Endocrinology Practice Questions

Q: Which of the following hormones is not stored in cells?

Cortisol. ***Cortisol*** - Cortisol is a **steroid hormone** that is synthesized from **cholesterol** on demand and is **not stored** in secretory vesicles or elsewhere within cells. - Being **lipophilic**, it diffuses freely across cell membranes immediately after synthesis. - Its release is regulated by the **hypothalamic-pituitary-adrenal (HPA) axis**, with synthesis and immediate secretion occurring upon stimulation. *Insulin* - Insulin is a **peptide hormone** synthesized as **proinsulin** and then cleaved into active insulin. - It is **stored in secretory granules** within pancreatic beta cells, allowing for rapid release in response to elevated blood glucose. *Thyroxine* - Thyroxine (T4) is a **thyroid hormone** that is synthesized from tyrosine and iodine. - It is **stored extracellularly** within the thyroid gland's follicles as part of a large protein called **thyroglobulin**. - Unlike cortisol (which is never stored), thyroxine has a **substantial storage pool** that can last weeks, though the storage is extracellular rather than intracellular. *Renin* - Renin is an **enzyme** produced by the **juxtaglomerular cells** of the kidney. - It is **stored in secretory granules** within these cells and released in response to decreased renal perfusion pressure or sympathetic stimulation.

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: 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 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: What is the half-life of the thyroid hormone triiodothyronine (T3)?

1 day. ***1 day*** - The **half-life of T3 (triiodothyronine)** is approximately **1 day (24 hours)**, making its biological effects relatively rapid compared to T4. - This shorter half-life contributes to its quicker onset and offset of action. *8 hours* - While reflecting a relatively short duration, **8 hours** is not the accepted half-life for T3. - This value is too short for T3, which has a more sustained biological effect. *6 hours* - A half-life of **6 hours** is too short for T3, which has a more sustained effect than such a rapid clearance would suggest. - This would imply a much faster metabolic turnover than observed clinically. *10 days* - **10 days** is longer than the actual **half-life of T4 (thyroxine)**, which is approximately **7 days**. - T4 serves as a prohormone and is more extensively protein-bound, contributing to its prolonged presence in circulation compared to T3.

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: For how long is Thyroxine stored in the thyroid follicle?

2-3 months. ***2-3 months*** - The thyroid gland stores a substantial amount of **thyroglobulin**, a precursor to **thyroid hormones**, within the **follicular lumen**. - This large storage capacity ensures a **reserve of hormones** sufficient for approximately **2 to 3 months** of normal physiological needs, even if thyroid hormone synthesis were to cease. *1-2 weeks* - This duration is too short for the thyroid's actual storage capacity; the gland is designed for a much longer reserve of **thyroid hormones**. - A 1-2 week supply would make the body highly vulnerable to **rapid onset of hypothyroidism** if synthesis were disrupted. *1-2 days* - This period is extremely short and does not reflect the significant storage capabilities of the thyroid gland, which is unique among endocrine glands for its large **extracellular storage** of hormones. - Such a limited reserve would lead to immediate and severe **hypothyroidism** with any interruption in hormone production. *3-4 years* - While the thyroid does store a considerable amount of hormone, a 3-4 year supply is an **overestimation of its storage capacity**. - The metabolic turnover and requirements of the body for thyroid hormones necessitate replenishment within a few months, rather than years.

Q: What is the body's first physiological response to hypoglycemia?

Decreased insulin. ***Decreased insulin*** - **Decreased insulin secretion** is the body's **first and earliest** physiological response to falling blood glucose levels, occurring at approximately **80-85 mg/dL**. - This represents the **primary defense mechanism** against hypoglycemia - by reducing insulin release from pancreatic beta cells, the body removes the most potent glucose-lowering stimulus. - This allows blood glucose to stabilize before it drops further, and occurs **before** any active counterregulatory hormones are released. - This is a critical **first-line defense** that prevents the need for more aggressive counterregulatory responses. *Increased glucagon* - **Glucagon** is the **second line of defense** against hypoglycemia, with secretion increasing at glucose levels around **65-70 mg/dL**. - While glucagon is the most important **active counterregulatory hormone** (stimulating glycogenolysis and gluconeogenesis), it is not the *first* response. - The temporal sequence is: insulin suppression occurs first, followed by glucagon release if glucose continues to fall. *Increased cortisol* - **Cortisol** is a late counterregulatory hormone, responding to more severe or prolonged hypoglycemia (glucose <65 mg/dL). - It promotes gluconeogenesis and reduces peripheral glucose utilization over hours, not minutes. - Along with growth hormone, cortisol provides sustained glucose elevation but is not an early response. *Increased norepinephrine* - **Norepinephrine** (and epinephrine) are part of the sympathetic/adrenomedullary response to hypoglycemia at approximately **65-70 mg/dL**. - These catecholamines provide important counterregulation but are activated after insulin suppression has already occurred. - They contribute to both glucose mobilization and the symptomatic (adrenergic) response to hypoglycemia.

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

Which of the following hormones is not stored in cells?

Accepted Answer

Cortisol

Answer

Thyroxin

Answer

Renin

Answer

Insulin

Question 2

Which hormone acts on JAK-STAT kinase receptor?

Accepted Answer

GH

Answer

TSH

Answer

Thyroxine

Answer

FSH

Question 3

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 4

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 5

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 6

What is the half-life of the thyroid hormone triiodothyronine (T3)?

Accepted Answer

1 day

Answer

8 hours

Answer

6 hours

Answer

10 days

Question 7

During starvation, which hormone level increases?

Accepted Answer

Ghrelin

Answer

Leptin

Answer

MSH

Answer

Insulin

Question 8

For how long is Thyroxine stored in the thyroid follicle?

Accepted Answer

2-3 months

Answer

1-2 weeks

Answer

1-2 days

Answer

3-4 years

Question 9

What is the body's first physiological response to hypoglycemia?

Accepted Answer

Decreased insulin

Answer

Increased glucagon

Answer

Increased cortisol

Answer

Increased norepinephrine

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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