All practice questions

8270 questions

All types8,270 Multiple choice4,249 Multiple select325 Numeric160 Matching1,849 Ordering1,687

A 72-year-old man is hospitalized due to 3 weeks of progressive fatigue, low-grade fevers, and shortness of breath with exertion. Six weeks ago, he underwent a transurethral resection of the prostate for benign prostatic hyperplasia. On physical examination, his temperature is 38.2°C (100.8°F), pulse is 94/min, blood pressure is 132/84 mm Hg, and respirations are 18/min. Cardiac auscultation reveals a new grade 3/6 holosystolic murmur loudest at the apex with radiation to the axilla. Examination of the extremities shows splinter hemorrhages under the fingernails of both hands.

Laboratory studies show:
Leukocyte count: 14,500/mm³
Hemoglobin: 10.8 g/dL
Platelets: 130,000/mm³
Blood urea nitrogen: 42 mg/dL
Serum creatinine: 2.1 mg/dL (baseline 1.1 mg/dL)

Transesophageal echocardiography demonstrates a 1.4-cm oscillating vegetation on the anterior leaflet of the mitral valve with moderate-to-severe mitral regurgitation. Empiric therapy with intravenous vancomycin and gentamicin is initiated. Two days later, three sets of blood cultures drawn prior to antibiotic administration are positive for *Enterococcus faecalis*. Antimicrobial susceptibility testing indicates the isolate is susceptible to ampicillin, penicillin, and vancomycin, and exhibits no high-level resistance to gentamicin. The patient remains hemodynamically stable.

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

Continue intravenous vancomycin and gentamicin

Switch to intravenous ampicillin and ceftriaxone

Switch to intravenous ampicillin and gentamicin

Switch to intravenous ampicillin monotherapy

Switch to intravenous daptomycin and linezolid

Show answer & explanation

Answer: Switch to intravenous ampicillin and ceftriaxone

Answer

The most appropriate next step is to switch to intravenous ampicillin and ceftriaxone, which provides required synergistic bactericidal activity without worsening the patient's acute kidney injury.

The correct answer is to switch to intravenous ampicillin and ceftriaxone. This patient has *Enterococcus faecalis* infective endocarditis, likely arising from his recent transurethral resection of the prostate (a classic risk factor due to genitourinary instrumentation). Enterococci are intrinsically tolerant to beta-lactam antibiotics because their primary penicillin-binding proteins (PBPs) have a low affinity for them. Therefore, cell wall synthesis inhibitors (like ampicillin) are merely bacteriostatic against Enterococci when used alone. To achieve the bactericidal activity necessary to cure endocarditis and sterilize the cardiac vegetations, synergistic combination therapy must be used.

Historically, the standard of care was ampicillin combined with an aminoglycoside (gentamicin). However, gentamicin is highly nephrotoxic. This patient has developed an acute kidney injury (serum creatinine increased from 1.1 mg/dL to 2.1 mg/dL). In patients with impaired renal function, the combination of ampicillin and ceftriaxone is the definitively preferred regimen. Ceftriaxone saturates specific PBPs (PBP2 and PBP3) that ampicillin does not effectively target, forcing the bacteria to rely on PBP5, which is then overwhelmed by ampicillin. This dual-beta-lactam therapy provides excellent bactericidal synergy against *E. faecalis* without the severe risk of aminoglycoside-induced nephrotoxicity.

Step-by-Step Solution

Identify the patient's primary diagnosis and the causative organism.

The patient has native valve infective endocarditis caused by Enterococcus faecalis, likely secondary to his recent genitourinary procedure.

Establishing the diagnosis and microbiologic etiology dictates the required duration and type of antimicrobial therapy.

Determine the required properties of antimicrobial therapy for this condition.

Infective endocarditis requires prolonged, bactericidal therapy to sterilize avascular heart valve vegetations. For Enterococcus, beta-lactam monotherapy is only bacteriostatic.

Enterococci are inherently tolerant to beta-lactams due to low-affinity penicillin-binding proteins (PBPs), so combination therapy is required to achieve a bactericidal effect.

Evaluate the patient's clinical status to select the safest synergistic regimen.

The patient has an acute kidney injury (creatinine 2.1 mg/dL, elevated from baseline). Therefore, the traditional synergistic agent, gentamicin (an aminoglycoside), is contraindicated due to its nephrotoxicity.

Ceftriaxone, when combined with ampicillin, provides excellent synergistic bactericidal activity against E. faecalis and avoids nephrotoxicity, making it the regimen of choice.

Key Concept

For Enterococcus faecalis infective endocarditis, the combination of ampicillin and ceftriaxone provides synergistic bactericidal activity and is the preferred regimen for patients with, or at high risk for, nephrotoxicity.

Question 1382Question →

A $48$ -year-old man is evaluated for resistant hypertension. His blood pressure is $168/104 \text{ mm Hg}$ despite strict adherence to maximum-dose amlodipine, lisinopril, and hydrochlorothiazide. He reports recent episodes of muscle cramping and significant fatigue. Laboratory studies reveal a serum potassium level of $2.9 \text{ mEq/L}$ and a serum sodium level of $146 \text{ mEq/L}$ . The physician suspects a specific endocrine etiology for his secondary hypertension. Arrange the following diagnostic and 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 sequence is: (1) Screening with plasma aldosterone-to-renin ratio, (2) Confirmatory saline suppression test, (3) Anatomical localization with adrenal CT, (4) Functional confirmation with adrenal venous sampling, and (5) Definitive treatment with unilateral adrenalectomy.

The diagnostic workup of primary hyperaldosteronism strictly follows a protocol designed to prevent the surgical removal of nonfunctioning adrenal incidentalomas. The cascade requires biochemical screening (aldosterone-to-renin ratio) to detect potential cases. Positive screens require biochemical confirmation (saline suppression test) to prove autonomy. Once confirmed, anatomical localization (CT scan) identifies structural abnormalities. However, because incidentalomas are highly prevalent in patients older than

35

, structural abnormalities must undergo functional lateralization (adrenal venous sampling) to prove the visible nodule is actively secreting aldosterone. Only after AVS lateralizes the hypersecretion to one gland is unilateral adrenalectomy indicated. If AVS shows bilateral hypersecretion, the patient is treated medically with mineralocorticoid receptor antagonists (e.g., spironolactone).

Step-by-Step Solution

Perform initial biochemical screening for primary hyperaldosteronism.

Obtain an early-morning plasma aldosterone concentration (PAC) and plasma renin activity (PRA).

Patients with resistant hypertension accompanied by spontaneous or diuretic-induced hypokalemia have a high pretest probability for primary hyperaldosteronism and require a screening PAC/PRA ratio.

Confirm autonomous aldosterone secretion.

Perform a suppression test, such as the intravenous saline infusion test.

The PAC/PRA ratio is highly sensitive but can yield false positives. A confirmatory test demonstrating the failure of aldosterone to suppress under volume expansion proves autonomous secretion.

Anatomically localize the suspected lesion.

Obtain a high-resolution CT scan of the abdomen.

Imaging distinguishes between bilateral adrenal hyperplasia, a unilateral adenoma, and rarer conditions like adrenocortical carcinoma. It must follow, not precede, biochemical confirmation.

Confirm functional lateralization of the hormone hypersecretion.

Perform bilateral adrenal venous sampling (AVS).

Because nonfunctioning adrenal adenomas (incidentalomas) are found in up to

10\%

of patients over age

40

, AVS is required to prove that the radiologically identified nodule is the actual source of aldosterone before removing the gland.

Provide definitive treatment for the identified pathology.

Proceed with unilateral laparoscopic adrenalectomy.

Surgery is the definitive cure for a biochemically active, functionally lateralized unilateral aldosterone-producing adenoma.

Key Concept

The precise, stepwise diagnostic and management algorithm for primary hyperaldosteronism.

Question 1383Question →

A 28-year-old woman is brought to the emergency department by her husband due to a 1-week history of worsening fatigue, facial rash, and shortness of breath that is exacerbated by deep inspiration. She was diagnosed with systemic lupus erythematosus (SLE) 4 years ago but stopped taking her prescribed mycophenolate mofetil and hydroxychloroquine 8 months ago. Her temperature is 38.6°C (101.5°F), blood pressure is 155/95 mmHg, heart rate is 110/min, and respiratory rate is 24/min. Physical examination reveals an erythematous rash across her cheeks and nasal bridge that spares the nasolabial folds. Lung auscultation demonstrates decreased breath sounds at the bilateral bases and a pleural friction rub. Mild jugular venous distention is present.

Laboratory studies show:

Laboratory Test	Result	Reference Range
Hemoglobin	9.2 g/dL	12.0–16.0 g/dL
Leukocyte count	2,800/mm³	4,500–11,000/mm³
Platelet count	95,000/mm³	150,000–400,000/mm³
Blood urea nitrogen	42 mg/dL	7–18 mg/dL
Serum creatinine	2.4 mg/dL	0.6–1.2 mg/dL
Thyroid-stimulating hormone (TSH)	1.1 mU/L	0.5–5.0 mU/L
Free T4	0.7 ng/dL	0.9–1.7 ng/dL

Arterial blood gas analysis on room air reveals:

Arterial Blood Gas	Result	Reference Range
pH	7.28	7.35–7.45
$pCO_2$	26 mmHg	35–45 mmHg
$pO_2$	88 mmHg	75–105 mmHg
$HCO_3^-$	12 mEq/L	22–28 mEq/L

Urinalysis shows 3+ protein, 20-30 red blood cells/hpf, and red blood cell casts. A urine culture obtained on admission grows >100,000 CFU/mL of *Escherichia coli* that is sensitive to amoxicillin, ceftriaxone, and nitrofurantoin. Blood cultures are pending.

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

Initiate high-dose intravenous methylprednisolone

Administer intravenous sodium bicarbonate for inadequately compensated metabolic acidosis

Initiate intravenous meropenem to treat the urinary tract infection and systemic symptoms

Administer intravenous furosemide and noninvasive ventilation for acute decompensated heart failure

Begin oral levothyroxine supplementation for suspected secondary hypothyroidism

Show answer & explanation

Answer: Initiate high-dose intravenous methylprednisolone

Answer

Initiate high-dose intravenous methylprednisolone

The patient is experiencing a severe, organ-threatening flare of systemic lupus erythematosus (SLE), characterized by proliferative lupus nephritis (acute kidney injury, proteinuria, red blood cell casts), serositis (pleuritic chest pain, friction rub, pleural effusions), and hematologic involvement (pancytopenia). The most appropriate next step in managing an acute, life-threatening SLE flare is the administration of high-dose intravenous glucocorticoids (e.g., methylprednisolone). Once the acute inflammation is controlled, a steroid-sparing immunosuppressant (e.g., cyclophosphamide or mycophenolate mofetil) will be initiated for induction therapy.

Step-by-Step Solution

Analyze the patient's clinical presentation and history.

The patient has a history of nonadherence to SLE medications and presents with a malar rash, pancytopenia, acute kidney injury with RBC casts (lupus nephritis), and pleurisy with effusions (serositis).

Identifying the underlying disease process is required to select the correct targeted therapy.

Evaluate the arterial blood gas using Winter's formula to determine if there is a mixed acid-base disorder.

Expected

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

mmHg. The patient's actual

pCO_2

is 26 mmHg, indicating adequate respiratory compensation for the metabolic acidosis.

This rules out a secondary respiratory acidosis and confirms sodium bicarbonate is not urgently indicated for uncompensated respiratory failure.

Interpret the thyroid function tests and urine culture in the context of critical illness.

The low free T4 with a normal TSH in an acutely ill patient indicates euthyroid sick syndrome. The *E. coli* UTI is sensitive to narrow-spectrum agents.

This rules out the need for levothyroxine and broad-spectrum antibiotics like meropenem.

Determine the definitive treatment for the primary pathology.

The patient is experiencing a severe, organ-threatening SLE flare, requiring immediate administration of high-dose intravenous corticosteroids.

Without rapid immunosuppression, the proliferative lupus nephritis and pancytopenia will worsen and potentially become fatal.

Key Concept

Severe, organ-threatening flares of Systemic Lupus Erythematosus (such as proliferative lupus nephritis or severe serositis) require immediate treatment with high-dose intravenous glucocorticoids.

Question 1384Question →

A 38-year-old man is brought to the emergency department by his partner due to severe headache, confusion, and fever for the past 24 hours. His medical history is significant for HIV, but he has not taken antiretroviral therapy for over a year. His last known CD4 cell count was 85/mm $^3$ . His temperature is 39.2°C (102.6°F), blood pressure is 110/70 mmHg, and heart rate is 115/min. He is lethargic but arousable to physical stimuli. Neurologic examination reveals marked nuchal rigidity. Funduscopic examination shows blurring of the optic disc margins bilaterally. Arrange the following diagnostic and therapeutic steps in the most appropriate chronological sequence for the immediate management of this patient.

Drag items to arrange them in the correct order

Show answer & explanation

Answer

The correct sequence of interventions is: 1) Obtain two sets of blood cultures, 2) Administer empiric intravenous antibiotics and dexamethasone, 3) Obtain a noncontrast CT scan of the head, and 4) Perform a lumbar puncture for cerebrospinal fluid analysis.

The patient has suspected bacterial meningitis with indications for a head CT prior to lumbar puncture (LP) due to papilledema, altered mental status, and an immunocompromised state (advanced HIV). According to current guidelines, the correct management sequence in this scenario is to immediately obtain blood cultures, immediately administer empiric antibiotics (and adjunctive dexamethasone), perform the head CT, and finally perform the LP. This protocol ensures that life-saving treatment is not delayed while awaiting imaging, while also mitigating the risk of cerebral herniation from the LP.

Step-by-Step Solution

Identify the patient's condition and risk factors.

The patient presents with classic signs of meningitis (fever, headache, nuchal rigidity) along with red flag features indicating potentially increased intracranial pressure (papilledema, altered mental status, and advanced HIV).

Recognizing red flag features dictates the sequencing of the diagnostic workup, specifically the need for neuroimaging prior to lumbar puncture.

Prioritize initial microbiologic sampling.

Obtain blood cultures as the absolute first step.

Drawing blood cultures takes only minutes and must be done before antimicrobials are introduced to preserve the diagnostic yield.

Determine the timing of medical therapy.

Administer empiric intravenous antibiotics and dexamethasone immediately following the blood draws.

Delaying antibiotics while waiting for a CT scan and lumbar puncture significantly increases mortality in bacterial meningitis.

Sequence the diagnostic neuroimaging and procedure.

Obtain a noncontrast CT scan of the head, followed by a lumbar puncture.

The CT scan is necessary to rule out mass effect before the lumbar puncture is safely performed, avoiding the risk of cerebral herniation.

Key Concept

Management sequence for suspected bacterial meningitis in patients with indications for cranial imaging prior to lumbar puncture.

Question 1385Question →

A 68-year-old woman is brought to the emergency department by her family due to a 24-hour history of fever, severe headache, and progressively worsening confusion. She has a medical history of rheumatoid arthritis and is currently on chronic immunosuppressive therapy with methotrexate and prednisone. On physical examination, her temperature is 39.2°C (102.6°F), blood pressure is 105/65 mmHg, and heart rate is 118/min. She is lethargic, oriented only to her own name, and exhibits marked nuchal rigidity. There are no clear focal neurologic deficits, but a thorough neurologic examination is limited by her altered mental status. Based on her clinical presentation and risk factors, arrange the following management steps in the most appropriate chronological sequence.

Drag items to arrange them in the correct order

Show answer & explanation

Answer

The correct sequence is: Obtain peripheral blood cultures, administer empiric intravenous antibiotics and dexamethasone, perform a non-contrast CT scan of the head, perform a lumbar puncture, and finally de-escalate targeted antimicrobial therapy based on culture results.

This patient presents with classic signs of bacterial meningitis. Because she is over 60 years old, actively immunocompromised, and presenting with altered mental status, she requires a head CT before a lumbar puncture to rule out elevated intracranial pressure and prevent herniation. In this scenario, it is critical not to delay life-saving treatment. Peripheral blood cultures must be obtained first to maximize diagnostic yield, immediately followed by the administration of empiric intravenous antibiotics and dexamethasone. Once therapy is initiated, the head CT is performed. If the CT shows no mass effect, a lumbar puncture is safely performed to obtain cerebrospinal fluid. Finally, broad-spectrum therapy is tailored and de-escalated based on the ultimate culture and susceptibility results.

Step-by-Step Solution

Identify the suspected diagnosis and assess indications for neuroimaging.

The patient has suspected bacterial meningitis with indications for a head CT prior to LP (age > 60, immunosuppression, and altered mental status).

Recognizing these risk factors dictates that a lumbar puncture must be delayed until a CT scan confirms it is safe to proceed without risking cerebral herniation.

Determine the necessary interventions prior to obtaining neuroimaging.

Blood cultures must be drawn, followed immediately by the administration of empiric antibiotics and dexamethasone.

To prevent devastating neurological outcomes or death, antibiotics must not be delayed for neuroimaging. Blood cultures are drawn just beforehand to ensure diagnostic yield is not compromised.

Determine the sequence of neuroimaging and the diagnostic procedure.

A non-contrast head CT is performed, followed subsequently by a lumbar puncture.

The CT scan rules out significant mass effect, making the subsequent lumbar puncture safe to perform for cerebrospinal fluid analysis.

Determine the final step in the clinical management pathway.

De-escalate and tailor antimicrobial therapy.

Once culture and susceptibility results return, broad-spectrum empiric therapy should be narrowed to targeted therapy to promote antibiotic stewardship and reduce toxicity.

Key Concept

In patients with suspected bacterial meningitis who possess risk factors for brain herniation (e.g., age > 60, immunocompromised state, altered mental status, new-onset seizure, or focal neurologic deficits), empiric antibiotics and dexamethasone must be administered immediately after drawing blood cultures, without waiting for a head CT or lumbar puncture.

Question 1386Question →

Match each pediatric patient's medical history or underlying condition with the specific vaccine that is absolutely contraindicated for them.

Click a left item, then click its matching right item

Show answer & explanation

Answer

The infant with intussusception matches with the Rotavirus vaccine. The infant with SCID matches with the MMR vaccine. The infant with an allergy to baker's yeast matches with the Hepatitis B vaccine. The child with unexplained encephalopathy matches with the DTaP vaccine.

Each patient's clinical history highlights a classic, absolute contraindication for a specific routine pediatric vaccine as per CDC and AAP guidelines. The rotavirus vaccine is avoided in those with a history of intussusception. Live vaccines (such as MMR and Varicella) are contraindicated in severe cellular immunodeficiencies like SCID. The Hepatitis B vaccine is cultivated in yeast and is contraindicated in patients with yeast anaphylaxis. Finally, the pertussis component of the DTaP vaccine is strictly contraindicated if an unexplained encephalopathy occurs within 7 days of receiving a prior dose.

Step-by-Step Solution

Analyze the contraindications for the rotavirus vaccine.

Identify that a history of intussusception absolutely contraindicates the rotavirus vaccine.

Rotavirus vaccine slightly increases the risk of intussusception in infants by serving as a lead point in the bowel.

Evaluate vaccine safety in patients with severe combined immunodeficiency (SCID).

Determine that live vaccines, such as the MMR vaccine, are strictly contraindicated.

SCID patients lack functional T-cells and are at high risk of fatal disseminated disease from live vaccine strains.

Review the components and manufacturing process of the Hepatitis B vaccine.

Note that it is derived from recombinant baker's yeast.

Anaphylaxis to baker's yeast means the Hepatitis B vaccine cannot be safely administered.

Identify the absolute contraindications associated with the DTaP vaccine.

Connect encephalopathy within 7 days of a previous dose specifically to the pertussis component.

This adverse event dictates the use of the DT vaccine rather than DTaP for future doses.

Key Concept

Absolute contraindications to specific routine pediatric immunizations.

Question 1387Question →

A $68$ -year-old man is brought to the emergency department by his daughter due to a $3$ -day history of progressively worsening headache, blurred vision, and confusion. He also reports having two episodes of severe epistaxis earlier in the week. Over the past several months, he has experienced fatigue and a $4.5\text{ kg}$ ( $10\text{ lb}$ ) weight loss. His temperature is $37.1^\circ\text{C}$ ( $98.8^\circ\text{F}$ ), blood pressure is $145/85\text{ mm Hg}$ , heart rate is $92/\text{min}$ , and respiratory rate is $16/\text{min}$ . Physical examination reveals bilateral cervical lymphadenopathy. Funduscopic examination shows dilated, tortuous retinal veins with scattered retinal hemorrhages. Neurologic examination shows an oriented but lethargic patient with no focal motor or sensory deficits. Laboratory studies show the following:

Laboratory Test	Result
Hemoglobin	$8.4\text{ g/dL}$
Mean corpuscular volume	$88\text{ fL}$
Leukocytes	$6,200/\text{mm}^3$
Platelets	$145,000/\text{mm}^3$
Calcium	$9.2\text{ mg/dL}$
Creatinine	$1.1\text{ mg/dL}$
Total protein	$10.5\text{ g/dL}$
Albumin	$3.8\text{ g/dL}$

Serum protein electrophoresis demonstrates a prominent monoclonal spike in the gamma-globulin region. Quantitative immunoglobulins reveal a markedly elevated IgM level. Which of the following is the most appropriate next step in management?

Plasma exchange

Packed red blood cell transfusion

Intravenous normal saline and furosemide

Hemodialysis

Intravenous ceftriaxone and vancomycin

Show answer & explanation

Answer: Plasma exchange

Answer

Plasma exchange

This patient's presentation of an elevated total protein with a large gamma gap, combined with an IgM monoclonal spike and lymphadenopathy, strongly suggests Waldenström macroglobulinemia (WM). The acute onset of headache, blurred vision, confusion, and epistaxis, along with the classic funduscopic finding of dilated, tortuous retinal veins (often described as 'sausage-link' veins), is pathognomonic for hyperviscosity syndrome. Because IgM is a massive pentameric immunoglobulin, extremely high concentrations significantly increase serum viscosity, which leads to sludging of blood in the microcirculation of the brain, eyes, and mucosal surfaces. The most appropriate and urgent next step in management is plasma exchange (plasmapheresis). This procedure rapidly clears the large IgM molecules from the circulation, immediately reversing the hyperviscosity and resolving the acute symptoms. Once the acute crisis is managed, definitive treatment with systemic chemotherapy or targeted therapies can be initiated.

Step-by-Step Solution

Analyze the clinical and laboratory findings to establish a diagnosis.

The patient has lymphadenopathy, an IgM monoclonal spike, and a large gamma gap (Total protein 10.5 g/dL minus Albumin 3.8 g/dL). This is diagnostic of Waldenström macroglobulinemia.

Differentiating Waldenström macroglobulinemia from Multiple Myeloma is crucial, as the latter typically presents with IgG/IgA spikes, hypercalcemia, and renal failure.

Identify the cause of the patient's acute symptoms.

The combination of headache, confusion, blurred vision, epistaxis, and tortuous retinal veins represents hyperviscosity syndrome.

IgM exists as a large pentamer; at high concentrations, it severely increases blood viscosity, leading to impaired microvascular transit and sludging in the central nervous system and retinal vessels.

Determine the most appropriate immediate intervention.

Select plasma exchange (plasmapheresis) as the next step in management.

Plasma exchange is the definitive acute treatment for hyperviscosity syndrome, as it mechanically removes the excess IgM from the circulation, rapidly resolving the life-threatening symptoms before chemotherapy is initiated.

Key Concept

The initial management of symptomatic hyperviscosity syndrome in Waldenström macroglobulinemia requires urgent plasma exchange to rapidly reduce serum IgM levels and prevent irreversible neurologic or ischemic complications.

Question 1388Question →

A 32-year-old woman comes to the clinic due to profound fatigue, generalized weakness, and amenorrhea. She delivered her first child 6 months ago. The delivery was complicated by a severe postpartum hemorrhage that required an emergent transfusion of $4$ units of packed red blood cells. Since the delivery, she has been unable to breastfeed her infant and her menses have not resumed. She reports frequent dizzy spells, especially when standing. Her blood pressure is $90/60 \text{ mm Hg}$ seated and $78/50 \text{ mm Hg}$ upon standing. Her pulse is $64/\text{min}$ . Physical examination shows loss of pubic and axillary hair, and a delayed relaxation phase of the deep tendon reflexes.

Laboratory studies show:

Laboratory Test	Result	Reference Range
Hemoglobin	$11.5 \text{ g/dL}$	$12.0 - 16.0 \text{ g/dL}$
Sodium	$132 \text{ mEq/L}$	$136 - 145 \text{ mEq/L}$
Potassium	$4.0 \text{ mEq/L}$	$3.5 - 5.0 \text{ mEq/L}$
Thyroid-stimulating hormone (TSH)	$1.2 \, \mu\text{U/mL}$	$0.4 - 4.0 \, \mu\text{U/mL}$
Free T4	$0.4 \text{ ng/dL}$	$0.9 - 2.4 \text{ ng/dL}$

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

Initiate levothyroxine therapy

Reassure the patient and repeat laboratory tests in 6 weeks

Measure serum prolactin level

Measure morning serum cortisol level

Measure serum thyroid-stimulating immunoglobulin

Show answer & explanation

Answer: Measure morning serum cortisol level

Answer

Measure morning serum cortisol level

The correct answer is to measure the morning serum cortisol level. This patient's presentation of severe postpartum hemorrhage followed by failure to lactate, amenorrhea, and fatigue is classic for Sheehan syndrome (ischemic necrosis of the anterior pituitary). Her laboratory results show central hypothyroidism (low Free T4 with inappropriately normal TSH) and dilutional hyponatremia, further supporting panhypopituitarism. Because the pituitary also produces ACTH, she is at high risk for central adrenal insufficiency. A critical principle in endocrinology is that thyroid hormone replacement (levothyroxine) increases the metabolic clearance of cortisol. If levothyroxine is given to a patient with untreated adrenal insufficiency, it can precipitate an acute, life-threatening adrenal crisis. Therefore, the adrenal axis MUST be evaluated (via morning cortisol or ACTH stimulation test) and, if deficient, treated with glucocorticoids before initiating levothyroxine.

Step-by-Step Solution

Interpret the thyroid laboratory studies.

The patient has a low Free T4 with an inappropriately normal TSH, which confirms the diagnosis of central (secondary) hypothyroidism rather than primary hypothyroidism.

In primary hypothyroidism, a low Free T4 would cause a compensatory elevation in TSH. An inappropriately normal or low TSH indicates a pituitary or hypothalamic failure.

Integrate the clinical history and physical examination findings.

The history of severe postpartum hemorrhage, combined with failure to lactate, amenorrhea, orthostatic hypotension, and central hypothyroidism, strongly suggests Sheehan syndrome (postpartum ischemic necrosis of the anterior pituitary).

Sheehan syndrome results in panhypopituitarism, causing deficiencies in prolactin, FSH/LH, TSH, and ACTH.

Identify the immediate life-threatening risk in panhypopituitarism.

The patient likely has central adrenal insufficiency (decreased ACTH leading to decreased cortisol). Note that aldosterone is preserved (normal potassium) because it is regulated by the renin-angiotensin-aldosterone system, not ACTH.

Failure to recognize and treat cortisol deficiency can lead to cardiovascular collapse and death.

Determine the correct sequence of hormone replacement.

The next best step is to measure the morning serum cortisol level (or perform a cosyntropin stimulation test) to evaluate the adrenal axis before giving any thyroid replacement.

Initiating levothyroxine accelerates the basal metabolic rate and increases the hepatic clearance of cortisol. In a patient with unrecognized adrenal insufficiency, this can rapidly precipitate an acute adrenal crisis.

Key Concept

In patients with suspected panhypopituitarism (such as Sheehan syndrome), the adrenal axis must be evaluated and treated with glucocorticoids before initiating levothyroxine therapy to prevent the precipitation of an acute adrenal crisis.

Question 1389Question →

A 52-year-old man is brought to the emergency department by emergency medical services after his daughter found him lethargic and confused in his apartment. The daughter reports that the patient has a history of severe osteoarthritis, major depressive disorder, and alcohol use disorder. He recently lost his job and has been drinking heavily for the past week. His current medications include fluoxetine and several over-the-counter pain relievers. On physical examination, the patient is difficult to arouse but withdraws from painful stimuli. His mucous membranes are dry.

Vital signs are as follows:
Temperature: 37.4°C (99.3°F)
Blood pressure: 105/65 mmHg
Heart rate: 112/min
Respiratory rate: 26/min
Oxygen saturation: 98% on room air

Laboratory studies reveal the following:

Serum chemistry:
Sodium: 142 mEq/L
Potassium: 3.4 mEq/L
Chloride: 106 mEq/L
Bicarbonate: 12 mEq/L
Blood urea nitrogen: 24 mg/dL
Creatinine: 1.2 mg/dL
Glucose: 88 mg/dL

Arterial blood gas (on room air):
pH: 7.44
PaCO $_2$ : 18 mmHg
PaO $_2$ : 102 mmHg

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

Measurement of serum salicylate concentration

Measurement of serum osmolal gap

Measurement of serum beta-hydroxybutyrate concentration

Calculation of the urine anion gap

Measurement of serum acetaminophen concentration

Show answer & explanation

Answer: Measurement of serum salicylate concentration

Answer

The most appropriate diagnostic step is the measurement of the serum salicylate concentration.

The correct answer is measurement of serum salicylate concentration. This patient's laboratory results demonstrate a mixed acid-base disorder characterized by a primary high anion gap metabolic acidosis and a concurrent primary respiratory alkalosis. The anion gap is elevated at 24 mEq/L (

142 - (106 + 12)

). According to Winter's formula, the expected PaCO

_2

for a bicarbonate of 12 mEq/L is

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

mmHg. Because the patient's measured PaCO

_2

(18 mmHg) is significantly lower than the expected range, a concurrent primary respiratory alkalosis is present. The combination of a high anion gap metabolic acidosis and a primary respiratory alkalosis is the classic hallmark of salicylate toxicity. Salicylates directly stimulate the medullary respiratory center (causing hyperventilation and respiratory alkalosis) and uncouple oxidative phosphorylation in mitochondria (causing lactic acidosis and ketoacidosis). Given the patient's history of major depressive disorder and access to over-the-counter pain relievers, an intentional overdose is highly likely.

Step-by-Step Solution

Calculate the serum anion gap to identify the primary metabolic disturbance.

Anion Gap =

142 - (106 + 12) = 24

mEq/L.

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

Apply Winter's formula to determine if respiratory compensation is appropriate.

Expected PaCO

_2

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

mmHg. The measured PaCO

_2

is 18 mmHg.

Comparing the measured PaCO

_2

to the expected PaCO

_2

detects concurrent respiratory acid-base disorders.

Synthesize the findings of HAGMA and the lower-than-expected PaCO

_2

The patient has a primary high anion gap metabolic acidosis AND a primary respiratory alkalosis.

Because the measured PaCO

_2

(18 mmHg) is significantly lower than the expected range (24-28 mmHg), there is an independent process driving hyperventilation.

Select the diagnostic test that corresponds to this specific mixed disorder.

Measurement of serum salicylate concentration is indicated.

Salicylate toxicity uniquely uncouples oxidative phosphorylation (causing lactic/ketoacidosis) and directly stimulates the medullary respiratory center (causing respiratory alkalosis).

Key Concept

Mixed Acid-Base Disorders and Salicylate Toxicity

Alternative Method

In addition to assessing the respiratory compensation, the Delta Ratio (

\Delta AG / \Delta HCO_3^-

) can be calculated to evaluate for a third concurrent metabolic disorder. Here, the

\Delta AG

24 - 12 = 12

, and the

\Delta HCO_3^-

24 - 12 = 12

. The ratio is

12/12 = 1.0

, which confirms a pure high anion gap metabolic acidosis without an additional secondary metabolic alkalosis or normal gap acidosis. This allows the clinician to focus exclusively on the respiratory derangement.

Estimated Time:2m 0s

Question 1390Question →

Match each patient's clinical presentation and laboratory profile, obtained during an episode of documented fasting hypoglycemia, to the most accurate pathophysiologic description of the underlying etiology.

Click a left item, then click its matching right item

Show answer & explanation

Answer

The accurate matching pairs exogenous insulin with a lack of connecting peptide, insulinoma with autonomous neuroendocrine proliferation, sulfonylurea ingestion with K-ATP channel closure, Doege-Potter syndrome with paraneoplastic IGF-II secretion, and adrenal insufficiency with counter-regulatory hormone failure.

The diagnostic workup of hypoglycemia relies on measuring insulin, C-peptide, proinsulin, and hypoglycemic agents during a hypoglycemic episode. Exogenous insulin lacks C-peptide. Endogenous hyperinsulinemia (high C-peptide) is split between secretagogue use (positive drug screen, K-ATP channel closure) and insulinoma (negative screen, autonomous tumor). Hypoglycemia with appropriately suppressed insulin points to non-beta cell tumors (IGF-II secretion) or counter-regulatory failure (adrenal insufficiency).

Step-by-Step Solution

Analyze the relationship between insulin and C-peptide in each profile.

Profiles with elevated insulin are either exogenous or endogenous. Profiles with suppressed insulin represent non-insulin-mediated hypoglycemia.

C-peptide is co-secreted 1:1 with endogenous insulin. Its presence or absence differentiates the source of excess insulin.

Evaluate the hyperinsulinemic profiles (elevated insulin).

The nurse has low C-peptide, indicating exogenous insulin. The 62-year-old and 70-year-old have high C-peptide, indicating endogenous production.

Exogenous pharmaceutical insulin does not contain C-peptide. Endogenous insulin production (tumors or drugs) secretes both.

Differentiate the endogenous hyperinsulinemic profiles.

The 70-year-old has a positive secretagogue screen, indicating sulfonylurea use. The 62-year-old has a negative screen and high proinsulin, indicating an insulinoma.

Sulfonylureas chemically stimulate the beta cells, while insulinomas are autonomous neuroendocrine tumors.

Evaluate the hypoinsulinemic (suppressed insulin) profiles.

The 58-year-old with a pleural tumor has elevated IGF-II (Doege-Potter syndrome). The 34-year-old with hyperpigmentation has failed cortisol response (Addison's disease).

Hypoglycemia normally suppresses insulin. If hypoglycemia persists, it is driven by insulin mimics (IGF-II) or a lack of counter-regulatory hormones (cortisol, glucagon, epinephrine).

Key Concept

Diagnostic differentiation of fasting hypoglycemia using the insulin, C-peptide, and counter-regulatory hormone axis

Estimated Time:2m 0s

Question 1391Question →

A $22$ -year-old man with a history of type 1 diabetes mellitus is brought to the emergency department due to lethargy, abdominal pain, and recurrent vomiting for the past $24$ hours. He recently had a viral respiratory tract infection. Vital signs show a temperature of $37.2^{\circ}\text{C}$ ( $99.0^{\circ}\text{F}$ ), blood pressure of $90/60$ mm Hg, pulse of $122$ /min, and respirations of $28$ /min with deep, sighing breathing. Point-of-care blood glucose is $520$ mg/dL. Intravenous access is established. Arrange the following acute management steps in the most appropriate chronological order.

Drag items to arrange them in the correct order

Show answer & explanation

Answer

The correct sequence is: rapid fluid resuscitation with normal saline, followed by establishing the serum potassium level, then initiating intravenous insulin, and finally adding dextrose to the fluids once glucose falls below

200

mg/dL.

The standard protocol for DKA management prioritizes addressing life-threatening volume depletion first. Therefore, a rapid infusion of

0.9\%

sodium chloride is the initial step. Next, because total body potassium is depleted in DKA and insulin drives potassium intracellularly, the serum potassium level must be obtained to ensure it is

> 3.3

mEq/L before starting insulin. Once potassium is confirmed safe, an intravenous regular insulin infusion is initiated to resolve the ketoacidosis. Finally, when the blood glucose drops to

200

mg/dL,

5\%

dextrose must be added to the intravenous fluids to prevent hypoglycemia while the insulin infusion continues in order to close the anion gap.

Step-by-Step Solution

Assess volume status and provide initial fluid resuscitation.

Administration of

0.9\%

sodium chloride restores intravascular volume.

Patients with DKA have profound fluid deficits (often

3

6

liters) due to osmotic diuresis. Reversing hypovolemic shock is the most immediate priority.

Evaluate baseline electrolyte levels, particularly potassium.

Serum potassium concentration is ascertained.

Total body potassium is depleted in DKA despite often normal or high serum levels. Because insulin shifts potassium into cells, it is unsafe to administer insulin without knowing if the patient requires concurrent potassium repletion.

Administer insulin therapy.

Continuous intravenous regular insulin is started.

Insulin stops ketogenesis, allowing the anion gap acidosis to resolve.

Adjust fluid composition based on glucose response.

5\%

dextrose is added to intravenous fluids.

Once blood glucose reaches

200

mg/dL, dextrose prevents hypoglycemia, allowing the insulin infusion to continue until ketones are cleared and the anion gap closes.

Key Concept

Chronological Management of Diabetic Ketoacidosis (DKA)

Estimated Time:1m 30s

Question 1392Question →

A 23-year-old man comes to the office to evaluate a progressively enlarging lump on the right side of his neck that he first noticed 6 weeks ago. He also reports drenching night sweats and a 6-kg (13-lb) unintentional weight loss over the past 2 months. His temperature is 37.8°C (100.0°F), blood pressure is 118/76 mm Hg, pulse is 84/min, and respirations are 14/min. Physical examination reveals a 4.5-cm, firm, non-tender, rubbery lymph node in the right supraclavicular region. There is no other cervical, axillary, or inguinal lymphadenopathy. The liver and spleen are not palpable. Complete blood count and comprehensive metabolic panel are within normal limits. Arrange the following steps in the most appropriate chronological order for the evaluation and initial management of this patient's condition.

Drag items to arrange them in the correct order

Show answer & explanation

Answer

The correct sequential order is: 1) Perform an excisional lymph node biopsy, 2) Obtain a whole-body PET-CT scan, 3) Assess baseline cardiopulmonary function, and 4) Initiate definitive multiagent systemic chemotherapy.

The evaluation of a patient presenting with high clinical suspicion for lymphoma follows a strict, sequential clinical pathway to ensure accurate diagnosis, appropriate staging, and patient safety. The absolute first requirement is obtaining a definitive histologic diagnosis through an excisional lymph node biopsy, as fine-needle aspiration disrupts the nodal architecture necessary for precise subtyping. Once the exact subtype (e.g., Hodgkin lymphoma) is known, the disease must be staged. A whole-body PET-CT scan is the standard imaging modality used to evaluate for additional nodal basins and extranodal involvement. The resulting stage dictates the specific chemotherapy regimen (such as ABVD). Because these regimens often include highly toxic agents like doxorubicin (cardiotoxic) and bleomycin (pulmonary toxic), baseline organ function must be formally assessed via echocardiography and pulmonary function testing. Finally, after diagnosis, staging, and safety parameters are fully secured, multiagent systemic chemotherapy can be safely initiated.

Step-by-Step Solution

Establish a definitive histologic diagnosis.

Excisional lymph node biopsy confirms the lymphoma subtype.

A tissue diagnosis is an absolute prerequisite before staging or treating any suspected malignancy. Excisional biopsy preserves nodal architecture, which is critical for lymphoma subtyping.

Stage the disease clinically.

Whole-body PET-CT scan delineates the extent of nodal and extranodal involvement.

Accurate staging determines the exact chemotherapy regimen needed, the number of cycles, and whether adjunctive radiation therapy will be required.

Perform pre-treatment baseline safety evaluation.

Echocardiography and pulmonary function tests establish baseline organ reserve.

Standard regimens like ABVD contain doxorubicin (cardiotoxic) and bleomycin (pulmonary toxic). Baseline function must be documented before these agents can be safely administered.

Commence targeted medical therapy.

Multiagent systemic chemotherapy is initiated safely and effectively.

Curative-intent treatment is the final step, proceeding only after diagnosis, staging, and safety assessments are strictly completed.

Key Concept

The evaluation of suspected lymphoma follows a strict sequence: histologic confirmation via excisional biopsy, followed by clinical staging via PET-CT, followed by pre-treatment organ function testing, and finally initiation of chemotherapy.

Estimated Time:1m 30s

Question 1393Question →

A 22-year-old woman with a history of type 1 diabetes mellitus presents to the emergency department with a 1-day history of nausea, vomiting, and diffuse abdominal pain. She missed several doses of her insulin because she was not feeling well. Her temperature is $37.2^\circ C$ ( $99.0^\circ F$ ), blood pressure is $105/65$ mmHg, heart rate is $118/min$ , and respiratory rate is $26/min$ . Physical examination reveals dry mucous membranes and diffuse abdominal tenderness without rebound or guarding.

Laboratory studies show:

Laboratory Study	Result
Serum sodium	$140$ mEq/L
Serum potassium	$4.5$ mEq/L
Serum chloride	$104$ mEq/L
Serum bicarbonate	$12$ mEq/L
Blood glucose	$450$ mg/dL
Serum creatinine	$1.2$ mg/dL

Which of the following is the expected arterial partial pressure of carbon dioxide ( $pCO_2$ ) if appropriate respiratory compensation has occurred in this patient?

12

mmHg

20

mmHg

26

mmHg

32

mmHg

40

mmHg

Show answer & explanation

Answer: $26$ mmHg

Answer

The expected arterial

pCO_2

26

mmHg.

The correct expected arterial

pCO_2

26

mmHg. This patient presents with diabetic ketoacidosis, which causes a primary anion gap metabolic acidosis. In the presence of a metabolic acidosis, the physiological response is hyperventilation to decrease arterial

pCO_2

and normalize the blood pH (respiratory compensation). The appropriate degree of respiratory compensation is calculated using Winter's formula: Expected

pCO_2 = 1.5 \times [HCO_3^-] + 8 \pm 2

. Using the patient's serum bicarbonate of

12

mEq/L, the expected

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

mmHg. A measured

pCO_2

within the range of

24

28

mmHg indicates a simple metabolic acidosis with appropriate compensation.

Step-by-Step Solution

Calculate the anion gap and identify the primary acid-base disturbance.

Anion Gap =

140 - (104 + 12) = 24

. The patient has an elevated anion gap metabolic acidosis (diabetic ketoacidosis).

Identifying the primary disturbance dictates which compensation formula to use.

Apply Winter's formula to determine expected respiratory compensation.

Expected

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

Winter's formula predicts the expected

pCO_2

response to a primary metabolic acidosis.

Calculate the specific expected value for this patient.

Expected

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

(Range:

24 - 28

mmHg).

Plugging in the patient's bicarbonate level of

12

mEq/L yields the target compensation.

Key Concept

Winter's formula for predicting appropriate respiratory compensation in primary metabolic acidosis

Question 1394Question →

A 68-year-old man presents to the emergency department with progressively worsening shortness of breath over the past 3 days. He has a history of ischemic cardiomyopathy with a reduced ejection fraction and severe chronic obstructive pulmonary disease. The patient reports waking up in the middle of the night gasping for air and has required three pillows to sleep comfortably. His temperature is $37.0^\circ\text{C}$ ( $98.6^\circ\text{F}$ ), blood pressure is $155/90$ mm Hg, pulse is $110$ /min, and respirations are $24$ /min. Oxygen saturation is $91\%$ on room air. Physical examination reveals an elevated jugular venous pressure, an S3 gallop, and diffuse bilateral crackles at the lung bases. There is 3+ bilateral pitting edema up to the mid-calves. Laboratory testing demonstrates a brain natriuretic peptide (BNP) level of $950$ pg/mL (normal: $<100$ pg/mL). Which of the following is the most appropriate next step in management?

Intravenous furosemide

Intravenous methylprednisolone

Oral azithromycin

Inhaled ipratropium

Oral amoxicillin-clavulanate

Show answer & explanation

Answer: Intravenous furosemide

Answer

Intravenous furosemide

The correct answer is intravenous furosemide. This patient's presentation of progressive dyspnea, orthopnea, elevated jugular venous pressure, an S3 gallop, bibasilar crackles, and severe pitting edema is the classic clinical picture of acute decompensated heart failure (ADHF). The markedly elevated brain natriuretic peptide (BNP) level further confirms this diagnosis over a primary pulmonary issue. The cornerstone of initial therapy for ADHF is the administration of intravenous loop diuretics, such as furosemide. These agents effectively reduce volume overload and alleviate pulmonary congestion by decreasing cardiac preload.

Step-by-Step Solution

Synthesize the patient's symptoms, physical examination, and laboratory findings to establish a diagnosis.

The patient has orthopnea, an S3 gallop, elevated jugular venous pressure, bibasilar crackles, pitting edema, and an elevated BNP level, which collectively diagnose acute decompensated heart failure.

Although the patient has a history of COPD, distinguishing between a COPD exacerbation and heart failure requires identifying signs of fluid overload, which are prominent here.

Determine the most appropriate initial management for the confirmed diagnosis.

Intravenous furosemide is selected as the next best step.

Intravenous loop diuretics rapidly induce diuresis and venodilation, decreasing cardiac preload and resolving pulmonary congestion in acute decompensated heart failure.

Key Concept

Acute decompensated heart failure is characterized by signs of volume overload (elevated jugular venous pressure, S3 gallop, peripheral edema) and is primarily managed with intravenous loop diuretics to rapidly reduce preload.

Question 1395Question →

A 72-year-old man is brought to the emergency department by emergency medical services due to severe, progressive shortness of breath over the past 48 hours. He also reports a cough productive of clear sputum and difficulty sleeping unless propped up on three pillows. His medical history is significant for severe chronic obstructive pulmonary disease (COPD), ischemic cardiomyopathy with a left ventricular ejection fraction of 35%, and hypothyroidism. He admits to missing his medications for the past two weeks.

Vital signs are temperature 37.1 °C (98.8 °F), blood pressure 162/94 mm Hg, pulse 115/min, and respirations 28/min. Oxygen saturation is 85% on room air.

Physical examination shows a patient in acute respiratory distress, using accessory muscles of respiration. Jugular venous distention is present up to 10 cm H2O. Lung auscultation reveals diffuse, bilateral expiratory wheezing and scattered crackles at the lung bases. Cardiovascular examination demonstrates a regular tachycardia with a prominent S3 gallop. There is 2+ bilateral lower extremity pitting edema.

Laboratory and diagnostic studies show:
Leukocyte count: 8,200/mm³
Thyroid-stimulating hormone (TSH): 0.3 µU/mL (Normal: 0.5–5.0 µU/mL)
Free T4: 0.8 ng/dL (Normal: 0.9–1.7 ng/dL)
Sputum culture (obtained 3 days ago at an outpatient clinic for a mild cough): heavy growth of *Streptococcus pneumoniae*, susceptible to amoxicillin.

Arterial blood gas analysis on room air:
$pH$ : $7.29$
$pCO_2$ : $56$ mm Hg
$pO_2$ : $52$ mm Hg
$HCO_3^-$ : $26$ mEq/L

A portable chest radiograph shows cardiomegaly, bilateral perihilar alveolar opacities, and prominent interlobular septa.

Which of the following is the most appropriate initial step in the management of this patient's respiratory distress?

Intravenous furosemide and noninvasive positive-pressure ventilation

Intravenous methylprednisolone and nebulized albuterol-ipratropium

Intravenous piperacillin-tazobactam and vancomycin

Intravenous sodium bicarbonate infusion

Intravenous levothyroxine and hydrocortisone

Show answer & explanation

Answer: Intravenous furosemide and noninvasive positive-pressure ventilation

Answer

The most appropriate initial step is the administration of intravenous furosemide and noninvasive positive-pressure ventilation.

The correct approach involves administering intravenous loop diuretics (furosemide) and initiating noninvasive positive-pressure ventilation (NPPV). This patient presents with classic signs of acute decompensated heart failure (ADHF), including an S3 gallop, jugular venous distention, orthopnea, and peripheral edema. The chest radiograph confirms cardiogenic pulmonary edema with cardiomegaly, perihilar opacities, and prominent interlobular septa (Kerley B lines). The diffuse wheezing heard on auscultation represents 'cardiac asthma,' which occurs when fluid accumulates in the peribronchial spaces, causing airway narrowing. Furthermore, the patient's arterial blood gas reveals an acute respiratory acidosis (

pH 7.29

pCO_2 56

mm Hg) due to impending respiratory failure from the increased work of breathing. NPPV (such as CPAP or BiPAP) is the ideal respiratory support for ADHF because it not only improves oxygenation but also increases intrathoracic pressure, thereby decreasing both cardiac preload and afterload. Concurrently, intravenous furosemide provides rapid diuresis and venodilation, further reducing preload.

Step-by-Step Solution

Analyze the patient's presentation and physical exam findings.

The patient presents with orthopnea, JVD, an S3 gallop, bilateral crackles, wheezing, and peripheral edema.

These signs collectively and strongly suggest acute decompensated heart failure (ADHF) with fluid overload, despite the history of COPD.

Evaluate the diagnostic data.

The chest radiograph shows cardiomegaly, perihilar alveolar opacities, and prominent interlobular septa (Kerley B lines). The ABG demonstrates acute respiratory acidosis with hypoxemia.

The imaging confirms cardiogenic pulmonary edema. The respiratory acidosis is driven by increased work of breathing and V/Q mismatch stemming from the pulmonary edema.

Determine the best immediate management.

Intravenous furosemide and noninvasive positive-pressure ventilation (NPPV) are indicated.

Furosemide provides rapid preload reduction through diuresis and venodilation, while NPPV improves oxygenation, decreases the work of breathing, and further reduces cardiac preload and afterload.

Key Concept

Differentiating acute decompensated heart failure from COPD exacerbation and managing cardiogenic pulmonary edema with preload reduction and noninvasive ventilation.

Estimated Time:1m 30s

Question 1396Question →

A $22$ -year-old man with type $1$ diabetes mellitus is brought to the emergency department due to nausea, vomiting, and confusion for the past $24$ hours. He has not taken his insulin for $2$ days. Vital signs show blood pressure $90/60$ mm Hg, heart rate $124$ /min, and respiratory rate $26$ /min with deep, sighing breaths. Laboratory evaluation reveals a serum glucose of $580$ mg/dL, potassium of $4.9$ mEq/L, bicarbonate of $11$ mEq/L, and an arterial pH of $7.18$ . Serum ketones are strongly positive. Arrange the following steps in the most appropriate sequence for the acute management and resolution of this patient's condition.

Drag items to arrange them in the correct order

Show answer & explanation

Answer

The correct sequence for DKA management is: IV normal saline, followed by IV regular insulin, adding dextrose when glucose drops, administering subcutaneous insulin once the gap closes, and finally stopping the IV insulin after a brief overlap.

The standard protocol for DKA resuscitation follows a strict physiological sequence. First, intravascular volume must be replaced with normal saline to prevent hemodynamic collapse. Second, once potassium is confirmed adequate, a continuous IV insulin infusion is started to halt ketone production. Third, because glucose drops faster than ketones clear, dextrose must be added to the IV fluids once glucose reaches 200-250 mg/dL to prevent hypoglycemia while the insulin infusion continues. Fourth, once the anion gap closes, subcutaneous basal insulin is administered. Finally, the IV insulin is discontinued 1-2 hours later to allow the subcutaneous depot to absorb, preventing a gap in insulin coverage that would trigger rebound ketoacidosis.

Step-by-Step Solution

Administer intravenous fluids (0.9% normal saline).

Restoration of intravascular volume and renal perfusion.

Patients with DKA have significant osmotic diuresis leading to profound dehydration. Administering insulin first would drive glucose and water into cells, potentially causing cardiovascular collapse.

Start continuous intravenous regular insulin.

Suppression of lipolysis and ketogenesis.

After confirming potassium is ≥3.3 mEq/L (the patient's is 4.9 mEq/L), insulin is required to drive potassium and glucose into cells and stop ketone production, resolving the anion gap acidosis.

Add 5% dextrose to intravenous fluids.

Prevention of severe hypoglycemia.

Serum glucose typically normalizes faster than the ketoacidosis resolves. When glucose falls to ≤200-250 mg/dL, dextrose is added so insulin can be safely continued until the anion gap closes.

Give subcutaneous long-acting insulin.

Establishment of basal insulin coverage.

Once the anion gap closes (≤12 mEq/L) and the patient tolerates oral intake, transition to a subcutaneous regimen begins.

Discontinue the IV insulin infusion.

Safe transition off continuous infusion without rebounding.

IV regular insulin has a half-life of only minutes. It must overlap with the subcutaneous dose by 1-2 hours to prevent immediate recurrence of ketogenesis.

Key Concept

Stepwise acute management of Diabetic Ketoacidosis (DKA)

Estimated Time:1m 30s

Question 1397Question →

Jugular venous pulse (JVP) analysis provides critical insights into right-sided heart hemodynamics and can distinguish between several life-threatening and chronic cardiovascular pathologies. Match each of the following abnormal JVP waveform findings with the specific clinical condition it most classically represents.

Click a left item, then click its matching right item

Show answer & explanation

Answer

The prominent 'x' descent with blunted 'y' descent matches Cardiac tamponade. The rapid 'y' descent matches Constrictive pericarditis. Intermittent cannon 'a' waves match Complete atrioventricular block. Absent 'a' waves match Atrial fibrillation. Prominent 'c-v' waves match Severe tricuspid regurgitation.

Each JVP finding corresponds directly to altered right heart hemodynamics: tamponade continuously prevents diastolic filling (blunted 'y'), constriction halts rapid filling abruptly (steep 'y'), AV dissociation creates intermittent atrial contraction against a closed valve (cannon 'a'), AF lacks synchronized atrial contraction (absent 'a'), and TR causes systolic backflow into the atrium (large 'c-v').

Step-by-Step Solution

Analyze the 'a' wave, which corresponds to active right atrial contraction.

Absent 'a' waves point to a lack of coordinated atrial contraction (atrial fibrillation). Intermittent giant 'a' waves indicate the atrium is contracting against a closed tricuspid valve (AV dissociation, such as complete AV block).

The 'a' wave occurs just before the first heart sound; analyzing its presence or amplification identifies primary electrical or mechanical atrial abnormalities.

Analyze the 'c' and 'v' waves and their relationship.

The fusion of 'c' and 'v' waves into a large systolic regurgitant wave indicates that ventricular blood is flowing back into the atrium during ventricular systole, which is classic for severe tricuspid regurgitation.

The 'v' wave normally represents slow atrial filling during ventricular systole; incompetent valves exaggerate this wave massively.

Evaluate the 'x' and 'y' descents to differentiate pericardial space diseases.

A blunted 'y' descent indicates restricted early diastolic filling (cardiac tamponade), whereas a rapid, steep 'y' descent (Friedreich sign) indicates rapid early filling that halts abruptly (constrictive pericarditis).

The 'y' descent represents early passive filling of the right ventricle when the tricuspid valve opens. The mechanics of the pericardial restriction dictate the speed of this filling.

Key Concept

Interpretation of jugular venous pulse (JVP) waveforms to diagnose structural, valvular, and electrical cardiac pathologies.

Question 1398Question →

A series of patients present to the primary care clinic for routine health screening and evaluation of liver function. As part of their workup, Hepatitis B serologic testing is performed. Match the following Hepatitis B serologic profiles with their most accurate clinical interpretation.

Click a left item, then click its matching right item

Show answer & explanation

Answer

The correct matches are: 1) Acute Hepatitis B infection is characterized by positive HBsAg and positive Anti-HBc IgM. 2) Resolved natural Hepatitis B infection shows positive Anti-HBc IgG and positive Anti-HBs. 3) Chronic Hepatitis B infection presents with positive HBsAg and positive Anti-HBc IgG, without Anti-HBs. 4) Immunity secondary to Hepatitis B vaccination demonstrates positive Anti-HBs only, without any core antibodies.

Matching correctly relies on systematically evaluating HBsAg (active disease marker), Anti-HBc (differentiates acute from chronic/resolved, and natural infection from vaccine immunity), and Anti-HBs (protective immunity marker).

Step-by-Step Solution

Analyze the status of the Hepatitis B surface antigen (HBsAg).

Positive HBsAg indicates active infection (acute or chronic), while negative HBsAg indicates no active infection.

HBsAg is the first serologic marker to appear in active infection and must clear for resolution.

Evaluate the Hepatitis B core antibody (Anti-HBc) type.

Anti-HBc IgM indicates acute infection, whereas Anti-HBc IgG indicates past or chronic infection. Absence of Anti-HBc in an immune patient indicates vaccination.

Core antibodies are formed only against the actual virus, never against the vaccine.

Check for the presence of the Hepatitis B surface antibody (Anti-HBs).

Positive Anti-HBs signifies immunity, either from natural resolution or from vaccination.

Anti-HBs is a neutralizing antibody that provides protective, long-term immunity.

Key Concept

Interpretation of Hepatitis B Serologic Panels

Question 1399Question →

Match each patient's clinical presentation with the most likely corresponding liver biopsy finding.

Click a left item, then click its matching right item

Show answer & explanation

Answer

Primary Biliary Cholangitis (PBC) matches with florid granulomatous duct destruction; Primary Sclerosing Cholangitis (PSC) matches with onion-skin periductal fibrosis; Alpha-1 antitrypsin deficiency matches with PAS-positive diastase-resistant globules; Autoimmune hepatitis matches with lymphoplasmacytic interface hepatitis; Nonalcoholic Steatohepatitis (NASH) matches with macrovesicular steatosis and ballooning.

Each clinical vignette provides classic epidemiological and laboratory clues for a specific liver pathology. Matching these correctly requires accurately diagnosing the condition based on the vignette, and then recalling the highly specific pathognomonic biopsy finding associated with that disease.

Step-by-Step Solution

Evaluate the first vignette (middle-aged woman, pruritus, AMA positive).

Diagnose Primary Biliary Cholangitis (PBC).

AMA positivity and cholestatic pattern in a middle-aged woman are classic for PBC, characterized by granulomatous destruction of bile ducts.

Evaluate the second vignette (young man, ulcerative colitis, MRCP strictures).

Diagnose Primary Sclerosing Cholangitis (PSC).

PSC is strongly associated with inflammatory bowel disease and presents with stricturing of biliary tree and 'onion-skin' fibrosis on biopsy.

Evaluate the third vignette (young man with panacinar emphysema and liver abnormalities).

Diagnose Alpha-1 antitrypsin deficiency.

The co-occurrence of early-onset lung and liver disease suggests alpha-1 antitrypsin deficiency, leading to PAS-positive globule accumulation in the liver.

Evaluate the fourth vignette (young woman, elevated transaminases, anti-smooth muscle antibodies).

Diagnose Autoimmune Hepatitis.

Autoimmune hepatitis presents with hypergammaglobulinemia and specific autoantibodies, showing lymphoplasmacytic interface hepatitis on histology.

Evaluate the fifth vignette (older obese man, metabolic syndrome, elevated transaminases).

Diagnose Nonalcoholic Steatohepatitis (NASH).

Metabolic syndrome risk factors without other causes of liver disease point to NASH, identified by steatosis, ballooning, and Mallory-Denk bodies.

Key Concept

Correlating clinical presentations of hepatobiliary diseases with their defining histopathological features.

Question 1400Question →

A 22-year-old man with type 1 diabetes mellitus is brought to the emergency department due to lethargy, nausea, vomiting, and diffuse abdominal pain for the past 24 hours. He recently had a viral upper respiratory infection. Temperature is 37.2°C (99.0°F), blood pressure is 90/60 mmHg, pulse is 125/min, and respirations are 28/min and deep. Mucous membranes are dry and capillary refill is prolonged. Laboratory studies show:

Laboratory test	Result
Serum glucose	650 mg/dL
Serum sodium	132 mEq/L
Serum potassium	3.1 mEq/L
Serum bicarbonate	10 mEq/L
Serum chloride	98 mEq/L
Arterial blood pH	7.15

Urine ketones are strongly positive.

Arrange the following management steps in the correct chronological order of administration for this patient according to standard diabetic ketoacidosis (DKA) protocols.

Drag items to arrange them in the correct order

Show answer & explanation

Answer

The correct sequence is: 1) Administer rapid IV 0.9% normal saline, 2) Administer IV potassium chloride, 3) Initiate continuous IV regular insulin, 4) Add 5% dextrose to IV fluids.

The standard sequence for DKA management requires aggressive initial fluid resuscitation with 0.9% normal saline. Following fluid initiation, potassium levels dictate the next step. If potassium is < 3.3 mEq/L, insulin must be withheld and intravenous potassium given first. Once potassium is ≥ 3.3 mEq/L, an IV insulin infusion is started to close the anion gap. Finally, when blood glucose reaches 200-250 mg/dL, dextrose is added to IV fluids to prevent hypoglycemia while insulin continues.

Step-by-Step Solution

Assess hemodynamic status and restore intravascular volume.

0.9% normal saline bolus is administered.

The patient exhibits signs of severe hypovolemic shock (hypotension, tachycardia, dry mucous membranes) due to profound osmotic diuresis. Immediate fluid resuscitation with isotonic saline is required to restore perfusion.

Evaluate the baseline serum potassium level before initiating insulin therapy.

Intravenous potassium chloride is administered.

The patient's initial potassium is dangerously low at 3.1 mEq/L. Patients in DKA have total body potassium depletion, and administering insulin immediately would drive extracellular potassium into the cells, risking fatal cardiac arrhythmias. Potassium must be replaced first.

Initiate insulin therapy once potassium levels are safe (≥ 3.3 mEq/L).

Continuous intravenous regular insulin infusion is started.

Insulin is essential to suppress lipolysis, halt ketogenesis, and correct the high anion gap metabolic acidosis. It is started only after hypovolemia and profound hypokalemia have been initially addressed.

Monitor blood glucose levels and adjust intravenous fluids accordingly.

5% dextrose is added to the intravenous fluids.

Once the serum glucose falls to approximately 200-250 mg/dL, dextrose must be added to the fluid regimen. This prevents hypoglycemia while allowing the continuation of the insulin infusion needed to fully close the anion gap.

Key Concept

Algorithm for Diabetic Ketoacidosis (DKA) management, specifically recognizing the critical threshold of serum potassium (< 3.3 mEq/L) that dictates withholding insulin until potassium is replenished.

PreviousPage 70 / 414Next

All practice questions

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

Alternative Method

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