Endocrinology Practice Questions

Q: Which hormone increases with age?

FSH. **Explanation:** The correct answer is **FSH (Follicle-Stimulating Hormone)**. **1. Why FSH increases with age:** As individuals age, there is a progressive decline in gonadal function (menopause in females and andropause in males). In females, the depletion of ovarian follicles leads to a significant decrease in **Estrogen and Inhibin**. Since Inhibin and Estrogen normally exert negative feedback on the anterior pituitary and hypothalamus, their absence leads to a compensatory, marked rise in **FSH** (and to a lesser extent, LH). FSH levels >40 mIU/mL are a diagnostic hallmark of menopause. **2. Why the other options are incorrect:** * **GH (Growth Hormone):** GH levels peak during puberty and decline steadily with age (somatopause), contributing to reduced muscle mass and increased adiposity in the elderly. * **Prolactin:** Prolactin levels generally remain stable or slightly decrease with age, particularly in postmenopausal women due to the lack of estrogenic stimulation of lactotrophs. * **Insulin:** While insulin *resistance* often increases with age (leading to Type 2 Diabetes), the actual basal insulin secretion and the pancreatic beta-cell response to glucose typically **decrease** or remain impaired due to islet cell atrophy. **3. High-Yield Clinical Pearls for NEET-PG:** * **Hormones that Decrease with Age:** GH, Melatonin, DHEA (Adrenopause), Testosterone, Estrogen, and Aldosterone. * **Hormones that Increase with Age:** FSH, LH, PTH (due to Vitamin D deficiency/renal decline), and Norepinephrine. * **Stable Hormones:** Thyroid hormones (T3/T4) generally remain stable, though the risk of hypothyroidism increases. * **Key Fact:** FSH is the most sensitive marker for the onset of menopause.

Q: Which of the following is NOT an action of GLP-1?

Increases gastric emptying. **Explanation:** Glucagon-like peptide-1 (GLP-1) is an **incretin hormone** secreted by the L-cells of the distal ileum and colon in response to food intake. Its primary physiological role is to lower postprandial blood glucose levels and promote satiety. **Why Option C is the correct answer:** GLP-1 actually **slows gastric emptying** (decreases gastric motility). By delaying the passage of food from the stomach to the duodenum, it slows the absorption of nutrients into the bloodstream, preventing rapid spikes in postprandial glucose. Therefore, "increasing gastric emptying" is physiologically incorrect. **Analysis of Incorrect Options:** * **A. Increases insulin release:** GLP-1 stimulates glucose-dependent insulin secretion from pancreatic beta cells. This is known as the "incretin effect." * **B. Decreases glucagon release:** It suppresses glucagon secretion from pancreatic alpha cells, which reduces hepatic glucose production. * **D. Reduces appetite:** GLP-1 acts on the hypothalamus to increase satiety and reduce food intake, contributing to weight loss. **High-Yield Clinical Pearls for NEET-PG:** * **Incretin Effect:** Oral glucose causes a much higher insulin response than intravenous glucose due to the release of GLP-1 and GIP. * **Degradation:** Endogenous GLP-1 is rapidly degraded by the enzyme **Dipeptidyl Peptidase-4 (DPP-4)**. * **Pharmacology:** GLP-1 agonists (e.g., Liraglutide, Semaglutide) are used to treat Type 2 Diabetes and obesity. They are contraindicated in patients with a history of Medullary Thyroid Carcinoma or MEN 2 syndrome.

Q: What is the main product of the fetal adrenal gland?

DHEA-S. **Explanation:** The fetal adrenal gland is a unique, highly active organ characterized by a massive **"fetal zone"** (comprising about 80% of the gland), which lacks the enzyme **3β-hydroxysteroid dehydrogenase (3β-HSD)**. 1. **Why DHEA-S is correct:** Due to the deficiency of 3β-HSD, the fetal adrenal cannot convert pregnenolone to progesterone. Instead, it shunts precursors toward the androgen pathway. It produces large quantities (up to 200 mg/day) of **Dehydroepiandrosterone sulfate (DHEA-S)**. This DHEA-S serves as the essential precursor for the placenta to synthesize **Estriol (E3)**, which is a key marker of fetal well-being. 2. **Why other options are incorrect:** * **Cortisol:** While the definitive zone produces some cortisol (essential for lung maturation), it is not the *main* product. Most fetal cortisol is actually derived from maternal sources or converted from cortisone. * **Testosterone:** While DHEA-S is an androgen precursor, the adrenal gland itself does not primarily secrete testosterone; this occurs mainly in the fetal Leydig cells of the testes. * **Progesterone:** The fetal adrenal cannot produce progesterone due to the lack of 3β-HSD. Progesterone is primarily supplied to the fetus by the **placenta**. **High-Yield Clinical Pearls for NEET-PG:** * **Size:** At birth, the fetal adrenal is disproportionately large (similar in size to the kidney) but undergoes rapid involution of the fetal zone post-delivery. * **Estriol (E3) Marker:** A sudden drop in maternal serum estriol indicates **fetal distress**, as its synthesis requires a functional fetal adrenal (to produce DHEA-S) and a functional fetal liver (for 16-hydroxylation). * **ACTH Control:** The fetal zone is primarily regulated by fetal ACTH and hCG.

Q: Growth hormone is not produced during which of the following conditions?

Paradoxical sleep. Growth hormone (GH) secretion is pulsatile and regulated by various physiological stimuli. Understanding the relationship between sleep architecture and metabolic states is crucial for NEET-PG. ### **Explanation of the Correct Answer** Growth hormone secretion is highly dependent on the stages of sleep. The primary surge of GH occurs during **Deep Sleep (Stage N3 of NREM sleep)**, specifically during the first few hours of the night. Conversely, during **Paradoxical Sleep (REM sleep)**, GH secretion is significantly inhibited. This is why GH levels are at their lowest during the REM phase, making Option D the correct answer. ### **Analysis of Incorrect Options** * **A. Deep Sleep:** This is the period of maximal GH secretion. The surge is linked to the onset of slow-wave sleep (SWS). * **B. Hypoglycemia:** Low blood glucose is a potent stimulator of GH. GH acts as a counter-regulatory hormone that increases blood glucose by antagonizing insulin and promoting gluconeogenesis. * **C. Low Free Fatty Acid (FFA):** GH promotes lipolysis. Therefore, a decrease in circulating FFAs acts as a stimulus for GH release, while high FFA levels inhibit it. ### **Clinical Pearls for NEET-PG** * **Stimulators of GH:** GHRH, Ghrelin (produced by the stomach), fasting/starvation, exercise, trauma, and amino acids (Arginine). * **Inhibitors of GH:** Somatostatin, Hyperglycemia, Obesity, and Somatomedins (IGF-1) via negative feedback. * **Gold Standard Test:** The Insulin Tolerance Test (ITT) is the gold standard for diagnosing GH deficiency because it induces hypoglycemia, which should normally trigger a GH surge. * **Screening Test:** IGF-1 levels are used for screening because GH levels fluctuate due to their pulsatile nature.

Q: What is the primary mechanism by which catecholamines stabilize blood glucose concentration during hypoglycemia?

Stimulation of gluconeogenesis in the liver.. ### Explanation **Correct Answer: D. Stimulation of gluconeogenesis in the liver.** **Mechanism:** Catecholamines (Epinephrine and Norepinephrine) act as counter-regulatory hormones during hypoglycemia. They primarily stabilize blood glucose by stimulating **hepatic gluconeogenesis** (the synthesis of glucose from non-carbohydrate precursors like lactate and amino acids) and **hepatic glycogenolysis**. Epinephrine activates $\beta_2$ receptors in the liver, increasing cAMP levels, which activates protein kinase A, leading to the induction of key gluconeogenic enzymes. **Analysis of Incorrect Options:** * **Option A:** While catecholamines do stimulate glycogen phosphorylase in muscles, muscle tissue lacks the enzyme **Glucose-6-Phosphatase**. Therefore, muscle glycogen is broken down into lactate (via glycolysis) rather than being released directly as free glucose into the blood. * **Option B:** Catecholamines **promote** glycogenolysis (breakdown of glycogen) to increase blood sugar; inhibiting it would worsen hypoglycemia. * **Option C:** Catecholamines actually **inhibit** insulin release (via $\alpha_2$ receptors) and stimulate glucagon release. Inhibiting insulin is crucial during hypoglycemia to prevent further glucose uptake by peripheral tissues. **High-Yield NEET-PG Pearls:** * **Dual Action:** Epinephrine increases glucose production (liver) and decreases glucose utilization (peripheral tissues). * **Receptor Specificity:** Hepatic glucose production is mediated by $\beta_2$ and $\alpha_1$ receptors, while the inhibition of insulin secretion is mediated by $\alpha_2$ receptors in pancreatic beta cells. * **Hierarchy of Response:** In hypoglycemia, the first line of defense is the suppression of insulin, followed by a rise in glucagon and epinephrine. Cortisol and Growth Hormone act later (4–6 hours) to maintain glucose levels.

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).

Question 1

Which of the following statements is true about estrogen?

Accepted Answer

Estradiol is the most potent among estradiol, estriol, and estrone.

Answer

Inhibits osteoblasts.

Answer

Decreases the expression of LDL receptors.

Answer

Is a C19 steroid.

Question 2

Which hormone increases with age?

Accepted Answer

FSH

Answer

GH

Answer

Prolactin

Answer

Insulin

Question 3

Which of the following is NOT an action of GLP-1?

Accepted Answer

Increases gastric emptying

Answer

Increases insulin release

Answer

Decreases glucagon release

Answer

Reduces appetite

Question 4

What is the main product of the fetal adrenal gland?

Accepted Answer

DHEA-S

Answer

Cortisol

Answer

Testosterone

Answer

Progesterone

Question 5

Growth hormone is not produced during which of the following conditions?

Accepted Answer

Paradoxical sleep

Answer

Deep sleep

Answer

Hypoglycemia

Answer

Low free fatty acid content in the body

Question 6

What is the primary mechanism by which catecholamines stabilize blood glucose concentration during hypoglycemia?

Accepted Answer

Stimulation of gluconeogenesis in the liver.

Answer

Stimulation of glycogen phosphorylase to release glucose from muscle.

Answer

Inhibition of glycogenolysis in the liver.

Answer

Stimulation of insulin release from the pancreas.

Question 7

Which of the following inhibits prolactin secretion?

Accepted Answer

Dopamine

Answer

Haloperidol

Answer

GABA (Gamma-aminobutyric acid)

Answer

Neurophysin

Question 8

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 9

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 10

Refeeding edema is due to increased release of-

Accepted Answer

Insulin

Answer

Growth hormone

Answer

Glucocorticoids

Answer

Thyroxine

Endocrinology — MCQs

Endocrinology — MCQs

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