Internal Medicine

3151 questions

Question 481Question →

Antimicrobial stewardship emphasizes selecting the appropriate agent, dose, and duration while minimizing unnecessary broad-spectrum coverage to prevent resistance. Match each of the following common infectious disease presentations with the most appropriate guideline-concordant initial management strategy.

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Items

A 28-year-old non-pregnant woman presenting with dysuria, urinary frequency, and suprapubic pain, without fever or costovertebral angle tenderness.
A 45-year-old otherwise healthy man with a 2.5 cm fluctuant, erythematous cutaneous abscess on his back and normal vital signs.
A 50-year-old healthy woman with unilateral, spreading erythema and warmth on her lower leg, without fluctuance, purulence, or systemic toxicity.
A 35-year-old previously healthy man presenting with a 3-day history of productive cough, fever, and focal crackles, with no medical comorbidities.

Matches

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Answer

Uncomplicated cystitis requires nitrofurantoin or fosfomycin; a simple cutaneous abscess requires only incision and drainage; non-purulent cellulitis is managed with targeted beta-lactams (e.g., cephalexin); and uncomplicated outpatient community-acquired pneumonia is treated with amoxicillin or doxycycline.
Each presentation is accurately matched to its guideline-recommended empiric therapy. The choices highlight key stewardship concepts: avoiding fluoroquinolones in simple cystitis, relying on source control for simple abscesses, targeting streptococci rather than MRSA in non-purulent cellulitis, and utilizing amoxicillin or doxycycline for uncomplicated outpatient pneumonia.

Step-by-Step Solution

1
Analyze the clinical presentation of the 28-year-old woman.
Identified as uncomplicated cystitis.
Choosing targeted agents like nitrofurantoin minimizes collateral damage and adheres to stewardship guidelines, avoiding fluoroquinolones.
2
Evaluate the 45-year-old man with a fluctuant abscess.
Identified as a simple abscess requiring incision and drainage without antibiotics.
Systemic antibiotics do not improve cure rates for small, simple abscesses without systemic signs, and their use increases the risk of adverse effects.
3
Assess the 50-year-old woman with spreading erythema.
Identified as non-purulent cellulitis, best treated with cephalexin or dicloxacillin.
Because non-purulent cellulitis is overwhelmingly caused by Streptococcus species, empiric MRSA coverage (e.g., vancomycin, linezolid) is unwarranted.
4
Review the 35-year-old man with acute respiratory symptoms.
Identified as outpatient community-acquired pneumonia (CAP) in a healthy host.
Guidelines recommend amoxicillin or doxycycline for outpatients without comorbidities or recent antibiotic exposure.

Key Concept

Antimicrobial stewardship and guideline-concordant empiric therapy for common outpatient infections.
Question 482Question →

A 6262-year-old woman is brought to the emergency department by her husband due to progressive confusion, profound weakness, and mild shortness of breath over the past 33 days. She has a history of estrogen receptor-positive breast cancer treated with lumpectomy and radiation 44 years ago. Two months ago, she developed severe back pain and was diagnosed with widespread osteolytic metastases. For the past week, she has been extremely thirsty, urinating frequently, and has not had a bowel movement in 44 days. Her husband reports she has become increasingly lethargic today.

Vital signs are: temperature 37.1∘C37.1^\circ\text{C} (98.8∘F98.8^\circ\text{F}), pulse 112112/min, blood pressure 88/5588/55 mm Hg, and respirations 1818/min.

Physical examination reveals dry mucous membranes and decreased skin turgor. The lungs are clear to auscultation. Heart sounds are rapid but regular. The abdomen is mildly distended with decreased bowel sounds. Neurologic examination shows a lethargic patient who is oriented to name only.

Laboratory studies show:
Laboratory TestResultReference Range
Hemoglobin10.210.2 g/dL12.0−15.512.0-15.5 g/dL
Leukocytes7,5007,500/mm3^34,500−11,0004,500-11,000/mm3^3
Sodium148148 mEq/L136−145136-145 mEq/L
Potassium4.14.1 mEq/L3.5−5.03.5-5.0 mEq/L
Calcium (total)14.814.8 mg/dL8.4−10.28.4-10.2 mg/dL
Albumin3.53.5 g/dL3.5−5.53.5-5.5 g/dL
Creatinine2.22.2 mg/dL0.6−1.10.6-1.1 mg/dL

Which of the following is the most appropriate initial step in the management of this patient's current condition?

Show answer & explanation

Answer: Intravenous infusion of 0.9% normal saline

Answer

The most appropriate initial step is the administration of an intravenous infusion of 0.9% normal saline.
The correct answer is the intravenous infusion of 0.9%0.9\% normal saline. This patient is presenting with a hypercalcemic crisis secondary to widespread osteolytic metastases from breast cancer. Severe hypercalcemia (typically >14>14 mg/dL) induces nephrogenic diabetes insipidus, leading to polyuria, profound dehydration, and acute kidney injury. This hypovolemia is evidenced by her hypotension, tachycardia, dry mucous membranes, and elevated sodium and creatinine. The absolute first step in managing severe hypercalcemia is aggressive volume resuscitation with isotonic saline (typically at 200−300200-300 mL/hr). This dilutes the serum calcium, restores the glomerular filtration rate (GFR), and increases the renal excretion of calcium. Once the patient is euvolemic, long-term treatments such as bisphosphonates (e.g., zoledronic acid) or calcitonin can be safely administered.

Step-by-Step Solution

1
Identify the primary medical emergency from the clinical presentation and laboratory data.
The patient has severe hypercalcemia (14.814.8 mg/dL) due to osteolytic metastases from breast cancer, complicated by severe dehydration and acute kidney injury.
Hypercalcemia causes nephrogenic diabetes insipidus, leading to massive polyuria, polydipsia, volume depletion, and subsequent acute kidney injury (creatinine 2.22.2 mg/dL) and hypotension.
2
Determine the priority of interventions for severe hypercalcemia of malignancy.
Immediate intravascular volume expansion must precede all other therapies.
Volume expansion with isotonic saline restores the glomerular filtration rate (GFR), dilutes serum calcium, and promotes the renal excretion of calcium.

Key Concept

The initial management of severe hypercalcemia of malignancy always begins with aggressive intravenous hydration using isotonic saline to restore intravascular volume and promote renal calcium excretion.
Question 483Question →

A 74-year-old man is hospitalized for the management of melena and severe symptomatic anemia. He has a notable medical history of essential hypertension, type 2 diabetes mellitus, and stage 3 chronic kidney disease. Upon admission, his hemoglobin level is 5.8 g/dL5.8 \text{ g/dL}, and he is prescribed three units of packed red blood cells. Approximately 30 minutes into the transfusion of the third unit, the patient reports sudden-onset shortness of breath and a dry cough.

Current vital signs include a temperature of 37.2∘C37.2^\circ\text{C} (99.0∘F99.0^\circ\text{F}), blood pressure of 178/96 mm Hg178/96 \text{ mm Hg}, heart rate of 115/min115/\text{min}, and respiratory rate of 26/min26/\text{min}. Pulse oximetry displays an oxygen saturation of 86%86\% while breathing room air.

Physical examination shows prominent jugular venous distention when the patient is seated at a 45-degree angle. Auscultation of the lungs reveals bilateral basilar crackles without any audible wheezing. Cardiac examination demonstrates a regular tachycardia with a prominent S3 gallop.

An arterial blood gas analysis on room air yields the following results:

pH: 7.287.28
PaCO 2_2: 56 mm Hg56 \text{ mm Hg}
PaO 2_2: 52 mm Hg52 \text{ mm Hg}
HCO 3−_3^-: 25 mEq/L25 \text{ mEq/L}

A portable chest radiograph displays bilateral pulmonary infiltrates, an enlarged cardiac silhouette, and widening of the vascular pedicle.

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

Show answer & explanation

Answer: Administer intravenous furosemide

Answer

The most appropriate next step in management is to administer intravenous furosemide to treat Transfusion-Associated Circulatory Overload (TACO).
The correct answer is to administer intravenous furosemide. This patient is experiencing Transfusion-Associated Circulatory Overload (TACO), a common complication of blood product administration, particularly in patients with underlying cardiac or renal disease (such as this patient's chronic kidney disease). TACO is characterized by acute respiratory distress, hypertension, tachycardia, and classic signs of volume overload, including jugular venous distention, an S3 gallop, and pulmonary crackles. Arterial blood gas analysis typically reveals hypoxemia and, in severe or fatiguing cases, an acute respiratory acidosis due to poor ventilation. Management involves immediately stopping the transfusion, providing supplemental oxygen or noninvasive ventilatory support, and administering loop diuretics like furosemide to reduce intravascular volume.

Step-by-Step Solution

1
Analyze the patient's presentation and vital signs during the blood transfusion.
The patient developed acute respiratory distress, hypoxemia, and significant hypertension (178/96 mm Hg178/96 \text{ mm Hg}) during the third unit of packed red blood cells.
Identifying the timeline and vital sign changes is critical for differentiating between types of acute transfusion reactions.
2
Evaluate the physical examination and radiographic findings.
The presence of jugular venous distention, an S3 gallop, bibasilar crackles, cardiomegaly, and a widened vascular pedicle indicates cardiogenic volume overload.
These findings distinguish volume overload from other pulmonary pathologies like ARDS, TRALI, or pneumonia.
3
Determine the optimal therapeutic intervention.
The patient is experiencing Transfusion-Associated Circulatory Overload (TACO) and requires immediate diuresis with intravenous furosemide.
Diuretics reduce the intravascular volume and hydrostatic pressure, rapidly resolving the pulmonary edema.

Key Concept

Transfusion-Associated Circulatory Overload (TACO) presents with respiratory distress, hypertension, and signs of cardiogenic pulmonary edema (JVD, S3 gallop) during or shortly after a blood transfusion, and is managed primarily with diuretics and respiratory support.
Question 484Question →

A 73-year-old man presents to the emergency department with severe, progressively worsening shortness of breath over the past 48 hours. His medical history is significant for ischemic cardiomyopathy with a left ventricular ejection fraction of 35%, severe chronic obstructive pulmonary disease, and stage 3 chronic kidney disease. The patient reports having to sleep upright in a chair to breathe. Temperature is 37.0°C (98.6°F), blood pressure is 168/94 mm Hg, pulse is 112/min, and respirations are 26/min. Pulse oximetry shows 86% on room air. Physical examination reveals use of accessory muscles of respiration. Jugular venous pressure is estimated at 10 cm H2OH_2O. Chest auscultation reveals bilateral basilar crackles extending to the mid-lung fields and prolonged expiration with diffuse end-expiratory wheezes. Lower extremities show 2+ pitting edema.

Laboratory results are as follows:
Sodium: 138 mEq/L
Potassium: 4.8 mEq/L
Chloride: 104 mEq/L
Bicarbonate: 16 mEq/L
Blood urea nitrogen: 42 mg/dL
Creatinine: 2.1 mg/dL (baseline 1.8 mg/dL)
Lactic acid: 3.8 mmol/L
Thyroid-stimulating hormone (TSH): 0.9 μ\mu U/mL (Normal: 0.4-4.0 μ\mu U/mL)
Free T4: 0.6 ng/dL (Normal: 0.9-1.7 ng/dL)

Arterial blood gas on room air:
pH: 7.30
PaCO2PaCO_2: 31 mm Hg
PaO2PaO_2: 54 mm Hg

Chest radiograph demonstrates cardiomegaly, bilateral hazy perihilar opacities, and cephalization of the pulmonary vessels without focal consolidation. Which of the following is the most appropriate next step in management?

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Answer: Intravenous furosemide and noninvasive positive pressure ventilation

Answer

Intravenous furosemide and noninvasive positive pressure ventilation
The correct choice directly addresses acute decompensated heart failure (ADHF) with cardiogenic pulmonary edema and hypoxemic respiratory failure. The patient's elevated jugular venous pressure, orthopnea, crackles, and classic chest radiograph findings (cardiomegaly, perihilar opacities) confirm fluid overload. Noninvasive positive pressure ventilation (NPPV) is indicated because it decreases the work of breathing and improves oxygenation, while simultaneously decreasing both preload and afterload. Intravenous loop diuretics (furosemide) are required to reduce the underlying volume overload.

Step-by-Step Solution

1
Identify the primary clinical syndrome from the patient's presentation.
The patient has elevated jugular venous pressure, orthopnea, bilateral crackles, pitting edema, and a chest radiograph showing cardiomegaly with perihilar opacities. This indicates Acute Decompensated Heart Failure (ADHF).
Recognizing the signs of cardiogenic pulmonary edema is necessary to select the correct initial treatment.
2
Differentiate the cause of wheezing in this specific patient.
Although the patient has a history of COPD, the wheezing is 'cardiac asthma' caused by peribronchial edema secondary to volume overload, rather than a primary COPD exacerbation.
Misinterpreting the wheezing leads to incorrect treatment with bronchodilators and steroids instead of diuretics.
3
Evaluate the acid-base status to rule out impending respiratory failure.
Using Winter's formula (1.5×[HCO3−]+81.5 \times [HCO_3^-] + 8), the expected PaCO2PaCO_2 is 1.5×16+8=32±21.5 \times 16 + 8 = 32 \pm 2 mm Hg. The patient's actual PaCO2PaCO_2 of 31 mm Hg indicates a simple metabolic acidosis (likely lactic acidosis from hypoperfusion) with appropriate respiratory compensation.
Confirming appropriate respiratory compensation prevents the incorrect assumption of a superimposed respiratory acidosis that might prompt premature intubation.
4
Select the most appropriate initial pharmacological and respiratory support.
Initiate intravenous furosemide for rapid diuresis and noninvasive positive pressure ventilation (NPPV) to improve oxygenation and decrease the work of breathing.
NPPV and loop diuretics are the first-line therapies for ADHF presenting with severe respiratory distress.

Key Concept

Management of Acute Decompensated Heart Failure (ADHF) and differentiation from COPD exacerbation
Estimated Time:1m 30s
Question 485Question →

Match each gastrointestinal disorder to its primary underlying pathophysiological mechanism of malabsorption or characteristic histologic finding.

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Items

Whipple disease
Celiac disease
Small intestinal bacterial overgrowth (SIBO)
Zollinger-Ellison syndrome
Terminal ileal Crohn disease

Matches

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Answer

Whipple disease matches with lymphatic obstruction by PAS-positive macrophages; Celiac disease matches with immune-mediated villous atrophy; SIBO matches with microbial deconjugation of bile salts; Zollinger-Ellison syndrome matches with inactivation of pancreatic enzymes by acid; Terminal ileal Crohn disease matches with impaired active transport of conjugated bile acids.
Each disorder represents a distinct pathophysiological category of malabsorption: mucosal injury (Celiac disease), lymphatic obstruction (Whipple disease), altered luminal pH inactivating enzymes (Zollinger-Ellison syndrome), microbial alteration of bile salts (SIBO), and disruption of enterohepatic circulation (Terminal ileal Crohn disease).

Step-by-Step Solution

1
Analyze the mechanism for Whipple disease.
Tropheryma whipplei causes PAS-positive macrophage infiltration in the lamina propria.
These macrophages physically block lymphatic drainage in the lacteals, preventing chylomicron absorption.
2
Analyze the mechanism for Celiac disease.
Gluten sensitivity leads to immune-mediated mucosal damage characterized by villous atrophy.
The physical loss of absorptive surface area directly impairs the uptake of all nutrients.
3
Analyze the mechanism for Small intestinal bacterial overgrowth (SIBO).
Enteric bacteria deconjugate bile acids prematurely in the upper gut.
Deconjugated bile acids are rapidly absorbed in the jejunum instead of the ileum, preventing adequate micelle formation for fat absorption.
4
Analyze the mechanism for Zollinger-Ellison syndrome.
Massive amounts of gastric acid enter the duodenum.
Pancreatic enzymes (especially lipase) require a neutral or alkaline pH to function; the acid denatures them, preventing luminal fat digestion.
5
Analyze the mechanism for Terminal ileal Crohn disease.
Inflammation destroys the specialized transport mechanisms for conjugated bile acids in the terminal ileum.
Failure of the enterohepatic circulation depletes the bile acid pool, impairing micelle formation and fat absorption.

Key Concept

Pathophysiological Mechanisms of Malabsorption
Question 486Question →

An ambulatory 29-year-old male construction worker presents to his primary care provider with a 6-month history of progressive fatigue, diminished libido, and a 6-kg (13-lb) weight gain. He states that he feels constantly sluggish and cold, even during warm weather. Fourteen months ago, he sustained a severe traumatic brain injury during a scaffolding collapse at work, which required a 3-week stay in the intensive care unit. His blood pressure is 105/70 mm Hg, and his pulse is 55/min. Physical examination reveals pale skin, sparse axillary and pubic hair, and a delayed relaxation phase of the deep tendon reflexes.

Laboratory studies show:

Laboratory TestResultReference Range
Thyroid-stimulating hormone (TSH)1.2 μU/mL1.2\ \mu\text{U/mL}0.5 - 5.0 μU/mL0.5\text{ - }5.0\ \mu\text{U/mL}
Free thyroxine (T4)0.3 ng/dL0.3\text{ ng/dL}0.9 - 2.4 ng/dL0.9\text{ - }2.4\text{ ng/dL}

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

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Answer: Magnetic resonance imaging of the brain

Answer

Magnetic resonance imaging of the brain
Magnetic resonance imaging of the brain is the correct next step because this patient has central (secondary) hypothyroidism as part of a broader post-traumatic hypopituitarism syndrome. His clinical presentation includes features of hypothyroidism (weight gain, delayed reflexes) and hypogonadism (sparse hair, low libido). The diagnosis of central hypothyroidism is confirmed by a low free T4 paired with an inappropriately normal TSH. The pituitary gland failed to increase TSH secretion in response to the low free T4. Severe traumatic brain injury is a known cause of anterior pituitary dysfunction due to direct tissue contusion, shearing of the pituitary stalk, or vascular injury. Once central hypothyroidism is identified biochemically, patients must undergo neuroimaging (MRI) of the hypothalamic-pituitary region and have other pituitary axes evaluated.

Step-by-Step Solution

1
Analyze the clinical presentation and physical examination.
The patient exhibits classic signs of hypothyroidism (fatigue, cold intolerance, weight gain, bradycardia, delayed reflexes) and hypogonadism (diminished libido, sparse body hair) 14 months after a severe traumatic brain injury.
Identifying the multi-axis endocrine deficits provides context for interpreting the laboratory results.
2
Interpret the thyroid function laboratory studies.
The free T4 is overtly low (0.3 ng/dL0.3\ \text{ng/dL}), but the TSH is inappropriately normal (1.2 μU/mL1.2\ \mu\text{U/mL}).
A normal or low TSH in the presence of a low free T4 indicates a failure of the pituitary gland to mount an appropriate compensatory response.
3
Determine the underlying diagnosis and select the next appropriate step.
The laboratory pattern confirms central (secondary) hypothyroidism, likely caused by post-traumatic hypopituitarism. The next step is to obtain a brain MRI and evaluate other anterior pituitary hormones.
Anatomical imaging of the hypothalamic-pituitary axis is required to evaluate for structural damage (e.g., stalk shearing, ischemic necrosis, or empty sella) resulting from the prior trauma.

Key Concept

Central (secondary) hypothyroidism presents with a low free T4 level and an inappropriately normal or low TSH. Following a traumatic brain injury, patients can develop post-traumatic hypopituitarism; the diagnosis requires evaluation of pituitary hormones and magnetic resonance imaging of the brain.
Question 487Question →

A 51-year-old man is currently hospitalized for the management of acute complicated diverticulitis. Four days ago, he presented with severe left lower quadrant abdominal pain, and a computed tomography scan revealed a 4.2-cm4.2\text{-cm} pericolic abscess. The abscess was successfully managed with computed tomography-guided percutaneous drainage. Due to a documented history of extended-spectrum beta-lactamase (ESBL) urinary tract infections, he was empirically started on intravenous meropenem upon admission.

Today, the patient reports feeling well and his abdominal pain has completely resolved. He is tolerating a regular diet without nausea. His temperature is 37.1∘C37.1^\circ\text{C} (98.8∘F98.8^\circ\text{F}), blood pressure is 122/78 mmHg122/78\text{ mmHg}, and pulse is 76/min76/\text{min}. His leukocyte count has decreased from 17,500/mm317,500/\text{mm}^3 at admission to 7,200/mm37,200/\text{mm}^3. The percutaneous drain output has been negligible for the past 24 hours, and the catheter was removed this morning.

The finalized abscess fluid culture demonstrates heavy growth of *Escherichia coli* and *Bacteroides fragilis*. Susceptibility testing of the *E. coli* isolate reveals sensitivity to amoxicillin-clavulanate, ceftriaxone, and ciprofloxacin, with no evidence of ESBL production.

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

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Answer: Discharge the patient with a prescription for oral amoxicillin-clavulanate

Answer

Discharge the patient with a prescription for oral amoxicillin-clavulanate.
This patient presented with complicated diverticulitis (pericolic abscess), which was appropriately managed with percutaneous drainage and empiric broad-spectrum antibiotics (meropenem) due to his ESBL history. Now, the patient has achieved clinical stability (afebrile, normal hemodynamics), adequate source control (drain removed after minimal output), and is tolerating an oral diet. These factors make him an ideal candidate for transition from intravenous to oral antibiotic therapy. The culture results demonstrate an absence of ESBL-producing organisms, allowing for the de-escalation of the carbapenem. Amoxicillin-clavulanate provides comprehensive and targeted coverage for both the isolated enteric gram-negative rod (E. coli) and the anaerobe (B. fragilis), perfectly aligning with antibiotic stewardship guidelines.

Step-by-Step Solution

1
Evaluate the patient's clinical trajectory and source control status.
The patient is afebrile, tolerating oral intake, has a normalized white blood cell count, and the abscess was successfully drained and removed.
Determines if the patient is eligible for transition from intravenous to oral antibiotic therapy.
2
Analyze the abscess culture and susceptibility results.
Cultures grew non-ESBL E. coli and B. fragilis, both of which are fully covered by narrower-spectrum agents.
Guides antibiotic de-escalation from empiric broad-spectrum therapy to targeted therapy.
3
Select the most appropriate oral step-down regimen.
Oral amoxicillin-clavulanate provides excellent coverage for both enteric gram-negative rods and anaerobes without providing unnecessary coverage.
Adheres to antibiotic stewardship principles by using the narrowest effective spectrum.

Key Concept

De-escalation of empiric broad-spectrum antibiotics to targeted, narrow-spectrum oral agents in patients with complicated diverticulitis once source control is achieved and culture data are available.
Estimated Time:1m 30s
Question 488Question →

Match the following high-resolution esophageal manometry (HRM) profiles based on the Chicago Classification to their most appropriate clinical diagnoses.

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Items

Elevated integrated relaxation pressure (IRP>15IRP > 15 mm Hg) and 100%100\% failed peristalsis.
Normal IRPIRP and ≥20%\ge 20\% premature swallows (distal latency <4.5< 4.5 seconds).
Normal IRPIRP and ≥20%\ge 20\% hypercontractile swallows (distal contractile integral >8,000> 8,000 mm Hg ⋅\cdot s ⋅\cdot cm).
Decreased resting lower esophageal sphincter (LES) pressure and absent peristalsis in the smooth muscle portion of the esophagus.

Matches

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Answer

The correct matches are: Elevated IRP with failed peristalsis corresponds to Achalasia; normal IRP with premature swallows corresponds to Distal esophageal spasm; normal IRP with hypercontractile swallows corresponds to Jackhammer esophagus; and decreased LES pressure with absent peristalsis corresponds to Systemic sclerosis.
The diagnosis of esophageal motility disorders relies on high-resolution manometry (HRM). Achalasia is defined by absent peristalsis and impaired LES relaxation (elevated IRPIRP). Distal esophageal spasm features normal LES relaxation but premature, rapid contractions. Jackhammer esophagus features normal relaxation but extremely high-amplitude, hypercontractile swallows. Systemic sclerosis causes smooth muscle atrophy in the lower two-thirds of the esophagus, resulting in absent peristalsis and a hypotensive LES, which differentiates it from achalasia.

Step-by-Step Solution

1
Assess the integrated relaxation pressure (IRPIRP) to evaluate lower esophageal sphincter (LES) function.
An elevated IRPIRP (>15> 15 mm Hg) indicates an outflow obstruction, typically pointing to achalasia.
Failure of the LES to relax is the hallmark of achalasia.
2
Evaluate the integrity and timing of peristalsis if the IRPIRP is normal.
Premature swallows indicate distal esophageal spasm, while absent peristalsis with a hypotensive LES suggests scleroderma.
Differentiation of motility disorders relies on contraction pattern (premature vs. absent) when outflow obstruction is ruled out.
3
Assess the vigor of contractions using the distal contractile integral (DCI).
A DCI >8,000> 8,000 mm Hg ⋅\cdot s ⋅\cdot cm indicates Jackhammer esophagus.
Extreme hypercontractility defines this specific motility disorder.

Key Concept

Diagnosis of esophageal motility disorders using Chicago Classification criteria on high-resolution manometry.
Question 489Question →

A 2424-year-old woman presents to the emergency department with a 22-day history of severe abdominal cramps and frequent, grossly bloody diarrhea. She recalls eating an undercooked hamburger at a picnic 44 days prior. Her temperature is 37.2∘C37.2^\circ\mathrm{C} (99.0∘F99.0^\circ\mathrm{F}), blood pressure is 110/70 mmHg110/70\text{ mmHg}, and pulse is 105/min105\text{/min}. Physical examination reveals diffuse abdominal tenderness without rebound or guarding. Suspecting an infection with enterohemorrhagic \textit{Escherichia coli} (EHEC), arrange the following clinical management steps in the most appropriate chronological order.

Drag items to arrange them in the correct order

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Answer

The correct sequence is: 1) Send stool for culture and Shiga toxin assay, 2) Initiate IV fluids and strictly withhold empiric antibiotics, 3) Monitor serial blood counts and renal function for HUS, 4) Initiate hemodialysis if refractory uremia develops.
The correct chronological management of suspected enterohemorrhagic E. coli begins with diagnostic testing (Shiga toxin assay) to confirm the etiology. The immediate therapeutic step is fluid resuscitation while strictly avoiding antibiotics, as their use increases Shiga toxin release and the risk of Hemolytic Uremic Syndrome (HUS). Following initial stabilization, the patient must be monitored with serial blood counts and renal function panels to detect the onset of HUS (thrombocytopenia, hemolytic anemia, acute kidney injury). Finally, if HUS progresses to severe or refractory renal failure, late-stage supportive care with hemodialysis is indicated.

Step-by-Step Solution

1
Initial Diagnostic Workup
Stool is sent for culture and Shiga toxin assay.
Identifying the specific pathogen is crucial because the presence of Shiga toxin dictates a specific divergence from standard infectious diarrhea protocols.
2
Primary Medical Management
Intravenous fluids are administered and antibiotics are withheld.
Empiric antibiotics cause bacterial cell lysis and increased Shiga toxin release, drastically increasing the risk of hemolytic uremic syndrome (HUS). Hydration protects the kidneys.
3
Surveillance for Complications
Serial monitoring of platelets, hemoglobin, schistocytes, and creatinine is performed.
EHEC infections carry a high risk of progressing to HUS, which presents with thrombocytopenia, microangiopathic hemolytic anemia, and acute kidney injury.
4
Management of Severe Complications
Hemodialysis is initiated if necessary.
In cases where HUS leads to severe, irreversible, or highly symptomatic acute kidney injury (e.g., refractory anuria), dialysis is the required supportive treatment.

Key Concept

Management of Shiga toxin-producing E. coli (EHEC) involves avoiding antibiotics to prevent Hemolytic Uremic Syndrome (HUS), utilizing aggressive fluid resuscitation, and monitoring for microangiopathic complications.
Question 490Question →

A 7171-year-old male is transported to the emergency room by emergency medical services after his family found him writhing in severe abdominal pain. He reports a 33-day history of colicky abdominal pain, intractable nausea, and bilious vomiting. He has not passed stool or flatus for the past 4848 hours. His medical history includes hypertension, hyperlipidemia, and an open partial colectomy performed 88 years ago. On arrival, his temperature is 39.4∘C39.4^\circ\text{C} (102.9∘F102.9^\circ\text{F}), blood pressure is 88/50 mmHg88/50\text{ mmHg}, pulse is 128/min128/\text{min}, and respiratory rate is 26/min26/\text{min}. Physical examination reveals a tensely distended abdomen. There is diffuse, severe tenderness to palpation with involuntary guarding and positive rebound tenderness. Auscultation reveals a complete absence of bowel sounds.

Laboratory studies show:

Laboratory TestResult
Leukocyte count22,500/mm322,500/\text{mm}^3 (18%18\% bands)
Hemoglobin13.8 g/dL13.8\text{ g/dL}
Platelet count245,000/mm3245,000/\text{mm}^3
Serum lactate6.2 mmol/L6.2\text{ mmol/L}

An upright abdominal radiograph displays multiple dilated loops of small bowel with prominent air-fluid levels and a complete absence of gas in the colon and rectum.

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

Show answer & explanation

Answer: Urgent exploratory laparotomy

Answer

The most appropriate next step in management is urgent exploratory laparotomy.
The correct answer is urgent exploratory laparotomy. This patient presents with cardinal signs of a mechanical small bowel obstruction (colicky pain, bilious vomiting, obstipation) and a history of prior abdominal surgery, which is a major risk factor for adhesive disease. Crucially, he also demonstrates 'red flag' signs of a complicated obstruction. These include hemodynamic instability (hypotension, tachycardia), high fever, generalized peritonitis (guarding, rebound tenderness), marked leukocytosis with a left shift, and elevated serum lactate. These findings strongly suggest that the bowel has progressed to ischemia, strangulation, or frank necrosis. Complicated small bowel obstruction is an absolute surgical emergency that requires immediate exploratory laparotomy for definitive source control and resection of any necrotic bowel segments.

Step-by-Step Solution

1
Analyze the patient's symptoms, surgical history, and initial imaging.
The clinical triad of colicky pain, vomiting, and obstipation, combined with prior abdominal surgery and radiographic evidence of dilated loops with air-fluid levels, establishes the diagnosis of a mechanical small bowel obstruction (SBO).
Identifying the primary underlying structural pathology is the first step in abdominal emergencies.
2
Evaluate vital signs, physical examination findings, and laboratory data for complications.
The patient is hemodynamically unstable (hypotension, tachycardia) with high fever, generalized peritonitis (rebound tenderness, guarding), marked leukocytosis with a left shift, and severe lactic acidosis.
These 'red flag' findings indicate that the obstruction is complicated by bowel ischemia, strangulation, or perforation.
3
Determine the appropriate management pathway based on the presence of these complications.
Because there are clear signs of a complicated obstruction, conservative management is bypassed in favor of immediate surgical exploration.
Ischemic or perforated bowel is a surgical emergency requiring immediate operative source control to prevent sepsis and death.

Key Concept

Management of Complicated Small Bowel Obstruction (SBO)
Estimated Time:1m 30s
Question 491Question →

An inpatient oncology service evaluates a 29-year-old man who developed a sudden fever. He is currently on day 12 of induction chemotherapy for acute myeloid leukemia. He reports feeling profoundly fatigued but denies cough, shortness of breath, dysuria, abdominal pain, or diarrhea. Vital signs show a temperature of 38.9°C (102.0°F), blood pressure of 118/74 mm Hg, pulse of 98/min, and respirations of 16/min. Physical examination reveals clear lung fields bilaterally, no cardiac murmurs, and a non-tender abdomen. The insertion site of his right internal jugular central venous catheter is clean, dry, and intact with no surrounding erythema, induration, or purulent discharge. Laboratory studies are significant for a leukocyte count of 300/mm3300/\text{mm}^3 with 10%10\% neutrophils (Absolute Neutrophil Count = 30/mm330/\text{mm}^3). Which of the following is the most appropriate next step in the management of this patient?

Show answer & explanation

Answer: Obtain blood cultures and initiate intravenous cefepime

Answer

Obtain blood cultures and initiate intravenous cefepime.
This patient has high-risk febrile neutropenia, defined by an absolute neutrophil count <500/mm3< 500/\text{mm}^3 (here 30/mm330/\text{mm}^3) alongside profound expected immunosuppression from acute myeloid leukemia induction therapy. In high-risk febrile neutropenia, the most common life-threatening pathogens include Gram-negative organisms, particularly Pseudomonas aeruginosa. The standard of care is to immediately draw blood cultures and begin empiric intravenous monotherapy with an anti-pseudomonal beta-lactam, such as cefepime, meropenem, or piperacillin-tazobactam. Gram-positive coverage (e.g., vancomycin) is not routinely recommended unless the patient exhibits hemodynamic instability, signs of severe catheter-related infection (erythema/purulence at the site), severe pneumonia, or known colonization with MRSA. Because this patient is hemodynamically stable and has a benign exam, cefepime monotherapy is the most appropriate next step.

Step-by-Step Solution

1
Calculate the Absolute Neutrophil Count (ANC) and identify the clinical syndrome.
ANC is 300×0.10=30/mm3300 \times 0.10 = 30/\text{mm}^3. Since ANC is <500/mm3< 500/\text{mm}^3 and the patient has a single oral temperature of ≥38.3°C\geq 38.3°C (101.0°F101.0°F), the diagnosis is neutropenic fever.
Establishing the diagnosis of febrile neutropenia dictates an immediate algorithm for life-saving empiric antibiotic therapy.
2
Stratify the patient's risk level to determine the route and setting of care.
The patient has a hematologic malignancy (AML) undergoing induction chemotherapy, anticipating prolonged (>7> 7 days) and profound (ANC <100/mm3< 100/\text{mm}^3) neutropenia. This classifies him as high-risk.
High-risk patients must be admitted (or remain inpatient) and receive intravenous, bactericidal antibiotics rather than oral step-down regimens.
3
Select the appropriate empiric antimicrobial regimen based on the patient's specific physical exam findings.
The patient has stable vital signs, clear lungs, and a benign central line insertion site. Monotherapy with an anti-pseudomonal beta-lactam (e.g., cefepime, piperacillin-tazobactam) is indicated. Vancomycin is not added.
Routine use of vancomycin in all febrile neutropenic patients increases toxicity and resistance. It is strictly reserved for those with hemodynamic instability, obvious catheter-site infection, skin/soft tissue infection, or severe pneumonia.

Key Concept

Empiric Management of High-Risk Febrile Neutropenia
Question 492Question →

A 45-year-old man is hospitalized due to severe acute pancreatitis secondary to alcohol use. He is admitted to the intensive care unit and managed with aggressive intravenous fluid resuscitation, analgesia, and enteral nutrition. On day 3 of hospitalization, the patient develops a temperature of 38.8∘C38.8^{\circ}\text{C} (101.8∘F101.8^{\circ}\text{F}). His blood pressure is 112/70 mmHg112/70\text{ mmHg}, pulse is 114/min114\text{/min}, and respirations are 22/min22\text{/min}. Physical examination shows a distended abdomen with severe epigastric tenderness but no rebound or guarding.

Laboratory studies show a leukocyte count of 18,500/mm318,500/\text{mm}^3 and a serum lipase of 1,200 U/L1,200\text{ U/L}. A contrast-enhanced CT scan of the abdomen reveals acute inflammation of the pancreas with a 6-cm6\text{-cm} area of non-enhancement in the pancreatic body and tail, consistent with >30%>30\% pancreatic necrosis. There is no gas observed within the necrotic collection. The gallbladder is surgically absent, and the biliary tree is not dilated. Blood, urine, and sputum cultures are obtained.

What is the most appropriate next step in management?

Show answer & explanation

Answer: Withhold antimicrobial therapy and continue supportive care

Answer

The most appropriate next step is to withhold antimicrobial therapy and continue supportive care.
In the early phase (specifically the first week) of severe acute pancreatitis, the development of fever, tachycardia, and leukocytosis is typically secondary to the systemic inflammatory response syndrome (SIRS) driven by massive cytokine release, rather than an active bacterial infection. Current gastroenterology guidelines strongly recommend against the routine use of prophylactic antibiotics for sterile pancreatic necrosis. Studies have shown that prophylactic antibiotics do not reduce mortality or the incidence of infected necrosis; instead, they increase the risk of opportunistic fungal infections and multi-drug resistant organisms. Infection of necrotic tissue usually occurs 77 to 1010 days after initial presentation and should be suspected when a patient clinically deteriorates after initial improvement, or when a CT scan demonstrates gas bubbles within the fluid collection.

Step-by-Step Solution

1
Analyze the timing of the patient's symptoms relative to disease onset.
The patient is on day 3 of severe acute pancreatitis with new-onset fever and leukocytosis.
Timing helps distinguish between Systemic Inflammatory Response Syndrome (SIRS), which peaks in the first week, and infected necrosis, which typically occurs 7-10 days after presentation.
2
Evaluate imaging findings for signs of active infection or alternate pathologies.
CT shows sterile necrosis (no gas) and there is no evidence of biliary obstruction.
Infected necrosis (gas on CT) or concurrent acute cholangitis would warrant immediate antibiotic therapy and possible procedural intervention.
3
Apply evidence-based gastroenterology guidelines for sterile pancreatic necrosis.
Prophylactic antibiotics are withheld, and supportive care is continued.
Guidelines recommend against prophylactic antibiotics because they do not improve outcomes and select for resistant organisms and fungal superinfections.

Key Concept

Management of acute necrotizing pancreatitis and indications for antimicrobial therapy.
Estimated Time:1m 15s
Question 493Question →

A 52-year-old woman presents to the emergency department with a 2-day history of left lower quadrant abdominal pain. The pain is constant and described as a dull ache. She reports mild nausea but no vomiting, diarrhea, or hematochezia. Her medical history is unremarkable, and she takes no daily medications. Temperature is 37.3°C (99.1°F), blood pressure is 128/82 mmHg, pulse is 84/min, and respirations are 14/min. Abdominal examination reveals focal tenderness in the left lower quadrant without guarding, rigidity, or rebound tenderness. Bowel sounds are normal. Laboratory testing shows a leukocyte count of 9,500/mm³ with a normal differential. A CT scan of the abdomen and pelvis with intravenous contrast demonstrates wall thickening and peri-colic fat stranding in the sigmoid colon. There is no evidence of an abscess, stricture, fistula, or free intraperitoneal air. The patient is able to tolerate oral fluids without difficulty. Which of the following is the most appropriate next step in management?

Show answer & explanation

Answer: Discharge home with a clear liquid diet and supportive care

Answer

Discharge home with a clear liquid diet and supportive care
The correct answer involves discharging the patient home with a clear liquid diet and supportive care. This patient presents with classic signs of acute uncomplicated diverticulitis, confirmed by a CT scan showing localized inflammation without complications such as an abscess, fistula, or free air. She is hemodynamically stable, afebrile, has a normal white blood cell count, and can tolerate oral intake. According to the American Gastroenterological Association (AGA) and other current societal guidelines, the routine use of antibiotics is no longer recommended for acute uncomplicated diverticulitis in immunocompetent patients without signs of systemic toxicity. Observational management with bowel rest (clear liquid diet) and close follow-up has been shown to be safe and effective, with no significant difference in complication rates, recurrence, or time to recovery compared to antibiotic therapy. This approach aligns with modern principles of antibiotic stewardship.

Step-by-Step Solution

1
Analyze the patient's clinical presentation and imaging findings.
The patient has left lower quadrant pain, normal vital signs, a normal leukocyte count, and CT findings of localized colonic wall thickening and fat stranding without complications.
To establish the diagnosis of acute uncomplicated diverticulitis and determine the severity of the disease.
2
Evaluate the indications for antibiotic therapy in this patient.
The patient is immunocompetent, has no signs of systemic inflammatory response syndrome (SIRS), and has no complications (abscess, perforation) on her CT scan.
To apply current guidelines which distinguish between patients who require antibiotics and those who can be safely managed observationally.
3
Determine the appropriate disposition and management plan.
The patient can tolerate oral intake and has mild disease, making her a candidate for outpatient management with a clear liquid diet and supportive care.
To provide evidence-based care while minimizing the risks of antibiotic resistance and adverse medication effects.

Key Concept

Management of acute uncomplicated diverticulitis
Estimated Time:1m 0s
Question 494Question →

Medical staff are reassessing a 6565-year-old female patient in the critical care ward due to increasing somnolence and tachypnea. The patient was hospitalized 7272 hours prior for septic shock complicating severe community-acquired pneumonia. Initial management included aggressive intravenous fluid resuscitation and empiric antimicrobial therapy with intravenous vancomycin and piperacillin-tazobactam. She has a past medical history of chronic obstructive pulmonary disease and left ventricular hypertrophy. Yesterday, her hemodynamics improved, allowing the discontinuation of vasopressor support. Today, the blood cultures obtained on admission demonstrate heavy growth of Streptococcus pneumoniae, which is reported as susceptible to ceftriaxone and penicillin.

Currently, the patient appears lethargic and is using accessory muscles of respiration. Current vital signs include a temperature of 37.8∘C37.8^\circ C (100.0∘F100.0^\circ F), blood pressure of 115/75 mmHg115/75\ mmHg, heart rate of 105/min105/min, and a respiratory rate of 30/min30/min. Pulse oximetry indicates an oxygen saturation of 90%90\% while receiving supplemental oxygen via a high-flow nasal cannula. Physical examination reveals diminished breath sounds bilaterally without jugular venous distention. A bedside point-of-care ultrasound demonstrates a collapsible inferior vena cava and a predominant A-line pattern bilaterally without significant B-lines.

Laboratory evaluation is notable for:
Sodium: 138 mEq/L138\ mEq/L
Chloride: 104 mEq/L104\ mEq/L
Bicarbonate: 15 mEq/L15\ mEq/L
Blood urea nitrogen: 32 mg/dL32\ mg/dL
Creatinine: 1.8 mg/dL1.8\ mg/dL

An arterial blood gas analysis reveals:
pHpH: 7.227.22
PaCO2PaCO_2: 38 mmHg38\ mmHg
PaO2PaO_2: 62 mmHg62\ mmHg
HCO3−HCO_3^-: 15 mEq/L15\ mEq/L

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

Select all that apply

Show answer & explanation

Answer: De-escalate the antimicrobial regimen to intravenous ceftriaxone; Commence non-invasive positive pressure ventilation

Answer

The correct steps are to de-escalate the antimicrobial regimen to intravenous ceftriaxone and commence non-invasive positive pressure ventilation.
The patient requires two critical interventions. First, her mixed metabolic and respiratory acidosis (Measured PaCO2>Expected PaCO2Measured\ PaCO_2 > Expected\ PaCO_2) paired with lethargy and accessory muscle use signals impending respiratory failure, mandating positive pressure ventilation. Second, best practices in infectious disease require de-escalating her empiric broad-spectrum coverage to a targeted narrow-spectrum agent (ceftriaxone) based on finalized, susceptible culture data.

Step-by-Step Solution

1
Analyze the patient's arterial blood gas utilizing Winter's formula to determine expected respiratory compensation.
The primary disorder is metabolic acidosis (pHpH 7.227.22, HCO3−HCO_3^- 15 mEq/L15\ mEq/L). Expected PaCO2=(1.5×15)+8=30.5±2 mmHgPaCO_2 = (1.5 \times 15) + 8 = 30.5 \pm 2\ mmHg. The measured PaCO2PaCO_2 (38 mmHg38\ mmHg) is higher than the expected range.
Identifying that the measured carbon dioxide tension exceeds the expected compensatory value uncovers a superimposed acute respiratory acidosis, indicating imminent respiratory failure.
2
Evaluate the clinical signs of respiratory distress and volume status in the context of the acid-base derangement.
The patient exhibits tachypnea, accessory muscle use, and somnolence. Bedside ultrasound and physical exam rule out acute decompensated heart failure. Positive pressure ventilation is indicated.
The failure to mount an adequate respiratory compensation alongside visible fatigue confirms that the patient's work of breathing is unsustainable without mechanical assistance.
3
Review the finalized blood culture data and modify the empiric treatment plan.
Cultures grew Streptococcus pneumoniae susceptible to ceftriaxone. Broad-spectrum agents (vancomycin and piperacillin-tazobactam) should be discontinued in favor of ceftriaxone.
De-escalating to a narrow-spectrum targeted antibiotic minimizes the risk of multidrug-resistant organism colonization and drug toxicity, adhering to core principles of antibiotic stewardship.

Key Concept

Management of acute mixed acid-base disorders indicating impending respiratory failure, and the timely application of targeted antimicrobial stewardship in the intensive care unit.
Question 495Question →

A 2929-year-old woman is brought to the emergency department by her husband due to severe dizziness, lethargy, and confusion that has worsened over the past 4848 hours. She gave birth to a healthy infant 55 months ago; the delivery was complicated by uterine atony and severe postpartum hemorrhage requiring emergent transfusion of 44 units of packed red blood cells. Since the delivery, she has been unable to breastfeed and has not resumed menstruation. Her pulse is 115115/min, and blood pressure is 82/5082/50 mm Hg. Physical examination reveals delayed capillary refill, dry mucous membranes, and loss of axillary and pubic hair. Laboratory studies show:

Serum sodium: 131131 mEq/L
Serum potassium: 4.14.1 mEq/L
Serum glucose: 5858 mg/dL
Thyroid-stimulating hormone (TSH): 0.30.3 mU/L (Normal: 0.50.5 - 5.05.0)
Free thyroxine (T4): 0.50.5 ng/dL (Normal: 0.90.9 - 1.71.7)

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

Show answer & explanation

Answer: Intravenous hydrocortisone

Answer

Intravenous hydrocortisone
The correct answer provides immediate glucocorticoid replacement (intravenous hydrocortisone). This patient's history of massive postpartum hemorrhage followed by failure to lactate and amenorrhea is the classic presentation of Sheehan syndrome (postpartum ischemic necrosis of the anterior pituitary). She now presents in an acute adrenal crisis (hypotension, hypoglycemia, hyponatremia) combined with central hypothyroidism (low TSH and low free T4). In any patient with panhypopituitarism, it is a critical rule of endocrinology that glucocorticoids must be administered before or simultaneously with levothyroxine. Thyroid hormone increases basal metabolic rate and hepatic clearance of cortisol; if levothyroxine is given first to a patient with adrenal insufficiency, it will precipitate or exacerbate a potentially fatal adrenal crisis.

Step-by-Step Solution

1
Identify the underlying pathology from the patient's obstetric history.
The history of severe postpartum hemorrhage, coupled with current failure to lactate (agalactia) and amenorrhea, strongly indicates Sheehan syndrome (ischemic necrosis of the pituitary gland).
Recognizing Sheehan syndrome establishes the clinical context of panhypopituitarism.
2
Interpret the laboratory findings and vital signs.
The low TSH and low free T4 confirm central hypothyroidism. The combination of hypotension, hypoglycemia, and hyponatremia in this context points to concurrent secondary adrenal insufficiency presenting as an acute adrenal crisis.
Identifying all hormonal deficiencies is critical for determining immediate management priorities in an unstable patient.
3
Determine the correct sequence of hormone replacement.
Glucocorticoids (intravenous hydrocortisone) must be administered immediately. Thyroid hormone replacement should be delayed until adrenal function is supported.
Administering levothyroxine accelerates the hepatic clearance of cortisol, which will rapidly deplete any remaining cortisol reserves and fatally worsen the acute adrenal crisis.

Key Concept

In patients with combined adrenal and thyroid insufficiency (such as panhypopituitarism from Sheehan syndrome), glucocorticoids MUST be replaced before thyroid hormone to prevent precipitating a fatal adrenal crisis.
Estimated Time:2m 0s
Question 496Question →

Match each patient's clinical presentation with the most likely corresponding finding on a peripheral blood smear.

Click a left item, then click its matching right item

Items

A 24-year-old man develops dark urine and fatigue three days after starting trimethoprim-sulfamethoxazole. Laboratory evaluation shows elevated unconjugated bilirubin and reduced haptoglobin.
A 38-year-old woman presents with confusion, fever, and petechiae. Laboratory evaluation shows severe thrombocytopenia, normal prothrombin and activated partial thromboplastin times, and elevated creatinine.
A 65-year-old man presents with severe back pain, fatigue, and constipation. Laboratory evaluation shows normocytic anemia, hypercalcemia, and an elevated total protein gap.
A 45-year-old strict vegan presents with progressive fatigue, impaired proprioception, and a smooth, red tongue. Laboratory evaluation shows a mean corpuscular volume of 115 fL.

Matches

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Answer

Patient 1 matches with degmacytes; Patient 2 matches with schistocytes; Patient 3 matches with stacked erythrocytes; Patient 4 matches with hypersegmented neutrophils.
Each clinical scenario presents hallmark signs of a distinct hematologic disorder that is definitively linked to a specific peripheral blood smear abnormality. G6PD deficiency results in oxidative red blood cell damage, leading to degmacytes (bite cells). TTP causes mechanical shearing of red blood cells in microthrombi, resulting in schistocytes. Multiple myeloma produces excess monoclonal proteins that alter red blood cell electrical charge, causing them to stack (Rouleaux formation). Vitamin B12 deficiency disrupts nuclear maturation in myeloid cell lines, leading to hypersegmented neutrophils.

Step-by-Step Solution

1
Evaluate the first vignette to identify the underlying condition.
The patient has sulfa-induced hemolytic anemia, highly suggestive of Glucose-6-phosphate dehydrogenase (G6PD) deficiency.
Identifying the disease allows for correlation with its hallmark peripheral smear finding, which is degmacytes (bite cells).
2
Evaluate the second vignette to identify the underlying condition.
The patient presents with the classic pentad of Thrombotic Thrombocytopenic Purpura (TTP): thrombocytopenia, microangiopathic hemolytic anemia, neurologic signs, renal impairment, and fever, with normal coagulation studies.
TTP is a microangiopathic hemolytic anemia that mechanically destroys red blood cells, leading to schistocytes.
3
Evaluate the third vignette to identify the underlying condition.
The patient has hypercalcemia, bone pain, and a high protein gap, which are classic signs of Multiple Myeloma.
Excess paraproteins in Multiple Myeloma neutralize red blood cell surface charges, leading to Rouleaux formation (stacked coins).
4
Evaluate the fourth vignette to identify the underlying condition.
The patient has dietary Vitamin B12 deficiency causing macrocytic anemia and subacute combined degeneration of the spinal cord.
Vitamin B12 deficiency impairs DNA synthesis, leading to megaloblastic changes such as hypersegmented neutrophils on the peripheral smear.

Key Concept

Peripheral blood smear findings are highly specific diagnostic clues for various hematologic disorders, reflecting underlying pathophysiology such as oxidative damage (G6PD), microangiopathy (TTP), paraproteinemia (Multiple Myeloma), or impaired DNA synthesis (B12 deficiency).
Estimated Time:1m 30s
Question 497Question →

A 2424-year-old woman is brought to the emergency department due to progressive confusion, nausea, vomiting, and severe abdominal pain over the past 2424 hours. She has a history of type 1 diabetes mellitus but reports running out of her medications three days ago. Her temperature is 37.2∘C37.2^\circ\text{C} (99.0∘F99.0^\circ\text{F}), blood pressure is 90/60 mmHg90/60\text{ mmHg}, pulse is 128/min128\text{/min}, and respirations are 26/min26\text{/min} and deep. Mucous membranes are dry. Laboratory studies show:

Blood glucose: 650 mg/dL650\text{ mg/dL}
Serum sodium: 132 mEq/L132\text{ mEq/L}
Serum potassium: 3.1 mEq/L3.1\text{ mEq/L}
Serum chloride: 98 mEq/L98\text{ mEq/L}
Serum bicarbonate: 11 mEq/L11\text{ mEq/L}
Arterial pH: 7.157.15
Serum ketones: Positive

Arrange the following therapeutic interventions in the correct chronological order for the evidence-based management of this patient's condition.

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Answer

The correct sequence is: Administer rapid intravenous 0.9% sodium chloride, followed by intravenous potassium chloride, then initiate continuous intravenous regular insulin infusion, subsequently add 5% dextrose to the maintenance intravenous fluids, and finally administer subcutaneous glargine insulin.
The management of diabetic ketoacidosis follows a strict chronological algorithm to maximize survival and prevent iatrogenic complications. Intravenous fluids (0.9% NaCl) are universally the first step to restore intravascular volume and renal perfusion. Second, the clinician must interpret the serum potassium level; because this patient's potassium is < 3.3 mEq/L, intravenous potassium chloride MUST be administered before insulin to avoid lethal intracellular shifting. Third, once potassium is safely replenished, intravenous regular insulin is started to correct the metabolic acidosis. Fourth, as blood glucose falls below 200 mg/dL, 5% dextrose is added to the fluids to prevent hypoglycemia, allowing the insulin infusion to continue until the anion gap closes. Finally, subcutaneous basal insulin is administered with a 1-to-2-hour overlap before discontinuing the intravenous drip to prevent rebound DKA.

Step-by-Step Solution

1
Assess the patient's hemodynamic status and initiate fluid resuscitation.
Rapid intravenous 0.9% sodium chloride is administered.
The patient is hypotensive, tachycardic, and severely dehydrated. Volume expansion is the most critical initial step to restore organ perfusion and lower serum counterregulatory hormones.
2
Evaluate the serum potassium level prior to initiating insulin therapy.
Intravenous potassium chloride is administered while holding insulin.
The patient's initial potassium is 3.1 mEq/L (below the critical threshold of 3.3 mEq/L). Insulin drives potassium into cells. Giving insulin first would precipitate severe hypokalemia, potentially causing respiratory muscle paralysis or fatal cardiac arrhythmias.
3
Initiate insulin therapy once potassium levels are safe.
Continuous intravenous regular insulin infusion is started.
With potassium adequately replaced, insulin is required to stop lipolysis, halt ketogenesis, and close the anion gap.
4
Monitor blood glucose closely while the insulin drip continues to resolve the acidosis.
5% dextrose is added to the intravenous fluids.
Blood glucose typically normalizes before the anion gap closes. When glucose drops below 200 to 250 mg/dL, dextrose must be added to prevent hypoglycemia while allowing the insulin drip to run until the acidosis resolves.
5
Transition the patient from intravenous to subcutaneous insulin.
Subcutaneous glargine insulin is administered.
Once the anion gap is closed and the patient is ready to eat, subcutaneous insulin is given. The intravenous infusion is continued for 1 to 2 hours afterward to prevent rebound ketoacidosis during the subcutaneous insulin onset.

Key Concept

Diabetic Ketoacidosis (DKA) Stepwise Management and the Potassium Trap
Question 498Question →

A 54-year-old man is brought to the emergency department by paramedics after being found stuporous in a local park. Beside him, paramedics found several empty bottles of antifreeze. His temperature is 36.5∘C36.5^\circ\text{C} (97.7∘F97.7^\circ\text{F}), blood pressure is 105/65 mmHg105/65\text{ mmHg}, pulse is 98/min98/\text{min}, and respirations are 14/min14/\text{min}. Physical examination reveals a lethargic patient who arouses to painful stimuli but is unable to answer questions. Cardiopulmonary examination is unremarkable.

The following laboratory results are obtained:

Laboratory TestResult
Serum sodium138 mEq/L138\text{ mEq/L}
Serum potassium4.8 mEq/L4.8\text{ mEq/L}
Serum chloride100 mEq/L100\text{ mEq/L}
Serum bicarbonate12 mEq/L12\text{ mEq/L}
Blood urea nitrogen24 mg/dL24\text{ mg/dL}
Serum creatinine1.5 mg/dL1.5\text{ mg/dL}

Arterial blood gas analysis on room air reveals:

ParameterResult
pH7.157.15
PaCO235 mmHg35\text{ mmHg}
PaO288 mmHg88\text{ mmHg}

Which of the following best describes this patient's primary acid-base disturbance(s)?

Show answer & explanation

Answer: High anion gap metabolic acidosis with a concurrent respiratory acidosis

Answer

High anion gap metabolic acidosis with a concurrent respiratory acidosis
The correct answer accurately identifies a mixed acid-base disorder. First, the low pH (7.157.15) and low serum HCO3−HCO_3^- (12 mEq/L12\text{ mEq/L}) establish a primary metabolic acidosis. Next, calculating the anion gap (Na+−(Cl−+HCO3−)Na^+ - (Cl^- + HCO_3^-)) yields 138−(100+12)=26 mEq/L138 - (100 + 12) = 26\text{ mEq/L}. An anion gap greater than 14 indicates a high anion gap metabolic acidosis (HAGMA), which is highly consistent with this patient's presentation of likely antifreeze (ethylene glycol) toxicity. To determine if the respiratory response is appropriate, Winter's formula is applied: Expected PaCO2=(1.5×HCO3−)+8±2PaCO_2 = (1.5 \times HCO_3^-) + 8 \pm 2. For this patient, the expected PaCO2=(1.5×12)+8±2=26±2 mmHgPaCO_2 = (1.5 \times 12) + 8 \pm 2 = 26 \pm 2\text{ mmHg} (range 24−28 mmHg24-28\text{ mmHg}). The measured PaCO2PaCO_2 is 35 mmHg35\text{ mmHg}, which is significantly higher than the expected range. An inappropriately elevated PaCO2PaCO_2 in the setting of a metabolic acidosis indicates a concurrent primary respiratory acidosis. This mixed disorder is classically seen in severe toxic alcohol ingestions due to CNS depression resulting in profound hypoventilation.

Step-by-Step Solution

1
Determine the primary acid-base disturbance based on pH and HCO3−HCO_3^-.
The pH is 7.157.15 (acidemia) and serum HCO3−HCO_3^- is 12 mEq/L12\text{ mEq/L} (low), indicating a primary metabolic acidosis.
Establishing the initial primary disorder is the first step in analyzing any arterial blood gas.
2
Calculate the anion gap to classify the metabolic acidosis.
Anion gap = Na+−(Cl−+HCO3−)=138−(100+12)=26 mEq/LNa^+ - (Cl^- + HCO_3^-) = 138 - (100 + 12) = 26\text{ mEq/L}. Since this is >14 mEq/L> 14\text{ mEq/L}, it is a high anion gap metabolic acidosis (HAGMA).
HAGMA has a specific differential diagnosis (e.g., MUDPILES) that is distinct from normal anion gap metabolic acidosis.
3
Calculate the expected PaCO2PaCO_2 using Winter's formula to check for respiratory compensation.
Expected PaCO2=(1.5×12)+8±2=26±2 mmHgPaCO_2 = (1.5 \times 12) + 8 \pm 2 = 26 \pm 2\text{ mmHg} (range: 24 to 28 mmHg24\text{ to }28\text{ mmHg}).
To determine if the body is appropriately compensating via hyperventilation or if a secondary respiratory disorder exists.
4
Compare the calculated expected PaCO2PaCO_2 with the measured PaCO2PaCO_2.
The measured PaCO2PaCO_2 (35 mmHg35\text{ mmHg}) is greater than the expected compensatory range (24−28 mmHg24-28\text{ mmHg}).
An inappropriately high PaCO2PaCO_2 in the setting of severe metabolic acidosis indicates a concurrent primary respiratory acidosis.

Key Concept

In a patient with metabolic acidosis, an inappropriately elevated PaCO2PaCO_2 compared to the calculated expected value using Winter's formula indicates a concurrent primary respiratory acidosis.
Estimated Time:1m 30s
Question 499Question →

A 6262-year-old woman presents to the emergency department with a sudden onset of right-sided chest pain that worsens with deep inspiration, accompanied by severe shortness of breath. Her symptoms started 22 hours ago. She recently returned from a 1212-hour international flight. Her medical history includes hypertension and osteoarthritis. She takes amlodipine and acetaminophen.

Upon evaluation, her temperature is 37.2∘C37.2^\circ\text{C} (99.0∘F99.0^\circ\text{F}), blood pressure is 118/76 mmHg118/76\text{ mmHg}, pulse is 118/min118/\text{min}, and respiratory rate is 26/min26/\text{min}. Oxygen saturation is 89%89\% on room air. Physical examination reveals clear lung fields bilaterally with no wheezing or crackles. Cardiac examination shows a regular, rapid rhythm with no murmurs, rubs, or gallops. The right calf is mildly swollen and tender to palpation compared to the left.

An arterial blood gas analysis on room air reveals:
pH: 7.527.52
PaCO2\text{PaCO}_2: 26 mmHg26\text{ mmHg}
PaO2\text{PaO}_2: 60 mmHg60\text{ mmHg}
HCO3−\text{HCO}_3^-: 21 mEq/L21\text{ mEq/L}

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

Show answer & explanation

Answer: Computed tomography angiography of the chest

Answer

The correct answer is computed tomography angiography of the chest.
Computed tomography angiography of the chest is the most appropriate next step. This patient's presentation is highly suspicious for an acute pulmonary embolism (PE), supported by her recent prolonged immobilization, unilateral calf swelling (suggestive of deep vein thrombosis), pleuritic chest pain, tachycardia, and hypoxemia. Her ABG demonstrates an acute respiratory alkalosis, which occurs in PE due to hypoxia-driven hyperventilation. For a hemodynamically stable patient with a high pretest probability of PE, CT pulmonary angiography is the diagnostic test of choice to confirm the presence of a thrombus.

Step-by-Step Solution

1
Synthesize the clinical presentation and risk factors.
The patient has acute pleuritic chest pain, dyspnea, tachycardia, hypoxia, and unilateral calf swelling following a long-haul flight.
These findings yield a high pretest probability (Wells score > 4) for an acute pulmonary embolism (PE).
2
Interpret the arterial blood gas (ABG) findings.
The ABG shows a high pH (7.527.52) and low PaCO2\text{PaCO}_2 (26 mmHg26\text{ mmHg}), indicating an acute respiratory alkalosis driven by hypoxia-induced hyperventilation.
This confirms a ventilation-perfusion mismatch typical of PE, ruling out primary metabolic acidosis or respiratory acidosis.
3
Determine the next best step for a hemodynamically stable patient with likely PE.
Diagnostic imaging with computed tomography (CT) pulmonary angiography of the chest should be ordered.
In hemodynamically stable patients with a high clinical suspicion of PE, definitive imaging is required to confirm the diagnosis before committing to long-term anticoagulation.

Key Concept

Diagnosis and initial management of acute pulmonary embolism
Estimated Time:1m 30s
Question 500Question →

A 38-year-old man presents to the clinic with a 3-month history of episodic, severe headaches accompanied by profuse sweating and a racing heartbeat. His blood pressure in the clinic is 178/104 mmHg, and his heart rate is 108/min. He has no other significant past medical history and takes no medications. Physical examination is unremarkable. Suspecting a specific catecholamine-secreting neuroendocrine tumor, the physician plans to evaluate and treat the patient. Arrange the following steps in the correct chronological order for the appropriate evidence-based diagnosis and management of this patient's condition.

Drag items to arrange them in the correct order

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Answer

The correct sequence is: establish the biochemical diagnosis (metanephrines), followed by anatomic localization (abdominal imaging), followed by medical optimization starting with alpha-blockade (phenoxybenzamine), followed by beta-blockade (propranolol), and concluding with definitive surgical resection (adrenalectomy).
The correct order follows the strictly tested standard of care for pheochromocytoma. First, the biochemical diagnosis must be established to avoid the diagnostic trap of adrenal incidentalomas. Second, anatomic localization with imaging is performed. Third, medical preparation for surgery is critical to prevent intraoperative hypertensive crises. This preparation mandates alpha-adrenergic blockade first (to control blood pressure and expand volume), followed by beta-adrenergic blockade (to control tachycardia). Finally, once the patient is medically optimized, definitive surgical resection is performed.

Step-by-Step Solution

1
Establish the biochemical diagnosis
Measurement of plasma fractionated free metanephrines.
Before any imaging, functioning tumors must be confirmed biochemically. This prevents the incidental discovery of non-functioning adrenal masses, which can lead to unnecessary interventions.
2
Localize the tumor anatomically
Perform a CT scan of the abdomen.
After confirming catecholamine excess, cross-sectional imaging is used to locate the pheochromocytoma to properly plan the surgical intervention.
3
Initiate medical optimization with alpha-blockade
Administration of phenoxybenzamine.
Alpha-blockade lowers systemic blood pressure and restores the chronically depleted intravascular volume. This step is absolutely required before beta-blockade can be considered.
4
Add beta-blockade for heart rate control
Administration of propranolol.
Beta-blockers control reflex tachycardia but must strictly be given only after adequate alpha-blockade to prevent a severe hypertensive crisis driven by unopposed alpha-adrenergic stimulation.
5
Definitive surgical treatment
Laparoscopic adrenalectomy.
Once the patient's blood pressure and heart rate are stabilized for 10-14 days with dual medical therapy, surgical removal of the tumor can be safely performed.

Key Concept

The chronological workup and management of pheochromocytoma requires biochemical confirmation before anatomic localization, and strict alpha-adrenergic blockade prior to beta-adrenergic blockade.
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