Endocrinology Practice Questions

Q: Which of the following inhibits prolactin secretion?

Dopamine. **Explanation:** The regulation of prolactin (PRL) is unique among anterior pituitary hormones because it is under **predominant tonic inhibition** by the hypothalamus. **1. Why Dopamine is Correct:** Dopamine is the primary **Prolactin-Inhibiting Hormone (PIH)**. It is secreted by the tuberoinfundibular dopaminergic (TIDA) neurons of the hypothalamus into the hypophyseal portal system. It binds to **D2 receptors** on the lactotrophs in the anterior pituitary, leading to the inhibition of adenylyl cyclase and a subsequent decrease in prolactin synthesis and secretion. **2. Analysis of Incorrect Options:** * **Haloperidol:** This is an antipsychotic medication that acts as a **D2 receptor antagonist**. By blocking the inhibitory effect of dopamine, it causes a rise in prolactin levels (**hyperprolactinemia**), often leading to side effects like galactorrhea and gynecomastia. * **GABA:** While GABA can exert some inhibitory influence on prolactin, it is not the primary physiological inhibitor. Its role is minor compared to the potent control exerted by dopamine. * **Neurophysin:** These are carrier proteins for oxytocin (Neurophysin I) and vasopressin (Neurophysin II). They are involved in the transport of hormones from the hypothalamus to the posterior pituitary and have no direct role in inhibiting prolactin. **High-Yield Clinical Pearls for NEET-PG:** * **The "Stalk Effect":** Any lesion that compresses the pituitary stalk (e.g., Craniopharyngioma) prevents dopamine from reaching the pituitary, resulting in **increased** prolactin levels. * **TRH Connection:** Thyrotropin-releasing hormone (TRH) acts as a prolactin-releasing factor. Therefore, in **primary hypothyroidism** (where TRH is elevated), patients may present with hyperprolactinemia. * **Drug of Choice:** For prolactinomas, the first-line treatment is medical management with dopamine agonists like **Cabergoline** (preferred due to longer half-life) or Bromocriptine.

Q: Glucagon is secreted by which cells?

Alpha cells of pancreas. **Explanation:** The pancreas is a dual-function organ containing endocrine units known as the **Islets of Langerhans**. These islets consist of several distinct cell types, each secreting specific hormones directly into the bloodstream to regulate metabolism. **1. Why Alpha Cells are Correct:** Glucagon is synthesized and secreted by the **Alpha (α) cells**, which constitute approximately 20% of the islet cells. Glucagon is a catabolic hormone; its primary role is to increase blood glucose levels during fasting states by stimulating **glycogenolysis** (breakdown of glycogen) and **gluconeogenesis** (synthesis of glucose) in the liver. **2. Analysis of Incorrect Options:** * **Beta (β) cells:** These are the most abundant cells (approx. 65-75%) in the islets. They secrete **Insulin**, which lowers blood glucose, and **Amylin**. * **Gamma (γ) cells (also known as F or PP cells):** These cells secrete **Pancreatic Polypeptide**, which helps regulate pancreatic exocrine secretions and gallbladder contraction. * **Delta (δ) cells (not listed but high-yield):** These secrete **Somatostatin**, which acts paratrinely to inhibit the secretion of both insulin and glucagon. **High-Yield NEET-PG Clinical Pearls:** * **Glucagonoma:** A rare tumor of alpha cells characterized by the "4 Ds": Diabetes mellitus, Dermatitis (Necrolytic Migratory Erythema), Deep vein thrombosis, and Depression. * **Glucagon as an Antidote:** It is the drug of choice for **Beta-blocker overdose** because it increases intracellular cAMP in the myocardium via non-adrenergic pathways, exerting a positive inotropic effect. * **Inhibitor:** Glucagon secretion is inhibited by high blood glucose levels and insulin (via paracrine action).

Q: Refeeding edema is due to increased release of-

Insulin. **Explanation:** **Refeeding edema** occurs when a patient who has been in a prolonged state of starvation or malnutrition (such as in Anorexia Nervosa or Marasmus) begins to consume carbohydrates again. **Why Insulin is the Correct Answer:** During starvation, insulin levels are low, and the body relies on ketone bodies and fatty acids. Upon refeeding, the sudden intake of carbohydrates triggers a **massive release of insulin**. Insulin has a potent **antinatriuretic effect** on the kidneys; it acts directly on the proximal convoluted tubule and the distal nephron to increase the reabsorption of sodium and water. This sudden expansion of extracellular fluid (ECF) volume leads to dependent edema and, in severe cases, heart failure. **Why Other Options are Incorrect:** * **Growth Hormone (GH):** While GH can cause some fluid retention, it is not the primary mediator of the acute fluid shifts seen in refeeding syndrome. * **Glucocorticoids (Cortisol):** Cortisol levels are typically elevated during the stress of starvation. Refeeding actually tends to normalize (decrease) cortisol levels rather than increase them. * **Thyroxine (T4):** Starvation often leads to "Euthyroid Sick Syndrome" (low T3). Refeeding helps restore thyroid function, but thyroxine does not cause acute sodium retention or edema. **Clinical Pearls for NEET-PG:** * **Refeeding Syndrome:** Characterized by the "Hallmark Triad" of **Hypophosphatemia, Hypokalemia, and Hypomagnesemia**. * **Mechanism of Hypophosphatemia:** Insulin drives phosphorus into cells for glycolysis and ATP production, leading to a dangerous drop in serum phosphorus levels. * **Management:** "Start low and go slow" with caloric intake and aggressively supplement electrolytes (especially Phosphorus and Thiamine).

Q: All the following factors stimulate growth hormone secretion except?

Increased blood glucose. **Explanation:** Growth Hormone (GH) secretion is pulsatile and regulated by the hypothalamus via Growth Hormone-Releasing Hormone (GHRH) and Somatostatin (GHIH). Its release is primarily triggered by states of energy deficiency or increased metabolic demand. **Why Increased Blood Glucose is the Correct Answer:** Hyperglycemia (increased blood glucose) acts as a potent **inhibitor** of GH secretion. When blood glucose levels are high, the body suppresses GH to prevent further glucose elevation, as GH is a "diabetogenic" hormone that decreases peripheral glucose uptake and increases gluconeogenesis. Conversely, **hypoglycemia** is a powerful stimulator of GH. **Analysis of Incorrect Options:** * **Deep Sleep (Stage 3 & 4 NREM):** The largest peak of GH secretion occurs roughly 60 minutes after the onset of deep sleep. This is why adequate sleep is critical for growth in children. * **Increased Blood Amino Acids:** High levels of amino acids (especially Arginine) stimulate GH secretion. This promotes protein synthesis and tissue growth, utilizing the available building blocks. * **Exercise:** Physical stress and exercise are potent physiological stimuli for GH release, mediated by increased sympathetic activity and the need for fuel mobilization (lipolysis). **High-Yield Clinical Pearls for NEET-PG:** 1. **Gherlin:** Produced by the stomach, it is the only peripheral hormone that directly stimulates GH secretion (the "hunger hormone"). 2. **Somatomedins (IGF-1):** GH acts on the liver to produce IGF-1, which exerts negative feedback on GH secretion. 3. **L-Dopa & Clonidine:** Both are pharmacological stimulators used in clinical "GH stimulation tests" to diagnose deficiency. 4. **Obesity:** GH secretion is significantly **decreased** in obese individuals.

Q: What is the effect of steroids on calcium?

Increased excretion of calcium from the kidney. **Explanation:** Glucocorticoids (steroids) exert a significant **antagonistic effect on calcium metabolism**, primarily leading to a reduction in total body calcium. 1. **Why Option C is Correct:** Steroids directly inhibit calcium reabsorption in the renal tubules. By decreasing tubular reabsorption, they promote **hypercalciuria** (increased excretion of calcium in the urine). This is a key mechanism used clinically to treat hypercalcemia (e.g., in sarcoidosis or Vitamin D toxicity). 2. **Why Option B is Incorrect:** Steroids actually **decrease** the intestinal absorption of calcium. They antagonize the actions of Vitamin D in the gut and inhibit the expression of calbindin (the calcium-binding protein), leading to reduced calcium uptake. 3. **Why Option A is Incorrect:** Because steroids decrease gut absorption and increase renal excretion, the net effect is a **decrease in plasma calcium levels** (hypocalcemia). This drop in plasma calcium triggers a secondary rise in Parathyroid Hormone (PTH), which then mobilizes calcium from the bones. **Clinical Pearls for NEET-PG:** * **Steroid-Induced Osteoporosis:** The combination of decreased gut absorption, increased renal loss, and secondary hyperparathyroidism leads to increased osteoclast activity and bone resorption. * **Vitamin D Antagonism:** Steroids are the treatment of choice for **Vitamin D toxicity** because they counteract Vitamin D’s effect on the gut and kidneys. * **Growth:** In children, the chronic use of steroids can lead to growth retardation partly due to these alterations in calcium and bone metabolism.

Q: Which hormone inhibits both resorption and formation of bone?

Glucocorticoids. **Explanation:** Glucocorticoids have a profound, dual inhibitory effect on bone metabolism, making them a common cause of secondary osteoporosis. 1. **Why Glucocorticoids are correct:** * **Inhibition of Formation:** They directly inhibit **osteoblast** proliferation and differentiation. They also increase osteoblast and osteocyte apoptosis, leading to a significant decrease in bone formation. * **Stimulation of Resorption:** While they primarily inhibit formation, they also promote bone resorption by increasing the expression of **RANKL** and decreasing **Osteoprotegerin (OPG)**, which activates osteoclasts. * *Note:* In the context of this specific physiological question, Glucocorticoids are unique because they suppress the cellular activity of the "Bone Remodeling Unit" as a whole, though the net result is rapid bone loss. 2. **Why other options are incorrect:** * **Estrogen:** Inhibits bone resorption (by inducing osteoclast apoptosis) but generally supports bone maintenance; it does not inhibit formation. * **Vitamin D (Calcitriol):** Primarily promotes bone mineralization (formation) by increasing intestinal Calcium and Phosphate absorption. While it can stimulate osteoclasts at high levels, its physiological role is bone health. * **Parathormone (PTH):** Increases bone resorption (via RANKL) to raise serum calcium. Intermittent low doses actually *stimulate* bone formation (anabolic effect), which is the basis for Teriparatide therapy. **High-Yield NEET-PG Pearls:** * **Glucocorticoid-Induced Osteoporosis (GIO):** This is the most common drug-induced osteoporosis. The most rapid bone loss occurs within the first 6 months of therapy. * **Mechanism:** Glucocorticoids also decrease intestinal calcium absorption and increase renal calcium excretion, leading to secondary hyperparathyroidism. * **Bisphosphonates** are the first-line treatment for preventing GIO.

Q: Breastfeeding is maximized during sleep. What is the physiological reason for this phenomenon?

Prolactin levels are elevated during sleep.. **Explanation:** The correct answer is **A. Prolactin levels are elevated during sleep.** **Physiological Basis:** Prolactin is the primary hormone responsible for the synthesis and secretion of milk (lactogenesis). Its secretion follows a distinct **circadian rhythm** and is highly influenced by the sleep-wake cycle. Prolactin levels begin to rise shortly after the onset of sleep, reaching their peak during the early morning hours (REM and non-REM stages). This nocturnal surge occurs independently of the suckling stimulus, though suckling further enhances release via the neuroendocrine reflex. Therefore, the physiological increase in prolactin during sleep ensures maximal milk production capacity during the night and early morning. **Analysis of Incorrect Options:** * **Option B:** While rest is beneficial for maternal well-being, "rest" itself is not the primary physiological driver of milk synthesis; the hormonal milieu (prolactin) is the definitive factor. * **Option C:** Proximity may facilitate the *opportunity* for feeding, but it does not explain the underlying *physiological* mechanism of increased milk availability. * **Option D:** This is incorrect because prolactin secretion is highly dependent on sleep status and the circadian clock. **NEET-PG High-Yield Pearls:** * **Source:** Prolactin is secreted by **Lactotrophs** (Acidophils) in the Anterior Pituitary. * **Inhibitory Control:** Unlike most pituitary hormones, Prolactin is under tonic inhibition by **Dopamine** (Prolactin-Inhibiting Hormone) from the hypothalamus. * **Stimulatory Factors:** TRH (Thyrotropin-releasing hormone) and Oxytocin can stimulate prolactin release. * **Clinical Correlation:** Night-time breastfeeding is often encouraged to maintain a high milk supply and can also prolong **lactational amenorrhea** due to the inhibitory effect of prolactin on GnRH.

Question 1

Which of the following inhibits prolactin secretion?

Accepted Answer

Dopamine

Answer

Haloperidol

Answer

GABA (Gamma-aminobutyric acid)

Answer

Neurophysin

Question 2

Glucagon is secreted by which cells?

Accepted Answer

Alpha cells of pancreas

Answer

Beta cells of pancreas

Answer

Gamma cells of pancreas

Answer

None of the above

Question 3

All of the following statements regarding calcium are true except:

Accepted Answer

Intestinal calcium absorption efficiency is inversely related to calcium intake.

Answer

It serves as a second messenger for the actions of many hormones.

Answer

Tubular reabsorption of calcium is regulated by parathyroid hormone.

Answer

Ionized calcium in the plasma exerts physiological effects.

Question 4

Refeeding edema is due to increased release of-

Accepted Answer

Insulin

Answer

Growth hormone

Answer

Glucocorticoids

Answer

Thyroxine

Question 5

All the following factors stimulate growth hormone secretion except?

Accepted Answer

Increased blood glucose

Answer

Deep sleep

Answer

Increased blood amino acids

Answer

Exercise

Question 6

What is the effect of steroids on calcium?

Accepted Answer

Increased excretion of calcium from the kidney

Answer

Increased plasma calcium level

Answer

Increased absorption of calcium from the gut

Answer

None of the above

Question 7

Which hormone inhibits both resorption and formation of bone?

Accepted Answer

Glucocorticoids

Answer

Estrogen

Answer

Vitamin D

Answer

Parathormone

Question 8

Breastfeeding is maximized during sleep. What is the physiological reason for this phenomenon?

Accepted Answer

Prolactin levels are elevated during sleep.

Answer

Maternal and infant rest promotes increased milk production.

Answer

The infant's proximity to the mother during sleep facilitates a continuous feeding reflex.

Answer

Breastfeeding frequency is independent of sleep status.

Question 9

Which of the following statements regarding insulin is true?

Accepted Answer

Insulin is composed of two chains linked by three disulfide bonds.

Answer

Insulin circulates in the blood bound to RBCs.

Answer

Insulin is synthesized by the alpha cells of the islets of Langerhans.

Answer

The elimination half-life of insulin is 60 minutes after subcutaneous injection.

Question 10

All of the following are caused by accidental transection of the pituitary stalk, except:

Accepted Answer

Diabetes mellitus

Answer

Polyuria

Answer

Galactorrhea

Answer

Diabetes insipidus

Endocrinology — MCQs

Endocrinology — MCQs

On this page

Practice by Chapter

Want unlimited practice?