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USMLE STEP3 Exam Questions
Step3 (Page 9 )

Updated On: 2-Mar-2026
Page 9 of 162
PDF with 804 Questions

A 68-year-old White male, with a history of hypertension, an 80 pack-year history of tobacco use and emphysema, is brought into the ER because of 4 days of progressive confusion and lethargy. His wife notes that he takes amlodipine for his hypertension. He does not use over-the-counter (OTC) medications, alcohol, or drugs. Furthermore, she indicates that he has unintentionally lost approximately 30 lbs in the last 6 months. His physical examination shows that he is afebrile with a blood pressure of 142/85, heart rate of 92 (no orthostatic changes), and a room-air O2 saturation of 91%. He is 70 kg. The patient appears cachectic. He is arousable but lethargic and unable to follow any commands. His mucous membranes are moist, heart rate regular without murmurs or a S3/S4 gallop, and extremities without any edema. His pulmonary examination shows mildly diminished breath sounds in the right lower lobe with wheezing bilaterally. The patient is unable to follow commands during neurologic examination but moves all his extremities spontaneously. Laboratory results are as follows:

Blood
Sodium: 109
Potassium: 3.8
Chloride: 103
CO2: 33
BUN: 17
Creatinine: 1.1
Glucose: 95
Urine osmolality: 600
Plasma osmolality: 229
White blood cell (WBC): 8000
Hgb: 15.8
Hematocrit (HCT): 45.3
Platelets: 410
Arterial blood gas: pH 7.36/pCO2 60/pO2 285
A chest x-ray (CXR) reveals a large right hilar mass.

Which of the following is the correct statement regarding the treatment of hyponatremia?

  1. Desmopressin acetate (DDAVP), used in conjunction with intravenous saline, will help correct the serum sodium.
  2. Correction of sodium slowly by 3 meq/day will prevent any subsequent neurologic injury.
  3. Correction of serum sodium by 15 meq over 24 hours could lead to permanentneurologic injury.
  4. Diuretics should be avoided in the treatment of hyponatremia.
  5. Potassium should always be added to IV saline solutions when treating both hyponatremia and hypokalemia.

Answer(s): C

Explanation:

The patient has hypotonic hyponatremia, which can lead to increased water shifting into the brain, resulting in cerebral edema. This patient has nothing in history or physical examination to suggest a stroke or the presence of sepsis as the etiology of his altered mental status. Central pontine myelinolysis is a potentially devastating neurologic complication that can result from the treatment of hyponatremia, not hyponatremia itself. While respiratory acidosis could potentially contribute to this patient's change in mental status, cerebral edema due to hypotonicity is the most likely etiology. The patient's laboratory studies indicate a low plasma osmolality with an inappropriately increased urine osmolality. With this degree of hypotonicity, the urine should be maximally dilute (osmolality of <100 mOsmol/kg H2O). The high urine osmolality suggests the presence of antidiuretic hormone. In psychogenic polydipsia, the urine would be maximally dilute. Choice C is unlikely since his physical examination does not suggest volume depletion; furthermore, the patient is taking a calcium channel blocker, not a diuretic, for the treatment of his hypertension. Decreased expression of renal collecting duct water channels would lead to water wasting and, thus, the development of diabetes insipidus and hypernatremia. The patient has symptomatic hypotonic hyponatremia with signs of cerebral edema.

This requires immediate attention. Choices A, C, and E are essentially hypotonic solutions which should be withheld in patients with hyponatremia. The serum sodium in this case should be increased by at least 5% for the treatment of cerebral edema. The use of 0.9% saline would require nearly 5 L of infusate to address this cerebral edema. This could lead to pulmonary edema and volume overload. The use of hypertonic saline (3% saline) is the ideal solution to use in this scenario, as the infusion of 3% saline will correct the symptoms while avoiding volume overload. As in all cases of hyponatremia management, frequent serum sodium assays are necessary in order to avoid too rapid of a correction, which could result in neurologic injury--pontine myelinolysis.



A 53-year-old Black male, with a history of hypertension, hepatitis C, and newly diagnosed nonsmall cell lung cancer, undergoes his first round of chemotherapy, which includes cisplatin. You are called to see this patient 5 days into his hospitalization for oliguria and laboratory abnormalities. Other than the chemotherapy, he is receiving lansoprazole, acetaminophen, and an infusion of D5-- 0.9% normal saline at 50 mL/h. On examination, his BP is 98/60 and heart rate is irregular, between 40 and 50 bpm. His physical examination shows a middle-aged male in no acute distress. His cardiac examination is unremarkable, his lungs show bibasilar crackles, and the abdominal examination is positive for a palpable spleen tip without any hepatomegaly or abdominal tenderness. He has trace bilateral ankle edema. His distal pulses are irregular. The neurologic examination was unremarkable. His laboratory (serum sample) results are as follows



Which electrolyte/acid-base abnormality is most likely responsible for the findings on physical examination?

  1. hypernatremia
  2. hyperkalemia
  3. metabolic acidosis
  4. hyperphosphatemia
  5. hyperuricemia

Answer(s): B

Explanation:

The patient has tumor lysis syndrome. The destruction of malignant cells by chemotherapeutic agents will lead to the release of intracellular contents, including potassium, phosphorus, and uric acid (from nucleic acids). This can result in hyperkalemia, hyperuricemia, and hyperphosphatemia. Hyperkalemia will produce significant ECG abnormalities, including peaked T waves and widened QRS complexes. The presence of bradycardia and irregular heart rate on physical examination are suggestive of the cardiac effects of hyperkalemia, which can lead to lifethreatening arrhythmias if not addressed. Patients with tumor lysis syndrome can develop a severe hyperuricemia. The kidneys are responsible for the excretion of uric acid. In acidic urine, the uric acid can crystallize in collecting tubules, resulting in intratubular obstruction and acute kidney failure. Calcium oxalate stones are not a part of this entity. Cisplatin can cause renal potassium and magnesium losses, which is not the case in this patient. The laboratory data suggest the release of intracellular contents (high LDH, uric acid, potassium, and phosphate) and the diagnosis of urate nephropathy as the cause of his acute kidney failure. As mentioned before, hyperkalemia will produce significant ECG abnormalities, including peaked T waves and widened QRS complexes. Prominent U waves are found in hypokalemia, not hyperkalemia. Atrial fibrillation is not typically seen in hyperkalemia.



A 53-year-old Black male, with a history of hypertension, hepatitis C, and newly diagnosed nonsmall cell lung cancer, undergoes his first round of chemotherapy, which includes cisplatin. You are called to see this patient 5 days into his hospitalization for oliguria and laboratory abnormalities. Other than the chemotherapy, he is receiving lansoprazole, acetaminophen, and an infusion of D5-- 0.9% normal saline at 50 mL/h. On examination, his BP is 98/60 and heart rate is irregular, between 40 and 50 bpm. His physical examination shows a middle-aged male in no acute distress. His cardiac examination is unremarkable, his lungs show bibasilar crackles, and the abdominal examination is positive for a palpable spleen tip without any hepatomegaly or abdominal tenderness. He has trace bilateral ankle edema. His distal pulses are irregular. The neurologic examination was unremarkable. His laboratory (serum sample) results are as follows



What is the most likely etiology of this patient's acute renal failure?

  1. renal tubular deposition of uric acid
  2. calcium oxalate kidney stones causing partial urinary tract obstruction
  3. renal tubular injury due to cisplatin
  4. ischemic acute tubular necrosis from a decreased cardiac output
  5. type II cryoglobulinemia due to hepatitis C

Answer(s): A

Explanation:

The patient has tumor lysis syndrome. The destruction of malignant cells by chemotherapeutic agents will lead to the release of intracellular contents, including potassium, phosphorus, and uric acid (from nucleic acids). This can result in hyperkalemia, hyperuricemia, and hyperphosphatemia. Hyperkalemia will produce significant ECG abnormalities, including peaked T waves and widened QRS complexes. The presence of bradycardia and irregular heart rate on physical examination are suggestive of the cardiac effects of hyperkalemia, which can lead to lifethreatening arrhythmias if not addressed. Patients with tumor lysis syndrome can develop a severe hyperuricemia. The kidneys are responsible for the excretion of uric acid. In acidic urine, the uric acid can crystallize in collecting tubules, resulting in intratubular obstruction and acute kidney failure. Calcium oxalate stones are not a part of this entity. Cisplatin can cause renal potassium and magnesium losses, which is not the case in this patient. The laboratory data suggest the release of intracellular contents (high LDH, uric acid, potassium, and phosphate) and the diagnosis of urate nephropathy as the cause of his acute kidney failure. As mentioned before, hyperkalemia will produce significant ECG abnormalities, including peaked T waves and widened QRS complexes. Prominent U waves are found in hypokalemia, not hyperkalemia. Atrial fibrillation is not typically seen in hyperkalemia



A 53-year-old Black male, with a history of hypertension, hepatitis C, and newly diagnosed nonsmall cell lung cancer, undergoes his first round of chemotherapy, which includes cisplatin. You are called to see this patient 5 days into his hospitalization for oliguria and laboratory abnormalities. Other than the chemotherapy, he is receiving lansoprazole, acetaminophen, and an infusion of D5-- 0.9% normal saline at 50 mL/h. On examination, his BP is 98/60 and heart rate is irregular, between 40 and 50 bpm. His physical examination shows a middle-aged male in no acute distress. His cardiac examination is unremarkable, his lungs show bibasilar crackles, and the abdominal examination is positive for a palpable spleen tip without any hepatomegaly or abdominal tenderness. He has trace bilateral ankle edema. His distal pulses are irregular. The neurologic examination was unremarkable. His laboratory (serum sample) results are as follows



What would be the most likely finding on this patient's ECG?

  1. shortened P-R segment
  2. prominent U wave
  3. widened QRS complexes
  4. flattened T waves
  5. atrial fibrillation

Answer(s): C

Explanation:

The patient has tumor lysis syndrome. The destruction of malignant cells by chemotherapeutic agents will lead to the release of intracellular contents, including potassium, phosphorus, and uric acid (from nucleic acids). This can result in hyperkalemia, hyperuricemia, and hyperphosphatemia. Hyperkalemia will produce significant ECG abnormalities, including peaked T waves and widened QRS complexes. The presence of bradycardia and irregular heart rate on physical examination are suggestive of the cardiac effects of hyperkalemia, which can lead to lifethreatening arrhythmias if not addressed. Patients with tumor lysis syndrome can develop a severe hyperuricemia. The kidneys are responsible for the excretion of uric acid. In acidic urine, the uric acid can crystallize in collecting tubules, resulting in intratubular obstruction and acute kidney failure. Calcium oxalate stones are not a part of this entity. Cisplatin can cause renal potassium and magnesium losses, which is not the case in this patient. The laboratory data suggest the release of intracellular contents (high LDH, uric acid, potassium, and phosphate) and the diagnosis of urate nephropathy as the cause of his acute kidney failure. As mentioned before, hyperkalemia will produce significant ECG abnormalities, including peaked T waves and widened QRS complexes. Prominent U waves are found in hypokalemia, not hyperkalemia. Atrial fibrillation is not typically seen in hyperkalemia



A 53-year-old Black male, with a history of hypertension, hepatitis C, and newly diagnosed nonsmall cell lung cancer, undergoes his first round of chemotherapy, which includes cisplatin. You are called to see this patient 5 days into his hospitalization for oliguria and laboratory abnormalities. Other than the chemotherapy, he is receiving lansoprazole, acetaminophen, and an infusion of D5-- 0.9% normal saline at 50 mL/h. On examination, his BP is 98/60 and heart rate is irregular, between 40 and 50 bpm. His physical examination shows a middle-aged male in no acute distress. His cardiac examination is unremarkable, his lungs show bibasilar crackles, and the abdominal examination is positive for a palpable spleen tip without any hepatomegaly or abdominal tenderness. He has trace bilateral ankle edema. His distal pulses are irregular. The neurologic examination was unremarkable. His laboratory (serum sample) results are as follows



Which of the following would be a part of the IMMEDIATE treatment strategy in this patient?

  1. atropine 1 mg IV
  2. calcium chloride, given IV
  3. 50 g of Kayexalate, given orally
  4. 10 units of regular insulin, given subcutaneously
  5. one ampule of glucagon, given IV

Answer(s): B

Explanation:

The patient has tumor lysis syndrome. The destruction of malignant cells by chemotherapeutic agents will lead to the release of intracellular contents, including potassium, phosphorus, and uric acid (from nucleic acids). This can result in hyperkalemia, hyperuricemia, and hyperphosphatemia. Hyperkalemia will produce significant ECG abnormalities, including peaked T waves and widened QRS complexes. The presence of bradycardia and irregular heart rate on physical examination are suggestive of the cardiac effects of hyperkalemia, which can lead to lifethreatening arrhythmias if not addressed. Patients with tumor lysis syndrome can develop a severe hyperuricemia. The kidneys are responsible for the excretion of uric acid. In acidic urine, the uric acid can crystallize in collecting tubules, resulting in intratubular obstruction and acute kidney failure. Calcium oxalate stones are not a part of this entity. Cisplatin can cause renal potassium and magnesium losses, which is not the case in this patient. The laboratory data suggest the release of intracellular contents (high LDH, uric acid, potassium, and phosphate) and the diagnosis of urate nephropathy as the cause of his acute kidney failure. As mentioned before, hyperkalemia will produce significant ECG abnormalities, including peaked T waves and widened QRS complexes. Prominent U waves are found in hypokalemia, not hyperkalemia. Atrial fibrillation is not typically seen in hyperkalemia



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