Endocrinology Practice Questions

Q: Steroid hormone that directly binds to intracellular cytoplasmic receptors

Glucocorticoids. ***Glucocorticoids*** - **Glucocorticoids** are **steroid hormones** that are **lipid-soluble** and can easily pass through the cell membrane to bind to **intracellular cytoplasmic receptors**. - This binding leads to the formation of a hormone-receptor complex that translocates to the nucleus to regulate **gene expression**. - This is the classic mechanism of action for steroid hormones. *Thyroxine* - **Thyroxine (T4)** is a **thyroid hormone**, **not a steroid hormone** - it is derived from tyrosine amino acids. - Although it does bind to intracellular receptors, it does not meet the criteria of being a steroid hormone as asked in the question. - Thyroxine primarily binds to nuclear receptors rather than cytoplasmic receptors. *Calcitonin* - **Calcitonin** is a **peptide hormone**, not a steroid hormone, that primarily binds to **cell surface receptors** on target cells like osteoclasts and renal tubule cells. - As a large, **water-soluble** molecule, it cannot directly cross the cell membrane to bind to intracellular receptors. *Vasopressin* - **Vasopressin**, also known as **antidiuretic hormone (ADH)**, is a **peptide hormone**, not a steroid hormone, that acts on **cell surface receptors** in the kidneys and blood vessels. - Its **hydrophilic** nature prevents it from penetrating the cell membrane to bind to intracellular receptors.

Q: All of the following hormones have cell surface receptors except:

Thyroxine. ***Thyroxine*** - **Thyroxine** (T4) is a **lipid-soluble thyroid hormone** that readily crosses the cell membrane to bind to **intracellular nuclear receptors** in the nucleus. - This binding leads to changes in gene expression, which then mediates its metabolic effects. - Unlike peptide hormones, thyroid hormones do not require cell surface receptors. *Insulin* - **Insulin** is a **peptide hormone** that binds to specific **cell surface receptors** (tyrosine kinase receptors) on target cells. - This binding initiates a signaling cascade that regulates glucose uptake and metabolism. *Adrenalin* - **Adrenalin** (epinephrine) is a **catecholamine hormone** that binds to **G protein-coupled receptors (GPCRs)** on the cell surface. - This binding triggers intracellular signaling pathways, leading to the "fight-or-flight" response. *Growth Hormone* - **Growth hormone** is a **protein hormone** that binds to **cell surface receptors** (cytokine receptors) on target cells. - This interaction activates the JAK-STAT signaling pathway, promoting growth and metabolism.

Q: The anterior pituitary is mainly composed of which of the following secretory cells?

Somatotrope. ***Somatotrope*** - **Somatotropes** are the most abundant cell type in the anterior pituitary, constituting about 50% of the gland's cells. - They produce and secrete **growth hormone (GH)**, which is crucial for growth, metabolism, and body composition. *Lactotrope* - **Lactotropes** produce **prolactin (PRL)**, which is involved in lactation. - They make up about 15-20% of the anterior pituitary cells, a significant but not the main proportion. *Corticotrope* - **Corticotropes** secrete **adrenocorticotropic hormone (ACTH)**, which stimulates the adrenal glands. - They constitute approximately 15-20% of the anterior pituitary cells, similar to lactotropes. *Thyrotrope* - **Thyrotropes** produce **thyroid-stimulating hormone (TSH)**, regulating thyroid function. - They are the least abundant cell type, making up only about 5% of the anterior pituitary cells.

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

Antilipolysis. ***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.

Q: Insulin secretion is induced by following EXCEPT:

Somatostatin. ***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.

Q: True about Parathyroid hormone:

Stimulates 1,25-D3 formation. ***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**.

Q: Stress hyperglycemia occurs due to all except -

Decreased level of norepinephrine. ***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.

Q: Thyroid peroxidase will help in all the following except:

Iodide trapping. ***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.

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

Free form. ***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.

Q: Decreased calcium levels lead to

Increased parathormone. ***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 1

Steroid hormone that directly binds to intracellular cytoplasmic receptors

Accepted Answer

Glucocorticoids

Answer

Thyroxine

Answer

Calcitonin

Answer

Vasopressin

Question 2

All of the following hormones have cell surface receptors except:

Accepted Answer

Thyroxine

Answer

Insulin

Answer

Adrenalin

Answer

Growth Hormone

Question 3

The anterior pituitary is mainly composed of which of the following secretory cells?

Accepted Answer

Somatotrope

Answer

Lactotrope

Answer

Corticotrope

Answer

Thyrotrope

Question 4

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

Accepted Answer

Antilipolysis

Answer

Na+ retention

Answer

decreases insulin

Answer

Lipolysis

Question 5

Insulin secretion is induced by following EXCEPT:

Accepted Answer

Somatostatin

Answer

Estrogens

Answer

Growth hormone

Answer

Placental lactogen

Question 6

True about Parathyroid hormone:

Accepted Answer

Stimulates 1,25-D3 formation

Answer

Inhibits Ca2+ absorption from the intestines

Answer

It is steroidal in nature

Answer

All of the options

Question 7

Stress hyperglycemia occurs due to all except -

Accepted Answer

Decreased level of norepinephrine

Answer

Increased level of ACTH

Answer

Insulin resistance

Answer

Increased level of cortisol

Question 8

Thyroid peroxidase will help in all the following except:

Accepted Answer

Iodide trapping

Answer

Iodide to iodine

Answer

Secretion of thyroglobulin into colloid

Answer

Binding thyroglobulin

Question 9

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

Accepted Answer

Free form

Answer

Bound to neurophysin-I

Answer

Bound to neurophysin-II

Answer

Bound to plasma albumin

Question 10

Decreased calcium levels lead to

Accepted Answer

Increased parathormone

Answer

Increased 24,25 dihydroxycholecalciferol

Answer

Increased 1,25 dihydroxycholecalciferol

Answer

Decreased calcitonin

Endocrinology — MCQs

Endocrinology — MCQs

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