Internal Medicine

3151 questions

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A 62-year-old man with myelodysplastic syndrome is receiving a transfusion of packed red blood cells for symptomatic anemia (hemoglobin $7.2$ g/dL). Thirty minutes into the infusion, he reports the sudden onset of severe flank pain, chills, and shortness of breath. His temperature is $39.2^\circ \text{C}$ ( $102.6^\circ \text{F}$ ), blood pressure is $85/50$ mm Hg, pulse is $118$ /min, and respiratory rate is $24$ /min. Physical examination reveals diaphoresis, and dark-colored urine is noted in his Foley catheter bag.

Arrange the following steps in the most appropriate sequential order for the immediate management of this patient's suspected acute hemolytic transfusion reaction.

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Answer

The correct sequence is to first stop the transfusion immediately, then maintain intravenous access with normal saline using new tubing, perform a bedside clerical check, and finally send the blood product and patient samples to the blood bank.

The clinical presentation of fever, chills, hypotension, flank pain, and dark urine (hemoglobinuria) shortly after starting a blood transfusion is highly indicative of an acute hemolytic transfusion reaction (AHTR), most commonly caused by ABO incompatibility due to a clerical error. The immediate, step-by-step management is strictly protocolized to minimize harm. The absolute first step is to stop the transfusion to prevent further exposure. Second, intravenous access must be maintained for aggressive hydration to prevent acute kidney injury; crucially, the existing tubing must be disconnected and replaced with new tubing for normal saline to avoid flushing residual incompatible blood into the patient. Third, a bedside clerical check of the patient's ID and the blood product label should be performed to quickly identify obvious errors. Finally, the remaining blood product, attached tubing, and fresh patient blood and urine samples are sent to the blood bank for definitive testing (including a direct antiglobulin test, plasma free hemoglobin, and repeat crossmatch).

Step-by-Step Solution

Stop the transfusion immediately.

Prevents any further infusion of the incompatible blood product.

Immediate cessation is the most critical intervention to limit the severity of the hemolytic reaction and minimize immune-mediated organ damage.

Maintain IV access with normal saline using new tubing.

Ensures a patent intravenous route for aggressive fluid resuscitation.

The patient is hypotensive and at risk for acute tubular necrosis. The old tubing must be disconnected, not flushed, to prevent pushing residual incompatible blood into the circulation.

Perform a bedside clerical check.

Identifies potential ABO incompatibility due to misidentification.

Clerical error (e.g., giving the wrong blood to the wrong patient) is the leading cause of fatal acute hemolytic transfusion reactions and must be rapidly identified.

Send samples to the blood bank.

Initiates formal laboratory investigation.

Definitive diagnosis requires laboratory testing of the remaining blood product and fresh patient samples (including a direct antiglobulin test and repeat crossmatching).

Key Concept

The sequential management algorithm for acute hemolytic transfusion reactions prioritizes immediately stopping exposure, securing safe IV access for resuscitation, identifying clerical errors, and sending samples for diagnostic confirmation.

Question 902Question →

A clinic focuses on the evaluation and management of severe and resistant hypertension. Match each patient's clinical presentation with the most appropriate initial diagnostic test for their suspected secondary cause of hypertension.

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Answer

The scenarios match their respective diagnostic tests as follows: The patient with hypokalemia requires an aldosterone-to-renin ratio; the patient with episodic headaches and sweating requires plasma free metanephrines; the young woman with a bruit requires CT angiography; and the patient with metabolic and bone abnormalities requires a dexamethasone suppression test.

Each patient's clinical presentation aligns perfectly with a specific secondary cause of hypertension (primary hyperaldosteronism, pheochromocytoma, fibromuscular dysplasia, and Cushing syndrome, respectively), dictating the targeted initial diagnostic tests provided in the correct pairs.

Step-by-Step Solution

Analyze the first clinical vignette for key features of secondary hypertension.

Identified drug-resistant hypertension with spontaneous or diuretic-induced hypokalemia, pointing to primary hyperaldosteronism.

Recognizing the classic presentation of primary hyperaldosteronism dictates the selection of the aldosterone-to-renin ratio as the initial screen.

Evaluate the second vignette for episodic symptoms.

Identified the triad of headache, sweating, and tachycardia with hypertensive emergencies, indicating pheochromocytoma.

Pheochromocytoma requires biochemical screening for catecholamine excess using plasma free metanephrines.

Assess the third vignette involving a young patient with a specific physical exam finding.

Identified severe hypertension in a young female with a subauricular bruit, highly suggestive of fibromuscular dysplasia.

FMD requires vascular imaging, making CT angiography or duplex ultrasound the appropriate initial diagnostic step.

Analyze the fourth vignette for systemic signs of endocrine dysfunction.

Identified hypertension accompanied by diabetes, bruising, and osteoporosis, characterizing Cushing syndrome.

Cushing syndrome requires demonstration of hypercortisolism, best initially screened with a low-dose dexamethasone suppression test.

Key Concept

Identification of distinct secondary causes of hypertension and selection of their appropriate initial screening modalities.

Question 903Question →

A 65-year-old man is evaluated in the hospital on day 3 of admission for community-acquired pneumonia. He was initially started on empiric intravenous ceftriaxone and azithromycin. His past medical history is notable for hypertension and type 2 diabetes mellitus. Today, he reports feeling much better and has a good appetite. His temperature is $37.1^\circ\text{C}$ ( $98.8^\circ\text{F}$ ), blood pressure is $128/78\text{ mmHg}$ , pulse is $78/\text{min}$ , and respiratory rate is $14/\text{min}$ . Pulse oximetry shows $96\%$ on room air. Physical examination reveals significantly decreased crackles at the right lower lung base compared to admission. The patient is tolerating an oral diet. Blood cultures obtained on admission show no growth. A sputum culture obtained on admission has grown *Streptococcus pneumoniae*. Susceptibility testing indicates the organism is highly susceptible to penicillin, amoxicillin, ceftriaxone, and levofloxacin, but resistant to azithromycin. Which of the following is the most appropriate next step in the management of this patient?

Transition to oral amoxicillin

Transition to oral levofloxacin

Transition to oral amoxicillin-clavulanate

Continue intravenous ceftriaxone

Continue intravenous ceftriaxone and azithromycin

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Answer: Transition to oral amoxicillin

Answer

Transition to oral amoxicillin

This patient was admitted for community-acquired pneumonia and has demonstrated significant clinical improvement. He is now afebrile, hemodynamically stable, and tolerating oral intake. According to the principles of antibiotic stewardship, patients who are clinically stable on intravenous antibiotics should be transitioned to oral therapy. Furthermore, the sputum culture has identified Streptococcus pneumoniae that is susceptible to penicillin and amoxicillin. The most appropriate action is to de-escalate (narrow the spectrum) from empiric ceftriaxone to targeted oral amoxicillin therapy to minimize collateral damage to the microbiome and reduce the risk of resistance.

Step-by-Step Solution

Evaluate the patient's clinical stability and current route of administration.

The patient is afebrile, hemodynamically stable, improving clinically, and successfully tolerating an oral diet.

Clinical stability criteria determine if a patient is ready to transition safely from intravenous to oral antibiotic therapy.

Analyze the sputum culture and susceptibility results.

The responsible pathogen is Streptococcus pneumoniae, which is susceptible to narrow-spectrum beta-lactams like amoxicillin and penicillin.

De-escalation of broad-spectrum empiric therapy must be guided by final culture and sensitivity data.

Select the most appropriate targeted oral agent.

Oral amoxicillin is chosen as the definitive therapy.

It provides targeted, narrow-spectrum coverage against the identified pathogen, minimizes collateral damage to the patient's microbiome, and facilitates prompt hospital discharge.

Key Concept

Antibiotic stewardship principles mandate de-escalating broad-spectrum empiric therapy to targeted, narrow-spectrum oral agents once clinical stability is achieved and culture susceptibilities are known.

Estimated Time:1m 0s

Question 904Question →

A 55-year-old man who underwent a coronary artery bypass graft surgery five days ago develops acute swelling and pain in his right calf. His platelet count has dropped from $250,000/\text{mm}^3$ postoperatively to $90,000/\text{mm}^3$ today. He has been receiving subcutaneous unfractionated heparin for deep vein thrombosis prophylaxis. A venous duplex ultrasound confirms a new right lower extremity deep vein thrombosis. He is clinically suspected of having heparin-induced thrombocytopenia (HIT). Arrange the following pathophysiologic steps in the correct chronological order detailing the development of this patient's condition.

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Answer

The correct chronological sequence is: 1) Heparin binds to PF4; 2) IgG antibodies are generated against the complex; 3) IgG binds to the heparin-PF4 complex; 4) The immune complex binds to platelet Fc receptors; 5) Platelets activate, cause thrombosis, and are consumed.

Heparin-induced thrombocytopenia (HIT) Type 2 is a prothrombotic, immune-mediated disorder. The sequence begins when exogenous heparin binds to endogenous platelet factor 4 (PF4), forming a highly immunogenic neoantigen. The body responds by creating IgG autoantibodies against this complex. These newly formed IgG antibodies bind to the circulating heparin-PF4 complexes. The Fc portion of these IgG antibodies then binds to and cross-links Fc-gamma-RIIA receptors on the surface of platelets. This intense cross-linking results in widespread platelet activation. Activated platelets release procoagulant microparticles, leading to a severe hypercoagulable state and thrombosis. Concurrently, the activated and antibody-coated platelets are rapidly cleared by the reticuloendothelial system (primarily the spleen), resulting in the characteristic drop in platelet count (thrombocytopenia). Therefore, the paradoxical presentation of thrombosis in the setting of thrombocytopenia is a direct result of this immune-mediated platelet activation and consumption.

Step-by-Step Solution

Identify the underlying diagnosis based on the clinical presentation.

The patient has a drop in platelets >50% and a new thrombosis 5 days after starting heparin, which is classic for Heparin-Induced Thrombocytopenia (HIT) Type 2.

Recognizing the condition is necessary to determine its underlying pathophysiologic mechanism.

Determine the initiating molecular event of HIT Type 2.

The sequence begins with the binding of administered heparin to endogenous platelet factor 4 (PF4).

This interaction creates the neoantigen that triggers the immune response.

Trace the subsequent immune system response.

The immune system recognizes the neoantigen and produces IgG antibodies, which then bind to the heparin-PF4 complexes.

Antibody formation and binding must occur before cellular activation can take place.

Identify how the immune complexes interact with cells.

The IgG-heparin-PF4 complexes bind to Fc-gamma-RIIA receptors on the platelet surface.

This binding bridges the humoral immune response to cellular activation.

Determine the final clinical consequences of this cellular interaction.

Platelets become activated (causing thrombosis) and are eventually removed from circulation (causing thrombocytopenia).

This explains the paradoxical presentation of thrombosis in the setting of low platelets.

Key Concept

Pathophysiology of Heparin-Induced Thrombocytopenia (HIT) Type 2

Estimated Time:1m 0s

Question 905Question →

A 28-year-old female patient with established systemic lupus erythematosus comes to the office reporting recent-onset leg swelling and foamy urine. Her blood pressure is $150/92$ mm Hg. Urinalysis reveals 3+ protein and the presence of red blood cell casts. Arrange the following steps in the most appropriate clinical sequence for the evaluation and management of this patient's new complication.

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Answer

The correct sequence is: quantify proteinuria, perform renal biopsy, initiate induction therapy, and finally transition to maintenance therapy.

The correct clinical sequence for managing suspected lupus nephritis begins with non-invasive confirmation of renal disease (quantifying proteinuria and assessing creatinine). Because the clinical presentation does not reliably predict the histopathologic class, a renal biopsy must be performed next. The biopsy results guide the initiation of aggressive induction therapy for severe disease (Classes III/IV). Finally, after 3 to 6 months of successful induction, the patient is transitioned to a lower-dose, less toxic maintenance therapy to sustain remission.

Step-by-Step Solution

Identify the clinical presentation.

The patient has systemic lupus erythematosus with new edema, hypertension, and red blood cell casts, indicating active glomerulonephritis (lupus nephritis).

Recognizing the complication dictates the immediate need for a structured renal workup.

Determine the initial diagnostic step.

Quantify the proteinuria and assess renal function via non-invasive testing.

Non-invasive confirmation of severity is required before exposing the patient to the risks of invasive testing.

Determine the definitive diagnostic step.

Perform a percutaneous renal biopsy.

Clinical features alone cannot reliably differentiate the histologic classes of lupus nephritis (Classes I through VI), which require vastly different treatments.

Determine the initial therapeutic intervention.

Initiate induction therapy.

Active, severe lupus nephritis (e.g., Class III or IV) requires aggressive, high-dose immunosuppression to prevent irreversible nephron loss.

Determine the long-term management strategy.

Transition to maintenance therapy.

Once remission is achieved (usually after 3-6 months), stepping down to a less toxic maintenance regimen prevents disease flares while minimizing medication toxicity.

Key Concept

Sequential evaluation and stepwise pharmacologic management of Lupus Nephritis

Estimated Time:1m 0s

Question 906Question →

A 64-year-old man presents to the emergency department due to a 2-week history of progressive dyspnea on exertion, orthopnea, and a persistent dry cough. His medical history includes seropositive rheumatoid arthritis, type 2 diabetes mellitus, and a 35-pack-year smoking history. His joint disease was previously inadequately controlled with methotrexate monotherapy, prompting the addition of adalimumab 6 months ago, which has successfully induced clinical remission.

On physical examination, his temperature is $37.4^\circ C$ ( $99.3^\circ F$ ), blood pressure is $148/90\ mmHg$ , heart rate is $108/min$ , and respiratory rate is $24/min$ . Pulse oximetry shows $91\%$ on room air. Jugular venous distention is prominent up to the angle of the mandible while the patient is seated at a 45-degree angle. Auscultation reveals diffuse bilateral expiratory wheezes and coarse crackles at the lung bases. Bilateral 2+ pitting edema is noted up to the mid-calves.

Laboratory results:
Leukocytes: $8,500/mm^3$
Hemoglobin: $11.2\ g/dL$
Brain natriuretic peptide (BNP): $840\ pg/mL$ (Normal $< 100$ )
Thyroid-stimulating hormone (TSH): $3.8\ \mu U/mL$ (Normal $0.5 - 5.0$ )

Arterial blood gas (room air):
pH: $7.48$
$PaCO_2$ : $31\ mmHg$
$PaO_2$ : $64\ mmHg$
$HCO_3^-$ : $23\ mEq/L$

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

Discontinue adalimumab and initiate intravenous furosemide

Administer systemic corticosteroids, nebulized ipratropium-albuterol, and oral azithromycin

Start empirical intravenous piperacillin-tazobactam and vancomycin

Administer intravenous sodium bicarbonate to correct the metabolic derangement

Initiate oral levothyroxine and order a transthoracic echocardiogram

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Answer: Discontinue adalimumab and initiate intravenous furosemide

Answer

The most appropriate management is to discontinue adalimumab and initiate intravenous furosemide.

The correct approach is to discontinue adalimumab and initiate intravenous furosemide. This patient presents with classic signs of acute decompensated heart failure (ADHF), including orthopnea, elevated jugular venous pressure, pulmonary crackles, pitting edema, and a highly elevated BNP. The wheezing he is experiencing is likely 'cardiac asthma' caused by peribronchial edema rather than a primary airway disease. A crucial element of his presentation is the initiation of adalimumab 6 months ago. Adalimumab is a tumor necrosis factor-alpha (TNF-alpha) inhibitor used in the treatment of rheumatoid arthritis. TNF-alpha inhibitors carry a well-documented risk of causing new-onset heart failure or exacerbating existing left ventricular dysfunction. They are contraindicated in patients with moderate to severe heart failure. Therefore, the most appropriate management must involve not only acute diuresis with a loop diuretic (e.g., furosemide) to reduce preload and relieve pulmonary congestion, but also the immediate discontinuation of the offending biologic agent.

Step-by-Step Solution

Evaluate the clinical signs, symptoms, and laboratory data to establish the primary acute diagnosis.

The combination of orthopnea, prominent JVD, bibasilar crackles, pedal edema, and a markedly elevated BNP (

840\ pg/mL

) confirms a diagnosis of acute decompensated heart failure (ADHF).

Accurate identification of the acute presentation is required to avoid confounding diagnoses like COPD exacerbation (despite the wheezing or 'cardiac asthma').

Review the patient's pharmacologic history for potential triggers of the acute decompensation.

The patient was started on adalimumab 6 months ago for refractory rheumatoid arthritis.

Identifying drug-induced etiologies is a critical step in the comprehensive management of heart failure, particularly in rheumatologic patients on biologic disease-modifying antirheumatic drugs (DMARDs).

Recall the adverse effect profile of the identified biologic agent.

Adalimumab is a TNF-alpha inhibitor. TNF-alpha inhibitors are known to worsen latent left ventricular dysfunction or cause new-onset heart failure.

Understanding the toxicity profile of TNF-alpha inhibitors dictates the necessity of removing the offending agent.

Formulate the comprehensive next best step in management.

Management includes diuresis with intravenous furosemide for the acute volume overload and immediate discontinuation of adalimumab.

Treating the symptoms without addressing the underlying pharmacologic trigger would result in continued myocardial toxicity and recurrent heart failure.

Key Concept

Tumor necrosis factor-alpha (TNF-alpha) inhibitors (e.g., adalimumab, infliximab, etanercept) can cause new-onset heart failure or exacerbate underlying cardiac dysfunction. Patients presenting with heart failure while on these agents must have the medication discontinued.

Estimated Time:2m 0s

Question 907Question →

A $28$ -year-old man presents to the clinic with a $3$ -month history of a painless, slowly enlarging mass in his right supraclavicular region. He also reports an unintentional weight loss of $6\text{ kg}$ ( $13\text{ lbs}$ ) and drenching night sweats over the past month. Physical examination reveals a $4\text{-cm}$ , firm, non-tender, and mobile lymph node in the right supraclavicular fossa. The remainder of the examination, including abdominal palpation, is unremarkable. A complete blood count and comprehensive metabolic panel are within normal limits.

Arrange the following clinical steps in the most appropriate chronological order for the definitive evaluation and management of this patient's suspected condition.

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Answer

The correct sequence is: Excisional biopsy -> Histopathologic confirmation -> PET/CT staging -> Baseline organ function testing (Echo/PFTs) -> Initiation of chemotherapy.

The management of highly suspected Hodgkin lymphoma follows a strict, sequential clinical protocol. First, an excisional lymph node biopsy is mandatory, as fine-needle aspiration destroys the critical tissue architecture needed for lymphoma classification. Following the biopsy, histopathologic review establishes the definitive diagnosis by confirming the presence of Reed-Sternberg cells. Once the diagnosis is secured, the patient must undergo staging with an 18F-FDG PET/CT scan to determine the anatomic extent of the disease, which dictates the number of chemotherapy cycles and the role of radiotherapy. Before starting the standard ABVD (doxorubicin, bleomycin, vinblastine, dacarbazine) regimen, baseline organ function must be assessed due to the known cardiotoxicity of doxorubicin and the pulmonary toxicity of bleomycin. Therefore, an echocardiogram and pulmonary function tests are required pre-treatment steps. Finally, with diagnosis, staging, and safety parameters established, systemic combination chemotherapy is initiated.

Step-by-Step Solution

Evaluate the clinical presentation of 'B symptoms' and painless supraclavicular lymphadenopathy.

Identify the immediate need for an intact tissue sample, prioritizing an excisional lymph node biopsy.

Lymphoma diagnosis requires visualization of the entire lymph node architecture, which is inherently destroyed by fine-needle aspiration techniques.

Analyze the excised lymph node tissue.

Establish the definitive diagnosis of classic Hodgkin lymphoma via the identification of Reed-Sternberg cells.

Therapeutic and staging algorithms cannot proceed without a confirmed histologic subtype.

Map the anatomic distribution of the confirmed malignancy.

Order a whole-body 18F-FDG PET/CT scan for clinical staging.

The stage of the disease (Ann Arbor classification) determines the intensity and duration of the required chemotherapy.

Evaluate the patient's physiological capacity to tolerate the indicated treatment.

Perform an echocardiogram and pulmonary function tests.

The standard ABVD regimen includes doxorubicin and bleomycin, requiring baseline cardiac ejection fraction and pulmonary diffusion capacity measurements prior to exposure.

Begin definitive medical management.

Initiate systemic ABVD combination chemotherapy.

Treatment is administered safely and effectively only after the diagnostic, staging, and safety prerequisite steps are complete.

Key Concept

Algorithmic diagnosis, staging, and pre-treatment evaluation of Hodgkin Lymphoma.

Estimated Time:1m 30s

Question 908Question →

Match each clinical presentation with its corresponding primary acid-base disorder.

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Answer

The clinical scenarios correctly match their respective primary acid-base disturbances based on the primary driver of the pH change: bicarbonate loss in diarrhea (normal gap acidosis), CO2 blow-off in asthma (respiratory alkalosis), acid loss in vomiting (metabolic alkalosis), and lactic acid buildup in sepsis (high gap acidosis).

Each presentation classically alters the acid-base balance through a specific physiologic mechanism. Diarrhea causes direct bicarbonate loss (normal AG metabolic acidosis). Hyperventilation from an acute asthma attack blows off CO2 (respiratory alkalosis). Severe vomiting removes gastric acid and volume (metabolic alkalosis). Poor perfusion from septic shock generates systemic lactate (high AG metabolic acidosis).

Step-by-Step Solution

Assess the pH in each scenario to determine if the primary disorder is an acidosis (pH

< 7.35

) or an alkalosis (pH

> 7.45

Identifies the fundamental directional disturbance of the acid-base derangement.

Provides the baseline needed to categorize the primary process before evaluating compensation.

Evaluate the PaCO

_2

and serum bicarbonate levels to identify if the primary etiology is respiratory or metabolic.

Differentiates metabolic conditions (driven by bicarbonate) from respiratory conditions (driven by carbon dioxide).

Determines which physiological system is responsible for the abnormal pH.

For patients presenting with metabolic acidosis, evaluate the calculated anion gap using the formula:

Na^+ - (Cl^- + HCO_3^-)

Categorizes the acidosis as either a normal or high anion gap metabolic acidosis.

Narrows down the differential diagnosis significantly, such as distinguishing diarrhea (normal gap) from lactic acidosis (high gap).

Key Concept

Basic interpretation of primary acid-base disorders requires assessing the pH, identifying the primary alteration in PaCO2 or bicarbonate, and calculating the anion gap in all cases of metabolic acidosis.

Question 909Question →

A medical student is reviewing serologic markers for various autoimmune diseases. Match each specific autoantibody below to the rheumatologic condition with which it is most strongly associated.

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Answer

Anti-CCP matches with Rheumatoid arthritis; Anti-dsDNA matches with Systemic lupus erythematosus (SLE); Anti-centromere matches with Limited cutaneous systemic sclerosis; Anti-Ro/SSA matches with Sjögren syndrome.

Each autoantibody serves as a specific diagnostic marker for a distinct rheumatologic condition. Anti-CCP is specific for rheumatoid arthritis, anti-dsDNA for SLE, anti-centromere for limited cutaneous systemic sclerosis, and anti-Ro/SSA for Sjögren syndrome.

Step-by-Step Solution

Identify the disease association for anti-CCP.

Anti-CCP is linked to Rheumatoid arthritis.

It is a highly specific marker for RA that helps differentiate it from other inflammatory arthritides.

Identify the disease association for anti-dsDNA.

Anti-dsDNA is linked to Systemic lupus erythematosus (SLE).

It is a specific marker for SLE that often fluctuates with disease flares.

Identify the disease association for anti-centromere.

Anti-centromere is linked to Limited cutaneous systemic sclerosis.

It is the primary autoantibody found in patients with the limited form of systemic sclerosis.

Identify the disease association for anti-Ro/SSA.

Anti-Ro/SSA is linked to Sjögren syndrome.

It is frequently tested during the diagnostic workup for sicca symptoms characteristic of Sjögren syndrome.

Key Concept

Autoantibody profiles are essential in the diagnosis and classification of rheumatologic diseases.

Question 910Question →

A 64-year-old man comes to the emergency department reporting progressive facial swelling and shortness of breath over the past two weeks. He notes that the swelling is worse in the morning when he wakes up and improves slightly throughout the day. The patient has a 40-pack-year smoking history and has not seen a physician in ten years. Vital signs are temperature 37.1°C (98.8°F), blood pressure 135/85 mmHg, pulse 98/min, and respirations 18/min. Physical examination reveals plethora and edema of the face and neck. Prominent, distended superficial veins are visible across the anterior chest wall. Auscultation of the lungs reveals decreased breath sounds over the right upper lung field. Which of the following is the most likely cause of this patient's presentation?

Obstruction of blood flow through the superior vena cava

Acute exacerbation of chronic obstructive pulmonary disease

Volume overload from acute decompensated heart failure

Mucopolysaccharide deposition due to severe hypothyroidism

Mast cell degranulation causing acute angioedema

Show answer & explanation

Answer: Obstruction of blood flow through the superior vena cava

Answer

Obstruction of blood flow through the superior vena cava

The correct answer accurately identifies the pathophysiology of Superior Vena Cava (SVC) syndrome. This patient's presentation—progressive facial and neck edema, plethora, and distended collateral veins on the anterior chest—is the classic hallmark of SVC obstruction. Given his heavy smoking history and decreased breath sounds in the right upper lung, the most likely etiology is a right-sided bronchogenic carcinoma compressing the SVC. The swelling is often worse in the morning due to lying supine overnight, which further compromises venous return.

Step-by-Step Solution

Analyze the patient's demographics and risk factors.

The patient is a 64-year-old man with a 40-pack-year smoking history.

Identifies the patient as being at exceptionally high risk for lung malignancies.

Evaluate the key physical examination findings.

The exam shows facial plethora, neck edema, and distended superficial chest veins, alongside right-sided decreased breath sounds.

These specific signs point directly to impaired venous return from the head and upper torso.

Synthesize findings to determine the most likely mechanism.

The combination of symptoms strongly suggests an external compression of the superior vena cava, an oncologic emergency known as SVC syndrome.

A right lung tumor is likely compressing the SVC, leading to venous backflow and engorgement of collateral veins.

Key Concept

Superior vena cava (SVC) syndrome is an oncologic emergency presenting with facial and neck swelling, plethora, and distended chest veins, most commonly caused by bronchogenic carcinoma compressing the SVC.

Question 911Question →

A 65-year-old man with a history of deceased-donor renal transplantation 2 years ago is brought to the emergency department by his family due to a 24-hour history of high fever, severe generalized headache, and progressive confusion. His current medications include tacrolimus, mycophenolate mofetil, and prednisone. His temperature is 39.2°C (102.6°F), blood pressure is 105/65 mm Hg, pulse is 112/min, and respirations are 20/min. Physical examination is notable for marked nuchal rigidity and a Glasgow Coma Scale score of 11. Neurological examination reveals a new mild left-sided hemiparesis. Arrange the following steps in the most appropriate chronological sequence for the acute diagnostic and therapeutic management of this patient.

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Answer

The correct sequence of management is: Obtain peripheral blood cultures, followed by immediate administration of empiric dexamethasone and broad-spectrum antibiotics (including ampicillin), then perform a CT scan of the head, followed by a lumbar puncture, and finally adjust antimicrobial therapy based on culture results.

The algorithm for suspected bacterial meningitis depends on the presence or absence of specific 'red flag' criteria. Normally, the sequence is: Blood cultures → Lumbar puncture → Antibiotics. However, if the patient has altered mental status, new-onset seizures, papilledema, focal neurological deficits, is severely immunocompromised, or is >60 years old, a head CT is required prior to LP. Because a CT scan introduces a significant time delay, the revised sequence becomes: Blood cultures → Dexamethasone + Empiric antibiotics → CT head → Lumbar puncture → Tailor therapy based on cultures. This patient meets multiple criteria for a pre-LP CT scan (age > 60, transplant recipient, GCS 11, hemiparesis), necessitating immediate antibiotic administration directly after blood cultures.

Step-by-Step Solution

Identify the clinical syndrome and immediate life-threatening risk.

The patient presents with the classic triad (fever, neck stiffness, altered mental status) of acute bacterial meningitis.

Rapid recognition dictates an emergent, algorithmic approach to minimize neurological morbidity and mortality.

Assess for indications requiring neuroimaging prior to lumbar puncture.

The patient has four absolute indications for a CT scan prior to LP: age > 60, immunocompromised state (transplant recipient), altered mental status (GCS 11), and focal neurologic deficit (hemiparesis).

Performing an LP in the presence of increased intracranial pressure from a space-occupying lesion can precipitate fatal brain herniation.

Determine the timing of antibiotic administration.

Because the required CT scan will delay the lumbar puncture, antibiotics and adjunctive dexamethasone must be administered immediately after blood cultures are drawn, without waiting for neuroimaging or CSF analysis.

Delaying antibiotics in acute bacterial meningitis significantly increases mortality. The sequence MUST prioritize treatment over obtaining a definitive CSF culture when imaging is required.

Determine the empiric antibiotic regimen.

The regimen must include vancomycin (for resistant S. pneumoniae), a 3rd-generation cephalosporin (for N. meningitidis and H. influenzae), and ampicillin.

Ampicillin is essential to cover Listeria monocytogenes, which is highly prevalent in patients who are immunocompromised (e.g., organ transplant on mycophenolate/tacrolimus) and those over age 50.

Key Concept

In patients with suspected bacterial meningitis who have indications for a CT scan before lumbar puncture (e.g., focal deficit, altered mental status, immunocompromise), blood cultures must be drawn and empiric antibiotics administered immediately, prior to neuroimaging and LP.

Question 912Question →

A 58-year-old woman comes to the clinic for follow-up of fatigue and joint pain. She has a 6-year history of rheumatoid arthritis, currently treated with methotrexate and low-dose prednisone. She reports that her fatigue has progressively worsened over the past three months, limiting her daily activities. Over the same period, she has experienced increased morning stiffness lasting up to 2 hours and worsening swelling in her hands and wrists. She has no history of gastrointestinal bleeding or melena. Vital signs are normal. Physical examination reveals active synovitis with swelling and tenderness in the bilateral metacarpophalangeal and proximal interphalangeal joints.

Laboratory studies show:

Laboratory Parameter	Result	Reference Range
Hemoglobin	$9.2 \text{ g/dL}$	$12.0-16.0 \text{ g/dL}$
Mean corpuscular volume	$86 \text{ \mu m}^3$	$80-100 \text{ \mu m}^3$
Leukocyte count	$8,400/\text{mm}^3$	$4,500-11,000/\text{mm}^3$
Platelet count	$410,000/\text{mm}^3$	$150,000-400,000/\text{mm}^3$
Serum iron	$30 \text{ \mu g/dL}$	$50-170 \text{ \mu g/dL}$
Total iron-binding capacity (TIBC)	$220 \text{ \mu g/dL}$	$250-450 \text{ \mu g/dL}$
Ferritin	$480 \text{ ng/mL}$	$10-150 \text{ ng/mL}$
Erythrocyte sedimentation rate	$85 \text{ mm/h}$	$0-20 \text{ mm/h}$
Serum creatinine	$0.9 \text{ mg/dL}$	$0.6-1.2 \text{ mg/dL}$

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

Escalation of disease-modifying antirheumatic therapy

Initiation of oral ferrous sulfate therapy

Administration of an erythropoiesis-stimulating agent

Referral for bone marrow aspiration and biopsy

Transfusion of packed red blood cells

Show answer & explanation

Answer: Escalation of disease-modifying antirheumatic therapy

Answer

The most appropriate next step is escalation of disease-modifying antirheumatic therapy.

The correct answer is the escalation of disease-modifying antirheumatic therapy. This patient presents with a normocytic anemia characterized by a low serum iron, low total iron-binding capacity (TIBC), and an elevated ferritin level. This profile is the classic presentation of anemia of chronic disease (also known as anemia of inflammation). The underlying pathogenesis involves inflammation-induced hepatic production of hepcidin. Hepcidin binds to ferroportin (the iron export channel) on macrophages and enterocytes, leading to its degradation. This prevents the release of iron into the serum, resulting in iron sequestration (high ferritin) and reduced available serum iron for erythropoiesis. The most effective and appropriate management for anemia of chronic disease is to treat the underlying inflammatory disorder. In this case, the patient has active rheumatoid arthritis that is inadequately controlled on her current regimen. Escalating her immunosuppressive therapy will reduce inflammation, decrease hepcidin levels, and subsequently improve her hemoglobin.

Step-by-Step Solution

Analyze the patient's clinical presentation and complete blood count.

The patient has a normocytic anemia (hemoglobin

9.2 \text{ g/dL}

, MCV

86 \text{ \mu m}^3

) in the setting of poorly controlled rheumatoid arthritis (indicated by active synovitis and an elevated ESR of

85 \text{ mm/h}

Establishing the presence of active inflammation is crucial for contextualizing the anemia.

Interpret the iron studies.

Serum iron is low, TIBC is low, and ferritin is elevated.

These findings definitively differentiate anemia of chronic disease (where iron is sequestered in macrophages) from true iron deficiency anemia (which would present with high TIBC and low ferritin).

Determine the appropriate management based on the diagnosis.

The primary treatment for anemia of chronic disease is to address the underlying inflammatory condition.

Treating the rheumatoid arthritis will reduce hepatic hepcidin production, restoring normal iron mobilization and enabling proper erythropoiesis.

Key Concept

The definitive treatment for anemia of chronic disease (anemia of inflammation) is optimization of the underlying inflammatory condition, which reduces hepcidin levels and resolves iron sequestration.

Question 913Question →

Match the following classic dermatological findings with the infectious disease they most accurately represent.

Click a left item, then click its matching right item

Show answer & explanation

Answer

The correct matches are: Erythema migrans with Lyme disease, centripetal maculopapular rash with Rocky Mountain spotted fever, dermatomal vesicular rash with Herpes zoster, and the 'slapped cheek' appearance with Erythema infectiosum.

Each of these dermatological findings is a classic, highly specific manifestation of its respective infectious disease. Recognizing these visual patterns allows clinicians to promptly initiate targeted therapy (e.g., doxycycline for Lyme disease or Rocky Mountain spotted fever) often before confirmatory laboratory results are available.

Step-by-Step Solution

Analyze the targetoid (bull's-eye) rash description.

Identified as erythema migrans, matching Lyme disease.

Erythema migrans is the hallmark clinical sign of early Lyme disease, allowing for a clinical diagnosis without initial serologic testing.

Analyze the rash starting on the wrists and ankles and spreading centrally.

Identified as the classic rash pattern for Rocky Mountain spotted fever.

This distinct centripetal pattern (extremities to trunk) is a key diagnostic clue for Rickettsia rickettsii infection.

Analyze the unilateral, painful, vesicular rash in a single dermatome.

Identified as shingles, matching Herpes zoster.

Varicella-zoster virus remains latent in nerve ganglia and its reactivation strictly follows dermatomal lines, not crossing the midline.

Analyze the 'slapped cheek' rash followed by a reticular pattern.

Identified as Fifth disease, matching Erythema infectiosum.

This biphasic rash pattern in a child is pathognomonic for Parvovirus B19 infection.

Key Concept

Recognition of classic dermatological manifestations of infectious diseases.

Estimated Time:45s

Question 914Question →

A 28-year-old woman with a known history of systemic lupus erythematosus (SLE) presents to the nephrology clinic with new-onset hypertension, progressive lower extremity edema, and foamy urine. Laboratory evaluation reveals a serum creatinine of 1.7 mg/dL, a serum albumin level of 2.6 g/dL, and a urine protein-to-creatinine ratio of 3.8 g/g. Urinalysis demonstrates dysmorphic red blood cells and red blood cell casts.

Assuming the patient initially follows a standard favorable clinical trajectory but eventually experiences a severe, treatment-resistant flare several years later, arrange the following clinical interventions in the correct chronological sequence of her long-term management.

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Answer

The correct sequence is: 1) Renal biopsy, 2) Induction therapy, 3) Document response at 3-6 months, 4) Maintenance therapy, 5) Escalation for refractory relapse.

The standard sequence for managing active lupus nephritis requires establishing a histological baseline via biopsy before committing to highly toxic induction therapy. Induction (e.g., high-dose steroids and mycophenolate) aims to rapidly halt inflammation. The efficacy of this phase must be evaluated after 3 to 6 months. Once a response is documented, the patient is safely stepped down to maintenance therapy to minimize long-term toxicity. Finally, if the disease relapses and proves refractory years later, escalation to salvage agents like voclosporin or rituximab is indicated.

Step-by-Step Solution

Identify the need for a definitive tissue diagnosis in a patient presenting with signs of active, severe lupus nephritis.

Place the performance of a renal biopsy as the initial step.

Empiric treatment without classifying the specific WHO/ISN histological class is inappropriate, as the class dictates the treatment protocol.

Determine the immediate pharmacological management following histological confirmation of proliferative lupus nephritis.

Place the initiation of high-dose induction therapy as the second step.

Rapid, aggressive immunosuppression is required to halt immune-mediated renal damage and induce remission.

Establish the timeframe for evaluating the efficacy of the initial intense treatment phase.

Place the documentation of clinical response at 3 to 6 months as the third step.

Induction therapy regimens require several months to achieve maximal clinical effect; premature alteration of therapy should be avoided.

Select the appropriate ongoing management strategy once disease remission is achieved.

Place the transition to lower-dose maintenance therapy as the fourth step.

Maintenance therapy uses lower medication doses to sustain remission while reducing the risk of long-term toxicity, such as opportunistic infections.

Formulate a plan for a subsequent severe, treatment-resistant disease flare.

Place the escalation to calcineurin inhibitors or biologics as the final step.

Advanced, targeted therapies are reserved for salvage treatment in patients who eventually relapse and become refractory to standard regimens.

Key Concept

The standard management algorithm for proliferative lupus nephritis follows a strict sequence: diagnostic renal biopsy, intense induction therapy, formal assessment of response, transition to less toxic maintenance therapy, and ultimately, targeted escalation for refractory relapses.

Estimated Time:1m 30s

Question 915Question →

A 68-year-old man with a history of castration-resistant metastatic prostate cancer is brought to the emergency department by his family. He reports a 5-day history of progressively worsening, severe thoracic back pain that is exacerbated by coughing and laying flat. Over the past 12 hours, he has developed profound weakness in both legs and an inability to urinate. His temperature is 37.2°C (99.0°F), blood pressure is 142/86 mmHg, and pulse is 92/min. Neurological examination reveals 2/5 motor strength in the bilateral lower extremities, decreased pinprick sensation below the umbilicus, and absent patellar and Achilles reflexes. Anal sphincter tone is markedly diminished. Post-void residual bladder volume is 600 mL.

Arrange the following management steps in the most appropriate chronological sequence for this patient:

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Show answer & explanation

Answer

The correct chronological sequence is: 1) Administer high-dose intravenous dexamethasone, 2) Obtain an urgent MRI of the entire spine, 3) Review imaging findings with neurosurgery and radiation oncology, 4) Initiate definitive surgical decompression or external beam radiotherapy.

The correct sequence for managing suspected malignant epidural spinal cord compression (MESCC) with neurological deficits begins with immediate medical stabilization to preserve nerve function, followed by diagnostic imaging, and finally definitive therapy. When a patient presents with back pain and overt neurological deficits (such as paraparesis, a sensory level, and bowel/bladder dysfunction), the absolute first step is the administration of high-dose intravenous dexamethasone. This intervention reduces peritumoral vasogenic edema and immediately decreases pressure on the spinal cord. Once steroids are empirically administered, an urgent MRI of the entire spine is obtained to confirm the diagnosis and assess for multiple lesions. After the lesion is radiographically defined, multidisciplinary consultation with neurosurgery and radiation oncology is required to formulate a treatment plan. Finally, definitive treatment is executed, which involves surgical decompression or external beam radiotherapy depending on spinal stability and tumor histology.

Step-by-Step Solution

Recognize the clinical syndrome of an oncologic emergency.

The patient has malignant epidural spinal cord compression (MESCC) with active neurologic deficits (paraparesis, sensory level, urinary retention).

History of metastatic prostate cancer combined with progressive back pain and rapidly evolving myelopathy is the classic presentation of MESCC.

Determine the most urgent initial therapeutic intervention.

Administer high-dose intravenous dexamethasone immediately.

Corticosteroids rapidly reduce peritumoral vasogenic edema and decrease pressure on the spinal cord. They must be given immediately to prevent permanent paralysis before any diagnostic imaging delays.

Identify the confirmatory diagnostic test.

Obtain an urgent MRI of the entire spine.

MRI is the gold standard to localize the compression. The entire spine must be imaged because up to 30% of these patients have multiple concurrent asymptomatic epidural metastases.

Formulate a definitive treatment plan.

Consult specialists, then proceed with surgery or radiation.

Once the anatomy is defined on MRI, a multidisciplinary team determines if the patient is best suited for surgical decompression or targeted external beam radiotherapy.

Key Concept

In patients with suspected malignant epidural spinal cord compression presenting with neurological deficits, systemic glucocorticoids must be administered immediately prior to confirmatory imaging to preserve neurologic function.

Estimated Time:1m 30s

Question 916Question →

A $34$ -year-old woman is brought to the emergency department by her partner due to confusion and difficulty speaking that began this morning. Over the past three days, she has experienced fatigue, generalized weakness, and subjective fever. She has no significant past medical history and takes no medications. Her temperature is $38.4^\circ\text{C}$ ( $101.1^\circ\text{F}$ ), blood pressure is $145/88\text{ mmHg}$ , pulse is $112/\text{min}$ , and respiratory rate is $18/\text{min}$ . Physical examination reveals scleral icterus and scattered petechiae over the lower extremities. Neurological examination is notable for fluctuating lethargy and expressive aphasia.

Laboratory studies show the following:

Laboratory Test	Result	Reference Range
Hemoglobin	$7.8\text{ g/dL}$	$12.0$ - $15.5\text{ g/dL}$
Mean corpuscular volume	$92\text{ fL}$	$80$ - $100\text{ fL}$
Platelets	$18,000/\text{mm}^3$	$150,000$ - $400,000/\text{mm}^3$
Leukocytes	$8,400/\text{mm}^3$	$4,500$ - $11,000/\text{mm}^3$
Blood urea nitrogen	$38\text{ mg/dL}$	$7$ - $18\text{ mg/dL}$
Serum creatinine	$2.4\text{ mg/dL}$	$0.6$ - $1.2\text{ mg/dL}$
Total bilirubin	$4.1\text{ mg/dL}$	$0.1$ - $1.2\text{ mg/dL}$
Indirect bilirubin	$3.2\text{ mg/dL}$	$0.1$ - $0.8\text{ mg/dL}$
Lactate dehydrogenase	$1,450\text{ U/L}$	$100$ - $250\text{ U/L}$
Prothrombin time	$13\text{ seconds}$	$11$ - $15\text{ seconds}$
Activated partial thromboplastin time	$32\text{ seconds}$	$25$ - $40\text{ seconds}$

A peripheral blood smear demonstrates numerous fragmented red blood cells. Which of the following is the most critical initial intervention for this patient?

Centrifugal separation of the patient's plasma and replacement with donor plasma

Transfusion of pooled donor apheresis platelets

Intravenous administration of broad-spectrum antimicrobial therapy

Intravenous infusion of pooled human immune globulin

Initiation of continuous venovenous hemofiltration

Show answer & explanation

Answer: Centrifugal separation of the patient's plasma and replacement with donor plasma

Answer

Centrifugal separation of the patient's plasma and replacement with donor plasma

The correct answer describes plasma exchange (plasmapheresis), which is the primary, life-saving treatment for Thrombotic Thrombocytopenic Purpura (TTP). TTP is a thrombotic microangiopathy typically caused by severely reduced activity of the von Willebrand factor (vWF)-cleaving protease ADAMTS13, most commonly due to an acquired autoantibody. This deficiency leads to the accumulation of ultra-large vWF multimers that consume platelets and form microthrombi in small blood vessels, causing diffuse end-organ ischemia. The classic pentad of TTP includes microangiopathic hemolytic anemia (MAHA), thrombocytopenia, acute kidney injury, neurologic changes, and fever. Immediate plasma exchange is therapeutic because it simultaneously removes the offending circulating ADAMTS13 autoantibodies and replenishes functional ADAMTS13 enzyme from the donor plasma.

Step-by-Step Solution

Analyze the clinical presentation and physical examination findings.

The patient presents with an acute onset of fever, altered mental status, expressive aphasia, and petechiae, indicating a systemic disease process involving the central nervous system and platelets.

Identifying the affected organ systems helps narrow the differential diagnosis for acute systemic illness.

Evaluate the laboratory values and peripheral blood smear.

Labs reveal severe thrombocytopenia, acute kidney injury, and non-immune hemolytic anemia (elevated LDH, indirect hyperbilirubinemia, and schistocytes). Coagulation studies (PT and aPTT) are strictly within normal limits.

Normal coagulation studies distinguish this microangiopathic process from Disseminated Intravascular Coagulation (DIC).

Synthesize the findings to formulate a definitive diagnosis.

The classic pentad of fever, neurological abnormalities, thrombocytopenia, microangiopathic hemolytic anemia, and renal insufficiency confirms the diagnosis of Thrombotic Thrombocytopenic Purpura (TTP).

Recognizing this pentad (or the essential dyad of MAHA and thrombocytopenia) is necessary to diagnose TTP, a true hematologic emergency.

Determine the most appropriate initial life-saving intervention.

Plasma exchange is the primary treatment, acting to remove the circulating ADAMTS13 autoantibodies and replenish the deficient functional enzyme.

Without immediate plasma exchange, mortality from TTP approaches 90% due to progressive organ ischemia.

Key Concept

Diagnosis and emergent management of Thrombotic Thrombocytopenic Purpura (TTP)

Question 917Question →

A 26-year-old man presents to the clinic with a 4-day history of a severely swollen, painful right knee, bilateral conjunctival injection, and pain at the left posterior heel. He reports having had a severe diarrheal illness three weeks ago after a camping trip. The patient's vital signs are within normal limits. Arrange the following diagnostic and therapeutic steps in the optimal chronological sequence for managing this patient's condition.

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Answer

The correct sequence of management for this patient begins with performing a diagnostic arthrocentesis to rule out joint infection. Once a sterile inflammatory fluid confirms the diagnosis of reactive arthritis, initial therapy with high-dose NSAIDs is started. If localized symptoms persist, intra-articular glucocorticoids are administered. Finally, if the disease becomes chronic (lasting more than 3-6 months), systemic therapy is escalated to DMARDs like sulfasalazine.

The correct sequence strictly follows the clinical algorithm for acute mono/oligoarthritis suspected to be reactive arthritis: immediate exclusion of a life-threatening or joint-destroying infection (arthrocentesis), formal diagnosis confirmation (sterile fluid + clinical triad), first-line systemic anti-inflammatory therapy (NSAIDs), step-up local therapy for refractory symptoms (intra-articular steroids), and long-term disease modification (DMARDs) if the condition becomes chronic.

Step-by-Step Solution

Perform diagnostic arthrocentesis of the right knee.

Evaluation of synovial fluid for cell count, Gram stain, and culture.

To definitively rule out septic arthritis, which is a critical diagnosis to exclude in any patient with a new-onset, acutely swollen joint.

Establish the clinical diagnosis of reactive arthritis.

Confirmation of the diagnosis based on the sterile inflammatory synovial fluid and the classic clinical features following an enteric infection.

Accurate diagnosis dictates the appropriate immunosuppressive or anti-inflammatory management pathway.

Initiate high-dose nonsteroidal anti-inflammatory drugs (NSAIDs).

Reduction of acute joint inflammation and symptomatic relief.

NSAIDs are the established first-line medical therapy for the acute phase of reactive arthritis.

Administer an intra-articular glucocorticoid injection.

Targeted suppression of localized inflammation in the right knee.

Indicated as step-up therapy when systemic NSAIDs provide inadequate relief for monoarticular or oligoarticular involvement.

Escalate to systemic disease-modifying antirheumatic drugs (DMARDs) such as sulfasalazine.

Long-term immune modulation and prevention of joint damage.

Indicated for the subset of patients whose reactive arthritis progresses to a chronic phase lasting beyond 3 to 6 months.

Key Concept

The sequential diagnostic and therapeutic pathway for reactive arthritis requires ruling out joint infection via arthrocentesis first, followed by step-wise medical management starting with NSAIDs, escalating to intra-articular steroids for refractory local disease, and utilizing DMARDs for chronic disease.

Question 918Question →

Match each clinical presentation with its most characteristic peripheral blood smear finding.

Click a left item, then click its matching right item

Show answer & explanation

Answer

The asymptomatic older male with marked lymphocytosis matches with fragile leukocyte remnants (smudge cells). The patient with pancytopenia and circulating blasts matches with linear azurophilic granules (Auer rods). The young man with sulfa-induced hemolysis matches with semicircular erythrocyte defects (bite cells). The woman with confusion, fever, acute kidney injury, and thrombocytopenia matches with mechanically sheared erythrocytes (schistocytes).

Peripheral blood smear evaluation is critical for distinguishing hematologic pathologies. Smudge cells indicate the fragile monoclonal B-cells of CLL. Auer rods are pathognomonic for myeloblasts in AML. Bite cells indicate splenic phagocytosis of oxidized hemoglobin seen in G6PD deficiency. Schistocytes represent the mechanical destruction of erythrocytes characteristic of microangiopathic hemolytic anemias like TTP.

Step-by-Step Solution

Evaluate the first vignette describing an asymptomatic elderly patient with significant incidental lymphocytosis.

Diagnose Chronic Lymphocytic Leukemia (CLL), which pairs with smudge cells due to the characteristic fragility of the malignant lymphocytes.

Identifying the classic demographic and lab presentation of CLL isolates its specific morphologic marker.

Analyze the second vignette featuring pancytopenia and circulating blasts in a middle-aged adult.

Diagnose Acute Myeloid Leukemia (AML), which pairs with Auer rods.

Auer rods are pathognomonic for myeloblasts in AML and help distinguish it from acute lymphoblastic leukemia (ALL).

Assess the third vignette involving acute hemolysis triggered by a sulfa antibiotic.

Diagnose Glucose-6-Phosphate Dehydrogenase (G6PD) deficiency, which pairs with bite cells (degmacytes).

Sulfa drugs induce oxidative stress in G6PD deficiency, causing Heinz body formation; splenic removal of these bodies produces bite cells.

Examine the final vignette showing the classic pentad of fever, neurologic changes, renal failure, and thrombocytopenia.

Diagnose Thrombotic Thrombocytopenic Purpura (TTP), which pairs with schistocytes.

TTP is a microangiopathic hemolytic anemia (MAHA) where microthrombi shear red blood cells as they pass through small vessels.

Key Concept

Recognizing the pathognomonic peripheral blood smear findings associated with highly tested hematologic and oncologic disorders.

Question 919Question →

A $52$ -year-old man is evaluated for persistent fever. He was admitted $20$ days ago for acute myeloid leukemia induction chemotherapy, which resulted in profound bone marrow suppression. Ten days ago, his absolute neutrophil count dropped to $50/\text{mm}^3$ and he developed a fever of $39.1^\circ\text{C}$ ( $102.4^\circ\text{F}$ ). Blood cultures were drawn, and empiric intravenous cefepime was initiated. He remained febrile, and $5$ days ago, intravenous vancomycin was added.

Today, his temperature is $38.6^\circ\text{C}$ ( $101.5^\circ\text{F}$ ). He reports new-onset right-sided pleuritic chest pain. His absolute neutrophil count remains at $50/\text{mm}^3$ . Repeated blood cultures drawn prior to the initiation of antibiotics and $5$ days ago have shown no growth. A non-contrast computed tomography scan of the chest reveals a $3\text{ cm}$ dense macronodule surrounded by a halo of ground-glass attenuation in the right upper lobe. Serum galactomannan testing is strongly positive, and intravenous voriconazole is initiated.

Which of the following is the most appropriate next step regarding this patient's antibacterial regimen?

Continue cefepime and discontinue vancomycin

Discontinue both cefepime and vancomycin

Continue both cefepime and vancomycin

Switch cefepime to meropenem and continue vancomycin

Continue vancomycin and discontinue cefepime

Show answer & explanation

Answer: Continue cefepime and discontinue vancomycin

Answer

Continue cefepime and discontinue vancomycin

The correct approach is to continue cefepime and discontinue vancomycin. This patient has febrile neutropenia complicated by a new diagnosis of invasive pulmonary aspergillosis. According to IDSA guidelines, in high-risk patients with profound neutropenia (ANC < 500/mm³), the initial empiric antipseudomonal beta-lactam (in this case, cefepime) must be continued until the ANC recovers to ≥ 500/mm³ and is trending upward. This is crucial because the patient remains at extreme risk for rapidly fatal Gram-negative bacterial sepsis, regardless of whether a secondary fungal pathogen has been identified as the source of the prolonged fever. Conversely, vancomycin is not recommended for routine empiric therapy in febrile neutropenia unless specific indications exist. When added empirically for persistent fever, it should be promptly discontinued if blood cultures remain negative after 48-72 hours. Since this patient's cultures have been negative for 5 days, continuing vancomycin represents poor antibiotic stewardship.

Step-by-Step Solution

Identify the cause of the patient's persistent fever and new symptoms.

The patient has developed invasive pulmonary aspergillosis, evidenced by the chest CT 'halo sign' and strongly positive serum galactomannan assay.

Establishing the etiology of the fever is necessary to determine the appropriate targeted antimicrobial therapy (voriconazole).

Determine the required duration of empiric Gram-negative antibacterial therapy in this host.

Cefepime must be continued until the absolute neutrophil count recovers to at least 500/mm³.

Patients with profound neutropenia remain at extreme risk for life-threatening Gram-negative sepsis (e.g., Pseudomonas aeruginosa) from endogenous flora. Guidelines mandate continuing the empiric antipseudomonal beta-lactam until marrow recovery, even when a secondary fungal infection is diagnosed.

Apply antibiotic stewardship principles to the empiric Gram-positive coverage.

Vancomycin should be discontinued immediately.

Vancomycin was added empirically for persistent fever. Because blood cultures have remained sterile after 5 days, there is no evidence of a Gram-positive infection. Continuing it increases toxicity and the risk of resistance.

Key Concept

In febrile neutropenia, empiric antipseudomonal beta-lactam therapy must be continued until marrow recovery (ANC ≥ 500/mm³), even if a specific fungal pathogen is identified. Empiric vancomycin should be discontinued if blood cultures remain negative after 48-72 hours.

Question 920Question →

A 62-year-old woman is evaluated in the emergency department for a 24-hour history of confusion and fever. She was brought from a skilled nursing facility where she is recovering from an ischemic stroke. Her medical history includes chronic obstructive pulmonary disease (COPD) and diet-controlled type 2 diabetes mellitus. Medications include aspirin and inhaled tiotropium.

Vital signs are temperature 38.6°C (101.5°F), blood pressure 82/50 mm Hg, pulse 122/min, and respirations 24/min. Pulse oximetry is 94% on room air.

Physical examination reveals a lethargic and disoriented patient. Mucous membranes are dry. Lung auscultation reveals mild, diffuse end-expiratory wheezing without crackles. Cardiac examination shows tachycardia with a regular rhythm. The abdomen is soft, but right costovertebral angle tenderness is present.

Laboratory results are as follows:
Leukocytes: 16,500/mm³ (15% bands)
Sodium: 138 mEq/L
Potassium: 4.8 mEq/L
Bicarbonate: 16 mEq/L
Creatinine: 2.1 mg/dL (baseline 0.9 mg/dL)
Lactate: 4.2 mmol/L
TSH: 0.1 mU/L (Normal 0.4-4.0 mU/L)
Free T4: 0.6 ng/dL (Normal 0.9-1.7 ng/dL)

Arterial blood gas on room air:
pH: 7.30
PaCO2: 32 mm Hg
PaO2: 78 mm Hg

A urine culture collected 2 days ago at the nursing facility for dysuria has just resulted, showing >100,000 CFU/mL of *Escherichia coli* sensitive to ceftriaxone, ciprofloxacin, and nitrofurantoin.

A chest radiograph shows hyperinflated lungs and flattened diaphragms with no focal consolidations or pulmonary venous congestion.

The patient is immediately started on intravenous ceftriaxone. Over the next 2 hours, she receives 3 liters of intravenous normal saline. Reassessment shows a blood pressure of 78/48 mm Hg and a pulse of 118/min.

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

Initiate intravenous norepinephrine

Switch antibiotic therapy to intravenous meropenem

Administer intravenous furosemide

Administer intravenous sodium bicarbonate

Initiate intravenous levothyroxine

Show answer & explanation

Answer: Initiate intravenous norepinephrine

Answer

Initiate intravenous norepinephrine

This patient is presenting with septic shock secondary to acute pyelonephritis. According to Surviving Sepsis Campaign guidelines, initial resuscitation for sepsis with hypotension or a lactate ≥ 4.0 mmol/L requires rapid administration of at least 30 mL/kg of intravenous crystalloids. This patient received 3 liters of normal saline (adequate for an average adult) but remains profoundly hypotensive with a blood pressure of 78/48 mm Hg (Mean Arterial Pressure [MAP] =

58

mm Hg). For fluid-refractory septic shock, the immediate next step is the initiation of vasopressors to maintain a MAP

\geq 65

mm Hg. Norepinephrine is the first-line vasopressor of choice.

Step-by-Step Solution

Diagnose the primary condition

The patient has septic shock secondary to pyelonephritis, evidenced by fever, CVA tenderness, leukocytosis, positive urine culture, lactic acidosis, and severe hypotension.

Identifying the etiology of the shock state is necessary to guide appropriate resuscitation and antimicrobial therapy.

Evaluate the response to initial therapy

The patient received 3 liters of intravenous crystalloid (standard 30 mL/kg fluid challenge for sepsis), but her blood pressure remains 78/48 mm Hg (MAP = 58 mm Hg).

Hemodynamic reassessment determines if the patient is fluid-responsive or fluid-refractory.

Determine the next pharmacological intervention

Initiate a vasopressor (norepinephrine) to achieve a target MAP of ≥ 65 mm Hg.

In fluid-refractory septic shock, vasopressors are indicated immediately after adequate fluid resuscitation to prevent prolonged organ hypoperfusion.

Key Concept

Management of fluid-refractory septic shock

Estimated Time:1m 30s

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