Endocrinology — MCQs

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 391: What is the primary effect of calcitonin?

A. Bone deposition (Correct Answer)
B. Bone resorption
C. Increases intestinal absorption of calcium
D. Decreases intestinal absorption of calcium

Explanation: **Explanation:** Calcitonin is a peptide hormone secreted by the **parafollicular cells (C-cells)** of the thyroid gland. Its primary function is to lower plasma calcium levels when they are elevated (hypercalcemia). **Why Option A is correct:** Calcitonin acts as a "hypocalcemic" hormone. It achieves this primarily by inhibiting the activity of **osteoclasts** (cells that break down bone). By suppressing bone resorption, it shifts the balance toward **bone deposition** (mineralization), effectively moving calcium from the blood into the bone matrix. **Why the other options are incorrect:** * **Option B:** Bone resorption is the primary effect of **Parathyroid Hormone (PTH)**. PTH stimulates osteoclasts to break down bone and release calcium into the blood. Calcitonin is the physiological antagonist to PTH in this regard. * **Options C & D:** Intestinal absorption of calcium is primarily regulated by **1,25-dihydroxyvitamin D3 (Calcitriol)**. While calcitonin has a minor inhibitory effect on calcium absorption in the gut, it is not its primary or most significant mechanism of action. **High-Yield Clinical Pearls for NEET-PG:** * **The "Emergency" Hormone:** Calcitonin acts rapidly but is considered a short-term regulator of calcium compared to PTH and Vitamin D. * **Marker for Malignancy:** Serum calcitonin levels are used as a specific tumor marker for **Medullary Thyroid Carcinoma (MTC)**. * **Therapeutic Use:** Due to its ability to inhibit osteoclasts, exogenous calcitonin (often salmon calcitonin) is used clinically to treat **Paget’s disease** and severe hypercalcemia. * **Renal Effect:** Calcitonin also increases the renal excretion of calcium and phosphate (phosphaturic effect).

Question 392: Which of the following does not depend on insulin via GLUT4 for glucose uptake?

A. Brain (Correct Answer)
B. Skeletal muscles
C. Cardiac muscles
D. Adipose tissue

Explanation: **Explanation:** The uptake of glucose into cells is mediated by **Glucose Transporters (GLUT)**. These are divided into two categories: those that are insulin-independent and those that are insulin-dependent. **Why the Brain is the Correct Answer:** The brain is a vital organ that requires a continuous supply of glucose regardless of insulin levels. Glucose uptake in the brain (specifically across the blood-brain barrier and into neurons) is mediated primarily by **GLUT1** and **GLUT3**. These transporters are **insulin-independent**, ensuring the brain receives fuel even during fasting or hypoglycemic states. **Why the Other Options are Incorrect:** * **Skeletal Muscle & Cardiac Muscle:** These tissues primarily utilize **GLUT4**. In the resting state, GLUT4 is stored in intracellular vesicles. Upon insulin binding to its receptor, these vesicles translocate to the cell membrane to allow glucose entry. Therefore, glucose uptake here is highly **insulin-dependent**. (Note: Exercise can also trigger GLUT4 translocation in skeletal muscle via insulin-independent pathways). * **Adipose Tissue:** Like muscle, adipocytes rely on **GLUT4** for glucose uptake to facilitate triglyceride synthesis. This process is strictly regulated by insulin. **NEET-PG High-Yield Pearls:** * **GLUT4** is the **only** insulin-dependent glucose transporter. * **GLUT1:** Found in RBCs, Blood-Brain Barrier, and kidneys. * **GLUT2:** A high-capacity, bidirectional transporter found in **Liver, Pancreas (B-cells), and Small Intestine**. It acts as a glucose sensor. * **GLUT5:** Primarily a **fructose** transporter found in the small intestine and spermatozoa. * **SGLT1/2:** These are sodium-glucose co-transporters (active transport) found in the small intestine and proximal convoluted tubule of the kidney, respectively.

Question 393: Thyroid-stimulating hormone (TSH) secreted from the pituitary gland is under control by which of the following mechanisms?

A. Thyrotropin-releasing hormone (TRH) and negative feedback from T3 and T4 (Correct Answer)
B. Releasing factors similar to those controlling cortisol secretion
C. Releasing factors that bypass the neurohypophysis to act on the anterior pituitary
D. Thyrotropin-releasing hormone (TRH) only

Explanation: **Explanation:** The regulation of Thyroid-stimulating hormone (TSH) follows the classic **Hypothalamic-Pituitary-Thyroid (HPT) axis** model. 1. **Why Option A is Correct:** TSH secretion is primarily stimulated by **Thyrotropin-releasing hormone (TRH)**, a tripeptide synthesized in the paraventricular nucleus of the hypothalamus. However, the system is self-regulating via a **negative feedback loop**. High levels of free T3 and T4 in the blood inhibit both the synthesis of TRH in the hypothalamus and the sensitivity of thyrotropes in the anterior pituitary to TRH. This ensures hormonal homeostasis. 2. **Why Incorrect Options are Wrong:** * **Option B:** Cortisol is regulated by the HPA axis (CRH and ACTH). While both are anterior pituitary hormones, their releasing factors and feedback triggers are distinct. * **Option C:** Releasing factors for the anterior pituitary (adenohypophysis) travel through the **hypophyseal portal system**, not the neurohypophysis (posterior pituitary). The neurohypophysis stores ADH and Oxytocin. * **Option D:** This is incomplete. While TRH is the primary stimulator, the negative feedback from peripheral thyroid hormones is equally essential for physiological regulation. **Clinical Pearls for NEET-PG:** * **Primary Hypothyroidism:** Low T3/T4 leads to a loss of negative feedback, resulting in **elevated TSH** (the most sensitive screening test). * **Secondary Hypothyroidism:** Low T3/T4 with low or inappropriately normal TSH suggests a pituitary or hypothalamic pathology. * **Wolff-Chaikoff Effect:** An autoregulatory phenomenon where high iodine intake transiently inhibits thyroid hormone synthesis. * **Somatostatin and Dopamine:** Both can inhibit TSH secretion, though they are not the primary regulators.

Question 394: Which of the following is NOT an appetite suppressant?

A. Melanocyte stimulating hormone
B. Melanocyte corticotropic releasing hormone
C. Neuropeptide Y (Correct Answer)
D. Leptin

Explanation: **Explanation:** The regulation of appetite occurs primarily in the **Arcuate Nucleus (ARC)** of the hypothalamus, which contains two distinct sets of neurons: the **Orexigenic** (appetite-stimulating) and **Anorexigenic** (appetite-suppressing) pathways. **Why Neuropeptide Y (NPY) is the correct answer:** Neuropeptide Y is one of the most potent **orexigenic** peptides known. It is co-released with Agouti-related peptide (AgRP) from the ARC. When activated, NPY stimulates food intake, reduces energy expenditure, and promotes fat storage. Therefore, it is an appetite stimulant, not a suppressant. **Analysis of Incorrect Options (Appetite Suppressants):** * **Melanocyte Stimulating Hormone (α-MSH):** This is an anorexigenic peptide derived from Pro-opiomelanocortin (POMC). It acts on MC3 and MC4 receptors in the hypothalamus to inhibit feeding. * **Corticotropin-Releasing Hormone (CRH):** Produced in the paraventricular nucleus, CRH acts as a potent anorexigenic signal, typically reducing food intake during stress responses. * **Leptin:** Produced by adipocytes, Leptin is the "satiety hormone." It crosses the blood-brain barrier to inhibit NPY/AgRP neurons (stimulants) and excite POMC neurons (suppressants), leading to long-term energy balance. **High-Yield Clinical Pearls for NEET-PG:** * **Vagus Nerve:** The primary neural pathway for short-term satiety signals (like CCK) from the gut to the brain. * **Ghrelin:** The only major peripheral hormone that **stimulates** hunger (produced by P/D1 cells of the stomach). * **POMC Deficiency:** Leads to hyperphagia, early-onset obesity, and red hair (due to lack of MSH). * **Mnemonic for ARC:** **N**PY/AgRP = **N**o (stop) fasting/Start eating; **P**OMC/CART = **P**ause eating.

Question 395: Calcitonin levels are increased in which of the following conditions?

A. Hyperthyroidism
B. Hyperparathyroidism (Correct Answer)
C. Hypoparathyroidism
D. Cushing Syndrome

Explanation: **Explanation:** **Correct Option: B. Hyperparathyroidism** The primary stimulus for the secretion of **Calcitonin** (produced by the parafollicular C-cells of the thyroid gland) is **Hypercalcemia**. In Hyperparathyroidism, there is an excess of Parathyroid Hormone (PTH), which leads to elevated serum calcium levels through increased bone resorption and renal calcium reabsorption. As a physiological feedback mechanism, the body increases Calcitonin levels to counteract this hypercalcemia by inhibiting osteoclast activity and promoting renal calcium excretion. **Analysis of Incorrect Options:** * **A. Hyperthyroidism:** This involves excess T3/T4 from follicular cells. While severe thyrotoxicosis can occasionally cause mild hypercalcemia due to increased bone turnover, it is not a primary or classic cause for elevated Calcitonin. * **C. Hypoparathyroidism:** This condition results in **Hypocalcemia**. Low serum calcium levels inhibit the secretion of Calcitonin. * **D. Cushing Syndrome:** Excess glucocorticoids generally lead to decreased bone formation and can cause secondary hyperparathyroidism due to decreased intestinal calcium absorption, but they do not directly stimulate Calcitonin secretion. **High-Yield Clinical Pearls for NEET-PG:** * **Tumor Marker:** Calcitonin is the most sensitive tumor marker for **Medullary Carcinoma of the Thyroid (MCT)**. * **Antagonist:** Calcitonin acts as a physiological antagonist to PTH, but its role in human calcium homeostasis is much weaker than PTH. * **Therapeutic Use:** Exogenous Calcitonin (Salmon calcitonin) is used clinically to treat **Paget’s disease** and severe hypercalcemia. * **Stimuli:** Besides hypercalcemia, GI hormones like **Gastrin** are potent stimulators of Calcitonin secretion.

Question 396: Which of the following is a consequence of adrenal insufficiency?

A. A rise in plasma sodium/potassium ratio
B. Low blood pressure (Correct Answer)
C. Increased breakdown of protein
D. A fall in extra-cellular fluid volume

Explanation: **Explanation:** Adrenal insufficiency (Addison’s disease) results from the deficiency of adrenocortical hormones, primarily **aldosterone** (mineralocorticoid) and **cortisol** (glucocorticoid). **Why "Low blood pressure" is correct:** Hypotension is a hallmark of adrenal insufficiency due to two main mechanisms: 1. **Mineralocorticoid deficiency:** Lack of aldosterone leads to "salt wasting" (failure to reabsorb $Na^+$ and water in the distal tubules), causing hypovolemia. 2. **Glucocorticoid deficiency:** Cortisol is essential for maintaining vascular tone; it sensitizes vascular smooth muscle to the pressor effects of catecholamines. Without it, peripheral vascular resistance drops, leading to hypotension. **Analysis of Incorrect Options:** * **A. A rise in plasma sodium/potassium ratio:** In adrenal insufficiency, aldosterone deficiency causes hyponatremia (low $Na^+$) and hyperkalemia (high $K^+$). Therefore, the $Na^+/K^+$ ratio **falls**, it does not rise. * **C. Increased breakdown of protein:** Cortisol is a catabolic hormone. In its absence, protein breakdown actually **decreases**. Patients often present with muscle weakness due to impaired carbohydrate metabolism rather than excessive proteolysis. * **D. A fall in extra-cellular fluid volume:** While ECF volume does decrease, **Low blood pressure** is considered the more direct clinical "consequence" and a primary diagnostic sign. *Note: In many standardized exams, if both are present, hypotension is the prioritized clinical manifestation.* **NEET-PG High-Yield Pearls:** * **Hyperpigmentation:** Seen in primary adrenal insufficiency due to increased ACTH (which has MSH-like activity), specifically in skin creases and buccal mucosa. * **Electrolyte Triad:** Hyponatremia, Hyperkalemia, and Metabolic Acidosis. * **Cosyntropin Stimulation Test:** The gold standard for diagnosis. * **Adrenal Crisis:** An emergency characterized by profound hypotension, dehydration, and shock, often triggered by stress or infection.

Question 397: The blood glucose level in diabetes mellitus is decreased by the removal of which endocrine gland?

A. Thyroid
B. Parathyroids
C. Anterior pituitary (Correct Answer)
D. Posterior pituitary

Explanation: **Explanation:** The correct answer is **Anterior Pituitary**. This phenomenon is historically known as the **Houssay Phenomenon**. **Why the Anterior Pituitary is correct:** The anterior pituitary secretes several "diabetogenic" hormones, most notably **Growth Hormone (GH)** and **Adrenocorticotropic Hormone (ACTH)**. * **Growth Hormone** decreases peripheral glucose uptake and increases gluconeogenesis. * **ACTH** stimulates the adrenal cortex to release **Cortisol**, which significantly raises blood glucose levels by promoting gluconeogenesis and antagonizing insulin action. In a diabetic individual, removing the anterior pituitary (hypophysectomy) eliminates these insulin-antagonistic effects, leading to a marked increase in insulin sensitivity and a subsequent decrease in blood glucose levels. **Why the other options are incorrect:** * **Thyroid:** While Thyroid hormones ($T_3, T_4$) increase glucose absorption from the gut, their effect on overall glycemic control in diabetes is less direct and potent compared to the pituitary-adrenal axis. * **Parathyroids:** These glands regulate calcium and phosphate homeostasis via Parathyroid Hormone (PTH) and have no significant direct role in glucose metabolism. * **Posterior Pituitary:** This gland stores and releases ADH (Vasopressin) and Oxytocin. These hormones primarily regulate water balance and uterine contractions/milk ejection, respectively, and do not significantly influence blood glucose levels. **High-Yield Clinical Pearls for NEET-PG:** * **Houssay Phenomenon:** The spontaneous improvement of diabetes mellitus following the destruction of the anterior pituitary (e.g., due to Sheehan’s syndrome or a pituitary tumor). * **Diabetogenic Hormones:** Growth Hormone, Cortisol, Glucagon, and Epinephrine. * **Insulin-like Growth Factor (IGF-1):** While GH is diabetogenic, its mediator IGF-1 has insulin-like effects; however, the direct anti-insulin effect of GH predominates in the blood.

Question 398: Which iodinated compound is present in the maximum concentration in the thyroid?

A. Monoiodotyrosine (MIT)
B. Diiodotyrosine (DIT) (Correct Answer)
C. Triiodothyronine (T3)
D. Reverse T3

Explanation: **Explanation:** The synthesis of thyroid hormones occurs within the thyroglobulin molecule in the follicular lumen. The process involves the iodination of tyrosine residues (organification) followed by the coupling of these residues. **1. Why DIT is the correct answer:** During the organification process, iodine is added to tyrosine residues to form **Monoiodotyrosine (MIT)** and **Diiodotyrosine (DIT)**. Statistically and biochemically, the formation of DIT is more prevalent than MIT. When these precursors couple, two DIT molecules join to form T4 (Thyroxine), while one MIT and one DIT join to form T3. Because T4 is the primary secretory product of the thyroid (produced in a much higher ratio than T3), the thyroid gland maintains a significantly higher pool of **DIT** as the precursor. In the thyroid gland, the concentration gradient follows the order: **DIT > MIT > T4 > T3.** **2. Analysis of Incorrect Options:** * **MIT (Option A):** While abundant, MIT is present in lower concentrations than DIT because the majority of tyrosine residues undergo double iodination. * **T3 (Option B):** T3 is the most biologically active hormone but is produced in much smaller quantities within the gland compared to its precursors. * **Reverse T3 (Option D):** rT3 is a metabolically inactive product formed primarily by the peripheral deiodination of T4 in tissues, not stored in high concentrations within the thyroid gland. **High-Yield Clinical Pearls for NEET-PG:** * **Iodine Trap:** The Sodium-Iodide Symporter (NIS) is the secondary active transport mechanism that initiates this process. * **Wolff-Chaikoff Effect:** A transient reduction in thyroid hormone synthesis due to ingestion of a large amount of iodine. * **Thyroglobulin:** It is the storage form of thyroid hormones; one molecule of thyroglobulin contains approximately 30 T4 molecules and a vast excess of DIT/MIT.

Question 399: Pulsatile release of GnRH is important for?

A. Gonadotrophin stimulation (Correct Answer)
B. Ovulation induction
C. GnRH feedback inhibition
D. Gonadotropin downregulation

Explanation: **Explanation:** The secretion of **Gonadotropin-Releasing Hormone (GnRH)** from the hypothalamus is inherently **pulsatile**. This intermittent release is physiological and essential for the stimulation of the anterior pituitary to secrete LH (Luteinizing Hormone) and FSH (Follicle-Stimulating Hormone). **1. Why Option A is Correct:** The pituitary GnRH receptors require a "rest period" between pulses to remain sensitive. Pulsatile GnRH (occurring every 60–90 minutes) prevents the internalization of receptors, thereby maintaining the synthesis and release of **Gonadotrophins**. **2. Why Other Options are Incorrect:** * **Option B:** While pulsatile GnRH eventually leads to ovulation, its *direct* physiological function is the stimulation of gonadotrophs. Ovulation is a secondary downstream effect of the LH surge. * **Option C:** Feedback inhibition is primarily mediated by ovarian/testicular steroids (estrogen, progesterone, testosterone) acting on the hypothalamus and pituitary, not by the pulsatility of GnRH itself. * **Option D:** **Continuous (non-pulsatile)** administration of GnRH leads to the **downregulation** and desensitization of GnRH receptors. This suppresses the pituitary-gonadal axis. **Clinical Pearls for NEET-PG:** * **GnRH Agonists (e.g., Leuprolide, Goserelin):** When given continuously, they cause "chemical castration." This is used clinically to treat **prostate cancer, endometriosis, and precocious puberty**. * **Kallmann Syndrome:** Characterized by the failure of GnRH neurons to migrate, leading to hypogonadotropic hypogonadism and anosmia. * **Pulse Frequency:** High-frequency pulses favor **LH** release, while low-frequency pulses favor **FSH** release.

Question 400: Which of the following is an anabolic hormone?

A. Corticosteroids
B. Glucagon
C. Insulin (Correct Answer)
D. Somatostatin

Explanation: **Explanation:** **Insulin** is the primary **anabolic hormone** of the body. It is secreted by the beta cells of the pancreas in response to high blood glucose levels (the fed state). Its primary role is to promote the storage of nutrients and the synthesis of complex molecules. * **Why Insulin is correct:** Insulin stimulates **glycogenesis** (glycogen synthesis in liver and muscle), **lipogenesis** (fatty acid synthesis in adipose tissue), and **protein synthesis** (by increasing amino acid uptake). It simultaneously inhibits catabolic processes like glycogenolysis and gluconeogenesis. **Analysis of Incorrect Options:** * **Corticosteroids (e.g., Cortisol):** These are primarily **catabolic** in peripheral tissues. They promote protein breakdown in muscles and lipolysis in extremities to provide substrates for gluconeogenesis in the liver. * **Glucagon:** Known as a "counter-regulatory" hormone, it is **catabolic**. It raises blood glucose by stimulating glycogenolysis and gluconeogenesis in the liver during fasting states. * **Somatostatin:** This is an **inhibitory hormone**. In the pancreas, it inhibits the secretion of both insulin and glucagon; it does not directly promote the synthesis of energy stores. **High-Yield Clinical Pearls for NEET-PG:** * **The "Anabolic Trio":** Insulin, Growth Hormone (GH), and Testosterone are the major anabolic hormones. Note: While GH is anabolic for proteins, it is catabolic for fats (lipolytic). * **Insulin-Independent Glucose Uptake:** Occurs in the **BRICK L** (Brain, RBCs, Intestine, Cornea, Kidney, Liver). * **GLUT-4:** The only insulin-dependent glucose transporter, found primarily in skeletal muscle and adipose tissue.

Practice by Chapter

Principles of Endocrine Regulation

Practice Questions

Hypothalamus and Pituitary Gland

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Thyroid Physiology

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Adrenal Cortex and Medulla

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Pancreatic Hormones and Glucose Metabolism

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Calcium and Phosphate Homeostasis

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Growth Hormone and Growth Factors

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Endocrine Regulation of Metabolism

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Hormone Receptors and Signaling

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Assessment of Endocrine Function

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