Endocrinology — MCQs
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The major source of estrogen after menopause is?
Which set of hormones exclusively utilizes nuclear receptors?
Which of the following is true about somatostatin, insulin, and glucagon?
In surgical stress all hormones are increased except:
Aldosterone secretion is maximally stimulated by?
All of the following statements about Insulin like Growth factor - 1 are true, except:
Insulin-mediated transport of glucose is seen in:
Prolactin is synthesized in
During the metabolism of iodine in thyroid synthesis, Wolff-Chaikoff effect is seen due to:
The blood levels of 1,25 dihydroxycholecalciferol are positively regulated by:-
Endocrinology Indian Medical PG Practice Questions and MCQs
Question 721: The major source of estrogen after menopause is?
- A. Aromatization of androgens in granulosa cells of the ovary
- B. Adrenal production of estrogens
- C. Aromatization of androgens in theca cells of ovary
- D. Aromatization of androgens in adipose tissue (Correct Answer)
Explanation: ***Aromatization of androgens in adipose tissue*** - After menopause, ovarian function declines significantly, reducing direct **estrogen production**. - **Adipose tissue** becomes the primary site for the conversion of adrenal androgens (like androstenedione) into estrogens, predominantly **estrone**, via the enzyme **aromatase**. *Aromatization of androgens in granulosa cells of the ovary* - **Granulosa cells** are the primary site of estrogen production in the **premenopausal ovary**, converting androgens from theca cells into estradiol. - After menopause, granulosa cell function and numbers decline significantly, ceasing their role as a major estrogen source. *Adrenal production of estrogens* - The **adrenal glands** primarily produce **androgens** (like DHEA and androstenedione) which are then converted to estrogens in peripheral tissues, especially after menopause. - They do not directly produce significant amounts of estrogen themselves. *Aromatization of androgens in theca cells of ovary* - **Theca cells** in the premenopausal ovary predominantly produce **androgens** (androstenedione and testosterone) under the influence of LH. - These androgens are then transported to granulosa cells for aromatization; theca cells themselves do not produce estrogen.
Question 722: Which set of hormones exclusively utilizes nuclear receptors?
- A. Estrogen, Thyroxine, Insulin
- B. Cortisol, Aldosterone, TSH
- C. Progesterone, Testosterone, Glucagon
- D. Vitamin D, Retinoic acid, Progesterone (Correct Answer)
Explanation: ***Vitamin D, Retinoic acid, Progesterone*** - **Vitamin D**, **retinoic acid**, and **progesterone** are all **lipid-soluble molecules** that can readily cross the cell membrane and bind to **intracellular nuclear receptors**. - Their binding to nuclear receptors directly influences **gene transcription** and protein synthesis. *Estrogen, Thyroxine, Insulin* - While **estrogen** and **thyroxine** utilize nuclear receptors, **insulin** is a peptide hormone that binds to **cell surface receptors**. - **Insulin** activates a signal transduction cascade, rather than directly influencing gene transcription via nuclear receptors. *Cortisol, Aldosterone, TSH* - **Cortisol** and **aldosterone** are steroid hormones that bind to nuclear receptors. - However, **TSH (Thyroid Stimulating Hormone)** is a peptide hormone that binds to **G protein-coupled receptors** on the cell surface of thyroid cells. *Progesterone, Testosterone, Glucagon* - **Progesterone** and **testosterone** are steroid hormones that utilize nuclear receptors. - **Glucagon** is a peptide hormone that binds to **G protein-coupled receptors** on the cell surface of target cells, primarily hepatocytes.
Question 723: Which of the following is true about somatostatin, insulin, and glucagon?
- A. Glucagon blocks insulin and Somatostatin release.
- B. Somatostatin blocks release of insulin and glucagon. (Correct Answer)
- C. Insulin increases glucagon release.
- D. Somatostatin stimulates insulin.
Explanation: ***Somatostatin blocks release of insulin and glucagon.*** - **Somatostatin** acts as a paracrine inhibitor within the **islets of Langerhans**, suppressing the secretion of both **insulin** from beta cells and **glucagon** from alpha cells. - This inhibitory action helps to modulate and fine-tune nutrient absorption and utilization following a meal, preventing excessive fluctuations in blood glucose levels. *Glucagon blocks insulin and Somatostatin release.* - **Glucagon's primary role** is to raise blood glucose by stimulating **hepatic glucose production**, not to block the release of insulin or somatostatin. - In fact, glucagon can stimulate **somatostatin release**, which then acts to inhibit glucagon secretion, forming a negative feedback loop. *Insulin increases glucagon release.* - **Insulin and glucagon** have opposing roles in glucose regulation; insulin's main function is to lower blood glucose, while glucagon raises it. - High insulin levels typically **suppress glucagon secretion**, as the body needs to lower glucose, not raise it further. *Somatostatin stimulates insulin.* - **Somatostatin** is a potent **inhibitor** of insulin release, not a stimulator. - This inhibitory effect helps to prevent rapid and excessive insulin secretion, which could lead to hypoglycemia.
Question 724: In surgical stress all hormones are increased except:
- A. Insulin (Correct Answer)
- B. Epinephrine
- C. ACTH
- D. Cortisol
Explanation: ***Insulin*** - While other **stress hormones** increase, **insulin** levels typically **decrease** or remain stable due to increased **insulin resistance** during surgical stress. - This physiological response aims to maintain **blood glucose** levels for energy during heightened metabolic demands. *Epinephrine* - **Epinephrine** (adrenaline) is a key **catecholamine** released during surgical stress, leading to a "fight or flight" response. - It increases **heart rate**, **blood pressure**, and promotes **gluconeogenesis** to supply quick energy. *ACTH* - **Adrenocorticotropic hormone (ACTH)** is released from the **pituitary gland** in response to surgical stress. - **ACTH** stimulates the adrenal cortex to produce **cortisol**, a critical stress hormone. *Cortisol* - **Cortisol** levels significantly rise during surgical stress, mediated by **ACTH** release. - It plays a crucial role in **modulating inflammation**, **glucose metabolism**, and maintaining **hemodynamic stability**.
Question 725: Aldosterone secretion is maximally stimulated by?
- A. Exogenous steroids
- B. ACTH
- C. Hypernatremia
- D. Hyperkalemia (Correct Answer)
Explanation: ***Hyperkalemia*** - **Hyperkalemia is the most potent direct stimulator** of aldosterone secretion from the zona glomerulosa cells of the adrenal cortex. - Even a small increase in serum potassium (0.1 mEq/L) can significantly increase aldosterone synthesis and secretion. - This is a crucial homeostatic mechanism to promote **renal potassium excretion** via principal cells in the collecting duct, normalizing serum potassium levels. - **Mechanism**: K+ directly depolarizes zona glomerulosa cells → opens voltage-gated Ca2+ channels → increases intracellular Ca2+ → stimulates aldosterone synthesis. *Exogenous steroids* - Exogenous glucocorticoids **suppress the hypothalamic-pituitary-adrenal (HPA) axis** through negative feedback. - They do not stimulate aldosterone secretion; instead, they reduce endogenous corticosteroid production. - Some synthetic steroids may have mineralocorticoid activity themselves, but they don't stimulate endogenous aldosterone. *ACTH* - ACTH has only a **permissive role** in aldosterone secretion, not a primary regulatory role. - While ACTH is required for maintaining the structural integrity of the zona glomerulosa, it is **not the maximal stimulator**. - ACTH primarily regulates **cortisol synthesis** from the zona fasciculata. - The major physiological regulators of aldosterone are **hyperkalemia** and **angiotensin II** (via the renin-angiotensin system). *Hypernatremia* - **Hypernatremia inhibits aldosterone secretion** rather than stimulating it. - Since aldosterone's primary action is to increase sodium reabsorption, elevated sodium levels signal the body to reduce aldosterone to prevent further sodium retention. - This is part of the negative feedback mechanism for sodium homeostasis.
Question 726: All of the following statements about Insulin like Growth factor - 1 are true, except:
- A. Mainly secreted by the pancreas (Correct Answer)
- B. Required for skeletal and cartilage growth
- C. Secretion is stimulated by Growth Hormone
- D. Also known as Somatomedin C
Explanation: ***Mainly secreted by the pancreas*** - **Insulin-like Growth Factor-1 (IGF-1)** is primarily produced by the **liver** in response to **growth hormone (GH)** stimulation, not the pancreas. - While the pancreas does produce some growth factors and hormones, IGF-1 synthesis is predominantly hepatic. *Required for skeletal and cartilage growth* - IGF-1 is a crucial mediator of **growth hormone's effects**, playing a significant role in **linear growth, bone formation**, and **cartilage maintenance**. - It promotes **cell proliferation** and differentiation in various tissues, including bone and cartilage. *Secretion is stimulated by Growth Hormone* - **Growth hormone (GH)** from the pituitary gland stimulates the liver and other tissues to produce IGF-1. - IGF-1 then mediates many of the growth-promoting actions of GH. *Also known as Somatomedin C* - **Somatomedin C** is an older name for **Insulin-like Growth Factor-1 (IGF-1)**. - This term reflects its **growth-promoting actions** and its similarity in structure to **insulin**.
Question 727: Insulin-mediated transport of glucose is seen in:
- A. Seen in adipose tissue (Correct Answer)
- B. Main Mechanism in RBCs
- C. All are true
- D. Via GLUT-2
Explanation: ***Seen in adipose tissue*** - **Adipose tissue** (fat cells) and muscle cells significantly increase their uptake of glucose in response to **insulin**. - This transport is mediated by **GLUT4 transporters**, which are translocated to the cell membrane upon insulin binding. *Main Mechanism in RBCs* - **Red blood cells (RBCs)** primarily utilize **GLUT1 transporters** for glucose uptake. - **GLUT1** is constitutive and **insulin-independent**, meaning its activity is not regulated by insulin. *All are true* - This option is incorrect because the statement regarding RBCs is false, making the collective "all are true" statement inaccurate. *Via GLUT-2* - **GLUT2** is a primary transporter in the **liver, pancreatic β-cells, intestinal epithelial cells**, and **kidney**. - While it facilitates glucose transport, **GLUT2 is insulin-independent** and has a low affinity but high capacity for glucose, primarily involved in sensing and buffering glucose levels rather than insulin-mediated uptake in peripheral tissues.
Question 728: Prolactin is synthesized in
- A. Thalamus
- B. Pituitary (Correct Answer)
- C. Hypothalamus
- D. Pineal gland
Explanation: ***Pituitary*** - Prolactin is primarily synthesized and secreted by the **lactotroph cells** located in the **anterior pituitary gland**. - Its main function is to stimulate **milk production** (lactation) in mammals. *Thalamus* - The thalamus is a large mass of **gray matter** located in the dorsal part of the diencephalon, primarily involved in relaying **sensory and motor signals**, and the regulation of consciousness and sleep. - It does not have a role in hormone synthesis like prolactin. *Hypothalamus* - The hypothalamus produces **releasing and inhibiting hormones** that regulate the pituitary gland, including **prolactin-inhibiting hormone (PIH)**, which is primarily dopamine. - It does not directly synthesize prolactin itself. *Pineal gland* - The pineal gland is primarily responsible for producing **melatonin**, which regulates **sleep-wake cycles** (circadian rhythm). - It has no role in the synthesis of prolactin.
Question 729: During the metabolism of iodine in thyroid synthesis, Wolff-Chaikoff effect is seen due to:
- A. Inhibition of organic binding of iodide (Correct Answer)
- B. Inhibition of iodide trapping mechanism
- C. Inhibition of cAMP response of TSH
- D. Inhibition of proteolysis of Thyroglobulin
Explanation: ***Inhibition of organic binding of iodide*** - The **Wolff-Chaikoff effect** is a temporary inhibition of thyroid hormone synthesis that occurs when a large amount of inorganic iodide is ingested. This high concentration of iodide specifically inhibits the **organification of iodide** (the incorporation of iodide into tyrosyl residues of thyroglobulin). - This effect essentially “pauses” the process of combining iodide with a protein to form thyroid hormones, thus preventing acute iodine overload from leading to excessive hormone production. *Inhibition of iodide trapping mechanism* - Iodide trapping refers to the active transport of iodide into the thyroid follicular cells via the **sodium-iodide symporter (NIS)**. The Wolff-Chaikoff effect does not primarily inhibit this mechanism; rather, it occurs after iodide has already entered the cell. - While very high doses of iodide for prolonged periods can eventually downregulate NIS, the primary acute mechanism of the Wolff-Chaikoff effect is not the inhibition of iodide uptake. *Inhibition of cAMP response of TSH* - **TSH (Thyroid Stimulating Hormone)** acts via **cAMP** to stimulate various steps in thyroid hormone synthesis, including iodide trapping, organification, and hormone release. The Wolff-Chaikoff effect is a direct response of the thyroid gland to excess iodide, independent of TSH signaling. - This option describes a different regulatory mechanism related to TSH signaling rather than the direct impact of high iodide on synthesis. *Inhibition of proteolysis of Thyroglobulin* - **Proteolysis of thyroglobulin** is the final step in thyroid hormone release, where lysosomes cleave T3 and T4 from thyroglobulin and release them into circulation. The Wolff-Chaikoff effect primarily affects hormone synthesis (organification) rather than hormone release. - While prolonged high iodide levels could potentially have downstream effects, the acute and direct effect of Wolff-Chaikoff is upstream in the synthesis pathway.
Question 730: The blood levels of 1,25 dihydroxycholecalciferol are positively regulated by:-
- A. 25 OH cholecalciferol
- B. Magnesium
- C. PTH (Correct Answer)
- D. Calcium
Explanation: ***PTH*** - **Parathyroid hormone (PTH)** is the primary physiological regulator of 1,25-dihydroxycholecalciferol synthesis in the kidneys. - **PTH stimulates the 1-alpha-hydroxylase enzyme**, which converts 25-hydroxycholecalciferol to the active form, 1,25-dihydroxycholecalciferol. *25 OH cholecalciferol* - This is the **precursor molecule** to 1,25-dihydroxycholecalciferol, but its blood level directly reflects overall vitamin D status rather than actively regulating the active form. - While it is the substrate for activated vitamin D, it doesn't directly stimulate its own conversion; rather, **PTH is the key regulator of the conversion process**. *Magnesium* - **Magnesium is a cofactor for many enzymatic reactions**, including those involved in vitamin D metabolism and PTH secretion. - However, it does not directly regulate the blood levels of 1,25-dihydroxycholecalciferol; severe **magnesium deficiency can impair PTH secretion** and action, indirectly affecting vitamin D. *Calcium* - **High blood calcium levels (hypercalcemia) would inhibit PTH release**, thereby negatively regulating 1,25-dihydroxycholecalciferol production. - Conversely, **low calcium levels would stimulate PTH**, which in turn increases 1,25-dihydroxycholecalciferol synthesis to raise calcium levels.
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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