Endocrinology — MCQs

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 731: Insulin secretion is decreased by:

A. Adrenaline (Correct Answer)
B. Vagal stimulation
C. Glucagon
D. Glucose

Explanation: ***Adrenaline*** - **Adrenaline** (epinephrine) stimulates **alpha-2 adrenergic receptors** on pancreatic beta cells, which inhibits insulin secretion. - This mechanism is important during **stress** or **hypoglycemia** to prevent excessive insulin release and support glucose mobilization. *Vagal stimulation* - **Vagal stimulation** (parasympathetic nervous system) generally **increases** insulin secretion. - This effect is mediated by the release of **acetylcholine**, which acts on muscarinic receptors on beta cells. *Glucagon* - While glucagon's primary role is to **increase blood glucose**, it can also directly **stimulate insulin secretion** under certain physiological conditions. - This serves as a feedback loop to prevent excessive hyperglycemia following glucagon-mediated glucose release. *Glucose* - **Glucose** is the primary physiological stimulus for **insulin secretion**. - High blood glucose levels directly activate pancreatic beta cells, leading to insulin release to lower blood glucose.

Question 732: Due to fear which of the following hormones increases rapidly?

A. Growth hormones
B. Thyroid hormone
C. Corticosteroid
D. Epinephrine (Correct Answer)

Explanation: ***Epinephrine*** - **Epinephrine**, also known as adrenaline, is a hormone and neurotransmitter involved in the **"fight or flight" response** to stress, fear, or excitement. - When faced with fear, the **adrenal medulla** releases epinephrine, leading to rapid physiological changes like increased heart rate, blood pressure, and energy availability to prepare the body for immediate action. *Growth hormones* - **Growth hormone (GH)** primarily regulates growth, metabolism, and body composition. - While stress can influence GH secretion, a rapid increase in direct response to acute fear is not its primary function. *Thyroid hormone* - **Thyroid hormones (T3 and T4)** regulate metabolism, energy balance, and body temperature over a longer term. - Their primary role is not in the immediate, rapid physiological response to acute fear. *Corticosteroid* - **Corticosteroids**, such as cortisol, are released in response to stress, but their increase is typically more prolonged than the instant surge of epinephrine. - They play a role in modulating immune response and metabolism during stress but are not responsible for the immediate "fight or flight" reactions.

Question 733: The primary action of leptin is:

A. To increase food intake
B. To increase gastric contraction
C. To decrease food intake (Correct Answer)
D. To increase intestinal motility

Explanation: ***To decrease food intake*** - **Leptin** is a hormone primarily produced by **adipocytes (fat cells)** that acts on the hypothalamus to signal satiety and reduce hunger. - Higher levels of leptin indicate ample energy stores, leading to a **decrease in food intake** and an increase in energy expenditure. *To increase food intake* - This is the opposite of leptin's primary action; instead, hormones like **ghrelin** are known to increase food intake. - Leptin's role is to regulate long-term energy balance by **reducing appetite**. *To increase gastric contraction* - **Gastric contractions** are primarily regulated by neural and other hormonal signals (e.g., motilin, gastrin), not leptin. - Leptin's main target is the central nervous system to influence overall **appetite control**. *To increase intestinal motility* - Intestinal motility is primarily influenced by the **enteric nervous system** and hormones such as **serotonin** and **motilin**. - Leptin's action is more focused on **central regulation of satiety** rather than direct effects on gut movement.

Question 734: The function of which of the following is increased by an elevated parathyroid hormone concentration:

A. Action of osteoblasts only
B. Osteoclasts (Correct Answer)
C. Phosphate reabsorptive pathways in the renal tubules
D. Hepatic formation of 25-hydroxycholecalciferol

Explanation: ***Osteoclasts*** - **Parathyroid hormone (PTH)** primarily acts to increase serum calcium levels by stimulating **osteoclasts**, leading to bone resorption and release of calcium and phosphate into the bloodstream. - While PTH does not directly act on osteoclasts, it binds to receptors on osteoblasts, which then release factors that activate osteoclasts. *Action of osteoblasts only* - PTH indirectly affects **osteoblasts** by binding to their receptors, but this action primarily leads to **RANKL expression**, which then stimulates osteoclast activity, not a direct increase in osteoblastic bone formation. - Chronic elevation of PTH, as seen in primary hyperparathyroidism, can paradoxically lead to a net loss of bone mass due to increased osteoclastic activity. *Phosphate reabsorptive pathways in the renal tubules* - PTH actually **decreases reabsorption of phosphate** in the renal tubules, leading to phosphaturia. This helps to prevent calcium-phosphate precipitation by lowering serum phosphate levels while raising calcium. - This is a key mechanism by which PTH increases serum calcium—by both mobilizing it from bone and reducing its renal excretion, while simultaneously promoting renal phosphate excretion. *Hepatic formation of 25-hydroxycholecalciferol* - The **liver** is responsible for the hydroxylation of vitamin D3 (cholecalciferol) to **25-hydroxycholecalciferol (calcidiol)**, a process that is not directly regulated by PTH. - PTH primarily stimulates the **kidneys** to convert 25-hydroxycholecalciferol to its active form, **1,25-dihydroxyvitamin D (calcitriol)**, which then enhances intestinal calcium absorption.

Question 735: Function of leptin is:

A. Stimulation of AgRP
B. Decrease lipolysis
C. Reduce food intake (Correct Answer)
D. All of the options

Explanation: ***Reduce food intake*** - **Leptin** is a hormone secreted by **adipose tissue** that signals **satiety** to the brain, which leads to a reduction in energy intake and increased expenditure. - It acts on the **hypothalamus** to inhibit the production of neuropeptides that stimulate appetite and to stimulate the production of neuropeptides that suppress appetite. *Stimulation of AgRP* - **Agouti-related peptide (AgRP)** is a neuropeptide that **promotes feeding** and reduces energy expenditure. - Leptin's function is to **inhibit, not stimulate**, AgRP expression and activity, thus suppressing appetite. *Decrease lipolysis* - Leptin generally acts to **increase lipolysis** and lipid oxidation in peripheral tissues, rather than decrease it. - This action helps to reduce fat stores and increase energy expenditure, aligning with its role in weight regulation. *All of the options* - This option is incorrect because leptin's primary role is to **reduce food intake**, and it **inhibits AgRP** and generally **increases lipolysis**, contrary to the other choices. - Therefore, not all the listed functions are accurate descriptions of leptin's actions.

Question 736: Excessive production of aldosterone results in:

A. Potassium retention
B. Metabolic acidosis
C. Depressed plasma renin (Correct Answer)
D. Severe hypotension

Explanation: ***Depressed plasma renin*** - **Excessive aldosterone production** (primary hyperaldosteronism) independently leads to **sodium and water retention**, expanding extracellular fluid volume and consequently **suppressing renin secretion** via negative feedback. - While secondary hyperaldosteronism (e.g., due to renal artery stenosis) can involve high renin, primary aldosteronism is characterized by **low renin levels** because the adrenal glands are overproducing aldosterone autonomously. *Potassium retention* - Aldosterone's primary role in the kidney is to promote **sodium reabsorption** and **potassium excretion** in the principal cells of the collecting duct. - Therefore, excessive aldosterone typically leads to **hypokalemia** (low potassium levels) due to increased potassium loss, not retention. *Metabolic acidosis* - Aldosterone enhances the secretion of **hydrogen ions (H+)** in the intercalated cells of the collecting duct, helping to regulate acid-base balance. - Excessive aldosterone consequently leads to increased H+ excretion, which can result in **metabolic alkalosis**, not acidosis. *Severe hypotension* - Aldosterone promotes **sodium and water reabsorption**, leading to an increase in **blood volume** and **blood pressure**. - Therefore, excessive aldosterone production typically results in **hypertension** (high blood pressure), not hypotension.

Question 737: The arterial blood glucose concentration in normal humans after a meal is in the range of:

A. 120 to 140 mg/dL (Correct Answer)
B. 30 to 50 mg/dL
C. 50 to 70 mg/dL
D. 220 to 250 mg/dL

Explanation: ***120 to 140 mg/dL*** - After a meal, **carbohydrates** are digested into glucose, which is absorbed into the bloodstream, causing a physiological rise in blood glucose levels. - This range represents the normal **postprandial (after meal)** peak glucose concentration in healthy individuals before insulin brings it back down. *30 to 50 mg/dL* - This range is significantly **lower than normal** and indicates severe **hypoglycemia**, which can lead to symptoms like confusion, seizures, and loss of consciousness. - Such low levels are not seen in healthy individuals after a meal. *50 to 70 mg/dL* - This range represents **mild to moderate hypoglycemia**, which can cause symptoms such as sweating, tremors, and hunger. - While lower than normal, it is still not the typical post-meal glucose level in healthy individuals. *220 to 250 mg/dL* - This range is significantly **higher than normal** and indicates **hyperglycemia**, suggesting impaired glucose regulation. - Such levels after a meal are often seen in individuals with **diabetes mellitus** or impaired glucose tolerance.

Question 738: Iodine uptake is seen in the following organ:

A. Thyroid (Correct Answer)
B. Parathyroid
C. Ovary
D. All of the options

Explanation: ***Thyroid*** - The **thyroid gland** actively traps **iodine** from the bloodstream using the **sodium-iodide symporter (NIS)** to synthesize thyroid hormones, **T3** and **T4**. - This high affinity for iodine is exploited in diagnostic imaging (e.g., **radioactive iodine uptake test**) and therapeutic applications (e.g., **radioactive iodine ablation** for thyroid cancer). *Parathyroid* - The **parathyroid glands** are primarily involved in regulating **calcium** and **phosphate** metabolism, producing **parathyroid hormone (PTH)**. - They do not have a significant mechanism for **iodine uptake** or utilization. *Ovary* - The **ovaries** are endocrine glands responsible for producing **estrogen** and **progesterone** and are involved in female reproduction. - They do not exhibit significant **iodine uptake** as they do not use iodine for their primary hormonal functions. *All of the options* - This option is incorrect because while the **thyroid** actively takes up iodine, the **parathyroid glands** and **ovaries** do not. - Only organs involved in **thyroid hormone synthesis** or with specific iodine-transporting mechanisms show significant iodine uptake.

Question 739: If blood supply to hypothalamus is interrupted through median eminence which hormone will have normal secretion?

A. GH
B. TSH
C. Vasopressin (Correct Answer)
D. Prolactin

Explanation: ***Vasopressin (ADH)*** - Vasopressin is synthesized in the **supraoptic and paraventricular nuclei** of the hypothalamus - It travels down **axons** (hypothalamic-hypophyseal tract) to the **posterior pituitary** where it is stored and released - Its secretion is **NOT dependent on the hypophyseal portal system** that passes through the median eminence - Interruption of the portal blood supply through the median eminence affects only the **anterior pituitary hormones** - Vasopressin secretion would remain **completely normal** as it bypasses the portal system entirely *Prolactin* - Prolactin is an anterior pituitary hormone under **tonic inhibition** by dopamine from the hypothalamus - Dopamine reaches the anterior pituitary via the **portal system through the median eminence** - Interruption of this blood supply would **block dopamine delivery**, resulting in **increased prolactin secretion** (not normal) - This is the classic "stalk effect" seen in pituitary stalk lesions *GH* - Growth Hormone requires **GHRH (Growth Hormone-Releasing Hormone)** stimulation from the hypothalamus - GHRH travels via the **portal system** to stimulate the anterior pituitary - Portal disruption prevents GHRH delivery → **Decreased GH secretion** *TSH* - Thyroid-Stimulating Hormone requires **TRH (Thyrotropin-Releasing Hormone)** stimulation - TRH travels via the **portal system** to the anterior pituitary - Portal disruption prevents TRH delivery → **Decreased TSH secretion**

Question 740: Which is not an action of cortisol?

A. Mobilization of fatty acids
B. Increases liver and plasma proteins
C. Stimulation of gluconeogenesis
D. Increases the number of eosinophils (Correct Answer)

Explanation: ***Increases the number of eosinophils*** - Cortisol and other glucocorticoids actually cause a **decrease in the number of eosinophils** in circulation. - This effect is due to increased destruction of eosinophils and decreased production, contributing to their **immunosuppressive** actions. *Mobilization of fatty acids* - Cortisol plays a role in **lipid metabolism**, promoting the breakdown of fats from adipose tissue. - This leads to the **release of fatty acids** into the bloodstream for energy utilization, especially during stress or fasting. *Increases liver and plasma proteins* - Cortisol has an **anabolic effect on the liver**, promoting the synthesis of various proteins, including plasma proteins. - This contributes to maintaining protein levels in the body, although its overall effect on protein metabolism can be catabolic in muscle. *Stimulation of gluconeogenesis* - Cortisol is a major **glucocorticoid**, meaning it increases blood glucose levels. - It achieves this by stimulating the liver to produce glucose from non-carbohydrate sources like amino acids and glycerol, a process known as **gluconeogenesis**.

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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