Internal Medicine

3151 questions

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

A 71-year-old man is transported to the emergency department from a local nursing facility due to the sudden onset of severe breathlessness and orthopnea that started 3 hours ago. He has a past medical history of severe chronic obstructive pulmonary disease (COPD) and ischemic cardiomyopathy with a left ventricular ejection fraction of $30\%$ .

Upon arrival, he is visibly agitated and using accessory muscles of respiration. Vital signs are:
- Temperature: $37.1^\circ\text{C}$ ( $98.8^\circ\text{F}$ )
- Blood pressure: $172/100\text{ mm Hg}$
- Heart rate: $118\text{/min}$ and regular
- Respiratory rate: $29\text{/min}$
- Oxygen saturation: $82\%$ on ambient air

Physical examination reveals jugular venous distention when sitting upright at 45 degrees. Chest auscultation demonstrates widespread expiratory wheezing mixed with fine bibasilar crackles. Cardiac auscultation reveals tachycardia and a prominent third heart sound (S3). There is 2+ bilateral pitting edema up to the knees.

Arterial blood gas analysis on ambient air shows:
- pH: 7.22
- $PaCO_2$ : $75\text{ mm Hg}$
- $PaO_2$ : $48\text{ mm Hg}$
- $HCO_3^-$ : $31\text{ mEq/L}$

Which of the following are the most appropriate initial steps in the management of this patient? (Select exactly two)

Select all that apply

Apply noninvasive positive-pressure ventilation

Administer a rapid-acting intravenous loop diuretic

Commence empiric broad-spectrum antibiotics and systemic corticosteroids

Infuse intravenous sodium bicarbonate to correct the acidemia

Administer high-dose nebulized bronchodilators as the primary therapy

Show answer & explanation

Answer: Apply noninvasive positive-pressure ventilation; Administer a rapid-acting intravenous loop diuretic

Answer

The most appropriate initial steps are applying noninvasive positive-pressure ventilation (NPPV) and administering a rapid-acting intravenous loop diuretic.

The correct interventions directly address the pathophysiology of acute decompensated heart failure (ADHF). Noninvasive positive-pressure ventilation (NPPV) provides positive intrathoracic pressure, which decreases venous return (preload) and reduces left ventricular transmural pressure (afterload), thereby improving cardiac output. It also recruits fluid-filled alveoli, improving gas exchange and reducing the work of breathing. Intravenous loop diuretics (e.g., furosemide) are indicated to rapidly reduce intravascular volume and alleviate venous congestion.

Step-by-Step Solution

Analyze the clinical presentation and physical examination findings.

The patient presents with severe respiratory distress, hypertension, JVD, an S3 gallop, bibasilar crackles, and peripheral edema.

These are classic signs of acute decompensated heart failure (ADHF) with volume overload. The wheezing represents 'cardiac asthma' secondary to peribronchial edema, not necessarily a primary COPD exacerbation.

Interpret the arterial blood gas (ABG) results.

The ABG shows acidemia (pH 7.22), severe hypercapnia (

PaCO_2

75\text{ mm Hg}

), hypoxemia (

PaO_2

48\text{ mm Hg}

), and an elevated bicarbonate (

HCO_3^-

31\text{ mEq/L}

This indicates an acute-on-chronic respiratory acidosis. The elevated bicarbonate reflects baseline chronic

CO_2

retention from severe COPD, while the acute drop in pH is driven by the sudden rise in

PaCO_2

due to alveolar flooding from cardiogenic pulmonary edema.

Determine the optimal immediate interventions based on the diagnosis.

The patient requires immediate support for oxygenation and ventilation, along with aggressive volume removal.

NPPV effectively supports ventilation, reduces the work of breathing, and provides favorable hemodynamic effects (decreased preload and afterload). Intravenous loop diuretics are required to rapidly treat the volume overload.

Key Concept

The initial management of acute decompensated heart failure (ADHF) complicated by acute hypercapnic respiratory failure prioritizes noninvasive positive-pressure ventilation (NPPV) and intravenous loop diuretics, while differentiating 'cardiac asthma' from a primary COPD exacerbation.

Question 22Question →

A 64-year-old man is evaluated in the intensive care unit for a persistent fever. He was admitted 8 days ago after a severe motor vehicle collision that resulted in multiple rib fractures, a pulmonary contusion, and a splenectomy. He has been mechanically ventilated since admission. Three days ago, he developed a temperature of 38.9°C (102.0°F), increased purulent endotracheal secretions, and increased oxygen requirements. A chest radiograph revealed a new right lower lobe consolidation. He was empirically started on intravenous cefepime, vancomycin, and amikacin. Today, his temperature is 37.4°C (99.3°F), and his oxygen requirements have decreased. The endotracheal aspirate culture from three days ago has grown Pseudomonas aeruginosa (>100,000 CFU/mL). Susceptibility testing shows the isolate is susceptible to cefepime, meropenem, piperacillin-tazobactam, and amikacin, but resistant to ciprofloxacin. No other organisms, including Staphylococcus aureus, have grown. Blood cultures obtained prior to antibiotic initiation are negative. Which of the following is the most appropriate next step in this patient's pharmacotherapy?

Discontinue vancomycin and amikacin, and continue cefepime

Discontinue vancomycin, and continue cefepime and amikacin

Discontinue amikacin, and continue cefepime and vancomycin

Continue cefepime, vancomycin, and amikacin

Discontinue current antibiotics, and initiate meropenem

Show answer & explanation

Answer: Discontinue vancomycin and amikacin, and continue cefepime

Answer

The most appropriate next step is to discontinue vancomycin and amikacin, and continue therapy with cefepime alone.

The correct answer is to discontinue vancomycin and amikacin, and continue cefepime alone. This patient initially presented with ventilator-associated pneumonia (VAP) and appropriately received broad-spectrum empiric therapy targeting MRSA (vancomycin) and resistant Gram-negative organisms, including Pseudomonas (cefepime and amikacin). At 48 to 72 hours, when culture data return, therapy must be de-escalated. Because no MRSA was isolated, vancomycin can be safely discontinued. Furthermore, although empiric double antipseudomonal coverage is standard for critically ill patients at risk for multidrug-resistant organisms, definitive therapy should utilize a single active beta-lactam agent once susceptibilities are confirmed. Continuing an aminoglycoside like amikacin offers no survival benefit for definitive therapy and exposes the patient to nephrotoxicity and ototoxicity.

Step-by-Step Solution

Identify the patient's clinical diagnosis and indication for antibiotics.

The patient has ventilator-associated pneumonia (VAP) as evidenced by fever, purulent secretions, new lung consolidation, and positive respiratory cultures after >48 hours of mechanical ventilation.

Establishing the diagnosis determines the appropriate treatment guidelines to apply.

Analyze the culture and susceptibility results relative to the empiric antibiotic regimen.

Cultures grew only Pseudomonas aeruginosa susceptible to cefepime. Methicillin-resistant Staphylococcus aureus (MRSA) was not isolated.

Empiric therapy must be adjusted based on definitive microbiological data to prevent antibiotic resistance and drug toxicity.

Apply principles of antibiotic stewardship to de-escalate the regimen.

Vancomycin should be stopped because MRSA is absent. Amikacin should be stopped because combination therapy for Pseudomonas is only required empirically; definitive therapy requires only a single active beta-lactam agent (cefepime).

Guidelines recommend transitioning from broad-spectrum empiric therapy to targeted monotherapy once susceptibilities are known.

Key Concept

In the management of ventilator-associated pneumonia, empiric broad-spectrum therapy (e.g., MRSA coverage and double antipseudomonal coverage) should be promptly de-escalated to a single targeted agent once culture and susceptibility results are available and the patient is clinically improving.

Estimated Time:1m 30s

Question 23Question →

A $38$ -year-old woman is brought to the emergency department by her husband due to sudden-onset confusion, agitation, and strange behavior that began this morning. For the past $3$ days, she has complained of profound fatigue, generalized weakness, and subjective fevers. She has no significant past medical history and takes no medications. Her temperature is $38.2^\circ\text{C}$ ( $100.8^\circ\text{F}$ ), pulse is $112\text{/min}$ , blood pressure is $142/88\text{ mmHg}$ , and respiratory rate is $18\text{/min}$ . Physical examination reveals a confused and agitated woman. There are numerous non-blanching, pinpoint erythematous macules on her bilateral lower extremities. Neurological examination reveals no focal motor or sensory deficits, but she is oriented only to person.

Laboratory studies reveal:
Hemoglobin: $7.4\text{ g/dL}$
Platelet count: $22,000/\mu\text{L}$
Leukocyte count: $9,200/\mu\text{L}$
Creatinine: $2.2\text{ mg/dL}$
Total bilirubin: $3.8\text{ mg/dL}$
Indirect bilirubin: $3.1\text{ mg/dL}$
Thyroid-stimulating hormone (TSH): $4.8\text{ }\mu\text{U/mL}$ (Normal: $0.4-4.0\text{ }\mu\text{U/mL}$ )

A peripheral blood smear demonstrates numerous fragmented red blood cells.

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

Transfuse pooled donor platelets

Administer intravenous ceftriaxone and vancomycin

Initiate therapeutic plasma exchange

Administer intravenous haloperidol and arrange psychiatric admission

Defer interventions until informed consent is obtained from the patient's parents

Show answer & explanation

Answer: Initiate therapeutic plasma exchange

Answer

The correct answer is to initiate therapeutic plasma exchange.

The correct answer is to initiate therapeutic plasma exchange. This patient presents with the classic pentad of Thrombotic Thrombocytopenic Purpura (TTP): fever, microangiopathic hemolytic anemia (schistocytes, elevated indirect bilirubin, anemia), thrombocytopenia, renal insufficiency (elevated creatinine), and neurologic symptoms (confusion, agitation). TTP is a life-threatening hematologic emergency caused by severe deficiency of the von Willebrand factor (vWF)-cleaving protease ADAMTS13, leading to unchecked platelet aggregation and microvascular thrombosis. Therapeutic plasma exchange (plasmapheresis) is the definitive next step in management as it removes the offending autoantibodies and replenishes functional ADAMTS13.

Step-by-Step Solution

Analyze the patient's clinical presentation and vitals.

38

-year-old woman presents with acute-onset confusion, fever (

38.2^\circ\text{C}

), and petechiae.

To identify the primary organ systems involved (neurologic and dermatologic/hematologic) in an acutely ill patient.

Interpret the laboratory findings and peripheral blood smear.

Labs reveal severe thrombocytopenia (

22,000/\mu\text{L}

), anemia (

7.4\text{ g/dL}

) with elevated indirect bilirubin, acute kidney injury (creatinine

2.2\text{ mg/dL}

), and schistocytes on smear.

To confirm the presence of Microangiopathic Hemolytic Anemia (MAHA) and differentiate it from other causes of thrombocytopenia.

Synthesize findings to establish the most likely diagnosis.

The combination of MAHA, thrombocytopenia, fever, renal dysfunction, and neurologic abnormalities represents the classic pentad of Thrombotic Thrombocytopenic Purpura (TTP).

To select the appropriate life-saving intervention, as TTP requires immediate, specialized treatment.

Determine the best next step in management based on the diagnosis of TTP.

Therapeutic plasma exchange must be initiated immediately.

Plasma exchange removes autoantibodies against ADAMTS13 and provides the functional enzyme, reversing the microvascular thrombosis.

Key Concept

Diagnosis and emergent management of Thrombotic Thrombocytopenic Purpura (TTP) with therapeutic plasma exchange.

Estimated Time:1m 30s

Question 24Question →

Match each clinical presentation of a newly diagnosed HIV patient with the most appropriate timing and rationale for initiating antiretroviral therapy (ART).

Click a left item, then click its matching right item

Show answer & explanation

Answer

The patient with cryptococcal meningitis matches with deferring ART

2

10

weeks to prevent fatal CNS IRIS. The patient with tuberculosis and a CD4 count

< 50

matches with initiating ART within

2

weeks to maximize survival. The patient with tuberculosis and a CD4 count

> 50

matches with initiating ART between

2

and

8

weeks. The patient with CMV retinitis matches with deferring ART

1

2

weeks to prevent vision-threatening immune recovery uveitis.

The timing of ART initiation in the setting of acute opportunistic infections requires a delicate balance between rapidly restoring immune function to improve survival and avoiding Immune Reconstitution Inflammatory Syndrome (IRIS). For cryptococcal meningitis, the risk of fatal CNS IRIS is unacceptably high, necessitating a

2

10

week delay. For tuberculosis, the survival benefit of very early ART (within

2

weeks) outweighs the risk of TB-IRIS only in profoundly immunosuppressed patients (CD4

< 50

). For TB patients with CD4 counts

> 50

, ART should be delayed

2

8

weeks. For CMV retinitis, a

1

2

week delay is required to prevent immune recovery uveitis and subsequent blindness.

Step-by-Step Solution

Identify the underlying opportunistic infection (OI) for each patient based on the clinical presentation and diagnostic findings.

Patient 1 has cryptococcal meningitis, Patient 2 has active pulmonary tuberculosis, Patient 3 has active pulmonary tuberculosis, and Patient 4 has CMV retinitis.

Recognizing the specific OI is the critical first step because antiretroviral therapy (ART) initiation guidelines are inherently disease-specific.

Determine the patient's CD4 count for those with tuberculosis.

Patient 2 has a CD4 count

< 50

cells/

\text{mm}^3

, whereas Patient 3 has a CD4 count

> 50

cells/

\text{mm}^3

For active tuberculosis, the optimal timing of ART depends heavily on the degree of immunosuppression to balance the survival benefit against the risk of Immune Reconstitution Inflammatory Syndrome (IRIS).

Apply the guideline-based timing for ART initiation for each specific OI and CD4 category.

Cryptococcal meningitis requires a

2

10

week delay; TB with CD4

< 50

requires ART within

2

weeks; TB with CD4

> 50

requires ART in

2

8

weeks; CMV retinitis requires a

1

2

week delay.

Following these specific guidelines minimizes the risk of fatal or organ-threatening IRIS while maximizing overall patient survival.

Key Concept

Timing of Antiretroviral Therapy (ART) Initiation in HIV-Associated Opportunistic Infections

Question 25Question →

A 22-year-old man presents to the emergency department complaining of severe chest pain and difficulty breathing for the past 48 hours. He has a known history of homozygous sickle cell disease (HbSS). Vital signs show a temperature of 39.1°C (102.4°F), blood pressure of 92/58 mm Hg, heart rate of 128/min, and respiratory rate of 34/min. Pulse oximetry is 83% while receiving high-flow oxygen via a non-rebreather mask. Physical examination reveals severe respiratory distress, scleral icterus, and bilateral dullness to percussion with widespread crackles. A portable chest radiograph displays new diffuse, multilobar alveolar infiltrates.

Laboratory analysis reveals the following:

Laboratory Test	Result
Hemoglobin	6.9 g/dL (baseline 8.5 g/dL)
Leukocytes	24,000/mm³
Platelets	380,000/mm³
Reticulocytes	15%

The patient has been started on intravenous fluids, broad-spectrum antibiotics (ceftriaxone and azithromycin), and adequate pain management. Which of the following is the most appropriate next step in management?

Administer intravenous furosemide

CT angiography of the chest

Exchange blood transfusion

Simple red blood cell transfusion

Switch to intravenous piperacillin-tazobactam

Show answer & explanation

Answer: Exchange blood transfusion

Answer

Exchange blood transfusion is the most appropriate next step in management for this patient with severe acute chest syndrome.

The correct answer is exchange blood transfusion. This patient is presenting with acute chest syndrome (ACS), a life-threatening complication of sickle cell disease characterized by fever, chest pain, new pulmonary infiltrates, and hypoxemia. His presentation is severe, evidenced by multilobar infiltrates and profound hypoxemia (83% on a non-rebreather mask). The management of severe ACS requires an exchange blood transfusion. This procedure removes the patient's sickled red blood cells (HbS) and replaces them with normal red blood cells (HbA), rapidly improving oxygenation and halting the vaso-occlusive cycle without significantly raising overall blood viscosity. Simple transfusion is typically reserved for mild cases where the hemoglobin has dropped significantly but hypoxemia is less severe.

Step-by-Step Solution

Identify the primary diagnosis based on the clinical presentation.

The patient with sickle cell disease presents with fever, chest pain, new pulmonary infiltrates, and severe hypoxemia, establishing the diagnosis of Acute Chest Syndrome (ACS).

Recognizing ACS is critical as it is a major cause of mortality in sickle cell patients and requires specific, rapid intervention.

Determine the severity of the acute chest syndrome.

The presence of multilobar infiltrates, severe hypoxemia (SpO2 83% on high-flow oxygen), and hemodynamic instability indicates severe ACS.

Severity classification dictates the choice between a simple red blood cell transfusion and an exchange transfusion.

Select the appropriate targeted intervention for severe ACS.

Exchange blood transfusion is indicated rather than a simple transfusion.

Exchange transfusion rapidly decreases the percentage of hemoglobin S and improves oxygen-carrying capacity without significantly increasing overall blood viscosity, avoiding the exacerbation of vaso-occlusion.

Key Concept

Severe acute chest syndrome in sickle cell disease requires exchange blood transfusion to rapidly reduce hemoglobin S levels and improve oxygenation without causing hyperviscosity.

Question 26Question →

A 68-year-old man is brought to the emergency department by emergency medical services due to severe, acute-onset shortness of breath and chest tightness that awoke him from sleep 1 hour ago. He has a history of ischemic cardiomyopathy with a left ventricular ejection fraction of 35%, chronic obstructive pulmonary disease, hypertension, and erectile dysfunction. His current medications include aspirin, lisinopril, carvedilol, tiotropium, and sildenafil. He reports taking a dose of sildenafil 10 hours ago. The patient is diaphoretic and in severe respiratory distress, struggling to speak in full sentences. His temperature is 37.1°C (98.8°F), blood pressure is 210/115 mmHg, pulse is 115/min, and respiratory rate is 32/min with an oxygen saturation of 84% on room air. Physical examination reveals jugular venous distension 12 cm above the sternal angle. Cardiac auscultation reveals a regular tachycardia with a prominent S3 gallop. Lung auscultation reveals diffuse bilateral expiratory wheezes and crackles at the lung bases. Electrocardiogram shows sinus tachycardia with left ventricular hypertrophy and non-specific ST-segment changes. Which of the following is the most appropriate next step in management?

Application of non-invasive positive pressure ventilation and administration of intravenous furosemide

Administration of intravenous nitroglycerin and intravenous furosemide

Administration of nebulized albuterol, ipratropium, and intravenous methylprednisolone

Administration of intravenous metoprolol and non-invasive positive pressure ventilation

Immediate endotracheal intubation and administration of intravenous furosemide

Show answer & explanation

Answer: Application of non-invasive positive pressure ventilation and administration of intravenous furosemide

Answer

Application of non-invasive positive pressure ventilation and administration of intravenous furosemide

The patient presents with sympathetic crashing acute pulmonary edema, a form of acute decompensated heart failure (ADHF) characterized by acute severe hypertension, respiratory distress, and flash pulmonary edema. The wheezing represents 'cardiac asthma' resulting from peribronchial edema. The immediate goals of therapy are to improve oxygenation and reduce ventricular preload and afterload. Non-invasive positive pressure ventilation (NIPPV) is the ideal first-line respiratory support because it decreases the work of breathing, improves oxygenation, and beneficially decreases both left ventricular preload and afterload. Intravenous loop diuretics (such as furosemide) are indicated to assist with fluid offloading. Although intravenous vasodilators, primarily nitroglycerin, are standard therapy for rapid afterload reduction in hypertensive ADHF, they are strictly contraindicated in this patient. The patient ingested sildenafil, a phosphodiesterase-5 (PDE-5) inhibitor, 10 hours ago. PDE-5 inhibitors block the degradation of cyclic GMP (cGMP), while nitrates increase the production of cGMP via nitric oxide. Co-administering these medications within 24 hours leads to massive cGMP accumulation, resulting in profound and potentially fatal hypotension. Therefore, combining NIPPV with intravenous furosemide provides safe and effective preload and afterload reduction without risking a catastrophic drug interaction.

Step-by-Step Solution

Diagnose the primary cause of acute respiratory distress based on clinical findings.

Acute decompensated heart failure (sympathetic crashing acute pulmonary edema).

The presence of severe hypertension, hypoxia, orthopnea, an S3 gallop, JVD, and bibasilar crackles points to a cardiogenic etiology. The wheezing represents cardiac asthma, not a primary COPD exacerbation.

Review the patient's medication history for potential drug interactions before initiating standard heart failure therapy.

The patient took sildenafil 10 hours ago.

Standard therapy for hypertensive acute pulmonary edema includes afterload reduction with nitrates (e.g., nitroglycerin). However, nitrates are absolutely contraindicated within 24 hours of sildenafil use.

Determine the safest and most effective alternative interventions for immediate stabilization.

Initiate non-invasive positive pressure ventilation (NIPPV) and administer intravenous loop diuretics.

NIPPV rapidly improves oxygenation and decreases both left ventricular preload and afterload, serving as a non-pharmacologic afterload reducer. Furosemide aids in volume offloading without interacting with PDE-5 inhibitors.

Key Concept

Management of acute decompensated heart failure with concurrent phosphodiesterase-5 inhibitor use

Question 27Question →

Match each clinical presentation and laboratory finding with the most likely underlying nephrological diagnosis.

Click a left item, then click its matching right item

Show answer & explanation

Answer

The correct matches are: Acyclovir use with needle-shaped crystals correlates to Crystal-induced acute kidney injury. Rheumatoid arthritis with apple-green birefringence correlates to AA Amyloidosis. Post-angiography AKI with livedo reticularis correlates to Atheroembolic renal disease. Lithium use with lack of ADH response correlates to Nephrogenic diabetes insipidus. Tenofovir use with glycosuria and hypophosphatemia correlates to Proximal (Type 2) renal tubular acidosis.

Each vignette provides pathognomonic clues for a specific renal pathology. Acyclovir is notorious for precipitating in renal tubules. Chronic inflammatory conditions drive serum amyloid A overproduction leading to AA amyloidosis. Invasive vascular procedures can dislodge cholesterol crystals causing atheroembolic disease with systemic features. Lithium commonly impairs the collecting duct's response to ADH. Finally, tenofovir is a known cause of Fanconi syndrome, manifesting as a generalized proximal tubular dysfunction.

Step-by-Step Solution

Analyze the first clinical vignette involving intravenous acyclovir.

Identify the rapid onset of acute kidney injury accompanied by needle-shaped crystals.

Recognizing the crystalluria points directly to crystal-induced intratubular obstruction caused by the drug.

Evaluate the second vignette detailing rheumatoid arthritis and nephrotic syndrome.

Identify the pathognomonic finding of apple-green birefringence with Congo red stain.

This specific histological finding, combined with a chronic inflammatory state, confirms AA Amyloidosis.

Examine the third vignette describing acute kidney injury following coronary angiography.

Identify the delayed onset, livedo reticularis, and eosinophilia.

These are the classic systemic signs of cholesterol embolization (atheroembolic renal disease), distinguishing it from contrast-induced nephropathy.

Assess the fourth vignette involving lithium therapy and polyuria.

Recognize the lack of urinary concentration following both water deprivation and desmopressin administration.

This establishes resistance to ADH at the renal level, confirming nephrogenic diabetes insipidus rather than central diabetes insipidus.

Review the fifth vignette detailing tenofovir use and multiple metabolic derangements.

Identify the combination of normoglycemic glycosuria, hypophosphatemia, and non-anion gap metabolic acidosis.

This combination indicates a generalized proximal tubule defect (Fanconi syndrome), leading to Proximal (Type 2) RTA.

Key Concept

Differentiation of complex nephrological syndromes based on specific medication toxicities, systemic disease manifestations, and pathognomonic biopsy or urinary findings.

Question 28Question →

A 36-year-old woman is evaluated in the endocrinology clinic for a 9-month history of amenorrhea and bilateral milky nipple discharge. She has also experienced mild, dull frontal headaches over the past 3 months. She takes no medications, and a urine pregnancy test performed in the clinic is negative. Menarche occurred at age 13, and her menses were previously regular. Her body mass index (BMI) is $24 \text{ kg/m}^2$ . Vital signs are within normal limits. Physical examination confirms bilateral galactorrhea. Visual field testing by confrontation reveals intact peripheral vision in both eyes.

Laboratory studies show the following:
Prolactin: $68 \text{ ng/mL}$ (Normal: $4$ - $23 \text{ ng/mL}$ )
Thyroid-stimulating hormone (TSH): $1.8 \ \mu\text{U/mL}$ (Normal: $0.4$ - $4.2 \ \mu\text{U/mL}$ )
Free thyroxine (T4): $1.1 \text{ ng/dL}$ (Normal: $0.9$ - $1.7 \text{ ng/dL}$ )
Insulin-like growth factor-1 (IGF-1): $180 \text{ ng/mL}$ (within normal limits for age)
Morning cortisol: $14 \ \mu\text{g/dL}$ (Normal: $5$ - $25 \ \mu\text{g/dL}$ )

Magnetic resonance imaging (MRI) of the brain reveals a $1.8$ -cm homogeneous sellar mass with suprasellar extension. The mass is compressing the pituitary stalk and abutting the optic chiasm.

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

Transsphenoidal surgical resection

Initiation of cabergoline therapy

Initiation of levothyroxine therapy

Serial observation with repeat MRI of the brain in 6 months

Intravenous hydrocortisone administration

Show answer & explanation

Answer: Transsphenoidal surgical resection

Answer

Transsphenoidal surgical resection

The correct answer is transsphenoidal surgical resection because the patient has a clinically non-functioning pituitary macroadenoma causing symptomatic mass effect. While her prolactin is elevated, the level (

68 \text{ ng/mL}

) is far too low for a

1.8

-cm true prolactinoma, which typically secretes prolactin at levels

> 200 \text{ ng/mL}

. Instead, the mild hyperprolactinemia is due to the "stalk effect"—the large tumor compresses the pituitary stalk, disrupting the normal delivery of inhibitory dopamine from the hypothalamus to the lactotrophs. Because dopamine agonists (e.g., cabergoline) are ineffective at shrinking non-functioning adenomas, surgery is the treatment of choice to relieve headaches and prevent impending visual loss from optic chiasm compression.

Step-by-Step Solution

Evaluate the clinical and laboratory presentation.

The patient has a

1.8

-cm pituitary mass with mildly elevated prolactin (

68 \text{ ng/mL}

) and normal thyroid, IGF-1, and cortisol levels.

Establishing the biochemical activity of the pituitary mass is essential for accurate diagnosis and management.

Correlate the tumor size with the prolactin level.

A true prolactinoma measuring

1.8 \text{ cm}

(a macroadenoma) would expectedly produce prolactin levels

> 200 \text{ ng/mL}

(often

> 1000 \text{ ng/mL}

). The level of

68 \text{ ng/mL}

is disproportionately low for the tumor size.

Tumor size in prolactinomas correlates directly with hormone secretion. A mismatch suggests a different etiology for the hyperprolactinemia.

Identify the mechanism of hyperprolactinemia.

The mild prolactin elevation is caused by the "stalk effect"—the

1.8

-cm non-functioning macroadenoma is compressing the pituitary stalk, blocking the delivery of inhibitory dopamine from the hypothalamus to the lactotrophs.

Understanding the stalk effect confirms the diagnosis of a clinically non-functioning pituitary adenoma rather than a prolactinoma.

Determine the appropriate management for the confirmed diagnosis.

Dopamine agonists do not reliably shrink non-functioning adenomas. Because the mass is large, abutting the optic chiasm, and causing headaches, surgical resection is required.

Surgical decompression is the definitive treatment for symptomatic non-functioning macroadenomas to relieve mass effect and preserve vision.

Key Concept

Discordance between a large pituitary mass size and a mildly elevated prolactin level (< 200 ng/mL) indicates a non-functioning adenoma causing stalk compression, which requires surgery, rather than a prolactinoma, which is treated medically.

Question 29Question →

A 67-year-old woman is brought to the emergency department by her daughter due to increasing confusion, rapid breathing, and generalized weakness that started yesterday. The daughter notes that the patient has been complaining of a "constant buzzing" in her ears for the past 24 hours. The patient has a history of ischemic cardiomyopathy with a left ventricular ejection fraction of 35%, type 2 diabetes mellitus, and severe bilateral knee osteoarthritis. Her current medications include metoprolol, lisinopril, empagliflozin, and several over-the-counter analgesics that she has been taking frequently due to a recent pain flare.

Vital signs are:
Temperature: 38.3°C (100.9°F)
Heart rate: 118/min
Respiratory rate: 32/min
Blood pressure: 105/65 mm Hg
Oxygen saturation: 97% on room air

Physical examination reveals a disoriented patient taking deep, rapid breaths. Chest auscultation demonstrates scattered bilateral basilar crackles. Cardiac examination shows a regular, rapid rhythm with no murmurs, gallops, or jugular venous distention. Trace bilateral pedal edema is present.

Laboratory results:
Serum sodium: 142 mEq/L
Serum potassium: 3.4 mEq/L
Serum chloride: 100 mEq/L
Serum bicarbonate: 14 mEq/L
Blood urea nitrogen: 32 mg/dL
Serum creatinine: 1.6 mg/dL (baseline 1.1 mg/dL)

Arterial blood gas on room air:
pH: 7.46
PaCO2: 20 mm Hg
PaO2: 88 mm Hg

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

Intravenous sodium bicarbonate

Endotracheal intubation and mechanical ventilation

Intravenous furosemide

Intravenous ceftriaxone and azithromycin

Measurement of serum thyroid-stimulating hormone

Show answer & explanation

Answer: Intravenous sodium bicarbonate

Answer

Intravenous sodium bicarbonate

The correct intervention is intravenous sodium bicarbonate. This patient's presentation of tinnitus, hyperthermia, noncardiogenic pulmonary edema, altered mental status, and a history of excessive over-the-counter analgesic use is highly suspicious for salicylate toxicity. The diagnosis is confirmed by her arterial blood gas and basic metabolic panel, which reveal the hallmark mixed acid-base disorder of salicylate poisoning: a primary respiratory alkalosis (due to direct stimulation of the medullary respiratory center) and a primary high anion gap metabolic acidosis (due to uncoupling of oxidative phosphorylation and accumulation of organic acids). Intravenous sodium bicarbonate acts to alkalinize both the serum and the urine. Serum alkalinization keeps the salicylate molecule in its ionized (deprotonated) state, preventing it from crossing the blood-brain barrier and causing central nervous system toxicity. Urine alkalinization promotes 'ion trapping' in the renal tubules, significantly increasing renal clearance of the drug.

Step-by-Step Solution

Analyze the arterial blood gas (ABG) to determine the primary acid-base disorder.

The pH is 7.46 (alkalemia). The

PaCO_2

is 20 mm Hg (low). The

HCO_3^-

is 14 mEq/L (low). Since the pH is high and the

PaCO_2

is low, the primary disorder is a respiratory alkalosis.

Establishing the initial primary disorder is the first step in diagnosing complex acid-base abnormalities.

Calculate expected compensation to evaluate for mixed acid-base disorders.

For acute respiratory alkalosis, expected

HCO_3^-

drops by 2 mEq/L for every 10 mm Hg drop in

PaCO_2

. The

PaCO_2

dropped by 20 (from 40 to 20), so

HCO_3^-

should drop by 4. Expected

HCO_3^- = 24 - 4 = 20

mEq/L. The actual

HCO_3^-

is 14 mEq/L. Because the actual bicarbonate is much lower than the expected compensatory level, there is a concomitant primary metabolic acidosis.

Whenever actual compensatory values differ significantly from expected values, a secondary primary disorder is present.

Calculate the anion gap to characterize the metabolic acidosis.

Anion Gap (AG)

= Na^+ - (Cl^- + HCO_3^-) = 142 - (100 + 14) = 28

mEq/L. This confirms a high anion gap metabolic acidosis (HAGMA).

HAGMA narrows the differential diagnosis to specific causes such as ketoacidosis, lactic acidosis, renal failure, or ingestions (MUDPILES).

Synthesize the laboratory data with the clinical presentation.

The patient has a primary respiratory alkalosis + primary HAGMA. Clinically, she presents with tinnitus ('buzzing' in ears), hyperthermia, tachypnea, and noncardiogenic pulmonary edema (crackles without JVD/S3) after taking over-the-counter analgesics. This is the classic presentation of severe salicylate (aspirin) toxicity.

Salicylates directly stimulate the medullary respiratory center (causing respiratory alkalosis) and later uncouple oxidative phosphorylation (causing lactic acidosis/HAGMA).

Determine the definitive treatment for the diagnosed condition.

The treatment for severe salicylate toxicity is intravenous sodium bicarbonate.

Sodium bicarbonate alkalinizes the blood, keeping salicylate in its ionized form so it cannot cross the blood-brain barrier. It also alkalinizes the urine, trapping the salicylate ion in the renal tubules and promoting its excretion.

Key Concept

Diagnosis and management of a mixed primary respiratory alkalosis and primary high anion gap metabolic acidosis secondary to salicylate toxicity.

Question 30Question →

A 38-year-old woman is hospitalized for a 1-week history of severe lower back pain, generalized weakness, and recurrent chills. Her medical history is significant for intravenous drug use. Her temperature is $39.2^\circ C$ ( $102.6^\circ F$ ), blood pressure is $112/68 \text{ mm Hg}$ , and pulse is $115/\text{min}$ . Physical examination reveals a new III/VI holosystolic murmur loudest at the cardiac apex. There is pronounced point tenderness over the lower lumbar spine, but no focal neurologic deficits are present. Laboratory studies show a leukocyte count of $15,200/\mu L$ . Magnetic resonance imaging of the spine demonstrates abnormal signal intensity in the L4-L5 intervertebral disc and adjacent vertebral bodies, consistent with discitis and osteomyelitis. Blood cultures are drawn, and empiric therapy with intravenous vancomycin and cefepime is initiated. On hospital day 3, the patient's fever has improved. A transesophageal echocardiogram reveals a 1.4-cm vegetation on the mitral valve. Blood cultures are finalized and grow *Staphylococcus aureus* that is resistant to penicillin but susceptible to oxacillin, cefazolin, daptomycin, and vancomycin. Which of the following is the most appropriate next step in pharmacotherapy?

Discontinue the current regimen and initiate intravenous cefazolin

Discontinue cefepime and continue intravenous vancomycin

Continue both intravenous vancomycin and cefepime

Discontinue the current regimen and initiate intravenous daptomycin

Discontinue the current regimen and initiate oral linezolid

Show answer & explanation

Answer: Discontinue the current regimen and initiate intravenous cefazolin

Answer

Discontinue the current regimen and initiate intravenous cefazolin

For severe, deep-seated infections caused by methicillin-susceptible *Staphylococcus aureus* (MSSA), such as left-sided infective endocarditis and vertebral osteomyelitis, targeted beta-lactam antibiotics (e.g., cefazolin, nafcillin, or oxacillin) are the definitive treatment of choice. Clinical data consistently demonstrate that these beta-lactams are superior to vancomycin for MSSA, leading to more rapid clearance of bacteremia and lower rates of treatment failure and mortality. Therefore, the principles of antimicrobial stewardship and optimal clinical care dictate prompt de-escalation from empiric broad-spectrum coverage to a narrow-spectrum beta-lactam once susceptibilities confirm MSSA.

Step-by-Step Solution

Interpret the blood culture susceptibilities.

The organism is Staphylococcus aureus susceptible to oxacillin.

Oxacillin susceptibility defines the isolate as methicillin-susceptible Staphylococcus aureus (MSSA).

Determine the optimal antibiotic class for MSSA bacteremia, endocarditis, and osteomyelitis.

Narrow-spectrum, anti-staphylococcal beta-lactams are the treatment of choice.

Clinical evidence consistently shows that anti-staphylococcal penicillins (nafcillin, oxacillin) or first-generation cephalosporins (cefazolin) have superior efficacy, lower mortality rates, and lower relapse rates compared to vancomycin for MSSA infections.

Select the appropriate management step based on principles of antibiotic stewardship.

De-escalate the empiric broad-spectrum regimen to intravenous cefazolin.

De-escalation improves patient outcomes by utilizing the most effective targeted therapy while minimizing unnecessary broad-spectrum exposure (reducing toxicity and resistance).

Key Concept

Targeted antimicrobial therapy (de-escalation) for methicillin-susceptible Staphylococcus aureus (MSSA) bacteremia and endocarditis.

Question 31Question →

Paramedics bring an 81-year-old female to the acute care unit from her assisted living facility. Staff members called for help after noticing she was acting confused and breathing rapidly since she woke up. Her medical history is notable for severe osteoarthritis, hypertension, and diet-controlled type 2 diabetes mellitus. According to the facility's notes, she had been complaining of a constant "ringing" sound in her ears for the past 48 hours and self-administering extra over-the-counter analgesics for knee pain.

On arrival, her temperature is 37.1°C (98.8°F), blood pressure is 135/85 mm Hg, pulse is 112/min, and respirations are 28/min. Oxygen saturation is 96% on ambient air.

The patient appears mildly lethargic and is oriented only to person. Her mucous membranes are notably dry. Auscultation of the chest reveals a rapid, regular heart rate with no murmurs, and breath sounds are clear in all lung fields. The abdomen is non-tender. Trace pitting edema is noted at the ankles.

Laboratory evaluation demonstrates:
Sodium: 142 mEq/L
Potassium: 3.9 mEq/L
Chloride: 102 mEq/L
Bicarbonate: 14 mEq/L
Blood urea nitrogen: 24 mg/dL
Creatinine: 1.2 mg/dL
Glucose: 105 mg/dL

Arterial blood gas analysis on ambient air reveals:
pH: 7.42
pCO2: 20 mm Hg
pO2: 92 mm Hg

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

Intravenous furosemide

Nebulized albuterol and ipratropium

Intravenous piperacillin-tazobactam

Intravenous sodium bicarbonate

Intravenous 0.9% sodium chloride and supportive observation

Show answer & explanation

Answer: Intravenous sodium bicarbonate

Answer

Intravenous sodium bicarbonate

This patient's clinical presentation (tinnitus, confusion, tachypnea) and laboratory findings (mixed high anion gap metabolic acidosis and primary respiratory alkalosis) are highly characteristic of salicylate toxicity. Salicylates directly stimulate the medullary respiratory center, causing early primary respiratory alkalosis. As toxicity progresses, the uncoupling of oxidative phosphorylation leads to the accumulation of organic acids, resulting in a concomitant high anion gap metabolic acidosis. This mixed disorder often keeps the pH near normal (e.g., 7.42). The next best step in management is to administer intravenous sodium bicarbonate. This alkalinizes the urine (target pH

\ge 7.5

), which converts lipophilic salicylic acid into its ionized, lipophobic form (salicylate). This 'ion trapping' prevents renal tubular reabsorption and significantly enhances the excretion of the toxin.

Step-by-Step Solution

Calculate the anion gap.

\text{Na}^+ - (\text{Cl}^- + \text{HCO}_3^-) = 142 - (102 + 14) = 26 \text{ mEq/L}

To identify the presence of a primary high anion gap metabolic acidosis.

Apply Winter's formula to determine the expected pCO2.

Expected

\text{pCO}_2 = (1.5 \times 14) + 8 = 29 \pm 2 \text{ mm Hg}

. The measured

\text{pCO}_2

20 \text{ mm Hg}

To assess whether respiratory compensation is appropriate or if a secondary acid-base disorder is present.

Synthesize the clinical and laboratory data.

The patient has a mixed high anion gap metabolic acidosis and primary respiratory alkalosis, accompanied by tinnitus and confusion in the setting of excessive analgesic use.

This triad of findings is pathognomonic for salicylate (aspirin) toxicity.

Determine the appropriate management.

Administer intravenous sodium bicarbonate.

To alkalinize the urine, which traps salicylate in its ionized form and enhances renal excretion.

Key Concept

Adults with salicylate toxicity classically present with a mixed high anion gap metabolic acidosis and primary respiratory alkalosis; the next best step in management is urine alkalinization with intravenous sodium bicarbonate.

Estimated Time:2m 0s

Question 32Question →

A 72-year-old man with a history of chronic obstructive pulmonary disease (COPD) and hypertension is brought to the emergency department for severe, worsening shortness of breath over the past 24 hours. He reports that his breathing is especially difficult when he lies down to sleep, forcing him to sleep in a recliner chair. He denies fever, chills, or any change in the volume or color of his sputum. Blood pressure is 155/92 mm Hg, pulse is 108/min, and respirations are 26/min. Pulse oximetry shows 88% on room air. Physical examination reveals distended jugular veins, bilateral crackles at the lung bases, and an S3 gallop. There is 2+ bilateral lower extremity pitting edema.

Arterial blood gas analysis on room air shows:

Parameter	Value
pH	7.28
PaCO2	60 mm Hg
HCO3-	27 mEq/L

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

Intravenous furosemide

Inhaled albuterol and systemic glucocorticoids

Intravenous piperacillin-tazobactam

Intravenous sodium bicarbonate

Empiric oral azithromycin

Show answer & explanation

Answer: Intravenous furosemide

Answer

Intravenous furosemide is the most appropriate next step in management.

The correct answer is intravenous furosemide because the patient's presentation is classic for acute decompensated heart failure (ADHF). Despite his history of COPD, findings such as orthopnea (sleeping in a recliner), an S3 gallop, jugular venous distention, and pitting edema indicate severe volume overload and left ventricular dysfunction. Intravenous loop diuretics like furosemide rapidly decrease intravascular volume, relieving pulmonary congestion and improving respiratory mechanics. The respiratory acidosis seen on his blood gas will improve once the underlying pulmonary edema is resolved.

Step-by-Step Solution

Analyze the patient's symptoms and vital signs.

The patient has severe dyspnea, orthopnea, hypoxemia, and significant hypertension.

To identify the acuity and exact nature of the respiratory distress.

Evaluate the physical examination findings.

Findings include jugular venous distention, bibasilar crackles, an S3 gallop, and bilateral lower extremity pitting edema.

These specific signs help differentiate between possible causes of dyspnea in a patient with multiple comorbidities.

Synthesize findings to form a definitive diagnosis.

The combination of orthopnea, JVD, an S3 gallop, and edema strongly points to acute decompensated heart failure (ADHF) leading to cardiogenic pulmonary edema, despite the history of COPD.

Accurate diagnosis is required before initiating targeted therapy.

Determine the appropriate initial management.

Intravenous loop diuretics (such as furosemide) should be administered to rapidly reduce volume overload and relieve pulmonary congestion.

This is the standard, high-yield first-line treatment for ADHF.

Key Concept

Patients with a history of COPD can present with dyspnea due to acute decompensated heart failure (ADHF). Key differentiating features pointing to ADHF include orthopnea, jugular venous distention (JVD), an S3 gallop, and peripheral edema, which should be managed primarily with intravenous loop diuretics.

Estimated Time:1m 0s

Question 33Question →

A $65$ -year-old man presents to the clinic with a $3$ -month history of progressive difficulty swallowing both solids and liquids. He reports frequent regurgitation of undigested food, especially at night, and an unintended weight loss of $8$ kg ( $17.6$ lb) during this period. His medical history is significant for hypertension and a $40$ -pack-year smoking history. Vital signs are within normal limits. Physical examination is unremarkable. A barium esophagram demonstrates esophageal dilation with symmetric, smooth tapering at the gastroesophageal junction. Upper gastrointestinal endoscopy shows retained food debris in the esophageal body but normal overlying mucosa; the endoscope passes easily into the stomach with gentle pressure. High-resolution esophageal manometry demonstrates absent peristalsis in the esophageal body and a high integrated relaxation pressure, indicating failure of the lower esophageal sphincter to relax upon swallowing. Which of the following is the most appropriate next step in management?

Endoscopic ultrasound of the gastroesophageal junction

Laparoscopic Heller myotomy

Initiation of intravenous piperacillin-tazobactam

24-hour ambulatory esophageal pH monitoring

Empiric trial of a high-dose proton pump inhibitor

Show answer & explanation

Answer: Endoscopic ultrasound of the gastroesophageal junction

Answer

Endoscopic ultrasound of the gastroesophageal junction

The patient's clinical and diagnostic findings (absent peristalsis, high integrated relaxation pressure, and a 'bird's beak' appearance) are highly indicative of an achalasia motility pattern. However, primary achalasia typically has a prolonged, indolent course in younger patients. This patient's advanced age (

>60

years), short symptom duration (

<6

months), profound weight loss, and significant smoking history strongly suggest pseudoachalasia. Pseudoachalasia is most commonly caused by a malignancy (e.g., gastric adenocarcinoma) infiltrating the gastroesophageal junction and myenteric plexus. Standard endoscopy often appears normal because the tumor may be submucosal or cause extrinsic compression. Therefore, the most appropriate next step is an endoscopic ultrasound (or computed tomography scan) to evaluate for a submucosal tumor before initiating definitive achalasia therapy.

Step-by-Step Solution

Analyze the clinical presentation and diagnostic findings.

The patient has dysphagia to solids and liquids, a 'bird's beak' appearance on esophagram, and manometry showing absent peristalsis and incomplete lower esophageal sphincter relaxation.

To establish the primary manometric diagnosis of an achalasia-like motility disorder.

Evaluate the patient's demographics and history for atypical features.

The patient has advanced age (

>60

years), rapid onset of symptoms (

<6

months), and severe weight loss.

Primary achalasia typically presents in younger patients with an indolent course, whereas these rapid-onset red flags strongly suggest a secondary cause, known as pseudoachalasia.

Determine the next best diagnostic step to evaluate for secondary causes.

An endoscopic ultrasound of the gastroesophageal junction is the most appropriate next step.

Standard endoscopy can easily miss submucosal infiltrating tumors (like gastric adenocarcinoma) that cause pseudoachalasia. Endoscopic ultrasound is highly sensitive for detecting these lesions.

Key Concept

Patients presenting with an achalasia motility pattern who have clinical red flags (age

>60

years, rapid symptom onset

<6

months, and profound weight loss) must be evaluated for pseudoachalasia (malignancy) using endoscopic ultrasound or computed tomography before initiating definitive therapy.

Estimated Time:2m 30s

Question 34Question →

A 54-year-old woman with a long-standing history of severe alcohol use disorder is brought to the emergency department by emergency medical services after vomiting large amounts of bright red blood at home. On arrival, she is lethargic and confused. Her blood pressure is 82/50 mm Hg, and her pulse is 128/min. Physical examination reveals marked scleral icterus, multiple spider angiomas on the chest, and a visibly distended abdomen with shifting dullness. The emergency physician suspects acute variceal hemorrhage as the cause of her instability. Arrange the following management steps in the most appropriate chronological sequence for this patient.

Drag items to arrange them in the correct order

Show answer & explanation

Answer

The correct chronological sequence is: 1) Establish large-bore IV access and fluid resuscitation, 2) Administer IV octreotide and prophylactic antibiotics, 3) Perform urgent EGD for variceal ligation, and 4) Evaluate for TIPS placement if the bleeding is refractory.

The algorithmic approach to suspected variceal hemorrhage prioritizes patient survival through physiological stabilization before mechanical intervention. Establishing large-bore intravenous access and administering fluids addresses the immediate, life-threatening hypovolemic shock. Vasoactive agents (octreotide) and prophylactic antibiotics (ceftriaxone) are the next most rapid and effective means to lower portal pressure and prevent infection-related mortality, respectively, and can be administered simultaneously while preparing the endoscopy suite. Endoscopy is the definitive primary treatment (via band ligation) but requires a stabilized patient. Finally, TIPS is a highly invasive salvage procedure utilized only when the aforementioned primary therapies fail to control the bleeding.

Step-by-Step Solution

Assess the patient's hemodynamic status and immediate life threats.

The patient is in hypovolemic shock (blood pressure 82/50 mm Hg, pulse 128/min) due to acute upper gastrointestinal hemorrhage.

Recognizing shock dictates that immediate life-saving stabilization (ABCs) must precede definitive diagnostic or therapeutic procedures.

Determine the initial medical management for suspected variceal bleeding in cirrhosis.

Vasoactive drugs (e.g., octreotide) and prophylactic antibiotics (e.g., ceftriaxone) should be administered immediately upon suspicion.

Octreotide reduces portal venous pressure to slow bleeding, and prophylactic antibiotics significantly reduce the risk of mortality and bacterial infections, which are common triggers and fatal complications of variceal bleeding.

Determine the timing of endoscopic and radiologic interventions.

EGD is the primary definitive treatment but is performed only after initial stabilization. TIPS is reserved strictly for treatment failure.

Performing endoscopy on an unstable patient increases the risk of cardiovascular collapse and aspiration. TIPS carries a high risk of hepatic encephalopathy and is used only as salvage therapy.

Key Concept

The management of acute variceal hemorrhage requires a strict stepwise algorithm: 1) hemodynamic stabilization, 2) pharmacotherapy with vasoactive agents and prophylactic antibiotics, 3) endoscopic intervention, and 4) salvage therapy with TIPS only for refractory cases.

Question 35Question →

A 38-year-old woman comes to the clinic due to a 3-month history of worsening fatigue, generalized weakness, and a 4.5-kg (10-lb) weight gain despite a decreased appetite. She also reports feeling constantly cold and having increasingly irregular menstrual cycles. Her temperature is 36.1°C (97.0°F), blood pressure is 100/65 mm Hg, and pulse is 54/min. Physical examination shows dry skin and delayed relaxation of the deep tendon reflexes. Laboratory studies show a thyroid-stimulating hormone (TSH) level of 0.1 $\mu$ U/mL (normal: 0.5-5.0 $\mu$ U/mL) and a free thyroxine (T4) level of 0.4 ng/dL (normal: 0.9-1.7 ng/dL). Which of the following is the most likely cause of this patient's findings?

Autoimmune destruction of the thyroid gland

Thyroid-stimulating immunoglobulin production

Compression of pituitary thyrotrophs

Exogenous levothyroxine consumption

Decreased peripheral conversion of T4 to T3

Show answer & explanation

Answer: Compression of pituitary thyrotrophs

Answer

Compression of pituitary thyrotrophs, leading to central (secondary) hypothyroidism.

The correct answer identifies the etiology of central hypothyroidism. This patient has classic hypothyroid symptoms (fatigue, cold intolerance, weight gain, bradycardia), which correlates with her low free T4 level. However, her TSH is inappropriately suppressed rather than elevated. This lack of appropriate pituitary response indicates a central cause of hypothyroidism, most commonly resulting from a pituitary macroadenoma that causes mass effect and compression of normal thyrotrophs.

Step-by-Step Solution

Analyze the patient's symptoms and vital signs.

The patient presents with fatigue, weight gain, cold intolerance, bradycardia, and delayed deep tendon reflexes.

Identifying the clinical syndrome is the first step; these findings strongly suggest a hypothyroid state.

Interpret the thyroid function tests.

The free T4 is abnormally low, confirming hypothyroidism. The TSH is also abnormally low.

Normally, a low T4 should trigger an elevated TSH via negative feedback. An inappropriately low TSH in the setting of low T4 localizes the defect to the anterior pituitary or hypothalamus.

Determine the most likely etiology for the laboratory pattern.

The pattern indicates central hypothyroidism, which is most often caused by a pituitary mass.

A nonfunctioning pituitary adenoma can compress normal pituitary thyrotrophs, leading to decreased TSH production and subsequent hypothyroidism. This also commonly causes menstrual irregularities via compression of gonadotrophs or hyperprolactinemia due to stalk compression.

Key Concept

Central (secondary) hypothyroidism is characterized by clinical signs of hypothyroidism combined with a low free T4 and an inappropriately normal or low TSH.

Question 36Question →

A $64$ -year-old woman is evaluated in the emergency department for severe shortness of breath and increasing leg swelling over the past week. She has a history of severe chronic obstructive pulmonary disease (COPD) requiring home oxygen therapy. Her temperature is $37.0^\circ\text{C}$ ( $98.6^\circ\text{F}$ ), blood pressure is $105/68\text{ mm Hg}$ , pulse is $118\text{ /min}$ , and respirations are $28\text{ /min}$ . Jugular venous pulsation is visible at $15\text{ cm H}_2\text{O}$ . Cardiac examination reveals a prominent parasternal heave and a loud $P_2$ . Lung auscultation shows significantly prolonged expiration and diffuse wheezing, with no crackles. The liver edge is palpable $4\text{ cm}$ below the right costal margin and is tender. Moderate pitting edema is present in the lower extremities. Arterial blood gas on $2\text{ L/min}$ supplemental oxygen shows:

pH: $7.31$
$PaCO_2$ : $62\text{ mm Hg}$
$PaO_2$ : $54\text{ mm Hg}$
$HCO_3^-$ : $31\text{ mEq/L}$

A trial of non-invasive positive pressure ventilation (NIPPV) is initiated for acute-on-chronic hypercapnic respiratory failure. Ten minutes later, the patient becomes lethargic and her blood pressure drops precipitously to $70/40\text{ mm Hg}$ . Which of the following is the most appropriate immediate next step in management?

Remove the non-invasive positive pressure ventilation mask

Perform emergent endotracheal intubation

Administer an intravenous bolus of furosemide

Initiate an intravenous infusion of sodium bicarbonate

Administer intravenous piperacillin-tazobactam and vancomycin

Show answer & explanation

Answer: Remove the non-invasive positive pressure ventilation mask

Answer

Remove the non-invasive positive pressure ventilation mask

The correct answer identifies that the sudden onset of profound hypotension following the initiation of non-invasive positive pressure ventilation (NIPPV) is due to a precipitous drop in venous return. The patient's physical exam (JVD, hepatomegaly, edema, clear lungs) reveals severe right ventricular failure (cor pulmonale) secondary to COPD. The failing right ventricle requires high filling pressures (preload) to maintain adequate stroke volume. When NIPPV is applied, the positive pressure is transmitted to the intrathoracic cavity, compressing the intrathoracic veins and sharply reducing venous return. This sudden loss of preload drastically drops right ventricular output, leading to reduced left ventricular filling and systemic shock. The immediate, life-saving intervention is to remove the NIPPV mask to restore venous return.

Step-by-Step Solution

Analyze the patient's baseline clinical presentation.

The patient has signs of isolated right ventricular failure (JVD, parasternal heave, hepatomegaly, peripheral edema, clear lungs) secondary to chronic lung disease. This confirms a diagnosis of cor pulmonale.

Establishing the baseline hemodynamic state is required to predict how the patient will respond to cardiopulmonary interventions.

Evaluate the arterial blood gas results.

The ABG shows a pH of 7.31, PaCO2 of 62, and HCO3- of 31, indicating acute-on-chronic respiratory acidosis. NIPPV is a standard appropriate initial therapy for this gas exchange derangement.

Understanding the indication for NIPPV clarifies why it was started, setting up the subsequent complication.

Identify the mechanism of the sudden hemodynamic collapse after NIPPV initiation.

NIPPV delivers positive pressure to the airways, which transmits to the intrathoracic cavity. Increased intrathoracic pressure compresses the vena cava, reducing venous return (preload) to the right atrium.

Connecting the intervention to its physiological consequence is necessary to identify the cause of the shock.

Determine the effect of reduced preload on a failing right ventricle.

A failing right ventricle (cor pulmonale) is highly dependent on elevated filling pressures to maintain stroke volume. The sudden reduction in preload leads to a precipitous drop in right ventricular output, subsequent loss of left ventricular filling, and profound systemic hypotension.

This explains why the blood pressure dropped to 70/40 mm Hg and why the patient became lethargic.

Select the appropriate immediate intervention.

The inciting cause of the shock must be immediately reversed by removing the NIPPV mask to restore negative intrathoracic pressure and venous return.

Reversing the mechanical obstruction to venous return is the only way to immediately restore cardiac output in this scenario.

Key Concept

Patients with right ventricular failure (cor pulmonale) are highly dependent on adequate preload; initiating positive pressure ventilation increases intrathoracic pressure, which can precipitously reduce venous return and cause profound hypotensive shock.

Estimated Time:2m 0s

Question 37Question →

A 54-year-old man presents to the clinic with a 3-month history of profound fatigue, intermittent joint pain in his hands, and a recurrent rash on his lower legs. He has a past medical history of a brief period of intravenous drug use in his early twenties. He currently takes no medications. Vital signs are within normal limits. Physical examination reveals a non-blanching, palpable purpuric rash over the bilateral shins and ankles. There is mild symmetric tenderness and swelling of the metacarpophalangeal and proximal interphalangeal joints.

Laboratory evaluation is as follows:

Test	Result	Reference Range
Hemoglobin	$12.4\text{ g/dL}$	$13.5-17.5\text{ g/dL}$
Platelets	$185,000/\text{mm}^3$	$150,000-400,000/\text{mm}^3$
Creatinine	$1.7\text{ mg/dL}$	$0.6-1.2\text{ mg/dL}$
AST	$58\text{ U/L}$	$10-40\text{ U/L}$
ALT	$72\text{ U/L}$	$10-40\text{ U/L}$
Rheumatoid factor	Positive	Negative
Complement C3	$105\text{ mg/dL}$	$80-160\text{ mg/dL}$
Complement C4	$6\text{ mg/dL}$	$15-45\text{ mg/dL}$

Urinalysis shows 2+ protein, $15-20$ red blood cells/hpf, and occasional red blood cell casts.

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

Antineutrophil cytoplasmic antibody assay

Testing for hepatitis C virus RNA

Antinuclear antibody assay

Testing for hepatitis B surface antigen

Blood cultures and transesophageal echocardiography

Show answer & explanation

Answer: Testing for hepatitis C virus RNA

Answer

Testing for hepatitis C virus RNA

The correct answer is testing for hepatitis C virus RNA. This patient exhibits the classic features of mixed cryoglobulinemia syndrome (MCS): palpable purpura, arthralgias, and immune-complex mediated glomerulonephritis (nephritic syndrome). The laboratory findings of a positive rheumatoid factor (an IgM antibody against IgG) and an isolated low C4 with a normal C3 are the pathophysiological hallmarks of this condition. More than 90% of MCS cases are secondary to chronic hepatitis C virus infection, making HCV screening the most essential next step in diagnostic evaluation.

Step-by-Step Solution

Analyze the clinical presentation and physical examination findings.

The patient has the classic triad of palpable purpura, weakness (fatigue), and arthralgias, along with nephritic syndrome (RBC casts, elevated creatinine, proteinuria).

Identifying this triad points strongly toward a systemic small-to-medium vessel vasculitis or immune-complex mediated disease.

Interpret the specific immunological laboratory profile.

The labs show a positive rheumatoid factor (RF), a normal C3 level, and a severely depressed C4 level.

In this context, the RF is actually an IgM autoantibody directed against the Fc portion of IgG. These form immune complexes (cryoglobulins) that robustly activate the classical complement pathway, leading to marked consumption of C4 but often sparing C3.

Determine the underlying etiology of the suspected diagnosis (Mixed Cryoglobulinemia Syndrome).

Mixed cryoglobulinemia is overwhelmingly associated with chronic Hepatitis C virus (HCV) infection.

Chronic immune stimulation by HCV drives the clonal expansion of B cells that produce cryoglobulins. Testing for HCV RNA is the most critical next diagnostic step to confirm the etiology before initiating antiviral and/or immunosuppressive therapy.

Key Concept

Mixed cryoglobulinemia syndrome presents with palpable purpura, arthralgias, and glomerulonephritis. It is characterized immunologically by a positive rheumatoid factor and an isolated low C4, and requires testing for its most common underlying cause: chronic hepatitis C virus infection.

Estimated Time:1m 30s

Question 38Question →

Match each patient's clinical presentation with the myositis-specific autoantibody that is most strongly associated with their clinical phenotype.

Click a left item, then click its matching right item

Show answer & explanation

Answer

The correct pairings map the cancer-associated dermatomyositis presentation to Anti-TIF1-γ, the antisynthetase syndrome presentation to Anti-Jo-1, the immune-mediated necrotizing myopathy to Anti-SRP, and the classic, highly steroid-responsive dermatomyositis to Anti-Mi-2.

Each myositis-specific autoantibody defines a distinct clinical subgroup. Anti-TIF1-γ is linked to malignancy; Anti-Jo-1 to antisynthetase syndrome (ILD, mechanic's hands); Anti-SRP to profound, rapidly progressive necrotizing myopathy; and Anti-Mi-2 to classic, steroid-responsive dermatomyositis.

Step-by-Step Solution

Analyze the first clinical vignette for distinctive features.

The patient has dermatomyositis signs (heliotrope rash) alongside clear symptoms of a malignancy (weight loss, lung mass).

Identifying the paraneoplastic nature of the presentation isolates Anti-TIF1-γ as the most appropriate autoantibody.

Analyze the second clinical vignette for syndromic patterns.

The patient exhibits interstitial lung disease and mechanic's hands.

These are the hallmark findings of antisynthetase syndrome, which is driven by antibodies against aminoacyl-tRNA synthetases, most notably Anti-Jo-1.

Examine the third clinical vignette's biopsy and laboratory findings.

The presentation involves severe, rapid weakness with massive CK elevation and a non-inflammatory necrotizing biopsy.

This confirms immune-mediated necrotizing myopathy (IMNM), which is classically associated with Anti-SRP or Anti-HMGCR antibodies.

Review the fourth clinical vignette for classic diagnostic criteria.

The patient has classic cutaneous dermatomyositis that responds perfectly to standard corticosteroid therapy.

Anti-Mi-2 is linked to this classic presentation, predicting an excellent response to treatment and a low risk for severe systemic complications.

Key Concept

Myositis-specific autoantibodies and their corresponding distinct clinical phenotypes (antisynthetase syndrome, immune-mediated necrotizing myopathy, cancer-associated dermatomyositis).

Question 39Question →

A 58-year-old woman is hospitalized for the treatment of infective endocarditis. She initially presented with a 3-week history of low-grade fever, fatigue, and a new heart murmur. Her history is notable for a dental extraction one month prior. Transesophageal echocardiography on admission revealed a 7-mm vegetation on the mitral valve leaflet. Three sets of blood cultures grew *Streptococcus sanguinis* with a penicillin minimum inhibitory concentration (MIC) of 0.05 mcg/mL. She was started on a planned 2-week synergistic regimen of intravenous aqueous penicillin G and intravenous gentamicin. On day 5 of hospitalization, the patient reports feeling clinically improved and has been afebrile for 48 hours. However, laboratory studies show her serum creatinine has increased from a baseline of 0.8 mg/dL to 2.1 mg/dL. Her urine output has mildly decreased over the past 24 hours. Which of the following is the most appropriate modification to her antimicrobial regimen?

Discontinue gentamicin and continue intravenous penicillin G for a total 4-week course

Discontinue both antibiotics and initiate intravenous vancomycin for a total 4-week course

Decrease the dose of gentamicin and continue both antibiotics for a total 2-week course

Discontinue penicillin G and continue intravenous gentamicin for a total 2-week course

Discontinue both antibiotics and initiate oral amoxicillin for a total 4-week course

Show answer & explanation

Answer: Discontinue gentamicin and continue intravenous penicillin G for a total 4-week course

Answer

Discontinue gentamicin and continue intravenous penicillin G for a total 4-week course

The correct answer identifies that the patient has developed aminoglycoside-induced acute kidney injury. Standard treatment guidelines for native valve endocarditis caused by highly penicillin-susceptible viridans group streptococci (MIC ≤ 0.12 mcg/mL) offer two primary first-line regimens: 4 weeks of IV penicillin (or ceftriaxone) monotherapy, OR a 2-week synergistic course of IV penicillin (or ceftriaxone) combined with gentamicin. If a patient experiences significant nephrotoxicity or ototoxicity while on the 2-week synergistic regimen, the aminoglycoside must be discontinued immediately. To ensure complete eradication of the infection, the patient is then transitioned to the 4-week monotherapy protocol, counting the days already completed.

Step-by-Step Solution

Identify the primary complication occurring in the patient.

The patient has developed acute kidney injury (AKI), evidenced by a rise in serum creatinine from 0.8 mg/dL to 2.1 mg/dL and decreased urine output.

Recognizing the complication is essential to determining which medication is causing harm.

Determine the likely cause of the complication.

Gentamicin is a well-known nephrotoxic aminoglycoside and is the most likely culprit for the patient's intrinsic acute tubular necrosis.

Identifying the offending agent dictates the required therapeutic modification.

Select the appropriate alternative evidence-based regimen for the infection.

For native valve endocarditis caused by highly penicillin-susceptible viridans group streptococci (MIC ≤ 0.12 mcg/mL), a 4-week course of intravenous penicillin G monotherapy is equivalent in efficacy to the 2-week synergistic regimen.

Stopping the toxic agent and relying on the safe, targeted monotherapy protocol prevents further renal damage while ensuring the endocarditis is fully treated.

Key Concept

In patients receiving a 2-week synergistic course of penicillin and gentamicin for highly penicillin-susceptible viridans group streptococcal endocarditis who develop acute kidney injury, the aminoglycoside should be discontinued, and penicillin monotherapy should be extended to a full 4-week course.

Question 40Question →

Match each clinical scenario describing a medication adverse effect or monitoring requirement in a patient with a rheumatologic condition to the most likely responsible pharmacologic agent.

Click a left item, then click its matching right item

Show answer & explanation

Answer

The scenarios match with Tocilizumab (bowel perforation), Cyclophosphamide (bladder neoplasm), Infliximab (drug-induced lupus), Leflunomide (cholestyramine washout), and Hydroxychloroquine (maculopathy screening).

Each rheumatologic medication carries a distinct side effect and monitoring profile. Tocilizumab (IL-6 inhibitor) increases the risk of bowel perforation. Cyclophosphamide causes urothelial toxicity (hemorrhagic cystitis, bladder cancer) via its metabolite acrolein. Infliximab (TNF-alpha inhibitor) is classically associated with drug-induced lupus. Leflunomide is teratogenic and undergoes enterohepatic circulation, requiring cholestyramine for rapid clearance. Hydroxychloroquine causes retinal toxicity requiring rigorous OCT or visual field screening.

Step-by-Step Solution

Analyze the first scenario featuring bowel perforation on a biologic.

Identify Tocilizumab (IL-6 inhibitor) as the most likely causative agent.

IL-6 inhibition is uniquely associated with lower gastrointestinal perforation compared to other biologics.

Analyze the second scenario featuring a bladder neoplasm after IV infusions for lupus.

Identify Cyclophosphamide as the causative agent.

Cyclophosphamide metabolism produces acrolein, which is highly toxic to the urothelium and oncogenic.

Analyze the third scenario featuring drug-induced lupus on a biologic.

Identify Infliximab (TNF-alpha inhibitor) as the causative agent.

Anti-TNF agents are the most common biologics implicated in drug-induced lupus.

Analyze the fourth scenario featuring a teratogenic DMARD requiring cholestyramine washout.

Identify Leflunomide as the responsible agent.

Leflunomide undergoes extensive enterohepatic circulation, and cholestyramine binds the drug in the gut to accelerate its elimination.

Analyze the fifth scenario featuring regular OCT screening for maculopathy.

Identify Hydroxychloroquine as the responsible agent.

Hydroxychloroquine binds to melanin in the retinal pigment epithelium, leading to dose-dependent, irreversible retinal toxicity.

Key Concept

Adverse effects and screening requirements of rheumatologic pharmacotherapy

PreviousPage 2 / 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