SeanWu25/NEJM-AI_Benchmarking_Medical_Language_Models huggingface dataset:
Subject: Electrolytes and Acid-Base Disorders

An 88-year-old man with syndrome of inappropriate antidiuretic hormone secretion caused by small-cell lung cancer was being treated with ﬂuid restriction and urea, but his serum [Na+] did not improve sufﬁciently. Moreover, his diet-related quality of life was reduced by this treatment. Tolvaptan administration (15 mg/d) led to an appropriate improvement in serum [Na+] within the upper limit of correction. While initiating tolvaptan, the doctor repeatedly instructed the patient to drink water whenever he felt thirsty. At his initial follow-up visit, the patient reported he was drinking well, with good appetite and an improved diet-related quality of life. However, 2 weeks later, he visited a clinic because of lethargy. Vital signs: GCS: E4V5M6 (Eye response, opens eyes spontaneously; Verbal response, oriented, converses normally; Motor response, obeys commands); BP 100/ 60 mm Hg (supine position), pulse rate 65 beats/min, respiratory rate 14/min, SpO2 95% (room air), temperature 36.2 degree C, weight 70 kg (+2 kg)
Blood: total protein 6.3 g/dl, albumin 3.0 g/dl, BUN 40 mg/dl, creatinine 0.9 mg/dl, uric acid 5.0 mg/dl, Na+ 160 mmol/L, K+ 4.5 mmol/L, Cl- 120 mmol/L, glucose 100 mg/dl, osmolality 350 mOsm/kg H2O
Urine: Na+ 15 mmol/L, K+ 30 mmol/L, osmolality 120 mOsm/kg H2O
Hypernatremia was diagnosed and 5% dextrose in water was administered..
Question: Which ONE of the following is the MOST likely cause of this patient’s hypernatremia?
1. Aquaresis produced by tolvaptan
2. Decreased thirst in response to hypertonicity in the elderly
3. Loss of appetite
4. Mistakenly continued ﬂuid restriction
5. Partial improvement of syndrome of inappropriate antidiuretic hormone secretion because of treatment of small-cell lung cancer
Answer: B
Subject: Electrolytes and Acid-Base Disorders

A 59-year-old man with a medical history of type 2 diabetes mellitus, hypertension, coronary artery dis-ease, and bipolar disorder taking lithium is admitted to the intensive care unit with pneumonia and septic shock. On examination, the patient is sedated, receiving mechanical ventilation, with an FiO2 40%, positive end-expiratory pressure 8 cmH2O, BP 118/79 mm Hg, heart rate 91 beats/min. The results of heart and lung examination are unremarkable. There is no jugular venous distension, or peripheral edema. For the past 24 hours, his urine output was 1300 ml. Laboratory evaluation shows serum sodium 155 mmol/L, potassium 3.7 mmol/L, chloride 123 mmol/L, total CO2 25 mmol/L, BUN 24 mg/dl, serum creatinine 1.3 mg/dl (baseline creatinine 1 mg/dl), blood glucose 170 mg/dl, and urine osmolarity 629 mOsm/kg..
Question: Which ONE of the following answers is MOST likely the correct cause of the patient’s hyponatremia?
1. Hypernatremia is iatrogenic and requires intravenous or oral free water supplementation
2. Hypernatremia is secondary to lithium-induced partial nephrogenic diabetes insipidus
3. Hypernatremia is secondary to osmotic diuresis from hyperglycemia
4. Hypernatremia is secondary to lithium-induced complete nephrogenic diabetes insipidus
Answer: A
Subject: Electrolytes and Acid-Base Disorders

An 86-year-old woman with a medical history of hypertension, multi-infarct dementia, and atrial ﬁbrillation presents from a nursing home with mental status changes to the emergency department. On presentation, her BP is 106/58 mm Hg, heart rate is 90 beats/min (irregular), respiratory rate is 22/min, oxygen saturation is 97% and weight is 60 kg. On examination she has dry mucous membranes, she is oriented to name only, her lung and heart examination results are unremarkable, and there is no leg edema. Laboratory evaluation shows serum sodium 176 mmol/L, potassium 3.5 mmol/L, chloride 129 mmol/L, bicarbonate 35 mmol/L, creatinine 1.5 mg/dl (base-line creatinine 1.2 mg/dl, and urine osmolarity 655 mOsm/kg..
Question: Which is the correct statement regarding the rate of correction and amount of patient’s free water deﬁcit?
1. Assuming minimal ongoing free water losses, the infusion of 2 liters of free water would decrease the serum sodium concentration to approximately 155 mmol/L
2. Assuming 45% total body water content in this elderly woman, the free water deﬁcit is 3.5 L
3. A change in the serum sodium concentration of 1 mmol/L/h is likely safe and should not cause neurologic sequelae.
4. Assuming minimal ongoing free water losses, the infusion of 4 liters of free water would decrease the serum sodium concentration to approximately 154 mmol/L
Answer: D
Subject: Electrolytes and Acid-Base Disorders

A 44-year-old man with a medical history of pulmonary sarcoidosis has his condition evaluated for increased thirst and urination of 2 weeks duration. He takes maintenance 10 mg of prednisone. He has no other contributory medical history and does not take other medications. On examination, BP is 125/74 mm Hg, heart rate is 72 beats/min, and respiratory rate is 15/min. The lungs and heart examination results are unremarkable. Laboratory evaluation shows serum sodium 147 mmol/L, potassium 3.8 mmol/L, chloride 110 mmol/L, BUN 16 mg/dl, creatinine 1.1 mg/dl, calcium 8.7 mg/dl, albumin 4 g/dl, urine sodium 20 mmol/L, and urine osmolarity 115 mOsm/kg. The urine output exceeds 6 liters per day..
Question: What is the correct statement regarding the cause of and diagnostic workup for hypotonic polyuria?
1. The indirect water deprivation test will accurately differentiate between central diabetes insipidus and primary polydipsia
2. Hypertonic saline infusion test and resultant copeptin release will accurately differentiate between central diabetes insipidus and primary polydipsia
3. In the setting of sarcoidosis, nephrogenic diabetes insipidus due to hypercalcemia is the most likely cause of hypernatremia
4. Copeptin levels after a water deprivation test will accurately differentiate between central diabetes insipidus and primary polydipsia
Answer: B
Subject: Electrolytes and Acid-Base Disorders

A 40-year-old woman with a medical history of schizophrenia presents to the emergency department with tonic-clonic seizures. She is intubated on arrival. On examination, BP is 179/88 mm Hg, and heart rate 137 beats/min. Laboratory evaluation shows serum sodium 183 mmol/L, serum osmolality 363 mOsm/kg, potassium 3.6 mmol/L, chloride 128 mmol/L, blood glucose 115 mg/dl, BUN 22 mg/dl, creatinine 1.0 mg/dl. The patient’s family reports that she might have ingested 500 ml of triple-strength Japanese seasoning soy sauce 3 to 4 hours before seizure onset..
Question: Which of the following statements regarding the management of an acute salt intoxication is correct?
1. Goal serum sodium correction should not exceed more than 10 mmol/L in 24 hours or 0.5 mmol/L per hour to avoid the development of cerebral edema
2. Cerebral edema is unlikely to occur in this setting of acute hypernatremia, and rapid correction of serum Na to baseline should be undertaken
3. Acute hypernatremia allows for the formation of idiogenic osmoles counterbalancing the osmotic gradient between extracellular and intracellular compartments
4. Administration of free water at high rates is sufﬁcient to treat salt intoxication, and extracorporeal removal can cause too rapid a decrease in the serum sodium concentration
Answer: B
Subject: Electrolytes and Acid-Base Disorders

A 55-year-old man with a medical history of hypertension, type 2 diabetes mellitus, hyperlipidemia, and ESKD, receiving hemodialysis, is seen for a nephrology consultation in the neurologic intensive care unit, where he has been admitted for subarachnoid hemorrhage. The patient is intubated, is using minimal ventilatory settings, and does not require any sedation. His GCS score is 7. An external ventricular drain is placed, and the patient is given hypertonic saline infusion. BP 135/75, heart rate 67 beats/min. Laboratory evaluation shows sodium 147 mmol/L, potassium 6.0 mmol/L, chloride 108 mmol/l, total CO2 21 mmol/L, BUN 88 mg/dl, and creatinine 10.4 mg/dl. His last dialysis was performed 3 days ago. The patient is full code, and the family would like to pursue full medical and surgical management at this point..
Question: What is the optimal decision in regard to the renal replacement therapy for this patient?
1. Perform intermittent hemodialysis with regular blood and dialysate ﬂows because the patient is starting to experience electrolyte abnormalities, and rising BUN might contribute to worsening mental status
2. Begin continuous venovenous hemodiaﬁltration with isotonic bicarbonate replacement ﬂuid and discontinue hypertonic saline infusion
3. Begin continuous venovenous hemodiaﬁltration with standard sodium concentration dialysate and replacement ﬂuid; at the same time continue hypertonic saline infusion to maintain permissive hypernatremia
4. Hold off renal replacement therapy at this time and manage the electrolyte abnormalities medically
Answer: C
Subject: Electrolytes and Acid-Base Disorders

A 22-year old woman is referred for hypokalemia. The patient’s history indicates progressive weakness over the past 3 weeks and weight gain despite exercise and following a healthy balanced diet. The patient does not describe having diarrhea or vomiting, and she does not have a history of using over-the-counter (OTC) medications or herbal supplements. Her body mass index (BMI) is 19 kg/m2, and BP is 120/80 mm Hg. The results of physical examination are unremarkable. Laboratory evaluation shows plasma sodium 133 mEq/L, plasma potassium 2.7 mEq/L, plasma chloride 83 mEq/L, plasma bicarbonate 34 mEq/L, plasma BUN 6 mg/dl, plasma creatinine 0.6 mg/dl, arterial blood gases pH 7.46 and PCO2 44 mm Hg, urine electrolytes (mEq/L) [Na+] 70, urine [K+}, urine [Cl-] <15, urine pH8..
Question: What is the most likely cause of this patient’s hypokalemia?
1. Early (“continuous”) vomiting
2. Magnesium deﬁciency
3. Long-term laxative use
4. Remote diuretic use
Answer: A
Subject: Electrolytes and Acid-Base Disorders

A 32-year-old man with a history of cystic ﬁbrosis presents to the emergency department with progressive confusion and is unable to provide any medical history. His family informs that over the past few days, he had been painting a new roof in the heat of summer. On medication review, it is learned that the patient takes topiramate for migraine prophylaxis and inhaled tobramycin for Pseudomonas aeruginosa colonization. History is limited because of altered mental status. On examination, BP is 90/60 mm Hg and pulse is 100 beats/min. Mucous membranes are dry, and poor skin turgor is noted. Additional laboratory studies show plasma sodium 135 mEq/L, plasma potassium 2.2 mEq/L, plasma chloride 86 mEq/L, plasma bicarbonate 40 mEq/L, plasma BUN 56 mg/dl, plasma creatinine 2.3 mg/dl, plasma uric acid 12.2 mg/dl, plasma creatine kinase 676 U/L..
Question: What is the most likely pathophysiologic explanation for this patient's severe hypokalemia?
1. Inhibition of carbonic anhydrase in the proximal tubule
2. Activation of calcium-sensing receptor in the distal tubule
3. Metabolic alkalosis–induced transcellular shift of potassium out of the cells
4. Loss of potassium in the sweat glands from perspiration with extracellular ﬂuid volume depletion and secondary hyperaldosteronism
5. Urinary loss of bicarbonate by the intercalated cells
Answer: D
Subject: Electrolytes and Acid-Base Disorders

A 36-year-old man is referred to nephrology clinic for evaluation of hypokalemia. The patient described progressive fatigue and leg cramps over the past year since initiating intermittent fasting and adhering to a vegetarian diet. He takes magnesium supplements for the leg cramps but denies using other OTC medications, herbal supplements, or illicit drugs. The patient is sexually active and is taking pre-exposure prophylaxis, emtricitabine, and tenofovir to prevent HIV. He is afebrile, BP is 120/80 mm Hg, pulse is 80 beats/min, and respiratory rate is 16/min. The results of physical examination are unremarkable. Laboratory data: Plasma sodium 138 mEq/L, potassium 3.4 mEq/L, chloride 114 mEq/L, bicarbonate 15 mEq/L, BUN 28 mg/dl, creatinine 0.6 mg/dl, glucose 92 mg/dl, uric acid 2.3 mg/dl, serum phosphorus 1.9 mg/dl. Urine studies: pH 6, 1+ protein, 2+ glucose, no erythrocytes or leukocytes. The patient was admitted, and an intravenous hypotonic saline solution (0.45% NaCl) containing 75 mEq sodium bicarbonate was initiated at a rate of 1 mEq/kg per h. Spot urine and simultaneous plasma electrolytes were obtained to measure fractional excretion of HCO3-..
Question: What would you predict as the expected trend and values for pertinent laboratory data shown in the next series of choices?
1. Plasma K+ ↓, Plasma HCO3- ↑, Urine pH ↑", Fractional excretion of [HCO3-] 2%
2. Plasma K+ ↑, Plasma HCO3- ↑, Urine pH ↔, Fractional excretion of [HCO3-] 15%
3. Plasma K+ ↑, Plasma HCO3- ↓, Urine pH ↓, Fractional excretion of [HCO3-] 2%
4. Plasma K+ ↓, Plasma HCO3-↑, Urine pH ↑, Fractional excretion of [HCO3-] 15%
Answer: D
Subject: Electrolytes and Acid-Base Disorders

A 22-year-old woman is seen in a nephrology clinic for electrolyte abnormalities. The patient described having excessive muscle cramps after ballet lessons and indicates that she has been vigorously training for an upcoming dance competition. She denies current use of OTC medications, herbal supplements, or diuretics, and she speciﬁcally denies vomiting or diarrhea. There is a history of “idiopathic edema” for which she received hydrochlorothiazide 12.5 mg/d, but she categorically denies current use. Her sister has a history of Hashimoto thyroiditis, and her mother had a history of stroke. Her BP in the clinic is 110/60 mm Hg, and her BMI is 19 kg/m2. The results of physical examination are unremarkable. Blood chemistry: Plasma sodium 138 mEq/L, potassium 2.7 mEq/L, chloride 95 mEq/L, bicarbonate 32 mEq/L, creatinine 0.6 mg/dl, magnesium 1.3 mg/dl, aldosterone 20 ng/dl (high). Spot urine studies: K+/Cr ratio 32 mEq/g, Ca+2/Cr ratio 0.4mg/g (high), fractional excretion of Mg+2 3% (high)..
Question: What is the most likely cause of hypokalemia?
1. Abuse of laxatives
2. Surreptitious diuretic use
3. Herbal medicine containing glycyrrhizic acid
4. Remote vomiting
5. OTC thyroid supplementation
Answer: B
Subject: Electrolytes and Acid-Base Disorders

A 27-year-old man presents to a nephrology clinic for consultation. The patient was seen in the emergency department of a local hospital with profound muscle weakness, and a [K+] of 2.3 mEq/L was reported. The patient’s condition improved, and the discharge plasma [K+] was 4.1 mEq/L. This same sequence of events occurred 3 weeks later, and he is referred by the emergency department physician for evaluation of the recurrent hypokalemia. He has been describing increased salt-craving and frequent muscle cramps. His medical history is signiﬁcant for depression treated with selective serotonin reuptake inhibitor antidepressants. He denies the use of any OTC medications or herbal supplements. He has been taking magnesium oxide 400 mg four times a day and potassium chloride 20 mEq two times a day for several years. The patient is afebrile, with BP 100/70 mm Hg, pulse 78 beats/min, and respiratory rate 16/min. He appears euvolemic on examination. No sensory deﬁcits are noted, and muscle strength in the upper and lower extremities is 2/4. Electrocardiogram reveals “U” waves in limb leads II and V1. The plasma electrolytes at the time of this visit: Plasma sodium 139 mEq/L, potassium 2.7 mEq/L, chloride 95 mEq/L, bicarbonate 29 mEq/L, creatinine 0.7 mg/dl, magnesium 1.1 mEq/L. The patient is admitted to the hospital for diagnostic studies and treatment of hypokalemia. Spot urine studies obtained after stabilization are as follows: K+/Cr ratio 25 mEq/g, Ca+2/Cr ratio 0.04 mg/g, fractional excretion of Mg+2 5% (high)..
Question: What is the most likely cause of hypokalemia and hypomagnesemia?
1. Mutation in CLDN16 gene encoding claudin-16
2. Mutation in SLC12A3 gene encoding NCC in the distal tubule
3. Mutation in KCNJ1 gene encoding ROMK in collecting duct
4. Mutation in SLC12A1 gene encoding for NKCC2 in thick ascending limb of Henle
Answer: B
Subject: Electrolytes and Acid-Base Disorders

You are following up a 71-year-old man for CKD. He has long-standing diabetes and hypertension. His eGFR is 32 mL/min per 1.73, and his microalbumin-to-creatinine ratio is 1.7 grams. His serum potassium is 5.8 mEq/L and takes lisinopril 10 mg daily..
Question: Which of the following is the best approach to the management of his hyperkalemia?
1. Leave his regimen unchanged as recent studies have shown that low potassium confers higher cardiovascular risk and mortality than does high potassium
2. Avoid potassium-binding agents as they all have gastrointestinal side effects and are risky for long-term use
3. Initiate patiromer to allow continued treatment with renin-angiotensin system inhibitors.
4. Add ﬂudrocortisone to reduce potassium in this patient
Answer: C
Subject: Electrolytes and Acid-Base Disorders

A 16-year-old boy is referred for evaluation of hyperkalemia detected during emergency department evaluation of muscle weakness. He notes frequent episodes of muscle weakness since childhood, associated with physical exertion or exposure to cold. Episodes of weakness have worsened as he has gotten older and are associated with muscular pain after episodes. During the most recent episode his potassium was 6.5 mEq/L and was associated with electrocardiographic changes, with normal chloride, sodium, and bicarbonate. His condition was subsequently evaluated by his pediatrician, who noted normal potassium of 4.5 mEq/L and normal renin and aldosterone concentrations. The patient notes that his late father used to describe the exact same problem, as do his uncle and cousin. In addition, his younger sister is starting to have the same symptoms..
Question: What is the most likely underlying cause of hyperkalemia?
1. A loss of function mutation of the gene encoding the epithelial sodium channel
2. A mutation of WNK (with no lysine) kinase resulting in increased expression of the sodium-chloride (NCCT) cotransporter and inhibition of potassium channels in principal cells
3. A mutation in the SCNA4 gene for the alpha subunit of the skeletal muscle cell sodium channel
4. A mutation in genes encoding proteins that modulate WNK activity, including Kelch-like 3 and Cullin 3
Answer: C
Subject: Electrolytes and Acid-Base Disorders

You are invited to speak at a symposium sponsored by the Federal Emergency Management Agency (FEMA) on emergency preparedness in urban centers. A FEMA council member has heard that hyperkalemia is a major cause of death of victims with crush injury sustained as a result of being buried under rubble in earthquakes. She asks you how to best determine hyperkalemia, particularly when there are multiple victims and time to is limited..
Question: What is your response?
1. Measuring potassium in serum is faster than measuring potassium in whole blood
2. A deep learning algorithm using an electrocardiogram is able to exclude hyperkalemia with acceptable accuracy
3. Serum potassium is usually lower than plasma potassium
4. Measuring potassium in whole blood is not as accurate as measuring potassium in serum or plasma
Answer: B
Subject: Electrolytes and Acid-Base Disorders

A 79-year-old woman with ESKD routinely presents on Tuesday mornings with predialysis potassium 6.8 mEq/L. She undergoes dialysis three times weekly for 4 hours via a ﬁstula. Her Kt/V is 1.7..
Question: Which of the following is most likely to be an evidence-based approach to her hyperkalemia?
1. Sodium zirconium cyclosilicate should not be chosen as it is effective in reducing potassium in non-dialysis CKD patients but not in dialysis patients
2. Sodium zirconium cyclosilicate should be chosen for this patient rather than patiromer as it is less likely to cause edema
3. Sodium zirconium cyclosilicate also removes hydrogen ions and may increase serum bicarbonate
4. Sodium zirconium cyclosilicate works quickly and has been shown to provide added beneﬁt to insulin and glucose in the treatment of acute severe hyperkalemia
Answer: C
Subject: Electrolytes and Acid-Base Disorders

A 74-year-old man with type II diabetes mellitus and heart failure with reduced ejection fraction presents to the emergency department with a 1-week history of fatigue, vomiting, headache, and abdominal pain. He is found to have AKI, with creatinine increased to 2.3 mg/dl from baseline 1.2 mg/dl. Other laboratory results show Na+ 134 mEq/L, K+ 4.0 mEq/L, Cl- 98 mEq/L, HCO3- 15 mmol/L, BUN 68 mmol/L, glucose 196 mmol/L. Lactate is 1.5 mEq/L. On examination, he is in hemodynamically stable condition, with a mildly tender abdomen, but the results of physical examination are otherwise unremarkable. For his diabetes, he takes insulin and another oral antidiabetic medication that he cannot recall the name of. He reports that his blood sugars have been very well controlled, such that his insulin was recently reduced by 50%..
Question: In considering this case, which of the following statements is most accurate?
1. Metformin is the most likely culprit agent for acidosis in this case
2. The recent reduction in insulin dosing may be the precipitant for this clinical presentation
3. The patient’s near-normal blood glucose excludes ketoacidosis as a cause of this presentation
4. This patient should be given an intravenous infusion of isotonic bicarbonate
Answer: B
Subject: Electrolytes and Acid-Base Disorders

The internal medicine residency director asks you to lead a teaching session for medicine residents on drugs and the kidney. She references a patient recently admitted with zidovudine-induced metabolic acidosis and asks that you include an overview of drug-induced acidosis..
Question: With regard to drug-induced metabolic acidosis, which of the following is correct?
1. Topiramate is associated with urine crystals and with crystalline stone formation
2. Valproate is highly protein bound and is not amenable to removal with hemodialysis
3. Concomitant use of antibiotics has been associated with increased risk of pyroglutamic acidosis from acetaminophen use
4. Linezolid causes a non-anion gap by blocking carbonic anhydrase
Answer: C
Subject: Electrolytes and Acid-Base Disorders

A 37-year-old male patient with CKD stage IV comes for clinic follow-up. At last review, [HCO3] had decreased to 19 mEq/L, and NaHCO3 650 mg twice daily was initiated. Today, he reports abdominal bloating and some nausea after taking the medications. His BP is well controlled at 122/68 mm Hg, and on examination he has trace lower limb edema. He has read that NaHCO3 may promote ﬂuid retention and is reluctant to continue taking it. He asks for an explanation why it is necessary..
Question: Which of the following is correct with regard to treatment of metabolic acidosis in CKD?
1. A meta-analysis of treatment with NaHCO3 for metabolic acidosis did not show any increase in requirement for antihypertensive or diuretic agents
2. Increased ammoniagenesis resulting from acidosis leads to increases in endothelin-1 (ET-1) levels
3. In renal transplant recipients, metabolic acidosis has been associated with increased risk of graft failure, but not cardiovascular events
4. Alkali therapy has been shown to reduce urine ET-1 and aldosterone levels
Answer: D