Internal Medicine

3151 questions

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

A 28-year-old woman with a 3-year history of systemic lupus erythematosus (SLE) presents to the nephrology clinic with a 2-week history of worsening bilateral lower extremity edema, frothy urine, and new-onset headaches. Her home medications include hydroxychloroquine and naproxen. Her blood pressure is 162/98 mmHg. Physical examination reveals 2+ pitting edema up to the mid-calves and a faint erythematous malar rash. Recent laboratory studies show newly depressed C3 and C4 complement levels and a markedly elevated anti-dsDNA titer. Assuming the patient's clinical condition progresses as expected for a severe renal flare, arrange the following diagnostic and therapeutic steps in the correct chronological sequence for standard management.

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Answer

The correct sequence is: Obtain urinalysis/UPCR -> Perform renal biopsy -> Initiate induction therapy -> Transition to maintenance therapy.

The correct chronological management of suspected lupus nephritis begins with non-invasive biochemical confirmation via urinalysis and quantitative protein measurement. Because the histopathologic class of lupus nephritis dictates the necessity and intensity of immunosuppression, a renal biopsy is the mandatory next step prior to initiating aggressive systemic therapy. Once the class is established (e.g., diffuse proliferative lupus nephritis, Class IV), potent induction therapy is initiated to rapidly decrease inflammation. After remission is achieved—typically after 3 to 6 months—the patient is transitioned to a safer maintenance regimen to prevent relapses while avoiding the severe toxicities associated with prolonged induction therapy.

Step-by-Step Solution

Assess for biochemical evidence of renal involvement using urinalysis and a spot urine protein-to-creatinine ratio.

Confirms the presence of nephrotic or nephritic syndrome.

Establishes non-invasive proof of lupus nephritis before exposing the patient to the risks of an invasive procedure.

Perform a percutaneous renal biopsy.

Classifies the severity and chronicity of the renal lesions (Class I through VI).

Treatment regimens vary drastically based on histologic class; empiric induction is generally avoided without tissue diagnosis due to medication toxicity.

Start induction immunosuppression (e.g., high-dose glucocorticoids plus mycophenolate mofetil or cyclophosphamide).

Suppresses acute autoimmune activity and induces clinical remission.

Halts acute inflammatory damage to nephrons in severe proliferative lupus nephritis.

Switch to maintenance immunosuppression.

Maintains disease remission with a reduced side-effect profile.

Long-term use of high-dose corticosteroids and full-dose induction agents carries unacceptable risks of infection, malignancy, and metabolic derangements.

Key Concept

The standard management of lupus nephritis requires non-invasive biochemical screening, followed by histologic classification via biopsy, leading to intensive induction therapy and eventual transition to maintenance therapy.

Question 722Question →

An emergency medicine physician evaluates a $67$ -year-old man presenting with a $3$ -day history of progressively worsening shortness of breath and a change in his chronic cough, now producing yellow sputum.

His past medical history is notable for hypertension, diet-controlled type 2 diabetes mellitus, and a $50$ -pack-year smoking history. He has not had any recent hospitalizations.

Physical examination reveals a patient in moderate respiratory distress with a prolonged expiratory phase and diffuse expiratory wheezing. Jugular venous pressure is estimated at $6\text{ cm H}_2\text{O}$ (normal: $\le 8\text{ cm H}_2\text{O}$ ). Heart sounds are distant but regular, with no murmurs, rubs, or gallops. There is trace bilateral pedal edema.

A chest radiograph demonstrates hyperlucent lung fields, flattened hemidiaphragms, and an increased retrosternal airspace, without focal consolidations or vascular congestion.

The following laboratory and vital sign data are obtained on presentation:

Vital Signs & Laboratory Parameter	Value	Reference Range
Temperature	$37.9^\circ\text{C}$ ( $100.2^\circ\text{F}$ )	$36.5-37.3^\circ\text{C}$
Heart rate	$108/\text{min}$	$60-100/\text{min}$
Respiratory rate	$26/\text{min}$	$12-20/\text{min}$
Blood pressure	$142/86\text{ mmHg}$	$< 120/80\text{ mmHg}$
Oxygen saturation	$89\%$ (on $2\text{ L/min O}_2$ )	$\ge 95\%$
Leukocyte count	$11,500/\text{mm}^3$	$4,500-11,000/\text{mm}^3$
Brain natriuretic peptide (BNP)	$85\text{ pg/mL}$	$< 100\text{ pg/mL}$
Arterial pH	$7.29$	$7.35-7.45$
Arterial PaCO $_2$	$62\text{ mmHg}$	$35-45\text{ mmHg}$
Arterial PaO $_2$	$64\text{ mmHg}$	$75-105\text{ mmHg}$
Arterial HCO $_3^-$	$29\text{ mEq/L}$	$22-28\text{ mEq/L}$

Which of the following interventions are appropriate for the immediate management of this patient? (Select all that apply)

Select all that apply

Initiation of bilevel positive airway pressure therapy

Administration of systemic methylprednisolone

Intravenous administration of furosemide

Empiric administration of intravenous piperacillin-tazobactam and vancomycin

Administration of continuous intravenous sodium bicarbonate

Show answer & explanation

Answer: Initiation of bilevel positive airway pressure therapy; Administration of systemic methylprednisolone

Answer

The appropriate immediate management steps for this patient are the initiation of bilevel positive airway pressure therapy and the administration of systemic methylprednisolone.

The correct interventions focus on relieving severe bronchospasm, reducing airway inflammation, and reversing acute hypercapnic respiratory failure. Systemic glucocorticoids reduce inflammation and are a standard of care for all severe AECOPD presentations. Bilevel positive airway pressure (BiPAP) is specifically indicated because the patient has developed acute-on-chronic respiratory acidosis (pH

\le 7.35

and PaCO

_2

\ge 45\text{ mmHg}

) secondary to alveolar hypoventilation. BiPAP decreases the work of breathing, improves gas exchange, and significantly reduces mortality and the need for invasive mechanical ventilation in this population.

Step-by-Step Solution

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

The patient is experiencing an Acute Exacerbation of Chronic Obstructive Pulmonary Disease (AECOPD) likely triggered by an acute respiratory infection.

The patient has a

50

-pack-year smoking history, prolonged expiratory phase, diffuse wheezing, hyperinflated lungs on chest radiograph, and an acute worsening of dyspnea accompanied by increased purulent sputum production.

Interpret the arterial blood gas (ABG) and related diagnostic data.

The ABG reveals an acute-on-chronic respiratory acidosis (pH

7.29

, PaCO

_2

62\text{ mmHg}

, HCO

_3^-

29\text{ mEq/L}

). Furthermore, there is no evidence of concurrent decompensated heart failure (BNP is normal, and chest x-ray lacks vascular congestion).

Determining the severity of the acid-base derangement directly guides the required level of respiratory support.

Select evidence-based therapeutic interventions for hypercapnic AECOPD.

Non-invasive positive pressure ventilation (BiPAP), systemic glucocorticoids, inhaled bronchodilators, and targeted antibiotics are indicated.

BiPAP reverses hypercapnic respiratory failure and prevents intubation; systemic steroids significantly reduce airway inflammation and improve recovery time.

Key Concept

Management of severe acute exacerbations of chronic obstructive pulmonary disease (AECOPD) complicated by hypercapnic respiratory acidosis.

Question 723Question →

A $62$ -year-old man is evaluated in the hospital on hospital day $3$ . He originally presented with a $2$ -day history of fever, right flank pain, and dysuria. Medical history is significant for nephrolithiasis, for which he underwent a cystoscopy with stent placement $1$ week ago.

On admission, temperature was $38.9^\circ\text{C}$ ( $102.0^\circ\text{F}$ ), blood pressure was $104/62\text{ mmHg}$ , and pulse was $112/\text{min}$ . Laboratory studies showed a leukocyte count of $16,500/\mu\text{L}$ . He was empirically started on intravenous piperacillin-tazobactam.

Today (hospital day $3$ ), his temperature is $37.4^\circ\text{C}$ ( $99.3^\circ\text{F}$ ), blood pressure is $122/78\text{ mmHg}$ , and pulse is $84/\text{min}$ . Blood and urine cultures obtained on admission both grow *Enterobacter cloacae*. Antimicrobial susceptibility testing reveals the following:

* Ampicillin: Resistant
* Cefazolin: Resistant
* Ceftriaxone: Susceptible
* Cefepime: Susceptible
* Piperacillin-tazobactam: Susceptible
* Meropenem: Susceptible

Based on these results, which of the following is the most appropriate next step in the patient's antimicrobial management?

Transition to intravenous ceftriaxone

Transition to intravenous cefepime

Transition to intravenous meropenem

Continue intravenous piperacillin-tazobactam

Add intravenous gentamicin to the current regimen

Show answer & explanation

Answer: Transition to intravenous cefepime

Answer

The correct answer is to transition the patient to intravenous cefepime.

The correct next step is to transition the patient to intravenous cefepime. *Enterobacter cloacae* is an organism that intrinsically carries an inducible chromosomal *AmpC* beta-lactamase gene. In the setting of a high initial bacterial burden or invasive infection (such as bacteremia), treating this organism with a third-generation cephalosporin (e.g., ceftriaxone) can rapidly select for derepressed mutants that hyperproduce the AmpC enzyme, leading to subsequent clinical failure despite initial in vitro susceptibility. Cefepime, a fourth-generation cephalosporin, is highly stable against AmpC hydrolysis and is a weak inducer of the enzyme. According to current infectious disease guidelines, cefepime is the preferred definitive therapy for susceptible, high-risk AmpC producers. This choice maximizes clinical efficacy while adhering to antibiotic stewardship principles by sparing carbapenems.

Step-by-Step Solution

Analyze the clinical scenario and the microbiological data.

The patient has a urinary-source bacteremia caused by *Enterobacter cloacae*. He is clinically improving on empiric therapy, but definitive targeted therapy is now required based on culture susceptibilities.

Establishing the severity (invasive bacteremia) and the specific pathogen dictates the rules of antibiotic stewardship.

Identify the specific resistance mechanisms characteristic of the isolated organism.

*Enterobacter cloacae* is a classic high-risk producer of inducible chromosomal AmpC beta-lactamase.

Organisms with AmpC (like Enterobacter, Klebsiella aerogenes, and Citrobacter freundii) can rapidly develop resistance on therapy even if they initially test susceptible to certain antibiotics.

Evaluate the treatment options for an AmpC-producing organism.

Third-generation cephalosporins (ceftriaxone) and piperacillin-tazobactam are associated with clinical failure in invasive AmpC infections despite in vitro susceptibility. Cefepime and carbapenems (meropenem) remain clinically active.

Selecting an antibiotic that will not be hydrolyzed by the AmpC enzyme is critical for patient survival.

Apply antimicrobial stewardship principles to select the definitive agent.

Cefepime should be selected over meropenem since the isolate is susceptible to cefepime.

Carbapenems should be spared whenever possible to prevent the emergence of carbapenem-resistant Enterobacteriaceae (CRE). Cefepime provides the optimal balance of targeted efficacy and stewardship.

Key Concept

Definitive treatment of invasive infections caused by high-risk AmpC-producing Enterobacterales (e.g., *Enterobacter cloacae*) requires cefepime (when susceptible) to avoid clinical failure and spare carbapenem use.

Question 724Question →

A 68-year-old man is evaluated in the hospital on the third day of his admission for community-acquired pneumonia. He originally presented with a 3-day history of fever, productive cough, and shortness of breath. Chest radiography on admission showed a left lower lobe consolidation. He was empirically started on intravenous ceftriaxone and azithromycin. Today, he reports feeling much better and his cough has improved. He has been afebrile for the past 24 hours. His temperature is 37.1°C (98.8°F), blood pressure is 126/82 mm Hg, heart rate is 78/min, and respirations are 16/min. Pulse oximetry is 96% on ambient air. The patient is tolerating a regular diet. Blood cultures obtained on admission are sterile. Sputum culture has grown heavy *Streptococcus pneumoniae*. Susceptibility testing reveals the isolate is sensitive to penicillin, amoxicillin, ceftriaxone, levofloxacin, and vancomycin. Which of the following is the most appropriate next step in management?

Switch to oral amoxicillin

Switch to oral amoxicillin-clavulanate

Switch to oral levofloxacin

Continue intravenous ceftriaxone and discontinue azithromycin

Continue intravenous ceftriaxone and intravenous azithromycin

Show answer & explanation

Answer: Switch to oral amoxicillin

Answer

Switch to oral amoxicillin

The correct answer is to switch to oral amoxicillin. This patient was admitted with community-acquired pneumonia and appropriately started on an empiric regimen of intravenous ceftriaxone and azithromycin. By hospital day 3, he has met the criteria for clinical stability (afebrile, normal hemodynamics, tolerating oral intake) and is a candidate for transition to oral therapy. Sputum cultures have identified Streptococcus pneumoniae, a typical bacterial pathogen, rendering continued atypical coverage with azithromycin unnecessary. Furthermore, the isolate is sensitive to penicillin. According to the principles of antimicrobial stewardship, antibiotic therapy should be de-escalated to the narrowest effective agent. Oral amoxicillin is the targeted, narrow-spectrum drug of choice for penicillin-susceptible S. pneumoniae.

Step-by-Step Solution

Assess the patient's clinical stability for an intravenous-to-oral transition.

The patient is afebrile for 24 hours, hemodynamically stable, has a normal respiratory rate and oxygen saturation, and is tolerating a regular diet.

Patients hospitalized with community-acquired pneumonia should be transitioned to oral antibiotics as soon as they achieve clinical stability and can safely absorb oral medications, in order to facilitate early discharge and reduce catheter-related complications.

Evaluate the definitive microbiology and susceptibility results.

Sputum culture confirms an infection by Streptococcus pneumoniae that is fully sensitive to penicillin and amoxicillin.

Empiric broad-spectrum therapy must be de-escalated to a targeted regimen once the causative pathogen and its susceptibility profile are identified.

Select the most appropriate targeted oral antibiotic based on stewardship principles.

Oral amoxicillin is the optimal choice.

Amoxicillin provides excellent, narrow-spectrum coverage for penicillin-susceptible S. pneumoniae. Broad-spectrum agents or beta-lactamase inhibitors are unnecessary and inappropriate.

Key Concept

Patients hospitalized for community-acquired pneumonia should be transitioned from empirical intravenous therapy to targeted, narrow-spectrum oral antibiotics once they demonstrate clinical stability and a susceptible pathogen is identified.

Question 725Question →

A 45-year-old woman is newly diagnosed with moderate-to-severe, seropositive rheumatoid arthritis. She has no significant past medical history, normal hepatic and renal function, and no contraindications to standard pharmacotherapies. Assuming she requires continuous escalation of therapy due to inadequate responses at each step and ultimately develops severe, end-stage structural damage in her right knee over many years, arrange the following management steps in the correct chronological sequence.

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Answer

The correct sequence of management is: 1) Initiate conventional synthetic DMARD monotherapy with methotrexate, 2) Add a tumor necrosis factor (TNF) alpha inhibitor, 3) Switch to a biologic DMARD with a different mechanism of action, 4) Refer for surgical total joint arthroplasty.

The standard stepwise approach to rheumatoid arthritis begins with conventional synthetic DMARDs (methotrexate), escalates to a biologic DMARD (often a TNF inhibitor) upon inadequate response, switches to a non-TNF biologic upon subsequent failure, and ultimately relies on surgical joint replacement for irreversible, end-stage structural damage.

Step-by-Step Solution

Identify the appropriate first-line therapy for newly diagnosed, moderate-to-severe rheumatoid arthritis.

Methotrexate monotherapy is selected.

Methotrexate is the foundational initial disease-modifying agent due to its well-established long-term efficacy, safety profile, and cost-effectiveness.

Determine the next pharmacological step after an inadequate response to initial monotherapy.

Addition of a biologic DMARD (e.g., TNF inhibitor).

Guidelines recommend stepping up therapy by adding a biologic DMARD when disease activity remains unacceptably high despite maximally tolerated methotrexate.

Determine the management approach for a patient who fails initial biologic therapy.

Switch to a biologic with a different mechanism of action.

Cycling to a different class of biologic (non-TNF) is generally more effective than trying a second TNF inhibitor in cases of primary primary treatment failure.

Address end-stage, irreversible joint destruction.

Referral for total joint arthroplasty.

When pharmacological therapy cannot reverse existing structural damage and the patient suffers from intractable mechanical pain and dysfunction, surgical replacement is indicated.

Key Concept

Stepwise escalation of pharmacotherapy and surgical management in rheumatoid arthritis.

Estimated Time:1m 0s

Question 726Question →

Match each clinical presentation with its most likely underlying pathophysiological mechanism.

Click a left item, then click its matching right item

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Answer

Each clinical presentation is matched to its corresponding pathognomonic mechanism.

Each clinical vignette provides pathognomonic clues for a specific hematologic disorder. TTP is caused by ADAMTS13 deficiency; Primary Myelofibrosis involves marrow fibrosis from abnormal megakaryocytes; CLL is a CD5+ B cell neoplasm; G6PD deficiency involves defective generation of reduced glutathione; and Antiphospholipid Syndrome is driven by autoantibodies against phospholipid-binding proteins.

Step-by-Step Solution

Analyze the first presentation (fever, confusion, schistocytes, normal PT/PTT)

Diagnose Thrombotic Thrombocytopenic Purpura (TTP)

The combination of microangiopathic hemolytic anemia and thrombocytopenia with normal coagulation parameters points to ADAMTS13 deficiency.

Analyze the second presentation (splenomegaly, teardrop cells)

Diagnose Primary Myelofibrosis

Teardrop cells form as red blood cells squeeze through a fibrotic marrow space.

Analyze the third presentation (elderly patient, lymphadenopathy, smudge cells)

Diagnose Chronic Lymphocytic Leukemia (CLL)

Smudge cells are fragile neoplastic B cells that rupture easily during blood smear preparation.

Analyze the fourth presentation (hemolysis after sulfa drug exposure, bite cells)

Diagnose Glucose-6-Phosphate Dehydrogenase (G6PD) deficiency

Oxidative damage precipitates hemoglobin (Heinz bodies), which splenic macrophages 'bite' out, leading to hemolysis.

Analyze the fifth presentation (thrombosis, miscarriages, prolonged PTT)

Diagnose Antiphospholipid Syndrome

Lupus anticoagulant falsely prolongs PTT in vitro, but causes hypercoagulability and thrombosis in vivo.

Key Concept

Pathophysiological mechanisms of classic hematologic and oncologic disorders based on their peripheral smear and clinical presentations.

Question 727Question →

A physician evaluates a $32$ -year-old woman who presents with progressive fatigue, feeling persistently cold, and an unintentional $5\text{-kg}$ ( $11\text{-lb}$ ) weight gain over the past $8$ months. She states that she has not menstruated since the birth of her daughter $4$ years ago. Delivery was complicated by a massive hemorrhage that necessitated immediate blood transfusions, and she subsequently could not produce breast milk. Vital signs show a blood pressure of $96/60\text{ mm Hg}$ and a pulse of $58\text{/min}$ . Examination reveals pale, dry skin and a noticeable delay in the relaxation phase of her deep tendon reflexes. Initial laboratory tests display the following results:

Serum thyroid-stimulating hormone (TSH): $1.4\text{ \mu U/mL}$ (Normal: $0.5-5.0\text{ \mu U/mL}$ )
Serum free thyroxine (T4): $0.5\text{ ng/dL}$ (Normal: $0.9-1.7\text{ ng/dL}$ )

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

Measurement of morning serum cortisol

Initiation of levothyroxine therapy

Measurement of anti-thyroid peroxidase antibodies

Measurement of serum reverse triiodothyronine

Reassurance and repeat laboratory testing in

6

weeks

Show answer & explanation

Answer: Measurement of morning serum cortisol

Answer

The most appropriate next step is the measurement of morning serum cortisol to evaluate for concomitant adrenal insufficiency.

The correct answer is measurement of morning serum cortisol. This patient presents with central hypothyroidism (low free T4, normal TSH) and features of panhypopituitarism (amenorrhea, agalactia) following a severe postpartum hemorrhage. This constellation is classic for Sheehan syndrome (ischemic necrosis of the pituitary). Because the pituitary is damaged, she is at high risk for multiple hormone deficiencies, including adrenocorticotropic hormone (ACTH), which leads to secondary adrenal insufficiency. It is a critical safety principle in endocrinology that the adrenal axis must be assessed before initiating thyroid hormone replacement. Levothyroxine increases the basal metabolic rate and accelerates the hepatic clearance of cortisol. If levothyroxine is given to a patient with untreated adrenal insufficiency, the sudden increase in cortisol demand can precipitate a fatal acute adrenal crisis.

Step-by-Step Solution

Interpret the thyroid function tests.

The patient has a low free T4 with an inappropriately normal TSH.

This biochemical pattern confirms central (secondary) hypothyroidism rather than a primary thyroid gland failure.

Synthesize the laboratory findings with the clinical history.

The combination of central hypothyroidism, secondary amenorrhea, and failure to lactate following a postpartum hemorrhage indicates panhypopituitarism due to Sheehan syndrome.

Ischemic necrosis of the pituitary gland during delivery leads to multiple anterior pituitary hormone deficiencies, including TSH and ACTH.

Determine the safest management strategy.

Before treating the hypothyroidism, the adrenal axis must be evaluated by measuring morning serum cortisol.

Administering thyroid hormone increases cortisol metabolism. In a patient with undiagnosed ACTH deficiency, this will precipitate an acute, life-threatening adrenal crisis.

Key Concept

In patients with central hypothyroidism and suspected panhypopituitarism, concomitant adrenal insufficiency must be ruled out (or treated) before initiating levothyroxine therapy to avoid precipitating an acute adrenal crisis.

Question 728Question →

A 52-year-old man is evaluated in the hospital for fever. He was admitted 12 days ago for induction chemotherapy to treat acute myeloid leukemia. Two days ago, he developed a fever of $38.8^{\circ}\text{C}$ ( $101.8^{\circ}\text{F}$ ). At that time, his blood pressure was $108/68\text{ mm Hg}$ and pulse was $112/\text{min}$ . Laboratory studies showed an absolute neutrophil count (ANC) of $80/\mu\text{L}$ . Empiric intravenous cefepime and vancomycin were initiated after blood and urine cultures were obtained. Today, the patient reports feeling much better. He has been afebrile for the past 24 hours. His blood pressure is $122/78\text{ mm Hg}$ and pulse is $84/\text{min}$ . The central venous catheter site appears clean with no erythema or induration. Today's laboratory results show an ANC of $110/\mu\text{L}$ . Blood cultures drawn two days ago are positive for *Escherichia coli*. Susceptibility testing indicates the organism is susceptible to ceftriaxone, cefepime, piperacillin-tazobactam, and ciprofloxacin, and resistant to ampicillin. Which of the following is the most appropriate next step in the management of this patient's antibiotic therapy?

Discontinue vancomycin and continue cefepime

Discontinue vancomycin and cefepime, and begin ceftriaxone

Continue vancomycin and cefepime

Discontinue vancomycin and cefepime, and begin oral ciprofloxacin

Discontinue cefepime and continue vancomycin

Show answer & explanation

Answer: Discontinue vancomycin and continue cefepime

Answer

Discontinue vancomycin and continue cefepime

The correct action is to discontinue vancomycin and continue cefepime. The patient originally required empiric therapy for febrile neutropenia, which correctly included an anti-pseudomonal beta-lactam (cefepime). Vancomycin was likely added for possible catheter-related infection or initial instability. At 48 hours, blood cultures show only *E. coli*. According to standard guidelines for high-risk febrile neutropenia, empiric vancomycin should be discontinued if no Gram-positive pathogen is identified. However, despite the *E. coli* being susceptible to narrower agents like ceftriaxone, patients who remain profoundly neutropenic (ANC <

500/\mu\text{L}

) must be maintained on an anti-pseudomonal agent (like cefepime, meropenem, or piperacillin-tazobactam) to protect against secondary *Pseudomonas aeruginosa* infections until marrow recovery.

Step-by-Step Solution

Identify the primary clinical scenario and patient risk stratification.

The patient has high-risk febrile neutropenia (ANC <

500/\mu\text{L}

, hematologic malignancy undergoing induction) complicated by Gram-negative bacteremia.

Risk stratification determines the necessary breadth and duration of antimicrobial coverage.

Evaluate the need for continued Gram-positive (MRSA) coverage.

Vancomycin should be discontinued.

Empiric vancomycin is indicated initially for line-associated infections or hemodynamic instability, but must be stopped at 48 hours if no Gram-positive organisms are isolated to prevent resistance and toxicity.

Analyze the appropriate Gram-negative coverage given the culture results.

Although the isolated *E. coli* is susceptible to narrower agents like ceftriaxone, an anti-pseudomonal beta-lactam (cefepime) must be continued.

In high-risk febrile neutropenia, patients remain highly susceptible to fatal secondary infections, including *Pseudomonas aeruginosa*, until their ANC recovers to >

500/\mu\text{L}

. Standard targeted therapy is insufficient; empiric anti-pseudomonal coverage must be maintained simultaneously.

Key Concept

In high-risk febrile neutropenia with a documented non-pseudomonal Gram-negative infection, empiric anti-pseudomonal coverage must be maintained alongside targeted therapy until neutrophil recovery (ANC > 500/μL).

Question 729Question →

A $72$ -year-old woman is brought to the emergency department via ambulance due to a two-day history of worsening shortness of breath and orthopnea. She reports waking up gasping for air last night. She has a medical history of chronic obstructive pulmonary disease (COPD), diet-controlled type 2 diabetes mellitus, and a known pituitary microadenoma. Her home medications include a long-acting muscarinic antagonist and levothyroxine.

On triage, her temperature is $37.0^\circ\text{C}$ ( $98.6^\circ\text{F}$ ), blood pressure is $162/92$ mm Hg, pulse is $115$ /min, and respiratory rate is $28$ /min. Pulse oximetry shows an oxygen saturation of $85\%$ on room air. Physical examination reveals prominent jugular venous distention. Lung auscultation demonstrates diffuse fine crackles bilaterally with scattered expiratory wheezes. Cardiac examination reveals a regular tachycardia with a distinct $S_3$ gallop. The lower extremities have $2+$ pitting edema to the knees.

Laboratory results are as follows:

Test	Result
Sodium	$139$ mEq/L
Potassium	$4.2$ mEq/L
Chloride	$96$ mEq/L
Bicarbonate	$34$ mEq/L
Blood urea nitrogen	$32$ mg/dL
Creatinine	$1.4$ mg/dL
Thyroid-stimulating hormone (TSH)	$0.15$ $\mu$ U/mL (Normal: $0.5$ - $5.0$ $\mu$ U/mL)
Free thyroxine (T4)	$0.6$ ng/dL (Normal: $0.9$ - $1.7$ ng/dL)

Arterial blood gas on room air:

Test	Result
pH	$7.24$
PaCO2	$74$ mm Hg
PaO2	$52$ mm Hg

A portable chest radiograph displays an enlarged cardiac silhouette, prominent perihilar opacities, and bilateral blunting of the costophrenic angles. There is no lobar consolidation. The patient is placed on noninvasive positive pressure ventilation.

Which of the following is the most appropriate pharmacological intervention for this patient's acute presentation?

Intravenous loop diuretic administration

Administration of systemic methylprednisolone

Broad-spectrum coverage with vancomycin and cefepime

Intravenous infusion of sodium bicarbonate

Upward titration of current levothyroxine dosage

Show answer & explanation

Answer: Intravenous loop diuretic administration

Answer

Intravenous loop diuretic administration

The patient's clinical presentation is classic for acute decompensated heart failure (ADHF), characterized by volume overload (jugular venous distention, peripheral edema) and pulmonary edema (orthopnea, paroxysmal nocturnal dyspnea, crackles, and an S3 gallop). The chest radiograph confirms cardiomegaly and perihilar opacities. The expiratory wheezes represent 'cardiac asthma' due to peribronchial edema rather than a primary obstructive airway exacerbation. For patients presenting with ADHF and pulmonary edema, rapid preload reduction is essential. The most appropriate initial pharmacological therapy, in conjunction with noninvasive positive pressure ventilation, is an intravenous loop diuretic. This effectively promotes diuresis, decreases intravascular volume, and relieves pulmonary congestion.

Step-by-Step Solution

Synthesize the clinical and radiographic findings to identify the primary cause of acute respiratory failure.

The presence of orthopnea, an S3 gallop, jugular venous distention, and perihilar opacities confirms acute decompensated heart failure (ADHF) with pulmonary edema, despite the history of COPD and the presence of wheezing (cardiac asthma).

Accurate differentiation between ADHF and a COPD exacerbation dictates the immediate life-saving treatment pathway.

Interpret the arterial blood gas values in the context of the patient's underlying conditions.

The low pH, significantly elevated PaCO2, and elevated baseline bicarbonate indicate an acute-on-chronic respiratory acidosis secondary to pulmonary edema superimposed on chronic COPD.

Correct acid-base interpretation prevents the inappropriate administration of buffering agents like sodium bicarbonate, which can worsen respiratory acidosis.

Analyze the thyroid panel to determine its relevance to the acute presentation.

The low free T4 and low-normal TSH suggest central hypothyroidism related to the patient's pituitary microadenoma.

Recognizing this pattern prevents the misdiagnosis of primary hypothyroidism and avoids inappropriate dose adjustments during an acute cardiopulmonary crisis.

Select the most appropriate acute pharmacological management.

Administration of an intravenous loop diuretic is the correct next step to provide rapid diuresis and preload reduction.

Preload reduction is the cornerstone of therapy to relieve pulmonary congestion in patients presenting with ADHF.

Key Concept

Management of acute decompensated heart failure presenting with mixed cardiopulmonary symptoms.

Question 730Question →

A $31$ -year-old woman, gravida $2$ , para $0-1-0-0$ , at $11$ weeks gestation comes to the clinic for an initial prenatal visit. Her first pregnancy ended in a fetal demise at $22$ weeks gestation. She has a history of a left lower extremity deep venous thrombosis $3$ years ago following a transatlantic flight, for which she completed a $6$ -month course of warfarin. Today, she feels well. Blood pressure is $110/70$ mm Hg, and pulse is $84$ /min. Physical examination is unremarkable. Laboratory results are as follows:

Laboratory Test	Result	Reference Range
Hemoglobin	$11.2$ g/dL	$12.0-16.0$ g/dL (non-pregnant)
Platelet count	$125,000$ /mm $^3$	$150,000-400,000$ /mm $^3$
Serum bicarbonate	$20$ mEq/L	$22-28$ mEq/L
Arterial PCO $_2$	$30$ mm Hg	$35-45$ mm Hg
TSH	$0.2$ $\mu$ U/mL	$0.1-2.5$ $\mu$ U/mL (1st trimester)
Free T4	$1.3$ ng/dL	$0.8-2.0$ ng/dL
aPTT	$52$ seconds	$25-35$ seconds

Additional testing shows a positive rapid plasma reagin (RPR) but a negative fluorescent treponemal antibody absorption (FTA-ABS) test. Urinalysis shows trace protein. Which of the following is the most appropriate next step in management?

Subcutaneous low-molecular-weight heparin and oral low-dose aspirin

Intravenous ceftriaxone and oral azithromycin

Observation and routine prenatal care

Initiation of oral propylthiouracil

Administration of intravenous sodium bicarbonate

Show answer & explanation

Answer: Subcutaneous low-molecular-weight heparin and oral low-dose aspirin

Answer

Subcutaneous low-molecular-weight heparin and oral low-dose aspirin

This patient's clinical history (second-trimester fetal demise and unprovoked deep venous thrombosis) combined with her laboratory findings (prolonged aPTT and biologic false-positive RPR) is highly characteristic of Antiphospholipid Syndrome (APS). The false-positive RPR is caused by anticardiolipin antibodies, while the prolonged aPTT is an in vitro artifact caused by the lupus anticoagulant. Despite the in vitro prolongation, APS causes a severe hypercoagulable state in vivo. For pregnant patients with APS who have a history of prior thromboembolism, the standard of care is therapeutic-dose low-molecular-weight heparin (LMWH) and low-dose aspirin to prevent recurrent venous thromboembolism and severe obstetric complications (e.g., recurrent fetal demise, severe preeclampsia).

Step-by-Step Solution

Analyze the hematologic and infectious disease laboratory findings.

The patient has a prolonged aPTT and a false-positive RPR (positive RPR with negative FTA-ABS).

These findings are classic laboratory artifacts caused by circulating lupus anticoagulant (prolongs aPTT in vitro) and anticardiolipin antibodies (cross-reacts with RPR antigen).

Synthesize the laboratory findings with the patient's obstetric and medical history.

The combination of a prior DVT, a second-trimester fetal demise, and antiphospholipid antibodies confirms the diagnosis of Antiphospholipid Syndrome (APS).

APS diagnosis requires at least one clinical criterion (vascular thrombosis or specific pregnancy morbidity) and one laboratory criterion (lupus anticoagulant, anticardiolipin, or anti-beta-2-glycoprotein I antibodies).

Differentiate pathologic findings from the normal physiologic changes of pregnancy.

The mild anemia, low PCO2, low bicarbonate, and low TSH are all normal physiologic adaptations to pregnancy and do not require targeted therapy.

Progesterone causes central hyperventilation (respiratory alkalosis), hCG mildly suppresses TSH, and plasma volume expansion causes dilutional anemia.

Determine the appropriate management for a pregnant patient with APS and a history of thrombosis.

The patient requires therapeutic-dose low-molecular-weight heparin (LMWH) and low-dose aspirin.

Despite the prolonged aPTT in vitro, APS is a highly thrombophilic state in vivo. Anticoagulation is required to prevent recurrent maternal DVT and placental thrombosis leading to fetal demise.

Key Concept

Antiphospholipid Syndrome (APS) in pregnancy presents with a history of recurrent miscarriages or thrombosis, prolonged aPTT, and false-positive syphilis testing; it requires treatment with LMWH and low-dose aspirin.

Question 731Question →

Evaluate the following patient presentations, all of whom are found to have a non-anion gap metabolic acidosis. Match each patient's clinical and laboratory profile with the primary underlying pathophysiologic mechanism responsible for their condition.

Click a left item, then click its matching right item

Show answer & explanation

Answer

The correct pairings align the patient with nephrolithiasis and high urine pH to Type 1 RTA; the patient with myeloma and glycosuria to Type 2 RTA; the diabetic patient with hyperkalemia to Type 4 RTA; and the patient with a negative urine anion gap to gastrointestinal bicarbonate loss.

Each clinical vignette provides specific physiologic markers that pinpoint the source of the non-anion gap metabolic acidosis. Hyperkalemia isolates Type 4 RTA. Among the hypokalemic etiologies, an alkaline urine pH isolates Type 1 RTA. For the remaining hypokalemic and aciduric patients, a negative urine anion gap identifies extrarenal (GI) loss, while signs of Fanconi syndrome isolate Type 2 RTA.

Step-by-Step Solution

Analyze the potassium levels for each presentation of non-anion gap metabolic acidosis.

Three patients are hypokalemic, while the diabetic man is hyperkalemic.

Hyperkalemia in the setting of a non-anion gap metabolic acidosis is diagnostic of Type 4 RTA, separating it immediately from the other causes.

Evaluate the urine pH in the hypokalemic patients.

The woman with nephrolithiasis has a urine pH of 6.5, whereas the others have a urine pH < 5.5.

A persistently elevated urine pH (> 5.5) in the face of systemic acidosis indicates a failure of distal acidification, which is the mechanism of Type 1 RTA.

Assess the remaining two hypokalemic patients using additional diagnostic clues (urine anion gap and associated tubular defects).

The woman has a negative urine anion gap (indicating appropriate renal response to GI loss), while the man with myeloma has isolated glycosuria (indicating Fanconi syndrome / proximal tubule defect).

A negative urine anion gap confirms extrarenal bicarbonate loss. Generalized proximal tubule dysfunction (glycosuria, phosphaturia) confirms Type 2 RTA.

Key Concept

Differentiation of non-anion gap metabolic acidosis requires sequential evaluation of serum potassium, urine pH, and the urine anion gap to distinguish between gastrointestinal losses and the three main types of renal tubular acidosis.

Question 732Question →

A 24-year-old woman, G1P0 at 10 weeks gestation, comes to the clinic for her first prenatal visit. She feels well and has no significant past medical history. She is of Southeast Asian descent. She takes a daily prenatal vitamin. Blood pressure is 112/68 mmHg, and pulse is 78/min. Physical examination shows no abnormalities.

Laboratory studies reveal the following:

Test	Result	Normal Range
Hemoglobin	10.4 g/dL	12.0–15.5 g/dL
Mean corpuscular volume (MCV)	68 fL	80–100 fL
Red blood cell (RBC) count	5.6 million/mm $^3$	4.1–5.1 million/mm $^3$
Red cell distribution width (RDW)	12.8%	11.5%–14.5%
Serum iron	110 $\mu$ g/dL	60–170 $\mu$ g/dL
Total iron-binding capacity (TIBC)	310 $\mu$ g/dL	240–450 $\mu$ g/dL
Serum ferritin	125 ng/mL	15–200 ng/mL

Hemoglobin electrophoresis demonstrates:
- Hemoglobin A: 97.5%
- Hemoglobin A2: 2.0%
- Hemoglobin F: 0.5%

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

Evaluate the patient's partner with a complete blood count

Reassure the patient that these findings are secondary to normal pregnancy changes

Prescribe a therapeutic trial of oral ferrous sulfate

Perform molecular genetic testing of the patient's alpha-globin genes

Recommend immediate chorionic villus sampling

Show answer & explanation

Answer: Evaluate the patient's partner with a complete blood count

Answer

Evaluate the patient's partner with a complete blood count

The correct answer is to evaluate the patient's partner with a complete blood count (CBC). This patient presents with a microcytic anemia (hemoglobin 10.4 g/dL, MCV 68 fL). The initial step in evaluating microcytic anemia is an iron panel. This patient has normal iron studies (ferritin 125 ng/mL), effectively ruling out iron deficiency anemia. The combination of microcytosis, normal iron studies, elevated RBC count, and a normal red cell distribution width (RDW) is highly suggestive of thalassemia trait. Next, hemoglobin electrophoresis is performed to differentiate between alpha and beta-thalassemia trait. Beta-thalassemia trait is characterized by elevated Hemoglobin A2 (>3.5%). This patient's normal hemoglobin electrophoresis (HbA2 2.0%) rules out beta-thalassemia trait, leaving alpha-thalassemia trait as the presumed diagnosis.

Because this patient is of Southeast Asian descent, she is at high risk of carrying a 'cis' deletion of two alpha-globin genes (

--/\alpha\alpha

). If her partner also carries a two-gene deletion, the fetus is at a 25% risk of inheriting a four-gene deletion (

--/--

), leading to hemoglobin Barts and hydrops fetalis. To assess this risk, the most appropriate and cost-effective next step is to evaluate the partner's MCV with a simple CBC. If the partner's MCV is normal, the fetus is not at risk for hydrops fetalis, and further testing is unnecessary.

Step-by-Step Solution

Analyze the complete blood count and iron studies.

The patient has severe microcytic anemia (MCV 68 fL) with normal iron studies (ferritin 125 ng/mL), an elevated RBC count, and a normal RDW.

To rule out iron deficiency anemia, which is the most common cause of microcytic anemia in pregnancy, before considering hemoglobinopathies.

Interpret the hemoglobin electrophoresis.

Normal levels of HbA2 (2.0%) and HbF (0.5%).

To differentiate between beta-thalassemia trait (characterized by elevated HbA2 >3.5%) and alpha-thalassemia trait (characterized by a normal electrophoresis pattern in adults).

Determine the risk of severe fetal hemoglobinopathy.

The patient is of Southeast Asian descent and likely carries a cis-deletion (--/\alpha\alpha) alpha-thalassemia trait.

If the partner also carries a two-gene deletion, the fetus is at a 25% risk for hemoglobin Barts hydrops fetalis (--/--), which is fatal in utero.

Select the most cost-effective diagnostic next step.

Partner screening with a complete blood count (CBC).

If the partner has a normal MCV, the fetus cannot inherit a severe hemoglobinopathy, preventing the need for expensive maternal genetic testing or invasive fetal procedures.

Key Concept

In a pregnant patient with suspected alpha-thalassemia trait (microcytic anemia, normal iron studies, normal hemoglobin electrophoresis), the most appropriate next step is to screen the partner with a complete blood count to assess the risk of hemoglobin Barts hydrops fetalis.

Estimated Time:1m 30s

Question 733Question →

A 74-year-old woman is evaluated on postoperative day 3 following a left total knee arthroplasty. Her temperature is 38.1°C (100.6°F), blood pressure is 128/76 mm Hg, pulse is 82/min, and respirations are 14/min. The patient is ambulating with physical therapy and reports that her surgical pain is well controlled. An indwelling urinary catheter, placed during the surgery, was removed yesterday. She denies dysuria, urinary urgency, frequency, and flank pain. Physical examination shows a clean surgical incision without erythema, induration, or purulent drainage. The lungs are clear to auscultation. The calves are soft, non-tender, and symmetric. A urinalysis reveals 25 white blood cells/hpf and is positive for leukocyte esterase and nitrites. Which of the following is the most appropriate next step in management?

Reassurance and observation

Initiation of oral nitrofurantoin

Initiation of oral ciprofloxacin

Urine culture and initiation of intravenous ceftriaxone

Lower extremity venous duplex ultrasonography

Show answer & explanation

Answer: Reassurance and observation

Answer

Reassurance and observation is the correct management for this patient with asymptomatic bacteriuria and a normal postoperative fever.

The correct answer recommends reassurance and observation. The patient has asymptomatic bacteriuria (ASB), characterized by the presence of bacteria in the urine (suggested by positive nitrites) and pyuria (leukocyte esterase and white blood cells) without localizing signs or symptoms of a urinary tract infection, such as dysuria, frequency, urgency, or flank pain. Furthermore, her mild temperature elevation is a normal physiologic inflammatory response typical in the early postoperative period, often lasting up to 3 to 5 days. ASB is an expected finding following the removal of an indwelling urinary catheter. According to current infectious disease guidelines, ASB should not be screened for or treated with antibiotics except in specific populations, such as pregnant patients and those undergoing endoscopic urologic procedures associated with mucosal trauma. Providing antibiotic treatment for ASB in patients undergoing non-urologic surgery, including orthopedic joint replacement, does not reduce the rate of surgical site infection. Instead, it unnecessarily exposes the patient to adverse drug events, increases the risk of Clostridioides difficile infection, and drives antimicrobial resistance. Therefore, the most appropriate next step in management is observation.

Step-by-Step Solution

Evaluate the patient's clinical presentation and timeline.

The patient has a low-grade fever on postoperative day 3, without localized infectious symptoms or signs of deep vein thrombosis.

Mild fever in the early postoperative period (days 1-3) is frequently a normal physiologic inflammatory response rather than an infectious complication.

Interpret the urinalysis findings in the context of the patient's symptoms.

The patient has pyuria and bacteriuria but completely lacks urinary symptoms (no dysuria, urgency, or frequency).

The presence of bacteria and white blood cells in the urine without accompanying genitourinary symptoms confirms the diagnosis of asymptomatic bacteriuria, which is highly expected following recent catheter removal.

Determine the appropriate management for asymptomatic bacteriuria in this setting.

Antibiotic therapy is appropriately withheld, and the patient is observed.

Screening for or treating asymptomatic bacteriuria is not indicated in most patients (including post-arthroplasty) because it does not improve clinical outcomes and only increases the risk of antimicrobial resistance and adverse drug events.

Key Concept

Asymptomatic bacteriuria diagnosis and antibiotic stewardship

Estimated Time:1m 0s

Question 734Question →

A $34$ -year-old woman with a history of poorly controlled Graves disease is brought to the emergency department by her family due to profound confusion, severe agitation, and intractable vomiting. Her temperature is $39.4^\circ\text{C}$ ( $103.0^\circ\text{F}$ ), blood pressure is $160/70\text{ mm Hg}$ , pulse is $155/\text{min}$ and irregular, and respirations are $26/\text{min}$ . Physical examination reveals a diffuse, non-tender goiter, marked diaphoresis, a fine resting tremor, and bilateral proptosis. An electrocardiogram shows atrial fibrillation with rapid ventricular response. A clinical diagnosis of thyroid storm is made. Arrange the following management steps in the most appropriate chronological sequence to safely treat this patient.

Drag items to arrange them in the correct order

Show answer & explanation

Answer

The correct sequence for managing thyroid storm is to first control acute adrenergic symptoms with a beta-blocker, then block new hormone synthesis with a thionamide, subsequently block hormone release with an iodine solution (strictly after synthesis is blocked), reduce enterohepatic recycling of existing hormones, and finally plan for definitive surgical therapy once the patient is euthyroid.

Thyroid storm requires a highly specific, sequenced pharmacological approach. Initial management must focus on immediate life threats, namely cardiovascular collapse from adrenergic overdrive, which is managed with beta-blockers. Next, the production of new hormone is halted using a thionamide (propylthiouracil). Crucially, the release of already manufactured hormone is then blocked with an iodine solution. This iodine MUST be given at least one hour after the thionamide; otherwise, the iodine will serve as raw material to synthesize even more hormone. Adjunctive therapies like cholestyramine help clear circulating hormone. Definitive surgical management is exclusively reserved for the outpatient, euthyroid setting.

Step-by-Step Solution

Administer an intravenous beta-blocker (e.g., propranolol).

Decreases heart rate, blunts sympathetic hyperactivity, and prevents cardiovascular collapse.

Adrenergic overdrive is the most immediate life-threatening component of thyroid storm.

Administer a thionamide (e.g., propylthiouracil or methimazole).

Inhibits thyroid peroxidase, halting the production of new T3 and T4.

Synthesis must be stopped before the gland is exposed to high doses of exogenous iodine.

Administer an inorganic iodine solution (e.g., potassium iodide).

Inhibits the proteolytic release of preformed, stored thyroid hormone (the Wolff-Chaikoff effect).

Must be delayed until at least one hour after thionamide administration to avoid providing substrate for new hormone synthesis.

Administer a bile acid sequestrant (e.g., cholestyramine).

Binds thyroid hormones in the gastrointestinal tract.

Interrupts the enterohepatic circulation, thereby lowering circulating levels of pre-existing hormones.

Plan for definitive therapy (surgery or radioactive iodine).

Provides a permanent cure for the underlying Graves disease.

Can only be performed safely once the patient is fully stabilized and clinically euthyroid to prevent intraoperative storm.

Key Concept

In the management of thyroid storm, an iodine solution must only be administered AFTER a thionamide has been given to block thyroid hormone synthesis, preventing the Jod-Basedow phenomenon.

Question 735Question →

A $76$ -year-old woman is brought to the emergency department due to sudden-onset, severe abdominal pain that started $4$ hours ago. She has a medical history of hypertension, hyperlipidemia, type 2 diabetes mellitus, and paroxysmal atrial fibrillation. She was prescribed apixaban but admits to missing several doses over the past week. The patient also reports one episode of bilious vomiting at home. On arrival, her temperature is $38.4^\circ\text{C}$ ( $101.1^\circ\text{F}$ ), blood pressure is $88/56\text{ mm Hg}$ , and pulse is $122/\text{min}$ and irregularly irregular. Physical examination reveals a moderately distended abdomen with diffuse rigidity, involuntary guarding, and rebound tenderness. Bowel sounds are absent. Laboratory studies demonstrate a leukocyte count of $21,000/\text{mm}^3$ and a serum lactate level of $5.8\text{ mmol/L}$ (normal: $0.5-1.0\text{ mmol/L}$ ). Which of the following is the most appropriate next step in the management of this patient?

Emergency exploratory laparotomy

CT angiography of the abdomen

Nasogastric tube decompression and serial abdominal examinations

Intravenous piperacillin-tazobactam and admission to the intensive care unit

Measurement of arterial blood gases to calculate expected respiratory compensation

Show answer & explanation

Answer: Emergency exploratory laparotomy

Answer

Emergency exploratory laparotomy

The correct answer is emergency exploratory laparotomy. This patient's presentation of sudden-onset, severe abdominal pain in the setting of atrial fibrillation and missed anticoagulant doses is highly suspicious for acute mesenteric ischemia due to an arterial embolus (typically lodging in the superior mesenteric artery). While the classic early presentation involves 'pain out of proportion to physical exam findings,' this patient now demonstrates hemodynamic instability (hypotension, tachycardia) and frank peritonitis (rigid abdomen, involuntary guarding, rebound tenderness), accompanied by significantly elevated serum lactate. These clinical findings indicate that transmural bowel infarction and potential perforation have already occurred. In any patient with suspected acute mesenteric ischemia who develops peritonitis or hemodynamic instability, immediate surgical exploration (laparotomy) is required to resect necrotic bowel and restore perfusion. Delaying surgery to obtain confirmatory imaging or attempt medical management in this scenario significantly increases the risk of mortality.

Step-by-Step Solution

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

The patient has sudden-onset, severe abdominal pain with a history of paroxysmal atrial fibrillation and anticoagulant non-compliance, which is highly indicative of acute mesenteric ischemia due to an arterial embolus.

Recognizing the risk factors (atrial fibrillation) and classic symptom onset is the first step in formulating an accurate differential diagnosis.

Evaluate the patient's hemodynamic status and physical examination findings.

The patient is hemodynamically unstable (blood pressure

88/56\text{ mm Hg}

) and exhibits clear signs of peritonitis (diffuse rigidity, involuntary guarding, rebound tenderness).

Physical exam findings and vital signs are critical for determining whether the patient can safely undergo further diagnostic imaging or requires immediate surgical intervention.

Determine the most appropriate next step in management based on the presence of peritonitis and instability.

The presence of peritonitis and hemodynamic instability in suspected acute mesenteric ischemia mandates immediate emergency exploratory laparotomy.

Peritonitis indicates that transmural bowel infarction and potential perforation have already occurred. Delaying surgery for any reason significantly increases mortality.

Key Concept

Patients with suspected acute mesenteric ischemia who develop signs of peritonitis or hemodynamic instability require immediate emergency exploratory laparotomy to resect necrotic bowel.

Question 736Question →

A $46$ -year-old man presents to the clinic with an $8$ -month history of progressive fatigue, decreased libido, and generalized joint pain. He notes that the joint pain is most pronounced in the index and middle fingers of both hands. He also reports that his skin has become diffusely darker, despite working indoors year-round. He has no significant past medical history and takes no medications.

Physical examination reveals a firm liver edge palpable $3$ cm below the right costal margin. Testes are small and soft bilaterally. There is bony enlargement and tenderness over the second and third metacarpophalangeal joints of both hands.

Laboratory results are as follows:
Fasting blood glucose: $138$ mg/dL
Sodium: $139$ mEq/L
Potassium: $4.1$ mEq/L
Thyroid-stimulating hormone (TSH): $1.1$ $\mu$ U/mL (Normal: $0.5 - 5.0$ $\mu$ U/mL)
Free thyroxine (T4): $0.5$ ng/dL (Normal: $0.9 - 1.7$ ng/dL)
Total testosterone ( $8:00$ AM): $140$ ng/dL (Normal: $300 - 1000$ ng/dL)
Luteinizing hormone (LH): $1.2$ mIU/mL (Normal: $1.5 - 9.3$ mIU/mL)
Prolactin: $12$ ng/mL (Normal: $2 - 18$ ng/mL)

Which of the following is the most appropriate next step in establishing the underlying etiology of this patient's condition?

Measurement of transferrin saturation and serum ferritin

Magnetic resonance imaging of the brain

Measurement of anti-thyroid peroxidase antibodies

Cosyntropin stimulation test

Measurement of serum insulin-like growth factor 1

Show answer & explanation

Answer: Measurement of transferrin saturation and serum ferritin

Answer

Measurement of transferrin saturation and serum ferritin

The correct answer is measurement of transferrin saturation and serum ferritin. This patient's clinical presentation is classic for hereditary hemochromatosis, a systemic disorder characterized by excessive iron absorption and deposition in parenchymal organs. The 'bronze diabetes' triad includes skin hyperpigmentation and diabetes mellitus. Iron deposition in the liver causes hepatomegaly, and deposition in the synovium leads to a characteristic arthropathy of the second and third metacarpophalangeal joints. Furthermore, iron deposition in the anterior pituitary gland preferentially disrupts gonadotropin and thyrotropin secretion, leading to secondary hypogonadism (low testosterone with normal or low LH) and secondary hypothyroidism (low free T4 with inappropriately normal TSH). The most appropriate initial screening test for hemochromatosis is the measurement of serum iron studies.

Step-by-Step Solution

Interpret the patient's thyroid and gonadal laboratory results.

The patient has low free T4 and low testosterone with inappropriately normal TSH and LH levels.

To determine if the endocrine dysfunction is primary (end-organ failure) or secondary (central/pituitary failure).

Synthesize the central endocrine deficits with the systemic clinical findings.

The combination of secondary hypogonadism, secondary hypothyroidism, new-onset diabetes, hepatomegaly, hyperpigmentation, and specific second and third metacarpophalangeal arthropathy indicates an infiltrative systemic disease.

To identify the unifying underlying etiology.

Select the most appropriate initial diagnostic test for the suspected etiology.

Measurement of transferrin saturation and serum ferritin is the best initial step.

These are the standard screening tests for hereditary hemochromatosis before proceeding to confirmatory genetic testing.

Key Concept

Diagnosis of hereditary hemochromatosis presenting with anterior pituitary infiltration

Question 737Question →

A 65-year-old man is evaluated in the hospital for management of infective endocarditis. He was admitted three days ago after presenting with a one-week history of fevers, severe fatigue, and night sweats. His medical history is significant for hypertension and stage 3a chronic kidney disease with a baseline serum creatinine of 1.6 mg/dL.

Upon admission, multiple sets of blood cultures were obtained, and the patient was started on empiric intravenous vancomycin and piperacillin-tazobactam. Transthoracic echocardiography performed yesterday demonstrated a 1.2-cm mobile vegetation on the anterior leaflet of the native mitral valve.

Today, the microbiology laboratory finalizes the blood culture results, reporting that all four bottles are growing *Enterococcus faecalis*. The isolate is susceptible to ampicillin, vancomycin, gentamicin, and linezolid.

Based on current clinical guidelines, which of the following is the most appropriate definitive antimicrobial regimen for this patient?

Intravenous ampicillin and intravenous ceftriaxone

Intravenous ampicillin and intravenous gentamicin

Intravenous vancomycin and intravenous ceftriaxone

Intravenous ampicillin monotherapy

Intravenous piperacillin-tazobactam monotherapy

Show answer & explanation

Answer: Intravenous ampicillin and intravenous ceftriaxone

Answer

The most appropriate definitive regimen is the combination of intravenous ampicillin and intravenous ceftriaxone.

The correct answer is the combination of intravenous ampicillin and intravenous ceftriaxone. *Enterococcus faecalis* infective endocarditis requires a bactericidal regimen, which is achieved through dual antibiotic therapy. While ampicillin monotherapy is bacteriostatic against enterococci, the addition of a second agent provides synergistic bactericidal activity. Large clinical trials have demonstrated that the combination of ampicillin and ceftriaxone is equally effective as the historical standard (ampicillin plus an aminoglycoside) for treating *E. faecalis* endocarditis, but is associated with a significantly lower risk of nephrotoxicity. This remarkable synergy occurs because ceftriaxone saturates specific penicillin-binding proteins (PBPs) that ampicillin does not effectively target, leading to complete cell wall breakdown despite the organism's intrinsic resistance to cephalosporin monotherapy. Given this patient's pre-existing chronic kidney disease, avoiding nephrotoxic agents like gentamicin is critical, making ampicillin and ceftriaxone the definitive regimen of choice.

Step-by-Step Solution

Analyze the microbiological data and diagnosis.

The patient has native valve infective endocarditis caused by ampicillin-susceptible *Enterococcus faecalis*.

Establishing the precise pathogen and its susceptibility profile is required to transition from empiric broad-spectrum therapy to targeted therapy.

Determine the pharmacological requirements for treating enterococcal endocarditis.

A synergistic, bactericidal regimen is necessary because beta-lactam monotherapy (like ampicillin alone) is only bacteriostatic against enterococci.

Endocarditis is an endovascular infection with high bacterial density that requires bactericidal action for complete pathogen eradication and clinical cure.

Evaluate the patient's comorbidities to select the safest and most effective synergistic regimen.

The patient has stage 3a chronic kidney disease. The combination of ampicillin and ceftriaxone provides the necessary bactericidal synergy without the nephrotoxicity associated with aminoglycosides.

Antibiotic stewardship involves selecting the most effective therapy while actively minimizing adverse effects based on patient-specific physiological factors.

Key Concept

Definitive management of *Enterococcus faecalis* infective endocarditis requires synergistic bactericidal therapy; the combination of ampicillin and ceftriaxone is a first-line regimen that is strongly preferred over ampicillin and gentamicin in patients with baseline renal impairment.

Question 738Question →

A 66-year-old man with a history of metastatic prostate cancer is brought to the emergency department due to progressively worsening mid-back pain over the past week and new-onset weakness in both legs that started 12 hours ago. He also reports being unable to urinate since this morning. His temperature is 37.1°C, blood pressure is 138/86 mmHg, pulse is 92/min, and respiratory rate is 16/min. Neurologic examination reveals 3/5 motor strength in the bilateral lower extremities, diminished pinprick sensation below the umbilicus, and 3+ patellar reflexes bilaterally. Anal sphincter tone is significantly decreased. A bedside ultrasound reveals a postvoid residual volume of 600 mL. Arrange the following steps in the most appropriate sequence for the evaluation and management of this patient's acute presentation.

Drag items to arrange them in the correct order

Show answer & explanation

Answer

The correct sequence of management for suspected malignant epidural spinal cord compression is to first administer intravenous dexamethasone, followed by obtaining an urgent MRI of the entire spine, consulting neurosurgery for operative decompression, and finally initiating localized external beam radiation therapy.

Malignant epidural spinal cord compression (MESCC) is an oncologic emergency classically presenting with worsening back pain, motor weakness, sensory level deficits, and autonomic dysfunction (e.g., urinary retention). When a patient presents with objective neurologic deficits highly suspicious for MESCC, the immediate first step is the administration of high-dose intravenous dexamethasone. This rapidly decreases peritumoral vasogenic edema, relieves pressure on the spinal cord, and protects neurologic function. Confirmatory imaging with an urgent whole-spine MRI must follow immediately after steroid administration. Once the lesion is characterized anatomically, surgical consultation is warranted to evaluate for operative decompression, which is generally superior to primary radiation for solid tumors causing structural instability or bony impingement. Finally, external beam radiation therapy is utilized either as primary definitive therapy (for poor surgical candidates or highly radiosensitive tumors like lymphoma) or as post-operative adjuvant therapy.

Step-by-Step Solution

Administer intravenous dexamethasone.

Decreases vasogenic edema around the spinal cord.

In cases with severe, objective neurologic deficits (e.g., paraparesis, bowel/bladder dysfunction), immediate administration of high-dose corticosteroids is the absolute highest priority to prevent irreversible spinal cord ischemia and permanent paralysis.

Obtain an urgent MRI of the entire spine.

Localizes the lesion and assesses the extent of compression.

MRI is the gold standard for diagnosing epidural spinal cord compression and is strictly required to plan definitive surgical or radiation therapy.

Consult neurosurgery for potential operative decompression.

Evaluates the patient for surgical intervention.

Surgical decompression provides immediate structural relief and is indicated for patients with spinal instability, bony compression, or radioresistant tumors (like prostate cancer), provided they are surgical candidates.

Initiate localized external beam radiation therapy.

Provides local tumor control and further relieves cord compression.

Radiation is utilized post-operatively to eliminate microscopic residual tumor, or as the primary modality if surgery is contraindicated.

Key Concept

In patients presenting with signs of malignant epidural spinal cord compression (back pain with neurologic deficits), empiric high-dose intravenous corticosteroids must be administered immediately, prior to obtaining confirmatory MRI.

Estimated Time:1m 30s

Question 739Question →

A 74-year-old woman is brought to the emergency department due to a 2-day history of progressively worsening shortness of breath and a persistent cough. Her medical history is significant for hypertension, type 2 diabetes mellitus, and a 45-pack-year smoking history. She currently smokes half a pack of cigarettes daily. The patient reports that her dyspnea worsens significantly when she lies flat in bed. Vital signs show a temperature of 37.0°C (98.6°F), blood pressure of 172/96 mm Hg, pulse of 114/min, and respiratory rate of 28/min. Pulse oximetry shows an oxygen saturation of 88% on room air. Physical examination reveals elevated jugular venous pressure. Lung auscultation demonstrates diffuse bilateral wheezing with crackles at the lung bases. Cardiac examination reveals a regular tachycardia with a prominent S3 gallop. Which of the following is the most appropriate initial pharmacologic therapy for this patient?

Intravenous furosemide

Intravenous methylprednisolone

Inhaled albuterol and ipratropium

Oral azithromycin

Intravenous piperacillin-tazobactam

Show answer & explanation

Answer: Intravenous furosemide

Answer

Intravenous furosemide

The correct answer is intravenous furosemide because this patient is presenting with acute decompensated heart failure (ADHF). Although her heavy smoking history and wheezing might initially suggest a COPD exacerbation, the classic signs of volume overload and left ventricular failure—including orthopnea, elevated jugular venous pressure, bibasilar crackles, and an S3 gallop—confirm cardiogenic pulmonary edema. The wheezing she is experiencing is known as 'cardiac asthma' and is caused by peribronchial edema secondary to the heart failure. Intravenous loop diuretics like furosemide are the first-line pharmacologic therapy for ADHF to rapidly reduce volume overload, decrease preload, and alleviate respiratory symptoms.

Step-by-Step Solution

Analyze the patient's presenting symptoms and physical exam findings.

The patient has acute dyspnea, orthopnea, hypoxia, elevated jugular venous pressure, bibasilar crackles, wheezing, and an S3 gallop.

Identifying the constellation of findings is necessary to determine the primary underlying pathology.

Differentiate between a chronic obstructive pulmonary disease (COPD) exacerbation and acute decompensated heart failure (ADHF).

Despite the significant smoking history and the presence of wheezing, findings such as elevated jugular venous pressure, orthopnea, and particularly an S3 gallop strongly confirm a cardiogenic etiology (ADHF) rather than a primary pulmonary exacerbation.

Wheezing can occur in heart failure ('cardiac asthma') due to peribronchial edema, making clinical differentiation critical to avoid incorrect management.

Select the appropriate initial pharmacologic therapy based on the established diagnosis of ADHF.

Intravenous furosemide (a loop diuretic) is selected.

Loop diuretics rapidly reduce volume overload and preload, relieving pulmonary congestion and improving respiratory symptoms in ADHF.

Key Concept

Differentiation and management of acute decompensated heart failure versus COPD exacerbation.

Question 740Question →

A $72$ -year-old man is brought to the emergency department by his family due to a $3$ -day history of worsening shortness of breath, generalized weakness, and increased production of clear sputum. He has a past medical history of ischemic cardiomyopathy with a left ventricular ejection fraction of $35\%$ and severe chronic obstructive pulmonary disease (COPD).

On arrival, he is obtunded and responds only to painful stimuli. His temperature is $37.1^\circ\text{C}$ ( $98.8^\circ\text{F}$ ), heart rate is $122/\text{min}$ , blood pressure is $76/48 \text{ mmHg}$ , respiratory rate is $30/\text{min}$ , and oxygen saturation is $84\%$ on room air. Physical examination reveals flat neck veins while supine. Cardiac examination shows a rapid, regular rhythm with no murmurs or gallops. Pulmonary auscultation reveals poor air movement and diffuse expiratory wheezing bilaterally, without crackles. His extremities are cool with a capillary refill time of $4$ seconds.

Laboratory results are as follows:

Component	Value
Sodium	$140 \text{ mEq/L}$
Chloride	$96 \text{ mEq/L}$
Bicarbonate	$24 \text{ mEq/L}$
Lactate	$6.5 \text{ mmol/L}$
Procalcitonin	$0.08 \text{ ng/mL}$ (normal $<0.1$ )

Arterial blood gas analysis on room air:

Component	Value
pH	$7.14$
$PaCO_2$	$75 \text{ mmHg}$
$PaO_2$	$48 \text{ mmHg}$

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

Select all that apply

Endotracheal intubation and invasive mechanical ventilation

Rapid intravenous infusion of isotonic crystalloids

Administration of intravenous furosemide

Administration of intravenous sodium bicarbonate

Initiation of intravenous piperacillin-tazobactam and vancomycin

Show answer & explanation

Answer: Endotracheal intubation and invasive mechanical ventilation; Rapid intravenous infusion of isotonic crystalloids

Answer

The most appropriate next steps are endotracheal intubation and invasive mechanical ventilation, and rapid intravenous infusion of isotonic crystalloids.

The patient presents in severe respiratory failure and shock. The correct approaches involve securing the airway and restoring perfusion. Endotracheal intubation and invasive mechanical ventilation are required because the patient is obtunded, unable to protect his airway, and has profound acidemia (

pH = 7.14

) driven by severe hypercapnia (

PaCO_2 = 75 \text{ mmHg}

). Non-invasive positive pressure ventilation (NIPPV) is contraindicated in patients with altered mental status and hemodynamic instability. Additionally, the patient is in hypovolemic shock, evidenced by hypotension (

76/48 \text{ mmHg}

), tachycardia, elevated lactate (

6.5 \text{ mmol/L}

), cool extremities, and flat neck veins. Rapid intravenous infusion of isotonic crystalloids is the critical first step to restore intravascular volume and improve tissue perfusion.

Step-by-Step Solution

Analyze the patient's hemodynamic and volume status.

The presence of hypotension, tachycardia, flat neck veins, cool extremities, and lactic acidosis indicates hypovolemic shock, rather than cardiogenic shock from his known heart failure.

Identifying the type of shock dictates initial fluid management, favoring crystalloid resuscitation over diuresis.

Evaluate the respiratory status and arterial blood gas.

The patient is obtunded with a

pH

7.14

and a

PaCO_2

75 \text{ mmHg}

, indicating severe acute-on-chronic respiratory failure.

This establishes the need for definitive airway management (intubation) rather than non-invasive ventilation, which is absolutely contraindicated in patients with altered mental status.

Calculate the anion gap and assess the acid-base pathophysiology.

The anion gap is

20 \text{ mEq/L}

(

140 - [96 + 24]

), indicating a high anion gap metabolic acidosis. The concurrent high

PaCO_2

confirms a mixed disorder.

Recognizing the respiratory component determines that bicarbonate administration would be harmful, as it would generate excess

CO_2

that the patient cannot expire.

Key Concept

Management of severe mixed acid-base disorders and undifferentiated shock in patients with concurrent COPD and heart failure.

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