Calcium and Phosphate Regulation — MCQs
In hypoparathyroidism:
The function of which of the following is increased by an elevated parathyroid hormone concentration:
Parathormone has all of the following effects, except -
Which of the following organs are involved in the synthesis and activation of vitamin D?
Which of the following causes hypocalcemia:
A young patient presents with muscle spasms, numbness in the hands and feet, seizures, and difficulty in breathing due to laryngospasm. His blood work reveals an electrolyte imbalance. What is the most likely cause of these manifestations?
Tetany in muscle occurs in spite of normal serum Ca2+ level. Which ion is responsible?
Why is carpopedal spasm seen in hyperventilation?
Which of the following substances is NOT typically found in gallstones?
Which of the following is a common consequence of gastrectomy?
Calcium and Phosphate Regulation 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: The function of which of the following is increased by an elevated parathyroid hormone concentration:
- A. Action of osteoblasts only
- B. Osteoclasts (Correct Answer)
- C. Phosphate reabsorptive pathways in the renal tubules
- D. Hepatic formation of 25-hydroxycholecalciferol
Explanation: ***Osteoclasts*** - **Parathyroid hormone (PTH)** primarily acts to increase serum calcium levels by stimulating **osteoclasts**, leading to bone resorption and release of calcium and phosphate into the bloodstream. - While PTH does not directly act on osteoclasts, it binds to receptors on osteoblasts, which then release factors that activate osteoclasts. *Action of osteoblasts only* - PTH indirectly affects **osteoblasts** by binding to their receptors, but this action primarily leads to **RANKL expression**, which then stimulates osteoclast activity, not a direct increase in osteoblastic bone formation. - Chronic elevation of PTH, as seen in primary hyperparathyroidism, can paradoxically lead to a net loss of bone mass due to increased osteoclastic activity. *Phosphate reabsorptive pathways in the renal tubules* - PTH actually **decreases reabsorption of phosphate** in the renal tubules, leading to phosphaturia. This helps to prevent calcium-phosphate precipitation by lowering serum phosphate levels while raising calcium. - This is a key mechanism by which PTH increases serum calcium—by both mobilizing it from bone and reducing its renal excretion, while simultaneously promoting renal phosphate excretion. *Hepatic formation of 25-hydroxycholecalciferol* - The **liver** is responsible for the hydroxylation of vitamin D3 (cholecalciferol) to **25-hydroxycholecalciferol (calcidiol)**, a process that is not directly regulated by PTH. - PTH primarily stimulates the **kidneys** to convert 25-hydroxycholecalciferol to its active form, **1,25-dihydroxyvitamin D (calcitriol)**, which then enhances intestinal calcium absorption.
Question 3: Parathormone has all of the following effects, except -
- A. Increased calcitriol synthesis
- B. Increased phosphate reabsorption in kidney (Correct Answer)
- C. Increased Ca+2 reabsorption in kidney
- D. Increased bone resorption
Explanation: ***Increased phosphate reabsorption in kidney*** - Parathormone (**PTH**) primarily functions to increase serum **calcium** levels. - One of its key actions is to promote **phosphate excretion** by decreasing phosphate reabsorption in the renal tubules, not increasing it. *Increased calcitriol synthesis* - **PTH** stimulates the renal 1-alpha-hydroxylase enzyme, which is crucial for converting 25-hydroxyvitamin D to its active form, **1,25-dihydroxyvitamin D (calcitriol)**. - This active form of **vitamin D** then enhances intestinal calcium absorption. *Increased Ca+2 reabsorption in kidney* - **PTH** directly acts on the renal tubules, particularly the distal tubule and collecting duct, to increase the **reabsorption of calcium**. - This prevents calcium loss from the body and contributes to raising serum calcium levels. *Increased bone resorption* - **PTH** stimulates osteoclasts, leading to the breakdown of bone and the release of **calcium** and phosphate into the bloodstream. - This process, known as **bone resorption**, is a significant mechanism by which PTH increases serum calcium.
Question 4: Which of the following organs are involved in the synthesis and activation of vitamin D?
- A. Liver and Skin
- B. Skin and Kidney
- C. Kidney and Liver
- D. All of the options (Correct Answer)
Explanation: ***All of the options*** - The **skin** synthesizes an inactive form of vitamin D (**cholecalciferol**) upon exposure to **UVB radiation**. - The **liver** performs the first hydroxylation step, converting **cholecalciferol** (vitamin D3) into **25-hydroxyvitamin D** (calcidiol). The **kidneys** then perform the final hydroxylation, converting **calcidiol** into the active form, **1,25-dihydroxyvitamin D** (calcitriol). *Liver and Skin* - While both the **liver** and **skin** play crucial roles in vitamin D metabolism, they do not encompass all necessary organs. - The **kidneys** are essential for the final activation step of vitamin D. *Skin and Kidney* - The **skin** synthesizes the precursor, and the **kidneys** perform the final activation step. - However, the **liver** is required for the initial hydroxylation of vitamin D. *Kidney and Liver* - The **kidney** is responsible for the final activation, and the **liver** for the initial hydroxylation. - This option misses the crucial role of the **skin** in the initial synthesis of vitamin D upon sun exposure.
Question 5: 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.
Question 6: A young patient presents with muscle spasms, numbness in the hands and feet, seizures, and difficulty in breathing due to laryngospasm. His blood work reveals an electrolyte imbalance. What is the most likely cause of these manifestations?
- A. Respiratory Alkalosis (Correct Answer)
- B. Metabolic Alkalosis
- C. Respiratory Acidosis
- D. Metabolic Acidosis
Explanation: ***Respiratory Alkalosis*** - **Hyperventilation** (the likely underlying cause) leads to decreased partial pressure of carbon dioxide (**PCO2**), causing an increase in pH and **respiratory alkalosis**. - This **alkalosis** decreases **ionized calcium** levels by increasing calcium binding to albumin, leading to **hypocalcemia**. - **Hypocalcemia** causes increased neuromuscular excitability, resulting in **muscle spasms, numbness** (paresthesias), **seizures**, and **laryngospasm** (difficulty breathing). - This is the classic presentation of **hypocalcemic tetany** secondary to respiratory alkalosis. *Metabolic Alkalosis* - This imbalance is primarily characterized by an increase in **bicarbonate (HCO3-)** concentration, often due to **vomiting** or diuretic use. - While it can also cause alkalosis leading to **hypocalcemia** and similar neurological symptoms, the acute and severe presentation with prominent tetany and laryngospasm is more characteristic of **respiratory alkalosis**. - Metabolic alkalosis typically has a more gradual onset. *Respiratory Acidosis* - Caused by **hypoventilation**, leading to an increase in **PCO2** and a decrease in pH (acidosis). - **Acidosis increases ionized calcium**, so this would not cause hypocalcemic symptoms. - This condition typically manifests as **somnolence, confusion**, or CNS depression, not the neuromuscular excitability seen in this patient. *Metabolic Acidosis* - Characterized by a decrease in **bicarbonate (HCO3-)** and a decrease in pH, often due to conditions like **diabetic ketoacidosis** or **renal failure**. - **Acidosis increases ionized calcium**, making hypocalcemic tetany unlikely. - Symptoms usually include **Kussmaul breathing** (compensatory hyperventilation) and potential cardiac arrhythmias, which do not match this patient's presentation of tetany and laryngospasm.
Question 7: Tetany in muscle occurs in spite of normal serum Ca2+ level. Which ion is responsible?
- A. Mg2+
- B. K+
- C. Na+
- D. Ionized Ca2+ (Correct Answer)
Explanation: ***Ionized Ca2+*** - While total serum calcium might be normal, **tetany** is specifically caused by a decrease in the concentration of **ionized (free) calcium** in the extracellular fluid. - Ionized calcium is the physiologically active form of calcium responsible for neuromuscular excitability. *Mg2+* - **Hypomagnesemia** can exacerbate hypocalcemia and contribute to tetany, but it is not the primary ion directly responsible for tetany when **total serum calcium is normal**. - A deficiency in Mg2+ can impair the release of **parathyroid hormone** and reduce target organ responsiveness to PTH. *K+* - Abnormalities in **potassium levels** (hypokalemia or hyperkalemia) primarily affect cardiac and muscular excitability, leading to arrhythmias or muscle weakness/paralysis. - While electrolyte imbalances are interconnected, changes in potassium are not the direct cause of tetany due to calcium's role. *Na+* - **Sodium ions** are crucial for nerve impulse transmission and muscle contraction by establishing the resting membrane potential and initiating action potentials. - However, direct changes in sodium concentration do not typically cause tetany; rather, they can lead to neurological symptoms like seizures (hyponatremia) or altered mental status (hypernatremia).
Question 8: Why is carpopedal spasm seen in hyperventilation?
- A. Increased excretion of calcium in urine
- B. Increased plasma protein binding of Ca (Correct Answer)
- C. Increased sequestration of Ca in SER
- D. Ca utilized in bones
Explanation: ***Increased plasma protein binding of Ca*** - **Hyperventilation** leads to respiratory alkalosis due to excessive CO2 exhalation, increasing blood pH. - This elevated pH enhances the binding of **calcium to albumin**, decreasing the amount of free ionized calcium available. *Increased excretion of calcium in urine* - **Hyperventilation** itself does not directly lead to increased urinary calcium excretion; rather, it primarily affects the **distribution of calcium** within the bloodstream. - While prolonged alkalosis can affect renal handling of electrolytes, the immediate cause of carpopedal spasm is not urinary loss. *Increased sequestration of Ca in SER* - **Calcium sequestration** in the sarcoplasmic/endoplasmic reticulum (SER) is a process related to intracellular calcium handling and muscle contraction. - It is not the primary mechanism by which **hyperventilation-induced alkalosis** causes **hypocalcemia** and carpopedal spasm. *Ca utilized in bones* - Calcium is continuously exchanged between bone and the extracellular fluid, but **hyperventilation** does not immediately or significantly increase **bone utilization of calcium** to cause acute carpopedal spasm. - Bone serves as a reservoir, but the rapid onset of spasm points to changes in **circulating ionized calcium**.
Question 9: Which of the following substances is NOT typically found in gallstones?
- A. Cholesterol
- B. Oxalates (Correct Answer)
- C. Phosphate
- D. Carbonate
Explanation: ***Oxalates*** - Gallstones are primarily composed of **cholesterol**, **bile pigments**, and **calcium salts**, but they do not contain oxalates [1][2][3]. - Oxalates are more commonly associated with **kidney stones**, making this correct. *Carbonate* - Gallstones can contain **calcium carbonate**, particularly in certain types of stones, indicating that this option is incorrect. - These stones are formed in the **gallbladder**, often due to altered bile composition [2]. *Phosphate* - Some gallstones can contain **calcium phosphate**, especially in cases of infection or liver disease, which makes this option unsuitable. - Phosphate can contribute to the formation of **mixed stones** in the gallbladder. *Cholesterol* - In fact, the most common type of gallstone is the **cholesterol stone**, indicating that this option is incorrect [1][3]. - Cholesterol stones form when there is excessive **cholesterol** in the bile, leading to crystallization [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 882-883. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 403-404. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, p. 882.
Question 10: Which of the following is a common consequence of gastrectomy?
- A. Calcium deficiency
- B. Iron deficiency (Correct Answer)
- C. Steatorrhoea
- D. Fluid loss
Explanation: ***Iron deficiency*** - Gastrectomy often leads to **achlorhydria** or hypochlorhydria, reducing the conversion of **ferric iron** (Fe3+) to its more absorbable ferrous form (Fe2+). - Additionally, bypassing the duodenum, a primary site of iron absorption, further contributes to **iron malabsorption**. *Calcium deficiency* - While gastrectomy can contribute to calcium malabsorption due to reduced gastric acidity and faster transit, **iron deficiency** is typically a more direct and common initial consequence. - **Vitamin D deficiency**, often co-occurring with gastrectomy, is a more direct cause of **calcium malabsorption**. *Steatorrhoea* - **Steatorrhoea** (fat malabsorption) is more commonly associated with conditions affecting the **pancreas** or **small intestine** (e.g., celiac disease, chronic pancreatitis) rather than primarily gastrectomy unless there is significant bile salt malabsorption or rapid gastric emptying affecting nutrient mixing. - Although rapid transit post-gastrectomy can sometimes impair fat digestion, it's not the most common direct consequence compared to iron deficiency. *Fluid loss* - **Fluid loss** is usually an acute post-surgical complication or related to conditions causing vomiting or diarrhea, and not a common long-term consequence of gastrectomy itself. - While **dumping syndrome** can occur after gastrectomy, causing osmotic fluid shifts into the intestine, generalized chronic fluid loss is not a primary recognized long-term sequela.
Want unlimited practice?
Get full access to all questions, explanations, and performance tracking.
Start For Free