Endocrinology — MCQs

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 651: In trauma, which of the following hormones is/are increased? a) Epinephrine b) ACTH c) Glucagon d) Parathormone

A. bc
B. acd
C. bcd
D. abc (Correct Answer)

Explanation: ***abc*** - Trauma is a significant stressor that triggers the release of **epinephrine** (a), **ACTH** (b), and **glucagon** (c) as part of the body's **fight-or-flight response** and metabolic adaptation. - **Epinephrine** increases heart rate, blood pressure, and mobilizes energy stores; **ACTH** stimulates cortisol release to manage stress and inflammation; **glucagon** mobilizes glucose to provide energy for tissues. - **Parathormone** (d) is NOT significantly increased in acute trauma as it primarily regulates calcium homeostasis, not the acute stress response. *bc* - This option is incomplete as **epinephrine** (a) is also significantly increased during trauma due to the activation of the sympathetic nervous system. - While **ACTH** and **glucagon** are elevated, failing to include epinephrine underestimates the full hormonal response to trauma. *acd* - This option incorrectly includes **parathormone** (d) as a primary hormone elevated in acute trauma. While calcium regulation is important, parathormone's immediate increase is not a hallmark of the acute stress response. - It also omits **ACTH** (b), which is a key hormone in the stress axis response. *bcd* - This option incorrectly includes **parathormone** (d) which does not typically show a significant immediate increase during acute trauma. - It also omits **epinephrine** (a), a crucial component of the acute stress response mediated by sympathetic activation.

Question 652: GnRH is classified as a:

A. Steroid
B. Peptide (Correct Answer)
C. Amine
D. None of the options

Explanation: ***Correct: Peptide*** - **Gonadotropin-releasing hormone (GnRH)** is a **decapeptide**, meaning it is composed of ten amino acids. - As a **peptide hormone**, it exerts its effects by binding to specific receptors on target cells, typically initiating intracellular signaling cascades. *Incorrect: Steroid* - **Steroid hormones** are lipid-soluble molecules derived from cholesterol, such as **estrogen**, **testosterone**, or **cortisol**. - They typically bind to intracellular receptors and modulate gene expression, a mechanism distinct from GnRH. *Incorrect: Amine* - **Amine hormones** are derived from amino acids but are not peptides; examples include **catecholamines** (like epinephrine) and **thyroid hormones**. - These hormones often act via cell surface receptors, but their chemical structure is simpler than complex peptides like GnRH. *Incorrect: None of the options* - This option is incorrect because **peptide** accurately describes the biochemical nature of GnRH.

Question 653: Insulin increases the entry of glucose into which tissue primarily?

A. The mucosa of the small intestine
B. Renal tubular cells
C. All tissues
D. Skeletal muscle (Correct Answer)

Explanation: ***Skeletal muscle*** - Insulin significantly increases glucose uptake into **skeletal muscle** and adipose tissue by triggering the translocation of **GLUT4 transporters** to the cell membrane. - Skeletal muscle is the **primary site** for insulin-mediated glucose disposal, accounting for approximately **80% of postprandial glucose uptake** due to its large mass. - This is a key mechanism for **glucose disposal** from the blood, especially after a meal. *The mucosa of the small intestine* - Glucose absorption in the small intestine occurs via **SGLT1** and **GLUT2 transporters**, processes that are largely **insulin-independent**. - Small intestinal mucosal cells are responsible for absorbing dietary glucose, not for insulin-stimulated glucose uptake from the bloodstream. *Renal tubular cells* - Glucose reabsorption in renal tubules occurs primarily through **SGLT1** and **SGLT2 transporters** in the kidneys. - These processes are **insulin-independent** and are responsible for recovering glucose from the filtrate back into the blood. *All tissues* - While many tissues use glucose, not all of them rely on insulin to facilitate its entry. For example, the **brain**, liver, and **red blood cells** have insulin-independent glucose uptake mechanisms. - Only tissues like skeletal muscle and adipose tissue are **insulin-sensitive**, meaning their glucose uptake is directly stimulated by insulin via GLUT4 translocation.

Question 654: Insulin dependent glucose uptake occurs in:

A. Brain
B. Epithelial cells of small intestine
C. Muscle (Correct Answer)
D. Kidney

Explanation: ***Muscle*** - **Insulin** stimulates glucose uptake in **muscle cells** by promoting the translocation of **GLUT4 transporters** to the cell surface. - This process is crucial for removing glucose from the blood and storing it as **glycogen** in muscle tissue. - Along with **adipose tissue**, muscle is one of the **primary sites of insulin-dependent glucose uptake** in the body. *Brain* - The brain primarily uses **GLUT1** and **GLUT3 transporters** for glucose uptake, which are **insulin-independent**. - These transporters are always active, ensuring a continuous supply of glucose to the brain, regardless of insulin levels. *Epithelial cells of small intestine* - Glucose absorption in the small intestine initially occurs via **SGLT1** (sodium-glucose co-transporter 1) at the apical membrane and then exits into the bloodstream via **GLUT2** at the basolateral membrane. - This process is mainly regulated by the concentration gradient of glucose and sodium, not directly by **insulin**. *Kidney* - The kidneys reabsorb glucose from the filtrate primarily via **SGLT1** and **SGLT2** transporters in the renal tubules. - This reabsorption mechanism is **insulin-independent** and aims to conserve glucose, preventing its loss in urine.

Question 655: Hyperthyroid state is characterized by -

A. Decreased glycolysis
B. Increased cholesterol
C. Increased protein synthesis
D. Lipolysis (Correct Answer)

Explanation: ***Lipolysis (Correct)*** - **Thyroid hormones** have potent **lipolytic effects**, stimulating the breakdown of **triglycerides** into free fatty acids and glycerol - This increased fat catabolism is a key metabolic feature of hyperthyroidism and contributes to the **weight loss** commonly observed despite increased appetite - Enhanced lipolysis also explains the increased free fatty acid levels seen in hyperthyroid patients *Decreased glycolysis (Incorrect)* - **Thyroid hormones** increase overall metabolic rate, including **carbohydrate metabolism** - **Glycolysis** (glucose breakdown) is typically **increased**, not decreased, in hyperthyroid states - This increased glucose utilization contributes to the hypermetabolic state *Increased cholesterol (Incorrect)* - **Thyroid hormones** accelerate both the synthesis and catabolism of cholesterol, with a net effect of **increased cholesterol degradation and excretion** - **Serum cholesterol levels** are typically **decreased** in hyperthyroidism (often used as a metabolic marker) - Conversely, hypothyroidism is associated with hypercholesterolemia *Increased protein synthesis (Incorrect)* - While physiological levels of thyroid hormones support anabolic processes, **excessive thyroid hormone levels** in hyperthyroidism create a net **catabolic state** - This results in increased **protein breakdown (proteolysis)** exceeding synthesis - Clinical manifestations include **muscle weakness, muscle wasting**, and negative nitrogen balance

Question 656: Which gland secretes calcitonin for regulation of calcium metabolism?

A. Thyroid gland (Correct Answer)
B. Parathyroid gland
C. None of the glands
D. Both glands

Explanation: ***Thyroid gland*** - The **thyroid gland** contains specialized cells called **parafollicular cells** or C cells, which are responsible for secreting **calcitonin**. - **Calcitonin** plays a role in calcium metabolism by **lowering blood calcium levels** when they are too high, primarily by inhibiting osteoclast activity and stimulating calcium excretion by the kidneys. *Parathyroid gland* - The **parathyroid glands** secrete **parathyroid hormone (PTH)**, which has the opposite effect of calcitonin. - **PTH** acts to **raise blood calcium levels** by promoting bone resorption, increasing calcium reabsorption in the kidneys, and stimulating vitamin D activation. *None of the glands* - This option is incorrect because the **thyroid gland** is directly involved in producing calcitonin, a key hormone for calcium regulation. - Hormonal regulation of calcium is a vital physiological process orchestrated by specific endocrine glands. *Both glands* - While both the thyroid and parathyroid glands are crucial for **calcium homeostasis**, they secrete different hormones with opposing functions. - The thyroid secretes **calcitonin**, while the parathyroid secretes **parathyroid hormone**; they do not both secrete calcitonin.

Question 657: Melatonin is secreted from which cells of pineal gland?

A. Glial cells
B. Pinealocytes (Correct Answer)
C. Zymogen cells
D. Oncocytes

Explanation: ***Pinealocytes*** - **Pinealocytes** are the primary secretory cells within the **pineal gland** responsible for synthesizing and secreting **melatonin**. - These cells exhibit rhythmic activity, secreting more melatonin during periods of **darkness** to regulate the **sleep-wake cycle**. *Glial cells* - **Glial cells** (specifically astroglial cells and microglial cells) are present in the pineal gland but primarily provide **structural support** and **immune surveillance**, not melatonin synthesis. - Their main function is to maintain the **neural environment** and respond to injury or infection. *Zymogen cells* - **Zymogen cells** are typically found in glands like the pancreas or stomach, where they secrete **inactive enzyme precursors**. - They are not associated with the pineal gland or **melatonin production**. *Oncocytes* - **Oncocytes** are cells characterized by abundant **mitochondria** and are typically found in endocrine glands like the thyroid or parathyroid, often in **neoplastic conditions**. - They are not the **normal secretory cells** of the pineal gland.

Question 658: Leptin is secreted by?

A. Ovaries
B. Adipose tissue (Correct Answer)
C. Hypothalamus
D. Liver

Explanation: ***Adipose tissue*** - **Leptin** is a hormone primarily produced by **adipocytes** (fat cells) in adipose tissue. - Its main role is to regulate **energy balance** by signaling satiety to the brain, thereby reducing appetite and promoting energy expenditure. *Ovaries* - Ovaries primarily secrete **sex hormones** like **estrogen** and **progesterone**, which are crucial for female reproductive function. - While they play a role in metabolism, they are not the primary source of leptin. *Hypothalamus* - The **hypothalamus** is a region of the brain that **responds to leptin** and regulates many bodily functions, including appetite and metabolism, but it does not secrete leptin. - It integrates signals like leptin to maintain **homeostasis**. *Liver* - The liver is a central metabolic organ, involved in processes such as **glucose regulation**, protein synthesis, and detoxification. - While it produces many hormones and proteins, **leptin synthesis** is not one of its primary endocrine functions.

Question 659: Which one is an example of short loop negative feedback mechanism?

A. TRH inhibiting its release from hypothalamus
B. T3, T4 inhibiting TRH release from hypothalamus
C. T3, T4 inhibiting TSH release from anterior pituitary
D. TSH inhibiting TRH release from hypothalamus (Correct Answer)

Explanation: ***TSH inhibiting TRH release from hypothalamus*** - This is the **classic example of short-loop negative feedback** - **Short-loop feedback** occurs when a **pituitary hormone (TSH)** acts directly on the **hypothalamus** to inhibit the release of its corresponding **releasing hormone (TRH)** - This represents a **direct feedback** from the **anterior pituitary** back to the **hypothalamus** - **Key feature**: Involves only **two levels** of the endocrine axis (pituitary and hypothalamus) *TRH inhibiting its release from hypothalamus* - This describes **ultra-short loop (autocrine) feedback**, not short-loop feedback - In this mechanism, the **releasing hormone inhibits its own secretion** from the same cells - This is a **very localized, autocrine mechanism** rather than a true short-loop feedback - **Short-loop feedback** specifically requires a **pituitary hormone** acting back on the hypothalamus *T3, T4 inhibiting TRH release from hypothalamus* - This is an example of **long-loop negative feedback** - The **final hormone products (T3, T4)** from the **thyroid gland** inhibit the release of **TRH** from the **hypothalamus** - This feedback loop involves **three levels**: peripheral endocrine gland (thyroid), pituitary, and hypothalamus - **Key feature**: The **target organ hormone** feeds back to control higher centers *T3, T4 inhibiting TSH release from anterior pituitary* - This is another example of **long-loop negative feedback** - The **final hormone products (T3, T4)** from the **thyroid gland** inhibit **TSH** release from the **anterior pituitary** - This represents the **primary long-loop feedback** in the hypothalamic-pituitary-thyroid axis - This is the **most clinically significant feedback mechanism** in thyroid regulation

Question 660: Which of these hormones activate catalytic receptors?

A. All of these
B. Leptin
C. GH
D. IGF1 (Correct Answer)

Explanation: ***Correct: IGF1*** - **IGF-1** binds to the **IGF-1 receptor (IGF-1R)**, which is a **receptor tyrosine kinase (RTK)** with **intrinsic catalytic activity** [1]. - Upon IGF-1 binding, the receptor undergoes **autophosphorylation** and directly phosphorylates intracellular substrates through its own tyrosine kinase domain [2]. - This qualifies as a **true catalytic receptor** because the enzymatic activity is intrinsic to the receptor itself [3]. *Incorrect: Leptin* - Leptin binds to the **leptin receptor (Ob-R)**, which is a member of the **cytokine receptor family**. - This receptor **lacks intrinsic enzymatic activity** and instead signals through **associated Janus kinases (JAKs)** via the JAK-STAT pathway. - Since the catalytic activity comes from associated proteins (JAKs) rather than the receptor itself, this is **not classified as a catalytic receptor**. *Incorrect: GH* - **Growth Hormone (GH)** binds to the **GH receptor**, another member of the cytokine receptor superfamily. - Like the leptin receptor, the GH receptor **does not have intrinsic catalytic activity** but relies on associated JAKs for signal transduction via the JAK-STAT pathway. - This is **not a catalytic receptor** because the enzymatic function is provided by associated kinases, not the receptor itself. **Key Distinction:** - **Catalytic receptors** = Receptors with intrinsic enzymatic activity (e.g., receptor tyrosine kinases, receptor serine/threonine kinases) [1], [3] - **Cytokine receptors** = Receptors that recruit associated kinases but lack intrinsic catalytic domains

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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