Calcium and Bone Metabolism — MCQs
Parathyroid hormone (PTH) exerts its effect on calcium metabolism by acting on receptors present on the–
Intestinal absorption of calcium is mainly increased by?
Parathormone has all of the following effects, except -
Bone mass is reduced in all of the following conditions EXCEPT:
All of the following are the causes for hypercalcemia Except?
The symptoms of hyperparathyroidism include:
What is the most likely diagnosis in an individual with normal serum alkaline phosphatase, normal PTH, normal Vitamin D3, and elevated serum calcium?
Primary Hyperparathyroidism is associated with -
A female is on hormone replacement therapy for her menopausal symptoms. She is worried about her bone strength because her mom and sister had osteoporosis after the age of 50. All are given for prevention of osteoporosis along with hormonal replacement therapy, EXCEPT:
Epiphyseal dysgenesis is a feature of
Calcium and Bone Metabolism Indian Medical PG Practice Questions and MCQs
Question 1: Parathyroid hormone (PTH) exerts its effect on calcium metabolism by acting on receptors present on the–
- A. Macrophages
- B. Osteoblasts (Correct Answer)
- C. Osteoclasts
- D. None of the options
Explanation: ***Osteoblasts*** - **PTH receptors (PTH1R)** are primarily expressed on **osteoblasts**, not osteoclasts or osteocytes. - PTH binds to receptors on **osteoblasts**, which then stimulate **osteoclast differentiation and activity** indirectly through the **RANKL/RANK pathway**. - This is the **primary mechanism** by which PTH increases bone resorption and raises serum calcium levels. - Osteoblasts also mediate PTH's anabolic effects on bone when given intermittently. *Macrophages* - **Macrophages** are immune cells involved in inflammatory responses and phagocytosis. - They are not the primary target cells for PTH in calcium metabolism. - While they may play a role in bone remodeling, they lack the specific **PTH1R receptors** that mediate calcium regulation. *Osteoclasts* - **Osteoclasts** are the cells that actually resorb bone and release calcium. - However, **osteoclasts do NOT have PTH receptors**. - PTH acts **indirectly** on osteoclasts by first binding to osteoblast receptors, which then produce RANKL to stimulate osteoclast activity. *None of the options* - This is incorrect because **osteoblasts** are indeed the primary cells bearing PTH receptors for calcium metabolism.
Question 2: Intestinal absorption of calcium is mainly increased by?
- A. Calcitriol (Correct Answer)
- B. Parathormone
- C. Glucocorticoids
- D. ACTH
Explanation: ***Calcitriol*** - **Calcitriol** (1,25-dihydroxyvitamin D3) is the hormonally active form of vitamin D, which is essential for increasing **calcium absorption** from the intestines. - It stimulates the synthesis of **calcium-binding proteins** in intestinal epithelial cells, facilitating active transport of calcium. *Parathormone* - **Parathormone (PTH)** primarily regulates calcium by increasing its reabsorption in the **kidneys** and stimulating its release from **bones**. - While it indirectly promotes calcitriol synthesis, its *direct* effect on intestinal calcium absorption is minimal compared to calcitriol. *Glucocorticoids* - **Glucocorticoids** generally have an *inhibitory* effect on calcium absorption in the intestine and can also increase renal excretion of calcium. - Prolonged use can lead to **osteoporosis** due to their negative impact on bone formation and calcium balance. *ACTH* - **ACTH (adrenocorticotropic hormone)** primarily stimulates the adrenal cortex to produce **cortisol** and other glucocorticoids. - It has **no direct role** in regulating calcium absorption from the intestines.
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: Bone mass is reduced in all of the following conditions EXCEPT:
- A. Osteoporosis
- B. Osteopetrosis (Correct Answer)
- C. Hyperparathyroidism
- D. Osteomalacia
Explanation: **Osteopetrosis** - **Osteopetrosis**, also known as **marble bone disease**, is a rare genetic disorder characterized by **increased bone density** due to defective osteoclast function. - In this condition, osteoclasts are unable to resorb bone, leading to an excessive accumulation of bone tissue, resulting in **densified but brittle bones**. *Osteoporosis* - **Osteoporosis** is characterized by significantly **reduced bone mass** and microarchitectural deterioration of bone tissue [1]. - This leads to increased bone fragility and a higher risk of fractures, as the bone becomes porous and weak [2]. *Hyperparathyroidism* - **Hyperparathyroidism** causes **increased bone resorption** due to excessive parathyroid hormone (PTH) secretion. - PTH mobilizes calcium from the bones, leading to a **decrease in bone density** and potential bone cysts (**osteitis fibrosa cystica**) [3]. *Osteomalacia* - **Osteomalacia** is a condition where there is **defective mineralization of bone osteoid**, leading to softer bones [4]. - While the bone mass might appear structurally normal, the **mineral content is reduced**, making the bone weak and susceptible to bowing and fractures. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, pp. 1189-1191. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 665-666. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, p. 1194. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Bones, Joints, and Soft Tissue Tumors, pp. 1194-1195.
Question 5: All of the following are the causes for hypercalcemia Except?
- A. Thiazides
- B. Hyperparathyroidism
- C. Acute pancreatitis (Correct Answer)
- D. Hypervitaminosis of Vitamin D
Explanation: ***Acute pancreatitis*** - **Acute pancreatitis** is most commonly associated with **hypocalcemia**, not hypercalcemia [1]. - The likely mechanism for hypocalcemia in pancreatitis is the **saponification of calcium in necrotic fat** by free fatty acids released from local lipase activity [1]. *Thiazides* - **Thiazide diuretics** can cause a mild increase in calcium levels by **increasing calcium reabsorption in the distal renal tubule** [2]. - This effect is generally not severe enough to cause symptomatic hypercalcemia unless other underlying conditions are present. *Hyperparathyroidism* - **Primary hyperparathyroidism** is a common cause of hypercalcemia, due to the **overproduction of parathyroid hormone (PTH)** [2]. - PTH increases serum calcium by increasing **bone resorption**, renal calcium reabsorption, and intestinal calcium absorption [2]. *Hypervitaminosis of Vitamin D* - Excessive intake or production of **Vitamin D** leads to hypercalcemia by increasing **intestinal absorption of calcium** [2]. - It also enhances **bone resorption**, contributing to elevated serum calcium levels.
Question 6: The symptoms of hyperparathyroidism include:
- A. Polydipsia & polyuria
- B. Anorexia & weight loss
- C. Constipation & muscle weakness
- D. All of the options (Correct Answer)
Explanation: ***All of the options*** - **Hyperparathyroidism** leads to elevated **calcium levels** (hypercalcemia), which can manifest in a wide range of symptoms affecting multiple organ systems [1]. - The classic mnemonic for hypercalcemia symptoms is "**stones, bones, groans, and psychiatric overtones**," encompassing renal, skeletal, gastrointestinal, and neurological issues [1][2]. *Polydipsia & polyuria* - **Hypercalcemia** impairs the kidneys' ability to concentrate urine, leading to **nephrogenic diabetes insipidus** and subsequent **polyuria** (excessive urination) [1]. - The increased fluid loss from polyuria then triggers **polydipsia** (excessive thirst) to maintain hydration [1]. *Anorexia & weight loss* - Elevated calcium levels can cause **gastrointestinal symptoms** such as **anorexia** (loss of appetite), nausea, and vomiting [1]. - Chronic anorexia and associated GI disturbances can contribute to **weight loss** in patients with hyperparathyroidism. *Constipation & muscle weakness* - **Hypercalcemia** reduces the smooth muscle activity of the gastrointestinal tract, leading to decreased peristalsis and **constipation** [1]. - High calcium levels can also interfere with nerve and muscle function, resulting in generalized **muscle weakness** and fatigue [1].
Question 7: What is the most likely diagnosis in an individual with normal serum alkaline phosphatase, normal PTH, normal Vitamin D3, and elevated serum calcium?
- A. Nutritional rickets
- B. Hyperparathyroidism
- C. Multiple myeloma (Correct Answer)
- D. Vitamin D intoxication
Explanation: ***Multiple myeloma*** [4] - This condition is often associated with **osteolytic lesions** that lead to the release of calcium into the blood, causing **hypercalcemia**. - **PTH**, **alkaline phosphatase**, and **Vitamin D3** levels are typically normal in this scenario because their regulatory pathways are not primarily affected [1]. *Nutritional rickets* [2] - Characterized by **low calcium** and **phosphate levels**, usually with **elevated alkaline phosphatase** and **PTH** due to inadequate vitamin D or calcium intake [3]. - This patient exhibits **elevated serum calcium**, ruling out rickets. *Hyperparathyroidism* - Both **primary** and **secondary hyperparathyroidism** would present with **elevated PTH** levels, which is stated as normal in the case description [1]. - **Hypercalcemia** in hyperparathyroidism is caused by bone resorption and increased renal reabsorption of calcium, driven by high PTH [5]. *Vitamin D intoxication* - Would lead to **hypercalcemia** and **elevated Vitamin D3** levels, alongside **suppressed PTH** levels, which contradicts the described normal PTH and normal Vitamin D3 [1]. - The excessive vitamin D would increase calcium absorption from the gut and bone resorption not seen here.
Question 8: Primary Hyperparathyroidism is associated with -
- A. Increased serum PTH and Hypercalcemia (Correct Answer)
- B. Decreased serum PTH and Hyporcalcemia
- C. Decreased serum PTH and Hypercalcemia
- D. Increased serum PTH and Hyporcalcemia
Explanation: ***Increased serum PTH and Hypercalcemia*** - **Primary hyperparathyroidism** results from an autonomous overproduction of **parathyroid hormone (PTH)**, usually by an adenoma or hyperplasia [1]. - This excess PTH leads to increased calcium reabsorption from bones and kidneys, causing **hypercalcemia** [2][4]. *Decreased serum PTH and Hyporcalcemia* - This combination is characteristic of **hypoparathyroidism**, where insufficient PTH production leads to low calcium levels [3]. - Primary hyperparathyroidism, by definition, involves *increased* PTH [4]. *Decreased serum PTH and Hypercalcemia* - This might be seen in cases of **non-PTH-mediated hypercalcemia**, such as malignancy, where high calcium levels suppress normal PTH secretion [4]. - However, in primary hyperparathyroidism, PTH would be **elevated** [1]. *Increased serum PTH and Hyporcalcemia* - This scenario typically points to **secondary hyperparathyroidism**, where the parathyroid glands are overactive in response to chronic low calcium levels (e.g., due to **chronic kidney disease** or **Vitamin D deficiency**) [1][3]. - In primary hyperparathyroidism, the elevated PTH directly *causes* hypercalcemia [4].
Question 9: A female is on hormone replacement therapy for her menopausal symptoms. She is worried about her bone strength because her mom and sister had osteoporosis after the age of 50. All are given for prevention of osteoporosis along with hormonal replacement therapy, EXCEPT:
- A. Calcium
- B. Vitamin-E (Correct Answer)
- C. Vit.D
- D. None of the options
Explanation: ***Vitamin-E*** - **Vitamin-E** is an **antioxidant** vitamin that primarily protects cells from oxidative damage. - It does not play a direct role in **bone metabolism** or the prevention of osteoporosis. *Calcium* - **Calcium** is a fundamental component of bone tissue and is essential for maintaining **bone density** [1]. - Adequate calcium intake is crucial for **osteoporosis prevention**, especially in postmenopausal women [1], [2]. *Vit.D* - **Vitamin D** is essential for **calcium absorption** in the gut and its incorporation into bones. - Without sufficient Vitamin D, calcium cannot be effectively utilized, leading to compromised **bone health**. *None of the options* - This option is incorrect because Vitamin E does not contribute to osteoporosis prevention, making it the correct answer to the "EXCEPT" question. - Calcium and Vitamin D are both vital for bone strength, so stating that none of the options fit would be inaccurate [1].
Question 10: Epiphyseal dysgenesis is a feature of
- A. Hypoparathyroidism
- B. Hyperparathyroidism
- C. Hypothyroidism (Correct Answer)
- D. Hyperthyroidism
Explanation: ***Hypothyroidism*** - **Epiphyseal dysgenesis** (dysplastic or stippled epiphyses) is a classic radiographic feature of **congenital hypothyroidism**, particularly in infants and children [2]. - Reduced thyroid hormone levels impair normal bone development, leading to delayed bone maturation and abnormal epiphyseal ossification [2]. *Hypoparathyroidism* - This condition involves insufficient **parathyroid hormone (PTH)**, leading to **hypocalcemia** and **hyperphosphatemia** [1]. - Its effects on bone primarily involve increased bone density and sometimes basal ganglia calcification, not epiphyseal dysgenesis [1]. *Hyperparathyroidism* - Characterized by excessive **PTH**, which causes **hypercalcemia** and bone resorption. - Bone features include **osteitis fibrosa cystica** (brown tumors, subperiosteal resorption), which is distinct from epiphyseal dysgenesis. *Hyperthyroidism* - This condition is marked by excessive thyroid hormone, which can lead to **accelerated bone turnover** and increased risk of osteoporosis. - Unlike hypothyroidism, it does not cause epiphyseal dysgenesis; instead, it can lead to premature skeletal maturation.
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