Endocrinology — MCQs

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 711: Which of the following act through tyrosine kinase receptor:

A. GH
B. FSH
C. Glucagon
D. Insulin (Correct Answer)

Explanation: ***Insulin*** - **Insulin** binds to its specific receptor, which is a **tyrosine kinase receptor**, leading to autophosphorylation and activation of downstream signaling pathways. - This activation results in glucose uptake, metabolism, and storage in target cells. *GH* - **Growth Hormone (GH)** primarily acts through **JAK/STAT signaling pathways** after binding to its receptor, which is a cytokine receptor, not a direct tyrosine kinase receptor. - The GH receptor itself does not possess intrinsic tyrosine kinase activity but rather recruits and activates associated kinases. *FSH* - **Follicle-stimulating hormone (FSH)** mediates its effects by binding to a **G protein-coupled receptor (GPCR)** on target cells. - Activation of the **GPCR** leads to the generation of **cAMP** as a second messenger, which then modulates cellular processes. *Glucagon* - **Glucagon** also acts through a **G protein-coupled receptor (GPCR)** on liver cells. - Binding of glucagon to its receptor activates **adenylyl cyclase**, leading to an increase in **cAMP** levels and subsequently increased glycogenolysis and gluconeogenesis.

Question 712: Which of the following has growth hormone stimulating activity?

A. REM sleep
B. Ghrelin (Correct Answer)
C. IGF-1
D. Somatostatin

Explanation: **Ghrelin** - Ghrelin is a **peptide hormone** primarily produced in the stomach, often referred to as the "**hunger hormone**." - It directly stimulates the secretion of **growth hormone (GH)** from the anterior pituitary gland, acting as a natural **growth hormone secretagogue**. *REM sleep* - While a significant portion of **growth hormone (GH) secretion** occurs during sleep, it is predominantly associated with **slow-wave sleep (NREM stage 3 and 4)** rather than REM sleep. - REM sleep is primarily characterized by dreaming and muscle atonia, with less direct correlation to GH pulsatility. *IGF-1* - **Insulin-like growth factor 1 (IGF-1)** is a hormone primarily produced in the liver in response to growth hormone (GH). - IGF-1 actually exerts **negative feedback** on GH secretion, inhibiting its release rather than stimulating it. *Somatostatin* - **Somatostatin** is a peptide hormone produced in various tissues, including the hypothalamus and pancreas. - It acts as a **potent inhibitor** of growth hormone (GH) secretion from the anterior pituitary gland.

Question 713: Major hormone secreted by zona reticularis of adrenal cortex?

A. Aldosterone
B. Androgens (Correct Answer)
C. Glucocorticoids
D. Mineralocorticoids

Explanation: ***Androgens*** - The **zona reticularis** is the innermost layer of the adrenal cortex and is primarily responsible for the production of **adrenal androgens**, such as dehydroepiandrosterone (DHEA) and androstenedione. - These androgens contribute to secondary sexual characteristics, particularly in females, and can be converted to more potent androgens or estrogens in peripheral tissues. *Aldosterone* - **Aldosterone** is the primary **mineralocorticoid** and is secreted by the outermost layer of the adrenal cortex, the **zona glomerulosa**. - Its main role is to regulate **sodium and potassium balance** and **blood pressure** through its effects on the kidneys. *Glucocorticoids* - **Glucocorticoids**, with **cortisol** being the main one, are secreted by the middle layer of the adrenal cortex, the **zona fasciculata**. - They are involved in **glucose metabolism**, stress response, and immune system modulation. *Mineralocorticoids* - While androgens are steroid hormones, the term **mineralocorticoids** refers specifically to hormones like **aldosterone**, which are produced in the **zona glomerulosa**. - Their primary function is to regulate mineral balance, distinct from the sex hormone activity of androgens.

Question 714: Hypothalamus increases release of all hormones from the pituitary except ?

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

Explanation: ***Prolactin*** - The hypothalamus primarily **inhibits prolactin release** from the anterior pituitary via **dopamine** (prolactin-inhibiting hormone). - All other hormones listed (ACTH, TSH, FSH/LH, GH) are stimulated by their respective hypothalamic releasing hormones. *ACTH* - The hypothalamus **increases ACTH release** by secreting **corticotropin-releasing hormone (CRH)**, which acts on the anterior pituitary. - CRH stimulates corticotrophs to synthesize and release ACTH, which then acts on the adrenal glands. *TSH* - The hypothalamus **increases TSH release** by secreting **thyrotropin-releasing hormone (TRH)**, which stimulates thyrotrophs in the anterior pituitary. - TRH also has a minor stimulatory effect on prolactin release, but its primary role is TSH stimulation. *FSH* - The hypothalamus **increases FSH release** (along with LH) by secreting **gonadotropin-releasing hormone (GnRH)** in a pulsatile manner. - GnRH stimulates gonadotrophs in the anterior pituitary to produce and secrete both FSH and LH.

Question 715: What is the effect of inhibin B hormone?

A. Stimulates Sertoli cell proliferation
B. Inhibits FSH secretion from anterior pituitary (Correct Answer)
C. Directly stimulates seminiferous tubule development
D. Directly enhances spermatogenesis rate

Explanation: ***Inhibits FSH secretion from anterior pituitary*** - **Inhibin B** is a hormone produced by the **Sertoli cells** in males and **granulosa cells** in females. - Its primary function is to provide **negative feedback** to the anterior pituitary, specifically **inhibiting the release of follicle-stimulating hormone (FSH)**. *Stimulates Sertoli cell proliferation* - **FSH** (not inhibin B) is responsible for stimulating **Sertoli cell proliferation** and differentiation. - **Inhibin B** is produced by mature Sertoli cells, indicating their functional status rather than promoting their growth. *Directly stimulates seminiferous tubule development* - **FSH** and **testosterone** are the primary hormones crucial for the development and maintenance of the **seminiferous tubules**. - **Inhibin B** acts indirectly by regulating FSH, but it does not directly stimulate tubule development. *Directly enhances spermatogenesis rate* - While **inhibin B** production is correlated with the rate of spermatogenesis (it's high when spermatogenesis is active), it does not directly enhance the process. - **FSH** and **testosterone** are the direct hormonal regulators that enhance the rate of **spermatogenesis**.

Question 716: The hormone that links obesity and puberty

A. Ghrelin
B. Leptin (Correct Answer)
C. Thyroid hormone
D. Growth hormone

Explanation: ***Leptin*** - **Leptin** is a hormone produced by **adipose tissue** (fat cells) that signals satiety and plays a crucial role in regulating energy balance. Because it is directly proportional to the amount of body fat, higher levels associated with **obesity** can accelerate the onset of puberty. - High leptin levels are thought to signal to the **hypothalamus** that there are sufficient energy reserves for reproduction, thereby triggering the cascade of hormonal events necessary for **puberty**. *Ghrelin* - **Ghrelin** is an appetite-stimulating hormone primarily produced in the stomach, often referred to as the "**hunger hormone.**" - It does not directly link obesity with the initiation of puberty; its primary role is in short-term appetite regulation and energy homeostasis. *Thyroid hormone* - **Thyroid hormones** (T3 and T4) are essential for **growth, development**, and **metabolic rate**. - While thyroid dysfunction can affect overall growth and energy metabolism, it does not directly link obesity to the timing of puberty initiation. *Growth hormone* - **Growth hormone (GH)** is critical for linear growth during childhood and adolescence and influences metabolism. - While GH is vital for overall development, it does not directly mediate the connection between the *amount of adipose tissue* and the *onset of puberty* in the way leptin does.

Question 717: Regarding thyroid hormone all are true except:

A. T4 has the maximum plasma concentration
B. T3 is more avidly bound to nuclear receptors than T4
C. T3 is more active than T4
D. T4 has shorter half life than T3 (Correct Answer)

Explanation: ***T4 has shorter half-life than T3*** - This statement is incorrect because **T4 (thyroxine) has a significantly longer half-life (approximately 7 days)** compared to **T3 (triiodothyronine), which has a half-life of about 1-2 days**. - The longer half-life of T4 allows for a more stable and sustained effect, acting as a prohormone. *T4 has the maximum plasma concentration* - **T4 is secreted in much larger quantities from the thyroid gland than T3 (about 80% T4 vs. 20% T3)**, leading to a higher concentration in the plasma. - This high plasma concentration of T4 makes it the primary circulating thyroid hormone, mostly bound to plasma proteins. *T3 is more avidly bound to nuclear receptors than T4* - **T3 binds to nuclear thyroid hormone receptors with 10 to 15 times greater affinity than T4**, making it the more potent and biologically active form. - This stronger binding affinity is crucial for T3's direct physiological effects on target cells. *T3 is more active than T4* - **T3 is considered the metabolically active form of thyroid hormone**, directly mediating most physiological effects by binding to nuclear receptors. - T4 acts largely as a **prohormone**, being deiodinated in peripheral tissues to form T3, which then exerts metabolic activity.

Question 718: Which of the following compounds antagonizes the actions of insulin?

A. Substance P
B. Growth hormone (Correct Answer)
C. Neuropeptide Y
D. Vasoactive intestinal peptide

Explanation: ***Growth hormone*** - **Growth hormone (GH)** is a potent **anti-insulin hormone** that raises blood glucose by promoting **gluconeogenesis** and reducing glucose utilization by peripheral tissues. - It decreases **insulin sensitivity** in target tissues like muscle and adipose tissue, often leading to a temporary state of **insulin resistance**. *Substance P* - **Substance P** is a **neuropeptide** involved in pain transmission and inflammation, and its primary actions do not directly involve glucose metabolism or insulin antagonism. - While it can influence local metabolic processes, it does not exert systemic effects on insulin action. *Neuropeptide Y* - **Neuropeptide Y (NPY)** is a **neurotransmitter** primarily involved in stimulating appetite and reducing energy expenditure, playing a role in weight regulation. - Although it affects metabolic balance, NPY does not directly antagonize insulin's actions on glucose uptake or utilization. *Vasoactive intestinal peptide* - **Vasoactive intestinal peptide (VIP)** is a **neurotransmitter** and hormone that primarily affects smooth muscle relaxation, exocrine and endocrine secretions, and local blood flow. - It does not directly antagonize insulin's effects on glucose metabolism or directly impact insulin sensitivity in a significant way.

Question 719: Sympathetic stimulation has the following effect on insulin release

A. Inhibition followed by stimulation
B. No effect
C. Inhibition (Correct Answer)
D. Stimulation

Explanation: ***Inhibition*** - **Sympathetic nervous system** activation primarily leads to **inhibition** of insulin release through **alpha-2 adrenergic receptors** on pancreatic beta cells. - This effect is crucial during stress or exercise, as it helps to conserve glucose for vital organs by limiting its uptake into peripheral tissues. *Inhibition followed by stimulation* - While sympathetic activation primarily inhibits insulin release, there can be a **minor stimulatory effect** via **beta-2 adrenergic receptors** at higher concentrations of catecholamines or in specific physiological contexts, but the predominant initial effect is inhibition. - This option does not represent the primary and immediate action of typical sympathetic stimulation on insulin secretion. *No effect* - This is incorrect as the pancreatic beta cells are richly innervated by the **autonomic nervous system**, and sympathetic activity has a well-established direct influence on insulin secretion. - The body's need to regulate blood glucose tightly under stress or activity necessitates a direct effect from the sympathetic nervous system. *Stimulation* - **Stimulation of insulin release** is predominantly mediated by the **parasympathetic nervous system** (via acetylcholine) and high blood glucose levels. - Sympathetic stimulation generally exerts a counter-regulatory effect to ensure glucose availability during periods of increased demand.

Question 720: At the cellular level the physiological effects of human growth hormone are mediated by?

A. Insulin
B. Prolactin
C. Somatotropin
D. Insulin-like growth factors (Correct Answer)

Explanation: ***Insulin-like growth factors*** - The primary mechanism by which **growth hormone (GH)** exerts its physiological effects is by stimulating the production of **insulin-like growth factors (IGFs)**, particularly **IGF-1**. - **IGF-1** then mediates most of the **growth-promoting actions** of GH on target tissues through the **somatomedin hypothesis**. *Insulin* - **Insulin** is a hormone primarily involved in regulating **glucose metabolism** by promoting glucose uptake and utilization by cells. - While GH can influence **insulin sensitivity**, insulin itself does not mediate the primary growth-promoting effects of GH. *Prolactin* - **Prolactin** is a hormone primarily associated with **lactation** and **mammary gland development**. - It has distinct functions from growth hormone and does not mediate its growth-promoting actions. *Somatotropin* - **Somatotropin** is simply another name for **human growth hormone (hGH)** itself. - The question asks how the effects *of* growth hormone are mediated at the cellular level, implying a **downstream mediator**, not the hormone itself.

Practice by Chapter

Principles of Endocrine Regulation

Practice Questions

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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