Macrominerals (Na, K, Ca, Mg, P, Cl) — MCQs

10 questions

A 70-year-old man presents to his primary care physician for a general checkup. He states that he has been doing well and taking his medications as prescribed. He recently started a new diet and supplement to improve his health and has started exercising. The patient has a past medical history of diabetes, a myocardial infarction, and hypertension. He denies any shortness of breath at rest or with exertion. An ECG is performed and is within normal limits. Laboratory values are ordered as seen below. Serum: Na+: 139 mEq/L Cl-: 100 mEq/L K+: 6.7 mEq/L HCO3-: 25 mEq/L Glucose: 133 mg/dL Ca2+: 10.2 mg/dL Which of the following is the most likely cause of this patient's presentation?

A 32-year-old man with a history of chronic alcoholism presents to the emergency department with vomiting and diarrhea for 1 week. He states he feels weak and has had poor oral intake during this time. The patient is a current smoker and has presented many times to the emergency department for alcohol intoxication. His temperature is 97.5°F (36.4°C), blood pressure is 102/62 mmHg, pulse is 135/min, respirations are 25/min, and oxygen saturation is 99% on room air. On physical exam, he is found to have orthostatic hypotension and dry mucus membranes. Laboratory studies are ordered as seen below. Serum: Na+: 139 mEq/L Cl-: 101 mEq/L K+: 3.9 mEq/L HCO3-: 25 mEq/L BUN: 20 mg/dL Glucose: 99 mg/dL Creatinine: 1.1 mg/dL Ca2+: 9.8 mg/dL The patient is given normal saline, oral potassium, dextrose, thiamine, and folic acid. The following day, the patient seems confused and complains of diffuse weakness and muscle/bone pain. An ECG and head CT are performed and are unremarkable. Which of the following is the most likely explanation for this patient's new symptoms?

A 28-year-old African American woman presents to her primary care physician with two weeks of nausea, abdominal pain, and increased urination. She states she has had kidney stones in the past and is concerned because her current pain is different in character from what she had experienced then. In addition she reports increasing weakness and fatigue over the past several months as well as mild shortness of breath. Chest radiography shows bilateral hilar adenopathy. Which of the following processes is most likely responsible for her current symptoms?

A 69-year-old woman is brought to the emergency department because of fatigue and lethargy for 5 days. She has also had weakness and nausea for the last 3 days. She has sarcoidosis, major depressive disorder, and hypertension. She had a stroke 5 years ago. Current medications include aspirin, nifedipine, prednisolone, fluoxetine, and rosuvastatin, but she has not taken any of her medications for 7 days due to international travel. Her temperature is 36.1°C (96.9°F), pulse is 95/min, and blood pressure is 85/65 mm Hg. She is lethargic but oriented. Examination shows no other abnormalities. Her hemoglobin concentration is 13.4 g/dL and leukocyte count is 9,600/mm3. Both serum cortisol and ACTH levels are decreased. This patient is most likely to have which of the following additional laboratory abnormalities?

An investigator is studying the effects of hyperphosphatemia on calcium homeostasis. A high-dose phosphate infusion is administered intravenously to a healthy subject over the course of 3 hours. Which of the following sets of changes is most likely to occur in response to the infusion? $$$ Serum parathyroid hormone %%% Serum total calcium %%% Serum calcitriol %%% Urine phosphate $$$

A 70-year-old man is brought to the emergency department by his wife because of lethargy, confusion, and nausea for the past 2 days. He has previously been healthy and has no past medical history. His only medications are a daily multivitamin and acetaminophen, which he takes daily for hip pain. Vital signs are within normal limits. He is disoriented to place and time but recognizes his wife. The remainder of his physical examination shows no abnormalities. Laboratory studies show a hemoglobin concentration of 9.1 g/dL, a serum calcium concentration of 14.7 mg/dL, and a serum creatinine of 2.2 mg/dL (previously 0.9 mg/dL). Which of the following is the most likely underlying mechanism of this patient's condition?

A 55-year-old man with a history of congestive heart failure, hypertension, and hyperlipidemia presents to his primary care clinic. He admits he did not adhere to a low salt diet on a recent vacation. He now has progressive leg swelling and needs two pillows to sleep because he gets short of breath when lying flat. Current medications include aspirin, metoprolol, lisinopril, atorvastatin, and furosemide. His physician decides to increase the dosage and frequency of the patient’s furosemide. Which of the following electrolyte abnormalities is associated with loop diuretics?

An 8-year-old boy is brought to the pediatrician by his mother with nausea, vomiting, and decreased frequency of urination. He has acute lymphoblastic leukemia for which he received the 1st dose of chemotherapy 5 days ago. His leukocyte count was 60,000/mm3 before starting chemotherapy. The vital signs include: pulse 110/min, temperature 37.0°C (98.6°F), and blood pressure 100/70 mm Hg. The physical examination shows bilateral pedal edema. Which of the following serum studies and urinalysis findings will be helpful in confirming the diagnosis of this condition?

A 52-year-old man comes to the physician because of a 4-month history of fatigue, weakness, constipation, decreased appetite, and intermittent flank pain. He takes ibuprofen for knee and shoulder pain. Physical examination shows mild tenderness bilaterally in the costovertebral areas. His serum calcium concentration is 11.2 mg/dL, phosphorus concentration is 2.5 mg/dL, and N-terminal parathyroid hormone concentration is 830 pg/mL. Which of the following steps in vitamin D metabolism is most likely increased in this patient?

Q10

A 17-year-old girl with a BMI of 14.5 kg/m2 is admitted to the hospital for the treatment of anorexia nervosa. The patient is administered intravenous fluids and is supplied with 1,600 calories daily with an increase of 200 calories each day. On day 5 of treatment, the patient manifests symptoms of weakness and confusion, and dark brown urine. Which of the following clinical conditions is the most likely cause of the patient's symptoms?

Macrominerals (Na, K, Ca, Mg, P, Cl) US Medical PG Practice Questions and MCQs

Question 1: A 70-year-old man presents to his primary care physician for a general checkup. He states that he has been doing well and taking his medications as prescribed. He recently started a new diet and supplement to improve his health and has started exercising. The patient has a past medical history of diabetes, a myocardial infarction, and hypertension. He denies any shortness of breath at rest or with exertion. An ECG is performed and is within normal limits. Laboratory values are ordered as seen below. Serum: Na+: 139 mEq/L Cl-: 100 mEq/L K+: 6.7 mEq/L HCO3-: 25 mEq/L Glucose: 133 mg/dL Ca2+: 10.2 mg/dL Which of the following is the most likely cause of this patient's presentation?

A. Medication (Correct Answer)
B. Acute renal failure
C. Hemolysis
D. Dietary changes
E. Rhabdomyolysis

Explanation: ***Medication*** - The patient's **hyperkalemia** (K+ 6.7 mEq/L) despite feeling well, suggests a common side effect of medications, particularly those used for his pre-existing conditions like **hypertension** (**ACE inhibitors**, **ARBs**, **spironolactone**) and **diabetes**. - Medications are a frequent cause of asymptomatic electrolyte abnormalities, and given his complex medical history and the absence of acute symptoms, this is the most likely culprit. *Acute renal failure* - While acute renal failure can cause **hyperkalemia**, it typically presents with other symptoms such as **oliguria**, **fluid retention**, or other signs of organ dysfunction, which are not described. - The patient is reported to be "doing well" without **shortness of breath** or other acute complaints, making acute renal failure less likely as the primary cause of isolated hyperkalemia. *Hemolysis* - **Hemolysis** can release intracellular potassium, leading to **pseudohyperkalemia**, but it would typically be suspected in cases of **blood draw errors** or conditions causing red blood cell breakdown, none of which are indicated. - The patient's presentation does not include any signs or symptoms suggestive of red cell destruction. *Dietary changes* - While an extremely **high-potassium diet** or certain **supplements** could contribute to hyperkalemia, it is less common for dietary changes alone to cause such a significant elevation in a patient with normal organ function. - Given his medical history, medication-induced hyperkalemia is a more direct and common explanation. *Rhabdomyolysis* - **Rhabdomyolysis** involves the breakdown of muscle tissue, releasing potassium and other intracellular contents, but it is usually associated with significant **muscle pain**, **weakness**, and elevated **creatine kinase**. - The patient denies these symptoms and has no other indicators pointing towards severe muscle injury.

Question 2: A 32-year-old man with a history of chronic alcoholism presents to the emergency department with vomiting and diarrhea for 1 week. He states he feels weak and has had poor oral intake during this time. The patient is a current smoker and has presented many times to the emergency department for alcohol intoxication. His temperature is 97.5°F (36.4°C), blood pressure is 102/62 mmHg, pulse is 135/min, respirations are 25/min, and oxygen saturation is 99% on room air. On physical exam, he is found to have orthostatic hypotension and dry mucus membranes. Laboratory studies are ordered as seen below. Serum: Na+: 139 mEq/L Cl-: 101 mEq/L K+: 3.9 mEq/L HCO3-: 25 mEq/L BUN: 20 mg/dL Glucose: 99 mg/dL Creatinine: 1.1 mg/dL Ca2+: 9.8 mg/dL The patient is given normal saline, oral potassium, dextrose, thiamine, and folic acid. The following day, the patient seems confused and complains of diffuse weakness and muscle/bone pain. An ECG and head CT are performed and are unremarkable. Which of the following is the most likely explanation for this patient's new symptoms?

A. Hypomagnesemia
B. Hyponatremia
C. Hypoglycemia
D. Hypophosphatemia (Correct Answer)
E. Hypocalcemia

Explanation: **Hypophosphatemia** - **Hypophosphatemia** is common in **alcoholics**, often exacerbated by refeeding (administration of glucose and fluids). The patient's initial symptoms of weakness and muscle/bone pain after treatment suggest this condition. - Symptoms such as **confusion**, **diffuse weakness**, and **muscle/bone pain** are classic manifestations of severe hypophosphatemia as phosphorus is vital for muscle and nerve function, and bone health. *Hypomagnesemia* - While common in alcoholics and capable of causing weakness, **hypomagnesemia** typically presents with symptoms like **tremors**, **seizures**, and **cardiac arrhythmias**. - The patient's primary symptoms of confusion and diffuse muscle/bone pain are less characteristic of magnesium deficiency compared to phosphorus deficiency. *Hyponatremia* - The patient's initial sodium level was 139 mEq/L, which is within the normal range, making **hyponatremia** unlikely to be the cause of new symptoms. - While severe hyponatremia can cause confusion, it typically presents with other neurological symptoms like **headache** and **seizures**, which are not reported here. *Hypoglycemia* - The initial glucose level of 99 mg/dL was normal, and the patient received dextrose, making **hypoglycemia** an unlikely cause of the new symptoms. - Symptoms of hypoglycemia usually include **sweating**, **tremors**, and **palpitations**, in addition to confusion. *Hypocalcemia* - The patient's initial calcium level was 9.8 mg/dL, which is within the normal range, making **hypocalcemia** an unlikely cause of the new symptoms. - Symptoms of hypocalcemia typically include **tetany**, **paresthesias**, and a **prolonged QT interval** on EKG, none of which are described.

Question 3: A 28-year-old African American woman presents to her primary care physician with two weeks of nausea, abdominal pain, and increased urination. She states she has had kidney stones in the past and is concerned because her current pain is different in character from what she had experienced then. In addition she reports increasing weakness and fatigue over the past several months as well as mild shortness of breath. Chest radiography shows bilateral hilar adenopathy. Which of the following processes is most likely responsible for her current symptoms?

A. Osteoclast-driven bone resorption
B. Increased intestinal absorption of calcium (Correct Answer)
C. Ectopic parathyroid hormone release
D. Increased production of parathyroid hormone
E. Increased renal calcium reabsorption

Explanation: ***Increased intestinal absorption of calcium*** - The constellation of symptoms including **bilateral hilar adenopathy**, chronic fatigue, weakness, and hypercalcemia symptoms (nausea, abdominal pain, increased urination) in an African American woman is highly suggestive of **sarcoidosis**. - In sarcoidosis, activated macrophages within granulomas produce **1α-hydroxylase**, which converts **25-hydroxyvitamin D to 1,25-dihydroxyvitamin D (calcitriol)**, leading to increased intestinal absorption of calcium and subsequent hypercalcemia. *Osteoclast-driven bone resorption* - While hypercalcemia can result from increased osteoclast activity (e.g., in **malignancy** or **primary hyperparathyroidism**), sarcoidosis-associated hypercalcemia is primarily due to increased gut absorption of calcium. - The patient's history does not strongly point to significant bone destructive processes that would be the primary cause of her hypercalcemia. *Ectopic parathyroid hormone release* - **Ectopic PTH release** is characteristic of certain malignancies, such as squamous cell carcinoma, leading to **hypercalcemia of malignancy**. - This syndrome is typically associated with very high calcium levels and PTHrP (parathyroid hormone-related peptide) production, not the clinical picture of sarcoidosis. *Increased production of parathyroid hormone* - **Increased PTH production** (primary hyperparathyroidism) causes hypercalcemia by increasing bone resorption, renal calcium reabsorption, and renal production of calcitriol. - Although some symptoms overlap, the presence of **bilateral hilar adenopathy** and the absence of clear evidence for a parathyroid adenoma makes this less likely than sarcoidosis. *Increased renal calcium reabsorption* - While increased renal calcium reabsorption contributes to hypercalcemia, in the context of sarcoidosis, it is a secondary effect due to the overall calcium imbalance, not the primary mechanism. - The principal driver of hypercalcemia in this patient's likely condition is the **overproduction of active vitamin D** leading to increased intestinal absorption.

Question 4: A 69-year-old woman is brought to the emergency department because of fatigue and lethargy for 5 days. She has also had weakness and nausea for the last 3 days. She has sarcoidosis, major depressive disorder, and hypertension. She had a stroke 5 years ago. Current medications include aspirin, nifedipine, prednisolone, fluoxetine, and rosuvastatin, but she has not taken any of her medications for 7 days due to international travel. Her temperature is 36.1°C (96.9°F), pulse is 95/min, and blood pressure is 85/65 mm Hg. She is lethargic but oriented. Examination shows no other abnormalities. Her hemoglobin concentration is 13.4 g/dL and leukocyte count is 9,600/mm3. Both serum cortisol and ACTH levels are decreased. This patient is most likely to have which of the following additional laboratory abnormalities?

A. Hyperglycemia
B. Hyperkalemia
C. Hyponatremia (Correct Answer)
D. Hypokalemia
E. Normal anion gap metabolic acidosis

Explanation: ***Hyponatremia*** - This patient has **secondary adrenal insufficiency** due to **HPA axis suppression** from chronic prednisolone use, precipitated by abrupt withdrawal after 7 days without medication. - **Both decreased cortisol and ACTH** confirm secondary (central) adrenal insufficiency, distinguishing it from primary adrenal insufficiency where ACTH would be elevated. - **Hyponatremia** develops due to **cortisol deficiency** impairing free water excretion, leading to dilutional hyponatremia—a hallmark laboratory finding in adrenal insufficiency. - Clinical features include **fatigue, lethargy, hypotension, nausea, and weakness**, consistent with adrenal crisis. *Hyperglycemia* - While **glucocorticoids** cause hyperglycemia, **cortisol deficiency** in adrenal insufficiency leads to **impaired gluconeogenesis** and a tendency toward **hypoglycemia**, not hyperglycemia. - The patient's presentation with hypotension and weakness is consistent with adrenal crisis, not hyperglycemia. *Hyperkalemia* - **Hyperkalemia** is characteristic of **primary adrenal insufficiency** (Addison's disease) due to **aldosterone deficiency** affecting the renin-angiotensin-aldosterone system. - In **secondary adrenal insufficiency**, the hypothalamic-pituitary axis is suppressed but the **renin-angiotensin-aldosterone system remains intact**, so aldosterone secretion is preserved and significant hyperkalemia does not occur. *Hypokalemia* - **Hypokalemia** is not a typical feature of adrenal insufficiency and is more commonly associated with diuretic use, primary hyperaldosteronism, or other conditions not present in this case. - The patient's condition reflects cortisol deficiency with preserved aldosterone function. *Normal anion gap metabolic acidosis* - **Normal anion gap metabolic acidosis** occurs in conditions like **renal tubular acidosis** or **diarrhea**, but is not a direct or common consequence of secondary adrenal insufficiency. - The acute presentation with hypotension and electrolyte disturbance (hyponatremia) is the primary metabolic derangement in this case.

Question 5: An investigator is studying the effects of hyperphosphatemia on calcium homeostasis. A high-dose phosphate infusion is administered intravenously to a healthy subject over the course of 3 hours. Which of the following sets of changes is most likely to occur in response to the infusion? $$$ Serum parathyroid hormone %%% Serum total calcium %%% Serum calcitriol %%% Urine phosphate $$$

A. ↑ ↓ ↓ ↑
B. ↓ ↑ ↑ ↓
C. ↑ ↑ ↑ ↑
D. ↓ ↓ ↓ ↓
E. ↑ ↑ ↑ ↓
F. ↑ ↓ ↑ ↑ (Correct Answer)

Explanation: ***↑ ↓ ↑ ↑*** - A high-dose phosphate infusion causes **hyperphosphatemia**, which leads to binding of ionized calcium and results in **hypocalcemia** (decreased serum total calcium). - The hypocalcemia stimulates the parathyroid glands to secrete **increased PTH**. - Elevated PTH stimulates 1α-hydroxylase in the kidneys, leading to **increased calcitriol** (active vitamin D) production to enhance intestinal calcium absorption and renal calcium reabsorption. - Both the high filtered load of phosphate and **PTH's phosphaturic effect** lead to **increased urinary phosphate excretion** as the kidneys attempt to restore phosphate balance. *↑ ↓ ↓ ↑* - This option correctly predicts increased PTH and increased urinary phosphate, but incorrectly suggests **decreased calcitriol**. - PTH stimulation would increase 1α-hydroxylase activity, leading to **increased calcitriol production**, not decreased. *↓ ↑ ↑ ↓* - This option incorrectly predicts **decreased PTH** following hyperphosphatemia. - Hyperphosphatemia causes hypocalcemia, which **stimulates PTH release**, not suppresses it. - An increase in serum total calcium is also incorrect, as phosphate binds calcium acutely. *↑ ↑ ↑ ↑* - While this option correctly predicts increased PTH and calcitriol, it incorrectly suggests **increased serum total calcium**. - Acute hyperphosphatemia causes calcium-phosphate binding, leading to **decreased ionized and total calcium**, which is the trigger for PTH release. - However, urinary phosphate would correctly increase in this scenario. *↓ ↓ ↓ ↓* - This option is completely incorrect as it suggests all parameters decrease. - Hyperphosphatemia triggers compensatory mechanisms including **increased PTH and calcitriol**, not decreases. - Urinary phosphate must **increase** to excrete the excess phosphate load, not decrease. *↑ ↑ ↑ ↓* - This option incorrectly combines increased serum total calcium with **decreased urinary phosphate**. - In hyperphosphatemia, urinary phosphate excretion **must increase** due to both the filtered load and PTH's phosphaturic effect. - Additionally, acute phosphate binding would **decrease** serum calcium initially, though compensatory mechanisms attempt to restore it.

Question 6: A 70-year-old man is brought to the emergency department by his wife because of lethargy, confusion, and nausea for the past 2 days. He has previously been healthy and has no past medical history. His only medications are a daily multivitamin and acetaminophen, which he takes daily for hip pain. Vital signs are within normal limits. He is disoriented to place and time but recognizes his wife. The remainder of his physical examination shows no abnormalities. Laboratory studies show a hemoglobin concentration of 9.1 g/dL, a serum calcium concentration of 14.7 mg/dL, and a serum creatinine of 2.2 mg/dL (previously 0.9 mg/dL). Which of the following is the most likely underlying mechanism of this patient's condition?

A. Increased serum levels of 1,25-hydroxyvitamin D
B. Excessive consumption of calcium
C. Excess PTH secretion from parathyroid glands
D. Ectopic PTHrP release
E. Overproliferation of plasma cells (Correct Answer)

Explanation: ***Overproliferation of plasma cells*** - The patient presents with **hypercalcemia** (14.7 mg/dL), acute **kidney injury** (creatinine 2.2 mg/dL from 0.9 mg/dL), and **anemia** (hemoglobin 9.1 g/dL). These three findings, especially in an elderly patient, strongly suggest **multiple myeloma**, which is characterized by the overproliferation of plasma cells in the bone marrow. - The overproliferation of plasma cells in multiple myeloma leads to the production of **osteoclast-activating factors**, resulting in increased bone resorption and subsequent hypercalcemia. *Increased serum levels of 1,25-hydroxyvitamin D* - While **elevated vitamin D levels** can cause hypercalcemia, it typically occurs due to excessive supplementation or granulomatous diseases (e.g., sarcoidosis). There is no history of either in this patient. - This mechanism would not explain the accompanying **anemia** or **acute kidney injury** (beyond what hypercalcemia itself might induce), which are prominent features here. *Excessive consumption of calcium* - **Milk-alkali syndrome**, caused by excessive intake of calcium and absorbable alkali, can lead to hypercalcemia, metabolic alkalosis, and renal insufficiency. - However, the patient's history does not indicate excessive calcium intake, and this etiology would not typically explain significant **anemia**. *Excess PTH secretion from parathyroid glands* - **Primary hyperparathyroidism** results in increased PTH, leading to hypercalcemia and often low or normal phosphate. While it can cause kidney stones and bone issues, it does not typically cause **anemia** or the rapid progression of kidney injury seen here. - The patient's creatinine has doubled in a short period, which is more suggestive of an acute insult or a systemic disease like myeloma, rather than chronic changes from primary hyperparathyroidism. *Ectopic PTHrP release* - **Parathyroid hormone-related protein (PTHrP)** can be ectopically secreted by various malignancies (e.g., squamous cell carcinoma of the lung, renal cell carcinoma), leading to **humoral hypercalcemia of malignancy**. - While this can cause **hypercalcemia** and related kidney issues, it typically does not directly cause **anemia** in the same way as multiple myeloma, where **bone marrow infiltration** by plasma cells directly suppresses hematopoiesis. The constellation of hypercalcemia, anemia, and acute kidney injury points more specifically to multiple myeloma.

Question 7: A 55-year-old man with a history of congestive heart failure, hypertension, and hyperlipidemia presents to his primary care clinic. He admits he did not adhere to a low salt diet on a recent vacation. He now has progressive leg swelling and needs two pillows to sleep because he gets short of breath when lying flat. Current medications include aspirin, metoprolol, lisinopril, atorvastatin, and furosemide. His physician decides to increase the dosage and frequency of the patient’s furosemide. Which of the following electrolyte abnormalities is associated with loop diuretics?

A. Hyperchloremia
B. Hypocalcemia
C. Hypermagnesemia
D. Hypouricemia
E. Hypokalemia (Correct Answer)

Explanation: ***Hypokalemia*** - **Loop diuretics** are most commonly associated with **hypokalemia**, which is one of their most clinically significant electrolyte disturbances. - Loop diuretics inhibit the **Na-K-2Cl cotransporter** in the thick ascending limb, increasing sodium delivery to the collecting duct. - This stimulates **aldosterone-mediated potassium secretion** via principal cells, leading to increased urinary potassium loss. - **Clinical significance**: Hypokalemia can cause muscle weakness, cardiac arrhythmias, and potentiates digoxin toxicity—particularly important in heart failure patients. *Hyperchloremia* - Loop diuretics cause **hypochloremia**, not hyperchloremia. - Chloride reabsorption is blocked in the thick ascending limb, leading to increased chloride excretion. *Hypocalcemia* - Loop diuretics increase **urinary calcium excretion** (hypercalciuria) by reducing the positive luminal charge needed for paracellular calcium reabsorption. - However, this typically does **not cause clinically significant hypocalcemia** in most patients. - In contrast, thiazide diuretics decrease calcium excretion. *Hypermagnesemia* - Loop diuretics cause **hypomagnesemia**, not hypermagnesemia. - They disrupt the positive lumen potential necessary for magnesium reabsorption in the thick ascending limb. *Hypouricemia* - Loop diuretics cause **hyperuricemia**, not hypouricemia. - They compete with uric acid for secretion in the proximal tubule, promoting uric acid reabsorption and decreasing its excretion.

Question 8: An 8-year-old boy is brought to the pediatrician by his mother with nausea, vomiting, and decreased frequency of urination. He has acute lymphoblastic leukemia for which he received the 1st dose of chemotherapy 5 days ago. His leukocyte count was 60,000/mm3 before starting chemotherapy. The vital signs include: pulse 110/min, temperature 37.0°C (98.6°F), and blood pressure 100/70 mm Hg. The physical examination shows bilateral pedal edema. Which of the following serum studies and urinalysis findings will be helpful in confirming the diagnosis of this condition?

A. Hyperuricemia, hyperkalemia, hyperphosphatemia, and urinary monoclonal spike
B. Hyperkalemia, hyperphosphatemia, hypocalcemia, hyperuricemia, urine supernatant pink, and positive for heme
C. Hyperkalemia, hyperphosphatemia, hypocalcemia, and extremely elevated creatine kinase (MM)
D. Hyperuricemia, hyperkalemia, hyperphosphatemia, lactic acidosis, and oxalate crystals
E. Hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia, and urate crystals in the urine (Correct Answer)

Explanation: ***Hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia, and urate crystals in the urine*** - This patient's presentation following chemotherapy, particularly with a high pre-treatment leukocyte count, is highly suggestive of **tumor lysis syndrome (TLS)**. TLS is characterized by rapid tumor cell breakdown, releasing intracellular contents into the bloodstream. - The **four cardinal laboratory findings** of TLS are **hyperuricemia** (from nucleic acid breakdown), **hyperkalemia** (from intracellular potassium release), **hyperphosphatemia** (from intracellular phosphate release), and **hypocalcemia** (secondary to calcium-phosphate precipitation). The presence of **urate crystals in the urine** confirms the renal effects of uric acid overload, leading to acute kidney injury. *Hyperuricemia, hyperkalemia, hyperphosphatemia, and urinary monoclonal spike* - While **hyperuricemia, hyperkalemia, and hyperphosphatemia** are consistent with tumor lysis syndrome, a **urinary monoclonal spike** is typically associated with multiple myeloma or other plasma cell dyscrasias, not tumor lysis syndrome. - The patient's history of acute lymphoblastic leukemia and recent chemotherapy points away from a monoclonal gammopathy. - This option is also missing the key finding of **hypocalcemia**. *Hyperkalemia, hyperphosphatemia, hypocalcemia, hyperuricemia, urine supernatant pink, and positive for heme* - **Hyperkalemia, hyperphosphatemia, hyperuricemia, and hypocalcemia** are indeed the four cardinal metabolic abnormalities of TLS. However, a **pink urine supernatant and positive heme** indicate **hemoglobinuria** or **myoglobinuria**, pointing towards hemolysis or rhabdomyolysis, respectively. - While TLS can lead to acute kidney injury, these specific urinalysis findings are not typical for TLS. The expected urinary finding would be **urate crystals**, not heme pigments. *Hyperkalemia, hyperphosphatemia, hypocalcemia, and extremely elevated creatine kinase (MM)* - **Hyperkalemia, hyperphosphatemia, and hypocalcemia** are consistent with TLS. However, **extremely elevated creatine kinase (MM)** is a hallmark of **rhabdomyolysis**, a condition involving breakdown of skeletal muscle. - This option is also missing **hyperuricemia**, which is a cardinal feature of TLS. - There is no clinical indication for rhabdomyolysis in this patient's presentation. *Hyperuricemia, hyperkalemia, hyperphosphatemia, lactic acidosis, and oxalate crystals* - While **hyperuricemia, hyperkalemia, and hyperphosphatemia** are characteristic of TLS, this option is missing **hypocalcemia**, one of the four cardinal metabolic abnormalities. - Additionally, the presence of **oxalate crystals** in the urine is typically associated with **ethylene glycol poisoning** or primary hyperoxaluria, not tumor lysis syndrome. **Urate crystals**, not oxalate crystals, are expected due to the rapid breakdown of purines in TLS. - **Lactic acidosis** can occur in severe TLS but is not a defining laboratory criterion.

Question 9: A 52-year-old man comes to the physician because of a 4-month history of fatigue, weakness, constipation, decreased appetite, and intermittent flank pain. He takes ibuprofen for knee and shoulder pain. Physical examination shows mild tenderness bilaterally in the costovertebral areas. His serum calcium concentration is 11.2 mg/dL, phosphorus concentration is 2.5 mg/dL, and N-terminal parathyroid hormone concentration is 830 pg/mL. Which of the following steps in vitamin D metabolism is most likely increased in this patient?

A. Ergocalciferol → 25-hydroxyergocalciferol
B. 7-dehydrocholesterol → cholecalciferol
C. 25-hydroxycholecalciferol → 1,25-dihydroxycholecalciferol (Correct Answer)
D. 25-hydroxycholecalciferol → 24,25-dihydroxycholecalciferol
E. Cholecalciferol → 25-hydroxycholecalciferol

Explanation: ***25-hydroxycholecalciferol → 1,25-dihydroxycholecalciferol*** - This patient presents with **hypercalcemia** (11.2 mg/dL), **hypophosphatemia** (2.5 mg/dL), and a markedly **elevated N-terminal parathyroid hormone (PTH)** concentration (830 pg/mL), which are classic findings for **primary hyperparathyroidism**. - In primary hyperparathyroidism, elevated PTH directly stimulates the **renal 1-alpha-hydroxylase enzyme**, increasing the conversion of **25-hydroxycholecalciferol** (calcidiol) to its active form, **1,25-dihydroxycholecalciferol** (calcitriol), which raises calcium levels. *Ergocalciferol → 25-hydroxyergocalciferol* - This step involves the **hepatic 25-hydroxylase enzyme** converting dietary vitamin D2 (ergocalciferol) to its storage form, which is not primarily regulated by PTH in the context of hyperparathyroidism. - While essential for vitamin D activation, this conversion rate is usually adequate and not the primary increased step responsible for the hypercalcemic state in this patient's presentation. *7-dehydrocholesterol → cholecalciferol* - This process is the **cutaneous synthesis of vitamin D3 (cholecalciferol)**, which is dependent on UV light exposure and is not directly regulated by PTH. - This initial step of vitamin D synthesis occurs in the skin and is upstream of the metabolic pathway influenced by PTH. *25-hydroxycholecalciferol → 24,25-dihydroxycholecalciferol* - This conversion produces an **inactive form of vitamin D** and is catalyzed by the **24-hydroxylase enzyme**. - This enzyme activity is typically **suppressed by high PTH** and **increased by high levels of 1,25-dihydroxycholecalciferol**, serving to degrade excess active vitamin D; therefore, this step would likely be decreased, not increased, in primary hyperparathyroidism. *Cholecalciferol → 25-hydroxycholecalciferol* - This is the **hepatic 25-hydroxylation** of vitamin D3, producing 25-hydroxycholecalciferol (calcidiol), the major circulating form of vitamin D. - While critical for producing the substrate for further activation, this step is not the *most likely increased* step in response to high PTH in primary hyperparathyroidism.

Question 10: A 17-year-old girl with a BMI of 14.5 kg/m2 is admitted to the hospital for the treatment of anorexia nervosa. The patient is administered intravenous fluids and is supplied with 1,600 calories daily with an increase of 200 calories each day. On day 5 of treatment, the patient manifests symptoms of weakness and confusion, and dark brown urine. Which of the following clinical conditions is the most likely cause of the patient's symptoms?

A. Hypercalcemia
B. Thiamine deficiency
C. Hyperkalemia
D. Hypophosphatemia (Correct Answer)
E. Hypermagnesemia

Explanation: ***Hypophosphatemia*** - The symptoms of **weakness, confusion, and dark brown urine** during refeeding in an anorexic patient strongly suggest **refeeding syndrome**, which is mainly driven by severe **hypophosphatemia**. The dark brown urine indicates **rhabdomyolysis**, a classic sign of severe electrolyte disturbances in this context. - Rapid reintroduction of carbohydrates leads to an insulin surge, driving **phosphate, potassium, and magnesium** intracellularly. This causes a precipitous drop in serum phosphate levels, impairing ATP production and cellular function, leading to muscular weakness, cardiac dysfunction, and neurological symptoms. *Hypercalcemia* - **Hypercalcemia** is not typically a direct complication of refeeding syndrome and would not explain the constellation of symptoms, especially **rhabdomyolysis**. - Symptoms usually include **constipation, polyuria, polydipsia, and bone pain**, which are different from those presented. *Thiamine deficiency* - **Thiamine deficiency** can occur in refeeding syndrome, leading to **Wernicke-Korsakoff syndrome** marked by confusion, ataxia, and ophthalmoplegia. However, it does not typically cause **dark brown urine** due to rhabdomyolysis, which is a hallmark of severe hypophosphatemia. - While possible, it is less likely to be the *most likely* single cause for all presented symptoms, especially the musculoskeletal and renal manifestations. *Hyperkalemia* - **Hyperkalemia** is unlikely in refeeding syndrome; instead, **hypokalemia** is a common electrolyte disturbance as potassium shifts intracellularly with insulin secretion. - Symptoms of hyperkalemia include **cardiac arrhythmias and muscle weakness**, but it does not cause rhabdomyolysis or dark urine in this context. *Hypermagnesemia* - **Hypermagnesemia** is also not a typical complication of refeeding syndrome; instead, **hypomagnesemia** can occur due to intracellular shifting. - Symptoms of hypermagnesemia include **hypotension, bradycardia, muscle weakness, and respiratory depression**, which do not align with the patient's presentation.

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free