Endocrinology — MCQs
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Insulin is required for glucose transport in all of the following tissues except:
What is the primary effect of GLP-1 on insulin secretion?
Which hormone, together with the catecholamines, enhances the tone of vascular smooth muscle and assists in elevating blood pressure?
The hypothalamus produces several releasing peptides. Which releasing peptide is responsible for the release of adrenocorticotropic hormone (ACTH) from the pituitary?
Which of the following inhibit gonadotropin-releasing hormone pulse secretion?
Enteroinsular axis is mediated through:
Which hormone directly lowers blood calcium levels?
Increased insulin is characterized by all of the following, except:
What is the effect of cortisol on bone metabolism?
Intake of exogenous steroids causes
Endocrinology Indian Medical PG Practice Questions and MCQs
Question 851: Insulin is required for glucose transport in all of the following tissues except:
- A. RBC (Correct Answer)
- B. Skeletal muscles
- C. Adipose tissue
- D. Heart muscles
Explanation: ***RBC*** - **Red blood cells** transport glucose via **GLUT1 transporters**, which are insulin-independent. - This ensures a constant supply of glucose to RBCs for their energy needs, regardless of insulin levels. *Skeletal muscles* - **Skeletal muscle cells** rely on **GLUT4 transporters** for glucose uptake, which are highly **insulin-dependent**. - During exercise, muscle contraction can also stimulate GLUT4 translocation, increasing glucose uptake even without high insulin levels. *Adipose tissue* - **Adipose tissue** also primarily uses **GLUT4 transporters** for glucose uptake, making it highly **insulin-dependent**. - Insulin promotes glucose conversion into fatty acids for storage within adipocytes. *Heart muscles* - **Cardiac muscle cells** also use **GLUT4 transporters** for a significant portion of their glucose uptake, therefore exhibiting **insulin dependence**. - While they can utilize fatty acids as a primary energy source, glucose uptake increases in response to insulin, particularly during periods of high demand.
Question 852: What is the primary effect of GLP-1 on insulin secretion?
- A. Increased aldosterone secretion by adrenal
- B. Increased PTH secretion
- C. Increased insulin secretion from beta-cells of pancreas (Correct Answer)
- D. Increased testosterone secretion from Leydig cells
Explanation: ***Increased insulin secretion from beta-cells of pancreas*** - **Glucagon-like peptide-1 (GLP-1)** is an **incretin hormone** that stimulates **glucose-dependent insulin secretion** from pancreatic beta-cells. - This effect is crucial for maintaining **glucose homeostasis**, especially after a meal. *Increased aldosterone secretion by adrenal* - **Aldosterone secretion** is primarily regulated by the **renin-angiotensin-aldosterone system (RAAS)** and potassium levels, not directly by GLP-1. - Aldosterone's main function is to regulate **sodium and water balance** and **blood pressure**. *Increased PTH secretion* - **Parathyroid hormone (PTH)** secretion is primarily regulated by **serum calcium levels**. - Its main role is to maintain **calcium homeostasis** by affecting bone, kidney, and intestine. *Increased testosterone secretion from Leydig cells* - **Testosterone secretion** from Leydig cells is primarily regulated by **luteinizing hormone (LH)** from the pituitary gland. - GLP-1 has no direct significant role in **gonadal steroidogenesis**.
Question 853: Which hormone, together with the catecholamines, enhances the tone of vascular smooth muscle and assists in elevating blood pressure?
- A. Parathyroid hormone (PTH)
- B. Glucagon (GCG)
- C. Thyroxine (T4)
- D. Cortisol (Correct Answer)
Explanation: ***Cortisol*** - **Cortisol** potentiates the effects of **catecholamines** on **vascular smooth muscle**, leading to increased vasoconstriction and **elevated blood pressure**. - This **synergistic action** is crucial for maintaining vascular tone and immediate blood pressure regulation during stress. *Parathyroid hormone (PTH)* - **PTH** primarily regulates **calcium and phosphate** homeostasis by acting on bone, kidneys, and indirectly on the intestines. - It does not directly cause vasoconstriction or significantly interact with catecholamines to elevate blood pressure. *Glucagon (GCG)* - **Glucagon's** main role is to increase **blood glucose levels** by stimulating hepatic **glycogenolysis** and gluconeogenesis. - While it can have some chronotropic and inotropic effects on the heart, it is not a primary vasoconstrictor or a significant enhancer of catecholamine-mediated vascular tone. *Thyroxine (T4)* - **Thyroxine (T4)** and **triiodothyronine (T3)** play a broad role in **metabolism**, growth, and development. - While thyroid hormones can increase cardiac output and sensitivity to catecholamines, they do not directly enhance vascular smooth muscle tone in the same way cortisol does as a primary pressor.
Question 854: The hypothalamus produces several releasing peptides. Which releasing peptide is responsible for the release of adrenocorticotropic hormone (ACTH) from the pituitary?
- A. Somatostatin
- B. Corticotropin-releasing factor (CRF) (Correct Answer)
- C. Cortisol
- D. Corticosterone
Explanation: ***Corticotropin-releasing factor (CRF)*** - **Corticotropin-releasing factor** (CRF) is a hypothalamic releasing hormone that stimulates the **anterior pituitary gland** to secrete **adrenocorticotropic hormone (ACTH)**. - ACTH then acts on the adrenal cortex to stimulate the production of glucocorticoids, particularly **cortisol**. *Somatostatin* - **Somatostatin** is a hypothalamic hormone that primarily **inhibits** the release of growth hormone (GH) and thyroid-stimulating hormone (TSH) from the anterior pituitary. - It does not directly regulate the release of ACTH. *Corticosterone* - **Corticosterone** is a **glucocorticoid hormone** produced by the adrenal cortex, similar to cortisol, but it is not a hypothalamic releasing peptide. - It plays a role in stress response and metabolism but does not directly stimulate ACTH release from the pituitary; rather, its production is stimulated by ACTH. *Cortisol* - **Cortisol** is the primary **glucocorticoid** produced by the adrenal cortex in humans. - Its release is stimulated by ACTH, and it acts via a **negative feedback loop** to inhibit the release of both CRF from the hypothalamus and ACTH from the pituitary.
Question 855: Which of the following inhibit gonadotropin-releasing hormone pulse secretion?
- A. Prolactin (Correct Answer)
- B. Oxytocin
- C. Thyroxine
- D. Insulin
Explanation: ***Prolactin*** - Elevated levels of **prolactin** inhibit the pulsatile secretion of **gonadotropin-releasing hormone (GnRH)** from the hypothalamus. - This inhibition leads to decreased production of **luteinizing hormone (LH)** and **follicle-stimulating hormone (FSH)** from the pituitary, ultimately affecting gonadal function. *Thyroxine* - **Thyroxine** (thyroid hormone) primarily regulates metabolism and growth, and while it interacts with the reproductive axis, its direct effect is not typically the **inhibition of GnRH pulse secretion**. - Extreme thyroid dysfunction can indirectly impact reproductive hormones, but it's not the primary mechanism of GnRH inhibition. *Oxytocin* - **Oxytocin** is largely involved in **uterine contractions** during labor and **milk ejection** during lactation, and has roles in social bonding. - It does not directly inhibit the pulsatile release of **GnRH**. *Insulin* - **Insulin** is a key hormone in **glucose metabolism** and energy regulation. - While insulin resistance and hyperinsulinemia can affect reproductive function (e.g., in polycystic ovary syndrome, PCOS), it does not **directly inhibit GnRH pulse secretion**.
Question 856: Enteroinsular axis is mediated through:
- A. GLP-1 (Correct Answer)
- B. Nitric oxide
- C. Glucagon
- D. VIP
Explanation: ***GLP-1*** - **Glucagon-like peptide-1 (GLP-1)** is a key **incretin hormone** that mediates the enteroinsular axis by enhancing glucose-dependent insulin secretion from pancreatic beta cells. - It is released from intestinal L-cells in response to nutrient intake, linking nutrient sensing in the gut directly to pancreatic insulin secretion. *Glucagon* - **Glucagon** is a hormone primarily involved in raising **blood glucose** levels, released by pancreatic alpha cells, and acts in opposition to insulin. - While it plays a role in glucose homeostasis, it does not primarily mediate the **enteroinsular axis's** enhancement of insulin secretion. *Nitric oxide* - **Nitric oxide (NO)** is a gaseous signaling molecule involved in various physiological processes, including **vasodilation** and neurotransmission. - It is not considered a primary mediator of the **enteroinsular axis** or incretin effect. *VIP* - **Vasoactive intestinal peptide (VIP)** is a **neuropeptide** that acts as a neurotransmitter and neurohormone, involved in gut motility and secretion. - While it can influence pancreatic function, it is not the main mediator of the **enteroinsular axis** that links nutrient sensing in the gut to enhanced insulin secretion.
Question 857: Which hormone directly lowers blood calcium levels?
- A. Parathyroid hormone
- B. Calcitonin (Correct Answer)
- C. 1, 25-dihydroxycholecalciferol
- D. Vitamin D
Explanation: ***Calcitonin*** - **Calcitonin** is a hormone secreted by the **parafollicular C cells** of the thyroid gland. - Its primary function is to **lower blood calcium levels** by inhibiting osteoclast activity and promoting calcium excretion by the kidneys. - It is the only hormone that directly acts to **decrease serum calcium**. *Parathyroid hormone* - **PTH** is secreted by the parathyroid glands and has the **opposite effect** to calcitonin. - It **increases blood calcium levels** by stimulating osteoclast activity, increasing renal calcium reabsorption, and activating vitamin D. *1,25-dihydroxycholecalciferol* - This is the **active form of vitamin D**, also known as **calcitriol**. - Its main roles are to **increase blood calcium levels** by enhancing calcium absorption from the intestine and promoting bone resorption. *Vitamin D* - **Vitamin D** (cholecalciferol or ergocalciferol) is a precursor that needs to be metabolized into its active form, 1,25-dihydroxycholecalciferol. - Its ultimate effect (via its active form) is to **raise blood calcium levels**, not lower them.
Question 858: Increased insulin is characterized by all of the following, except:
- A. Hypoglycemia
- B. Enhanced fatty acid synthesis
- C. Increased Intracellular potassium
- D. Increased Glucagon secretion (Correct Answer)
Explanation: ***Increased Glucagon secretion*** - **Insulin** primarily functions to lower blood glucose, and its release is typically inhibited by factors that trigger **glucagon** secretion, which aims to raise blood glucose. - Increased insulin would generally lead to **decreased glucagon secretion** as the body attempts to maintain glucose homeostasis. *Increased Intracellular potassium* - Insulin promotes the uptake of **potassium** into cells, particularly muscle and liver cells, by stimulating the **Na+/K+ ATPase pump**. - This action helps to lower serum potassium levels and can be utilized therapeutically in cases of hyperkalemia. *Hypoglycemia* - **Insulin** is the primary hormone responsible for lowering blood glucose levels by promoting glucose uptake by cells and inhibiting hepatic glucose production. - Excess insulin, whether endogenous or exogenous, can lead to **hypoglycemia** if glucose intake does not match insulin action. *Enhanced fatty acid synthesis* - **Insulin** is an anabolic hormone that promotes energy storage, including the conversion of excess glucose into **fatty acids** in the liver and adipose tissue. - This process, known as lipogenesis, is a key mechanism by which insulin contributes to the storage of energy reserves.
Question 859: What is the effect of cortisol on bone metabolism?
- A. Decreased bone matrix (Correct Answer)
- B. Increases calcium absorption
- C. Stimulates osteoblast activity
- D. Increased bone matrix
Explanation: ***Decreased bone matrix*** - Cortisol **inhibits osteoblast activity** and **promotes osteoblast apoptosis**, leading to reduced production of bone matrix components like collagen - It also **increases osteoclast activity**, further contributing to bone breakdown and resulting in a net decrease in bone matrix - This mechanism is the primary cause of **glucocorticoid-induced osteoporosis** *Increases calcium absorption* - Cortisol actually **decreases intestinal calcium absorption** by reducing the sensitivity of the intestines to vitamin D - This effect contributes to **negative calcium balance** and exacerbates bone loss *Stimulates osteoblast activity* - Cortisol has an **inhibitory effect on osteoblast differentiation and function**, leading to reduced bone formation - This suppression of osteoblasts is the opposite of this option and directly contributes to weaker bones *Increased bone matrix* - This is incorrect as cortisol leads to **net bone loss**, not an increase, by inhibiting bone formation and accelerating bone resorption - An increase in bone matrix would require enhanced osteoblast activity, which is the opposite of cortisol's effect
Question 860: Intake of exogenous steroids causes
- A. Adrenal insufficiency (Correct Answer)
- B. Prolonged glucocorticoid exposure
- C. Catecholamine excess
- D. Hyperaldosteronism
Explanation: ***Adrenal insufficiency*** - Exogenous steroids suppress the **hypothalamic-pituitary-adrenal (HPA) axis** through **negative feedback mechanism**. - Chronic use leads to **decreased ACTH secretion**, causing **adrenal cortex atrophy** and **secondary adrenal insufficiency**. - The adrenal glands lose their ability to produce adequate **endogenous cortisol**, creating a state of functional adrenal insufficiency. - This is why **gradual tapering** is essential when discontinuing steroids to allow HPA axis recovery. *Prolonged glucocorticoid exposure* - This is not a consequence but rather a **description of the treatment itself** (tautological). - Taking exogenous steroids IS glucocorticoid exposure, not something it causes. - This option confuses the intervention with its consequences. *Catecholamine excess* - Catecholamines (epinephrine, norepinephrine) are produced by the **adrenal medulla**. - Exogenous steroids **do not affect** catecholamine production or secretion. - Catecholamine excess occurs in conditions like **pheochromocytoma**, unrelated to steroid use. *Hyperaldosteronism* - This involves **excessive aldosterone** production, causing **hypertension** and **hypokalemia**. - Most exogenous steroids are **glucocorticoids** with minimal mineralocorticoid activity. - While some synthetic steroids have mineralocorticoid effects at high doses, **hyperaldosteronism is not the primary consequence** of exogenous steroid intake.
Practice by Chapter
Principles of Endocrine Regulation
Practice Questions
Hypothalamus and Pituitary Gland
Practice Questions
Thyroid Physiology
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Adrenal Cortex and Medulla
Practice Questions
Pancreatic Hormones and Glucose Metabolism
Practice Questions
Calcium and Phosphate Homeostasis
Practice Questions
Growth Hormone and Growth Factors
Practice Questions
Endocrine Regulation of Metabolism
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Hormone Receptors and Signaling
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Assessment of Endocrine Function
Practice Questions
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