Internal Medicine

3151 questions

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

A 68-year-old man is evaluated in the hospital for decreased urine output. He was admitted 3 days ago for severe gastroenteritis and has had poor oral intake. His blood pressure is $96/60 \text{ mm Hg}$ and heart rate is $112/\text{min}$ . Physical examination reveals dry oral mucosa and delayed capillary refill. Laboratory studies show:

Parameter	Value
Serum sodium	$140 \text{ mEq/L}$
Blood urea nitrogen	$60 \text{ mg/dL}$
Serum creatinine	$2.5 \text{ mg/dL}$
Urine sodium	$14 \text{ mEq/L}$
Urine creatinine	$50 \text{ mg/dL}$

Based on these laboratory findings, what is the patient's calculated fractional excretion of sodium (expressed as a percentage)?

Show answer & explanation

Answer: 0.5

Answer

0.5

The calculated fractional excretion of sodium is 0.5%. A value less than 1% indicates appropriate renal sodium avidity in the setting of decreased renal perfusion, confirming prerenal acute kidney injury due to severe volume depletion from gastroenteritis.

Step-by-Step Solution

Identify the FeNa formula

FeNa = \frac{U_{Na} \times P_{Cr}}{P_{Na} \times U_{Cr}} \times 100

This formula normalizes sodium excretion to glomerular filtration rate to evaluate acute kidney injury.

Extract laboratory values

U_{Na} = 14

P_{Cr} = 2.5

P_{Na} = 140

U_{Cr} = 50

These variables are required to calculate the fractional excretion.

Calculate the numerator

14 \times 2.5 = 35

Represents the product of urine sodium and plasma creatinine.

Calculate the denominator

140 \times 50 = 7000

Represents the product of plasma sodium and urine creatinine.

Compute final percentage

(\frac{35}{7000}) \times 100 = 0.5

Yields the fractional excretion expressed as a percentage.

Key Concept

Calculation of Fractional Excretion of Sodium (FeNa)

Estimated Time:1m 0s

Question 2862Question →

A 35-year-old woman comes to the clinic for evaluation of profound fatigue, a 6-kg (13.2-lb) weight gain, and feeling constantly cold over the past 8 months. She also reports that her menstrual periods have been absent for the past 6 months. Her last pregnancy was 4 years ago and was uncomplicated. She takes no medications. Vital signs show a blood pressure of 110/70 mm Hg and a heart rate of 56/min. Physical examination reveals dry, pale skin and delayed relaxation of the deep tendon reflexes. A urine pregnancy test is negative. Laboratory evaluation shows:

Laboratory Test	Result	Reference Range
TSH	1.2 µU/mL	0.5–5.0 µU/mL
Free T4	0.4 ng/dL	0.9–1.7 ng/dL

Which of the following is the most likely underlying mechanism for this patient's clinical presentation?

Compression of the anterior pituitary by a benign neoplasm

Autoimmune destruction of the thyroid gland

Excessive ovarian androgen production leading to chronic anovulation

Physiologic increase in circulating hormone-binding globulins

Inadequate dietary consumption of iodine

Show answer & explanation

Answer: Compression of the anterior pituitary by a benign neoplasm

Answer

The most likely mechanism is compression of the anterior pituitary by a benign neoplasm (causing central hypothyroidism and hypogonadism).

The patient's clinical presentation of fatigue, weight gain, cold intolerance, bradycardia, and delayed deep tendon reflexes is highly characteristic of hypothyroidism. In a healthy hypothalamic-pituitary-thyroid (HPT) axis, a drop in free T4 removes negative feedback on the pituitary, resulting in a compensatory elevation in TSH. In this patient, the free T4 is clearly low, but the TSH is inappropriately normal. This discordance indicates a failure at the level of the pituitary gland or hypothalamus, known as central (or secondary) hypothyroidism. The concomitant presentation of amenorrhea suggests multiple pituitary axes are involved (panhypopituitarism). The most common cause of panhypopituitarism in an adult is a non-functioning pituitary adenoma compressing the anterior pituitary gland.

Step-by-Step Solution

Analyze the clinical presentation.

The patient has symptoms of a hypometabolic state (fatigue, weight gain, cold intolerance, bradycardia, delayed reflexes) and amenorrhea.

Identifying the affected organ systems guides the interpretation of the laboratory data.

Interpret the thyroid laboratory profile.

Free T4 is overtly low, but the TSH is within the normal reference range (1.2 µU/mL).

A healthy pituitary should respond to a low T4 by secreting massive amounts of TSH. An inappropriately normal TSH in the face of low T4 indicates central (secondary) hypothyroidism.

Synthesize the findings to determine the underlying mechanism.

The combination of central hypothyroidism and secondary amenorrhea (hypogonadotropic hypogonadism) strongly points to a structural pituitary lesion, such as a non-functioning pituitary adenoma.

Mass effect from a benign neoplasm compresses the thyrotroph and gonadotroph cells, leading to decreased secretion of multiple anterior pituitary hormones.

Key Concept

Central (secondary) hypothyroidism is characterized by a low free T4 and an inappropriately normal or low TSH. When combined with other pituitary hormone deficiencies (e.g., amenorrhea), a structural pituitary lesion should be highly suspected.

Estimated Time:1m 15s

Question 2863Question →

During morning rounds, the internal medicine team evaluates a male patient in his late fifties who was admitted three days prior for community-acquired pneumonia. On presentation to the emergency department, his temperature was $39.2^\circ\text{C}$ ( $102.6^\circ\text{F}$ ) and chest imaging revealed a right lower lobe consolidation. Initial empiric therapy with intravenous ceftriaxone and oral azithromycin was instituted.

Currently, the patient reports significant symptomatic improvement, noting decreased cough and resolution of shortness of breath. He is comfortably eating a regular diet. His vital signs show a temperature of $37.2^\circ\text{C}$ ( $99.0^\circ\text{F}$ ), blood pressure of $124/82\text{ mm Hg}$ , heart rate of $78/\text{min}$ , and respiratory rate of $16/\text{min}$ .

A high-quality sputum specimen collected prior to antibiotic administration has grown heavy *Streptococcus pneumoniae*. Antimicrobial susceptibility testing indicates that the organism is sensitive to penicillin, amoxicillin, ceftriaxone, and levofloxacin, but demonstrates resistance to macrolides.

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

Discontinue current antibiotics and initiate oral amoxicillin

Discontinue current antibiotics and initiate oral amoxicillin-clavulanate

Discontinue current antibiotics and initiate oral levofloxacin

Continue intravenous ceftriaxone and discontinue oral azithromycin

Discontinue current antibiotics and initiate oral linezolid

Show answer & explanation

Answer: Discontinue current antibiotics and initiate oral amoxicillin

Answer

The most appropriate next step is to discontinue the current antibiotics and initiate oral amoxicillin.

The correct answer is to transition the patient to oral amoxicillin. This patient has community-acquired pneumonia and is now clinically stable (afebrile, normal vitals, tolerating oral intake). Standard of care dictates transitioning such patients from intravenous to oral therapy. Because the sputum culture grew Streptococcus pneumoniae that is susceptible to penicillin and amoxicillin, antimicrobial stewardship principles strongly mandate de-escalating from the empiric broad-spectrum regimen (ceftriaxone and azithromycin) to a targeted, narrow-spectrum agent. High-dose oral amoxicillin is the drug of choice for penicillin-susceptible S. pneumoniae.

Step-by-Step Solution

Evaluate the patient's clinical trajectory to determine the appropriate route of administration.

The patient is afebrile, hemodynamically stable, and tolerating a regular diet.

Patients with community-acquired pneumonia who demonstrate clinical stability and intact gastrointestinal absorption should be transitioned from intravenous to oral antibiotics to facilitate discharge.

Analyze the microbiological culture and susceptibility data.

The pathogen is identified as Streptococcus pneumoniae, which is susceptible to penicillin and amoxicillin.

Empiric broad-spectrum therapy must be de-escalated to targeted therapy once a specific pathogen and its susceptibility profile are known.

Apply antimicrobial stewardship principles to select the optimal oral agent.

Oral amoxicillin is selected over broader alternatives.

Amoxicillin provides excellent targeted coverage for penicillin-susceptible S. pneumoniae with a narrow spectrum, minimizing the risk of adverse effects and antimicrobial resistance.

Key Concept

Antimicrobial stewardship in pneumonia involves transitioning clinically stable patients from empiric intravenous broad-spectrum therapy to the narrowest-spectrum effective oral agent based on culture data.

Estimated Time:1m 15s

Question 2864Question →

A 42-year-old woman is brought to the emergency department by her husband due to severe agitation, palpitations, vomiting, and high fever. She has a history of Graves disease but stopped taking her antithyroid medications three months ago. Her temperature is 39.7°C (103.5°F), blood pressure is 155/75 mmHg, and heart rate is 148/min and regular. Physical examination reveals a fine hand tremor, significant diaphoresis, lid lag, and a diffusely enlarged, non-tender thyroid gland. An electrocardiogram demonstrates sinus tachycardia. The clinical diagnosis of thyroid storm is suspected. Arrange the following interventions in the most appropriate chronological order of administration for this patient's acute to long-term management.

Drag items to arrange them in the correct order

Show answer & explanation

Answer

The correct sequence is the administration of intravenous propranolol, followed by propylthiouracil (PTU), then potassium iodide solution, and finally radioactive iodine ablation.

The management of thyroid storm requires a strict, stepwise pharmacological approach. Intravenous propranolol is given immediately to control severe adrenergic symptoms and decrease peripheral T4-to-T3 conversion. Next, a thionamide (such as propylthiouracil) is given to halt the synthesis of new thyroid hormone. Approximately 1 to 2 hours after the thionamide is given, an iodine solution (such as potassium iodide) is administered; the delay is critical to ensure synthesis is blocked so the iodine is not used to create new hormone. Instead, the iodine acutely inhibits the release of preformed hormone via the Wolff-Chaikoff effect. Finally, after the patient is stabilized and euthyroid (often weeks later), definitive therapy such as radioactive iodine ablation can be safely performed.

Step-by-Step Solution

Identify the immediate life-threatening pathophysiology.

The patient is experiencing thyroid storm with severe adrenergic hyperactivity (tachycardia, fever, agitation).

Immediate symptom control with a beta-blocker (propranolol) is required before addressing the thyroid gland directly. Propranolol also uniquely inhibits peripheral T4 to T3 conversion.

Determine the sequence to halt thyroid hormone production and release.

Propylthiouracil (PTU) must be administered prior to potassium iodide.

PTU blocks the synthesis of new thyroid hormone. If iodine is given first, the hyperactive thyroid will use the iodine substrate to synthesize large amounts of new hormone, acutely worsening the thyrotoxicosis.

Determine the timing for blocking hormone release.

Administer potassium iodide at least 1 hour after PTU.

Once the synthetic pathway is blocked by PTU, iodine can be safely administered to leverage the Wolff-Chaikoff effect, which acutely inhibits the release of pre-stored thyroid hormone.

Determine the timing for definitive treatment.

Radioactive iodine ablation is scheduled as an outpatient procedure.

Definitive therapy is contraindicated during an acute thyroid storm and is only performed once the patient is stabilized and rendered euthyroid on medical therapy.

Key Concept

The precise sequential management of thyroid storm requires beta-blockade, followed by thionamides (to block synthesis), followed 1-2 hours later by iodine (to block release), and later, definitive therapy.

Question 2865Question →

A 59-year-old man with a history of alcoholic cirrhosis and esophageal varices is hospitalized due to generalized abdominal pain and a low-grade fever. On admission, his temperature is 38.1 °C (100.6 °F), blood pressure is 105/65 mmHg, and heart rate is 98/min. Physical examination reveals scleral icterus, spider angiomata, and a distended abdomen with shifting dullness and diffuse mild tenderness.

A diagnostic paracentesis yields cloudy ascitic fluid with a leukocyte count of 1,200/mm³ and a neutrophil count of 950/mm³. He is immediately started on intravenous albumin and empiric intravenous piperacillin-tazobactam.

On hospital day 3, the patient is afebrile and reports significant improvement in his abdominal pain. Ascitic fluid cultures from admission grow *Klebsiella pneumoniae*. Susceptibility testing indicates the isolate is resistant to ampicillin, but susceptible to ceftriaxone, cefotaxime, ciprofloxacin, and piperacillin-tazobactam. Blood cultures show no growth.

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

De-escalate antimicrobial therapy to intravenous ceftriaxone

Continue intravenous piperacillin-tazobactam for a total 14-day course

Escalate antimicrobial therapy to intravenous meropenem

Add intravenous vancomycin to the current regimen

Discontinue all antimicrobial therapy immediately

Show answer & explanation

Answer: De-escalate antimicrobial therapy to intravenous ceftriaxone

Answer

De-escalate antimicrobial therapy to intravenous ceftriaxone

The correct action is to de-escalate antimicrobial therapy to intravenous ceftriaxone. This patient's absolute neutrophil count of 950/mm³ confirmed the diagnosis of spontaneous bacterial peritonitis (SBP). While empiric therapy with piperacillin-tazobactam may occasionally be utilized in patients with critical illness or healthcare-associated SBP, antimicrobial stewardship mandates tailoring the regimen once susceptibilities are known. The *Klebsiella pneumoniae* isolate is susceptible to ceftriaxone, a targeted third-generation cephalosporin that is the standard of care for SBP. De-escalating therapy minimizes the ecological pressure for multidrug-resistant organisms while effectively treating the underlying infection.

Step-by-Step Solution

Identify the primary diagnosis based on the clinical presentation and initial ascitic fluid analysis.

The patient has Spontaneous Bacterial Peritonitis (SBP), confirmed by an absolute neutrophil count greater than 250/mm³ (950/mm³) in the ascitic fluid.

Accurate diagnosis establishes the baseline severity and directs the initial need for empiric antimicrobial therapy and albumin.

Evaluate the patient's clinical trajectory in conjunction with the microbiological culture and susceptibility data.

The patient is clinically improving. Ascitic fluid cultures isolated *Klebsiella pneumoniae*, which is susceptible to ceftriaxone, cefotaxime, ciprofloxacin, and piperacillin-tazobactam.

Integrating clinical response with definitive microbiological data is necessary to adjust empiric therapy to definitive therapy.

Apply the principles of antimicrobial stewardship to select the definitive treatment regimen.

De-escalate the current broad-spectrum regimen (piperacillin-tazobactam) to a narrower, targeted agent (ceftriaxone) to complete a typical 5 to 7-day treatment course.

Using the narrowest effective spectrum minimizes toxicity, preserves the normal microbiome, and reduces the risk of generating multidrug-resistant organisms.

Key Concept

In patients with spontaneous bacterial peritonitis who are clinically improving, initial broad-spectrum empiric antibiotics should be de-escalated to targeted, narrow-spectrum therapy (such as a third-generation cephalosporin) as soon as culture and susceptibility results are available, in accordance with antimicrobial stewardship.

Estimated Time:1m 30s

Question 2866Question →

A 29-year-old woman, gravida 1 para 0, at 28 weeks gestation is brought to the emergency department due to sudden-onset, severe shortness of breath and a cough productive of pink-tinged sputum. She immigrated to the United States two years ago and has not received routine prenatal care. Vital signs show a blood pressure of 110/70 mmHg, a pulse of 118/min, and a respiratory rate of 28/min. Oxygen saturation is 88% on room air. Physical examination reveals a gravid uterus consistent with dates. Auscultation of the lungs demonstrates bilateral basilar crackles. Cardiac examination reveals a loud first heart sound (S1) and a low-pitched, rumbling mid-diastolic murmur heard best at the cardiac apex. Which of the following underlying mechanisms best explains the acute onset of this patient's respiratory symptoms?

Increased left atrial pressure secondary to shortened ventricular diastole

Progesterone-mediated stimulation of central respiratory centers

Upward displacement of the diaphragm reducing total lung capacity

Bronchial smooth muscle constriction and mucosal inflammation

Systemic vasodilation leading to compensatory right ventricular overload

Show answer & explanation

Answer: Increased left atrial pressure secondary to shortened ventricular diastole

Answer

Increased left atrial pressure secondary to shortened ventricular diastole

This patient's physical examination findings of a loud S1 and a mid-diastolic rumbling murmur at the apex are classic for mitral stenosis (MS), most commonly a sequela of prior rheumatic fever. Patients with mild-to-moderate MS may remain asymptomatic until placed under physiologic stress. The hemodynamic changes of pregnancy—specifically the substantial expansion of plasma volume and the normal elevation in resting heart rate—frequently precipitate acute decompensation in these patients. Because flow across a stenotic mitral valve is highly dependent on the duration of diastole, the physiologic tachycardia of pregnancy shortens diastolic filling time. This prevents adequate emptying of the left atrium, resulting in a severe, acute increase in left atrial and pulmonary venous pressures. This elevated hydrostatic pressure causes transudation of fluid into the alveolar spaces (pulmonary edema), leading to her acute presentation of hypoxia, crackles, and pink-tinged sputum.

Step-by-Step Solution

Identify the cardiac pathology based on physical exam findings.

The loud S1 and low-pitched mid-diastolic rumbling murmur at the apex indicate mitral stenosis (MS), likely rheumatic in origin given her immigration history.

Accurate interpretation of the murmur is required to understand the underlying cardiovascular vulnerability.

Recognize the clinical syndrome.

Acute dyspnea, hypoxia, bilateral crackles, and pink-tinged frothy sputum strongly suggest acute pulmonary edema (decompensated heart failure).

Differentiating cardiogenic pulmonary edema from normal pregnancy dyspnea or primary lung disease is essential for identifying the mechanism.

Connect the cardiac pathology with the physiologic changes of pregnancy.

Pregnancy naturally increases blood volume and resting heart rate. In mitral stenosis, a faster heart rate shortens diastolic filling time, rapidly elevating left atrial pressure and causing fluid transudation into the alveoli.

The question requires identifying the specific physiologic trigger that caused the previously stable MS to decompensate into acute pulmonary edema.

Key Concept

Patients with mitral stenosis are highly susceptible to acute pulmonary edema during pregnancy because the physiologic increase in heart rate (tachycardia) shortens diastole, preventing adequate left atrial emptying and causing a severe backup of pressure into the pulmonary circulation.

Question 2867Question →

A 32-year-old woman comes to the clinic reporting profound fatigue, weight loss, and lightheadedness upon standing over the past 3 months. She delivered a healthy infant 4 months ago. Her delivery was complicated by severe uterine atony and hemorrhage, requiring massive fluid resuscitation and the transfusion of 3 units of packed red blood cells. Since the delivery, she has been unable to breastfeed and has not resumed menstruation. Her blood pressure is 92/58 mm Hg and pulse is 95/min. Laboratory studies show:

Test	Result	Normal Range
Serum sodium	131 mEq/L	136-145 mEq/L
Serum potassium	4.1 mEq/L	3.5-5.0 mEq/L
Thyroid-stimulating hormone (TSH)	1.1 mU/L	0.5-5.0 mU/L
Free thyroxine (T4)	0.5 ng/dL	0.9-2.4 ng/dL

The physician suspects a thyroid disorder and considers initiating levothyroxine therapy. Which of the following is the most appropriate next step in management prior to initiating this medication?

Measure early morning serum cortisol

Measure serum thyroid peroxidase antibodies

Obtain an MRI of the brain

Perform an ultrasound of the thyroid gland

Measure serum prolactin

Show answer & explanation

Answer: Measure early morning serum cortisol

Answer

Measure early morning serum cortisol

The correct answer is measuring early morning serum cortisol. This patient’s history of severe postpartum hemorrhage followed by failure to lactate, amenorrhea, profound fatigue, and hypotension is the classic clinical presentation of Sheehan syndrome (ischemic necrosis of the pituitary gland). Her laboratory findings of a low free T4 and an inappropriately normal TSH confirm central hypothyroidism. Because the anterior pituitary is damaged, she likely also has central adrenal insufficiency (decreased ACTH leading to decreased cortisol). Thyroid hormone increases the hepatic clearance of cortisol and elevates the overall basal metabolic rate. Therefore, initiating levothyroxine in a patient with untreated adrenal insufficiency can acutely deplete their limited cortisol reserves and precipitate a life-threatening adrenal crisis. The integrity of the hypothalamic-pituitary-adrenal (HPA) axis must always be evaluated—typically starting with an early morning serum cortisol level—before administering thyroid hormone replacement.

Step-by-Step Solution

Interpret the clinical presentation.

The history of massive postpartum hemorrhage, lactation failure, amenorrhea, fatigue, and hypotension strongly suggests Sheehan syndrome (postpartum pituitary necrosis).

Severe blood loss and hypovolemia cause ischemic necrosis of the physiologically enlarged pituitary gland during pregnancy.

Analyze the laboratory findings.

A low free T4 with an inappropriately normal TSH indicates central hypothyroidism. Mild hyponatremia with a normal potassium level suggests central adrenal insufficiency.

The necrotic pituitary gland fails to secrete TSH and ACTH. Aldosterone secretion is preserved because it relies primarily on the renin-angiotensin-aldosterone system rather than ACTH, keeping potassium levels normal.

Determine the necessary sequence of treatment.

Adrenal function must be assessed (and treated if deficient) before thyroid hormone replacement is initiated.

Levothyroxine increases the basal metabolic rate and the hepatic clearance of cortisol. If administered to a patient with unrecognized adrenal insufficiency, it can rapidly deplete remaining cortisol reserves and precipitate a life-threatening adrenal crisis.

Key Concept

In patients with suspected panhypopituitarism and central hypothyroidism (e.g., Sheehan syndrome), evaluation for central adrenal insufficiency with a serum cortisol level is strictly required before initiating levothyroxine therapy in order to prevent an acute adrenal crisis.

Question 2868Question →

A 62-year-old man presents to a rural emergency department with crushing substernal chest pain that began 45 minutes ago. His blood pressure is $130/80\text{ mmHg}$ , and his heart rate is $88/\text{min}$ . An electrocardiogram reveals $4\text{ mm}$ ST-segment elevations in leads II, III, and aVF. The hospital does not have a cardiac catheterization laboratory. The nearest percutaneous coronary intervention (PCI)-capable center is 150 minutes away by helicopter due to current weather conditions.

Arrange the following management steps in the most appropriate chronological order according to standard guidelines.

Drag items to arrange them in the correct order

Show answer & explanation

Answer

The correct sequence begins with immediate dual antiplatelet therapy, followed by intravenous fibrinolysis (due to a transfer time >120 minutes). The patient is then transferred to a PCI-capable center, where coronary angiography is ultimately performed.

In the management of acute STEMI at a non-PCI capable facility, the critical decision point is the anticipated first medical contact-to-device time. Because the transfer time in this scenario is 150 minutes (well beyond the 120-minute threshold), the patient must receive a fibrinolytic agent within 30 minutes of arrival. Dual antiplatelet therapy is administered immediately upon presentation. After fibrinolysis, the patient is transferred to a PCI-capable center for coronary angiography (pharmacoinvasive strategy).

Step-by-Step Solution

Identify the diagnosis and immediate pharmacologic needs.

The patient has an acute inferior STEMI and requires immediate dual antiplatelet therapy (aspirin and a P2Y12 inhibitor).

To inhibit further platelet aggregation and prevent propagation of the coronary thrombus as early as possible.

Evaluate the expected time to primary percutaneous coronary intervention (PCI).

The patient is at a non-PCI capable center, and the expected transport time is 150 minutes.

The 120-minute threshold for first medical contact-to-device time determines whether primary PCI or fibrinolysis is the initial reperfusion strategy.

Determine the appropriate initial reperfusion strategy at the current facility.

Intravenous fibrinolytic therapy must be administered.

Because the transfer time exceeds 120 minutes, guidelines mandate administering fibrinolytics within 30 minutes of arrival to minimize total ischemic time.

Determine the post-fibrinolytic disposition.

Transfer the patient to a PCI-capable facility.

All patients receiving fibrinolytics require transfer for a pharmacoinvasive strategy.

Determine the definitive procedural management at the receiving center.

Perform coronary angiography.

To assess coronary anatomy and intervene on the culprit lesion, either immediately if lysis failed or routinely within 2-24 hours if successful.

Key Concept

Management of ST-segment elevation myocardial infarction (STEMI) at a non-PCI capable center.

Estimated Time:1m 30s

Question 2869Question →

A 58-year-old man suddenly collapses while walking in the hospital lobby. He is unresponsive, lacks a palpable pulse, and is not breathing. The emergency response team arrives and attaches a cardiac monitor, which reveals ventricular fibrillation. According to the Advanced Cardiac Life Support (ACLS) algorithm for adult cardiac arrest, arrange the following subsequent management steps in the correct chronological sequence.

Drag items to arrange them in the correct order

Show answer & explanation

Answer

The correct sequence for managing ventricular fibrillation is: deliver the first defibrillation shock, resume CPR and establish IV access, deliver a second shock, administer epinephrine during the next CPR cycle, and finally deliver a third shock followed by amiodarone.

The Advanced Cardiac Life Support (ACLS) algorithm for shockable rhythms dictates an alternating sequence of shocks and medications interposed with continuous 2-minute cycles of high-quality CPR. The sequence strictly follows: Shock 1 → CPR (establish IV) → Shock 2 → CPR (administer Epinephrine) → Shock 3 → CPR (administer Amiodarone). This maximizes coronary perfusion pressure while utilizing electrical and pharmacological therapies to terminate the arrhythmia.

Step-by-Step Solution

Recognize ventricular fibrillation and immediately deliver the first unsynchronized shock.

Depolarizes the myocardium in an attempt to allow the sinus node to reset.

Early defibrillation is the single most important intervention for survival in shockable cardiac arrest rhythms.

Resume CPR immediately for 2 minutes and obtain IV/IO access.

Maintains coronary and cerebral perfusion.

Pulse checks immediately after shocks cause detrimental delays in perfusion; CPR must be initiated instantly.

Perform a rhythm check and deliver a second shock if ventricular fibrillation persists.

Attempts electrical cardioversion a second time for refractory arrhythmias.

Repeated electrical therapy is required when the initial shock does not terminate the fibrillation.

Administer epinephrine 1 mg during the subsequent 2 minutes of CPR.

Increases aortic diastolic pressure.

Epinephrine is given after the second shock to enhance coronary and cerebral blood flow during CPR, increasing the likelihood of successful subsequent defibrillation.

Deliver a third shock and administer an antiarrhythmic like amiodarone.

Suppresses ventricular irritability.

Antiarrhythmics are indicated for ventricular fibrillation that is refractory to CPR, shocks, and vasopressors.

Key Concept

Advanced Cardiac Life Support (ACLS) Pulseless Arrest Algorithm for Shockable Rhythms

Question 2870Question →

A $28$ -year-old man comes to the clinic due to a $4$ -week history of abdominal pain, non-bloody diarrhea, and a $4$ -kg ( $8.8$ -lb) weight loss. He has $4$ to $5$ loose bowel movements daily. The abdominal pain is cramping in nature and localizes to the right lower quadrant. He has a history of mild asthma. Vital signs are temperature $37.3^\circ\text{C}$ ( $99.1^\circ\text{F}$ ), pulse $86/\text{min}$ , and blood pressure $118/76\text{ mmHg}$ . Physical examination reveals a soft, non-distended abdomen with moderate tenderness to deep palpation in the right lower quadrant. There is no rebound tenderness, guarding, or palpable mass. Bowel sounds are normal.

Laboratory studies show:

Test	Result	Normal Range
Hemoglobin	$11.2\text{ g/dL}$	$13.5$ - $17.5\text{ g/dL}$
Leukocyte count	$9,400/\text{mm}^3$	$4,500$ - $11,000/\text{mm}^3$
C-reactive protein	$35\text{ mg/L}$	$< 5\text{ mg/L}$

Stool studies for ova and parasites, routine bacterial pathogens, and *Clostridioides difficile* toxin are negative. A recent colonoscopy performed $2$ months ago for chronic diarrhea showed patchy areas of mucosal inflammation, erythema, and deep ulcerations in the terminal ileum, with a normal-appearing colon.

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

Prescribe a course of ciprofloxacin and metronidazole

Start intravenous methylprednisolone

Recommend a high-fiber diet and oral loperamide

Initiate oral budesonide therapy

Refer the patient for an elective ileocecal resection

Show answer & explanation

Answer: Initiate oral budesonide therapy

Answer

Initiate oral budesonide therapy

The most appropriate next step in management is to initiate oral budesonide therapy. This patient is experiencing a mild-to-moderate flare of Crohn disease, which is localized to the terminal ileum. Budesonide is a potent glucocorticoid that is specifically formulated to release in the distal ileum and right colon. Because it undergoes extensive first-pass hepatic metabolism, it effectively reduces localized mucosal inflammation while causing significantly fewer systemic side effects compared to conventional systemic corticosteroids like prednisone. Therefore, it is the first-line agent for inducing remission in this specific clinical scenario.

Step-by-Step Solution

Identify the patient's primary diagnosis and current disease status.

The patient has a mild-to-moderate flare of Crohn disease localized to the terminal ileum.

He presents with subacute non-bloody diarrhea, right lower quadrant abdominal pain, and weight loss, and recent colonoscopy confirmed terminal ileum involvement without signs of strictures or peritonitis.

Determine the appropriate pharmacotherapy based on disease location and severity.

Oral budesonide is the treatment of choice.

Budesonide is a glucocorticoid with high first-pass hepatic metabolism, providing targeted topical therapy to the terminal ileum and right colon while minimizing systemic side effects.

Key Concept

Oral budesonide is the first-line treatment for inducing remission in patients with mild-to-moderate Crohn disease that is confined to the terminal ileum and/or right colon.

Question 2871Question →

Correlate each of the described clinical scenarios with its characteristic pattern of thyroid function testing.

Click a left item, then click its matching right item

Show answer & explanation

Answer

1 matches with the inflammatory high T4/low uptake profile; 2 matches with the high reverse T3 profile; 3 matches with the low thyroglobulin profile; 4 matches with the isolated high TSH profile.

The correct matches require distinguishing the pathophysiologic mechanisms of varying thyroid states. Subacute thyroiditis presents with a painful goiter, high T4, low TSH, high ESR, and low radioiodine uptake due to glandular destruction. Euthyroid sick syndrome is an adaptive response to severe illness, showing low T3 and high reverse T3 due to altered peripheral conversion. Factitious thyrotoxicosis shows high T4 and low TSH, but uniquely low thyroglobulin because exogenous hormone suppresses endogenous gland function. Subclinical hypothyroidism features isolated TSH elevation with normal T4, often discovered via hyperlipidemia.

Step-by-Step Solution

Analyze the clinical scenario of the post-viral painful thyroid.

Identified as subacute granulomatous (de Quervain) thyroiditis.

The inflammation causes release of preformed hormones and decreased iodine uptake, with elevated inflammatory markers.

Evaluate the critically ill patient in the intensive care unit.

Identified as euthyroid sick syndrome.

Severe illness alters peripheral deiodination, reducing T3 and increasing reverse T3 without primary thyroid pathology.

Assess the healthcare worker with thyrotoxicosis and a nonpalpable gland.

Identified as factitious thyrotoxicosis (exogenous thyroid hormone intake).

Exogenous hormone suppresses TSH and thyroglobulin production, while the gland atrophies.

Examine the asymptomatic patient with new hyperlipidemia.

Identified as subclinical hypothyroidism.

Mild thyroid dysfunction often first presents with elevated TSH, normal T4, and altered lipid metabolism.

Key Concept

Differentiation of thyroid disorders based on integrated laboratory profiles, including TSH, free T4, T3, reverse T3, thyroglobulin, and radioiodine uptake.

Question 2872Question →

A 19-year-old woman is brought to the emergency department by her college roommate due to confusion, nausea, and ringing in her ears that started 4 hours ago. The roommate reports that the patient was distraught after a recent argument, and an empty bottle of over-the-counter pain medication was found on her desk. Vital signs show a temperature of $37.8^\circ$ C ( $100.0^\circ$ F), blood pressure of $110/70$ mmHg, pulse of $115$ /min, and respiratory rate of $28$ /min. Physical examination reveals an oriented but lethargic patient. Lungs are clear to auscultation. Laboratory studies are obtained and show the following:

Serum sodium: $142$ mEq/L
Serum potassium: $4.0$ mEq/L
Serum chloride: $104$ mEq/L
Serum bicarbonate: $14$ mEq/L
Blood urea nitrogen: $18$ mg/dL
Serum creatinine: $0.9$ mg/dL

Arterial blood gas (room air):
pH: $7.42$
pCO $_2$ : $20$ mmHg
pO $_2$ : $105$ mmHg

Based on the laboratory results, which of the following best describes this patient's acid-base disturbance?

High anion gap metabolic acidosis and concurrent primary respiratory alkalosis

High anion gap metabolic acidosis with appropriate respiratory compensation

Primary respiratory alkalosis with appropriate metabolic compensation

High anion gap metabolic acidosis and concurrent primary respiratory acidosis

Normal anion gap metabolic acidosis and concurrent primary respiratory alkalosis

Show answer & explanation

Answer: High anion gap metabolic acidosis and concurrent primary respiratory alkalosis

Answer

High anion gap metabolic acidosis and concurrent primary respiratory alkalosis

This patient presents with tinnitus, nausea, tachypnea, and an empty medication bottle, a classic vignette for salicylate (aspirin) toxicity. Salicylates cause a characteristic mixed acid-base disorder. First, calculate the anion gap:

142 - (104 + 14) = 24

mEq/L. Because the gap is

> 12

mEq/L, there is a primary high anion gap metabolic acidosis (HAGMA). Next, determine if the respiratory compensation is appropriate using Winter's formula: expected pCO

_2

(1.5 \times 14) + 8 \pm 2 = 29 \pm 2

mmHg (range

27-31

mmHg). The patient's actual pCO

_2

20

mmHg, which is significantly lower than the expected compensatory range. A pCO

_2

that is lower than expected indicates the presence of a superimposed primary respiratory alkalosis, caused by the direct stimulatory effect of salicylates on the medullary respiratory center.

Step-by-Step Solution

Calculate the serum anion gap.

Anion Gap =

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

142 - (104 + 14)

24

mEq/L.

An elevated anion gap (> 12 mEq/L) establishes the presence of a primary high anion gap metabolic acidosis (HAGMA).

Apply Winter's formula to determine the expected respiratory compensation.

Expected pCO

_2

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

(1.5 \times 14) + 8 \pm 2

29 \pm 2

mmHg (range

27-31

mmHg).

Winter's formula determines if the patient's respiratory response accurately compensates for the metabolic acidosis.

Compare the expected pCO2 to the measured pCO2.

The measured pCO

_2

20

mmHg, which is less than the expected range of

27-31

mmHg.

Because the measured pCO2 is lower than the expected compensatory range, there is an excessive respiratory drive indicating an additional primary respiratory alkalosis.

Key Concept

Interpretation of mixed acid-base disorders using the anion gap and Winter's formula

Question 2873Question →

A 28-year-old man presents to the emergency department with a 4-day history of high fevers, chills, and sharp, pleuritic chest pain. He also reports a cough productive of scant, blood-tinged sputum. His temperature is $39.1^\circ\text{C}$ ( $102.4^\circ\text{F}$ ), blood pressure is $112/68\text{ mmHg}$ , pulse is $118/\text{min}$ , and respiratory rate is $22/\text{min}$ . Oxygen saturation is $94\%$ on room air. Physical examination reveals prominent needle track marks on his forearms. Cardiac auscultation demonstrates a grade $3/6$ holosystolic murmur at the left lower sternal border; the murmur's intensity increases significantly during inspiration. Pulmonary auscultation reveals scattered crackles in both lung fields. A chest radiograph demonstrates multiple bilateral peripheral nodular opacities, several of which have central cavitation. Three sets of blood cultures are obtained. Which of the following is the most appropriate initial pharmacotherapy for this patient?

Intravenous vancomycin

Intravenous ceftriaxone and azithromycin

Oral isoniazid, rifampin, pyrazinamide, and ethambutol

Intravenous heparin infusion

Intravenous ampicillin-sulbactam

Show answer & explanation

Answer: Intravenous vancomycin

Answer

Intravenous vancomycin

The patient's presentation of high fever, intravenous drug use, a tricuspid regurgitation murmur (holosystolic at the left lower sternal border, augmenting with inspiration), and cavitary pulmonary lesions is highly characteristic of right-sided infective endocarditis complicated by septic pulmonary emboli. Staphylococcus aureus, including methicillin-resistant strains (MRSA), is the most common etiologic agent in this population. Empiric therapy with an agent that provides robust MRSA coverage, such as intravenous vancomycin, is necessary immediately after obtaining blood cultures.

Step-by-Step Solution

Analyze the patient's demographic risk factors and presenting vital signs.

The patient is a young intravenous drug user presenting with acute fever, tachycardia, and hypoxemia.

Identifying risk factors helps prioritize infectious etiologies such as endovascular infections.

Evaluate the physical examination findings, specifically the cardiac auscultation.

A holosystolic murmur at the left lower sternal border that augments with inspiration indicates tricuspid regurgitation.

Right-sided murmurs classically increase with inspiration (Carvallo sign) due to increased venous return to the right heart.

Interpret the radiographic findings in the context of the clinical picture.

Multiple cavitating peripheral nodular opacities in the lungs represent septic pulmonary emboli.

Vegetations on the tricuspid valve can dislodge and travel to the pulmonary vasculature, causing localized infarction and abscess formation.

Synthesize a diagnosis and determine the optimal empiric antibiotic regimen.

The diagnosis is right-sided infective endocarditis. Empiric therapy must cover Staphylococcus aureus (including MRSA).

Staphylococcus aureus is responsible for the vast majority of right-sided endocarditis cases in intravenous drug users, requiring broad-spectrum Gram-positive coverage with intravenous vancomycin until cultures result.

Key Concept

Right-sided infective endocarditis in intravenous drug users commonly presents with tricuspid regurgitation and septic pulmonary emboli, requiring empiric coverage for MRSA with intravenous vancomycin.

Estimated Time:1m 30s

Question 2874Question →

A 68-year-old man comes to the emergency department complaining of worsening shortness of breath, a persistent nonproductive cough, and swelling in his legs over the past 4 days. He has a 40-pack-year smoking history and a medical history of hypertension, hyperlipidemia, and type 2 diabetes mellitus. His current medications include amlodipine, lisinopril, atorvastatin, and metformin. His temperature is $37.1^\circ\text{C}$ ( $98.8^\circ\text{F}$ ), blood pressure is $162/92\text{ mmHg}$ , pulse is $106/\text{min}$ , and respirations are $24/\text{min}$ . Pulse oximetry shows an oxygen saturation of $92\%$ on room air. Physical examination reveals a patient in mild respiratory distress using accessory muscles of respiration. Jugular venous pressure is elevated at $12\text{ cm H}_2\text{O}$ . Lung auscultation reveals bilateral diffuse expiratory wheezes and dullness to percussion at both bases. Cardiac examination shows a regular rhythm, tachycardia, and a third heart sound (S3). Trace bilateral pitting edema is present up to the ankles. An electrocardiogram shows sinus tachycardia with no acute ischemic changes. Which of the following is the most appropriate initial therapy for this patient's current condition?

Intravenous furosemide

Inhaled albuterol and oral prednisone

Intravenous metoprolol

Oral azithromycin

Inhaled tiotropium

Show answer & explanation

Answer: Intravenous furosemide

Answer

Intravenous furosemide

This patient presents with signs and symptoms of acute decompensated heart failure (ADHF), including progressive dyspnea, elevated jugular venous pressure, an S3 gallop, and peripheral edema. The presence of expiratory wheezes in this context is often referred to as 'cardiac asthma.' This occurs because increased pulmonary capillary hydrostatic pressure leads to fluid transudation into the pulmonary interstitium, causing peribronchial edema and narrowing of the small airways. The dullness to percussion at the lung bases suggests the presence of bilateral pleural effusions, another classic sign of ADHF. The most appropriate initial management for ADHF with signs of severe volume overload is an intravenous loop diuretic, such as furosemide, which rapidly reduces intravascular volume and relieves pulmonary congestion.

Step-by-Step Solution

Analyze the patient's risk factors and presenting symptoms.

The patient has progressive dyspnea, nonproductive cough, and leg swelling. He has risk factors for both cardiovascular disease (hypertension, diabetes) and pulmonary disease (40-pack-year smoking history).

Establishing the differential diagnosis between acute decompensated heart failure (ADHF) and chronic obstructive pulmonary disease (COPD) exacerbation is necessary.

Evaluate the physical examination findings.

Elevated jugular venous pressure, an S3 gallop, dullness to percussion at the lung bases (indicating pleural effusions), and lower extremity pitting edema are present.

These findings strongly point toward volume overload and biventricular heart failure, distinguishing the presentation from primary lung disease despite the presence of wheezing (cardiac asthma).

Determine the most appropriate initial management for the confirmed diagnosis.

Intravenous loop diuretics (e.g., furosemide) should be administered.

Loop diuretics provide rapid diuresis and mild venodilation, which decreases preload, resolving pulmonary edema and relieving respiratory distress in ADHF.

Key Concept

Differentiating acute decompensated heart failure ('cardiac asthma') from a COPD exacerbation based on physical exam findings (S3 gallop, elevated jugular venous pressure) is critical for selecting the correct initial therapy of intravenous loop diuretics.

Question 2875Question →

An emergency medical responder brings a 73-year-old retired construction worker to the emergency department after his wife noticed severe swelling in his legs and progressive difficulty breathing over the past three weeks. The patient has a 50-pack-year smoking history but has not been evaluated by a physician in more than a decade. Vital signs show a temperature of 37.1°C, blood pressure of 138/84 mm Hg, pulse of 108/min, and respiratory rate of 24/min. Oxygen saturation is 88% on room air.

Physical examination reveals an increased anteroposterior diameter of the chest. Lung auscultation demonstrates globally decreased breath sounds with a prolonged expiratory phase. Jugular venous pressure is visibly elevated to 11 cm H2O and features a prominent *a* wave. Cardiac examination reveals a pronounced impulse along the left lower sternal border. A soft, high-pitched, blowing, early diastolic murmur is heard best at the second left intercostal space. The liver edge is palpable 4 cm below the right costal margin, and there is 2+ bilateral pitting edema extending to the knees.

A portable chest radiograph demonstrates hyperlucent lung fields, flattened diaphragms, and prominent central pulmonary arteries without pleural effusions or pulmonary infiltrates. Electrocardiography shows right axis deviation and peaked P waves in lead II.

Which of the following is the most likely initiating mechanism for this patient's cardiac findings?

Global alveolar hypoxia triggering pulmonary arterial vasoconstriction

Chronically elevated left ventricular end-diastolic pressure transmitting backward

Thromboembolic occlusion of the proximal and distal pulmonary arterial tree

Idiopathic proliferation of the intimal layer in small pulmonary muscular arteries

Primary structural degradation of the pulmonary valve leaflets

Show answer & explanation

Answer: Global alveolar hypoxia triggering pulmonary arterial vasoconstriction

Answer

Global alveolar hypoxia triggering pulmonary arterial vasoconstriction

The correct option correctly identifies the initiating mechanism for cor pulmonale (right heart failure secondary to chronic lung disease). In chronic obstructive pulmonary disease (COPD), alveolar hypoxia induces localized pulmonary vasoconstriction, a physiological reflex designed to shunt blood away from poorly ventilated alveoli toward better-ventilated ones. However, in severe COPD, widespread alveolar hypoxia results in global pulmonary vasoconstriction. Over time, this chronic vasoconstriction leads to structural vascular remodeling, permanently increased pulmonary vascular resistance, and severe pulmonary hypertension. The right ventricle hypertrophies (manifesting as a right ventricular heave, right axis deviation, and a prominent jugular 'a' wave) to overcome this elevated afterload, eventually leading to right-sided heart failure (hepatomegaly, peripheral edema) and dilation of the pulmonary valve ring (causing the high-pitched early diastolic Graham Steell murmur of pulmonary regurgitation).

Step-by-Step Solution

Analyze the patient's respiratory presentation and imaging.

The patient has a 50-pack-year smoking history, barrel chest, prolonged expiratory phase, hypoxia, and hyperlucent lungs with flattened diaphragms on chest radiograph.

These findings definitively establish a primary diagnosis of severe, chronic obstructive pulmonary disease (COPD).

Analyze the cardiovascular examination findings.

Elevated JVP with a prominent 'a' wave, a left lower sternal border impulse (right ventricular heave), hepatomegaly, peripheral edema, and a Graham Steell murmur (early diastolic murmur of pulmonary regurgitation). ECG shows right axis deviation and right atrial enlargement.

These findings indicate right ventricular hypertrophy and right-sided heart failure. The lack of pulmonary edema or left-sided murmurs suggests the right heart failure is isolated and secondary to pulmonary pathology.

Synthesize the findings to identify the pathophysiological link.

The combination of severe COPD and isolated right heart failure is known as cor pulmonale.

To answer the question, the specific mechanism linking COPD to right heart failure must be identified.

Identify the initiating mechanism of cor pulmonale in COPD.

Chronic alveolar hypoxia triggers localized pulmonary vasoconstriction (a compensatory reflex to optimize ventilation-perfusion matching). In severe COPD, this hypoxia is global, leading to widespread vasoconstriction, vascular remodeling, increased pulmonary vascular resistance, and pulmonary hypertension.

This elevated afterload forces the right ventricle to hypertrophy and eventually fail, leading to the clinical signs observed.

Key Concept

Cor Pulmonale Pathophysiology

Estimated Time:2m 0s

Question 2876Question →

A 48-year-old man is brought to the emergency department due to excruciating lower chest and upper abdominal pain that began 2 hours ago. The pain started abruptly after several episodes of forceful retching and vomiting following heavy alcohol consumption. His temperature is $38.2^\circ\text{C}$ ( $100.8^\circ\text{F}$ ), blood pressure is $105/65\text{ mmHg}$ , pulse is $118/\text{min}$ , and respirations are $24/\text{min}$ . Physical examination reveals diaphoresis and acute distress. Palpation of the anterior neck and supraclavicular area elicits a crackling sensation. Cardiac auscultation reveals a crunching sound synchronous with the heartbeat.

Arrange the following diagnostic and therapeutic steps in the most appropriate sequential order for managing this patient, assuming the initial contrast study is non-diagnostic but clinical suspicion remains high.

Drag items to arrange them in the correct order

Show answer & explanation

Answer

The correct sequence is: Obtain an upright chest radiograph -> Perform a water-soluble contrast esophagram -> Perform a barium contrast esophagram -> Proceed with emergency surgical repair and mediastinal drainage.

The patient's presentation of severe chest pain following forceful retching, combined with subcutaneous emphysema and Hamman sign (mediastinal crunch), is the classic presentation of Boerhaave syndrome (spontaneous transmural perforation of the esophagus). The management requires a specific, rapid sequence to confirm the diagnosis while minimizing iatrogenic harm. A chest radiograph is the most appropriate first screening test to identify pneumomediastinum. However, an esophagram is required to confirm the diagnosis and locate the tear for surgery. A water-soluble contrast study is always performed first; if it leaks into the mediastinum, it is easily absorbed and causes minimal tissue reaction. Because water-soluble contrast can miss small perforations, a negative result in a highly suspicious case must be followed by a barium study, which is more sensitive but carries a high risk of chemical mediastinitis if a large leak is present. Once the tear is confirmed and localized, urgent surgical intervention with primary repair and drainage is required.

Step-by-Step Solution

Diagnose the underlying condition based on the clinical presentation.

The patient has Boerhaave syndrome (effort rupture of the esophagus), indicated by Mackler triad (vomiting, lower thoracic pain, subcutaneous emphysema) and Hamman sign (mediastinal crunch).

Recognizing the high likelihood of an esophageal perforation dictates an urgent need for sequential diagnostic testing that avoids causing further harm.

Determine the best initial rapid screening test.

An upright chest radiograph.

It is fast, non-invasive, and can quickly reveal secondary signs of perforation such as pneumomediastinum or pleural effusions.

Select the safest initial confirmatory test to localize the perforation.

A water-soluble contrast esophagram.

Water-soluble contrast minimizes the risk of severe mediastinal inflammation if it leaks through a large defect.

Determine the next step if the water-soluble study is negative but suspicion is high.

A barium contrast esophagram.

Water-soluble contrast has a notable false-negative rate for small perforations. Barium is more sensitive and must be used to definitively rule out a tear, but only after a large leak has been excluded.

Identify the definitive treatment.

Emergency surgical repair and mediastinal drainage.

Once the perforation is located, surgical intervention is required to repair the defect and prevent fatal sepsis.

Key Concept

Diagnostic and therapeutic sequence for Boerhaave syndrome

Question 2877Question →

A 42-year-old man is brought to the emergency department by ambulance after being found unresponsive in his garage. His wife reports that he has a history of major depressive disorder and recently lost his job. On physical examination, he is unarousable. Blood pressure is 115/75 mm Hg, pulse is 112/min, and respirations are 24/min and deep.

Laboratory studies show:
Serum sodium: 140 mEq/L
Serum potassium: 4.6 mEq/L
Serum chloride: 105 mEq/L
Serum bicarbonate: 10 mEq/L
Blood urea nitrogen (BUN): 28 mg/dL
Serum creatinine: 1.8 mg/dL
Serum glucose: 108 mg/dL
Measured serum osmolality: 320 mOsm/kg H2O

What is this patient's serum osmolar gap in mOsm/kg H2O?

Show answer & explanation

Answer: 24

Answer

The correct osmolar gap is 24 mOsm/kg H2O.

The serum osmolar gap is the difference between the measured serum osmolality and the calculated serum osmolality. The calculated osmolality is determined using the formula:

2 \times [Na^+] + \frac{[Glucose]}{18} + \frac{[BUN]}{2.8}

. For this patient, the calculated osmolality is

2(140) + \frac{108}{18} + \frac{28}{2.8} = 280 + 6 + 10 = 296

mOsm/kg H2O. The measured osmolality is 320 mOsm/kg H2O. Therefore, the osmolar gap is

320 - 296 = 24

mOsm/kg H2O. A normal osmolar gap is generally

\le 10

mOsm/kg H2O. An elevated osmolar gap in the setting of a high anion gap metabolic acidosis (anion gap = 140 - (105 + 10) = 25 mEq/L) strongly suggests toxic alcohol ingestion, such as ethylene glycol or methanol.

Step-by-Step Solution

Calculate the expected serum osmolality.

Expected osmolality = 296 mOsm/kg H2O.

To determine if unmeasured osmoles (such as toxic alcohols) are present, the calculated osmolality must be compared to the measured osmolality.

Calculate the osmolar gap.

Osmolar gap = 24 mOsm/kg H2O.

The gap is the difference between the measured and calculated serum osmolality (

320 - 296 = 24

Key Concept

Calculation of the serum osmolar gap in the evaluation of high anion gap metabolic acidosis and suspected toxic alcohol ingestion.

Question 2878Question →

A 45-year-old man presents to the emergency department complaining of a 4-week history of productive cough, intermittent hemoptysis, drenching night sweats, and an unintentional 5-kg (11-lb) weight loss. He recently emigrated from a country with a high prevalence of tuberculosis. His temperature is 38.2°C (100.8°F), blood pressure is 120/78 mm Hg, pulse is 92/min, and respiratory rate is 18/min. A portable chest radiograph performed in the triage area reveals a cavitary lesion in the right upper lobe. The patient is currently sitting in a standard shared emergency department waiting area. Arrange the following steps in the most appropriate sequential order for the management of this patient.

Drag items to arrange them in the correct order

Show answer & explanation

Answer

The correct sequence is: Transfer to an airborne infection isolation room, collect three sputum specimens, initiate an empiric four-drug regimen, and finally narrow the regimen based on susceptibility results.

In a patient presenting with classic signs of active pulmonary tuberculosis (cavitary lesion, hemoptysis, weight loss), the absolute first priority is infection control via airborne isolation to protect staff and other patients. Following isolation, microbiological confirmation and susceptibility testing require the collection of sputum specimens for AFB smear and culture. Once diagnostics are secured, a standard empiric four-drug regimen (isoniazid, rifampin, pyrazinamide, ethambutol) is initiated. Finally, the regimen is narrowed to fewer drugs based on the final susceptibility results to adhere to antimicrobial stewardship and reduce medication toxicity.

Step-by-Step Solution

Identify the immediate public health and safety risk.

The patient has signs highly suspicious for active pulmonary tuberculosis and is currently in a shared space.

Airborne transmission poses a severe risk to others; thus, immediate placement in a negative-pressure airborne infection isolation room is the absolute first step.

Determine the necessary diagnostic workup prior to treatment.

Collection of three sputum specimens for AFB smear and culture is prioritized.

Cultures provide definitive diagnosis and crucial susceptibility data. They must be drawn before starting antibiotics to avoid false-negative results.

Select the initial therapeutic intervention.

Start the standard intensive phase therapy with isoniazid, rifampin, pyrazinamide, and ethambutol.

Empiric multidrug therapy is required to adequately treat the pathogen and prevent the emergence of drug resistance.

Plan the long-term management strategy.

De-escalate the regimen based on final culture and susceptibility results.

Narrowing the antibiotic spectrum minimizes adverse drug effects once pathogen sensitivities are definitively confirmed.

Key Concept

The management sequence for suspected active pulmonary tuberculosis prioritizes public health via infection control, followed by diagnostic microbiological sampling, empiric multi-drug therapy, and eventually targeted de-escalation.

Estimated Time:1m 0s

Question 2879Question →

Match each of the following dynamic auscultation findings with the most likely underlying structural or valvular pathology.

Click a left item, then click its matching right item

Show answer & explanation

Answer

The dynamic auscultation findings accurately map to hypertrophic cardiomyopathy (louder with Valsalva), mitral valve prolapse (later with squatting), aortic stenosis (softer with Valsalva), and mitral regurgitation (louder with handgrip).

Each maneuver predictably alters cardiac hemodynamics (preload and afterload), which changes the intensity or timing of murmurs depending on their underlying anatomical mechanism.

Step-by-Step Solution

Evaluate the murmur that becomes louder with the Valsalva maneuver.

The Valsalva maneuver decreases preload. A murmur that intensifies with decreased left ventricular volume is characteristic of hypertrophic cardiomyopathy.

Decreased left ventricular volume exacerbates the dynamic outflow tract obstruction.

Evaluate the murmur with a click that occurs later with squatting.

Squatting increases both preload and afterload, enlarging left ventricular volume. This delays leaflet prolapse in mitral valve prolapse.

A larger left ventricular volume keeps the mitral leaflets tense for a longer period before they prolapse into the left atrium.

Evaluate the crescendo-decrescendo murmur that decreases with the Valsalva maneuver.

Decreased preload results in a lower stroke volume across the aortic valve, which softens the murmur of aortic stenosis.

Most forward-flow murmurs decrease in intensity when preload is reduced.

Evaluate the holosystolic murmur that increases with sustained handgrip.

Handgrip increases afterload, which raises the backward pressure gradient. This amplifies retrograde flow and murmur intensity in mitral regurgitation.

Higher systemic vascular resistance forces more blood back through the incompetent mitral valve.

Key Concept

Hemodynamic effects of dynamic auscultation maneuvers on structural heart murmurs

Estimated Time:1m 30s

Question 2880Question →

A 62-year-old man is brought to the emergency department by his wife due to progressive confusion, lethargy, and worsening shortness of breath over the past 48 hours. He has a history of alcohol-associated cirrhosis, heart failure with preserved ejection fraction, and hypothyroidism. Home medications include lactulose, nadolol, spironolactone, furosemide, and levothyroxine. His wife notes that he doubled his furosemide dose three days ago because his abdomen felt "tighter than usual."

Vital signs are:
Temperature: 37.1°C (98.8°F)
Blood pressure: 105/65 mm Hg
Pulse: 98/min
Respirations: 22/min
Oxygen saturation: 94% on room air

Physical examination reveals a lethargic man who is oriented only to person. Scleral icterus and multiple spider angiomata are present. Breath sounds are diminished at the right lung base with dullness to percussion. The abdomen is markedly distended and tense, with shifting dullness. When the patient holds his arms outstretched with wrists extended, a coarse, flapping tremor is observed.

Laboratory results:
Sodium: 131 mEq/L
Potassium: 2.7 mEq/L
Chloride: 88 mEq/L
Bicarbonate: 35 mEq/L
Blood urea nitrogen: 38 mg/dL
Creatinine: 1.5 mg/dL
Leukocyte count: 7,500/mm³
Hemoglobin: 11.2 g/dL
Platelets: 85,000/mm³
TSH: 2.1 µU/mL (Normal: 0.4-4.0 µU/mL)
Free T4: 1.2 ng/dL (Normal: 0.8-1.8 ng/dL)

Arterial blood gas on room air:
pH: 7.51
PaCO2: 45 mm Hg
PaO2: 70 mm Hg

A diagnostic paracentesis yields clear yellow fluid with a neutrophil count of 120/mm³. Chest radiography reveals a small right-sided pleural effusion without focal consolidations.

In addition to optimizing his lactulose therapy, which of the following is the most appropriate next step in the management of this patient?

Administration of intravenous potassium chloride

Intravenous ceftriaxone

Intravenous furosemide and noninvasive positive-pressure ventilation

Intravenous acetazolamide

Intravenous levothyroxine

Show answer & explanation

Answer: Administration of intravenous potassium chloride

Answer

The correct answer is the administration of intravenous potassium chloride.

The correct answer focuses on reversing the specific precipitant of the patient's hepatic encephalopathy. In patients with cirrhosis, hypokalemia triggers increased renal ammonia production. Concurrently, diuretic-induced metabolic alkalosis favors the conversion of ammonium (NH4+) to ammonia (NH3). Because NH3 is uncharged, it readily crosses the blood-brain barrier, worsening encephalopathy. Repleting potassium chloride corrects both the hypokalemia and the associated hypochloremic metabolic alkalosis, halting this pathophysiologic cascade.

Step-by-Step Solution

Identify the primary clinical syndrome.

The patient has a flapping tremor (asterixis), lethargy, and a history of cirrhosis, which is diagnostic of an acute episode of hepatic encephalopathy (HE).

Recognizing the acute life-threatening complication guides the search for the precipitating cause.

Analyze the laboratory data to identify the trigger for the HE episode.

The labs reveal severe hypokalemia (K+ 2.7 mEq/L) and metabolic alkalosis (pH 7.51, HCO3 35 mEq/L) following excessive furosemide use.

Common precipitants for HE include GI bleeding, infection, and electrolyte disturbances. The paracentesis ruled out Spontaneous Bacterial Peritonitis (neutrophils < 250/mm³).

Connect the electrolyte derangements to the pathophysiology of hepatic encephalopathy.

Intracellular potassium depletion increases renal ammonia production. Furthermore, metabolic alkalosis shifts the equilibrium of ammonium (NH4+) toward uncharged ammonia (NH3), which freely crosses the blood-brain barrier.

Understanding this mechanism confirms that the hypokalemia and alkalosis are directly causing the worsening mental status.

Select the appropriate intervention.

Intravenous potassium chloride must be administered to replete the potassium deficit and provide chloride to help resolve the metabolic alkalosis.

Correcting the underlying precipitant is the cornerstone of HE management alongside ammonia-lowering therapies like lactulose.

Key Concept

Hypokalemia and metabolic alkalosis strongly precipitate hepatic encephalopathy by increasing renal ammoniagenesis and facilitating the diffusion of ammonia (NH3) across the blood-brain barrier.

Estimated Time:1m 30s

PreviousPage 144 / 158Next

Internal Medicine

Answer

Step-by-Step Solution

Key Concept

Common Mistakes

Answer

Step-by-Step Solution

Key Concept

Common Mistakes

Answer

Step-by-Step Solution

Key Concept

Common Mistakes

Answer

Step-by-Step Solution

Key Concept

Common Mistakes

Answer

Step-by-Step Solution

Key Concept

Common Mistakes

Answer

Step-by-Step Solution

Key Concept

Common Mistakes

Answer

Step-by-Step Solution

Key Concept

Common Mistakes

Answer

Step-by-Step Solution

Key Concept

Common Mistakes

Answer

Step-by-Step Solution

Key Concept

Common Mistakes

Answer

Step-by-Step Solution

Key Concept

Common Mistakes

Answer

Step-by-Step Solution

Key Concept

Common Mistakes

Answer

Step-by-Step Solution

Key Concept

Common Mistakes

Answer

Step-by-Step Solution

Key Concept

Common Mistakes

Answer

Step-by-Step Solution

Key Concept

Common Mistakes

Answer

Step-by-Step Solution

Key Concept

Common Mistakes

Answer

Step-by-Step Solution

Key Concept

Common Mistakes

Answer

Step-by-Step Solution

Key Concept

Common Mistakes

Answer

Step-by-Step Solution

Key Concept

Common Mistakes

Answer

Step-by-Step Solution

Key Concept

Common Mistakes

Answer

Step-by-Step Solution

Key Concept