Disorders of Calcium and Phosphate Metabolism — MCQs
In hypoparathyroidism:
Which of the following statements about hypercalcemia in sarcoidosis is false?
Which hormone is released when serum calcium levels decrease?
A patient is on a low calcium diet for 8 weeks. Which of the following increases to maintain serum calcium levels?
All are symptoms of hypocalcemia except
A 23-year-old woman undergoes total thyroidectomy for carcinoma of the thyroid gland. On the second postoperative day, she begins to complain of a tingling sensation in her hands and appears anxious, later complaining of muscle cramps. Which of the following is the most appropriate initial management strategy?
A 71-year-old man develops dysphagia for both solids and liquids and weight loss of 60 lb over the past 6 months. He undergoes endoscopy, demonstrating a distal esophageal lesion, and biopsies are consistent with squamous cell carcinoma. He is scheduled for neoadjuvant chemoradiation followed by an esophagectomy. Preoperatively he is started on total parenteral nutrition, given his severe malnutrition reflected by an albumin of less than 1. Which of the following is most likely to be a concern initially in starting total parenteral nutrition in this patient?
Which of the following is a feature of tumor lysis syndrome?
Why is citrate phosphate dextrose (CPD) better than acid citrate dextrose (ACD) for storage of blood?
What is the initial treatment of choice for managing secondary hyperparathyroidism in patients with renal osteodystrophy?
Disorders of Calcium and Phosphate Metabolism Indian Medical PG Practice Questions and MCQs
Question 1: In hypoparathyroidism:
- A. Plasma calcium is high and inorganic phosphorous low
- B. Plasma calcium and inorganic phosphorous are low
- C. Plasma calcium is low and inorganic phosphorous high (Correct Answer)
- D. Plasma calcium and inorganic phosphorous are high
Explanation: ***Plasma calcium is low and inorganic phosphorous high*** - **Hypoparathyroidism** is characterized by insufficient parathyroid hormone (PTH) production, leading to decreased bone resorption and reduced renal reabsorption of calcium [1]. This results in **hypocalcemia** (low plasma calcium) [1]. - PTH also promotes renal excretion of phosphate [2]. With insufficient PTH, renal phosphate excretion is impaired, leading to **hyperphosphatemia** (high inorganic phosphorus) [1]. *Plasma calcium is high and inorganic phosphorous low* - This profile is characteristic of **primary hyperparathyroidism**, where excessive PTH causes increased bone resorption and renal calcium reabsorption (high calcium), and increased renal phosphate excretion (low phosphorus). - It directly contradicts the defining features of hypoparathyroidism [1]. *Plasma calcium and inorganic phosphorous are low* - While plasma calcium is low in hypoparathyroidism, plasma inorganic phosphorus is characteristically high, not low [1]. - A combination of low calcium and low phosphorus can be seen in conditions like **vitamin D deficiency** (osteomalacia), but not directly in pure hypoparathyroidism [1]. *Plasma calcium and inorganic phosphorous are high* - This combination of high calcium and high phosphorus is uncommon and not typically seen in either hypoparathyroidism or hyperparathyroidism. - It could potentially indicate conditions like **milk-alkali syndrome** or **vitamin D intoxication**, but not hypoparathyroidism, which is defined by low calcium [1].
Question 2: Which of the following statements about hypercalcemia in sarcoidosis is false?
- A. PTHrP level is increased
- B. Parathormone level is increased (Correct Answer)
- C. Oral steroids are useful
- D. Calcitriol level is increased
Explanation: ***Parathormone level is increased*** - In **sarcoidosis-associated hypercalcemia**, the parathormone (PTH) level is typically **low or suppressed**. [1] - This is because the hypercalcemia is due to **extra-renal 1-$\alpha$ hydroxylation** of 25-hydroxyvitamin D to 1,25-dihydroxyvitamin D (calcitriol) by macrophages in granulomas, not primary hyperparathyroidism. [1] *PTHrP level is increased* - This statement is **false** for sarcoidosis. Elevated **parathyroid hormone-related peptide (PTHrP)** is a common cause of hypercalcemia in **malignancy**, particularly squamous cell carcinomas, but not in sarcoidosis. - Hypercalcemia in sarcoidosis is **PTH-independent** and not mediated by PTHrP. [1] *Oral steroids are useful* - This statement is **true**. **Corticosteroids** (like oral prednisone) are effective in treating hypercalcemia in sarcoidosis. - They work by **inhibiting the activity of 1-$\alpha$ hydroxylase** in alveolar macrophages and reducing intestinal calcium absorption. *Calcitriol level is increased* - This statement is **true**. In sarcoidosis, activated **macrophages within granulomas** aberrantly express **1-$\alpha$ hydroxylase**. [1] - This leads to the **extra-renal synthesis of calcitriol** (1,25-dihydroxyvitamin D), which increases intestinal calcium absorption and bone resorption, causing hypercalcemia. [1]
Question 3: Which hormone is released when serum calcium levels decrease?
- A. Parathormone (Correct Answer)
- B. Calcitonin
- C. Thyroxine
- D. Adrenaline
Explanation: ***Parathormone*** - **Parathormone (PTH)** is released from the **parathyroid glands** in response to **low serum calcium levels**. - Its primary function is to **increase serum calcium** by stimulating bone resorption, increasing renal reabsorption of calcium, and enhancing intestinal absorption of calcium (indirectly via vitamin D activation). *Calcitonin* - **Calcitonin** is released from the **thyroid gland** in response to **high serum calcium levels**. - Its main action is to **lower serum calcium** by inhibiting osteoclast activity and increasing renal calcium excretion. *Thyroxine* - **Thyroxine (T4)** is a thyroid hormone primarily involved in **metabolism**, growth, and development. - It does **not directly regulate** serum calcium levels. *Adrenaline* - **Adrenaline (epinephrine)** is a hormone released from the **adrenal glands** in response to stress. - It plays a role in the "fight or flight" response, affecting heart rate, blood pressure, and glucose metabolism, but **not calcium regulation**.
Question 4: A patient is on a low calcium diet for 8 weeks. Which of the following increases to maintain serum calcium levels?
- A. Active 24,25 dihydroxy cholecalciferol
- B. PTH (Correct Answer)
- C. Serum phosphate level
- D. Calcitonin
Explanation: ***PTH*** - **Parathyroid hormone (PTH)** is the primary regulator of calcium homeostasis and the key hormone that **increases in response to hypocalcemia** (low serum calcium). - In a patient on a low calcium diet for 8 weeks, **PTH secretion increases** to maintain normal serum calcium levels. - PTH acts through three main mechanisms: increasing **bone resorption** (releasing calcium from bone), enhancing renal **calcium reabsorption** in the distal tubule, and stimulating the production of **active vitamin D (1,25-dihydroxycholecalciferol)** which increases intestinal calcium absorption. *Active 24,25 dihydroxy cholecalciferol* - **24,25-dihydroxycholecalciferol** is a relatively **inactive metabolite** of vitamin D and represents a pathway of vitamin D catabolism, not activation. - The **active form** of vitamin D that increases calcium absorption is **1,25-dihydroxycholecalciferol (calcitriol)**, whose production is stimulated by PTH. - This metabolite does **not increase** in response to hypocalcemia as a compensatory mechanism. *Serum phosphate level* - A low calcium diet would **not directly lead to an increase in serum phosphate levels**. - In fact, PTH (which increases in response to low calcium) typically causes a **decrease in serum phosphate** by promoting renal phosphate excretion (phosphaturic effect). - High phosphate levels can actually exacerbate hypocalcemia by forming insoluble calcium-phosphate complexes. *Calcitonin* - **Calcitonin** is released from the thyroid parafollicular cells (C cells) in response to **high serum calcium levels** (hypercalcemia). - It acts to **lower** calcium by inhibiting osteoclast activity and reducing renal calcium reabsorption. - In hypocalcemia (low calcium diet), calcitonin secretion would **decrease, not increase**, making this the opposite of what occurs to maintain calcium homeostasis.
Question 5: All are symptoms of hypocalcemia except
- A. laryngospasm
- B. Trousseau sign
- C. Peaked p waves (Correct Answer)
- D. Chvostek sign
Explanation: ***Peaked p waves*** - **Peaked P waves** are associated with **right atrial enlargement** or **hyperkalemia**, not hypocalcemia [1]. - In hypocalcemia, the **QT interval** on an electrocardiogram is typically **prolonged**, not the P wave morphology altered this way. *laryngospasm* - **Laryngospasm** is a serious manifestation of **severe hypocalcemia** due to increased neuromuscular excitability. - It can lead to airway obstruction and is part of the tetany experienced in low calcium states. *Trousseau sign* - **Trousseau's sign** is a classic indicator of **latent tetany** in hypocalcemia, elicited by inflating a blood pressure cuff above systolic pressure for several minutes. - This maneuver induces **carpal spasm** (flexion of the wrist and metacarpophalangeal joints, extension of the interphalangeal joints, and adduction of the thumb). *Chvostek sign* - **Chvostek's sign** is another clinical sign of **hypocalcemia**, elicited by tapping on the facial nerve just anterior to the earlobe. - A positive sign results in **twitching of the ipsilateral facial muscles**, indicating increased neuromuscular irritability.
Question 6: A 23-year-old woman undergoes total thyroidectomy for carcinoma of the thyroid gland. On the second postoperative day, she begins to complain of a tingling sensation in her hands and appears anxious, later complaining of muscle cramps. Which of the following is the most appropriate initial management strategy?
- A. 10 mL of 10% magnesium sulfate intravenously
- B. Oral vitamin D
- C. 100 mg oral Synthroid
- D. Continuous infusion of calcium gluconate (Correct Answer)
Explanation: ***Continuous infusion of calcium gluconate*** - The patient's symptoms of **tingling sensation in hands**, **anxiety**, and **muscle cramps** after a total thyroidectomy are highly suggestive of **hypocalcemia**, likely due to iatrogenic hypoparathyroidism. - An initial bolus followed by a **continuous infusion of calcium gluconate** is the most appropriate management for symptomatic hypocalcemia to rapidly replete calcium levels and prevent further complications. *10 mL of 10% magnesium sulfate intravenously* - While **hypomagnesemia** can sometimes cause refractory hypocalcemia, it is not the primary electrolyte abnormality indicated by these specific symptoms following thyroidectomy. - Administering magnesium sulfate as the initial and sole treatment would fail to address the underlying **calcium deficiency** directly and might delay appropriate management. *Oral vitamin D* - **Oral vitamin D** is used for chronic management of hypocalcemia, as it helps improve calcium absorption. - However, it has a slow onset of action and is not suitable for the **acute and symptomatic hypocalcemia** that requires immediate intervention. *100 mg oral Synthroid* - **Synthroid (levothyroxine)** is thyroid hormone replacement therapy, indicated for hypothyroidism following thyroidectomy. - While necessary for long-term management, it does not address the **acute symptoms of hypocalcemia** and would be inappropriate as an initial treatment for this emergent condition.
Question 7: A 71-year-old man develops dysphagia for both solids and liquids and weight loss of 60 lb over the past 6 months. He undergoes endoscopy, demonstrating a distal esophageal lesion, and biopsies are consistent with squamous cell carcinoma. He is scheduled for neoadjuvant chemoradiation followed by an esophagectomy. Preoperatively he is started on total parenteral nutrition, given his severe malnutrition reflected by an albumin of less than 1. Which of the following is most likely to be a concern initially in starting total parenteral nutrition in this patient?
- A. Hypophosphatemia (Correct Answer)
- B. Hypoglycemia
- C. Hyperkalemia
- D. Hypermagnesemia
Explanation: ***Hypophosphatemia*** * This patient with severe malnutrition (albumin <1, 60lb weight loss) is at high risk for **refeeding syndrome** when TPN is initiated [1]. * Upon refeeding, **insulin release** causes intracellular shifts of electrolytes, particularly phosphate, leading to severe hypophosphatemia [1]. * *Hypoglycemia* * TPN contains dextrose, which typically causes **hyperglycemia**, not hypoglycemia, especially given its continuous infusion. * Hypoglycemia would be more likely if TPN was abruptly discontinued, causing a rapid drop in glucose levels as basal insulin continues to be secreted. * *Hyperkalemia* * Refeeding syndrome typically causes a rapid **intracellular shift of potassium**, leading to **hypokalemia**, not hyperkalemia [1]. * Hyperkalemia would be a concern in patients with renal insufficiency or those receiving potassium-sparing diuretics. * *Hypermagnesemia* * Similar to potassium and phosphate, refeeding syndrome usually causes an **intracellular shift of magnesium**, leading to **hypomagnesemia** [1]. * Hypermagnesemia is rare and typically seen in patients with severe renal failure or excessive exogenous magnesium intake (e.g., antacids).
Question 8: Which of the following is a feature of tumor lysis syndrome?
- A. Metabolic alkalosis (a rise in blood pH)
- B. Hypokalemia (a decrease in blood potassium levels)
- C. Hypocalcemia (a decrease in blood calcium levels) (Correct Answer)
- D. Hypophosphatemia (a decrease in blood phosphate levels)
Explanation: ***Hypocalcemia (a decrease in blood calcium levels)*** - **Hypocalcemia** in tumor lysis syndrome results from the precipitation of calcium with excessive phosphate released from lysed tumor cells. - The elevated phosphate levels bind to calcium, forming **calcium phosphate crystals** that can deposit in tissues, further lowering serum calcium. *Metabolic alkalosis (a rise in blood pH)* - Tumor lysis syndrome typically leads to **metabolic acidosis**, not alkalosis, due to the release of acidic intracellular metabolites like uric acid and phosphate. - The accumulation of these acidic compounds overwhelms the body's buffering systems, decreasing blood pH. *Hypokalemia (a decrease in blood potassium levels)* - Tumor lysis syndrome is characterized by **hyperkalemia**, an increase in blood potassium, as potassium is a major intracellular cation released during cell lysis. - The rapid breakdown of numerous tumor cells dumps vast amounts of intracellular potassium into the bloodstream. *Hypophosphatemia (a decrease in blood phosphate levels)* - Tumor lysis syndrome causes **hyperphosphatemia**, an elevation in blood phosphate levels, because phosphate is abundantly present within tumor cells and is released upon their destruction. - This excessive release of intracellular phosphate is a hallmark biochemical feature of the syndrome.
Question 9: Why is citrate phosphate dextrose (CPD) better than acid citrate dextrose (ACD) for storage of blood?
- A. Maintains pH stability during storage
- B. Contains phosphate and dextrose (Correct Answer)
- C. Prevents hemolysis in stored blood
- D. Reduces metabolic activity in stored blood
Explanation: ***Contains phosphate and dextrose*** - CPD contains **phosphate**, which acts as a buffer and helps maintain crucial 2,3-bisphosphoglycerate (2,3-BPG) levels in red blood cells, improving oxygen delivery capacity. - The presence of **dextrose** provides a substrate for glycolysis, which is essential for ATP production and red blood cell viability during storage. - This combination allows CPD to extend blood storage life to approximately **35 days** compared to ACD's **21 days**. *Maintains pH stability during storage* - Both ACD and CPD help maintain pH stability due to their **citrate** content, which acts as an anticoagulant and buffer. - However, CPD's phosphate component offers superior buffering capacity, but pH maintenance alone is not the primary distinguishing advantage. - This is a shared characteristic of both solutions, not the key reason CPD is preferred. *Prevents hemolysis in stored blood* - Both CPD and ACD prevent hemolysis by chelating **calcium**, which prevents coagulation and maintains red blood cell integrity. - While both solutions successfully prevent hemolysis, this is not the distinguishing feature that makes CPD superior. - The primary advantage of CPD lies in its better support of red blood cell metabolism and viability through phosphate and dextrose. *Reduces metabolic activity in stored blood* - This is **incorrect** - the purpose of anticoagulant solutions is to preserve blood components, not to reduce metabolic activity. - The dextrose in CPD is provided precisely to **fuel essential metabolic activity** (glycolysis) to sustain red blood cells during storage. - While refrigeration at 1-6°C slows metabolism, CPD actively supports rather than reduces the metabolic processes necessary for RBC survival.
Question 10: What is the initial treatment of choice for managing secondary hyperparathyroidism in patients with renal osteodystrophy?
- A. Cinacalcet
- B. Bisphosphonates
- C. Calcium restriction
- D. Phosphate binders (Correct Answer)
Explanation: ***Phosphate binders*** - **Phosphate binders** are the initial treatment because **hyperphosphatemia** is the primary driver of secondary hyperparathyroidism in renal disease, triggering parathyroid hormone (PTH) release [1]. - They work by binding dietary phosphate in the gastrointestinal tract, preventing its absorption and thus lowering serum phosphate levels [1]. *Cinacalcet* - **Cinacalcet** is a calcimimetic that increases the sensitivity of calcium-sensing receptors on the parathyroid gland, reducing **PTH secretion** [1]. - It is often used if **phosphate binders** and **vitamin D analogs** are insufficient in controlling PTH, making it a second-line treatment [1]. *Bisphosphonates* - **Bisphosphonates** are used to treat osteoporosis by inhibiting osteoclast activity and reducing bone resorption. - They are generally contraindicated in advanced renal osteodystrophy due to concerns about adynamic bone disease and are not an initial treatment for **secondary hyperparathyroidism**. *Calcium restriction* - While restricting dietary calcium might seem intuitive, **hypocalcemia** is often a problem in renal disease due to impaired vitamin D activation [1]. - Overly restricting calcium can worsen hypocalcemia, which would further stimulate PTH release, thus it is not an initial treatment for **secondary hyperparathyroidism**.
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