Internal Medicine

3151 questions

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

A 71-year-old woman is evaluated in the hospital during the night shift for acute-onset shortness of breath. She was admitted two days ago for acute pyelonephritis and has been receiving intravenous ceftriaxone alongside aggressive intravenous fluid resuscitation. Currently, she is visibly distressed and prefers to sit upright on the edge of the bed. Her temperature is 37.1°C (98.8°F), blood pressure is 158/92 mm Hg, pulse is 106/min, and respirations are 26/min. Pulse oximetry shows 88% on room air. Physical examination reveals prominent jugular venous distention. Lung auscultation demonstrates bilateral crackles extending to the mid-lung fields, with no wheezing. Cardiac examination reveals a regular rhythm, normal S1 and S2, and a distinct third heart sound (S3). There is 2+ bilateral lower extremity pitting edema. Which of the following is the most appropriate next step in management of this patient's current symptoms?

Intravenous furosemide

Inhaled albuterol

Intravenous piperacillin-tazobactam

Intravenous normal saline bolus

Oral metoprolol

Show answer & explanation

Answer: Intravenous furosemide

Answer

Intravenous furosemide

The correct answer is intravenous furosemide. This patient is presenting with classic signs of acute decompensated heart failure (ADHF) precipitated by aggressive intravenous fluid resuscitation. The combination of orthopnea (preferring to sit upright), hypoxia, jugular venous distention, bibasilar crackles, a distinct S3 gallop, and lower extremity edema strongly points to severe volume overload leading to acute pulmonary edema. The most appropriate initial step in management for ADHF with signs of volume overload is the administration of an intravenous loop diuretic, such as furosemide. This rapidly decreases intravascular volume, reduces ventricular preload, and relieves pulmonary congestion, thereby improving the patient's respiratory status.

Step-by-Step Solution

Analyze the clinical presentation and physical examination findings.

The patient presents with orthopnea, hypoxia, jugular venous distention, bibasilar crackles, and an S3 gallop after receiving aggressive intravenous fluids.

Identifying the constellation of signs and symptoms is necessary to determine the underlying etiology of the new-onset respiratory distress.

Establish the most likely diagnosis.

The clinical picture strongly indicates acute decompensated heart failure resulting from iatrogenic volume overload.

Distinguishing cardiogenic pulmonary edema from other causes of inpatient dyspnea directly guides the acute management.

Determine the most appropriate initial management.

Intravenous furosemide is selected as the initial treatment.

Loop diuretics are the first-line therapy to rapidly reduce intravascular volume and alleviate pulmonary congestion in acute decompensated heart failure.

Key Concept

Diagnosis and initial management of acute decompensated heart failure presenting with volume overload.

Estimated Time:1m 0s

Question 2582Question →

A $64$ -year-old man presents to the urgent care clinic due to a $3$ -day history of worsening shortness of breath. He reports that his baseline chronic cough has increased in frequency, and his sputum has changed from small amounts of clear mucus to copious amounts of thick, yellow-green phlegm. The patient has a history of severe chronic obstructive pulmonary disease (COPD) and uses daily inhaled tiotropium and as-needed albuterol. He smoked a pack of cigarettes daily for $40$ years but quit $2$ years ago. His temperature is $37.3^\circ\text{C}$ ( $99.1^\circ\text{F}$ ), blood pressure is $132/84\text{ mm Hg}$ , pulse is $92/\text{min}$ , and respiratory rate is $20/\text{min}$ . Pulse oximetry is $94\%$ on room air. He is speaking in full sentences and is in no acute distress. Lung auscultation reveals a prolonged expiratory phase with diffuse bilateral wheezing, but no crackles are heard. Cardiovascular examination shows no jugular venous distension and no lower extremity edema. The physician administers nebulized albuterol and ipratropium and prescribes a $5$ -day course of oral prednisone. Which of the following is the most appropriate additional step in management?

Prescribe oral azithromycin

Administer intravenous piperacillin-tazobactam

Administer intravenous vancomycin

Prescribe oral furosemide

Obtain an arterial blood gas to calculate expected respiratory compensation

Show answer & explanation

Answer: Prescribe oral azithromycin

Answer

Prescribe oral azithromycin

The correct step is to prescribe an oral antibiotic such as azithromycin. This patient is experiencing an acute exacerbation of chronic obstructive pulmonary disease (AECOPD). The standard outpatient management of AECOPD includes optimizing bronchodilator therapy (e.g., short-acting beta-agonists and muscarinic antagonists) and administering a short course of systemic glucocorticoids (e.g., oral prednisone) to reduce airway inflammation. Additionally, antibiotics are indicated when a patient has increased sputum purulence along with either increased dyspnea or increased sputum volume. Since this patient exhibits all three cardinal symptoms, an antibiotic is highly recommended to target common respiratory pathogens (e.g., Haemophilus influenzae, Moraxella catarrhalis, Streptococcus pneumoniae). A macrolide (azithromycin) or an advanced-generation cephalosporin is an appropriate, targeted choice for an uncomplicated outpatient exacerbation.

Step-by-Step Solution

Identify the patient's clinical syndrome.

The patient has an acute exacerbation of chronic obstructive pulmonary disease (AECOPD).

He presents with acute worsening of respiratory symptoms (dyspnea, cough, sputum changes) beyond normal day-to-day variations.

Assess the severity and cardinal symptoms to determine the need for antibiotics.

The patient has all three cardinal symptoms: increased dyspnea, increased sputum volume, and increased sputum purulence.

Current guidelines recommend antibiotics for AECOPD if the patient has all three cardinal symptoms, or two cardinal symptoms if one of them is increased sputum purulence.

Select the appropriate pharmacotherapy for a stable outpatient.

A narrow-spectrum oral antibiotic such as a macrolide (e.g., azithromycin) is the most appropriate choice.

The patient lacks risk factors for Pseudomonas aeruginosa or poor outcomes, so broad-spectrum intravenous antibiotics are not indicated.

Key Concept

Patients presenting with an uncomplicated acute exacerbation of COPD (AECOPD) who exhibit increased sputum purulence along with increased dyspnea and/or sputum volume should be treated with short-acting bronchodilators, systemic glucocorticoids, and a targeted oral antibiotic such as a macrolide.

Estimated Time:50s

Question 2583Question →

A 42-year-old woman is evaluated in the intensive care unit for persistent hypoxemia. She was admitted 3 days ago for severe acute pancreatitis and was intubated yesterday due to acute respiratory distress syndrome (ARDS). She is receiving a continuous intravenous infusion of fentanyl for analgesia and lactated Ringer solution. She has no other medical conditions.

The patient is sedated and paralyzed with a neuromuscular blocking agent.

Vital signs are temperature 37.9°C (100.2°F), pulse 118/min, and blood pressure 112/68 mm Hg.
Physical examination shows a jugular venous pressure of 6 cm H2O. Lung auscultation reveals bilateral diffuse crackles.

Hemodynamic monitoring shows a pulmonary capillary wedge pressure of 11 mm Hg and a cardiac index of 3.4 L/min/m2.

A chest radiograph demonstrates bilateral diffuse alveolar opacities.

Laboratory results are as follows:
Leukocyte count: 15,500/mm3
Thyroid-stimulating hormone (TSH): 1.1 µU/mL (Normal: 0.4–4.0 µU/mL)
Free T4: 0.6 ng/dL (Normal: 0.8–2.7 ng/dL)

A recent CT scan of the abdomen shows pancreatic necrosis without evidence of gas or infection. Blood cultures are sterile.

Arterial blood gas analysis on mechanical ventilation (Volume-assist control, Tidal volume 6 mL/kg ideal body weight, Respiratory rate 24/min, PEEP 8 cm H2O, FiO2 0.80):
pH: 7.30
pCO2: 52 mm Hg
pO2: 54 mm Hg
HCO3: 25 mEq/L

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

Increase the positive end-expiratory pressure

Administer intravenous furosemide

Administer intravenous sodium bicarbonate

Initiate intravenous meropenem

Administer intravenous levothyroxine

Show answer & explanation

Answer: Increase the positive end-expiratory pressure

Answer

Increase the positive end-expiratory pressure

The correct answer is to increase the positive end-expiratory pressure. This patient has Acute Respiratory Distress Syndrome (ARDS) secondary to severe acute pancreatitis. ARDS is characterized by severe hypoxemia (a

PaO_2/FiO_2

ratio < 300), bilateral alveolar opacities, and a normal pulmonary capillary wedge pressure indicating non-cardiogenic pulmonary edema. In ARDS, the primary driver of hypoxemia is extensive intrapulmonary shunting due to widespread alveolar collapse. Increasing PEEP recruits these collapsed alveoli, maintains them open at the end of expiration, increases the functional residual capacity, and improves ventilation-perfusion matching. According to standard ARDS Network protocols, a patient requiring an

FiO_2

of 0.80 should have their PEEP increased (typically to 14-20 cm

H_2O

) to optimize oxygenation and allow for a subsequent reduction in toxic oxygen levels.

Step-by-Step Solution

Identify the patient's primary condition based on the clinical presentation and data.

Severe hypoxemia (

PaO_2

54 mm Hg on 80%

FiO_2

) with bilateral lung opacities and a normal pulmonary capillary wedge pressure indicates Acute Respiratory Distress Syndrome (ARDS).

This establishes the framework for ventilator management.

Evaluate the current ventilator settings and the primary physiological deficit.

The patient is on a highly toxic

FiO_2

(0.80) but a relatively low PEEP (8 cm

H_2O

) for this degree of hypoxemia.

ARDS hypoxemia is driven by intrapulmonary shunting from alveolar collapse.

Determine the next best step to improve oxygenation.

Increasing the PEEP will recruit collapsed alveoli and improve ventilation-perfusion matching.

Standard ARDS Network protocols recommend upward titration of PEEP before increasing

FiO_2

to toxic levels.

Key Concept

In Acute Respiratory Distress Syndrome (ARDS), severe hypoxemia is managed by increasing Positive End-Expiratory Pressure (PEEP) to recruit collapsed alveoli, rather than excessively increasing

FiO_2

Estimated Time:1m 30s

Question 2584Question →

A 62-year-old man is evaluated in the intensive care unit for ongoing management of ventilator-associated pneumonia. He was intubated 6 days ago for severe acute respiratory distress syndrome. Three days ago, he developed a new fever, increased purulent endotracheal secretions, and worsening oxygenation. At that time, empiric intravenous vancomycin, cefepime, and ciprofloxacin were initiated. Today, his temperature is 37.2°C (99.0°F), leukocyte count has decreased from 16,000/mm³ to 9,500/mm³, and his oxygen requirements have significantly improved. Blood cultures have shown no growth. Endotracheal aspirate culture from three days ago grows Pseudomonas aeruginosa. Susceptibility testing shows the isolate is susceptible to cefepime, piperacillin-tazobactam, and ciprofloxacin. A methicillin-resistant Staphylococcus aureus (MRSA) nasal polymerase chain reaction screen performed on admission was negative, and no Gram-positive organisms are seen on the respiratory culture Gram stain. Which of the following is the most appropriate next step in antibiotic management?

Discontinue vancomycin and ciprofloxacin, and continue cefepime monotherapy

Discontinue vancomycin, and continue both cefepime and ciprofloxacin

Continue vancomycin, cefepime, and ciprofloxacin for a full 7-day course

Discontinue the current regimen and switch to intravenous meropenem

Discontinue cefepime and ciprofloxacin, and continue vancomycin monotherapy

Show answer & explanation

Answer: Discontinue vancomycin and ciprofloxacin, and continue cefepime monotherapy

Answer

Discontinue vancomycin and ciprofloxacin, and continue cefepime monotherapy

The most appropriate action is to discontinue vancomycin and ciprofloxacin, and continue cefepime monotherapy. This patient has ventilator-associated pneumonia (VAP) and is improving clinically. The respiratory culture has grown Pseudomonas aeruginosa susceptible to cefepime. The principles of antimicrobial stewardship dictate that broad-spectrum empiric therapy should be de-escalated to targeted therapy once microbiological data is available. Because there is no evidence of MRSA, vancomycin should be discontinued. Furthermore, routine double anti-pseudomonal coverage for definitive therapy is not recommended for patients who are clinically improving; a single active beta-lactam (like cefepime) is sufficient and minimizes toxicity.

Step-by-Step Solution

Evaluate the clinical response to empiric therapy.

The patient's temperature, leukocyte count, and oxygenation have all improved.

Clinical stability dictates whether de-escalation of antibiotics is safe.

Review microbiological data to target therapy.

Cultures isolate Pseudomonas aeruginosa susceptible to cefepime, with no evidence of MRSA.

Empiric broad-spectrum therapy must be narrowed to target the specific pathogen causing the infection.

Determine the optimal definitive antibiotic regimen.

Discontinue vancomycin (no MRSA) and ciprofloxacin (double coverage not needed), leaving cefepime monotherapy.

Guidelines recommend monotherapy for definitive treatment of susceptible P. aeruginosa in patients who are not in septic shock or at high risk for mortality.

Key Concept

De-escalation of empiric antimicrobial therapy in ventilator-associated pneumonia involves transitioning to targeted monotherapy based on culture susceptibilities and discontinuing unneeded empiric agents like MRSA coverage.

Question 2585Question →

A $72$ -year-old man is evaluated in the intensive care unit for worsening abdominal pain, progressive distension, and high fever. He was admitted $8$ days ago for a complicated urinary tract infection and has been receiving intravenous ceftriaxone. Three days ago, he developed profuse, watery diarrhea, which abruptly ceased this morning. His temperature is $39.1^\circ\text{C}$ ( $102.4^\circ\text{F}$ ), blood pressure is $82/50\text{ mmHg}$ , and pulse is $128\text{/min}$ . Physical examination reveals a markedly distended, tympanic abdomen with diffuse tenderness and absent bowel sounds.

Laboratory studies show:

Test	Result	Reference Range
Leukocyte count	$34,000\text{/mm}^3$	$4,000-11,000\text{/mm}^3$
Serum creatinine	$2.9\text{ mg/dL}$	$0.6-1.2\text{ mg/dL}$ (Baseline: $1.0\text{ mg/dL}$ )
Serum lactate	$4.5\text{ mmol/L}$	$0.5-1.0\text{ mmol/L}$

A stool nucleic acid amplification test is positive for *Clostridioides difficile*. A portable plain abdominal radiograph demonstrates a transverse colon diameter of $10.5\text{ cm}$ , loss of haustral markings, and no evidence of free air.

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

Enteral vancomycin and intravenous metronidazole

Intravenous vancomycin and enteral metronidazole

Enteral fidaxomicin monotherapy

Intravenous meropenem

Conservative management with nasogastric decompression and intravenous fluids

Show answer & explanation

Answer: Enteral vancomycin and intravenous metronidazole

Answer

The most appropriate next step in pharmacotherapy is the administration of enteral vancomycin and intravenous metronidazole.

This patient is presenting with fulminant *Clostridioides difficile* infection (CDI) complicated by an ileus and toxic megacolon. Fulminant CDI is characterized by severe systemic toxicity, manifesting as hypotension, shock, ileus, or megacolon. In the presence of a functional ileus—indicated by absent bowel sounds, abrupt cessation of diarrhea, and massive colonic dilation—orally administered antibiotics may not effectively transit to the colon. Therefore, the standard of care is combination therapy: high-dose enteral vancomycin (administered orally or via a nasogastric tube, frequently supplemented with vancomycin enemas) plus intravenous metronidazole. Intravenous metronidazole is uniquely beneficial because it is secreted directly from the bloodstream into the colonic mucosa, providing systemic coverage that complements the direct intraluminal effect of the enteral vancomycin.

Step-by-Step Solution

Assess the severity of the Clostridioides difficile infection.

The patient has fulminant disease, defined by hypotension (

82/50\text{ mmHg}

), shock (elevated lactate), severe leukocytosis (

34,000\text{/mm}^3

), and acute kidney injury.

Severity classification dictates the initial choice and route of antimicrobial therapy.

Identify complications modifying drug delivery.

The physical exam (absent bowel sounds, cessation of diarrhea) and radiograph (

10.5\text{ cm}

colonic dilation) indicate an ileus and toxic megacolon.

An ileus prevents orally administered medications from transiting effectively to the site of infection in the colon.

Select the appropriate targeted pharmacotherapy.

Dual therapy with enteral vancomycin (often given via nasogastric tube and supplemented by vancomycin enemas) combined with intravenous metronidazole is required.

IV metronidazole provides systemic delivery to the colonic mucosa, bypassing the ileus, while enteral vancomycin works intraluminally.

Key Concept

Management of fulminant Clostridioides difficile infection complicated by toxic megacolon

Question 2586Question →

Match the following classic liver biopsy histological findings to the most appropriate chronic hepatobiliary disorder.

Click a left item, then click its matching right item

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Answer

Autoimmune hepatitis matches with a lymphoplasmacytic infiltrate and interface hepatitis. Primary sclerosing cholangitis matches with concentric periductal 'onion-skin' fibrosis. Alpha-1 antitrypsin deficiency matches with PAS-positive, diastase-resistant globules. Hereditary hemochromatosis matches with extensive hemosiderin deposition. Primary biliary cholangitis matches with granulomatous destruction of interlobular bile ducts.

Definitive diagnosis of chronic hepatobiliary diseases often requires liver biopsy when clinical and serological findings are indeterminate or overlapping. Each of these five conditions presents with highly specific, defining histological features that distinguish them from one another.

Step-by-Step Solution

Evaluate the histological hallmark for autoimmune hepatitis.

Matched to lymphoplasmacytic infiltrate with prominent interface hepatitis.

The pathogenesis is driven by cell-mediated autoimmunity, leading to plasma cell predominance and inflammation spreading from the portal tracts into the parenchyma (interface hepatitis).

Evaluate the histological hallmark for primary sclerosing cholangitis.

Matched to concentric periductal fibrosis with an 'onion-skin' appearance.

Chronic inflammation leads to stricturing and obliterative fibrosis of both intrahepatic and extrahepatic bile ducts, classically forming concentric rings of fibrous tissue.

Evaluate the histological hallmark for alpha-1 antitrypsin deficiency.

Matched to periportal hepatocytes containing PAS-positive, diastase-resistant globules.

Misfolded alpha-1 antitrypsin protein polymerizes and becomes trapped in the hepatocyte endoplasmic reticulum, resisting breakdown by diastase.

Evaluate the histological hallmark for hereditary hemochromatosis.

Matched to extensive hemosiderin deposition primarily within hepatocytes.

A defect in the HFE gene causes excessive intestinal iron absorption, resulting in hepatic iron storage that can be visualized using a Prussian blue stain.

Evaluate the histological hallmark for primary biliary cholangitis.

Matched to florid duct lesions with granulomatous destruction of interlobular bile ducts.

The condition involves T-cell-mediated autoimmune granulomatous destruction specifically targeting the small, interlobular intrahepatic bile ducts.

Key Concept

Histological hallmarks of chronic and autoimmune liver diseases

Question 2587Question →

A 62-year-old man presents to the emergency department with sudden-onset, severe, tearing chest pain that radiates directly to his back between his scapulae. The pain started 30 minutes ago while he was watching television. His medical history is significant for poorly controlled essential hypertension and a 40-pack-year smoking history. His temperature is 37.0°C (98.6°F), blood pressure is 210/110 mm Hg in the right arm and 170/95 mm Hg in the left arm, heart rate is 112/min, and respiratory rate is 20/min. Physical examination reveals an early diastolic decrescendo murmur at the right upper sternal border. An electrocardiogram shows sinus tachycardia with no ischemic changes. A chest radiograph reveals a widened mediastinum. Based on the most likely diagnosis, arrange the following management steps in the most appropriate chronological sequence.

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Answer

The correct sequential order for managing suspected acute aortic dissection is to first initiate intravenous beta-blockade, followed by intravenous vasodilator therapy, then obtain confirmatory imaging, and finally obtain a surgical consultation for definitive repair.

The correct sequence prioritizes immediate anti-impulse therapy to prevent aortic rupture, followed by diagnostic confirmation, and ultimately definitive surgical management. Beta-blockers must explicitly precede vasodilators.

Step-by-Step Solution

Identify the clinical presentation as highly suspicious for an acute aortic dissection.

The patient has tearing chest pain, asymmetric blood pressures, a widened mediastinum, and a new aortic regurgitation murmur.

Recognizing the classic signs of aortic dissection is necessary to rapidly initiate life-saving anti-impulse therapy.

Determine the first priority in medical stabilization.

Heart rate must be lowered first using an intravenous beta-blocker (e.g., esmolol) to a target of < 60/min.

Beta-blockers decrease left ventricular contractility (dP/dt) and reduce the shear stress on the aortic wall, minimizing the chance of further dissection or rupture.

Determine the next step in medical stabilization.

Add an intravenous vasodilator (e.g., sodium nitroprusside) to lower systolic blood pressure to 100-120 mm Hg.

Vasodilators must only be given after beta-blockade to prevent reflex sympathetic activation and worsening of the dissection.

Determine the role of diagnostic imaging.

Safely transport the hemodynamically optimized patient to obtain a CTA of the chest.

Imaging is necessary to confirm the diagnosis and classify the extent of the dissection (Stanford Type A vs. Type B).

Determine the definitive treatment based on presentation.

Consult cardiothoracic surgery.

The early diastolic murmur indicates aortic valve involvement (Stanford Type A), which requires emergent operative repair.

Key Concept

In acute aortic dissection, medical therapy must be sequenced with intravenous beta-blockers administered before vasodilators to prevent reflex tachycardia and increased aortic shear stress, followed by confirmatory imaging and appropriate surgical management.

Estimated Time:1m 30s

Question 2588Question →

Match each clinical presentation of dysphagia and chest pain to its most characteristic high-resolution esophageal manometry finding.

Click a left item, then click its matching right item

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Answer

Systemic sclerosis pairs with absent peristalsis and diminished LES pressure; Achalasia pairs with absent peristalsis and incomplete LES relaxation; Diffuse esophageal spasm pairs with premature simultaneous contractions; Hypercontractile esophagus pairs with high-amplitude coordinated contractions.

Esophageal motility disorders frequently present with overlapping symptoms of dysphagia, regurgitation, and non-cardiac chest pain. High-resolution manometry is the gold standard for differentiating these conditions based on two primary metrics: peristaltic integrity (coordination and amplitude) and lower esophageal sphincter (LES) dynamics (resting pressure and relaxation). Systemic sclerosis causes smooth muscle fibrosis leading to a weak LES; achalasia is caused by neuronal degeneration leading to a non-relaxing LES; diffuse esophageal spasm causes uncoordinated contractions; and hypercontractile esophagus causes excessively strong but coordinated contractions.

Step-by-Step Solution

Diagnose the underlying condition for each clinical vignette based on the provided symptoms and physical findings.

The vignettes represent systemic sclerosis (CREST syndrome features), achalasia, diffuse esophageal spasm (DES), and hypercontractile esophagus, respectively.

Accurate clinical diagnosis is a prerequisite for anticipating the expected diagnostic test findings on high-resolution manometry.

Correlate each diagnosed motility disorder with its specific pathophysiologic mechanism and manometric pattern.

Systemic sclerosis = hypotensive LES + aperistalsis. Achalasia = failure of LES relaxation + aperistalsis. DES = premature simultaneous contractions. Hypercontractile esophagus = high-amplitude peristaltic contractions.

High-resolution manometry directly measures the specific neuromuscular deficits responsible for each condition's symptoms.

Key Concept

Pathophysiology and manometric findings of esophageal motility disorders

Question 2589Question →

Match each etiology of thyrotoxicosis to its characteristic laboratory and radioactive iodine uptake (RAIU) diagnostic profile.

Click a left item, then click its matching right item

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Answer

Graves disease matches with diffusely increased RAIU; Exogenous thyroid hormone matches with decreased RAIU and decreased thyroglobulin; Subacute thyroiditis matches with decreased RAIU and increased thyroglobulin; Toxic multinodular goiter matches with heterogeneous (patchy) increased RAIU.

The matching correctly pairs each underlying pathophysiology with its diagnostic hallmark. RAIU maps the gland's synthetic activity, separating hyper-synthesizing disorders from destructive/exogenous ones. Thyroglobulin further differentiates endogenous destructive processes (high) from exogenous hormone suppression (low).

Step-by-Step Solution

Confirm the presence of thyrotoxicosis.

All profiles demonstrate decreased TSH and increased Free T4.

This establishes the primary biochemical state before differentiating the underlying cause.

Evaluate the radioactive iodine uptake (RAIU) pattern.

RAIU distinguishes conditions with increased hormone synthesis (high uptake) from those with hormone release/exogenous sources (low uptake).

High/normal uptake points to Graves or toxic nodular disease. Low uptake points to thyroiditis, iodine load, or exogenous sources.

Differentiate high RAIU conditions by uptake distribution.

Diffuse uptake indicates Graves disease, whereas patchy/heterogeneous uptake indicates toxic multinodular goiter.

Graves involves global gland stimulation by antibodies, whereas TMNG involves localized autonomous nodules.

Differentiate low RAIU conditions using serum thyroglobulin.

High thyroglobulin indicates thyroiditis (follicular destruction), whereas low thyroglobulin indicates exogenous intake.

Thyroglobulin is co-secreted with endogenous thyroid hormone. Its absence confirms the thyrotoxicosis is from an external source.

Key Concept

Differentiation of thyrotoxicosis etiologies using radioactive iodine uptake (RAIU) and serum thyroglobulin levels.

Estimated Time:1m 30s

Question 2590Question →

A 68-year-old man with a history of type 2 diabetes mellitus is brought to the emergency department by his daughter due to progressive confusion and lethargy over the past three days. He recently had a mild upper respiratory infection. On physical examination, his temperature is $37.2^\circ\text{C}$ ( $99.0^\circ\text{F}$ ), blood pressure is $95/60\text{ mm Hg}$ , and heart rate is $118/\text{min}$ . The patient appears lethargic and has dry mucous membranes with delayed capillary refill.

Laboratory results are as follows:

Serum sodium: $132 \text{ mEq/L}$
Serum potassium: $3.1 \text{ mEq/L}$
Serum chloride: $98 \text{ mEq/L}$
Serum bicarbonate: $22 \text{ mEq/L}$
Blood urea nitrogen: $48 \text{ mg/dL}$
Serum creatinine: $1.9 \text{ mg/dL}$
Serum glucose: $940 \text{ mg/dL}$
Arterial blood gas (room air): pH $7.35$ , pCO $_2$ $40 \text{ mm Hg}$ , pO $_2$ $88 \text{ mm Hg}$

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

Initiation of normal saline and potassium chloride

Initiation of normal saline and continuous intravenous regular insulin

Initiation of normal saline, potassium chloride, and continuous intravenous regular insulin

Initiation of half-normal saline and continuous intravenous regular insulin

Initiation of normal saline and intravenous sodium bicarbonate

Show answer & explanation

Answer: Initiation of normal saline and potassium chloride

Answer

Initiation of normal saline and potassium chloride

This patient presents with Hyperosmolar Hyperglycemic State (HHS), characterized by extreme hyperglycemia, hyperosmolality, dehydration, and altered mental status without severe acidosis. The initial management of both HHS and Diabetic Ketoacidosis (DKA) focuses on aggressive fluid resuscitation with isotonic (

0.9\%

) normal saline to restore intravascular volume and tissue perfusion. Simultaneously, electrolyte levels, particularly potassium, must be carefully assessed before starting insulin. Although patients often have a total body potassium deficit due to osmotic diuresis, serum potassium levels can appear falsely normal or elevated due to extracellular shifts caused by insulin deficiency and hypertonicity. In this patient, the serum potassium is already markedly low at

3.1 \text{ mEq/L}

. Administering insulin will drive potassium back into the cells, further lowering the serum level and risking life-threatening complications such as cardiac arrhythmias and respiratory muscle weakness. Therefore, the strict guideline is to withhold insulin if serum potassium is

< 3.3 \text{ mEq/L}

. The appropriate next step is to initiate vigorous hydration with normal saline and add intravenous potassium chloride until the potassium level definitively rises above

3.3 \text{ mEq/L}

, at which point insulin can be safely introduced.

Step-by-Step Solution

Diagnose the primary condition based on clinical presentation and laboratory results.

The patient has Hyperosmolar Hyperglycemic State (HHS).

Characterized by severe hyperglycemia (glucose > 600 mg/dL), hyperosmolality, and altered mental status without significant ketoacidosis (normal pH, normal bicarbonate).

Evaluate the patient's fluid status and electrolyte derangements.

The patient has significant volume depletion (hypotension, tachycardia, acute kidney injury) and severe hypokalemia (potassium < 3.3 mEq/L).

Osmotic diuresis from extreme hyperglycemia leads to profound total body water and electrolyte deficits, including potassium.

Determine the sequence of therapeutic interventions.

Administer intravenous normal saline and potassium chloride, but strictly hold insulin.

Insulin therapy drives potassium intracellularly. Giving insulin when serum potassium is < 3.3 mEq/L can cause fatal arrhythmias or respiratory muscle paralysis.

Key Concept

In the management of DKA and HHS, insulin must be held if serum potassium is below

3.3 \text{ mEq/L}

to prevent life-threatening hypokalemia. Fluid resuscitation and potassium replacement are the immediate priorities.

Question 2591Question →

A 52-year-old man is brought to the emergency department by his wife due to a 24-hour history of severe generalized headache, high fever, and progressive confusion. His temperature is 39.4°C (102.9°F), blood pressure is 142/88 mmHg, and heart rate is 112/min. On physical examination, he is lethargic and oriented only to person. Neck flexion produces involuntary hip and knee flexion. Ophthalmoscopic examination reveals bilateral optic disc swelling with blurred margins. Arrange the following management steps in the most appropriate chronological order for this patient.

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Answer

The correct sequence is: Obtain peripheral blood cultures, followed by administration of empiric intravenous antibiotics and dexamethasone, followed by a non-contrast CT scan of the head, and finally a lumbar puncture.

The correct sequence prioritizes life-saving interventions while minimizing procedural risks. Blood cultures are drawn first to optimize pathogen detection. Because the patient has papilledema and altered mental status (red flags for elevated intracranial pressure), a lumbar puncture cannot be safely performed without first obtaining a CT scan of the head to rule out a focal mass lesion. However, the time required to complete the CT scan would cause an unacceptable delay in therapy; therefore, empiric antibiotics and dexamethasone must be administered immediately after blood cultures are obtained and before the patient is sent to the radiology department. Once the CT scan confirms the absence of a mass effect, a lumbar puncture can be safely performed to analyze the cerebrospinal fluid.

Step-by-Step Solution

Identify the primary diagnosis and recognize high-risk features.

The patient has signs of bacterial meningitis (fever, headache, confusion, positive Brudzinski sign) along with signs of elevated intracranial pressure (papilledema, altered mental status).

Recognizing elevated intracranial pressure is critical because it dictates that a CT scan must be performed before a lumbar puncture to prevent uncal or tonsillar herniation.

Determine the timing of antimicrobial therapy relative to diagnostic imaging.

Antibiotics and corticosteroids must be given prior to the CT scan and lumbar puncture.

Delaying antibiotics for imaging in suspected bacterial meningitis significantly increases mortality and neurologic morbidity.

Establish the sequence for initial blood tests and therapy.

Blood cultures are drawn just before antibiotic administration.

This maximizes the diagnostic yield from the blood cultures without causing a clinically significant delay in antibiotic administration.

Key Concept

In patients with suspected bacterial meningitis who have indications for a CT scan prior to lumbar puncture (e.g., papilledema, altered mental status, focal neurologic deficits), empiric antibiotics and dexamethasone must be administered immediately after blood cultures are drawn and before the CT scan is performed.

Estimated Time:1m 0s

Question 2592Question →

Emergency medical services bring a 58-year-old male to the emergency department due to the abrupt onset of excruciating, tearing chest pain radiating to his interscapular region. He has a history of poorly controlled hypertension. Vital signs show a blood pressure of $215/115$ mm Hg in his right arm and $180/95$ mm Hg in his left arm. His heart rate is $112$ /min. Physical examination reveals a faint early diastolic decrescendo murmur at the right upper sternal border. An initial portable chest radiograph demonstrates a widened mediastinum.

Arrange the following management steps in the optimal chronological sequence to minimize the risk of catastrophic complications and ensure appropriate definitive care.

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Show answer & explanation

Answer

The correct sequence is: 1) Initiate an intravenous beta-blocker, 2) Initiate an intravenous vasodilator, 3) Obtain urgent CTA of the aorta, and 4) Transfer to the operating room for emergent surgical repair.

The management of an acute aortic dissection prioritizes hemodynamic stabilization to prevent propagation of the intimal tear, followed by definitive diagnosis and surgical intervention. Intravenous beta-blockers must be administered first to lower the heart rate to approximately

60

/min and decrease the rate of rise of left ventricular pressure (dP/dt), which reduces aortic wall shear stress. Only after adequate beta-blockade is achieved should an intravenous vasodilator be administered to lower the systolic blood pressure to a target of

100-120

mm Hg. Once the patient is medically stabilized, urgent CTA is performed to confirm the diagnosis and delineate the anatomy. Because this patient has signs of a Stanford Type A dissection (aortic regurgitation murmur, right arm blood pressure discrepancy), emergent surgical repair is the final, definitive step.

Step-by-Step Solution

Identify the suspected diagnosis

Acute Stanford Type A aortic dissection

The patient presents with tearing chest pain, asymmetric blood pressures, a murmur of aortic regurgitation, and a widened mediastinum.

Determine the first pharmacological intervention

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

Reduces heart rate and left ventricular dP/dt, minimizing shear stress on the aortic wall and preventing propagation of the dissection flap.

Determine the second pharmacological intervention

Administer an intravenous vasodilator (e.g., nitroprusside)

Given strictly after beta-blockade to reduce systolic blood pressure to

100-120

mm Hg. Giving it beforehand would cause reflex tachycardia and increase shear stress.

Determine the appropriate diagnostic imaging

Perform computed tomography angiography (CTA) of the aorta

Once the patient is hemodynamically stabilized, noninvasive imaging is required to define the exact anatomy and extent of the dissection for surgical planning.

Determine the definitive treatment

Transfer to the operating room for surgical repair

Type A dissections have a high mortality rate due to rupture and tamponade, requiring emergent surgical intervention.

Key Concept

Chronological management of acute aortic dissection (anti-impulse therapy followed by imaging and surgery)

Estimated Time:1m 30s

Question 2593Question →

A 64-year-old man arrives at the emergency department via ambulance with sudden-onset, severe "tearing" chest pain that radiates to his back. His blood pressure is 215/115 mm Hg in the right arm and 175/95 mm Hg in the left arm. His heart rate is 118/min and regular. Physical examination reveals a new early diastolic decrescendo murmur at the right upper sternal border. An electrocardiogram shows sinus tachycardia and voltage criteria for left ventricular hypertrophy. Chest radiography demonstrates a widened mediastinum. The clinical team suspects an acute type A aortic dissection. Arrange the following steps in the correct order for the most appropriate management of this patient.

Drag items to arrange them in the correct order

Show answer & explanation

Answer

The correct sequence is: 1) Administer an intravenous beta-blocker, 2) Administer an intravenous vasodilator, 3) Obtain a computed tomography (CT) angiography, 4) Consult cardiothoracic surgery.

The management of an acute aortic dissection requires strict, stepwise coordination. The absolute first priority is medical stabilization (anti-impulse therapy). An intravenous beta-blocker is administered first to decrease heart rate (target < 60/min) and reduce left ventricular contractility (dP/dt), which lowers the shear stress on the aortic wall. Once the heart rate is controlled, an intravenous vasodilator is added if the systolic blood pressure remains elevated above the target of 100-120 mm Hg. Following hemodynamic stabilization, definitive imaging with CT angiography is performed to confirm the diagnosis and map the anatomy. Finally, because this patient has signs of ascending aorta involvement (Type A) indicated by the new aortic regurgitation murmur, emergent cardiothoracic surgical repair is required.

Step-by-Step Solution

Administer intravenous esmolol.

Heart rate and left ventricular contractility are reduced.

Decreases aortic wall shear stress and prevents dissection propagation; this must strictly precede vasodilators to prevent reflex tachycardia.

Administer intravenous sodium nitroprusside.

Systolic blood pressure is further reduced to a target of 100-120 mm Hg.

Provides additional blood pressure control to minimize aortic wall stress, only after the heart rate is adequately lowered.

Perform CT angiography of the chest.

The presence, type, and extent of the aortic dissection are confirmed.

Definitive imaging is required to differentiate a Stanford Type A from a Type B dissection and map the anatomy for surgical planning.

Consult cardiothoracic surgery.

The patient is taken for emergent surgical repair.

Type A aortic dissections (involving the ascending aorta, as suggested by the aortic regurgitation murmur) carry a high risk of fatal complications like rupture and require immediate surgery.

Key Concept

The stepwise management of acute aortic dissection (anti-impulse therapy sequencing).

Question 2594Question →

During morning rounds on the inpatient hematology-oncology unit, a 42-year-old woman is evaluated for a new-onset fever. She was admitted seven days ago for induction chemotherapy to treat acute myeloid leukemia. Her temperature is 38.9°C (102.0°F), blood pressure is 118/74 mm Hg, pulse is 92/min, and respiratory rate is 16/min. The patient reports feeling fatigued but denies cough, dysuria, abdominal pain, or skin changes. Physical examination reveals a clean peripherally inserted central catheter site with no surrounding erythema, warmth, or induration. The lungs are clear to auscultation. Laboratory studies show a hemoglobin of 8.2 g/dL, platelet count of 45,000/mm³, and an absolute neutrophil count of 300/mm³. Renal and hepatic function panels are within normal limits. Blood and urine cultures have been obtained. Which of the following is the most appropriate initial pharmacotherapy for this patient?

Intravenous cefepime

Intravenous cefepime and vancomycin

Intravenous ceftriaxone and azithromycin

Intravenous vancomycin and fluconazole

Oral ciprofloxacin and amoxicillin-clavulanate

Show answer & explanation

Answer: Intravenous cefepime

Answer

Intravenous cefepime

The most appropriate initial therapy for high-risk febrile neutropenia is monotherapy with an intravenous antipseudomonal beta-lactam, such as cefepime, meropenem, or piperacillin-tazobactam. This patient is at high risk due to induction chemotherapy for acute myeloid leukemia. Her clinical presentation lacks indications for empiric MRSA coverage (e.g., hemodynamic instability, pneumonia, or signs of a catheter site infection), making monotherapy the standard of care.

Step-by-Step Solution

Identify the primary clinical syndrome.

The patient has neutropenic fever, defined by a single oral temperature of ≥ 38.3°C (101.0°F) and an absolute neutrophil count (ANC) < 500/mm³.

Recognizing febrile neutropenia is critical as it is a medical emergency requiring prompt empiric antibiotics.

Risk-stratify the patient to determine the required route and setting of therapy.

The patient is classified as high-risk because she is an inpatient undergoing induction chemotherapy for acute myeloid leukemia, which typically results in prolonged and profound neutropenia.

High-risk patients require hospital admission (or continued hospitalization) and intravenous broad-spectrum antibiotics.

Select the appropriate empiric antimicrobial regimen based on risk and clinical signs.

Intravenous antipseudomonal beta-lactam monotherapy (e.g., cefepime) is selected.

There are no indications to add Gram-positive/MRSA coverage (such as hemodynamic instability, catheter-site infection, or pneumonia). Adding vancomycin unnecessarily violates antibiotic stewardship principles.

Key Concept

High-risk febrile neutropenia must be treated empirically with an intravenous antipseudomonal beta-lactam; routine addition of vancomycin is not indicated unless specific criteria for MRSA coverage are present.

Question 2595Question →

A 34-year-old man is brought to the emergency department by emergency medical services after his partner witnessed him having an episode of rhythmic limb jerking and loss of consciousness lasting approximately 5 minutes. On arrival, he is deeply lethargic and only moans to painful stimuli. His temperature is $37.2^\circ\text{C}$ ( $99.0^\circ\text{F}$ ), blood pressure is $118/76$ mmHg, pulse is $112$ /min, and respirations are $12$ /min. Physical examination reveals a laceration on the lateral aspect of his tongue and generalized muscle tenderness.

Laboratory studies show:
Sodium: $140$ mEq/L
Potassium: $4.6$ mEq/L
Chloride: $104$ mEq/L
Bicarbonate: $12$ mEq/L
Blood urea nitrogen: $16$ mg/dL
Creatinine: $1.1$ mg/dL
Glucose: $118$ mg/dL

Arterial blood gas (room air):
pH: $7.17$
pCO $_2$ : $34$ mmHg
pO $_2$ : $78$ mmHg

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

High anion gap metabolic acidosis with appropriate respiratory compensation

High anion gap metabolic acidosis and concurrent respiratory alkalosis

High anion gap metabolic acidosis and concurrent respiratory acidosis

High anion gap metabolic acidosis and concurrent normal anion gap metabolic acidosis

Normal anion gap metabolic acidosis and concurrent respiratory acidosis

Show answer & explanation

Answer: High anion gap metabolic acidosis and concurrent respiratory acidosis

Answer

High anion gap metabolic acidosis and concurrent respiratory acidosis

The correct answer accurately synthesizes the laboratory data. First, the patient has an acidemia (pH 7.17) driven by a low bicarbonate (12 mEq/L), indicating a primary metabolic acidosis. The anion gap is calculated as

140 - (104 + 12) = 24

, confirming a high anion gap metabolic acidosis, which is classically seen following generalized tonic-clonic seizures due to intense muscle exertion producing lactic acid. Next, appropriate respiratory compensation must be evaluated using Winter's formula:

pCO_2 = (1.5 \times 12) + 8 \pm 2 = 26 \pm 2

mmHg. The patient's measured pCO2 is 34 mmHg. Since the measured pCO2 is higher than the expected range of 24-28 mmHg, the patient has a concurrent, superimposed respiratory acidosis. This is clinically consistent with the patient's low respiratory rate of 12/min and deep lethargy, representing a post-ictal depression of the central respiratory drive.

Step-by-Step Solution

Determine the primary acid-base disorder by looking at the pH and bicarbonate.

The pH is 7.17 (acidemia) and the bicarbonate is 12 mEq/L (low), which indicates a primary metabolic acidosis.

Establishing the primary disturbance directs the choice of subsequent diagnostic formulas.

Calculate the serum anion gap using the formula:

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

AG = 140 - (104 + 12) = 140 - 116 = 24

. The normal range is typically 10-14, so this is a high anion gap metabolic acidosis.

Determining the anion gap identifies the cause of the metabolic acidosis (e.g., lactic acidosis from the recent seizure).

Calculate the expected respiratory compensation using Winter's formula:

Expected\ pCO_2 = (1.5 \times HCO_3^-) + 8 \pm 2

Expected\ pCO_2 = (1.5 \times 12) + 8 \pm 2 = 18 + 8 \pm 2 = 26 \pm 2

mmHg. The expected pCO2 range is 24 to 28 mmHg.

Winter's formula determines if the respiratory system has appropriately compensated for the primary metabolic acidosis.

Compare the expected pCO2 to the measured pCO2 on the arterial blood gas.

The measured pCO2 is 34 mmHg, which is significantly higher than the expected range of 24-28 mmHg.

Because the measured pCO2 is higher than the expected compensatory range, the patient is retaining carbon dioxide (likely due to a post-ictal depressed respiratory drive), indicating a concurrent respiratory acidosis.

Key Concept

Interpretation of a mixed acid-base disorder requires calculating the anion gap to identify unmeasured anions and applying Winter's formula to determine if respiratory compensation for a metabolic acidosis is appropriate.

Question 2596Question →

Emergency medical responders rush a $62$ -year-old male to the trauma bay for abrupt-onset dyspnea, left-sided pleuritic chest pain, and near-syncope that began two hours ago. The patient arrived yesterday from a transpacific business trip. His past medical history includes essential hypertension and hypercholesterolemia. Initial assessment reveals a blood pressure of $82/50$ mm Hg, a heart rate of $134$ /min, and a respiratory rate of $32$ /min. Pulse oximetry displays an oxygen saturation of $86\%$ despite administration of high-flow supplemental oxygen. Physical examination is notable for prominent jugular venous distention and a palpable parasternal heave. Auscultation of the lungs is unremarkable. An expedited point-of-care echocardiogram is performed, showing marked right ventricular enlargement, interventricular septal bowing into the left ventricle, and severe hypokinesis of the right ventricular free wall with relative apical sparing.

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

Select all that apply

Administer intravenous alteplase

Initiate a norepinephrine infusion

Administer intravenous furosemide

Administer intravenous sodium bicarbonate

Initiate empirical intravenous vancomycin and cefepime

Show answer & explanation

Answer: Administer intravenous alteplase; Initiate a norepinephrine infusion

Answer

The correct interventions are to administer intravenous alteplase and initiate a norepinephrine infusion.

The clinical vignette describes a patient with a massive pulmonary embolism, characterized by sudden-onset dyspnea, clear lungs, right ventricular strain, and hemodynamic instability (obstructive shock). For massive pulmonary embolism, the administration of systemic thrombolytics (such as alteplase) is the standard of care to rapidly dissolve the clot, reduce pulmonary vascular resistance, and relieve right ventricular afterload. Concurrently, vasopressor support is necessary to maintain systemic blood pressure and right ventricular perfusion; a norepinephrine infusion is the preferred agent as it increases systemic vascular resistance without excessively overdistending the right ventricle.

Step-by-Step Solution

Analyze the patient's clinical presentation and bedside imaging.

The patient has sudden-onset dyspnea, hypotension, jugular venous distention, clear lungs, and McConnell's sign on echocardiogram following prolonged immobilization.

These findings confirm a massive (hemodynamically unstable) pulmonary embolism causing acute right ventricular failure and obstructive shock.

Determine the indication for reperfusion therapy.

Select intravenous alteplase.

Systemic thrombolysis is the standard of care for massive pulmonary embolism to rapidly relieve the pulmonary artery obstruction and decrease right ventricular afterload.

Select the appropriate hemodynamic support.

Select norepinephrine infusion.

Norepinephrine increases systemic vascular resistance, maintaining right ventricular perfusion pressure without excessively overdistending the right ventricle, which is superior to aggressive fluid loading.

Key Concept

Management of massive pulmonary embolism requires immediate hemodynamic support with vasopressors (e.g., norepinephrine) and rapid reduction of right ventricular afterload via systemic thrombolysis (e.g., alteplase) or embolectomy.

Question 2597Question →

A 62-year-old man with a history of alcohol-related cirrhosis is brought to the emergency department by his family due to worsening confusion and increased abdominal swelling over the past 3 days. His temperature is 38.2°C (100.8°F), pulse is 98/min, and blood pressure is 100/60 mm Hg. Physical examination reveals scleral icterus and a distended abdomen with a positive fluid wave. There is diffuse, mild abdominal tenderness without rebound or guarding. Neurologic examination shows bilateral asterixis. Laboratory studies show a serum albumin of 2.5 g/dL and creatinine of 1.4 mg/dL. A diagnostic paracentesis is performed, yielding cloudy fluid with the following analysis:

Parameter	Value
Total protein	1.1 g/dL
Albumin	0.5 g/dL
Leukocyte count	700/mm³
Neutrophils	60%

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

Intravenous cefotaxime

Intravenous piperacillin-tazobactam

Intravenous vancomycin

Oral rifaximin and lactulose

Urgent exploratory laparotomy

Show answer & explanation

Answer: Intravenous cefotaxime

Answer

Intravenous cefotaxime

The most appropriate next step in management is the administration of an intravenous third-generation cephalosporin, such as cefotaxime. This patient with a history of cirrhosis presents with fever, abdominal pain, and altered mental status (hepatic encephalopathy), which are hallmark clinical signs of spontaneous bacterial peritonitis (SBP). The diagnosis of SBP is established when the absolute polymorphonuclear (PMN) cell count in the ascitic fluid is

\geq 250\text{/mm}^3

. In this scenario, the PMN count is calculated by multiplying the total leukocyte count by the neutrophil percentage (

700 \times 0.60 = 420\text{/mm}^3

). Because SBP is most frequently caused by enteric Gram-negative organisms (such as *Escherichia coli* and *Klebsiella pneumoniae*) and occasionally Gram-positive organisms (such as *Streptococcus pneumoniae*), empiric therapy with an intravenous third-generation cephalosporin provides the optimal targeted antimicrobial coverage and achieves excellent concentrations in the ascitic fluid.

Step-by-Step Solution

Analyze the ascitic fluid results to calculate the absolute polymorphonuclear (PMN) cell count.

The PMN count is calculated by multiplying the total leukocyte count by the percentage of neutrophils (

700 \times 0.60 = 420\text{/mm}^3

An absolute PMN count is required to differentiate sterile ascites from infected ascites.

Interpret the PMN count in the clinical context of a patient with cirrhosis, ascites, fever, and encephalopathy.

A PMN count

\geq 250\text{/mm}^3

establishes the diagnosis of Spontaneous Bacterial Peritonitis (SBP).

SBP is a severe infection of ascitic fluid without an obvious intra-abdominal surgically treatable source, commonly triggering hepatic encephalopathy.

Select the appropriate evidence-based empiric pharmacotherapy for SBP.

An intravenous third-generation cephalosporin, such as cefotaxime, is the treatment of choice.

This class provides excellent coverage against the most common causative organisms, which are enteric Gram-negative bacteria (e.g., E. coli, Klebsiella).

Key Concept

Spontaneous bacterial peritonitis (SBP) is diagnosed by an ascitic fluid absolute polymorphonuclear (PMN) cell count of

\geq 250\text{/mm}^3

and requires prompt empiric therapy with an intravenous third-generation cephalosporin.

Question 2598Question →

Emergency medical services bring a $61$ -year-old woman to the resuscitation bay immediately after she collapsed at home. She regained consciousness after a few minutes but currently complains of severe, abrupt-onset dyspnea and right-sided chest pain. Her surgical history is notable for an uncomplicated right total hip arthroplasty performed three weeks ago.

Vital signs are temperature $37.9^{\circ}$ C ( $100.2^{\circ}$ F), blood pressure $72/46$ mmHg, heart rate $134$ /min, and respiratory rate $28$ /min. Oxygen saturation is $85\%$ on ambient air. Physical examination shows elevated jugular venous pressure and a loud pulmonary component of the second heart sound ( $P_2$ ). The lungs are clear to auscultation bilaterally. The right calf exhibits mild asymmetric edema.

A rapid bedside echocardiogram reveals severe right ventricular dilation with marked hypokinesis of the free wall and normal apical contractility.

Arterial blood gas analysis on ambient air shows:

pH: $7.22$
$PaCO_2$ : $28$ mmHg
$PaO_2$ : $54$ mmHg
$HCO_3^-$ : $11$ mEq/L

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

Administer intravenous alteplase

Transport the patient for computed tomography pulmonary angiography

Administer intravenous furosemide

Administer intravenous sodium bicarbonate

Obtain blood cultures and start broad-spectrum antibiotics

Show answer & explanation

Answer: Administer intravenous alteplase

Answer

Administer intravenous alteplase

The correct next step is to administer intravenous alteplase. This patient presents with a massive pulmonary embolism (PE), defined by the presence of acute PE accompanied by hemodynamic instability (systolic blood pressure

< 90

mmHg). The classic triad of elevated jugular venous pressure, clear lungs, and hypotension points to obstructive shock. The bedside echocardiogram showing right ventricular free wall hypokinesis with apical sparing (McConnell's sign) provides sufficient diagnostic evidence in this unstable patient. For massive PE, systemic thrombolysis is the treatment of choice to quickly reduce the clot burden, lower pulmonary artery pressure, and restore right ventricular output. The mortality benefit of thrombolytics outweighs the risk of hemorrhage in this life-threatening scenario.

Step-by-Step Solution

Analyze the patient's hemodynamic status and clinical presentation.

The patient is in shock (blood pressure

72/46

mmHg) with severe hypoxia, recent surgery, and signs of right ventricular overload (elevated JVP, loud

P_2

Identifying hemodynamic instability dictates whether the patient can safely undergo definitive imaging or requires empiric bedside treatment.

Interpret the bedside echocardiogram and arterial blood gas findings.

Echocardiography shows classic McConnell's sign (RV free wall hypokinesis with apical sparing), strongly suggesting acute pulmonary embolism. ABG reveals severe metabolic acidosis with inadequate respiratory compensation (impending respiratory failure).

In unstable patients, bedside ultrasound provides critical diagnostic clues without the risk of transport.

Determine the optimal intervention for massive pulmonary embolism.

Systemic thrombolytic therapy (e.g., intravenous alteplase) is indicated to rapidly dissolve the clot and restore right ventricular output.

Standard anticoagulation (e.g., heparin) prevents further clot propagation but does not rapidly break down the existing obstruction causing the shock.

Key Concept

Management of massive pulmonary embolism involves rapid recognition via bedside echocardiography and prompt administration of systemic thrombolytics in hemodynamically unstable patients.

Question 2599Question →

Match each infectious disease clinical scenario with the most appropriate targeted antimicrobial therapy or post-exposure prophylaxis regimen.

Click a left item, then click its matching right item

Show answer & explanation

Answer

Meningitis contact matches with single-dose ciprofloxacin; Pregnant patient with Lyme disease matches with amoxicillin; Primary syphilis matches with intramuscular penicillin G benzathine; HIV needle stick exposure matches with 28-day course of tenofovir-emtricitabine plus dolutegravir.

Each clinical scenario requires a specific, guideline-directed antimicrobial approach. Meningococcal close contacts need ciprofloxacin, rifampin, or ceftriaxone. Pregnant patients with Lyme disease should receive amoxicillin to avoid teratogenic effects. Primary syphilis is definitively treated with intramuscular penicillin G benzathine. High-risk occupational HIV exposures require a 28-day course of a 3-drug antiretroviral regimen.

Step-by-Step Solution

Evaluate the first scenario for meningococcal exposure prophylaxis.

Identify that sharing oral secretions with a meningococcal meningitis patient is a high-risk exposure requiring prophylaxis with ciprofloxacin, rifampin, or ceftriaxone.

Chemoprophylaxis prevents secondary cases among close contacts by rapidly eradicating nasopharyngeal carriage.

Assess the pregnant patient presenting with a targetoid rash.

Diagnose early localized Lyme disease (erythema migrans) and select amoxicillin.

Doxycycline is typically contraindicated in pregnancy due to fetal risks, making amoxicillin the first-line safe alternative.

Analyze the presentation of a painless penile ulcer.

Diagnose primary syphilis and select intramuscular penicillin G benzathine.

Penicillin remains the curative and definitive first-line treatment for early syphilis.

Evaluate the occupational HIV exposure risk.

Classify the hollow-bore needle stick from an uncontrolled HIV patient as high-risk, warranting full 3-drug post-exposure prophylaxis for 28 days.

A 3-drug regimen maximizes the prevention of viral integration and establishment of systemic infection after a significant exposure.

Key Concept

Appropriate selection of targeted antimicrobial therapy and prophylaxis depends on the specific pathogen, patient characteristics (e.g., pregnancy status), and the specific nature of the exposure.

Question 2600Question →

Correlate the following clinical conditions with their most characteristic acid-base and electrolyte laboratory profile.

Click a left item, then click its matching right item

Show answer & explanation

Answer

Surreptitious vomiting is matched with low urine chloride metabolic alkalosis; Primary hyperaldosteronism with high urine chloride metabolic alkalosis and hypertension; Thiazide abuse with high urine chloride metabolic alkalosis and normotension; Severe acute diarrhea with normal anion gap metabolic acidosis.

Surreptitious vomiting causes saline-responsive alkalosis (low urine chloride). Thiazide abuse causes saline-resistant alkalosis (high urine chloride) with volume depletion. Primary hyperaldosteronism causes saline-resistant alkalosis (high urine chloride) with volume expansion (hypertension). Diarrhea causes a non-anion gap metabolic acidosis due to direct gastrointestinal base loss.

Step-by-Step Solution

Differentiate the causes of hypokalemic metabolic alkalosis based on blood pressure.

Hypertension points to mineralocorticoid excess (Primary hyperaldosteronism). Normotension or hypotension points to volume contraction (vomiting or diuretic use).

Volume status helps narrow down the etiology of metabolic alkalosis.

Differentiate the volume-contracted causes of metabolic alkalosis using urine chloride.

Urine chloride

< 20

mEq/L indicates an extrarenal cause of chloride loss where the kidneys are functioning properly to retain chloride (surreptitious vomiting). Urine chloride

> 20

mEq/L indicates renal chloride wasting (thiazide diuretic abuse).

Urine chloride distinguishes saline-responsive (extrarenal) from saline-resistant (renal) chloride losses.

Identify the primary acid-base disorder caused by severe lower gastrointestinal fluid loss.

Loss of bicarbonate-rich fluid results in a normal anion gap metabolic acidosis.

Unlike gastric fluid which is acidic, lower gastrointestinal fluid is rich in bicarbonate and potassium.

Key Concept

Differentiation of acid-base disorders using volume status, blood pressure, and urine chloride.

Estimated Time:1m 30s

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