Endocrinology — MCQs

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 821: The primary site of vasopressin synthesis is

A. Supraoptic nucleus (Correct Answer)
B. Preoptic nucleus
C. Paraventricular nucleus
D. Posterior pituitary

Explanation: ***Supraoptic nucleus*** - The **supraoptic nucleus** of the hypothalamus is the **primary site** for the synthesis of **vasopressin** (also known as antidiuretic hormone or ADH). - Approximately **80% of vasopressin** is produced by the neurosecretory cells in this nucleus. - The synthesized vasopressin is transported down axons to the posterior pituitary for storage and release. *Preoptic nucleus* - The **preoptic nucleus** is involved in various homeostatic functions, including **thermoregulation** and **sleep regulation**, but not the synthesis of vasopressin. - While it has neuronal connections to the hypothalamus, it does not produce ADH. *Paraventricular nucleus* - The **paraventricular nucleus** also synthesizes **both vasopressin and oxytocin**, accounting for approximately **20% of vasopressin production**. - While it does produce vasopressin, the **supraoptic nucleus remains the primary site**, making it the correct answer to this question. - The PVN also plays important roles in stress response and various autonomic functions. *Posterior pituitary* - The **posterior pituitary** (neurohypophysis) is responsible for the **storage and release** of vasopressin and oxytocin, not their synthesis. - These hormones are produced in the hypothalamic nuclei (supraoptic and paraventricular) and then transported down axonal tracts to the posterior pituitary.

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: For how long is Thyroxine stored in the thyroid follicle?

A. 1-2 weeks
B. 1-2 days
C. 2-3 months (Correct Answer)
D. 3-4 years

Explanation: ***2-3 months*** - The thyroid gland stores a substantial amount of **thyroglobulin**, a precursor to **thyroid hormones**, within the **follicular lumen**. - This large storage capacity ensures a **reserve of hormones** sufficient for approximately **2 to 3 months** of normal physiological needs, even if thyroid hormone synthesis were to cease. *1-2 weeks* - This duration is too short for the thyroid's actual storage capacity; the gland is designed for a much longer reserve of **thyroid hormones**. - A 1-2 week supply would make the body highly vulnerable to **rapid onset of hypothyroidism** if synthesis were disrupted. *1-2 days* - This period is extremely short and does not reflect the significant storage capabilities of the thyroid gland, which is unique among endocrine glands for its large **extracellular storage** of hormones. - Such a limited reserve would lead to immediate and severe **hypothyroidism** with any interruption in hormone production. *3-4 years* - While the thyroid does store a considerable amount of hormone, a 3-4 year supply is an **overestimation of its storage capacity**. - The metabolic turnover and requirements of the body for thyroid hormones necessitate replenishment within a few months, rather than years.

Question 824: Growth hormone level is highest during

A. Sleep (Correct Answer)
B. Hypoglycemia
C. Fasting
D. Exercise

Explanation: ***Sleep*** - Growth hormone (GH) secretion is **pulsatile**, with the largest and most consistent pulses occurring during **slow-wave sleep** (deep sleep). - This nocturnal surge contributes significantly to the overall daily GH output and is crucial for growth and metabolic regulation. *Hypoglycemia* - While **hypoglycemia** is a potent stimulus for GH release, it is an acute stress response rather than a state where GH levels are consistently highest. - The body's primary response to hypoglycemia is to raise blood glucose, and while GH helps, it is not the peak physiological secretion time. *Fasting* - **Prolonged fasting** can increase GH secretion as a mechanism to mobilize fat stores and conserve glucose. - However, the peak levels due to fasting are generally less pronounced than the dramatic surge observed during deep sleep. *Exercise* - **Vigorous exercise** can acutely stimulate GH release, particularly with sustained effort. - This increase is typically transient and not as high or consistently cyclical as the secretion during nocturnal sleep.

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: 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 827: Which of the following hormones does not mediate its action through cAMP?

A. Glucagon
B. Follicle stimulating hormone
C. Estrogen (Correct Answer)
D. Luteinizing hormone

Explanation: ***Estrogen*** - **Estrogen** is a **steroid hormone** that mediates its action by binding to intracellular receptors, forming a complex that directly influences gene transcription. - Steroid hormones, due to their **lipophilicity**, can cross the cell membrane and do not typically rely on cell surface receptors or second messengers like cAMP. *Glucagon* - **Glucagon** acts on a **G protein-coupled receptor (GPCR)**, specifically a Gs-coupled receptor, leading to the activation of adenylyl cyclase. - This activation increases the intracellular concentration of **cAMP**, which then activates protein kinase A to mediate its effects, primarily on glucose metabolism. *Follicle stimulating hormone* - **FSH** binds to a **GPCR** on target cells, activating the Gs protein pathway. - This activation stimulates **adenylyl cyclase** and increases intracellular **cAMP** levels, which are critical for its role in gamete development. *Luteinizing hormone* - **LH**, like FSH, binds to a cell surface **GPCR** that activates the Gs protein. - This leads to the stimulation of **adenylyl cyclase** and an increase in **cAMP**, mediating its effects on steroidogenesis and ovulation.

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: 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.

Question 830: 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.

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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