Internal Medicine

3151 questions

Question 341Question →

A 72-year-old male is brought to the emergency department experiencing severe, progressive right knee pain and swelling that commenced roughly 12 hours prior. His medical background is significant for hypertension, diet-controlled type 2 diabetes mellitus, and osteoarthritis. Four days ago, he underwent an uncomplicated laparoscopic cholecystectomy and was discharged home the following day. His current temperature is 38.4°C (101.1°F), blood pressure is 135/85 mm Hg, and pulse is 98/min. Physical examination of the right lower extremity demonstrates a visibly swollen, markedly warm, and erythematous knee. The patient shouts in pain with even minimal passive range of motion. Plain radiography of the affected joint reveals medial joint space narrowing, subchondral sclerosis, and a distinct linear calcification within the articular cartilage. Which of the following is the most appropriate next step in management?

Show answer & explanation

Answer: Arthrocentesis of the right knee

Answer

Arthrocentesis of the right knee
The correct next step in management for a patient with a new-onset, acutely swollen, painful, and warm joint accompanied by fever is diagnostic arthrocentesis. Although this patient's radiograph demonstrates chondrocalcinosis (linear calcification of the articular cartilage), which is highly indicative of calcium pyrophosphate deposition (CPPD) disease (pseudogout), an acute pseudogout flare cannot be reliably distinguished from septic arthritis on clinical grounds alone. Both conditions can present with severe monoarticular pain, erythema, swelling, and systemic fever, and both can be triggered by recent physiological stressors such as surgery. Because septic arthritis is a medical emergency that can cause irreversible cartilage destruction within 24 to 48 hours, synovial fluid must be aspirated and analyzed (for cell count, Gram stain, and culture) before any targeted or empiric therapy is initiated. If synovial fluid analysis reveals positively birefringent rhomboid crystals and negative cultures, the diagnosis of pseudogout is confirmed and appropriate anti-inflammatory therapy can be started.

Step-by-Step Solution

1
Identify the primary clinical problem and vital sign abnormalities.
The patient has an acute, warm, swollen, and severely painful monoarticular arthritis accompanied by a new postoperative fever (38.4°C).
Recognizing the constellation of acute joint inflammation with systemic fever is critical for triaging the urgency of the condition.
2
Analyze the provided diagnostic data (radiograph) in the clinical context.
The radiograph demonstrates chondrocalcinosis, a hallmark of calcium pyrophosphate deposition (CPPD) disease, which can cause acute pseudogout flares often triggered by surgery or medical illness.
While imaging points to a crystalline etiology, imaging alone cannot rule out a concurrent or alternative infectious process.
3
Determine the most critical condition to exclude and the test required to do so.
Septic arthritis is a joint-destroying emergency that can mimic pseudogout perfectly. Arthrocentesis with synovial fluid analysis (cell count, Gram stain, and culture) is mandatory before initiating any treatment.
Missing a septic joint leads to rapid cartilage destruction and sepsis. Therefore, fluid aspiration is always the definitive next step.

Key Concept

In any patient presenting with an acute, warm, swollen joint and fever, septic arthritis must be definitively excluded via arthrocentesis and synovial fluid analysis, even if there is radiographic evidence suggesting a crystal arthropathy such as pseudogout.
Question 342Question →

A 64-year-old female patient is currently hospitalized for the treatment of acute pyelonephritis. She initially presented to the emergency department three days ago with severe right-sided flank pain, dysuria, and a temperature of 39.2∘C39.2^\circ\text{C} (102.6∘F102.6^\circ\text{F}). Blood cultures were drawn, and empiric intravenous ceftriaxone was initiated. The admission blood cultures show no growth to date. However, the urine culture obtained prior to antibiotic administration has grown >105>10^5 colony-forming units/mL of *Escherichia coli*. The susceptibility report is as follows:

Antimicrobial AgentResult
AmoxicillinResistant
CefazolinResistant
CeftriaxoneResistant
CefepimeResistant
CiprofloxacinResistant
ErtapenemSusceptible
MeropenemSusceptible
NitrofurantoinSusceptible
Trimethoprim-sulfamethoxazoleSusceptible

Today, the patient reports that her flank pain has nearly resolved. Her current 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 heart rate is 78/min78/\text{min}. She is tolerating a regular diet without nausea.

Based on the culture results and the patient's clinical progress, which of the following is the most appropriate next step in the pharmacologic management of this patient?

Show answer & explanation

Answer: Transition to oral trimethoprim-sulfamethoxazole

Answer

Transition to oral trimethoprim-sulfamethoxazole
The correct response identifies that this patient has acute pyelonephritis caused by an Extended-Spectrum Beta-Lactamase (ESBL)-producing strain of E. coli, evidenced by resistance to ceftriaxone and cefepime. Because the patient is now afebrile, hemodynamically stable, and able to tolerate an oral diet, she is an excellent candidate for step-down therapy from intravenous to oral antibiotics. This transition minimizes hospital length of stay and reduces the risks associated with intravenous catheters. Trimethoprim-sulfamethoxazole is the optimal choice; the isolate is highly susceptible, and the medication achieves excellent concentrations in both the urine and the renal parenchyma.

Step-by-Step Solution

1
Interpret the antibiotic susceptibility profile.
The E. coli isolate is resistant to third- and fourth-generation cephalosporins, indicating it is an Extended-Spectrum Beta-Lactamase (ESBL) producer.
Accurate identification of the resistance mechanism dictates which antibiotic classes can be safely used.
2
Assess the patient's current clinical stability.
The patient is afebrile, hemodynamically stable, and tolerating an oral diet.
Clinical stability determines whether the patient must remain on intravenous therapy or can be transitioned to an oral regimen.
3
Select the appropriate targeted oral agent based on pharmacokinetics.
Trimethoprim-sulfamethoxazole is selected because it is susceptible and penetrates renal tissue, whereas nitrofurantoin does not.
Pyelonephritis requires antibiotics that achieve high tissue concentrations in the kidneys, not just the lower urinary tract.

Key Concept

Management of acute pyelonephritis caused by Extended-Spectrum Beta-Lactamase (ESBL)-producing Enterobacteriaceae involves transitioning clinically stable patients to highly bioavailable oral antibiotics with adequate renal tissue penetration, such as trimethoprim-sulfamethoxazole, to promote antibiotic stewardship and avoid unnecessary intravenous carbapenem use.
Estimated Time:1m 30s
Question 343Question →

Match each clinical infectious disease vignette with its most appropriate targeted pharmacotherapy or first-line treatment regimen.

Click a left item, then click its matching right item

Items

A 45-year-old man with poor dentition presents with a chronic, indurated submandibular mass and multiple sinus tracts exuding yellowish purulent discharge. Microscopy of the exudate shows branching, non-acid-fast, Gram-positive bacilli.
A 58-year-old renal transplant recipient presents with fever, focal seizures, and a cavitary lung lesion. Sputum microscopy demonstrates filamentous, branching, Gram-positive rods that are weakly acid-fast.
A 65-year-old man with acute myeloid leukemia develops profound neutropenia and persistent fever despite broad-spectrum antibacterials. Chest CT reveals a dense pulmonary macronodule surrounded by a ground-glass halo.
A 32-year-old man with advanced HIV presents with a 2-week history of insidious headache and lethargy. Cerebrospinal fluid analysis reveals elevated opening pressure and encapsulated yeast organisms on an India ink preparation.
A 72-year-old woman is evaluated for acute-onset altered mental status and fever. Cerebrospinal fluid analysis shows neutrophilic pleocytosis. Gram stain reveals intracellular and extracellular Gram-positive bacilli with tumbling motility.

Matches

Show answer & explanation

Answer

Vignette 1 matches with Penicillin G/Amoxicillin, Vignette 2 matches with Trimethoprim-sulfamethoxazole, Vignette 3 matches with Voriconazole, Vignette 4 matches with Amphotericin B and flucytosine, and Vignette 5 matches with Ampicillin.
Each specific pathogen presentation is correctly matched with its guideline-directed targeted antimicrobial therapy based on strict microbiological characteristics (Gram stain, acid-fastness, India ink) and classic clinical syndromes.

Step-by-Step Solution

1
Analyze the first vignette for key diagnostic microbiological and clinical features.
Identified cervicofacial mass with sinus tracts and branching non-acid-fast bacilli as an Actinomyces infection.
To determine the underlying pathogen and recall its specific targeted treatment (Penicillin).
2
Analyze the second vignette for key diagnostic microbiological and clinical features.
Identified pulmonary and CNS involvement in a transplant patient with weakly acid-fast branching bacilli as a Nocardia infection.
To differentiate from Actinomyces and select the correct antimicrobial therapy (TMP-SMX).
3
Analyze the third vignette for key radiologic and host-factor features.
Identified neutropenic fever with a chest CT 'halo sign' as invasive pulmonary aspergillosis.
To recognize this severe opportunistic fungal pneumonia which necessitates Voriconazole therapy.
4
Analyze the fourth vignette for key neurologic and fluid-analysis features.
Identified subacute meningitis in an immunocompromised patient with encapsulated yeast as a Cryptococcal infection.
To select the appropriate synergistic induction regimen of Amphotericin B and flucytosine.
5
Analyze the fifth vignette for key demographic and microscopic features.
Identified meningitis in an elderly patient with Gram-positive motile bacilli as Listeria monocytogenes.
To recall that Listeria possesses intrinsic resistance to standard empiric cephalosporins, requiring the addition of Ampicillin.

Key Concept

Diagnosis and targeted pharmacotherapy of specific opportunistic and severe infectious diseases
Question 344Question →

A 45-year-old man presents to the clinic complaining of profound fatigue, a 6-kg (13.2-lb) weight loss, and generalized weakness over the past 4 months. He also notes decreased libido and occasional dizziness when standing. Two years ago, he sustained a severe traumatic brain injury in a motor vehicle collision that required a 3-week stay in the intensive care unit. His blood pressure is 102/62 mm Hg while supine and 84/52 mm Hg upon standing. Heart rate is 86/min. Physical examination reveals loss of axillary and pubic hair, and delayed relaxation of deep tendon reflexes. Laboratory studies show:

* Sodium: 131 mEq/L131 \text{ mEq/L}
* Potassium: 4.0 mEq/L4.0 \text{ mEq/L}
* Thyroid-stimulating hormone (TSH): 2.2 μU/mL2.2 \text{ } \mu\text{U/mL} (Normal: 0.4–4.0 μU/mL0.4–4.0 \text{ } \mu\text{U/mL})
* Free T4: 0.5 ng/dL0.5 \text{ ng/dL} (Normal: 0.9–1.7 ng/dL0.9–1.7 \text{ ng/dL})

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

Show answer & explanation

Answer: Measurement of early morning serum cortisol

Answer

Measurement of early morning serum cortisol is the most appropriate next step to rule out concurrent central adrenal insufficiency before starting thyroid hormone replacement.
The correct answer addresses the critical need to evaluate for central adrenal insufficiency in a patient presenting with central hypothyroidism (indicated by low free T4 and normal TSH) following a traumatic brain injury. Administering levothyroxine before confirming and replacing cortisol in panhypopituitarism increases cortisol metabolism and can trigger a life-threatening adrenal crisis.

Step-by-Step Solution

1
Analyze the thyroid function tests.
The patient has a low free T4 but a normal TSH.
This discordant pattern (inappropriately normal TSH) indicates secondary (central) hypothyroidism rather than primary thyroid failure.
2
Integrate the clinical history and physical exam findings.
History of severe traumatic brain injury, fatigue, weight loss, orthostatic hypotension, hyponatremia, and loss of body hair.
These findings point to panhypopituitarism, including central adrenal insufficiency (explaining the hyponatremia and orthostasis without hyperkalemia) and hypogonadotropic hypogonadism.
3
Determine the sequence of management.
The hypothalamic-pituitary-adrenal axis must be evaluated before replacing thyroid hormone.
Levothyroxine increases the metabolic clearance of cortisol. If levothyroxine is given to a patient with untreated adrenal insufficiency, it can precipitate an acute, potentially fatal adrenal crisis. Therefore, an early morning serum cortisol level must be checked first.

Key Concept

In patients with central hypothyroidism (often part of panhypopituitarism), the hypothalamic-pituitary-adrenal axis must be evaluated with a serum cortisol level (and treated if necessary) before initiating levothyroxine therapy to prevent an adrenal crisis.
Question 345Question →

Review the clinical vignettes below, which present various mechanisms of renal and systemic acid-base derangements. Which classic arterial blood gas and serum chemistry profile is most strongly associated with each patient's presentation?

Click a left item, then click its matching right item

Items

A young female with a history of recurrent self-induced vomiting who develops extreme volume depletion and profound weakness.
A middle-aged male with a high-output ileostomy who develops severe lethargy and signs of moderate dehydration.
A young male with type 1 diabetes mellitus who disconnected his insulin pump and subsequently developed deep, rapid respirations.
An elderly male with advanced chronic obstructive pulmonary disease who develops increasing somnolence during an acute respiratory exacerbation.
A young adult female exhibiting tinnitus, tachypnea, and altered mental status shortly after intentionally consuming excessive doses of over-the-counter analgesics.

Matches

Show answer & explanation

Answer

The correct matches pair the specific mechanism of acid-base disturbance with its hallmark laboratory profile. The patient with vomiting has a hypokalemic metabolic alkalosis. The patient with an ileostomy has a normal anion gap acidosis. The patient in diabetic ketoacidosis has an elevated anion gap acidosis with hyperkalemia. The COPD patient has an acute-on-chronic respiratory acidosis. The patient with aspirin toxicity has a dual presentation of an elevated anion gap acidosis and independent respiratory-driven alkalemia.
Matching questions require correctly identifying the physiological consequences of each clinical event. Vomiting uniquely causes a hypokalemic metabolic alkalosis due to direct acid loss. Lower gastrointestinal losses (ileostomy) cause a normal anion gap acidosis due to direct bicarbonate wasting. Ketoacidosis produces a severe elevated anion gap acidosis accompanied by hyperkalemia due to extracellular shifts. Chronic respiratory failure acute exacerbations cause acute-on-chronic respiratory acidosis. Salicylate toxicity uniquely produces a dual-primary disorder: a respiratory-driven alkalemia from central stimulation and an elevated anion gap acidosis from cellular toxicity.

Step-by-Step Solution

1
Calculate the serum anion gap (AG=Na+−(Cl−+HCO3−)AG = \text{Na}^+ - (\text{Cl}^- + \text{HCO}_3^-)) for each provided laboratory profile to categorize the metabolic disturbances.
The third and fifth profiles reveal elevated anion gaps (26 mEq/L26 \text{ mEq/L} and 25 mEq/L25 \text{ mEq/L} respectively). The second profile reveals a normal anion gap (11 mEq/L11 \text{ mEq/L}).
Identifying the anion gap is the critical first step in determining the etiology of any metabolic acidosis.
2
Evaluate the patient with severe vomiting and volume depletion.
Gastric acid loss generates a severe metabolic alkalosis with compensatory hypoventilation. This perfectly corresponds to the first profile featuring a pH\text{pH} of 7.527.52, elevated bicarbonate, and profound hypochloremia.
Vomiting classically leads to a hypokalemic, hypochloremic metabolic alkalosis due to direct acid loss and secondary hyperaldosteronism from volume contraction.
3
Analyze the patient with a high-output ileostomy.
This patient loses massive amounts of bicarbonate from the lower GI tract, producing a hyperchloremic, normal anion gap acidosis, matching the second profile.
Gastrointestinal fluid below the stomach is rich in bicarbonate; its excessive loss forces the kidneys to retain chloride to maintain electroneutrality.
4
Assess the patient with insulin deprivation (diabetic ketoacidosis).
DKA produces an elevated anion gap acidosis. The profound acidemia (pH\text{pH} 7.227.22), elevated gap (26 mEq/L26 \text{ mEq/L}), and hyperkalemia (6.1 mEq/L6.1 \text{ mEq/L}) despite total body potassium depletion match the third profile.
Insulin deficiency leads to unchecked lipolysis and ketone body production, while extracellular potassium shifts occur due to lack of insulin and profound acidemia.
5
Examine the patient with an acute COPD exacerbation.
This presentation is characterized by acute-on-chronic respiratory acidosis. The fourth profile demonstrates a severely elevated pCO2\text{pCO}_2 (70 mmHg70 \text{ mmHg}) and acidemia, with chronically retained bicarbonate (31 mEq/L31 \text{ mEq/L}).
Chronic hypercapnia leads to renal bicarbonate retention over days to weeks. An acute exacerbation spikes the pCO2\text{pCO}_2 further, dropping the pH precipitously.
6
Determine the acid-base consequence of aspirin toxicity in the final patient.
Salicylates directly stimulate the respiratory center (driving pCO2\text{pCO}_2 down) while uncoupling oxidative phosphorylation (elevating the anion gap). This dual pathology matches the fifth profile, which shows a normal-to-alkalemic pH (7.427.42) despite a very low bicarbonate (13 mEq/L13 \text{ mEq/L}) and an elevated anion gap.
The presence of two competing, simultaneous primary disorders (respiratory alkalemia and metabolic acidemia) is the hallmark of adult salicylate poisoning.

Key Concept

Pathophysiological correlation of complex clinical presentations with their expected arterial blood gas and serum electrolyte profiles.
Question 346Question →

Match each of the following patient laboratory profiles to the most likely underlying pathophysiologic mechanism.

(Reference ranges: Serum Calcium: 8.4-10.2 mg/dL; Intact PTH: 10-65 pg/mL; Phosphorus: 2.5-4.5 mg/dL; 24-hour urine calcium: 100-300 mg/day).

Click a left item, then click its matching right item

Items

Serum Calcium: 11.2 mg/dL, Intact PTH: 55 pg/mL, 24-hr urine calcium: 45 mg/day
Serum Calcium: 11.8 mg/dL, Intact PTH: 8 pg/mL, 1,25-dihydroxyvitamin D: elevated, Phosphorus: 3.8 mg/dL
Serum Calcium: 12.5 mg/dL, Intact PTH: 5 pg/mL, Phosphorus: 2.1 mg/dL, PTHrP: elevated
Serum Calcium: 11.5 mg/dL, Intact PTH: 120 pg/mL, Phosphorus: 2.2 mg/dL, 24-hr urine calcium: 350 mg/day
Serum Calcium: 7.5 mg/dL, Intact PTH: 110 pg/mL, Phosphorus: 2.1 mg/dL, Alkaline phosphatase: 250 U/L

Matches

Show answer & explanation

Answer

The accurate diagnostic match depends on differentiating PTH-dependent states (primary hyperparathyroidism, FHH) from PTH-independent states (malignancy, granulomatous disease) and identifying secondary responses to hypocalcemia (vitamin D deficiency).
Each laboratory profile distinctly isolates a core mechanism of calcium homeostasis disruption: a shifted CaSR set-point (FHH), unregulated endogenous hormone production (Primary HPT), ectopic vitamin D activation (Sarcoidosis), ectopic peptide secretion (HHM), or appropriate secondary response to nutrient deficiency (Osteomalacia).

Step-by-Step Solution

1
Evaluate the intact PTH level relative to serum calcium.
Identifies if the condition is PTH-mediated (high/normal PTH with high calcium) or PTH-independent (suppressed PTH with high calcium).
Normal physiological response to hypercalcemia is complete suppression of PTH. Unsuppressed PTH indicates the parathyroid gland is the source or the set-point is altered.
2
For PTH-dependent hypercalcemia, check the 24-hour urine calcium.
Differentiates Primary Hyperparathyroidism (high/normal urine calcium) from Familial Hypocalciuric Hypercalcemia (very low urine calcium).
Both present with high calcium and unsuppressed PTH, but FHH features a mutant CaSR that increases renal calcium reabsorption.
3
For PTH-independent hypercalcemia, evaluate PTHrP and vitamin D metabolites.
Differentiates humoral hypercalcemia of malignancy (high PTHrP) from granulomatous diseases (high 1,25-dihydroxyvitamin D).
Different ectopic mechanisms cause the hypercalcemia, requiring distinct therapeutic interventions.

Key Concept

Differential diagnosis of calcium and phosphorus metabolic disorders using intact PTH, urine calcium, and specific systemic markers.
Question 347Question →

An otherwise healthy 2626-year-old male is evaluated in the outpatient clinic due to a 44-day history of a swollen, painful, and warm right knee. He also reports recent onset of left heel pain that worsens with walking. For the past week, he has experienced bilateral eye redness and a "gritty" sensation. Three weeks prior to this visit, the patient had a self-limited episode of fever, abdominal cramps, and watery diarrhea that resolved after a few days. His current temperature is 37.4∘C37.4^\circ\text{C} (99.3∘F99.3^\circ\text{F}), blood pressure is 122/78122/78 mmHg, and pulse is 8686/min. Physical examination shows a large effusion in the right knee with restricted range of motion secondary to pain. There is marked tenderness at the insertion of the left Achilles tendon. Bilateral conjunctival injection is noted without purulent discharge. Arthrocentesis of the right knee yields 4040 mL of cloudy yellow fluid. Synovial fluid analysis reveals a leukocyte count of 35,000/mm335,000/\text{mm}^3 with 80%80\% neutrophils. Gram stain shows no organisms, and polarized light microscopy demonstrates no crystals. Which of the following is the most appropriate next step in the management of this patient?

Show answer & explanation

Answer: Prescription of oral naproxen

Answer

Prescription of oral naproxen
This patient's presentation of asymmetric oligoarthritis, enthesitis (Achilles tendon tenderness), and conjunctivitis shortly after a diarrheal illness is highly characteristic of reactive arthritis. It is a seronegative spondyloarthropathy that typically occurs 11 to 44 weeks after a gastrointestinal (e.g., Salmonella, Shigella, Campylobacter) or genitourinary (e.g., Chlamydia trachomatis) infection. The joint aspirate shows an inflammatory pattern (WBC between 2,0002,000 and 50,000/mm350,000/\text{mm}^3) with a negative Gram stain, typical of this sterile, immune-mediated condition. The cornerstone of initial therapy for the joint symptoms is a high-dose nonsteroidal anti-inflammatory drug (NSAID) such as naproxen, ibuprofen, or indomethacin.

Step-by-Step Solution

1
Identify the clinical syndrome based on the patient's history and physical findings.
The patient presents with an acute asymmetric oligoarthritis, enthesitis (Achilles tendon tenderness), and conjunctivitis following a recent diarrheal illness.
Recognizing the classic triad of symptoms following an enteric infection points strongly to reactive arthritis (formerly Reiter syndrome).
2
Evaluate the synovial fluid analysis results.
The fluid is inflammatory (leukocyte count of 35,000/mm³) but non-purulent (negative Gram stain and no crystals).
This confirms an inflammatory arthritis rather than a crystal-induced or grossly purulent bacterial septic arthritis, supporting the diagnosis of a seronegative spondyloarthropathy.
3
Determine the initial step in management for this condition.
The most appropriate next step is to initiate systemic anti-inflammatory treatment with an NSAID.
NSAIDs are the recognized first-line therapy for the acute joint symptoms of reactive arthritis.

Key Concept

Reactive arthritis is a seronegative spondyloarthropathy characterized by the triad of arthritis, conjunctivitis, and urethritis/enthesitis following a gastrointestinal or genitourinary infection; initial management of the arthritis is with high-dose NSAIDs.
Question 348Question →

A clinical quality committee is reviewing antimicrobial prescribing practices within the gastroenterology and hepatology department. Match the following patient scenarios with the most appropriate, guideline-concordant initial pharmacological management to promote effective care and antimicrobial stewardship.

Click a left item, then click its matching right item

Items

A stable 45-year-old with CT-confirmed uncomplicated acute diverticulitis and no systemic toxicity
A cirrhotic patient presenting with ascites, fever, and ascitic fluid showing 350350 polymorphonuclear cells/mm3mm^3
A hospitalized patient developing profuse watery diarrhea and a positive stool toxin assay for Clostridioides difficile
A patient with advanced cirrhosis being discharged after successfully recovering from an episode of spontaneous bacterial peritonitis

Matches

Show answer & explanation

Answer

Uncomplicated diverticulitis is managed with observation; active spontaneous bacterial peritonitis requires intravenous cefotaxime; initial Clostridioides difficile infection is treated with oral fidaxomicin; and secondary spontaneous bacterial peritonitis prophylaxis uses oral trimethoprim-sulfamethoxazole.
Each management strategy directly aligns with current evidence-based guidelines optimizing patient outcomes while minimizing unnecessary broad-spectrum antimicrobial exposure. Matching the clinical severity and specific pathogen risks to the narrowest effective intervention is the cornerstone of gastrointestinal infectious disease management.

Step-by-Step Solution

1
Analyze the diverticulitis scenario.
Identify that the patient is stable with uncomplicated disease, warranting observation without antibiotics.
Routine antibiotics in uncomplicated cases do not improve outcomes and worsen antimicrobial resistance.
2
Evaluate the ascitic fluid findings in the febrile cirrhotic patient.
Confirm spontaneous bacterial peritonitis due to a PMN count greater than 250/mm3250/mm^3, requiring immediate intravenous third-generation cephalosporins.
Untreated spontaneous bacterial peritonitis has a high mortality rate and requires immediate broad-spectrum empirical coverage.
3
Assess the diarrheal presentation and stool assay.
Identify an active Clostridioides difficile infection requiring targeted oral therapy.
Oral fidaxomicin (or oral vancomycin) is the standard of care for initial episodes.
4
Determine the outpatient needs for a patient who just recovered from spontaneous bacterial peritonitis.
Initiate lifelong secondary prophylactic oral antibiotics.
The recurrence rate of spontaneous bacterial peritonitis is extremely high without ongoing daily prophylaxis.

Key Concept

Antimicrobial stewardship and appropriate targeted therapy for gastrointestinal and hepatologic infections
Question 349Question →

A 66-year-old retired mechanic is brought to the clinic by his daughter after experiencing difficulty walking over the past 24 hours. He reports a two-week history of dull, continuous pain in his mid-thoracic region that worsens when he lies flat in bed. His past medical history is significant for non-small cell lung cancer treated with radiation and chemotherapy two years ago. On neurologic examination, he demonstrates 3/5 strength in the bilateral lower extremities, diminished sensation to pinprick below the umbilicus, and symmetric hyperreflexia at the patellae and ankles. Rectal examination reveals decreased sphincter tone. Vital signs are within normal limits except for a temperature of 37.8°C (100.0°F). Laboratory results reveal a normal leukocyte count and a serum calcium level of 9.2 mg/dL. Which of the following is the most appropriate initial step in the management of this patient?

Show answer & explanation

Answer: Intravenous dexamethasone administration

Answer

Immediate administration of intravenous dexamethasone.
The correct answer is intravenous dexamethasone administration. This patient's presentation of progressively worsening thoracic back pain that is exacerbated by recumbency, accompanied by acute bilateral lower extremity weakness, sensory level deficits, and bowel/bladder dysfunction in the setting of a known solid malignancy, is highly concerning for neoplastic epidural spinal cord compression (ESCC). In cases of suspected ESCC, intravenous glucocorticoids must be given immediately upon clinical suspicion to reduce vasogenic edema, alleviate pressure on the spinal cord, and preserve neurological function. Steroids must be administered prior to obtaining confirmatory imaging.

Step-by-Step Solution

1
Identify the clinical syndrome from the patient's presentation.
The patient exhibits red flag signs for neoplastic epidural spinal cord compression (ESCC): back pain worse with lying down, lower extremity motor weakness, sensory level deficits, and bowel/bladder dysfunction, all in the context of a previous solid organ malignancy.
Recognizing this oncologic emergency early is critical because neurologic recovery is directly tied to the neurologic status at the time treatment is initiated.
2
Determine the priority of management for suspected ESCC.
High-dose glucocorticoids (e.g., dexamethasone) must be administered immediately.
Corticosteroids rapidly decrease peritumoral vasogenic edema, thereby acutely relieving physical pressure on the spinal cord and preventing irreversible ischemia and paralysis.
3
Plan the subsequent sequence of care.
Arrange for an urgent magnetic resonance imaging (MRI) of the entire spine after steroid administration.
While imaging is required to confirm the diagnosis and guide definitive treatment (such as surgical decompression or targeted radiation therapy), diagnostic tests should never delay the initial medical stabilization of the spinal cord.

Key Concept

The initial management of suspected neoplastic epidural spinal cord compression requires the immediate administration of high-dose intravenous glucocorticoids (like dexamethasone) to reduce spinal cord edema and preserve neurologic function, even before confirmatory imaging is obtained.
Estimated Time:1m 0s
Question 350Question →

A 45-year-old woman is brought to the emergency department due to progressive muscle weakness. Over the past week, she has had difficulty rising from a chair and climbing stairs. She has a 5-year history of primary Sjögren syndrome, for which she uses artificial tears and saliva substitutes. Vital signs are within normal limits. Physical examination shows symmetric 3/5 muscle strength in the proximal upper and lower extremities, with decreased deep tendon reflexes.

Laboratory studies are obtained:

Laboratory TestResultReference Range
Serum sodium140 mEq/L136-145 mEq/L
Serum potassium2.1 mEq/L3.5-5.0 mEq/L
Serum chloride114 mEq/L95-105 mEq/L
Serum bicarbonate14 mEq/L22-28 mEq/L
Arterial pH7.287.35-7.45
Arterial pCO230 mmHg35-45 mmHg
Urine pH6.84.5-8.0

Which of the following best explains this patient's clinical presentation and laboratory findings?

Show answer & explanation

Answer: Impaired distal tubular secretion of hydrogen ions with appropriate respiratory compensation

Answer

Impaired distal tubular secretion of hydrogen ions with appropriate respiratory compensation
The correct answer accurately identifies that the patient has a non-anion gap metabolic acidosis (NAGMA) due to impaired distal tubular hydrogen secretion (Type 1 RTA) with appropriate respiratory compensation. The patient's anion gap is normal at 12 mEq/L12\ mEq/L. According to Winter's formula, the expected pCO2pCO_2 is (1.5×14)+8=29±2 mmHg(1.5 \times 14) + 8 = 29 \pm 2\ mmHg; the measured pCO2pCO_2 is 30 mmHg30\ mmHg, indicating full compensation. The combination of NAGMA, severe hypokalemia (causing the progressive muscle weakness), and an inappropriately basic urine pH (6.86.8) is classic for Type 1 (distal) RTA. This condition is highly associated with autoimmune disorders, particularly primary Sjögren syndrome, due to autoantibody-mediated damage to the alpha-intercalated cells in the distal collecting tubule.

Step-by-Step Solution

1
Calculate the anion gap to categorize the metabolic acidosis.
AG=Na+−(Cl−+HCO3−)=140−(114+14)=12 mEq/LAG = Na^+ - (Cl^- + HCO_3^-) = 140 - (114 + 14) = 12\ mEq/L
Identifying a normal anion gap metabolic acidosis (NAGMA) narrows the differential diagnosis to renal tubular acidosis (RTA), gastrointestinal bicarbonate loss, or iatrogenic causes.
2
Apply Winter's formula to evaluate respiratory compensation.
Expected pCO2=1.5×14+8±2=29±2 mmHgExpected\ pCO_2 = 1.5 \times 14 + 8 \pm 2 = 29 \pm 2\ mmHg. The patient's pCO2pCO_2 is 30 mmHg30\ mmHg.
This confirms there is appropriate physiological respiratory compensation and completely rules out any concurrent primary respiratory alkalosis or acidosis.
3
Analyze the urine pH and serum potassium in the context of NAGMA.
The urine pH is inappropriately basic (6.86.8), and the serum potassium is severely low (2.1 mEq/L2.1\ mEq/L).
A normal kidney should excrete acid (urine pH<5.5pH < 5.5) in the presence of metabolic acidosis. A high urine pH with NAGMA and severe hypokalemia points to Type 1 (distal) RTA.
4
Connect the pathophysiology to the patient's underlying autoimmune disease.
The patient's primary Sjögren syndrome is the underlying etiology for the Type 1 RTA.
Autoimmune damage to the alpha-intercalated cells of the distal tubule impairs hydrogen ion secretion. The resulting Type 1 RTA causes severe hypokalemia, which manifests as profound muscle weakness and diminished reflexes.

Key Concept

Type 1 (distal) renal tubular acidosis (RTA) is classically associated with autoimmune diseases, particularly Sjögren syndrome, and presents with a normal anion gap metabolic acidosis, severe hypokalemia, and an inappropriately basic urine pH (> 5.5).
Question 351Question →

A 7171-year-old man is evaluated in the emergency department for severe, progressive shortness of breath over the past two days. He has a complex medical history that includes ischemic cardiomyopathy and chronic obstructive pulmonary disease. On physical examination, he is tachypneic and sitting upright in bed. Auscultation of the lungs reveals diffuse bilateral expiratory wheezing with faint crackles at the bases. To help distinguish between a pulmonary and a cardiovascular etiology for his acute presentation, the physician orders a rapid serum laboratory test that measures a specific endogenous polypeptide. The test results show a markedly elevated concentration of this polypeptide, supporting acute decompensated heart failure as the primary cause of his symptoms.

What is the primary physiologic stimulus for the secretion of the polypeptide measured in this patient?

Show answer & explanation

Answer: Ventricular myocyte stretching

Answer

Ventricular myocyte stretching
The clinical scenario describes a patient with dyspnea of unclear etiology where a serum polypeptide confirms acute decompensated heart failure. This diagnostic polypeptide is Brain Natriuretic Peptide (BNP). The primary physiologic stimulus for the synthesis and secretion of BNP is the stretching of ventricular myocytes due to volume expansion and pressure overload. BNP acts to promote diuresis, natriuresis, and vasodilation to counteract this fluid overload.

Step-by-Step Solution

1
Identify the clinical dilemma and the diagnostic test used.
The patient has symptoms common to both COPD and heart failure (wheezing, dyspnea). The specific polypeptide measured to differentiate these conditions is Brain Natriuretic Peptide (BNP).
Wheezing can occur in heart failure (cardiac asthma), making clinical differentiation difficult. BNP is the standard biomarker used to confirm a cardiac etiology.
2
Determine the pathophysiologic trigger for the release of this biomarker.
BNP is synthesized and secreted by the ventricular myocardium in response to stretch and increased wall tension.
Volume overload in heart failure causes ventricular stretch, triggering BNP release to promote diuresis and vasodilation to counteract the overload.

Key Concept

Brain Natriuretic Peptide (BNP) is a hormone secreted primarily by ventricular myocytes in response to increased ventricular wall tension and stretching caused by volume or pressure overload.
Question 352Question →

A 62-year-old man is brought to the emergency department via ambulance due to the sudden onset of severe, tearing chest pain that radiates to his interscapular region. His blood pressure is 195/115 mm Hg in the right arm and 170/100 mm Hg in the left arm. Heart rate is 110/min. Physical examination reveals a new diastolic decrescendo murmur at the right upper sternal border. Arrange the following steps in the most appropriate chronological order for the initial evaluation and management of this patient.

Drag items to arrange them in the correct order

Show answer & explanation

Answer

The correct sequence is to first obtain a 12-lead electrocardiogram, then administer intravenous esmolol, followed by intravenous sodium nitroprusside, and finally perform a computed tomography angiography.
The sequence follows the standard protocol for suspected aortic dissection: immediate bedside rule-out of ST-elevation myocardial infarction (ECG), followed by sequential anti-impulse medical therapy (heart rate control with esmolol, then blood pressure control with nitroprusside), and finally definitive diagnostic imaging (CT angiography) once the patient is hemodynamically stable.

Step-by-Step Solution

1
Obtain a bedside 12-lead electrocardiogram.
Rules out ST-segment elevation myocardial infarction.
It is essential to quickly differentiate aortic dissection from acute coronary syndrome, because treatments for myocardial infarction (such as heparin and thrombolytics) are contraindicated in aortic dissection.
2
Administer intravenous esmolol.
Lowers heart rate and left ventricular contractility.
Beta-blockers reduce aortic wall shear stress and prevent the reflex tachycardia that would occur if a vasodilator were given first.
3
Administer intravenous sodium nitroprusside.
Lowers systolic blood pressure to the target range of 100-120 mm Hg.
Vasodilators provide necessary blood pressure control but must be given only after adequate beta-blockade is established to prevent worsening of the dissection.
4
Perform computed tomography angiography of the chest and abdomen.
Provides definitive diagnosis and identifies the extent of the dissection.
Imaging is required for definitive diagnosis and surgical planning, but the patient must be hemodynamically stabilized first to prevent dissection propagation during transport and scanning.

Key Concept

In the initial management of suspected acute aortic dissection, an electrocardiogram is obtained first to rule out myocardial infarction, followed by strict blood pressure and heart rate control (beta-blocker first, then vasodilator) prior to definitive imaging.
Question 353Question →

A 34-year-old woman comes to the clinic reporting a 6-month history of severe fatigue, a 5-kg (11-lb) weight gain, and generalized weakness. She also reports cold intolerance and irregular menstrual periods, with her last menses occurring 4 months ago. She has no significant past medical history and takes no medications. Blood pressure is 100/60 mmHg and pulse is 55/min. Physical examination shows a tired-appearing woman with dry skin. Deep tendon reflexes exhibit a delayed relaxation phase. Laboratory results are as follows:

TestResultReference Range
Thyroid-stimulating hormone (TSH)1.8 mIU/L0.4 - 4.2 mIU/L
Free thyroxine (T4)0.5 ng/dL0.8 - 2.7 ng/dL
Human chorionic gonadotropinNegativeNegative

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

Show answer & explanation

Answer: Check serum morning cortisol level

Answer

Check serum morning cortisol level
The correct next step is to check a serum morning cortisol level. This patient presents with classic symptoms of hypothyroidism (fatigue, weight gain, cold intolerance, delayed deep tendon reflexes) and has a correspondingly low free T4. However, her TSH is inappropriately normal rather than elevated. A normal or low TSH in the presence of a low free T4 is the biochemical hallmark of secondary (central) hypothyroidism, which is caused by a failure of the pituitary gland or hypothalamus. In any patient with suspected hypopituitarism, it is critical to evaluate for concurrent central adrenal insufficiency (low ACTH leading to low cortisol). Thyroid hormone replacement (levothyroxine) accelerates the basal metabolic rate and increases the hepatic clearance of cortisol. If levothyroxine is administered to a patient with unrecognized adrenal insufficiency, the sudden relative decrease in available cortisol can precipitate a life-threatening adrenal crisis. Therefore, the hypothalamic-pituitary-adrenal axis must be evaluated (usually with a morning serum cortisol level or an ACTH stimulation test) before initiating levothyroxine. If adrenal insufficiency is confirmed, glucocorticoids must be given before or simultaneously with levothyroxine.

Step-by-Step Solution

1
Interpret the thyroid function tests.
The patient has a low free T4 with an inappropriately normal TSH.
This pattern is diagnostic of secondary (central) hypothyroidism, indicating a pituitary or hypothalamic disorder rather than a primary thyroid gland failure.
2
Identify the risks associated with central hypothyroidism.
Patients with central hypothyroidism are at high risk for concurrent central adrenal insufficiency (panhypopituitarism).
The pituitary gland produces both TSH and ACTH; a pathological process damaging TSH production often affects ACTH production as well.
3
Determine the safest management sequence.
The adrenal axis must be evaluated before starting thyroid hormone replacement.
Administering levothyroxine increases the basal metabolic rate and hepatic clearance of cortisol. If given to a patient with unrecognized adrenal insufficiency, it can abruptly precipitate a life-threatening adrenal crisis.

Key Concept

In patients with central hypothyroidism (low free T4, normal/low TSH), the adrenal axis must be evaluated (e.g., with a morning cortisol level) before initiating levothyroxine to prevent precipitating an adrenal crisis.
Estimated Time:1m 0s
Question 354Question →

A 4848-year-old male arrives at the emergency department reporting an abrupt onset of severe, constant epigastric pain that radiates to his back. The pain began 44 hours ago after he consumed a heavy meal. He has experienced two episodes of nonbilious emesis since symptom onset. He has a history of hyperlipidemia and takes rosuvastatin. His temperature is 37.9∘C37.9^\circ\text{C} (100.2∘F100.2^\circ\text{F}), heart rate is 115/min115/\text{min}, blood pressure is 128/82 mmHg128/82\text{ mmHg}, and respiratory rate is 18/min18/\text{min}. Cardiopulmonary examination is unremarkable. Abdominal examination reveals decreased bowel sounds and significant epigastric tenderness without rebound or guarding.

Laboratory studies show:

TestValue
Leukocyte count14,500/mm314,500/\text{mm}^3
Total bilirubin1.0 mg/dL1.0\text{ mg/dL}
Alkaline phosphatase95 U/L95\text{ U/L}
Aspartate aminotransferase (AST)150 U/L150\text{ U/L}
Alanine aminotransferase (ALT)180 U/L180\text{ U/L}
Lipase4,500 U/L4,500\text{ U/L}

A right upper quadrant ultrasound reveals multiple mobile gallstones within the gallbladder. The common bile duct measures 4 mm4\text{ mm} in diameter, and there is no intrahepatic biliary dilation.

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

Show answer & explanation

Answer: Initiation of aggressive intravenous crystalloid hydration

Answer

Initiation of aggressive intravenous crystalloid hydration
The correct answer is the initiation of aggressive intravenous crystalloid hydration. This patient has acute gallstone pancreatitis, diagnosed by characteristic epigastric pain and a markedly elevated serum lipase level (greater than three times the upper limit of normal). The pathogenesis involves severe retroperitoneal inflammation that leads to massive third-spacing of fluids, causing intravascular volume depletion and pancreatic microcirculatory hypoperfusion. Early, aggressive intravenous volume expansion (typically with isotonic crystalloids like lactated Ringer solution) within the first 1212 to 2424 hours is the cornerstone of management to prevent progression to pancreatic necrosis and multiorgan failure.

Step-by-Step Solution

1
Analyze the clinical presentation and laboratory results.
The patient has severe epigastric pain radiating to the back, elevated lipase (4,500 U/L4,500\text{ U/L}), and evidence of gallstones on ultrasound, confirming the diagnosis of acute gallstone pancreatitis.
Establishing the correct diagnosis and etiology is the first step in determining appropriate management.
2
Evaluate for complications or indications for urgent invasive procedures.
The patient's total bilirubin and alkaline phosphatase are normal, and the common bile duct is not dilated. There is no evidence of ascending cholangitis or severe biliary obstruction.
This rules out the need for urgent endoscopic retrograde cholangiopancreatography (ERCP).
3
Determine the optimal supportive care strategy.
Aggressive intravenous fluid resuscitation, along with pain control, is the standard of care to prevent third-spacing hypovolemia and pancreatic necrosis.
Acute pancreatitis causes significant retroperitoneal fluid shifts, leading to microvascular hypoperfusion that worsens the inflammatory cascade.

Key Concept

The primary initial management for acute gallstone pancreatitis without evidence of cholangitis is supportive care, centered on aggressive intravenous fluid resuscitation. Prophylactic antibiotics and urgent ERCP are not indicated in the absence of infected necrosis or biliary obstruction.
Estimated Time:1m 15s
Question 355Question →

An emergency department evaluation is requested for a 58-year-old male presenting with progressively worsening shortness of breath and a cough producing frothy sputum over the past 48 hours. His medical history is significant for a 30-pack-year smoking habit and type 2 diabetes mellitus complicated by diabetic nephropathy. Upon arrival, he is in moderate respiratory distress.

Vital signs reveal a blood pressure of 185/110 mm Hg185/110 \text{ mm Hg}, pulse of 112/min112/\text{min}, and respiratory rate of 28/min28/\text{min}. Oxygen saturation is 88% on room air. Pulmonary auscultation reveals bilateral crackles extending to the mid-lung fields along with diffuse expiratory wheezing. Examination of the lower extremities shows 2+ bilateral pitting edema.

Laboratory evaluation reveals the following:
Serum sodium: 138 mEq/L138 \text{ mEq/L}
Serum potassium: 5.9 mEq/L5.9 \text{ mEq/L}
Serum chloride: 102 mEq/L102 \text{ mEq/L}
Serum bicarbonate: 12 mEq/L12 \text{ mEq/L}
Blood urea nitrogen: 92 mg/dL92 \text{ mg/dL}
Serum creatinine: 7.4 mg/dL7.4 \text{ mg/dL}

Arterial blood gas (room air):
pH: 7.227.22
pCO2p\text{CO}_2: 36 mm Hg36 \text{ mm Hg}
pO2p\text{O}_2: 58 mm Hg58 \text{ mm Hg}

Based on the clinical and laboratory findings, which of the following best describes this patient's current acid-base disorder and the primary cause of his respiratory distress?

Show answer & explanation

Answer: Metabolic acidosis with an elevated anion gap and a concurrent respiratory acidosis; distress is primarily due to acute volume overload

Answer

Metabolic acidosis with an elevated anion gap and a concurrent respiratory acidosis; distress is primarily due to acute volume overload
The patient has a metabolic acidosis with an elevated anion gap of 24, driven by his acute-on-chronic renal failure (uremia). Using Winter's formula (1.5×[HCO3−]+8±21.5 \times [\text{HCO}_3^-] + 8 \pm 2), the expected pCO2p\text{CO}_2 is 24−28 mm Hg24-28 \text{ mm Hg}. The measured pCO2p\text{CO}_2 of 36 mm Hg36 \text{ mm Hg} is substantially higher than this range, revealing a concurrent respiratory acidosis. The patient's profound hypertension, severe renal failure, crackles, pitting edema, and frothy sputum all indicate acute volume overload leading to pulmonary edema. The fluid accumulation in the lungs causes respiratory fatigue and CO2\text{CO}_2 retention, alongside 'cardiac asthma' (wheezing due to peribronchial edema).

Step-by-Step Solution

1
Calculate the serum anion gap to determine the primary metabolic disorder.
Anion gap = 138−(102+12)=24138 - (102 + 12) = 24.
Identifies the presence of a metabolic acidosis with an elevated anion gap, likely secondary to uremia given the markedly elevated BUN and creatinine.
2
Apply Winter's formula to determine the expected pCO2p\text{CO}_2 for appropriate respiratory compensation.
Expected pCO2=(1.5×12)+8±2=26±2 mm Hgp\text{CO}_2 = (1.5 \times 12) + 8 \pm 2 = 26 \pm 2 \text{ mm Hg}.
Evaluates if a secondary acid-base disorder is present alongside the primary metabolic acidosis.
3
Compare the measured pCO2p\text{CO}_2 to the calculated expected pCO2p\text{CO}_2.
The measured pCO2p\text{CO}_2 of 36 mm Hg36 \text{ mm Hg} is significantly higher than the expected range (24−28 mm Hg24-28 \text{ mm Hg}).
A higher-than-expected pCO2p\text{CO}_2 indicates a concurrent respiratory acidosis due to inadequate ventilation.
4
Analyze the physical exam findings to identify the cause of respiratory distress and the respiratory acidosis.
Severe hypertension, frothy sputum, bilateral crackles, pitting edema, and severe renal failure point directly to acute pulmonary edema.
Volume overload leads to pulmonary edema, which impairs gas exchange and causes respiratory fatigue. This explains both the wheezing ('cardiac asthma') and the concurrent respiratory acidosis.

Key Concept

Mixed acid-base disorders and differentiation of acute pulmonary edema from primary obstructive lung disease.
Question 356Question →

A 28-year-old man presents to the emergency department with a 3-week history of daily spiking fevers, reaching up to 39.6°C (103.3°F), typically occurring in the late afternoon. He reports a severe sore throat, profound fatigue, and worsening pain and swelling in his bilateral wrists and knees. He notes a faint, salmon-colored rash on his trunk that seems to appear only during his febrile episodes and resolves when his temperature normalizes. He had an uncomplicated appendectomy 4 weeks ago. He is also stressed because his employer is demanding his specific medical diagnosis to approve his prolonged sick leave.

Vital signs show a temperature of 39.5°C (103.1°F), blood pressure of 120/78 mm Hg, heart rate of 110/min, and respiratory rate of 16/min. Physical examination reveals swollen, tender wrists and a macular erythematous rash on the chest. The lungs are clear to auscultation. Laboratory studies reveal:

TestResult
Leukocyte count22,000/mm322,000/\text{mm}^3 (88%88\% neutrophils)
Hemoglobin11.2 g/dL11.2 \text{ g/dL}
Erythrocyte sedimentation rate110 mm/h110 \text{ mm/h}
Serum ferritin9,200 ng/mL9,200 \text{ ng/mL}

Rheumatoid factor and antinuclear antibody (ANA) tests are negative. Blood cultures drawn 3 days ago in the outpatient clinic are sterile. Which of the following is the most appropriate next step in the management of this patient?

Show answer & explanation

Answer: Initiate systemic corticosteroid therapy

Answer

The correct approach is to initiate systemic corticosteroid therapy.
This patient's presentation of quotidian (daily spiking) fevers, a transient salmon-colored rash appearing at the height of the fever, polyarthritis, significant leukocytosis, and markedly elevated serum ferritin is the classic presentation of adult-onset Still's disease (AOSD). The negative rheumatoid factor, negative ANA, and sterile blood cultures are typical and help rule out other connective tissue diseases or sepsis. For moderate-to-severe presentations of AOSD, systemic corticosteroids are the mainstay of initial therapy to suppress the severe autoinflammatory response.

Step-by-Step Solution

1
Analyze the clinical presentation.
The patient is a young adult presenting with quotidian (daily spiking) fevers, an evanescent salmon-colored rash, polyarthritis, marked leukocytosis, and extreme hyperferritinemia.
Identifying these key features is essential to form a differential diagnosis.
2
Formulate the most likely diagnosis.
The constellation of symptoms and lab findings represents the classic triad for adult-onset Still's disease (AOSD).
Negative sterile blood cultures, negative ANA/RF, and a remote surgical history make infectious, autoimmune, and postoperative etiologies highly unlikely.
3
Determine the appropriate management.
Systemic corticosteroids (or high-dose NSAIDs) should be initiated.
AOSD is an autoinflammatory disorder. For moderate-to-severe systemic manifestations (debilitating arthritis, prolonged high fevers), systemic corticosteroids are the standard first-line treatment to rapidly control inflammation.

Key Concept

Adult-onset Still's disease (AOSD) is a systemic autoinflammatory condition classically presenting with quotidian fevers, a transient salmon-colored maculopapular rash, polyarthritis, marked leukocytosis, and severe hyperferritinemia. Treatment requires immunosuppression.
Question 357Question →

For each of the following hospitalized patients presenting with severe, confirmed, or highly suspected infections, select the most appropriate definitive or targeted empiric intravenous antimicrobial therapy from the options provided.

Click a left item, then click its matching right item

Items

A 62-year-old patient developing ventilator-associated pneumonia; endotracheal aspirate culture grows extended-spectrum beta-lactamase (ESBL)-producing Klebsiella pneumoniae.
A 54-year-old patient with a central line-associated bloodstream infection; blood cultures isolate vancomycin-resistant Enterococcus faecium.
A 71-year-old patient with complicated pyelonephritis; urine and blood cultures grow Enterobacter cloacae demonstrating inducible AmpC beta-lactamase production.
A 48-year-old critically ill patient in the intensive care unit who develops new-onset septic shock and candidemia; fungal species identification is pending.

Matches

Show answer & explanation

Answer

The correct pairings match specific resistance mechanisms and pathogen profiles with their definitive antimicrobial therapy: ESBL Klebsiella with meropenem, VRE with daptomycin, AmpC Enterobacter with cefepime, and critically ill candidemia with micafungin.
Each clinical scenario requires a highly specific antimicrobial agent based on pathogen characteristics. Carbapenems (meropenem) are required for ESBL-producing organisms because they resist hydrolysis by these specific enzymes. Daptomycin is utilized for VRE because enterococci have inherent cephalosporin resistance, and VRE's altered peptidoglycan precursors render vancomycin ineffective. Cefepime avoids the induction of AmpC beta-lactamases seen in 'SPACE' organisms (like Enterobacter). Finally, echinocandins (micafungin) are the standard of care for empiric candidemia in the critically ill due to the high mortality associated with missing fluconazole-resistant strains.

Step-by-Step Solution

1
Analyze the pathogen and its specific resistance mechanism described in each clinical vignette.
Identified ESBL-producing Klebsiella, VRE, AmpC-producing Enterobacter, and empiric candidemia in a critically ill patient.
Accurate pathogen identification is required to select structurally stable and mechanism-appropriate antimicrobials.
2
Match the identified resistance mechanisms to the antimicrobial class capable of overcoming them.
ESBL requires carbapenems; VRE requires membrane depolarizers (daptomycin) or oxazolidinones (linezolid); AmpC requires 4th-generation cephalosporins (cefepime) or carbapenems; severe undifferentiated candidemia requires echinocandins.
Beta-lactamases hydrolyze specific antibiotic rings; matching ensures the chosen drug will not be deactivated and provides adequate bactericidal or fungicidal activity.

Key Concept

Selection of targeted antimicrobial therapy must account for specific molecular resistance mechanisms (e.g., ESBL, AmpC, VRE) and patient acuity (e.g., risk of azole-resistant Candida in the intensive care unit).
Question 358Question →

Match each patient's clinical presentation with the autoantibody most specific to or characteristic of their underlying diagnosis.

Click a left item, then click its matching right item

Items

A 32-year-old woman with recurrent second-trimester miscarriages, a new left lower extremity deep vein thrombosis, and an isolated prolonged partial thromboplastin time.
A 45-year-old woman with chronic fatigue, difficulty swallowing solid foods, thickened skin confined to her fingers and face, and severe episodic digital pallor in cold weather.
A 55-year-old woman with progressive difficulty standing from a seated position, an erythematous periorbital rash, and violaceous, scaling papules over her metacarpophalangeal joints.
A 40-year-old woman with a chronic sensation of 'sand in the eyes,' the need to drink water to swallow dry foods, and bilateral parotid gland enlargement.
A 28-year-old woman with a photosensitive facial rash sparing the nasolabial folds, pleuritic chest pain, diffuse joint aches, and new-onset proteinuria.

Matches

Show answer & explanation

Answer

The clinical vignettes match as follows: Antiphospholipid syndrome with Anticardiolipin antibodies, Limited cutaneous systemic sclerosis with Anti-centromere antibodies, Dermatomyositis with Anti-Jo-1 antibodies, Sjögren syndrome with Anti-Ro/SSA antibodies, and Systemic Lupus Erythematosus with Anti-double-stranded DNA antibodies.
Each autoantibody represents a highly specific serologic marker for the respective clinical syndrome, confirming the diagnosis based on the classic physical and historical findings provided in the vignettes.

Step-by-Step Solution

1
Analyze each patient's demographic profile, physical exam findings, and laboratory abnormalities to establish the most likely rheumatologic diagnosis.
Identify Antiphospholipid syndrome, Limited cutaneous systemic sclerosis, Dermatomyositis, Sjögren syndrome, and SLE respectively.
Accurate disease identification is prerequisite to determining the corresponding serologic marker.
2
Correlate the identified rheumatologic diseases with their classic highly specific autoantibodies.
Match each disease state to its targeted antibody profile.
Autoantibody profiles are essential for confirming clinical diagnoses and predicting systemic involvement in rheumatologic conditions.

Key Concept

Serologic markers and autoantibody profiles of systemic autoimmune and rheumatologic diseases.
Question 359Question →

A 55-year-old man presents to the clinic with a 4-month history of worsening fatigue, generalized weakness, and cold intolerance. He also reports a significant decrease in libido and difficulty achieving erections over the same period. The patient occasionally experiences mild, dull headaches but denies any changes in his vision. His blood pressure is 112/72 mm Hg112/72 \text{ mm Hg} and pulse is 56/min56/\text{min}. Physical examination is notable for dry skin, sparse body hair, and delayed relaxation of the deep tendon reflexes. Visual field testing is full to confrontation. Laboratory evaluation is performed, with the following results:

Laboratory TestResultReference Range
Thyroid-stimulating hormone (TSH)1.8 mIU/L1.8 \text{ mIU/L}0.5−5.0 mIU/L0.5 - 5.0 \text{ mIU/L}
Free thyroxine (T4)0.5 ng/dL0.5 \text{ ng/dL}0.9−1.7 ng/dL0.9 - 1.7 \text{ ng/dL}
Total testosterone (8 AM)145 ng/dL145 \text{ ng/dL}300−1000 ng/dL300 - 1000 \text{ ng/dL}

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

Show answer & explanation

Answer: Magnetic resonance imaging of the pituitary gland

Answer

Magnetic resonance imaging of the pituitary gland
The correct answer is magnetic resonance imaging of the pituitary gland. This patient's laboratory results demonstrate a low free T4 with a TSH that is well within the normal range. In primary hypothyroidism, a low free T4 removes negative feedback and triggers a compensatory rise in TSH (typically >10 mIU/L> 10 \text{ mIU/L}). An inappropriately normal or low TSH in the setting of low free T4 is the hallmark of central (secondary) hypothyroidism. Combined with symptoms of hypogonadism, a low morning testosterone level, and headaches, this patient likely has panhypopituitarism secondary to a compressive pituitary mass (such as a nonfunctioning pituitary macroadenoma). The best next step is to obtain a pituitary MRI to evaluate for structural disease. Note that it is also essential to assess the adrenal axis (e.g., via an 8 AM serum cortisol level) before initiating any thyroid hormone replacement.

Step-by-Step Solution

1
Evaluate the thyroid panel results.
The patient has a low free T4 with a TSH that is inappropriately in the normal range, indicating central (secondary) hypothyroidism.
Primary hypothyroidism would cause a compensatory elevation in TSH. A normal or low TSH in the setting of low free T4 localizes the pathology to the pituitary or hypothalamus.
2
Synthesize the laboratory findings with the clinical presentation.
The concurrent hypogonadism (low testosterone, decreased libido) and presence of headaches indicate multi-axis pituitary dysfunction, likely due to a compressive mass.
Panhypopituitarism often presents with sequential loss of anterior pituitary hormones, frequently caused by nonfunctioning pituitary adenomas in adults.
3
Determine the most appropriate diagnostic intervention.
Magnetic resonance imaging (MRI) of the pituitary is required.
Before initiating hormone replacement, the structural cause of the panhypopituitarism must be evaluated via imaging. Additionally, the adrenal axis must be assessed (e.g., 8 AM cortisol) to avoid precipitating an adrenal crisis.

Key Concept

Diagnosis and workup of central hypothyroidism and panhypopituitarism
Question 360Question →

A 55-year-old man presents to the emergency department with a 4-day history of profuse watery diarrhea. He reports orthostatic dizziness, generalized weakness, and a significantly reduced urine output over the past 24 hours. He has no significant past medical history and takes no medications. Vital signs show a temperature of 37.1∘C37.1^\circ\text{C} (98.8∘F98.8^\circ\text{F}), blood pressure of 88/55 mm Hg88/55\text{ mm Hg}, and a heart rate of 122/min122/\text{min}. Physical examination reveals dry mucous membranes, decreased skin turgor, and flat jugular veins.

Laboratory studies are as follows:

Serum
Sodium: 140 mEq/L140\text{ mEq/L}
Potassium: 3.2 mEq/L3.2\text{ mEq/L}
Chloride: 110 mEq/L110\text{ mEq/L}
Bicarbonate: 18 mEq/L18\text{ mEq/L}
Blood urea nitrogen (BUN): 60 mg/dL60\text{ mg/dL}
Creatinine: 2.5 mg/dL2.5\text{ mg/dL}

Urine
Sodium: 14 mEq/L14\text{ mEq/L}
Creatinine: 50 mg/dL50\text{ mg/dL}

What is this patient's fractional excretion of sodium (FeNaFe_{Na}) in percentage?

Show answer & explanation

Answer: 0.5

Answer

0.5
The fractional excretion of sodium (FeNaFe_{Na}) measures the percentage of filtered sodium that is eventually excreted in the urine. It is widely used to distinguish between prerenal acute kidney injury (AKI) and acute tubular necrosis (ATN). It is calculated using the formula: FeNa=UNa×PCrPNa×UCr×100Fe_{Na} = \frac{U_{Na} \times P_{Cr}}{P_{Na} \times U_{Cr}} \times 100. Plugging in the patient's laboratory values yields 14×2.5140×50×100=0.5%\frac{14 \times 2.5}{140 \times 50} \times 100 = 0.5\%. In the setting of oliguria, an FeNa<1%Fe_{Na} < 1\% typically indicates prerenal azotemia, representing an intact renal tubular mechanism trying to conserve sodium and water in response to hypovolemia (consistent with this patient's severe dehydration from diarrhea).

Step-by-Step Solution

1
Identify the values required for the FeNa calculation.
UNa=14U_{Na} = 14, PCr=2.5P_{Cr} = 2.5, PNa=140P_{Na} = 140, UCr=50U_{Cr} = 50
These specific variables are needed to use the FeNaFe_{Na} equation, which helps differentiate prerenal azotemia from intrinsic renal disease.
2
Apply the FeNa formula.
FeNa=14×2.5140×50×100Fe_{Na} = \frac{14 \times 2.5}{140 \times 50} \times 100
The standard formula requires multiplying the ratio of urine-to-plasma sodium by the ratio of plasma-to-urine creatinine.
3
Calculate the final percentage.
0.5%0.5\%
This calculation yields the final percentage, which is less than 1%1\% and highly indicative of a prerenal etiology.

Key Concept

Fractional Excretion of Sodium (FeNa) Calculation
PreviousPage 18 / 158Next
Internal Medicine Practice Questions — USMLE Step 2 CK — Page 18 | Examkin