Calcium and Phosphate Metabolism — MCQs
Which hormone is released when serum calcium levels decrease?
Tetany is seen in
The most important regulator of serum 1,25(OH)2 vitamin D concentration is:
Secondary hyperparathyroidism due to Vit D deficiency shows :
All of the following statements are true except:
Proper evaluation of serum calcium level requires estimation of:
Site of 25-hydroxylation of cholecalciferol
Hypocalcemia is characterized by all except
True about Parathyroid hormone:
Which of the following causes hypocalcemia:
Calcium and Phosphate Metabolism Indian Medical PG Practice Questions and MCQs
Question 1: 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 2: Tetany is seen in
- A. Respiratory alkalosis (Correct Answer)
- B. Respiratory acidosis
- C. Metabolic acidosis
- D. Hyperkalemia
Explanation: ***Respiratory alkalosis*** - **Respiratory alkalosis** is caused by **hyperventilation**, which leads to a decrease in arterial partial pressure of carbon dioxide (**PaCO2**). - This decrease in PaCO2 causes an increase in pH (alkalemia) and a shift in the albumin-bound calcium equilibrium, reducing the amount of **ionized calcium** in the blood, leading to symptoms of **hypocalcemia** such as tetany. *Respiratory acidosis* - **Respiratory acidosis** is characterized by an increase in PaCO2 and a decrease in pH due to inadequate ventilation, which would not typically cause tetany. - In fact, the acidosis would tend to increase **ionized calcium** levels, thereby counteracting any tendency towards symptoms of hypocalcemia. *Metabolic acidosis* - **Metabolic acidosis** involves a decrease in bicarbonate concentration and pH, often due to conditions like diabetic ketoacidosis or lactic acidosis. - Similar to respiratory acidosis, the acidic environment of **metabolic acidosis** tends to increase **ionized calcium** levels, making tetany unlikely. *Hyperkalemia* - **Hyperkalemia** refers to elevated potassium levels in the blood, which primarily affects cardiac and neuromuscular function. - While it can cause muscle weakness and cardiac arrhythmias, it does not directly lead to **tetany**, which is a sign of **hypocalcemia**.
Question 3: The most important regulator of serum 1,25(OH)2 vitamin D concentration is:
- A. Calcium levels in serum
- B. Magnesium levels in serum
- C. Parathyroid hormone (Correct Answer)
- D. 25-hydroxyvitamin D in serum
Explanation: ***Parathyroid hormone*** - **Parathyroid hormone (PTH)** directly stimulates the **kidney's 1-alpha hydroxylase** enzyme, which converts **25(OH)D** to its active form, **1,25(OH)2D (calcitriol)**. - This regulation is critical for maintaining **calcium and phosphate homeostasis**, with PTH levels increasing when serum calcium is low, thereby boosting 1,25(OH)2D production. *Calcium levels in serum* - While **low serum calcium** indirectly stimulates **PTH** release, which then regulates 1,25(OH)2 vitamin D, calcium itself is not the direct or most important regulator. - The direct regulatory action on the conversion enzyme is mediated by PTH. *Magnesium levels in serum* - **Magnesium** plays a cofactor role in various enzymatic reactions, including those involving vitamin D metabolism, but it is not a direct or primary regulator of **1,25(OH)2 vitamin D concentration**. - Severe **hypomagnesemia** can sometimes impair PTH secretion and action, indirectly affecting vitamin D, but this is a secondary effect. *25-hydroxyvitamin D in serum* - **25-hydroxyvitamin D** is the precursor to **1,25(OH)2 vitamin D**, and its availability limits the maximum potential production of the active form. - However, the *rate* of conversion into the active form and thus the *concentration* of 1,25(OH)2D is primarily dictated by PTH, not the precursor itself.
Question 4: Secondary hyperparathyroidism due to Vit D deficiency shows :
- A. Hypocalcemia (Correct Answer)
- B. Hypophosphatemia
- C. Hypercalcemia
- D. Hyperphosphatemia
Explanation: ***Hypocalcemia*** - **Vitamin D deficiency** leads to decreased intestinal absorption of calcium, causing **hypocalcemia** [3]. - This persistent **low serum calcium** is the primary stimulus for the parathyroid glands to increase PTH secretion, leading to secondary hyperparathyroidism [1], [2]. *Hypophosphatemia* - While PTH typically promotes phosphate excretion in the kidneys leading to hypophosphatemia, in **secondary hyperparathyroidism due to vitamin D deficiency**, the effect on phosphate can be variable [3]. - The goal of increased PTH is to raise calcium, and maintaining some level of phosphate is necessary for bone health and proper calcium regulation. Early or mild deficiency may not show significant hypophosphatemia. *Hypercalcemia* - **Hypercalcemia** is a characteristic feature of **primary hyperparathyroidism**, where the parathyroid glands autonomously overproduce PTH [1]. - In secondary hyperparathyroidism (due to vitamin D deficiency), the PTH is elevated in response to **low calcium**, and sustained significant hypercalcemia is not expected; in fact, the underlying problem is **hypocalcemia** [1]. *Hyperphosphatemia* - **PTH** generally acts to lower serum phosphate levels by promoting its renal excretion [2]. - Therefore, **hyperphosphatemia** is not typically observed in secondary hyperparathyroidism; rather, a more common finding would be normal or low phosphate due to the elevated PTH [3].
Question 5: All of the following statements are true except:
- A. 25–α hydroxylation takes place in liver
- B. 1–α hydroxylation takes place in kidney
- C. Daily requirement in the absence of sun–light is 450-600 IU/day
- D. 25(OH)D3 is the most active form of vitamin D (Correct Answer)
Explanation: ***25(OH)D3 is the most active form of vitamin D*** - This statement is incorrect. While **25(OH)D3 (calcifediol)** is the major circulating form of vitamin D, it is not the most active form. - The most active form of vitamin D is **1,25(OH)2D3 (calcitriol)**, which is formed by the 1-alpha hydroxylation of calcifediol in the kidneys. *25–α hydroxylation takes place in liver* - This statement is true. The initial hydroxylation of **vitamin D3 (cholecalciferol)** at the 25-position occurs in the liver, forming 25(OH)D3 (calcifediol). - This step is catalyzed by the enzyme **25-hydroxylase**. *1–α hydroxylation takes place in kidney* - This statement is true. The 25(OH)D3 produced in the liver is then transported to the kidneys, where it undergoes a second hydroxylation at the 1-alpha position. - This step, catalyzed by **1-alpha-hydroxylase**, forms the biologically active hormone 1,25(OH)2D3 (calcitriol). *Daily requirement in the absence of sun–light is 450-600 IU/day* - This statement is generally true. The recommended daily allowance (RDA) for vitamin D in adults, especially in the absence of sufficient sun exposure, typically ranges from **400 to 800 IU (international units)**, with 600 IU/day being a common guideline. - This requirement can vary based on age, geographical location, and other individual factors.
Question 6: Proper evaluation of serum calcium level requires estimation of:
- A. Urinary output
- B. Serum albumin (Correct Answer)
- C. Serum phosphorus
- D. Serum potassium
Explanation: ***Serum albumin*** - Approximately **40-45% of total serum calcium** is bound to plasma proteins, primarily **albumin** - Changes in albumin levels (e.g., hypoalbuminemia) significantly affect total calcium measurements - A **correction formula** is essential: Corrected Ca = Measured Ca + 0.8 × (4.0 - measured albumin in g/dL) - This allows accurate estimation of the physiologically active **ionized calcium** level - Without albumin correction, hypocalcemia may be falsely diagnosed in hypoalbuminemic states *Incorrect: Urinary output* - While urinary calcium excretion is important for assessing calcium balance, urinary output itself is not directly used to evaluate serum calcium levels - It reflects renal function and fluid status, not calcium-protein binding *Incorrect: Serum phosphorus* - Serum phosphorus is important in calcium-phosphate homeostasis, particularly in kidney disease or parathyroid disorders - However, phosphorus levels do not directly influence calcium binding to albumin - Not required for correcting total serum calcium measurements *Incorrect: Serum potassium* - Serum potassium is a critical electrolyte but does not impact the interpretation or correction of serum calcium measurements - Potassium plays a role in nerve and muscle function, distinct from calcium homeostasis and protein binding
Question 7: Site of 25-hydroxylation of cholecalciferol
- A. Liver (Correct Answer)
- B. Bone
- C. Pancreas
- D. Heart
Explanation: ***Liver*** - The **liver** is the site of **25-hydroxylation** of cholecalciferol (Vitamin D3) to form **25-hydroxycholecalciferol (calcidiol)**. - This reaction is catalyzed by **25-hydroxylase (CYP2R1)** in hepatocytes. - This is the **first step** in vitamin D activation; subsequent 1α-hydroxylation occurs in the **kidney** to form the active **calcitriol**. *Bone* - Bone is a **target organ** for active vitamin D (calcitriol) action, not a site of hydroxylation. - It responds to calcitriol for calcium homeostasis and bone remodeling. *Pancreas* - The pancreas has no role in vitamin D metabolism. - Its primary functions are digestive enzyme secretion and endocrine regulation (insulin, glucagon). *Heart* - The heart does not perform vitamin D hydroxylation. - While vitamin D receptors exist in cardiac tissue, the organ does not metabolize vitamin D.
Question 8: Hypocalcemia is characterized by all except
- A. Carpopedal spasm
- B. Hyperactive tendon reflexes
- C. Numbness and tingling of circumoral region
- D. Shortening of Q-T interval in ECG (Correct Answer)
Explanation: ***Shortening of Q-T interval in ECG*** - Hypocalcemia typically causes **prolongation of the QT interval** on an ECG due to delayed repolarization of ventricular myocardial cells. - A **shortened QT interval** is usually associated with hypercalcemia or conditions like short QT syndrome. *Carpopedal spasm* - This is a classic sign of hypocalcemia, known as **Trousseau's sign**, elicited by inflating a blood pressure cuff above systolic pressure, which causes spasm of the hand and foot. - It results from increased neuromuscular irritability due to lower calcium levels. *Hyperactive tendon reflexes* - Hypocalcemia leads to **increased neuromuscular excitability**, which manifests as hyperactive or brisk deep tendon reflexes. - This heightened reflex activity is a common neurological symptom of low calcium. *Numbness and tingling of circumoral region* - This symptom, known as **paresthesia**, is a very common and early manifestation of hypocalcemia. - It occurs due to the increased excitability of peripheral nerves caused by reduced extracellular calcium.
Question 9: True about Parathyroid hormone:
- A. Inhibits Ca2+ absorption from the intestines
- B. It is steroidal in nature
- C. Stimulates 1,25-D3 formation (Correct Answer)
- D. All of the options
Explanation: ***Stimulate 1, 25 D3 formation*** - Parathyroid hormone (PTH) stimulates the kidneys to convert **25-hydroxyvitamin D** to its active form, **1,25-dihydroxyvitamin D (calcitriol)**. - **Calcitriol** is essential for increasing calcium absorption from the intestines. *Inhibits Ca2+ absorption from the intestines* - This statement is **incorrect**; PTH directly and indirectly (via calcitriol) promotes **calcium absorption** from the intestines. - **PTH's primary role** is to *increase* plasma calcium levels, which includes enhancing intestinal absorption. *It is steroidal in nature* - This statement is **incorrect**; Parathyroid hormone is a **peptide hormone**, not a steroidal hormone. - Steroidal hormones are derived from **cholesterol** (e.g., cortisol, estrogen), while peptide hormones are chains of amino acids. *All of the options* - This option is incorrect because the other two statements regarding PTH's action are demonstrably **false**.
Question 10: Which of the following causes hypocalcemia:
- A. 1, 25-dihydroxycholecalciferol
- B. Parathormone
- C. Thyroid hormones
- D. Calcitonin (Correct Answer)
Explanation: ***Calcitonin*** - **Calcitonin** is a hormone secreted by the **parafollicular cells (C cells)** of the thyroid gland. - It **lowers serum calcium levels** by **inhibiting osteoclast activity** (preventing bone resorption) and **increasing renal calcium excretion**. - This is the only hormone among the options that causes hypocalcemia. *1,25-dihydroxycholecalciferol* - This is the **active form of vitamin D** (calcitriol), which **increases serum calcium levels**. - It promotes intestinal calcium absorption, enhances bone resorption, and increases renal calcium reabsorption. - Deficiency of this hormone leads to hypocalcemia, but the hormone itself raises calcium. *Parathormone* - **Parathyroid hormone (PTH)** is the primary regulator that **increases serum calcium levels**. - It stimulates **osteoclast activity** (releasing calcium from bone), increases renal calcium reabsorption, and promotes synthesis of 1,25-dihydroxycholecalciferol. - PTH acts opposite to calcitonin in calcium homeostasis. *Thyroid hormones* - **Thyroxine (T4) and triiodothyronine (T3)** primarily regulate metabolism and have **no direct role in calcium homeostasis**. - While severe thyroid dysfunction can indirectly affect bone turnover, thyroid hormones do not directly cause hypocalcemia.
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