Endocrinology — MCQs

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 291: Dehydration increases the plasma concentration of all the following hormones EXCEPT?

A. Vasopressin
B. Aldosterone
C. Angiotensin II
D. Atrial natriuretic peptide (Correct Answer)

Explanation: **Explanation:** The correct answer is **Atrial Natriuretic Peptide (ANP)**. Dehydration leads to a decrease in total blood volume (hypovolemia) and an increase in plasma osmolarity. The body’s primary goal during dehydration is to conserve water and sodium to restore blood pressure and volume. **Why ANP is the correct answer:** ANP is a hormone secreted by the atrial myocytes in response to **atrial stretch** (increased venous return/volume overload). Its primary function is to promote natriuresis (sodium excretion) and diuresis (water excretion) to lower blood pressure. In dehydration, the atria are "under-filled," leading to **decreased** atrial stretch; therefore, ANP secretion is inhibited. **Why the other options are incorrect:** * **Vasopressin (ADH):** Dehydration increases plasma osmolarity, which is sensed by hypothalamic osmoreceptors. This triggers the release of ADH to increase water reabsorption in the collecting ducts. * **Angiotensin II:** Hypovolemia causes decreased renal perfusion, stimulating the Juxtaglomerular (JG) apparatus to release Renin. Renin converts Angiotensinogen to Angiotensin I, which is then converted to Angiotensin II. * **Aldosterone:** Angiotensin II and increased plasma potassium stimulate the adrenal cortex to release Aldosterone, which promotes sodium and water retention to restore volume. **High-Yield Clinical Pearls for NEET-PG:** * **ANP vs. ADH:** Think of them as antagonists. ANP "wastes" salt/water (lowers BP), while ADH/Aldosterone "save" salt/water (raises BP). * **BNP (B-type Natriuretic Peptide):** Secreted by ventricles in response to pressure/volume overload; used clinically as a marker for Heart Failure. * **Stimulus for ADH:** Increased osmolarity is a more sensitive stimulus for ADH release than decreased volume.

Question 292: Calcitonin causes hypocalcemia by which of the following mechanisms?

A. Inhibiting bone resorption (Correct Answer)
B. Promoting osteolysis
C. Decreasing renal tubular reabsorption of calcium
D. Decreasing absorption of phosphorus

Explanation: **Explanation:** Calcitonin is a peptide hormone secreted by the **parafollicular cells (C-cells)** of the thyroid gland. Its primary physiological role is to lower plasma calcium levels, acting as a functional antagonist to Parathyroid Hormone (PTH). **Why Option A is correct:** The hallmark action of calcitonin is the **inhibition of bone resorption**. It achieves this by binding to specific receptors on **osteoclasts**, leading to a decrease in their absorptive activity and a reduction in their formation rate. By preventing the breakdown of the bone matrix, calcitonin stops the release of calcium and phosphate into the bloodstream, effectively causing hypocalcemia. **Analysis of Incorrect Options:** * **B. Promoting osteolysis:** This is incorrect as osteolysis (bone breakdown) is stimulated by PTH, not calcitonin. Calcitonin inhibits this process. * **C. Decreasing renal tubular reabsorption of calcium:** While calcitonin does have a mild phosphaturic and calciuric effect on the kidneys, its **primary and most potent** hypocalcemic effect is mediated through bone, not the renal tubules. * **D. Decreasing absorption of phosphorus:** Calcitonin actually increases the renal excretion of phosphorus (phosphaturia), but this is a secondary effect and not the mechanism by which it regulates calcium. **High-Yield Clinical Pearls for NEET-PG:** * **Stimulus:** Hypercalcemia is the primary stimulus for calcitonin secretion. * **Clinical Use:** Due to its ability to inhibit osteoclasts, synthetic calcitonin (Salmon calcitonin) is used clinically to treat **Paget’s disease**, severe hypercalcemia, and postmenopausal osteoporosis. * **Tumor Marker:** Serum calcitonin levels are a specific tumor marker for **Medullary Thyroid Carcinoma (MTC)**. * **Escape Phenomenon:** Prolonged exposure to calcitonin leads to a downregulation of receptors, causing the hormone to lose its effectiveness over time.

Question 293: What is the primary function of oxytocin?

A. Milk ejection (Correct Answer)
B. Milk secretion
C. Ovulation
D. Maintenance of pregnancy

Explanation: **Explanation:** **1. Why "Milk Ejection" is correct:** Oxytocin is a peptide hormone synthesized in the **paraventricular nuclei** of the hypothalamus and stored in the posterior pituitary. Its primary role in lactation is the **Milk Ejection Reflex (Let-down reflex)**. It acts on the **G-protein coupled receptors** of the **myoepithelial cells** surrounding the mammary alveoli, causing them to contract. This contraction forces milk from the alveoli into the larger ducts and sinuses, making it available for the infant. **2. Why other options are incorrect:** * **Milk secretion (B):** This is the primary function of **Prolactin**, which stimulates the alveolar epithelium to synthesize milk. A common mnemonic: **P**rolactin **P**roduces, **O**xytocin **O**usts (ejects). * **Ovulation (C):** Ovulation is triggered by the **LH surge** (Luteinizing Hormone) from the anterior pituitary. * **Maintenance of pregnancy (D):** This is primarily the role of **Progesterone** (the "hormone of pregnancy"), which decreases uterine excitability. Oxytocin, conversely, causes uterine contractions and is used to induce labor. **3. High-Yield Clinical Pearls for NEET-PG:** * **Stimulus:** The strongest stimulus for oxytocin release is **suckling** (mechanical stimulation of the nipple), followed by psychological triggers (hearing a baby cry). * **Uterine Action:** Oxytocin causes contraction of the **fundus** of the uterus. Clinically, it is the drug of choice for **Postpartum Hemorrhage (PPH)** prevention. * **Ferguson Reflex:** A neuroendocrine reflex where cervical stretching triggers oxytocin release, creating a positive feedback loop during labor. * **Other functions:** It is often called the "love hormone" or "bonding hormone" due to its role in social recognition and maternal-infant bonding.

Question 294: What is the direct action of parathyroid hormone (PTH)?

A. Controls the rate of 25-hydroxycholecalciferol formation
B. Controls the rate of calcium transport in the mucosa of the small intestine
C. Controls the rate of formation of calcium-binding protein
D. Controls the rate of formation of 1,25-dihydroxycholecalciferol (Correct Answer)

Explanation: **Explanation:** Parathyroid Hormone (PTH) is the primary regulator of calcium homeostasis. Its **direct** action on the kidneys involves stimulating the enzyme **1α-hydroxylase** in the proximal convoluted tubule. This enzyme converts 25-hydroxycholecalciferol [25(OH)D] into **1,25-dihydroxycholecalciferol [1,25(OH)₂D]**, also known as Calcitriol (the active form of Vitamin D). Therefore, Option D is the correct direct physiological effect. **Analysis of Incorrect Options:** * **Option A:** The formation of 25-hydroxycholecalciferol occurs in the **liver** via the enzyme 25-hydroxylase, which is not regulated by PTH. * **Options B & C:** These are **indirect** actions of PTH. PTH does not act directly on the intestine. Instead, the Calcitriol produced by the kidneys (under PTH influence) travels to the intestinal mucosa to increase the synthesis of **Calbindin** (calcium-binding protein), which subsequently facilitates calcium absorption. **High-Yield Clinical Pearls for NEET-PG:** * **PTH Renal Actions:** Increases Ca²⁺ reabsorption (Distal Tubule), decreases Phosphate reabsorption (Proximal Tubule - Phosphaturic effect), and increases 1α-hydroxylase activity. * **Bone Action:** PTH stimulates osteoblasts to release **RANKL**, which then activates osteoclasts (indirect bone resorption). * **Hypocalcemia:** The most potent stimulus for PTH release. * **Magnesium Paradox:** Mild hypomagnesemia stimulates PTH, but **severe hypomagnesemia inhibits PTH secretion** and causes PTH resistance, leading to refractory hypocalcemia.

Question 295: Androgen is secreted by which of the following cells?

A. Leydig cells (Correct Answer)
B. Sertoli cells
C. Cowper's glands
D. Intermediate cells

Explanation: **Explanation:** The correct answer is **Leydig cells**. **1. Why Leydig cells are correct:** Leydig cells, also known as **interstitial cells of Leydig**, are located in the connective tissue between the seminiferous tubules of the testes. Their primary function is the synthesis and secretion of **androgens**, predominantly **testosterone**. This process is stimulated by **Luteinizing Hormone (LH)** from the anterior pituitary. LH binds to G-protein coupled receptors on Leydig cells, increasing cAMP and activating protein kinase A, which promotes the conversion of cholesterol to pregnenolone (the rate-limiting step in steroidogenesis). **2. Why the other options are incorrect:** * **Sertoli cells:** Located within the seminiferous tubules, these are "nurse cells." They support spermatogenesis, form the blood-testis barrier, and secrete **Inhibin B** and **Androgen Binding Protein (ABP)** under the influence of FSH. They do not synthesize androgens but help concentrate them. * **Cowper’s glands (Bulbourethral glands):** These are accessory glands that secrete a clear, alkaline pre-ejaculate fluid to lubricate the urethra and neutralize acidic urine; they do not have an endocrine function. * **Intermediate cells:** This is a non-specific term often referring to cells in the vaginal epithelium or specific layers of the adrenal cortex (though not a standard term for androgen production). **Clinical Pearls for NEET-PG:** * **LH acts on Leydig cells** (Mnemonic: **L**H = **L**eydig). * **FSH acts on Sertoli cells** (Mnemonic: **F**SH = **S**ertoli). * **Blood-Testis Barrier:** Formed by tight junctions between Sertoli cells. * **Testosterone Feedback:** High levels of testosterone inhibit LH secretion via negative feedback on the hypothalamus and anterior pituitary.

Question 296: The breast is a hormonally responsive organ. Which statement about progesterone is NOT true?

A. Progesterone is produced in the ovary
B. Progesterone stimulates growth of the lobules and the acini
C. Progesterone causes an increase in interstitial fluid in the breast
D. Progesterone promotes growth of both the stroma and the duct system of the breast (Correct Answer)

Explanation: **Explanation:** The breast undergoes complex structural changes under the influence of various hormones. To answer this question, one must distinguish between the specific roles of **Estrogen** and **Progesterone**. **1. Why Option D is the Correct (False) Statement:** The growth of the **stroma** and the **ductal system** is primarily the function of **Estrogen**, not progesterone. Estrogen is responsible for the elongation of ducts and the deposition of fat that gives the breast its mass during puberty. Progesterone, while essential for breast development, acts later in the hierarchy to differentiate these structures. **2. Analysis of Other Options:** * **Option A (True):** Progesterone is produced by the **Corpus Luteum** in the ovary during the luteal phase of the menstrual cycle (and by the placenta during pregnancy). * **Option B (True):** The specific physiological role of progesterone in the breast is the **lobulo-alveolar development**. it stimulates the budding of alveoli (acini) and prepares them for potential secretory activity. * **Option C (True):** Progesterone is known to cause **fluid retention** and increased vascularity in the breast tissue. This explains the common clinical symptom of "cyclical mastalgia" or breast heaviness/tenderness experienced by many women during the premenstrual (luteal) phase. **High-Yield NEET-PG Pearls:** * **Estrogen:** Responsible for ductal growth (Mnemonic: **E**strogen = **E**longation of ducts). * **Progesterone:** Responsible for alveolar/lobular growth (Mnemonic: **P**rogesterone = **P**roliferation of acini). * **Prolactin:** Essential for the final stages of alveolar differentiation and milk production (lactogenesis). * **Synergy:** Complete development of the mammary glands into milk-secreting organs requires the synergistic action of Estrogen, Progesterone, Prolactin, Growth Hormone, and Glucocorticoids.

Question 297: After ovulation, the corpus luteum begins to regress after how many days?

A. 5 days
B. 10 days (Correct Answer)
C. 15 days
D. 20 days

Explanation: **Explanation:** The lifespan of the corpus luteum (CL) is the primary determinant of the length of the secretory phase of the menstrual cycle. Following ovulation (typically Day 14), the ruptured follicle transforms into the corpus luteum under the influence of Luteinizing Hormone (LH). **Why 10 days is correct:** The corpus luteum has a functional lifespan of approximately **10 to 12 days** in a non-pregnant cycle. If fertilization does not occur, the CL begins to regress (luteolysis) around Day 24 of a 28-day cycle. This regression leads to a sharp decline in progesterone and estrogen levels, eventually triggering menstruation. Therefore, the regression starts roughly **10 days after ovulation**. **Analysis of Incorrect Options:** * **Option A (5 days):** At 5 days post-ovulation, the corpus luteum is at its peak vascularity and functional activity, secreting maximum amounts of progesterone to prepare the endometrium for implantation. * **Option C (15 days):** By 15 days post-ovulation, menstruation has usually already begun. The CL has already transformed into the inactive fibrous tissue known as the *corpus albicans*. * **Option D (20 days):** This exceeds the total duration of the luteal phase (which is fixed at 14 days). **NEET-PG High-Yield Pearls:** * **Fixed Phase:** While the follicular phase varies, the **luteal phase is constant at 14 days**. * **Rescue Mechanism:** If pregnancy occurs, **Human Chorionic Gonadotropin (hCG)**, secreted by the syncytiotrophoblast, mimics LH and "rescues" the corpus luteum from regression, maintaining it for the first 8–10 weeks of pregnancy (until the placental shift). * **Hormone Profile:** The corpus luteum primarily secretes **Progesterone** (dominant) and Estrogen. It also secretes **Inhibin A**.

Question 298: Largest amounts of prostaglandins are seen in which of the following?

A. Seminal fluid (Correct Answer)
B. Cerebrospinal fluid
C. Blood
D. Urine

Explanation: **Explanation:** Prostaglandins (PGs) are a group of physiologically active lipid compounds derived from arachidonic acid. The term "prostaglandin" itself is derived from the **prostate gland**, as they were first isolated from human semen in the 1930s. **Why Seminal Fluid is Correct:** Seminal fluid contains the **highest concentration** of prostaglandins in the human body (approximately 100–300 µg/mL). They are primarily secreted by the **seminal vesicles**. In the female reproductive tract, these prostaglandins perform two critical functions: 1. They react with female cervical mucus to make it more receptive to sperm movement. 2. They induce reverse peristaltic contractions in the uterus and fallopian tubes to facilitate the transport of sperm toward the ovaries. **Why Other Options are Incorrect:** * **B. Cerebrospinal Fluid (CSF):** While PGs (especially PGD2 and PGE2) are present in the brain and play roles in sleep and fever regulation, their concentration in CSF is negligible compared to semen. * **C. Blood:** Prostaglandins act as **autacoids** (local hormones). They are rapidly metabolized and inactivated (especially in the lungs) during their first passage through circulation; hence, systemic blood levels are very low. * **D. Urine:** PGs found in urine are metabolites of systemic production or locally produced by the kidneys to regulate renal blood flow, but the total quantity is significantly lower than in seminal fluid. **High-Yield NEET-PG Pearls:** * **Primary Source:** Seminal vesicles (not the prostate, despite the name). * **Clinical Correlation:** Low levels of prostaglandins in semen are associated with **male infertility**. * **Aspirin Connection:** NSAIDs like Aspirin inhibit Cyclooxygenase (COX), the rate-limiting enzyme in prostaglandin synthesis.

Question 299: Which hormones are secreted by the adrenal medulla?

A. Glucagon
B. Cortisol
C. Norepinephrine (Correct Answer)
D. Insulin

Explanation: **Explanation:** The adrenal gland is divided into two distinct functional units: the outer cortex and the inner medulla. The **adrenal medulla** is embryologically derived from the neural crest and functions as a modified sympathetic ganglion. It contains **chromaffin cells** that synthesize and secrete catecholamines directly into the bloodstream in response to sympathetic stimulation. The primary hormones secreted are **Epinephrine (80%)** and **Norepinephrine (20%)**, along with trace amounts of dopamine. **Analysis of Options:** * **Norepinephrine (Correct):** It is a catecholamine synthesized from tyrosine in the chromaffin cells. It acts on alpha and beta-adrenergic receptors to mediate the "fight-or-flight" response. * **Cortisol (Incorrect):** This is a glucocorticoid secreted by the **Zona Fasciculata** of the adrenal cortex, not the medulla. * **Insulin & Glucagon (Incorrect):** These are pancreatic hormones. Insulin is secreted by the **Beta cells** and Glucagon by the **Alpha cells** of the Islets of Langerhans. **High-Yield NEET-PG Pearls:** 1. **Rate-limiting enzyme:** Tyrosine hydroxylase is the rate-limiting step in catecholamine synthesis. 2. **PNMT Enzyme:** The conversion of Norepinephrine to Epinephrine requires the enzyme *Phenylethanolamine N-methyltransferase* (PNMT), which is induced by high concentrations of cortisol draining from the cortex. 3. **Clinical Correlation:** A tumor of the chromaffin cells is called a **Pheochromocytoma**, typically presenting with the triad of episodic headaches, sweating, and palpitations due to excess catecholamine secretion. 4. **VMA:** Vanillylmandelic acid (VMA) is the primary urinary metabolite of norepinephrine and epinephrine, used as a diagnostic marker for medullary tumors.

Question 300: What is the half-life of the insulin receptor?

A. 3 hours
B. 7 hours (Correct Answer)
C. 12 hours
D. 24 hours

Explanation: **Explanation:** The insulin receptor is a large, transmembrane glycoprotein consisting of two $\alpha$ and two $\beta$ subunits. Like most cell surface receptors, it undergoes a continuous cycle of synthesis, internalization, and degradation. **Why 7 hours is correct:** The average half-life of a mature insulin receptor on the cell membrane is approximately **7 to 10 hours**. This turnover rate is a balance between the synthesis of new receptors in the endoplasmic reticulum/Golgi apparatus and their degradation. When insulin binds to the receptor, the entire complex is internalized via endocytosis. While much of the insulin is degraded, the receptors are either recycled back to the cell surface or degraded by lysosomes. **Analysis of Incorrect Options:** * **A. 3 hours:** This is too short for the insulin receptor. Such rapid turnover is usually seen in specific signaling proteins or secondary messengers, not structural transmembrane receptors. * **C. 12 hours & D. 24 hours:** These durations are longer than the physiological turnover observed in studies of adipocytes and hepatocytes. However, it is important to note that in states of **hyperinsulinemia** (like Type 2 Diabetes), the half-life can actually decrease because increased insulin binding triggers "downregulation" and accelerated degradation of the receptors. **High-Yield Clinical Pearls for NEET-PG:** * **Structure:** The insulin receptor is a **Tyrosine Kinase receptor** (Catalytic receptor). * **Downregulation:** Chronic exposure to high insulin levels (obesity/insulin resistance) decreases the number of receptors on the cell surface by increasing the rate of degradation, thereby shortening the effective half-life. * **Subunits:** The $\alpha$-subunit is extracellular (binds insulin), while the $\beta$-subunit spans the membrane and possesses the tyrosine kinase activity. * **GLUT-4:** Insulin binding triggers the translocation of GLUT-4 transporters to the membrane in skeletal muscle and adipose tissue.

Practice by Chapter

Principles of Endocrine Regulation

Practice Questions

Hypothalamus and Pituitary Gland

Practice Questions

Thyroid Physiology

Practice Questions

Adrenal Cortex and Medulla

Practice Questions

Pancreatic Hormones and Glucose Metabolism

Practice Questions

Calcium and Phosphate Homeostasis

Practice Questions

Growth Hormone and Growth Factors

Practice Questions

Endocrine Regulation of Metabolism

Practice Questions

Hormone Receptors and Signaling

Practice Questions

Assessment of Endocrine Function

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free