Endocrinology — MCQs

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 671: Which of the following actions of GH is mediated by IGF-1?

A. Na+ retention
B. decreases insulin
C. Antilipolysis (Correct Answer)
D. Lipolysis

Explanation: ***Antilipolysis*** * **Insulin-like growth factor 1 (IGF-1)**, stimulated by GH, plays a role in reducing **lipolysis** indirectly. * IGF-1 promotes **anabolic processes** and nutrient storage, which can lead to decreased fat breakdown. *Na+ retention* * **Na+ retention** is more directly influenced by hormones like **aldosterone** and **ADH**, not IGF-1. * While GH can exert some influence on fluid and electrolyte balance, this specific action is not primarily mediated by IGF-1. *decreases insulin* * IGF-1 and GH generally tend to **increase insulin sensitivity** in some tissues or antagonize insulin effects indirectly. * IGF-1's primary metabolic role is not to decrease insulin itself directly. *Lipolysis* * **Growth hormone (GH)** directly promotes **lipolysis**, breaking down fat for energy. * However, the question specifically asks for actions mediated by **IGF-1**, which has an opposite, antilipolytic effect.

Question 672: Insulin secretion is induced by following EXCEPT:

A. Somatostatin (Correct Answer)
B. Estrogens
C. Growth hormone
D. Placental lactogen

Explanation: ***Somatostatin*** - **Somatostatin** directly inhibits insulin secretion from pancreatic beta cells, acting as a paracrine regulator to modulate islet hormone release. - It binds to **somatostatin receptors (SSTRs)** on beta cells, leading to a reduction in cAMP and inhibition of voltage-gated calcium channels, thereby decreasing insulin exocytosis. *Estrogens* - **Estrogens** generally enhance insulin secretion and improve insulin sensitivity, especially during pregnancy or in response to high glucose levels. - They can increase **beta-cell mass** and survival, contributing to better glycemic control. *Growth hormone* - **Growth hormone (GH)** can indirectly induce insulin secretion by promoting insulin resistance, which necessitates increased insulin production to maintain normal glucose levels. - Chronically elevated GH, as seen in **acromegaly**, often leads to hyperinsulinemia and can even cause diabetes. *Placental lactogen* - **Human placental lactogen (hPL)** is a hormone produced during pregnancy that primarily increases maternal insulin resistance to ensure adequate glucose supply to the fetus. - This increased resistance compensatorily stimulates **maternal beta cells** to secrete more insulin, leading to hyperinsulinemia.

Question 673: Levels of which of the following hormones are increased in postmenopausal women:

A. FSH (Correct Answer)
B. Estrogen
C. Progesterone
D. Cortisol

Explanation: ***FSH*** - In postmenopausal women, the **ovaries cease to produce estrogen and progesterone**, leading to a loss of negative feedback on the hypothalamus and pituitary gland. - This results in a **significant increase in the secretion of Follicle-Stimulating Hormone (FSH)** and Luteinizing Hormone (LH) from the anterior pituitary as the body attempts to stimulate ovarian function. *Estrogen* - Estrogen levels **decrease significantly** during menopause as the ovaries stop producing ovarian follicles and ultimately cease ovulation. - The drop in estrogen is responsible for many menopausal symptoms, such as **hot flashes and vaginal dryness**. *Progesterone* - Progesterone levels also **decrease substantially** after menopause, as its primary source is the corpus luteum formed after ovulation, which no longer occurs. - The decline in progesterone contributes to the **irregular menstrual cycles** leading up to and during menopause. *Cortisol* - **Cortisol levels are not directly affected by menopause** in the same dramatic way as sex hormones. - Cortisol is a stress hormone produced by the adrenal glands, and its levels are primarily regulated by the **hypothalamic-pituitary-adrenal (HPA) axis**, which is distinct from the reproductive axis.

Question 674: True about Parathyroid hormone:

A. Inhibits Ca2+ absorption from the intestines
B. It is steroidal in nature
C. Stimulates 1,25-D3 formation (Correct Answer)
D. All of the options

Explanation: ***Stimulate 1, 25 D3 formation*** - Parathyroid hormone (PTH) stimulates the kidneys to convert **25-hydroxyvitamin D** to its active form, **1,25-dihydroxyvitamin D (calcitriol)**. - **Calcitriol** is essential for increasing calcium absorption from the intestines. *Inhibits Ca2+ absorption from the intestines* - This statement is **incorrect**; PTH directly and indirectly (via calcitriol) promotes **calcium absorption** from the intestines. - **PTH's primary role** is to *increase* plasma calcium levels, which includes enhancing intestinal absorption. *It is steroidal in nature* - This statement is **incorrect**; Parathyroid hormone is a **peptide hormone**, not a steroidal hormone. - Steroidal hormones are derived from **cholesterol** (e.g., cortisol, estrogen), while peptide hormones are chains of amino acids. *All of the options* - This option is incorrect because the other two statements regarding PTH's action are demonstrably **false**.

Question 675: Stress hyperglycemia occurs due to all except -

A. Increased level of ACTH
B. Decreased level of norepinephrine (Correct Answer)
C. Insulin resistance
D. Increased level of cortisol

Explanation: ***Decreased level of norepinephrine*** - **Norepinephrine** is a **catecholamine** that generally **increases blood glucose** by stimulating **glycogenolysis** and **gluconeogenesis**. - Therefore, a *decrease* in norepinephrine would *reduce* stress-induced hyperglycemia, making this the exception. *Increased level of ACTH* - **ACTH (Adrenocorticotropic Hormone)** stimulates the adrenal glands to release **cortisol**, which contributes significantly to stress hyperglycemia. - Increased ACTH levels therefore *promote* hyperglycemia in stress. *Insulin resistance* - **Insulin resistance** is a common feature during stress, where target cells become less responsive to insulin's effects. - This reduced insulin sensitivity leads to higher circulating glucose levels, contributing to hyperglycemia. *Increased level of cortisol* - **Cortisol** is a key **stress hormone** that promotes **gluconeogenesis** (production of glucose from non-carbohydrate sources) and **glycogenolysis** (breakdown of glycogen to glucose). - Elevated cortisol levels directly lead to an increase in blood glucose, causing hyperglycemia.

Question 676: Hormone primarily responsible for blood pressure regulation following acute blood loss is:

A. Aldosterone
B. ANP
C. Epinephrine
D. ADH (Correct Answer)

Explanation: ***ADH*** - **Antidiuretic hormone (ADH)**, also known as **vasopressin**, is released in response to decreased blood volume and pressure detected by **baroreceptors**. - Its primary role is to increase water reabsorption in the **renal collecting ducts** and cause **vasoconstriction**, both of which help restore blood volume and pressure. - This makes ADH the key **hormonal mechanism** for BP regulation following acute blood loss. *Aldosterone* - **Aldosterone** is crucial for long-term **blood pressure regulation** by increasing sodium and water reabsorption in the kidneys. - While important for volume restoration, its effects are **slower** (hours) and more focused on electrolyte balance rather than immediate BP stabilization after acute blood loss. *ANP* - **Atrial natriuretic peptide (ANP)** is released in response to **atrial stretch** due to increased blood volume and acts to lower blood pressure. - It promotes **vasodilation** and **sodium/water excretion**, counteracting the body's efforts to raise blood pressure after blood loss. - ANP levels are **suppressed** during hypovolemia. *Epinephrine* - **Epinephrine** increases heart rate and cardiac contractility, and causes vasoconstriction, providing an immediate increase in blood pressure. - However, it's primarily a **catecholamine** (not a classic hormone) part of the **sympathetic nervous system** response, and while it acts immediately, ADH provides the sustained hormonal BP regulation.

Question 677: Thyroid peroxidase will help in all the following except:

A. Iodide to iodine
B. Secretion of thyroglobulin into colloid
C. Iodide trapping (Correct Answer)
D. Binding thyroglobulin

Explanation: ***Iodide trapping*** - **Iodide trapping** is the correct answer as it is **NOT** a function of thyroid peroxidase (TPO). - **Iodide trapping** (or iodide pump) is the active transport of iodide into thyroid follicular cells, mediated by the **sodium-iodide symporter (NIS)**, a completely separate protein system. - This process concentrates iodide within the thyroid gland, which is essential before TPO can act. *Iodide to iodine* - **Thyroid peroxidase (TPO) DOES** catalyze the **oxidation of iodide (I-) to iodine (I2)** at the apical membrane. - This is one of the primary enzymatic functions of TPO, making this option incorrect for an "EXCEPT" question. *Secretion of thyroglobulin into colloid* - **Thyroglobulin (Tg)** is secreted into the colloid by **exocytosis**, not directly by TPO. - However, TPO is located at the apical membrane and **facilitates the iodination of thyroglobulin** that has been secreted into the colloid. - While TPO doesn't perform the secretion itself, it has a direct functional relationship with thyroglobulin in the colloid, unlike iodide trapping which is entirely separate from TPO function. *Binding thyroglobulin* - **Thyroid peroxidase (TPO) DOES** interact with and act upon **thyroglobulin** as its substrate. - TPO catalyzes the iodination of tyrosine residues on the thyroglobulin molecule to form **monoiodotyrosine (MIT)** and **diiodotyrosine (DIT)**, and subsequently couples these to form T3 and T4.

Question 678: In which of the following forms the Anti diuretic hormone (ADH) is circulated in plasma:

A. Bound to neurophysin-I
B. Bound to neurophysin-II
C. Free form (Correct Answer)
D. Bound to plasma albumin

Explanation: ***Correct: Free form*** - **ADH circulates in plasma predominantly in its free (unbound) form** to reach target tissues and bind to its receptors (V1 and V2 receptors). - Upon secretion from the posterior pituitary into the bloodstream, **ADH dissociates from neurophysin-II** and circulates freely in plasma. - The free form has a short plasma half-life of **5-20 minutes** and is the active form that exerts physiological effects on kidneys, blood vessels, and other target organs. - Only free hormone can bind to receptors; bound forms are inactive. *Incorrect: Bound to neurophysin-II* - **Neurophysin-II serves as a carrier protein during intracellular transport**, not plasma circulation. - It transports ADH from the hypothalamus (supraoptic and paraventricular nuclei) down the axons to the posterior pituitary for storage. - While co-secreted with ADH, **neurophysin-II and ADH rapidly dissociate upon release into plasma**. - This option confuses the transport/storage mechanism with the circulation form. *Incorrect: Bound to neurophysin-I* - **Neurophysin-I** is the specific carrier protein for **oxytocin**, not ADH. - It facilitates intracellular transport of oxytocin from hypothalamus to posterior pituitary. - ADH does not bind to neurophysin-I. *Incorrect: Bound to plasma albumin* - **Albumin** is a non-specific carrier protein for various lipophilic hormones (thyroid hormones, steroid hormones). - **ADH is a peptide hormone** that does not require albumin for transport or solubility. - ADH circulates freely in aqueous plasma without significant protein binding.

Question 679: Decreased calcium levels lead to

A. Increased parathormone (Correct Answer)
B. Increased 24,25 dihydroxycholecalciferol
C. Increased 1,25 dihydroxycholecalciferol
D. Decreased calcitonin

Explanation: ***Increased parathormone*** * **Hypocalcemia** is the **direct and primary stimulus** for the release of **parathyroid hormone (PTH)** from the parathyroid glands. * This is an **immediate physiological response** - calcium-sensing receptors on parathyroid cells directly detect low calcium and trigger PTH secretion. * PTH then acts to restore serum calcium levels by increasing bone resorption, renal reabsorption of calcium, and stimulating **calcitriol** synthesis. *Increased 24,25 dihydroxycholecalciferol* * **24,25-dihydroxycholecalciferol** is an inactive metabolite of vitamin D, produced when vitamin D levels are sufficient or high. * Its production is **downregulated** in hypocalcemia, as the body prioritizes conversion to active vitamin D (calcitriol) rather than inactive metabolites. *Increased 1,25 dihydroxycholecalciferol* * While **1,25-dihydroxycholecalciferol (calcitriol)** does increase in response to hypocalcemia, this is an **indirect, secondary response** mediated through PTH, not a direct effect of low calcium. * The pathway: Decreased calcium → **PTH release (direct)** → PTH stimulates renal 1α-hydroxylase → increased calcitriol synthesis (indirect). * The question asks what decreased calcium "leads to" - the most accurate answer is the **direct, immediate response** (PTH), not downstream secondary effects. *Decreased calcitonin* * **Calcitonin** is a hormone that *lowers* blood calcium levels, primarily by inhibiting osteoclast activity and increasing renal calcium excretion. * Its secretion is stimulated by **high serum calcium levels**, so in hypocalcemia, calcitonin secretion decreases due to absence of the stimulus. * However, this is a **passive response** (lack of stimulation) rather than an active compensatory mechanism like PTH release.

Question 680: A major causal factor in some cases of hypogonadism is:

A. Reduced secretion of gonadotropin-releasing hormone (GnRH) (Correct Answer)
B. Excess secretion of testicular activin by Sertoli cells
C. Hypersecretion of pituitary LH and FSH as the result of increased GnRH
D. Failure of the hypothalamus to respond to testosterone

Explanation: ***Reduced secretion of gonadotropin-releasing hormone (GnRH)*** - **Hypogonadotropic hypogonadism** is characterized by low levels of LH and FSH due to inadequate GnRH secretion from the hypothalamus, leading to decreased testosterone production. - This can be caused by various factors, including genetic conditions, hypothalamic tumors, or functional suppression from stress or severe illness. *Excess secretion of testicular activin by Sertoli cells* - **Activin** promotes FSH synthesis and secretion from the pituitary but is not a primary cause of hypogonadism. - While disruptions in activin/inhibin balance can affect spermatogenesis, it doesn't directly cause a systemic hypogonadal state through its direct effect on GnRH or gonadal function. *Hypersecretion of pituitary LH and FSH as the result of increased GnRH* - **Hypersecretion of LH and FSH** in response to increased GnRH would lead to **hypergonadism**, or at least eugonadism, not hypogonadism. - This scenario would stimulate excessive testosterone production, the opposite of hypogonadism. *Failure of the hypothalamus to respond to testosterone* - The hypothalamus, as well as the pituitary, are sensitive to **negative feedback from testosterone** to regulate GnRH and gonadotropin release. - A failure to respond to testosterone would typically lead to **increased GnRH and gonadotropin secretion** (as the feedback loop is broken), resulting in higher testosterone levels, which contradicts hypogonadism.

Practice by Chapter

Principles of Endocrine Regulation

Practice Questions

Hypothalamus and Pituitary Gland

Practice Questions

Thyroid Physiology

Practice Questions

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

Practice Questions

Hormone Receptors and Signaling

Practice Questions

Assessment of Endocrine Function

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free