Endocrinology — MCQs

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 811: Which of the following hormones is not stored in cells?

A. Thyroxin
B. Renin
C. Insulin
D. Cortisol (Correct Answer)

Explanation: ***Cortisol*** - Cortisol is a **steroid hormone** that is synthesized from **cholesterol** on demand and is **not stored** in secretory vesicles or elsewhere within cells. - Being **lipophilic**, it diffuses freely across cell membranes immediately after synthesis. - Its release is regulated by the **hypothalamic-pituitary-adrenal (HPA) axis**, with synthesis and immediate secretion occurring upon stimulation. *Insulin* - Insulin is a **peptide hormone** synthesized as **proinsulin** and then cleaved into active insulin. - It is **stored in secretory granules** within pancreatic beta cells, allowing for rapid release in response to elevated blood glucose. *Thyroxine* - Thyroxine (T4) is a **thyroid hormone** that is synthesized from tyrosine and iodine. - It is **stored extracellularly** within the thyroid gland's follicles as part of a large protein called **thyroglobulin**. - Unlike cortisol (which is never stored), thyroxine has a **substantial storage pool** that can last weeks, though the storage is extracellular rather than intracellular. *Renin* - Renin is an **enzyme** produced by the **juxtaglomerular cells** of the kidney. - It is **stored in secretory granules** within these cells and released in response to decreased renal perfusion pressure or sympathetic stimulation.

Question 812: What is the half-life of the thyroid hormone triiodothyronine (T3)?

A. 8 hours
B. 1 day (Correct Answer)
C. 6 hours
D. 10 days

Explanation: ***1 day*** - The **half-life of T3 (triiodothyronine)** is approximately **1 day (24 hours)**, making its biological effects relatively rapid compared to T4. - This shorter half-life contributes to its quicker onset and offset of action. *8 hours* - While reflecting a relatively short duration, **8 hours** is not the accepted half-life for T3. - This value is too short for T3, which has a more sustained biological effect. *6 hours* - A half-life of **6 hours** is too short for T3, which has a more sustained effect than such a rapid clearance would suggest. - This would imply a much faster metabolic turnover than observed clinically. *10 days* - **10 days** is longer than the actual **half-life of T4 (thyroxine)**, which is approximately **7 days**. - T4 serves as a prohormone and is more extensively protein-bound, contributing to its prolonged presence in circulation compared to T3.

Question 813: Which of the following statements about thyroid hormone receptors is correct?

A. They directly bind to thyrotropin-releasing hormone (TRH)
B. They directly bind to thyroid-stimulating hormone (TSH)
C. They cause nuclear transcription after binding with T4
D. They are intracellular receptors that mediate gene transcription after binding with T3 or T4, but their primary action is through T3. (Correct Answer)

Explanation: ***They are intracellular receptors that mediate gene transcription after binding with T3 or T4, but their primary action is through T3.*** - **Thyroid hormone receptors** are indeed **intracellular** and act as **ligand-activated transcription factors**, regulating gene expression. - While both **T3** and **T4** can bind, **T3 (triiodothyronine)** is the more potent and active form, binding with much higher affinity to the receptors to exert its primary metabolic effects. *They directly bind to thyrotropin-releasing hormone (TRH)* - **TRH (thyrotropin-releasing hormone)** is produced by the hypothalamus and acts on the **pituitary gland** to stimulate TSH release, not directly on thyroid hormone receptors. - Thyroid hormone receptors bind to thyroid hormones (**T3 and T4**), not to the hypothalamic releasing hormones like TRH. *They directly bind to thyroid-stimulating hormone (TSH)* - **TSH (thyroid-stimulating hormone)** is produced by the pituitary gland and primarily acts on receptors located on the **thyroid gland cells** to stimulate thyroid hormone synthesis and release. - Thyroid hormone receptors are distinct from TSH receptors and bind to the hormones themselves (**T3/T4**), not the stimulating hormone TSH. *Causes nuclear transcription after binding with T4* - While **T4 (thyroxine)** can bind to thyroid hormone receptors, it is primarily a **prohormone**. - T4 is largely converted to the more active **T3** within target cells, and **T3** is the main mediator of nuclear transcription through these receptors.

Question 814: Thyroid hormone binds to which receptor ?

A. Membrane
B. Cytoplasmic
C. Nuclear (Correct Answer)
D. None of the options

Explanation: ***Nuclear*** - Thyroid hormones, being **lipid-soluble**, readily diffuse across the **cell membrane** to bind to receptors located in the nucleus. - This binding directly influences **gene expression** and protein synthesis, mediating the hormone's effects. *Membrane* - Membrane receptors typically bind **water-soluble hormones** (e.g., peptide hormones, catecholamines) that cannot freely cross the cell membrane. - These interactions usually trigger a **second messenger cascade** within the cell. *Cytoplasmic* - While some **steroid hormones** bind to cytoplasmic receptors which then translocate to the nucleus, thyroid hormones bind directly to nuclear receptors. - Cytoplasmic receptors are located in the **cytosol** before their ligand-induced translocation. *None of the options* - This option is incorrect, as thyroid hormones have a specific and well-defined receptor location. - The direct action on **gene regulation** necessitates a nuclear receptor.

Question 815: Which of the following hormones does not increase in response to stress?

A. thyroxine (Correct Answer)
B. None of the options
C. ADH
D. GH

Explanation: ***Correct: Thyroxine*** - **Thyroxine (T4)** does not acutely increase in response to stress - Thyroid hormones are **not part of the immediate stress response** mediated by the HPA axis - During acute stress, **TSH may actually be suppressed** by elevated cortisol - Chronic stress can affect thyroid function, but there is **no immediate surge** in T4 levels like with other stress hormones *Incorrect: ADH* - **Antidiuretic hormone (ADH/vasopressin)** is a key stress hormone - Released rapidly in response to **physical stress, pain, hypovolemia**, and hypotension - Part of the **neurohypophyseal stress response** to maintain blood pressure and volume - Works alongside cortisol in the stress response *Incorrect: GH* - **Growth hormone** levels increase during **acute stress** (physical and psychological) - Stimulated by stress-induced activation of **GHRH** and suppression of somatostatin - Promotes **gluconeogenesis and lipolysis** during metabolic stress - Part of the counter-regulatory hormone response *Incorrect: None of the options* - This option is incorrect because **thyroxine is the correct answer** - Thyroxine does not acutely increase with stress, unlike ADH and GH

Question 816: Which hormone is primarily inhibited by the hypothalamus?

A. TSH
B. FSH
C. CRH
D. Prolactin (Correct Answer)

Explanation: ***Prolactin*** - The hypothalamus secretes **dopamine** (Prolactin Inhibiting Hormone), which tonically inhibits prolactin release from the anterior pituitary. - Unlike most other anterior pituitary hormones, prolactin's primary hypothalamic control is **inhibitory** rather than stimulatory. *TSH* - **Thyroid-stimulating hormone (TSH)** is *stimulated* by **Thyrotropin-Releasing Hormone (TRH)** from the hypothalamus. - The hypothalamus does not primarily inhibit TSH; rather, it promotes its release, which is then regulated by negative feedback from thyroid hormones. *FSH* - **Follicle-stimulating hormone (FSH)** is *stimulated* by **Gonadotropin-Releasing Hormone (GnRH)** from the hypothalamus. - The hypothalamus promotes FSH release, which is essential for gamete production and ovarian follicle development. *CRH* - **Corticotropin-Releasing Hormone (CRH)** is a hormone secreted by the **hypothalamus** itself. - CRH acts on the anterior pituitary to *stimulate* the release of **ACTH**, not inhibit another hormone.

Question 817: 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 818: 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 819: 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 820: 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**.

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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