Endocrinology — MCQs
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Which of the following is a calorigenic hormone?
TRH stimulation testing is useful in diagnosis of disorders of the following hormones?
Major androgen precursor from adrenal cortex is
Which is true about Sex hormone-binding globulin (SHBG):
GH secretion is increased during:
Parathormone has all of the following effects, except -
Which of the following is not an effect of insulin?
Acidophilic cells of anterior pituitary secrete?
Which hormone is converted into its active form in the liver?
Insulin acts by which pathway-
Endocrinology Indian Medical PG Practice Questions and MCQs
Question 691: Which of the following is a calorigenic hormone?
- A. Norepinephrine
- B. Epinephrine
- C. Thyroid hormones
- D. All of the options (Correct Answer)
Explanation: ***All of the options*** - **Norepinephrine**, **epinephrine**, and **thyroid hormones** all increase the **basal metabolic rate** and **heat production**, classifying them as calorigenic. - These hormones stimulate cellular metabolism, leading to increased **oxygen consumption** and **ATP hydrolysis**, which generates heat. *Norepinephrine* - **Norepinephrine** promotes increased **thermogenesis** through its effects on various tissues, particularly brown adipose tissue. - It enhances the breakdown of **fat stores** and **glucose** to generate heat, contributing to the body's overall energy expenditure. *Epinephrine* - **Epinephrine** rapidly increases the **metabolic rate** and heat production during stress or exercise through its beta-adrenergic effects. - It stimulates **glycogenolysis** and **lipolysis**, providing substrates for energy production and subsequent heat generation. *Thyroid hormones* - **Thyroid hormones** (T3 and T4) are major regulators of the **basal metabolic rate** in nearly all body tissues. - They increase the activity of the **Na+/K+ ATPase pump** and mitochondrial oxidative phosphorylation, both of which are significant sources of heat.
Question 692: TRH stimulation testing is useful in diagnosis of disorders of the following hormones?
- A. PTH
- B. ACTH
- C. Insulin
- D. Growth hormone (Correct Answer)
Explanation: ***Growth hormone*** - **TRH** (Thyrotropin-Releasing Hormone) normally stimulates the release of **TSH** and **prolactin** from the anterior pituitary, but **does not normally affect growth hormone**. - In certain pathological conditions like **acromegaly**, TRH can **paradoxically stimulate growth hormone release**, where GH levels abnormally increase instead of remaining unchanged. - This **paradoxical GH response to TRH** is used as a diagnostic test in suspected acromegaly patients, helping differentiate it from normal physiology. - Note: The primary uses of TRH stimulation are for assessing **TSH** (thyroid axis disorders) and **prolactin** (hyperprolactinemia), but among the given options, growth hormone is the relevant answer. *PTH* - **PTH** (Parathyroid Hormone) regulation is primarily controlled by **serum calcium levels**, not by TRH. - Disorders of PTH are diagnosed through **calcium, phosphate, and PTH measurements**, not TRH stimulation. *ACTH* - **ACTH** (Adrenocorticotropic Hormone) release is stimulated by **CRH** (Corticotropin-Releasing Hormone), not TRH. - Conditions involving ACTH are typically evaluated using **CRH stimulation tests** or **dexamethasone suppression tests**. *Insulin* - **Insulin** secretion by pancreatic beta cells is primarily regulated by **blood glucose levels**, not by TRH. - Insulin-related disorders are diagnosed through **glucose tolerance tests**, **C-peptide levels**, and **insulin measurements**.
Question 693: Major androgen precursor from adrenal cortex is
- A. Testosterone
- B. Dihydrotestosterone
- C. DHEA (Correct Answer)
- D. Androstenedione
Explanation: ***DHEA*** - **Dehydroepiandrosterone (DHEA)** is the most abundant and potent **androgen precursor** produced by the adrenal cortex. - It is then converted in peripheral tissues to more potent androgens like testosterone and dihydrotestosterone. *Testosterone* - While testosterone is a potent androgen, its primary source is the **gonads** (testes in males, ovaries in females), not the adrenal cortex. - The adrenal cortex produces only small amounts of testosterone directly. *Dihydrotestosterone* - **Dihydrotestosterone (DHT)** is the most potent androgen, but it is primarily formed in target tissues from **testosterone** via the enzyme **5-alpha-reductase**. - The adrenal cortex does not directly produce significant amounts of DHT. *Androstenedione* - **Androstenedione** is also an adrenal androgen precursor, but it is produced in smaller quantities and is less potent than DHEA. - While it can be converted to testosterone, **DHEA** is considered the major overall androgen precursor from the adrenal gland due to its abundance.
Question 694: Which is true about Sex hormone-binding globulin (SHBG):
- A. Stimulates the secretion of inhibin
- B. Binds testosterone with a higher affinity than estradiol (Correct Answer)
- C. Reduces the total amount of circulating testosterone
- D. Decreases the half-life of testosterone
Explanation: ***Binds testosterone with a higher affinity than estradiol*** - SHBG has a **higher binding affinity for androgens** (**testosterone** and dihydrotestosterone) than for estrogens like **estradiol**. - This difference in affinity is crucial for regulating the **bioavailability of sex hormones**. *Stimulates the secretion of inhibin* - **Inhibin** secretion is primarily stimulated by **follicle-stimulating hormone (FSH)** and local factors in the gonads, not by SHBG. - SHBG's main role is to transport sex steroids, not to directly stimulate other hormone productions. *Reduces the total amount of circulating testosterone* - SHBG **binds circulating testosterone**, but it does not *reduce* the total amount; rather, it *regulates the free fraction* of testosterone. - The liver produces SHBG, which then acts as a **carrier protein**, affecting the bioavailability of **sex hormones**. *Decreases the half-life of testosterone* - By binding to testosterone, SHBG **increases the half-life** of testosterone by protecting it from rapid metabolic degradation and excretion. - **Bound hormones** are less readily metabolized and excreted, thus prolonging their circulation time.
Question 695: GH secretion is increased during:
- A. Increases on prolonged fasting (Correct Answer)
- B. Greater in the early morning
- C. Greater in the evening
- D. Stimulates B-cells of pancreas directly
Explanation: ***Increases on prolonged fasting*** - Growth Hormone (GH) secretion **significantly increases during prolonged fasting** as a crucial **counter-regulatory mechanism**. - GH promotes **lipolysis** (fat breakdown) and **gluconeogenesis**, helping maintain blood glucose while preserving protein stores. - During fasting, GH levels can increase **5-fold or more**, working alongside cortisol and glucagon to maintain metabolic homeostasis. - This is a well-established physiological response critical for survival during food deprivation. *Greater in the early morning* - GH secretion follows a **circadian rhythm** with peak secretion during **deep slow-wave sleep (stage 3-4 NREM)**. - This peak typically occurs in the **first half of the night** (e.g., 11 PM - 2 AM), not specifically in the "early morning" hours (5-7 AM). - By early morning, GH levels are typically declining as sleep becomes lighter. *Greater in the evening* - GH secretion is **lowest during waking hours**, including the evening. - The major pulsatile release begins **after sleep onset**, not during evening wakefulness. *Stimulates B-cells of pancreas directly* - GH does **not directly stimulate pancreatic β-cells**. - GH has **diabetogenic effects** by promoting hepatic glucose output and inducing **insulin resistance** in peripheral tissues. - Any increase in insulin secretion is **indirect**, resulting from elevated blood glucose, not direct β-cell stimulation.
Question 696: Parathormone has all of the following effects, except -
- A. Increased calcitriol synthesis
- B. Increased phosphate reabsorption in kidney (Correct Answer)
- C. Increased Ca+2 reabsorption in kidney
- D. Increased bone resorption
Explanation: ***Increased phosphate reabsorption in kidney*** - Parathormone (**PTH**) primarily functions to increase serum **calcium** levels. - One of its key actions is to promote **phosphate excretion** by decreasing phosphate reabsorption in the renal tubules, not increasing it. *Increased calcitriol synthesis* - **PTH** stimulates the renal 1-alpha-hydroxylase enzyme, which is crucial for converting 25-hydroxyvitamin D to its active form, **1,25-dihydroxyvitamin D (calcitriol)**. - This active form of **vitamin D** then enhances intestinal calcium absorption. *Increased Ca+2 reabsorption in kidney* - **PTH** directly acts on the renal tubules, particularly the distal tubule and collecting duct, to increase the **reabsorption of calcium**. - This prevents calcium loss from the body and contributes to raising serum calcium levels. *Increased bone resorption* - **PTH** stimulates osteoclasts, leading to the breakdown of bone and the release of **calcium** and phosphate into the bloodstream. - This process, known as **bone resorption**, is a significant mechanism by which PTH increases serum calcium.
Question 697: Which of the following is not an effect of insulin?
- A. Increased glycogenolysis (Correct Answer)
- B. Increased transport of glucose into cells
- C. Induction of lipoprotein lipase
- D. Decreased gluconeogenesis
Explanation: ***Increased glycogenolysis*** - Insulin primarily **inhibits glycogenolysis** (the breakdown of glycogen) and promotes glycogen synthesis to lower blood glucose levels. - Thus, increased glycogenolysis is the opposite of an insulin effect. *Increased transport of glucose into cells* - Insulin **facilitates the uptake of glucose** into insulin-sensitive cells (muscle and adipose tissue) by promoting the translocation of GLUT4 transporters to the cell membrane. - This action helps to remove glucose from the bloodstream and reduce blood sugar. *Induction of lipoprotein lipase* - Insulin **activates lipoprotein lipase (LPL)**, an enzyme that breaks down triglycerides in chylomicrons and VLDL into free fatty acids for storage in adipose tissue. - This promotes energy storage after a meal. *Decreased gluconeogenesis* - Insulin **suppresses hepatic gluconeogenesis**, the process by which the liver synthesizes glucose from non-carbohydrate precursors. - This helps to reduce the liver's glucose output and lower blood glucose levels.
Question 698: Acidophilic cells of anterior pituitary secrete?
- A. ACTH
- B. GH (Correct Answer)
- C. TSH
- D. ADH
Explanation: ***GH*** - **Growth Hormone (GH)** is secreted by **somatotrophs**, which are a type of acidophilic cell in the anterior pituitary. - These cells stain readily with **acidic dyes** due to their abundant secretory granules. *ACTH* - **Adrenocorticotropic hormone (ACTH)** is secreted by **corticotrophs**, which are **basophilic cells** in the anterior pituitary. - Corticotrophs stain with basic dyes due to different intracellular granule content. *TSH* - **Thyroid-stimulating hormone (TSH)** is secreted by **thyrotrophs**, which are a type of **basophilic cell** in the anterior pituitary. - Basophilic cells are characterized by their affinity for basic dyes. *ADH* - **Antidiuretic hormone (ADH)**, also known as vasopressin, is produced by the **hypothalamus** and released from the **posterior pituitary**, not the anterior pituitary. - It is not secreted by acidophilic cells.
Question 699: Which hormone is converted into its active form in the liver?
- A. Corticosteroid
- B. Estradiol
- C. ACTH
- D. Thyroid hormone (Correct Answer)
Explanation: ***Thyroid hormone*** - The liver is a major site for the conversion of **thyroxine (T4)**, the primary hormone secreted by the thyroid gland, into its more active form, **triiodothyronine (T3)**. - This conversion, primarily through **deiodination**, is critical for thyroid hormone action in target tissues throughout the body. *Corticosteroid* - **Cortisol**, the main human corticosteroid, is directly secreted by the **adrenal cortex** in its active form. - While the liver metabolizes cortisol for excretion, it does not convert an inactive form into an active corticosteroid. *Estradiol* - **Estradiol** is primarily produced and secreted in its active form by the **ovaries** in premenopausal women. - The liver is involved in the metabolism and conjugation of estradiol for excretion, not its activation. *ACTH* - **Adrenocorticotropic hormone (ACTH)** is secreted by the **anterior pituitary gland** in its active form. - Its primary role is to stimulate the adrenal cortex to produce cortisol; it does not undergo activation in the liver.
Question 700: Insulin acts by which pathway-
- A. Tyrosine kinase (Correct Answer)
- B. Intrinsic ion channel
- C. JAK-STAT-Kinase
- D. Transcription factor
Explanation: ***Tyrosine kinase*** - Insulin binds to its receptor, a **receptor tyrosine kinase**, activating the intracellular tyrosine kinase domain. - This activation leads to the **autophosphorylation** of the receptor and subsequent phosphorylation of various intracellular substrates, initiating a signaling cascade. *Intrinsic ion channel* - This mechanism involves a receptor that is itself an **ion channel**, opening or closing to allow ions to pass through the cell membrane upon ligand binding. - Insulin's primary action is not to alter membrane permeability via direct ion channel modulation but rather to initiate an intracellular signaling cascade. *JAK-STAT-Kinase* - The **JAK-STAT pathway** is typically utilized by cytokine receptors (e.g., growth hormone, interleukins) that do not possess intrinsic kinase activity but activate associated soluble kinases like JAK. - Insulin signaling primarily utilizes its intrinsic tyrosine kinase activity rather than recruiting JAK kinases. *Transcription factor* - While insulin ultimately influences gene expression and thus the activity of **transcription factors**, it is not a transcription factor itself. - Insulin's initial binding and signaling occur at the cell surface via its receptor, leading to downstream events that *regulate* transcription factor activity.
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
Practice Questions
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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