Endocrinology — MCQs

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 811: Which hormone acts on JAK-STAT kinase receptor?

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

Explanation: ***GH*** - **Growth Hormone (GH)** binds to a **cytokine receptor** that lacks intrinsic tyrosine kinase activity and instead signals through associated **JAK-STAT kinases**. - This binding leads to **JAK phosphorylation**, which then phosphorylates and activates **STAT proteins**, regulating gene expression. *TSH* - **Thyroid-stimulating hormone (TSH)** acts on a **G protein-coupled receptor** to stimulate thyroid hormone production and release. - Its signaling pathway primarily involves the activation of **adenylyl cyclase** and increases in **cAMP**, not the JAK-STAT pathway. *Thyroxine* - **Thyroxine (T4)** is a **thyroid hormone** that primarily acts by binding to **intracellular nuclear receptors**, which then regulate gene transcription. - It directly influences gene expression, rather than signaling through cell surface receptors and kinase pathways like JAK-STAT. *FSH* - **Follicle-stimulating hormone (FSH)**, like TSH, signals through a **G protein-coupled receptor** on target cells in the gonads. - This activation primarily leads to an increase in **intracellular cAMP levels** to mediate its effects on gamete production and hormone synthesis.

Question 812: Which of the following actions of growth hormone (GH) is primarily mediated by insulin-like growth factor 1 (IGF-1)?

A. Lipolysis
B. Sodium retention
C. Linear growth and bone development (Correct Answer)
D. Insulin resistance

Explanation: ***Linear growth and bone development*** - **IGF-1 (Somatomedin C)** is the primary mediator of growth hormone's effects on **linear growth and skeletal development** - IGF-1 is produced primarily in the liver in response to GH stimulation - Acts on **epiphyseal growth plates** to promote chondrocyte proliferation and differentiation - Mediates **protein synthesis, muscle growth, and bone mineralization** - This represents the classic **somatomedin hypothesis** - GH stimulates IGF-1 production, which then mediates growth effects *Lipolysis* - Growth hormone **directly** promotes lipolysis through GH receptors on adipocytes - This leads to breakdown of triglycerides into free fatty acids and glycerol - This is a **direct metabolic effect** of GH, independent of IGF-1 *Insulin resistance* - GH **directly** induces insulin resistance through its own receptors - This is one of the **diabetogenic effects** of GH - While IGF-1 can influence insulin sensitivity, insulin resistance is primarily a **direct GH effect** *Sodium retention* - GH has **direct effects** on renal tubules to promote sodium and water retention - This antinatriuretic effect occurs through GH receptors in the kidney - Not primarily mediated by IGF-1

Question 813: 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 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: 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 816: 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 817: 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 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: 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 820: 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.

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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