Parathyroid Gland Disorders — MCQs
Parathyroid hormone (PTH) exerts its effect on calcium metabolism by acting on receptors present on the–
Hypophosphatemia is caused by-
Which of the following is not seen in MEN 2B syndrome?
The most common cause of severe hypercalcemia is
Hypophosphatemia 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 :
A 45-year-old woman complains of tingling in her hands and feet, 24 hours after removal of follicular thyroid carcinoma. Her symptoms rapidly progress to severe muscle cramps, laryngeal stridor, and convulsions. Which of the following laboratory findings would be expected in this patient prior to treatment?
Which of the following is used in the treatment of well-differentiated thyroid carcinoma?
A 55-year-old male patient presents to the clinic with left lower lip weakness following a recent parotid gland surgery. Considering the surgical history and current symptoms, what is the most likely site of the lesion causing this patient's condition?
Parathyroid Gland Disorders 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: Hypophosphatemia is caused by-
- A. Primary hyperthyroidism
- B. Primary hypothyroidism
- C. Hypoparathyroidism
- D. Primary hyperparathyroidism (Correct Answer)
Explanation: ***Primary hyperparathyroidism*** - In **primary hyperparathyroidism**, excessive parathyroid hormone (PTH) leads to increased **renal phosphate excretion** and inhibition of its reabsorption, resulting in hypophosphatemia [1][2]. - PTH's primary role is to raise **serum calcium**, but it indirectly lowers phosphate by acting on the kidneys and bones [3]. *Primary hyperthyroidism* - **Hyperthyroidism** typically causes an increase in **bone turnover**, but does not directly lead to **hypophosphatemia** as a primary feature. - While high thyroid hormone levels can affect calcium and phosphate metabolism, it's more commonly associated with hypercalcemia rather than hypophosphatemia. *Primary hypothyroidism* - **Hypothyroidism** can lead to altered bone metabolism, but it does not directly cause **hypophosphatemia**. - Renal phosphate handling is generally not significantly impaired in a way that would lead to low serum phosphate levels. *Hypoparathyroidism* - **Hypoparathyroidism** is characterized by deficient PTH production, which leads to **decreased renal phosphate excretion**, resulting in **hyperphosphatemia**, not hypophosphatemia [4]. - The lack of PTH also causes hypocalcemia due to reduced bone resorption and impaired renal calcium reabsorption.
Question 3: Which of the following is not seen in MEN 2B syndrome?
- A. Mucosal neuroma
- B. Marfanoid habitus
- C. Parathyroid adenoma (Correct Answer)
- D. Megacolon
Explanation: ***Parathyroid adenoma*** - **Parathyroid adenomas**, leading to hyperparathyroidism, are characteristic of **MEN 2A syndrome**, not MEN 2B [1]. - While both MEN 2A and 2B involve mutations in the **RET proto-oncogene**, the specific clinical manifestations differ significantly. *Megacolon* - **Megacolon** (due to intestinal ganglioneuromatosis) is a recognized feature of **MEN 2B syndrome**. - This condition involves abnormal nerve ganglion cells in the intestine, leading to motility issues. *Mucosal neuroma* - **Mucosal neuromas** on the tongue, lips, and eyelids are a hallmark clinical sign of **MEN 2B syndrome**. - These benign growths are often one of the earliest and most recognizable features. *Marfanoid habitus* - **Marfanoid habitus**, characterized by a tall, slender build with long limbs and arachnodactyly, is a common physical finding in **MEN 2B syndrome**. - This connective tissue abnormality helps distinguish MEN 2B from other MEN syndromes.
Question 4: The most common cause of severe hypercalcemia is
- A. Malignancy (Correct Answer)
- B. Vitamin D toxicity
- C. Sarcoidosis
- D. Chronic renal failure
Explanation: ***Malignancy*** - **Malignancy** is the most frequent cause of **severe hypercalcemia**, often resulting from **parathyroid hormone-related peptide (PTHrP) secretion** (humoral hypercalcemia of malignancy) or **bone metastases** causing osteolysis [1]. - Cancers like **squamous cell carcinoma**, **breast cancer**, **multiple myeloma**, and **renal cell carcinoma** are commonly associated with severe hypercalcemia [1]. *Vitamin D toxicity* - While vitamin D toxicity can cause hypercalcemia, it typically leads to **moderate hypercalcemia** and is less common as a cause of **severe hypercalcemia** compared to malignancy [1]. - It usually occurs due to **excessive intake of vitamin D supplements** or activated vitamin D [1]. *Sarcoidosis* - Sarcoidosis can cause hypercalcemia due to **extrarenal production of 1,25-dihydroxyvitamin D** by activated macrophages [1]. - However, the hypercalcemia in sarcoidosis is usually **mild to moderate** and rarely reaches the severity seen with malignancy [1]. *Chronic renal failure* - **Chronic renal failure** is more commonly associated with **hypocalcemia** due to impaired vitamin D activation and hyperparathyroidism [2], [3]. - While some patients with end-stage renal disease and **adynamic bone disease** or **tertiary hyperparathyroidism** can develop hypercalcemia, it is not the most common cause of *severe* hypercalcemia in the general population.
Question 5: Hypophosphatemia is seen in:
- A. Hyperthyroidism
- B. Hypoparathyroidism
- C. Hyperparathyroidism (Correct Answer)
- D. Pseudohypoparathyroidism
Explanation: ***Hyperparathyroidism*** - In **primary hyperparathyroidism**, the excess **parathyroid hormone (PTH)** leads to increased phosphate excretion by the kidneys [1], [4]. - This results in **hypophosphatemia** as the body attempts to maintain **calcium-phosphate balance**, often at the expense of phosphate levels [1]. *Hyperthyroidism* - While hyperthyroidism can affect **bone metabolism**, it is typically associated with **normal or slightly elevated phosphate levels**, not hypophosphatemia [3]. - The main electrolyte disturbances are usually related to **calcium** (e.g., hypercalcemia) due to increased bone turnover [3]. *Hypoparathyroidism* - **Hypoparathyroidism** is characterized by **low or absent PTH**, leading to decreased renal phosphate excretion. - This results in **hyperphosphatemia**, along with **hypocalcemia** [2]. *Pseudohypoparathyroidism* - In **pseudohypoparathyroidism**, there is **PTH resistance** at target tissues, even with high or normal PTH levels [2]. - This leads to symptoms resembling hypoparathyroidism, including **hyperphosphatemia** and **hypocalcemia** [2].
Question 6: 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 7: 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 8: A 45-year-old woman complains of tingling in her hands and feet, 24 hours after removal of follicular thyroid carcinoma. Her symptoms rapidly progress to severe muscle cramps, laryngeal stridor, and convulsions. Which of the following laboratory findings would be expected in this patient prior to treatment?
- A. Decreased serum calcium and decreased PTH (Correct Answer)
- B. Decreased serum calcium and increased PTH
- C. Increased serum calcium and decreased PTH
- D. Increased serum calcium and increased PTH
Explanation: ***Decreased serum calcium and decreased PTH*** - The symptoms of **tingling**, **muscle cramps**, **laryngeal stridor**, and **convulsions** are classic signs of **hypocalcemia**. [1] - Following thyroidectomy, **parathyroid glands** can be inadvertently removed or damaged, leading to **hypoparathyroidism**, which results in decreased parathyroid hormone (PTH) levels and subsequent hypocalcemia. [1] *Decreased serum calcium and increased PTH* - This pattern is characteristic of **secondary hyperparathyroidism**, where low calcium levels stimulate increased PTH production. [1] - However, in this case, the hypocalcemia is a direct result of parathyroid damage during surgery, leading to *decreased* PTH. *Increased serum calcium and decreased PTH* - This pattern is characteristic of **primary hyperparathyroidism**, where an adenoma or hyperplasia of the parathyroid glands causes excessive PTH production, leading to hypercalcemia. [1] - This patient is experiencing symptoms consistent with hypocalcemia, not hypercalcemia. *Increased serum calcium and increased PTH* - This combination is rare and could suggest conditions like **familial hypocalciuric hypercalcemia**, where inappropriately high PTH is seen despite elevated calcium. [1] - However, the patient's symptoms are of hypocalcemia, and the history points towards iatrogenic hypoparathyroidism.
Question 9: Which of the following is used in the treatment of well-differentiated thyroid carcinoma?
- A. I131 (Correct Answer)
- B. 99m Tc
- C. 32p
- D. MIBG
Explanation: ***I131*** - **Radioactive iodine (I131)** is specifically absorbed by **well-differentiated thyroid cancer cells** because these cells retain the ability to uptake iodine, unlike other types of cancer cells. - Used for **ablating residual thyroid tissue** after surgery and for treating **metastatic well-differentiated thyroid carcinoma** [1]. *99m Tc* - **Technetium-99m (99m Tc)** is primarily used for **diagnostic imaging** (e.g., thyroid scans, bone scans), not for therapeutic treatment of thyroid cancer. - It has a short half-life and emits gamma rays, making it suitable for imaging but generally not for delivering sustained radiation for therapeutic effect. *32p* - **Phosphorus-32 (32p)** is a beta-emitting radionuclide used in the treatment of certain hematological malignancies, such as **polycythemia vera**, and for palliative treatment of bone metastases. - It is not selectively taken up by thyroid cancer cells and therefore is not used in the treatment of thyroid carcinoma. *MIBG* - **Metaiodobenzylguanidine (MIBG)**, often labeled with I123 (diagnostic) or I131 (therapeutic), is used in the diagnosis and treatment of **neuroendocrine tumors** like **pheochromocytoma** and **neuroblastoma**. - Its uptake mechanism targets cells of neuroectodermal origin, which is distinct from the iodine uptake mechanism of thyroid cells.
Question 10: A 55-year-old male patient presents to the clinic with left lower lip weakness following a recent parotid gland surgery. Considering the surgical history and current symptoms, what is the most likely site of the lesion causing this patient's condition?
- A. Main trunk of facial nerve
- B. Temporal branch of facial nerve
- C. Parotid duct
- D. Marginal mandibular branch of the facial nerve (Correct Answer)
Explanation: ***Marginal mandibular branch of the facial nerve*** - This branch supplies the muscles around the lower lip, including the **depressor anguli oris** and **depressor labii inferioris**, which are responsible for lower lip movement. - Damage to this specific branch during **parotid gland surgery** is a common cause of isolated **lower lip weakness**, as it runs superficial to the submandibular gland and is vulnerable during dissections in this area. *Main trunk of facial nerve* - Injury to the main trunk would result in **widespread paralysis** of all facial muscles on the affected side, not just isolated lower lip weakness. - The main trunk emerges from the stylomastoid foramen and then enters the parotid gland before branching, so damage here would affect all subsequent branches. *Temporal branch of facial nerve* - This branch innervates muscles responsible for eyebrow movement and forehead wrinkling (e.g., **frontalis muscle**). - Damage to the temporal branch would cause inability to raise the eyebrow and smooth out the forehead, not lower lip weakness. *Parotid duct* - The parotid duct (Stensen's duct) is responsible for transporting saliva from the parotid gland to the oral cavity. - Injury to the parotid duct would lead to complications like **salivary fistula** or **sialocele**, but it does not carry motor innervation to facial muscles and would not cause weakness.
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