arthritis whose regimen was recently stepped up to include a biologic DMARD, the most likely culprit is a tumor necrosis factor (TNF)-alpha inhibitor (e.g., etanercept, adalimumab, infliximab). TNF-alpha inhibitors carry a black-box warning for causing new-onset heart failure or exacerbating existing cardiac disease. The most appropriate next step in management is to immediately discontinue the offending biologic agent and treat the fluid overload with an intravenous loop diuretic such as furosemide.

Step-by-Step Solution

Identify the primary clinical syndrome based on the patient's presentation and examination.

The combination of orthopnea, jugular venous distention, an S3 gallop, pulmonary crackles, and peripheral edema strongly indicates acute decompensated heart failure (ADHF).

Accurate diagnosis of the acute cardiopulmonary crisis is required before identifying the underlying trigger.

Connect the new-onset ADHF to the patient's recent medical history, specifically the medication changes.

The patient was recently started on a new biologic DMARD for rheumatoid arthritis. Tumor necrosis factor (TNF)-alpha inhibitors (e.g., etanercept, infliximab, adalimumab) are common biologic DMARDs that are known to cause or worsen heart failure.

Identifying the iatrogenic cause of the patient's deterioration is essential for proper management.

Determine the most appropriate immediate management for the acute condition and the offending agent.

The offending TNF-alpha inhibitor must be discontinued immediately, and standard ADHF therapy (intravenous loop diuretics like furosemide) should be initiated to offload volume.

Continuing the offending agent will worsen the heart failure, and immediate symptom relief requires diuresis.

Key Concept

Tumor necrosis factor (TNF)-alpha inhibitors can cause new-onset heart failure or exacerbate underlying cardiac dysfunction. In affected patients, the offending biologic must be discontinued and standard heart failure therapy initiated.

Question 1063Question →

Match each clinical scenario describing a high-risk infectious exposure with the most appropriate post-exposure prophylaxis (PEP) or management strategy.

Click a left item, then click its matching right item

Show answer & explanation

Answer

Match the HBV non-responder to HBIG + revaccination; the previously rabies-vaccinated patient to vaccine on days 0 and 3 only; the HIV occupational exposure to 28 days of 3-drug ART; and the oral contraceptive user exposed to meningococcus to ciprofloxacin or ceftriaxone.

Each high-risk exposure corresponds to a highly specific, evidence-based post-exposure protocol that accounts for prior host immunity, medication interactions, and occupational risk.

Step-by-Step Solution

Analyze the hepatitis B exposure scenario.

The worker is a documented non-responder to the first vaccine series and is exposed to a known positive source.

This determines the need for both immediate passive immunity (HBIG) and an attempt at developing active immunity (revaccination series).

Evaluate the rabies exposure scenario.

The patient has a history of a complete pre-exposure rabies vaccination series.

Prior vaccination alters the PEP protocol by eliminating the need for HRIG and reducing the active vaccine schedule to two doses (days 0 and 3).

Assess the HIV exposure.

The exposure is high-risk (deep laceration) from a known HIV-positive source.

Current guidelines mandate a full 3-drug regimen for 4 weeks for high-risk occupational exposures to HIV.

Review the meningococcal prophylaxis scenario.

The patient requires PEP but is actively taking oral contraceptives.

Rifampin induces CYP3A4, which can lead to contraceptive failure. An alternative agent like ciprofloxacin or ceftriaxone must be selected to avoid this drug-drug interaction.

Key Concept

Guideline-concordant post-exposure prophylaxis for specific high-yield occupational and environmental infectious exposures.

Estimated Time:2m 0s

Question 1064Question →

A 68-year-old man is brought to the emergency department by his daughter due to a 1-week history of progressively worsening lethargy, confusion, and severe mid-back pain. He has a past medical history of chronic obstructive pulmonary disease (COPD) and hypertension. For the past few days, he has also experienced severe constipation and increased urinary frequency. His temperature is $37.1^\circ\text{C}$ ( $98.8^\circ\text{F}$ ), blood pressure is $105/65\text{ mmHg}$ , heart rate is $108/\text{min}$ , and respiratory rate is $16/\text{min}$ . Physical examination reveals dry mucous membranes and diminished skin turgor. His lungs are clear to auscultation bilaterally. Neurologic examination shows a lethargic patient who is oriented only to person. There are no focal motor or sensory deficits. Initial laboratory studies show:

Laboratory test	Result
Hemoglobin	$8.4\text{ g/dL}$
Leukocyte count	$7,500/\mu\text{L}$
Platelet count	$160,000/\mu\text{L}$
Blood urea nitrogen	$65\text{ mg/dL}$
Serum creatinine	$3.2\text{ mg/dL}$
Serum calcium	$15.4\text{ mg/dL}$
Serum albumin	$3.6\text{ g/dL}$

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

Intravenous administration of furosemide

Intravenous administration of broad-spectrum antibiotics

Magnetic resonance imaging of the thoracic and lumbar spine

Intravenous administration of

0.9\%

saline

Initiation of urgent hemodialysis

Show answer & explanation

Answer: Intravenous administration of $0.9\%$ saline

Answer

The most appropriate initial step in management is the intravenous administration of 0.9% saline.

The correct answer is the intravenous administration of

0.9\%

saline. This patient's presentation of bone pain, acute renal failure, severe hypercalcemia, and anemia is highly suspicious for multiple myeloma. Regardless of the underlying etiology, severe hypercalcemia (defined as serum calcium

> 14\text{ mg/dL}

) is a medical emergency. High serum calcium causes nephrogenic diabetes insipidus, leading to profound polyuria, dehydration, and prerenal acute kidney injury. The absolute most critical first step in management is aggressive volume expansion with isotonic (

0.9\%

) saline. This restores intravascular volume, improves the glomerular filtration rate (GFR), and directly promotes the urinary excretion of calcium.

Step-by-Step Solution

Identify the primary clinical emergency.

The patient has symptomatic, severe hypercalcemia (

15.4\text{ mg/dL}

) manifesting as lethargy, confusion, constipation, and profound volume depletion (hypotension, tachycardia, dry mucous membranes, prerenal acute kidney injury).

Severe hypercalcemia (

> 14\text{ mg/dL}

) is a life-threatening medical emergency requiring immediate intervention before pursuing definitive diagnostic workups for the underlying cause, which in this case is highly suspicious for multiple myeloma.

Determine the first-line treatment for severe hypercalcemia.

Aggressive intravenous hydration with isotonic (

0.9\%

) saline.

Hypercalcemia induces nephrogenic diabetes insipidus, leading to severe polyuria and volume depletion. Volume expansion with normal saline restores intravascular volume, increases the glomerular filtration rate, and directly promotes renal calcium excretion.

Evaluate and rule out other interventions.

Loop diuretics, hemodialysis, and diagnostic imaging are inappropriate at this exact moment.

Diuretics worsen volume depletion if given before fluids. Dialysis is reserved for refractory cases or volume-overloaded states. Imaging does not take precedence over hemodynamic stabilization.

Key Concept

The initial management of severe hypercalcemia of malignancy focuses on aggressive intravenous hydration with normal saline to restore intravascular volume and promote urinary calcium excretion.

Question 1065Question →

A $54$ -year-old man is evaluated in the emergency department for a fever and chills that started $6$ hours ago. He has a history of diffuse large B-cell lymphoma and received his most recent cycle of chemotherapy $10$ days ago. His temperature is $39.1^\circ$ C ( $102.4^\circ$ F), blood pressure is $110/70$ mm Hg, pulse is $115$ /min, and respirations are $24$ /min. Physical examination is unremarkable, with no focal source of infection identified. His central venous port site appears clean without erythema or induration.

Laboratory results are as follows:

Laboratory Test	Result	Reference Range
Hemoglobin	$9.2$ g/dL	$13.5$ – $17.5$ g/dL
Platelet count	$90,000$ /mm $^3$	$150,000$ – $400,000$ /mm $^3$
Leukocyte count	$800$ /mm $^3$	$4,500$ – $11,000$ /mm $^3$
Absolute neutrophil count	$200$ /mm $^3$	$\geq 1,500$ /mm $^3$
Thyroid-stimulating hormone (TSH)	$1.1$ $\mu$ U/mL	$0.5$ – $5.0$ $\mu$ U/mL
Free thyroxine (T4)	$0.5$ ng/dL	$0.9$ – $1.7$ ng/dL

Arterial Blood Gas	Result	Reference Range
pH	$7.48$	$7.35$ – $7.45$
pCO $_2$	$29$ mm Hg	$35$ – $45$ mm Hg
HCO $_3^-$	$22$ mEq/L	$22$ – $28$ mEq/L

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

Obtain blood cultures and start intravenous cefepime

Obtain blood cultures and start intravenous vancomycin

Delay antibiotic therapy pending blood culture results

Initiate oral levothyroxine therapy

Administer intravenous sodium bicarbonate

Show answer & explanation

Answer: Obtain blood cultures and start intravenous cefepime

Answer

Obtain blood cultures and start intravenous cefepime

The correct answer is to obtain blood cultures and start an intravenous antipseudomonal beta-lactam such as cefepime. This patient has febrile neutropenia, defined as a single oral temperature of

\geq 38.3^\circ

C (

101^\circ

F) or a sustained temperature

\geq 38.0^\circ

C (

100.4^\circ

F) for

\geq 1

hour, accompanied by an absolute neutrophil count (ANC)

< 500

/mm

^3

. Because these patients lack a robust inflammatory response, bacterial infections can rapidly progress to overwhelming sepsis and death. The most critical initial step is to immediately draw blood cultures and administer empiric, broad-spectrum intravenous antibiotics. The initial antibiotic regimen must have activity against Pseudomonas aeruginosa, as it is associated with a rapidly fatal course in neutropenic patients. Cefepime, meropenem, or piperacillin-tazobactam are appropriate choices for initial monotherapy.

Step-by-Step Solution

Identify the primary life-threatening condition based on the presentation and complete blood count.

The patient has a temperature of

39.1^\circ

C and an absolute neutrophil count of

200

/mm

^3

, establishing the diagnosis of febrile neutropenia.

Febrile neutropenia is an oncologic emergency requiring immediate intervention to prevent rapid progression to sepsis.

Determine the most appropriate initial empiric management for high-risk febrile neutropenia.

Blood cultures must be drawn, followed immediately by the administration of broad-spectrum intravenous antibiotics with antipseudomonal activity (e.g., cefepime, meropenem, or piperacillin-tazobactam).

Patients with severe neutropenia cannot mount a sufficient inflammatory response, making them highly susceptible to fatal infections, particularly from Pseudomonas aeruginosa.

Evaluate the distracting laboratory abnormalities to rule out other immediate interventions.

The thyroid studies indicate euthyroid sick syndrome, and the arterial blood gas shows respiratory alkalosis secondary to fever/tachypnea. Neither requires specific targeted treatment.

Treating incidental physiologic adaptations or misinterpreting the acid-base status distracts from the life-saving step of administering antibiotics.

Key Concept

Management of febrile neutropenia requires immediate empiric administration of broad-spectrum intravenous antibiotics with antipseudomonal coverage, such as cefepime.

Estimated Time:1m 30s

Question 1066Question →

Emergency medical services bring a 59-year-old woman to the emergency department after her daughter found her unarousable at home. The daughter reports that the patient has had a productive cough, subjective fevers, and generalized weakness for the past three days. Medical history is significant for severe chronic obstructive pulmonary disease and type 2 diabetes mellitus. Her current temperature is 38.6°C (101.5°F), blood pressure is 88/54 mm Hg, pulse is 118/min, and respirations are 24/min and shallow. Pulse oximetry shows 84% on room air. On physical examination, the patient is obtunded and only withdraws to painful stimuli. Lung auscultation reveals diffuse coarse rhonchi bilaterally.

Laboratory test	Result
Arterial blood gas (room air)
pH	7.15
PaCO2	44 mm Hg
PaO2	52 mm Hg
Serum chemistry
Sodium	140 mEq/L
Potassium	4.8 mEq/L
Chloride	100 mEq/L
Bicarbonate	14 mEq/L
Blood urea nitrogen	32 mg/dL
Creatinine	1.8 mg/dL
Lactate	5.5 mmol/L

A peripheral intravenous line is established, and a bolus of isotonic crystalloid is initiated along with empiric ceftriaxone and azithromycin. Which of the following is the most appropriate next step in the management of this patient?

Endotracheal intubation

Trial of noninvasive positive-pressure ventilation

Intravenous sodium bicarbonate administration

Intravenous furosemide administration

Transition to piperacillin-tazobactam and vancomycin

Show answer & explanation

Answer: Endotracheal intubation

Answer

Endotracheal intubation

The correct answer is endotracheal intubation. This patient presents with septic shock (hypotension, fever, elevated lactate) secondary to pneumonia, leading to a high anion gap metabolic acidosis. Applying Winter's formula (

PaCO_2 = 1.5 \times [HCO_3^-] + 8 \pm 2

), the expected

PaCO_2

for a bicarbonate of 14 mEq/L is 29 mm Hg (range 27-31). Her actual

PaCO_2

is 44 mm Hg, which indicates a concurrent respiratory acidosis (failure to mount the appropriate respiratory compensation, likely due to COPD and altered sensorium). While noninvasive positive-pressure ventilation (NIPPV) is typically the initial respiratory intervention for hypercapnic respiratory failure in COPD exacerbations, this patient is obtunded. Altered mental status is an absolute contraindication to NIPPV due to the inability to protect the airway and the consequent high risk of aspiration. Therefore, she requires immediate definitive airway protection with endotracheal intubation.

Step-by-Step Solution

Analyze the acid-base status to determine the primary and secondary disorders.

Anion Gap =

140 - (100 + 14) = 26

. Expected

PaCO_2 = 1.5 \times 14 + 8 = 29 \pm 2

mm Hg. Actual

PaCO_2

is 44 mm Hg.

Identifying the acid-base disturbances is essential for understanding the etiology of the patient's deterioration. The high anion gap indicates a primary metabolic acidosis (lactic acidosis from sepsis), while the inappropriately elevated PaCO2 indicates a concurrent primary respiratory acidosis (hypoventilation).

Assess the severity of the respiratory failure and the patient's neurologic status.

The patient is acidemic (pH 7.15), hypoxic (PaO2 52 mm Hg), and obtunded (withdraws only to pain).

To determine the appropriate modality for ventilatory support. An obtunded patient cannot protect their airway.

Select the appropriate intervention prioritizing the ABCs (Airway, Breathing, Circulation).

Endotracheal intubation is selected over noninvasive ventilation.

Although noninvasive positive-pressure ventilation (NIPPV) is standard for COPD exacerbations with hypercapnia, altered mental status is an absolute contraindication due to aspiration risk.

Key Concept

Patients with mixed metabolic and respiratory acidosis presenting with altered mental status and hypercapnic respiratory failure require immediate endotracheal intubation, as altered mental status is an absolute contraindication to noninvasive positive-pressure ventilation.

Question 1067Question →

During a shift in the emergency department, you evaluate a febrile patient who reports recent intravenous drug use. Physical examination reveals splinter hemorrhages, Janeway lesions, and a prominent holosystolic murmur at the apex radiating to the axilla. Suspecting acute infective endocarditis, the medical team prepares to initiate care. Arrange the following diagnostic and therapeutic steps in the most appropriate chronological order.

Drag items to arrange them in the correct order

Show answer & explanation

Answer

The correct sequence is: 1) Obtain blood cultures, 2) Initiate empiric antibiotics, 3) Perform a TTE, and 4) Perform a TEE if necessary.

The fundamental principle in managing suspected acute infective endocarditis is to secure the microbiological diagnosis before administering therapies that could alter the results. Therefore, obtaining multiple sets of blood cultures is always the first step. Because acute endocarditis can lead to rapid valvular destruction and systemic embolization, empiric antibiotics must be started immediately after the cultures are drawn. Once medical therapy is initiated, structural assessment of the heart is performed using a transthoracic echocardiogram (TTE), which is the standard initial imaging modality. A transesophageal echocardiogram (TEE) provides superior visualization but is more invasive; thus, it is sequenced last and utilized primarily when the TTE is negative, non-diagnostic, or if there is a high suspicion of perivalvular extension (e.g., abscess).

Step-by-Step Solution

Secure microbiological diagnosis

Obtain blood cultures before starting antibiotics

Administering antibiotics first can sterilize the blood, making targeted therapy impossible.

Stabilize and treat the infection

Start empiric broad-spectrum intravenous antibiotics

Acute infective endocarditis is rapidly progressive; treatment cannot be delayed for imaging.

Visualize the valves non-invasively

Perform a transthoracic echocardiogram (TTE)

TTE is the initial imaging test of choice due to its non-invasive nature and high specificity.

Further characterize the anatomy if needed

Perform a transesophageal echocardiogram (TEE)

Used when TTE is inconclusive or to rule out complications like paravalvular abscesses.

Key Concept

In acute infective endocarditis, blood cultures must be drawn prior to empiric antibiotics, followed by initial non-invasive imaging (TTE), with invasive imaging (TEE) reserved for specific indications.

Question 1068Question →

A 68-year-old man presents to the clinic with progressive dyspnea and a nonproductive cough over the past week. He reports waking up several times at night feeling starved for air and has recently started using three pillows to sleep comfortably. His medical history includes hypertension, hyperlipidemia, and a 30-pack-year smoking history, though he quit 10 years ago. Current medications include amlodipine and atorvastatin. Blood pressure is 155/92 mm Hg, pulse is 96/min, and respirations are 22/min. Oxygen saturation is 92% on room air. Physical examination shows elevated jugular venous pressure. Lung auscultation reveals bibasilar crackles and mild expiratory wheezing. There is 2+ pitting edema in the bilateral lower extremities. Which of the following is the most appropriate next step in pharmacological management?

Intravenous furosemide

Oral prednisone

Inhaled albuterol and ipratropium

Oral azithromycin

Intravenous piperacillin-tazobactam

Show answer & explanation

Answer: Intravenous furosemide

Answer

Intravenous furosemide

The correct answer is intravenous furosemide. This patient's presentation of orthopnea (using multiple pillows), paroxysmal nocturnal dyspnea, elevated jugular venous pressure, bibasilar crackles, and bilateral lower extremity edema is classic for acute decompensated heart failure (ADHF). The presence of mild wheezing is also common in ADHF due to peribronchial edema, a phenomenon often referred to as 'cardiac asthma.' The mainstay of initial therapy for ADHF is reducing volume overload and cardiac preload with intravenous loop diuretics, such as furosemide.

Step-by-Step Solution

Analyze the patient's presentation and physical exam findings.

The patient exhibits orthopnea, paroxysmal nocturnal dyspnea, elevated jugular venous pressure, bibasilar crackles, and bilateral pitting edema.

These findings are the hallmark clinical signs of volume overload and acute decompensated heart failure (ADHF).

Determine the appropriate initial therapy for this diagnosis.

Loop diuretics, such as intravenous furosemide, should be administered.

Intravenous loop diuretics provide rapid symptom relief by increasing diuresis, reducing volume overload, and decreasing cardiac preload.

Key Concept

Diagnosis and initial management of acute decompensated heart failure, distinguishing it from a COPD exacerbation.

Question 1069Question →

A 55-year-old man comes to the urgent care clinic with sudden, severe pain and swelling in his right big toe that awoke him from sleep. He has a history of hypertension and recently recovered from a mild respiratory illness. Vital signs are within normal limits. Physical examination reveals a markedly erythematous, warm, and exquisitely tender right first metatarsophalangeal joint. Synovial fluid analysis shows a leukocyte count of 18,000/µL. Polarized light microscopy of the fluid reveals needle-shaped, negatively birefringent crystals, and the Gram stain is negative. Which of the following is the most appropriate initial management for this patient's current condition?

Oral colchicine

Intravenous cefazolin and admit to the hospital

Oral allopurinol

Intravenous furosemide

Surgical debridement of the joint

Show answer & explanation

Answer: Oral colchicine

Answer

Oral colchicine

The patient's presentation of podagra (inflammation of the first metatarsophalangeal joint) along with synovial fluid showing needle-shaped, negatively birefringent crystals confirms the diagnosis of an acute gout flare. First-line medical therapy for acute gout includes NSAIDs, colchicine, or glucocorticoids. Oral colchicine is highly effective when started early in the course of an attack.

Step-by-Step Solution

Analyze the patient's clinical presentation and synovial fluid results.

The patient has acute monoarticular arthritis of the first metatarsophalangeal joint (podagra) with negatively birefringent, needle-shaped crystals.

Identifying the crystals is the definitive step to differentiate between various causes of acute monoarthritis.

Diagnose the underlying condition.

The diagnosis is an acute gout flare, caused by monosodium urate crystal deposition.

Negatively birefringent needle-shaped crystals are pathognomonic for gout, whereas pseudogout would show weakly positively birefringent rhomboid crystals.

Determine the most appropriate initial therapy.

First-line therapies for acute gout include NSAIDs, colchicine, or systemic glucocorticoids.

These agents rapidly reduce acute inflammation. Urate-lowering therapies are generally not initiated during an acute flare without concurrent anti-inflammatory prophylaxis.

Key Concept

Diagnosis and acute management of gout

Question 1070Question →

A 32-year-old woman comes to the clinic due to progressive fatigue and decreased exercise tolerance over the past 4 months. She has no significant past medical history and takes no medications. The patient reports having heavy menstrual periods, often soaking a pad every 2 hours during the first 3 days of her cycle. Vital signs are within normal limits. Physical examination shows mild conjunctival pallor but no jaundice or organomegaly. Laboratory studies show:

Hemoglobin: 9.8 g/dL
Mean corpuscular volume (MCV): 74 fL
White blood cell count: 6,500/mm³
Platelet count: 410,000/mm³

Which of the following is the most appropriate initial diagnostic test for this patient?

Serum iron studies

Hemoglobin electrophoresis

Direct antiglobulin test

Vitamin B12 and folate levels

Bone marrow aspiration and biopsy

Show answer & explanation

Answer: Serum iron studies

Answer

Serum iron studies

The correct answer is serum iron studies. The patient presents with fatigue, conjunctival pallor, and heavy menstrual bleeding, along with laboratory evidence of a microcytic anemia (MCV < 80 fL) and reactive thrombocytosis. This clinical picture is highly suggestive of iron deficiency anemia secondary to chronic blood loss. The most appropriate initial step in the diagnostic workup of microcytic anemia is to check serum iron studies (including ferritin, iron, and total iron-binding capacity) to confirm iron deficiency before initiating therapy.

Step-by-Step Solution

Classify the patient's anemia based on the laboratory values.

The patient has a hemoglobin of 9.8 g/dL and an MCV of 74 fL, indicating a microcytic anemia.

Categorizing anemia by MCV narrows the differential diagnosis to microcytic, normocytic, or macrocytic causes.

Correlate the laboratory findings with the clinical history.

The history of heavy menstrual bleeding strongly points to chronic blood loss as the underlying cause of the microcytic anemia.

Chronic blood loss is the leading cause of iron deficiency anemia in premenopausal women.

Identify the standard diagnostic workup for the suspected condition.

The most appropriate next step is to obtain serum iron studies (including ferritin, serum iron, and total iron-binding capacity).

Noninvasive iron studies are required to formally diagnose iron deficiency before initiating supplementation.

Key Concept

Evaluation of microcytic anemia and diagnosis of iron deficiency

Question 1071Question →

An emergency medical services team brings a 68-year-old woman to the resuscitation bay in January due to progressive lethargy and generalized swelling over the past 48 hours. Two weeks ago, she experienced a mild upper respiratory tract infection. Her past medical history is notable for hypertension, hyperlipidemia, and a severe postpartum hemorrhage requiring multiple blood transfusions 38 years ago. Current medications include amlodipine and atorvastatin. Vital signs show a temperature of 34.2°C (93.6°F), blood pressure of 88/56 mm Hg, heart rate of 48/min, and respiratory rate of 8/min. Pulse oximetry is 90% on room air. Physical examination reveals a somnolent patient who only awakens to painful stimuli. Her face appears puffy with marked periorbital edema, and deep tendon reflexes exhibit significantly delayed relaxation. Lung fields are clear to auscultation.

Initial laboratory testing reveals the following:
Sodium: 124 mEq/L
Potassium: 4.1 mEq/L
Chloride: 92 mEq/L
Bicarbonate: 26 mEq/L

Arterial blood gas (room air):
pH: 7.24
PaCO2: 68 mm Hg
PaO2: 62 mm Hg

Thyroid-stimulating hormone (TSH): 1.5 mU/L (Normal: 0.5–5.0 mU/L)
Free T4: 0.3 ng/dL (Normal: 0.9–1.7 ng/dL)

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

Administer intravenous hydrocortisone prior to intravenous levothyroxine

Administer intravenous levothyroxine immediately to reverse the metabolic state

Administer an intravenous sodium bicarbonate infusion to rapidly correct the acidemia

Initiate non-invasive positive pressure ventilation and administer nebulized glycopyrrolate and arformoterol

Administer empiric intravenous cefepime and vancomycin alongside a rapid crystalloid bolus

Show answer & explanation

Answer: Administer intravenous hydrocortisone prior to intravenous levothyroxine

Answer

Administer intravenous hydrocortisone prior to intravenous levothyroxine

The correct sequence of therapy requires recognizing that this patient has myxedema coma caused by panhypopituitarism, likely Sheehan syndrome, given her history of severe postpartum hemorrhage and a thyroid panel showing central hypothyroidism (low Free T4, normal TSH). Because central adrenal insufficiency is concurrently present, administering levothyroxine alone will accelerate the metabolic clearance of cortisol and provoke a fatal acute adrenal crisis. Intravenous hydrocortisone must be given first to provide stress-dose steroid coverage.

Step-by-Step Solution

Identify the clinical syndrome

The patient is presenting with myxedema coma, evidenced by profound hypothermia, bradycardia, altered mental status, delayed deep tendon reflexes, and non-pitting edema.

Recognizing the life-threatening extreme of hypothyroidism is required to initiate emergency endocrine resuscitation.

Analyze the acid-base and electrolyte status

The patient has severe hyponatremia and acute uncompensated respiratory acidosis (low pH, high PaCO2) driven by hypoventilation.

This confirms the severity of the myxedema coma and rules out primary metabolic causes for the acidemia.

Interpret the thyroid panel

The patient has a low Free T4 (0.3 ng/dL) with an inappropriately normal TSH (1.5 mU/L).

This laboratory pattern indicates central (secondary) hypothyroidism rather than primary hypothyroidism (where TSH would be markedly elevated).

Synthesize the endocrine history

The history of severe postpartum hemorrhage 38 years ago, combined with central hypothyroidism, points to Sheehan syndrome (postpartum pituitary necrosis) leading to panhypopituitarism.

Panhypopituitarism implies concurrent deficiencies in other pituitary hormones, most critically ACTH, resulting in central adrenal insufficiency.

Determine the pharmacological sequence

Intravenous hydrocortisone must be administered before or simultaneously with intravenous levothyroxine.

Administering thyroid hormone increases basal metabolic rate and hepatic clearance of cortisol. In a patient with untreated adrenal insufficiency, this will precipitate a fatal acute adrenal crisis.

Key Concept

In patients with suspected panhypopituitarism (e.g., Sheehan syndrome) presenting with myxedema coma, glucocorticoids must be administered before thyroid hormone replacement to avoid precipitating an acute adrenal crisis.

Question 1072Question →

Match each classic physical examination finding with the most likely rheumatologic diagnosis.

Click a left item, then click its matching right item

Show answer & explanation

Answer

Bony DIP outgrowths correspond to osteoarthritis. Violaceous knuckle plaques correspond to dermatomyositis. Diffuse digit swelling with nail pitting corresponds to psoriatic arthritis. Symmetric MCP swelling with ulnar deviation corresponds to rheumatoid arthritis.

Each rheumatologic condition has a classic physical examination signature. Osteoarthritis causes osteophyte formation (Heberden nodes at DIP, Bouchard nodes at PIP). Dermatomyositis presents with pathognomonic skin findings like Gottron papules on the knuckles. Psoriatic arthritis often involves dactylitis (sausage digits) and nail changes due to enthesitis. Rheumatoid arthritis causes erosive, symmetric synovitis leading to ulnar deviation and subluxation at the MCP joints.

Step-by-Step Solution

Analyze the specific joint involvement and associated dermatologic findings for each presentation.

Identified distinct patterns pathognomonic for four major rheumatologic diseases.

Pattern recognition of physical exam findings is the primary step in diagnosing and differentiating rheumatologic conditions.

Key Concept

Physical examination hallmarks in rheumatologic diseases

Question 1073Question →

A medical student is reviewing common adverse effects of antihypertensive medications frequently prescribed in the primary care setting. Match each patient's clinical presentation to the antihypertensive medication most likely responsible for their symptoms.

Click a left item, then click its matching right item

Show answer & explanation

Answer

The correct matches align the persistent dry cough with Lisinopril, the pitting ankle edema with Amlodipine, the acute gout flare with Hydrochlorothiazide, and the fatigue with cold extremities with Metoprolol.

Each clinical presentation represents a classic, high-yield adverse effect of a primary antihypertensive drug class. Lisinopril (ACE inhibitor) causes a bradykinin-mediated cough. Amlodipine (calcium channel blocker) causes peripheral edema via precapillary vasodilation. Hydrochlorothiazide (thiazide diuretic) decreases renal uric acid excretion, precipitating gout. Metoprolol (beta-blocker) reduces cardiac output, leading to fatigue and cold extremities.

Step-by-Step Solution

Analyze the first presentation (dry cough).

Identified as a bradykinin-mediated adverse effect.

Points to an ACE inhibitor (Lisinopril).

Analyze the second presentation (pitting ankle edema).

Identified as a precapillary vasodilation effect.

Points to a dihydropyridine calcium channel blocker (Amlodipine).

Analyze the third presentation (acute gout flare).

Identified as a consequence of reduced renal uric acid clearance.

Points to a thiazide diuretic (Hydrochlorothiazide).

Analyze the fourth presentation (fatigue and cold extremities).

Identified as a result of reduced cardiac output and peripheral vasoconstriction.

Points to a beta-blocker (Metoprolol).

Key Concept

Adverse effects of first-line antihypertensive medications.

Question 1074Question →

A 62-year-old man is evaluated in the hematology-oncology unit for persistent daily fevers. He was admitted 14 days ago to undergo induction chemotherapy for acute myeloid leukemia. Four days ago, he developed a fever of 38.9°C (102.0°F) when his absolute neutrophil count (ANC) was 200/mm³. After blood cultures were obtained, empiric intravenous cefepime was initiated. Today, his temperature is 38.8°C (101.8°F), blood pressure is 118/76 mmHg, pulse is 98/min, and respiratory rate is 18/min. His current ANC is 100/mm³. The initial blood cultures have shown no growth after 96 hours. The patient now reports the onset of mild, right-sided pleuritic chest pain. Physical examination reveals normal heart sounds and clear lung fields bilaterally. His tunneled central venous catheter site appears clean with no surrounding erythema or induration. A non-contrast chest CT demonstrates a 2.5-cm dense nodule in the right upper lobe surrounded by a distinct rim of ground-glass opacity. Serum galactomannan and beta-D-glucan assays are drawn and pending. Which of the following is the most appropriate next step in management?

Initiate intravenous voriconazole

Initiate intravenous caspofungin

Replace cefepime with intravenous meropenem

Add intravenous vancomycin

Withhold further pharmacotherapy until fungal biomarkers return

Show answer & explanation

Answer: Initiate intravenous voriconazole

Answer

The most appropriate next step is to initiate intravenous voriconazole.

This patient's clinical picture is classic for invasive pulmonary aspergillosis (IPA). He has prolonged neutropenic fever unresponsive to broad-spectrum antibacterials, combined with a new onset of pleuritic chest pain and a defining 'halo sign' on his chest CT. The halo sign is caused by a central pulmonary nodule (representing tissue infarction) surrounded by a ring of ground-glass opacity (representing alveolar hemorrhage), which occurs due to the angioinvasive nature of Aspergillus. In profoundly immunocompromised patients, delayed treatment of invasive mold infections is associated with exceedingly high mortality. Therefore, the most appropriate next step is to initiate empiric antifungal therapy with a mold-active triazole, such as voriconazole or isavuconazole, while awaiting definitive diagnostic results like the serum galactomannan assay.

Step-by-Step Solution

Analyze the clinical timeline and immune status.

The patient has profound neutropenia (ANC < 500/mm³) and persistent fever for 4 days despite broad-spectrum antipseudomonal beta-lactam therapy (cefepime).

Persistent fever in a neutropenic patient beyond 4-7 days of appropriate antibacterial therapy raises the clinical suspicion for invasive fungal infections.

Interpret the new clinical and radiographic findings.

Pleuritic chest pain combined with a CT showing a pulmonary nodule surrounded by ground-glass opacity (the 'halo sign').

The 'halo sign' represents a central area of pulmonary infarction surrounded by alveolar hemorrhage, which is highly characteristic of angioinvasive fungi, primarily Aspergillus species.

Determine the standard of care intervention.

Selection of a mold-active triazole (voriconazole or isavuconazole) immediately, rather than waiting for serum galactomannan results.

Invasive pulmonary aspergillosis has a very high mortality rate in neutropenic patients; delaying therapy for definitive diagnostic test results is contraindicated.

Key Concept

Invasive Pulmonary Aspergillosis Management in Neutropenia

Estimated Time:1m 30s

Question 1075Question →

A 54-year-old woman is brought to the emergency department by her daughter after experiencing a witnessed generalized tonic-clonic seizure. The patient has a history of severe systemic lupus erythematosus and is currently managed with chronic cyclophosphamide and high-dose prednisone. Her temperature is 39.3°C (102.7°F), blood pressure is 142/88 mm Hg, and heart rate is 114/min. She is postictal and difficult to arouse. Neurologic examination is limited by her somnolence but reveals profound nuchal rigidity. Arrange the following diagnostic and therapeutic steps in the most appropriate sequential order for the immediate management of this patient.

Drag items to arrange them in the correct order

Show answer & explanation

Answer

The correct sequence is to first obtain peripheral blood cultures, immediately administer intravenous dexamethasone and empiric antimicrobial therapy, then perform a non-contrast CT scan of the head, followed by a lumbar puncture, and finally de-escalate the antimicrobial therapy based on microbiological data.

The correct management algorithm for suspected bacterial meningitis requires immediate assessment for indications to perform a CT scan before a lumbar puncture. These indications include immunocompromised state, history of central nervous system disease, new-onset seizure, papilledema, altered consciousness, and focal neurologic deficits. Because this patient is severely immunocompromised (chronic cyclophosphamide and prednisone) and presents with a new-onset seizure, a CT scan is mandatory. In such cases, it is critical not to delay therapy; peripheral blood cultures must be drawn immediately, followed by the administration of empiric broad-spectrum antibiotics and dexamethasone. Only after therapy is initiated should the patient be sent for a CT scan. Once the CT scan rules out significant mass effect, a lumbar puncture is performed safely. Finally, the broad-spectrum regimen is tailored based on the final microbiological culture and sensitivity results.

Step-by-Step Solution

Identify the indications for neuroimaging prior to lumbar puncture.

The patient's immunosuppressive regimen and new-onset seizure mandate a head CT to rule out mass effect.

Performing an unguided lumbar puncture in a patient with a potential mass lesion can precipitate fatal cerebral herniation.

Obtain blood cultures.

Microbiological samples are secured before the administration of antibiotics.

Antibiotics can rapidly sterilize the blood, severely reducing the diagnostic yield of subsequent cultures.

Administer empiric antibiotics and dexamethasone.

Life-saving antimicrobial therapy is initiated immediately.

Mortality increases significantly if antibiotics are delayed while waiting for a CT scan to be performed and read.

Perform the non-contrast head CT, followed by the lumbar puncture.

The safety of the lumbar puncture is confirmed, and cerebrospinal fluid is obtained for Gram stain and culture.

Provides definitive microbiological data to guide long-term directed therapy once it is safe to do so.

Key Concept

In patients with suspected bacterial meningitis who have indications for a CT scan prior to lumbar puncture (e.g., immunosuppression, new-onset seizure, focal neurologic deficit), blood cultures must be drawn and empiric antibiotics administered BEFORE the CT scan to prevent treatment delays.

Estimated Time:1m 30s

Question 1076Question →

A 72-year-old retired mechanic presents to the emergency department with a 3-day history of progressively worsening shortness of breath. He reports needing to sleep propped up on three pillows and has developed a new nocturnal cough producing frothy white sputum. His medical history includes severe chronic obstructive pulmonary disease (COPD), a myocardial infarction three years ago, and chronic fatigue. His only home medications are a tiotropium inhaler and aspirin.

Vital signs show a temperature of 37.0°C (98.6°F), blood pressure of 160/90 mm Hg, heart rate of 110/min, and respiratory rate of 26/min. Pulse oximetry is 88% on room air.

Physical examination reveals an anxious man using accessory muscles of respiration. Jugular venous pressure is measured at 10 cm $H_2O$ . Chest auscultation reveals diffuse bilateral expiratory wheezes and fine bibasilar crackles. An S3 gallop is heard at the cardiac apex. The lower extremities show bilateral 2+ pitting edema.

Initial laboratory studies show:
Leukocyte count: 8,500/ $mm^3$
Brain natriuretic peptide (BNP): 920 pg/mL (normal < 100)
Thyroid-stimulating hormone (TSH): 1.5 $\mu U/mL$ (normal: 0.5-5.0)
Free T4: 0.6 ng/dL (normal: 0.9-1.7)

Arterial blood gas on room air:
pH: 7.28
$PaCO_2$ : 58 mm Hg
$PaO_2$ : 54 mm Hg
$HCO_3^-$ : 26 mEq/L

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

Administration of oral prednisone and nebulized tiotropium

Initiation of intravenous meropenem therapy

Intravenous administration of bumetanide

Intravenous infusion of sodium bicarbonate

Initiation of oral levothyroxine therapy

Show answer & explanation

Answer: Intravenous administration of bumetanide

Answer

Intravenous administration of bumetanide

The correct intervention is the intravenous administration of a loop diuretic, such as bumetanide. The patient's clinical presentation is classic for acute decompensated heart failure (ADHF) with cardiogenic pulmonary edema. While he has a history of COPD, the combination of orthopnea, elevated jugular venous pressure, an S3 gallop, bibasilar crackles, and an elevated BNP level strongly confirms ADHF. The diffuse wheezing is a manifestation of peribronchial edema, often termed 'cardiac asthma.' Initial management of ADHF requires supplemental oxygen and rapid preload reduction using intravenous loop diuretics.

Step-by-Step Solution

Evaluate the primary cause of acute respiratory distress based on physical exam and laboratory findings.

Findings of orthopnea, elevated jugular venous pressure, an S3 gallop, bibasilar crackles, and an elevated brain natriuretic peptide (BNP) indicate acute decompensated heart failure (ADHF) with pulmonary edema.

Differentiating between ADHF and a COPD exacerbation is a critical first step, as both can present with dyspnea, hypoxia, and wheezing ('cardiac asthma').

Analyze the arterial blood gas results.

An acute, uncompensated respiratory acidosis is present, which is consistent with poor gas exchange secondary to severe pulmonary edema.

Understanding the primary acid-base disturbance ensures the clinician avoids treating secondary physiological compensations inappropriately.

Select the most appropriate initial pharmacological intervention.

Intravenous loop diuretics (such as bumetanide or torsemide) are indicated alongside supplemental oxygen.

Loop diuretics rapidly reduce intravascular volume and right-sided preload, effectively relieving pulmonary congestion and improving oxygenation.

Key Concept

Differentiating acute decompensated heart failure (cardiac asthma) from a COPD exacerbation, and initiating appropriate acute management with intravenous loop diuretics.

Estimated Time:1m 30s

Question 1077Question →

Match each classic clinical presentation to the most likely hematologic diagnosis.

Click a left item, then click its matching right item

Show answer & explanation

Answer

The patient with back pain and hypercalcemia matches Multiple myeloma. The young woman with a mediastinal mass matches Hodgkin lymphoma. The patient with massive splenomegaly and BCR-ABL1 matches Chronic myeloid leukemia. The asymptomatic elderly man with lymphocytosis matches Chronic lymphocytic leukemia.

Each clinical vignette provides pathognomonic or highly characteristic features for its respective malignancy. Multiple myeloma features CRAB criteria. Hodgkin lymphoma classically affects young adults with cervical and mediastinal adenopathy. Chronic myeloid leukemia is defined by the BCR-ABL1 translocation and often presents with splenomegaly. Chronic lymphocytic leukemia typically presents as an incidental extreme lymphocytosis in older adults.

Step-by-Step Solution

Analyze the first presentation (back pain, hypercalcemia, kidney injury).

Identifies the diagnosis as Multiple myeloma.

These symptoms fulfill the CRAB criteria (Calcium, Renal, Anemia, Bone) characteristic of this plasma cell dyscrasia.

Analyze the second presentation (young female, painless lymphadenopathy, mediastinal mass).

Identifies the diagnosis as Hodgkin lymphoma.

This matches the classic bimodal age distribution and typical nodal involvement of this lymphoma.

Analyze the third presentation (splenomegaly, BCR-ABL1 mutation).

Identifies the diagnosis as Chronic myeloid leukemia.

Early satiety from splenomegaly and the BCR-ABL1 mutation are the hallmark diagnostic features.

Analyze the fourth presentation (elderly, asymptomatic lymphocytosis).

Identifies the diagnosis as Chronic lymphocytic leukemia.

This is the most common presentation of CLL, often discovered incidentally on routine laboratory testing.

Key Concept

Classic clinical presentations of major hematologic malignancies

Question 1078Question →

A 48-year-old woman with a history of limited cutaneous systemic sclerosis presents to the clinic with worsening episodes of painful blanching and cyanosis in her fingers upon cold exposure. She states that these episodes are becoming more frequent and severe despite wearing insulated gloves and strictly avoiding cold temperatures. Her physical examination is notable for sclerodactyly and multiple telangiectasias on her face and hands. No digital ulcers are currently present, but capillary refill is delayed during an episode in the clinic. Arrange the following therapeutic interventions in the correct order of escalation for the management of this patient's Raynaud phenomenon, starting from the most appropriate initial pharmacologic treatment to the therapy of last resort for critical digital ischemia.

Drag items to arrange them in the correct order

Show answer & explanation

Answer

The correct escalation sequence is: 1) oral calcium channel blockers, 2) oral phosphodiesterase-5 inhibitors, 3) intravenous prostanoids, 4) surgical digital sympathectomy.

The standard of care for severe secondary Raynaud phenomenon follows a stepwise escalation: lifestyle modifications are followed by oral calcium channel blockers as first-line pharmacotherapy. If symptoms persist, a phosphodiesterase-5 inhibitor is added. For severe refractory disease with critical ischemia or digital ulcers, intravenous prostanoids are administered. Surgical digital sympathectomy is strictly a treatment of last resort for imminent tissue loss.

Step-by-Step Solution

Identify the underlying condition and the failure of initial conservative management.

The patient has secondary Raynaud phenomenon due to systemic sclerosis and has already failed lifestyle modifications (cold avoidance).

Confirming the failure of conservative measures justifies the initiation of pharmacologic therapy.

Determine the first-line pharmacologic agent for secondary Raynaud phenomenon.

Oral dihydropyridine calcium channel blockers (e.g., nifedipine, amlodipine) are selected as the initial medical intervention.

These agents promote vasodilation and are the most effective initial oral medications for reducing the frequency of attacks.

Identify the next step if first-line monotherapy is insufficient.

An oral phosphodiesterase-5 inhibitor (e.g., sildenafil) is added as second-line therapy.

PDE-5 inhibitors provide additional vasodilation through the nitric oxide pathway for patients with refractory symptoms.

Determine the intervention for severe, treatment-resistant disease or critical ischemia.

Intravenous prostanoids (e.g., epoprostenol) are utilized for severe ischemia or active digital ulceration.

IV prostanoids are potent vasodilators but require intravenous access and close monitoring, limiting their use to severe cases.

Identify the definitive treatment of last resort.

Surgical digital sympathectomy is placed at the end of the algorithm.

This is an invasive surgical procedure considered only for limb-threatening ischemia when maximal medical therapy has completely failed.

Key Concept

Stepwise escalation of therapy in secondary Raynaud phenomenon

Estimated Time:1m 30s

Question 1079Question →

A 65-year-old man presents to the clinic with a 3-week history of progressively worsening shortness of breath and swelling in his legs. He reports waking up in the middle of the night gasping for air and now requires three pillows to sleep comfortably. His medical history is significant for severe, erosive rheumatoid arthritis, chronic obstructive pulmonary disease, and hypertension. His medications include methotrexate, lisinopril, tiotropium, and acetaminophen. Three months ago, his rheumatologist added etanercept due to inadequately controlled joint symptoms. He has a 40-pack-year smoking history but quit 5 years ago. Vital signs show a temperature of 37.0°C (98.6°F), blood pressure of 145/85 mmHg, pulse of 96/min, and respiratory rate of 22/min. Pulse oximetry shows 94% on room air. Physical examination reveals distended jugular veins, bibasilar lung crackles, and 3+ bilateral pitting edema up to the knees. Cardiac auscultation reveals a regular rhythm with an S3 gallop. Joint examination shows chronic deformities but no acute inflammation. Which of the following is the most likely cause of this patient's current presentation?

Toxic effect of a biologic agent on ventricular function

Acute exacerbation of chronic obstructive pulmonary disease

Inflammatory interstitial pulmonary fibrosis

Opportunistic bacterial pneumonia

Idiosyncratic pulmonary reaction to methotrexate

Show answer & explanation

Answer: Toxic effect of a biologic agent on ventricular function

Answer

Toxic effect of a biologic agent on ventricular function

The patient's presentation of progressive dyspnea, orthopnea, paroxysmal nocturnal dyspnea, jugular venous distension, bibasilar crackles, an S3 gallop, and lower extremity edema is the classic clinical picture of acute decompensated heart failure (ADHF). Tumor necrosis factor (TNF)-alpha inhibitors, such as etanercept, infliximab, and adalimumab, are biologic disease-modifying antirheumatic drugs (DMARDs) used for severe rheumatoid arthritis. A well-documented and highly tested adverse effect of TNF-alpha inhibitors is the development of new-onset heart failure or the exacerbation of underlying heart failure. Therefore, these agents should be used with extreme caution or completely avoided in patients with moderate to severe heart failure. The addition of etanercept three months ago is the most likely culprit for his sudden ventricular dysfunction and subsequent volume overload.

Step-by-Step Solution

Analyze the clinical presentation and physical examination findings.

The patient presents with orthopnea, paroxysmal nocturnal dyspnea, jugular venous distension, bibasilar crackles, an S3 gallop, and severe pitting edema.

To establish the primary physiologic syndrome, which is acute decompensated heart failure characterized by profound volume overload.

Review the patient's medical history and recent medication changes.

The patient has a history of severe rheumatoid arthritis and recently started etanercept three months ago.

To identify potential triggers, etiologies, or iatrogenic causes for the new-onset heart failure.

Connect the medication profile to the clinical syndrome.

Etanercept is a TNF-alpha inhibitor, a class of drugs known to cause or worsen heart failure.

Recognizing this adverse effect identifies the most likely cause of the patient's acute decompensation, as TNF-alpha inhibitors are strictly contraindicated in moderate-to-severe heart failure.

Key Concept

Tumor necrosis factor (TNF)-alpha inhibitors (e.g., etanercept, infliximab, adalimumab) can cause new-onset heart failure or exacerbate underlying heart failure, and their use is contraindicated in patients with moderate to severe ventricular dysfunction.

Estimated Time:1m 30s

Question 1080Question →

A 65-year-old woman is brought to the emergency department due to progressive confusion, generalized weakness, and recurrent vomiting over the past 4 days. Her medical history is significant for breast cancer treated with a lumpectomy, radiation, and chemotherapy 6 years ago. Vital signs show a temperature of 37.1°C (98.8°F), blood pressure of 100/60 mm Hg, heart rate of 112/min, and respiratory rate of 14/min. Physical examination is notable for dry mucous membranes, delayed capillary refill, and lethargy.

Laboratory evaluation reveals the following:

Laboratory Test	Result	Reference Range
Serum calcium	15.6 mg/dL	8.4-10.2 mg/dL
Serum albumin	3.8 g/dL	3.5-5.0 g/dL
Serum creatinine	2.1 mg/dL	0.6-1.1 mg/dL

An electrocardiogram demonstrates a shortened QT interval.

Arrange the following management steps in the most appropriate temporal sequence for the acute stabilization and definitive therapy of this patient, from initial action to long-term management.

Drag items to arrange them in the correct order

Show answer & explanation

Answer

The correct sequential order is: 1) Initiate aggressive intravenous volume expansion with 0.9% normal saline, 2) Administer calcitonin, 3) Administer an intravenous bisphosphonate, 4) Direct systemic therapy against the underlying relapsed malignancy.

The proper sequence for managing severe symptomatic hypercalcemia (> 14 mg/dL) begins with aggressive intravenous hydration (isotonic saline) to reverse severe volume depletion and improve renal calcium excretion. Because hydration alone is insufficient, calcitonin is administered to rapidly lower calcium levels within hours. Intravenous bisphosphonates (like zoledronic acid) are given to provide a sustained reduction in serum calcium, but because they take 48-72 hours to achieve full effect and can be nephrotoxic in dehydrated patients, they are administered following initial volume expansion. Finally, treating the underlying malignancy provides definitive, long-term resolution of the condition.

Step-by-Step Solution

Assess the clinical presentation and laboratory data.

The patient has severe symptomatic hypercalcemia (calcium > 14 mg/dL) complicated by profound dehydration and acute kidney injury.

Identifying the severity of hypercalcemia and its physiological impact on volume status dictates the urgency and sequence of interventions.

Select the most critical initial stabilization measure.

Intravenous volume expansion with isotonic saline is chosen as the first step.

Hypercalcemia causes a nephrogenic diabetes insipidus-like state, leading to severe volume depletion. Restoring intravascular volume improves glomerular filtration and increases renal calcium clearance.

Select the rapid-acting pharmacological therapy.

Calcitonin is administered next.

Calcitonin acts rapidly (within hours) to inhibit osteoclast function, bridging the temporal gap before long-acting agents take full effect.

Select the long-acting pharmacological therapy.

An intravenous bisphosphonate is administered.

Bisphosphonates provide sustained calcium reduction but take 48-72 hours to reach maximum effect. They must follow initial hydration to reduce the risk of nephrotoxicity.

Determine the definitive long-term management.

Systemic therapy for the underlying malignancy is planned.

Treating the root cause (relapsed breast cancer) is essential to prevent recurrent hypercalcemia once the acute crisis is managed.

Key Concept

The acute management of severe symptomatic hypercalcemia requires sequential, targeted interventions: initial aggressive volume expansion, followed by rapid-acting agents (calcitonin), long-acting agents (bisphosphonates), and ultimately treating the underlying malignant cause.

Estimated Time:1m 30s

PreviousPage 54 / 158Next

Internal Medicine

Answer

Step-by-Step Solution

Key Concept

Common Mistakes

Answer

Step-by-Step Solution

Key Concept

Common Mistakes

Answer

Step-by-Step Solution

Key Concept

Common Mistakes

Answer

Step-by-Step Solution

Key Concept

Common Mistakes

Answer

Step-by-Step Solution

Key Concept

Common Mistakes

Answer

Step-by-Step Solution

Key Concept

Common Mistakes

Answer

Step-by-Step Solution

Key Concept

Common Mistakes

Answer

Step-by-Step Solution

Key Concept

Common Mistakes

Answer

Step-by-Step Solution

Key Concept

Common Mistakes

Answer

Step-by-Step Solution

Key Concept

Common Mistakes

Answer

Step-by-Step Solution

Key Concept

Common Mistakes

Answer

Step-by-Step Solution

Key Concept

Common Mistakes

Answer

Step-by-Step Solution

Key Concept

Common Mistakes

Answer

Step-by-Step Solution

Key Concept

Common Mistakes

Answer

Step-by-Step Solution

Key Concept

Common Mistakes

Answer

Step-by-Step Solution

Key Concept

Common Mistakes

Answer

Step-by-Step Solution

Key Concept

Common Mistakes

Answer

Step-by-Step Solution

Key Concept

Common Mistakes

Answer

Step-by-Step Solution

Key Concept

Common Mistakes

Answer

Step-by-Step Solution

Key Concept