Endocrinology Practice Questions

Q: Thyroid hormone binds to which receptor ?

Nuclear. ***Nuclear*** - Thyroid hormones, being **lipid-soluble**, readily diffuse across the **cell membrane** to bind to receptors located in the nucleus. - This binding directly influences **gene expression** and protein synthesis, mediating the hormone's effects. *Membrane* - Membrane receptors typically bind **water-soluble hormones** (e.g., peptide hormones, catecholamines) that cannot freely cross the cell membrane. - These interactions usually trigger a **second messenger cascade** within the cell. *Cytoplasmic* - While some **steroid hormones** bind to cytoplasmic receptors which then translocate to the nucleus, thyroid hormones bind directly to nuclear receptors. - Cytoplasmic receptors are located in the **cytosol** before their ligand-induced translocation. *None of the options* - This option is incorrect, as thyroid hormones have a specific and well-defined receptor location. - The direct action on **gene regulation** necessitates a nuclear receptor.

Q: Which of the following actions of growth hormone (GH) is primarily mediated by insulin-like growth factor 1 (IGF-1)?

Linear growth and bone development. ***Linear growth and bone development*** - **IGF-1 (Somatomedin C)** is the primary mediator of growth hormone's effects on **linear growth and skeletal development** - IGF-1 is produced primarily in the liver in response to GH stimulation - Acts on **epiphyseal growth plates** to promote chondrocyte proliferation and differentiation - Mediates **protein synthesis, muscle growth, and bone mineralization** - This represents the classic **somatomedin hypothesis** - GH stimulates IGF-1 production, which then mediates growth effects *Lipolysis* - Growth hormone **directly** promotes lipolysis through GH receptors on adipocytes - This leads to breakdown of triglycerides into free fatty acids and glycerol - This is a **direct metabolic effect** of GH, independent of IGF-1 *Insulin resistance* - GH **directly** induces insulin resistance through its own receptors - This is one of the **diabetogenic effects** of GH - While IGF-1 can influence insulin sensitivity, insulin resistance is primarily a **direct GH effect** *Sodium retention* - GH has **direct effects** on renal tubules to promote sodium and water retention - This antinatriuretic effect occurs through GH receptors in the kidney - Not primarily mediated by IGF-1

Q: Which hormone increases with age?

Parathormone. ***Parathormone*** - **Parathormone (PTH)** levels in the blood tend to increase with age, often due to a decline in renal function and reduced vitamin D synthesis, leading to compensatory hyperparathyroidism. - This age-related increase in PTH can contribute to **bone demineralization** and an increased risk of osteoporosis. *GH* - **Growth hormone (GH)** levels generally **decrease with age**, leading to a condition known as somatopause. - Reduced GH contributes to changes in body composition, such as increased adiposity and decreased lean muscle mass, as well as reduced bone density. *Prolactin* - **Prolactin** levels typically remain relatively stable or may slightly decrease with age in men, while in women they can fluctuate due to hormonal changes like menopause but do not show a consistent increase with age. - High prolactin levels are often associated with specific pathological conditions like **prolactinomas** rather than normal aging. *Insulin* - While **insulin resistance** often increases with age, leading to higher fasting insulin levels in some individuals, the overall picture of insulin secretion can be complex and is often influenced by factors such as diet, exercise, and genetics rather than solely age. - A *decline in pancreatic beta-cell function* with age can also lead to impaired insulin secretion in some elderly individuals, complicating the simple relationship between age and insulin levels.

Q: Which hormone acts on JAK-STAT kinase receptor?

GH. ***GH*** - **Growth Hormone (GH)** binds to a **cytokine receptor** that lacks intrinsic tyrosine kinase activity and instead signals through associated **JAK-STAT kinases**. - This binding leads to **JAK phosphorylation**, which then phosphorylates and activates **STAT proteins**, regulating gene expression. *TSH* - **Thyroid-stimulating hormone (TSH)** acts on a **G protein-coupled receptor** to stimulate thyroid hormone production and release. - Its signaling pathway primarily involves the activation of **adenylyl cyclase** and increases in **cAMP**, not the JAK-STAT pathway. *Thyroxine* - **Thyroxine (T4)** is a **thyroid hormone** that primarily acts by binding to **intracellular nuclear receptors**, which then regulate gene transcription. - It directly influences gene expression, rather than signaling through cell surface receptors and kinase pathways like JAK-STAT. *FSH* - **Follicle-stimulating hormone (FSH)**, like TSH, signals through a **G protein-coupled receptor** on target cells in the gonads. - This activation primarily leads to an increase in **intracellular cAMP levels** to mediate its effects on gamete production and hormone synthesis.

Q: During starvation, which hormone level increases?

Ghrelin. ***Ghrelin*** - **Ghrelin** is often referred to as the "hunger hormone" because its levels typically rise during fasting or periods of starvation. - It stimulates **appetite** and signals the brain to increase food intake, playing a crucial role in energy balance. *Leptin* - **Leptin** is a hormone produced by **adipose tissue** that signals satiety and helps regulate long-term energy balance. - During starvation, **leptin levels typically decrease** as fat stores are depleted, which further increases appetite and reduces energy expenditure. *MSH* - **Melanocyte-stimulating hormone (MSH)** is involved in skin pigmentation and appetite regulation, but its levels do not primarily increase in response to starvation. - While MSH can influence appetite, it is often seen to decrease appetite when present in higher concentrations, which is counterintuitive during starvation. *Insulin* - **Insulin** is a hormone produced by the **pancreas** that helps regulate blood glucose levels by promoting glucose uptake into cells. - During starvation, blood glucose levels decrease, leading to a **reduction in insulin secretion** to preserve glucose for vital organs like the brain.

Q: Which of the following hormones does not increase in response to stress?

thyroxine. ***Correct: Thyroxine*** - **Thyroxine (T4)** does not acutely increase in response to stress - Thyroid hormones are **not part of the immediate stress response** mediated by the HPA axis - During acute stress, **TSH may actually be suppressed** by elevated cortisol - Chronic stress can affect thyroid function, but there is **no immediate surge** in T4 levels like with other stress hormones *Incorrect: ADH* - **Antidiuretic hormone (ADH/vasopressin)** is a key stress hormone - Released rapidly in response to **physical stress, pain, hypovolemia**, and hypotension - Part of the **neurohypophyseal stress response** to maintain blood pressure and volume - Works alongside cortisol in the stress response *Incorrect: GH* - **Growth hormone** levels increase during **acute stress** (physical and psychological) - Stimulated by stress-induced activation of **GHRH** and suppression of somatostatin - Promotes **gluconeogenesis and lipolysis** during metabolic stress - Part of the counter-regulatory hormone response *Incorrect: None of the options* - This option is incorrect because **thyroxine is the correct answer** - Thyroxine does not acutely increase with stress, unlike ADH and GH

Q: The primary site of vasopressin synthesis is

Supraoptic nucleus. ***Supraoptic nucleus*** - The **supraoptic nucleus** of the hypothalamus is the **primary site** for the synthesis of **vasopressin** (also known as antidiuretic hormone or ADH). - Approximately **80% of vasopressin** is produced by the neurosecretory cells in this nucleus. - The synthesized vasopressin is transported down axons to the posterior pituitary for storage and release. *Preoptic nucleus* - The **preoptic nucleus** is involved in various homeostatic functions, including **thermoregulation** and **sleep regulation**, but not the synthesis of vasopressin. - While it has neuronal connections to the hypothalamus, it does not produce ADH. *Paraventricular nucleus* - The **paraventricular nucleus** also synthesizes **both vasopressin and oxytocin**, accounting for approximately **20% of vasopressin production**. - While it does produce vasopressin, the **supraoptic nucleus remains the primary site**, making it the correct answer to this question. - The PVN also plays important roles in stress response and various autonomic functions. *Posterior pituitary* - The **posterior pituitary** (neurohypophysis) is responsible for the **storage and release** of vasopressin and oxytocin, not their synthesis. - These hormones are produced in the hypothalamic nuclei (supraoptic and paraventricular) and then transported down axonal tracts to the posterior pituitary.

Q: Wolff–Chaikoff effect is due to?

Excess iodine intake. ***Excess iodine intake*** - The **Wolff-Chaikoff effect** is a phenomenon where a high intake of iodine acutely **inhibits thyroid hormone synthesis** and release. - This effect protects the body from excessive thyroid hormone production during periods of very high iodine availability. *Decreased iodination of MIT* - While the Wolff-Chaikoff effect does inhibit **iodination**, the direct cause is the excessive iodine itself, which triggers an autoregulatory shutdown. - Decreased iodination is a *consequence* of the high iodine leading to inhibition of thyroid peroxidase activity, but not the primary cause of the effect. *Suppression of TSH secretion* - **TSH (Thyroid Stimulating Hormone)** secretion is primarily regulated by negative feedback from thyroid hormones (T3 and T4) and TRH from the hypothalamus. - The Wolff-Chaikoff effect directly involves the thyroid gland's response to iodine and is not primarily mediated by TSH suppression. *Decreased conversion of T4 to T3* - The **conversion of T4 to T3** primarily occurs in peripheral tissues, mediated by deiodinase enzymes. - The Wolff-Chaikoff effect focuses on the inhibition of **iodine organification** and hormone release within the thyroid gland itself, not peripheral conversion.

Q: How does adrenaline affect insulin secretion?

Inhibition of beta cells. ***Inhibition of beta cells*** - **Adrenaline** (epinephrine) binds to **alpha-2 adrenergic receptors** on pancreatic beta cells, which are coupled to inhibitory G-proteins. - This binding leads to **decreased cAMP levels** and hyperpolarization of the beta cell membrane, ultimately inhibiting insulin release. *Stimulation of delta cells* - **Delta cells** produce **somatostatin**, which generally inhibits the secretion of insulin and glucagon. - While adrenaline can have various systemic effects, its primary direct action on insulin secretion is not through stimulating delta cells. *Stimulation of g cells* - **G cells** in the stomach produce **gastrin**, a hormone involved in gastric acid secretion. - Adrenaline's primary physiological role in glucose metabolism does not involve direct stimulation of G cells to influence insulin secretion. *Stimulation of beta cells* - **Stimulation of beta cells** would lead to increased insulin secretion. - Adrenaline's physiological role, particularly in **stress responses**, is to raise blood glucose, which is achieved in part by **reducing insulin availability** to ensure glucose enters the bloodstream rather than tissues.

Question 1

Thyroid hormone binds to which receptor ?

Accepted Answer

Nuclear

Answer

Membrane

Answer

Cytoplasmic

Answer

None of the options

Question 2

Which of the following actions of growth hormone (GH) is primarily mediated by insulin-like growth factor 1 (IGF-1)?

Accepted Answer

Linear growth and bone development

Answer

Lipolysis

Answer

Sodium retention

Answer

Insulin resistance

Question 3

Which hormone increases with age?

Accepted Answer

Parathormone

Answer

GH

Answer

Prolactin

Answer

Insulin

Question 4

Which hormone acts on JAK-STAT kinase receptor?

Accepted Answer

GH

Answer

TSH

Answer

Thyroxine

Answer

FSH

Question 5

During starvation, which hormone level increases?

Accepted Answer

Ghrelin

Answer

Leptin

Answer

MSH

Answer

Insulin

Question 6

Which of the following hormones does not increase in response to stress?

Accepted Answer

thyroxine

Answer

None of the options

Answer

ADH

Answer

GH

Question 7

Which of the following statements about thyroid hormone receptors is correct?

Accepted Answer

They are intracellular receptors that mediate gene transcription after binding with T3 or T4, but their primary action is through T3.

Answer

They directly bind to thyrotropin-releasing hormone (TRH)

Answer

They directly bind to thyroid-stimulating hormone (TSH)

Answer

They cause nuclear transcription after binding with T4

Question 8

The primary site of vasopressin synthesis is

Accepted Answer

Supraoptic nucleus

Answer

Preoptic nucleus

Answer

Paraventricular nucleus

Answer

Posterior pituitary

Question 9

Wolff–Chaikoff effect is due to?

Accepted Answer

Excess iodine intake

Answer

Decreased iodination of MIT

Answer

Suppression of TSH secretion

Answer

Decreased conversion of T4 to T3

Question 10

How does adrenaline affect insulin secretion?

Accepted Answer

Inhibition of beta cells

Answer

Stimulation of delta cells

Answer

Stimulation of G cells

Answer

Stimulation of beta cells

Endocrinology — MCQs

Endocrinology — MCQs

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