Endocrinology — MCQs

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 821: How does adrenaline affect insulin secretion?

A. Stimulation of delta cells
B. Stimulation of G cells
C. Inhibition of beta cells (Correct Answer)
D. Stimulation of beta cells

Explanation: ***Inhibition of beta cells*** - **Adrenaline** (epinephrine) binds to **alpha-2 adrenergic receptors** on pancreatic beta cells, which are coupled to inhibitory G-proteins. - This binding leads to **decreased cAMP levels** and hyperpolarization of the beta cell membrane, ultimately inhibiting insulin release. *Stimulation of delta cells* - **Delta cells** produce **somatostatin**, which generally inhibits the secretion of insulin and glucagon. - While adrenaline can have various systemic effects, its primary direct action on insulin secretion is not through stimulating delta cells. *Stimulation of g cells* - **G cells** in the stomach produce **gastrin**, a hormone involved in gastric acid secretion. - Adrenaline's primary physiological role in glucose metabolism does not involve direct stimulation of G cells to influence insulin secretion. *Stimulation of beta cells* - **Stimulation of beta cells** would lead to increased insulin secretion. - Adrenaline's physiological role, particularly in **stress responses**, is to raise blood glucose, which is achieved in part by **reducing insulin availability** to ensure glucose enters the bloodstream rather than tissues.

Question 822: Wolff–Chaikoff effect is due to?

A. Decreased iodination of MIT
B. Excess iodine intake (Correct Answer)
C. Suppression of TSH secretion
D. Decreased conversion of T4 to T3

Explanation: ***Excess iodine intake*** - The **Wolff-Chaikoff effect** is a phenomenon where a high intake of iodine acutely **inhibits thyroid hormone synthesis** and release. - This effect protects the body from excessive thyroid hormone production during periods of very high iodine availability. *Decreased iodination of MIT* - While the Wolff-Chaikoff effect does inhibit **iodination**, the direct cause is the excessive iodine itself, which triggers an autoregulatory shutdown. - Decreased iodination is a *consequence* of the high iodine leading to inhibition of thyroid peroxidase activity, but not the primary cause of the effect. *Suppression of TSH secretion* - **TSH (Thyroid Stimulating Hormone)** secretion is primarily regulated by negative feedback from thyroid hormones (T3 and T4) and TRH from the hypothalamus. - The Wolff-Chaikoff effect directly involves the thyroid gland's response to iodine and is not primarily mediated by TSH suppression. *Decreased conversion of T4 to T3* - The **conversion of T4 to T3** primarily occurs in peripheral tissues, mediated by deiodinase enzymes. - The Wolff-Chaikoff effect focuses on the inhibition of **iodine organification** and hormone release within the thyroid gland itself, not peripheral conversion.

Question 823: Which of the following statements about ghrelin is false?

A. Stimulates appetite
B. Stimulates growth
C. Produced by stomach cells
D. Directly regulates thyroid hormone secretion (Correct Answer)

Explanation: ***Directly regulates thyroid hormone secretion*** - **Ghrelin** does NOT directly regulate **thyroid hormone secretion** or the **hypothalamic-pituitary-thyroid (HPT) axis**. - Ghrelin's primary physiological roles are related to **appetite stimulation**, **growth hormone release**, and **energy balance**. - While there may be indirect metabolic interactions, ghrelin has no established direct regulatory role in **TSH** or **thyroid hormone** production. *Produced by stomach cells* - This statement is **true**; **ghrelin** is predominantly produced by **P/D1 cells** (also called X/A-like cells) in the **fundus of the stomach**. - These cells release ghrelin primarily when the stomach is empty, signaling hunger to the brain. *Stimulates appetite* - This statement is **true**; ghrelin is often referred to as the "**hunger hormone**" because it acts on the **arcuate nucleus** of the **hypothalamus** to increase food intake. - Its levels rise before meals and decrease after eating, playing a crucial role in the **short-term regulation of appetite**. *Stimulates growth* - This statement is **true**; **ghrelin** is a potent stimulator of **growth hormone (GH) release** from the **anterior pituitary gland**. - It acts on **growth hormone secretagogue receptors (GHS-R)** on **somatotrophs** to promote GH secretion, contributing to its role in **growth** and **metabolism**.

Question 824: Which of the following hormones is secreted by acidophils in the anterior pituitary gland?

A. GH (Correct Answer)
B. TSH
C. ACTH
D. FSH

Explanation: ***GH*** - **Growth Hormone (GH)** is secreted by **somatotrophs**, which are a type of acidophil cell in the anterior pituitary. - GH plays a crucial role in **growth**, **metabolism**, and cell reproduction. - **Note**: Prolactin is also secreted by acidophils (lactotrophs), but among the given options, only GH is an acidophil hormone. *TSH* - **Thyroid-stimulating hormone (TSH)** is secreted by **thyrotrophs**, which are **basophil** cells in the anterior pituitary. - TSH stimulates the **thyroid gland** to produce thyroid hormones. *ACTH* - **Adrenocorticotropic hormone (ACTH)** is secreted by **corticotrophs**, which are another type of **basophil** cell. - ACTH stimulates the **adrenal cortex** to secrete glucocorticoids. *FSH* - **Follicle-stimulating hormone (FSH)** is secreted by **gonadotrophs**, which are also **basophil** cells. - FSH is involved in the **development of follicles** in the ovaries and **spermatogenesis** in the testes.

Question 825: What is the major adrenal androgen produced by the adrenal glands?

A. Testosterone
B. 11-hydroxy derivative of androstenedione
C. Dehydroepiandrosterone (DHEA) (Correct Answer)
D. Cortisol

Explanation: ***Dehydroepiandrosterone (DHEA)*** - **Dehydroepiandrosterone (DHEA)**, or specifically **dehydroepiandrosterone sulfate (DHEA-S)**, is the major adrenal androgen produced by the adrenal cortex and is an important **17-ketosteroid** [1]. - Its production is controlled by **ACTH** and serves as a precursor for more potent androgens and estrogens in peripheral tissues. *Testosterone* - While testosterone is a potent androgen, the primary source in males is the **testes**, and in females, it's produced in smaller amounts by the **ovaries** and peripherally from adrenal androgens. - The adrenal glands produce only a **small fraction** of circulating testosterone directly; they primarily produce precursors like DHEA [1]. *11-hydroxy derivative of androstenedione* - **Androstenedione** is an adrenal androgen precursor, but its 11-hydroxy derivative is not typically referred to as the major adrenal androgen. - The most significant adrenal androgen is DHEA, which is then converted peripherally to other androgens including androstenedione [1]. *Cortisol* - **Cortisol** is the primary **glucocorticoid** produced by the adrenal glands, playing a critical role in stress response, metabolism, and immune function [2]. - While produced by the adrenal cortex, it is a **steroid hormone**, but its primary function is not androgenic; it is a glucocorticoid.

Question 826: Insulin is essential for glucose entry in?

A. Muscle cells (Correct Answer)
B. Beta cells of pancreas
C. Cortical neurons
D. Renal tubular cells

Explanation: ***Muscle cells*** - **Insulin** promotes glucose uptake into **muscle cells** by stimulating the translocation of **GLUT4 transporters** to the cell surface. - In the absence of insulin, **glucose uptake** into quiescent muscle cells is significantly reduced. *Cortical neurons* - **Neurons** in the brain, including cortical neurons, primarily utilize **GLUT1** and **GLUT3 transporters** for glucose uptake, which are **insulin-independent**. - This ensures a constant supply of glucose to the brain, even during periods of low insulin. *Beta cells of pancreas* - **Pancreatic beta cells** use **GLUT2 transporters** for glucose uptake, which are **insulin-independent** and have a high capacity. - This allows beta cells to sense glucose levels and regulate insulin secretion accordingly. *Renal tubular cells* - **Renal tubular cells** reabsorb glucose primarily through **sodium-glucose co-transporters (SGLTs)** and **GLUT2 transporters**, both of which are **insulin-independent**. - Their primary role is in maintaining glucose homeostasis by preventing glucose loss in urine.

Question 827: What is the body's first physiological response to hypoglycemia?

A. Decreased insulin (Correct Answer)
B. Increased glucagon
C. Increased cortisol
D. Increased norepinephrine

Explanation: ***Decreased insulin*** - **Decreased insulin secretion** is the body's **first and earliest** physiological response to falling blood glucose levels, occurring at approximately **80-85 mg/dL**. - This represents the **primary defense mechanism** against hypoglycemia - by reducing insulin release from pancreatic beta cells, the body removes the most potent glucose-lowering stimulus. - This allows blood glucose to stabilize before it drops further, and occurs **before** any active counterregulatory hormones are released. - This is a critical **first-line defense** that prevents the need for more aggressive counterregulatory responses. *Increased glucagon* - **Glucagon** is the **second line of defense** against hypoglycemia, with secretion increasing at glucose levels around **65-70 mg/dL**. - While glucagon is the most important **active counterregulatory hormone** (stimulating glycogenolysis and gluconeogenesis), it is not the *first* response. - The temporal sequence is: insulin suppression occurs first, followed by glucagon release if glucose continues to fall. *Increased cortisol* - **Cortisol** is a late counterregulatory hormone, responding to more severe or prolonged hypoglycemia (glucose <65 mg/dL). - It promotes gluconeogenesis and reduces peripheral glucose utilization over hours, not minutes. - Along with growth hormone, cortisol provides sustained glucose elevation but is not an early response. *Increased norepinephrine* - **Norepinephrine** (and epinephrine) are part of the sympathetic/adrenomedullary response to hypoglycemia at approximately **65-70 mg/dL**. - These catecholamines provide important counterregulation but are activated after insulin suppression has already occurred. - They contribute to both glucose mobilization and the symptomatic (adrenergic) response to hypoglycemia.

Question 828: Which of the following is NOT true about ghrelin?

A. Has anorexic effect (Correct Answer)
B. Stimulates growth hormone release
C. Secreted by gastric fundus cells
D. Increases gastric motility

Explanation: ***Has anorexic effect*** - Ghrelin is known as the **"hunger hormone"** because it stimulates appetite and has an **orexigenic effect**, meaning it increases food intake. - Therefore, stating that it has an **anorexic effect** (reduces appetite) is incorrect. *Stimulates growth hormone release* - Ghrelin is a **natural ligand** for the **growth hormone secretagogue receptor (GHSR)**. - This binding leads to the stimulation of **growth hormone (GH)** release from the pituitary gland. *Secreted by gastric fundus cells* - The primary source of ghrelin in the body is the **P/D1 cells** found in the mucosa of the **gastric fundus**. - Smaller amounts are also produced in the small intestine, pancreas, and hypothalamus. *Increases gastric motility* - Ghrelin is involved in regulating stomach function and can **increase gastric motility** and acid secretion. - This action helps to prepare the digestive system for incoming food.

Question 829: All of the following are actions of cortisol EXCEPT:

A. Increase blood amino acid
B. Increase liver amino acid
C. Decrease blood amino acid (Correct Answer)
D. Decrease liver amino acid

Explanation: ***Decrease blood amino acid*** - This is **NOT** an action of cortisol, making it the correct answer for this EXCEPT question. - Cortisol actually **increases** blood amino acids through **protein catabolism** in muscle and other peripheral tissues. - The catabolic effect mobilizes amino acids from structural proteins, **elevating blood amino acid levels** during stress. *Increase blood amino acid* - This **IS** a correct action of cortisol through **protein breakdown** in peripheral tissues. - Cortisol promotes proteolysis in muscle, releasing amino acids into circulation for use in gluconeogenesis and acute phase protein synthesis. *Increase liver amino acid* - This **IS** a correct action of cortisol as it promotes **hepatic uptake** of amino acids from the bloodstream. - These amino acids are utilized for **gluconeogenesis** and synthesis of plasma proteins in the liver. *Decrease liver amino acid* - This could be considered an action in the sense that cortisol promotes rapid **utilization** of amino acids for gluconeogenesis. - However, the net effect is increased amino acid **flux through** the liver rather than a decrease in availability, as cortisol simultaneously increases hepatic uptake.

Question 830: Laron dwarfism is due to:

A. GH deficiency
B. GHRH deficiency
C. GH receptor resistance (Correct Answer)
D. IGF-1 deficiency

Explanation: ***GH receptor resistance*** - **Laron dwarfism** is caused by a genetic defect in the **growth hormone (GH) receptor**, leading to cellular insensitivity to GH. - Despite normal or elevated GH levels, the body cannot respond to GH, resulting in impaired **insulin-like growth factor 1 (IGF-1)** production and stunted growth. *GH deficiency* - This would involve insufficient production of **growth hormone** from the pituitary gland. - In such cases, administration of exogenous GH would typically be effective, which is not the case in Laron dwarfism due to receptor resistance. *GHRH deficiency* - A deficiency in **growth hormone-releasing hormone (GHRH)** from the hypothalamus would lead to decreased GH secretion. - This would ultimately result in **GH deficiency**, but the primary defect in Laron syndrome is at the receptor level, not in GHRH or GH production. *IGF-1 deficiency* - While Laron dwarfism does result in functionally low **IGF-1** levels due to GH insensitivity, the primary defect is in the GH receptor, which *prevents* GH from stimulating IGF-1 production. - True primary **IGF-1 deficiency** (apart from GH resistance) is a less common cause of dwarfism and would not involve high GH levels.

Practice by Chapter

Principles of Endocrine Regulation

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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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