Endocrinology Practice Questions

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 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 does not stimulate growth hormone (GH) release?

Free fatty acids. ***Free fatty acids*** - High levels of **free fatty acids** in the bloodstream inhibit growth hormone (GH) secretion. - This occurs through a **negative feedback loop** at the level of the hypothalamus and pituitary gland. *Fasting* - **Fasting** (especially prolonged) is a potent stimulus for GH release, helping to mobilize fat stores and maintain **glucose homeostasis**. - During fasting, ghrelin levels increase, which further promotes GH secretion. *Exercise* - **Physical exercise** is a well-known physiological stimulus for GH release, contributing to muscle growth and repair. - The intensity and duration of exercise can influence the magnitude of GH secretion. *Stress* - Various forms of **stress**, including physical (e.g., trauma, surgery) and psychological stress, stimulate GH release. - This response is mediated in part by the **sympathetic nervous system** and increased cortisol 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: 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: Which of the following hormones does not mediate its action through cAMP?

Estrogen. ***Estrogen*** - **Estrogen** is a **steroid hormone** that mediates its action by binding to intracellular receptors, forming a complex that directly influences gene transcription. - Steroid hormones, due to their **lipophilicity**, can cross the cell membrane and do not typically rely on cell surface receptors or second messengers like cAMP. *Glucagon* - **Glucagon** acts on a **G protein-coupled receptor (GPCR)**, specifically a Gs-coupled receptor, leading to the activation of adenylyl cyclase. - This activation increases the intracellular concentration of **cAMP**, which then activates protein kinase A to mediate its effects, primarily on glucose metabolism. *Follicle stimulating hormone* - **FSH** binds to a **GPCR** on target cells, activating the Gs protein pathway. - This activation stimulates **adenylyl cyclase** and increases intracellular **cAMP** levels, which are critical for its role in gamete development. *Luteinizing hormone* - **LH**, like FSH, binds to a cell surface **GPCR** that activates the Gs protein. - This leads to the stimulation of **adenylyl cyclase** and an increase in **cAMP**, mediating its effects on steroidogenesis and ovulation.

Q: Which hormone is primarily inhibited by the hypothalamus?

Prolactin. ***Prolactin*** - The hypothalamus secretes **dopamine** (Prolactin Inhibiting Hormone), which tonically inhibits prolactin release from the anterior pituitary. - Unlike most other anterior pituitary hormones, prolactin's primary hypothalamic control is **inhibitory** rather than stimulatory. *TSH* - **Thyroid-stimulating hormone (TSH)** is *stimulated* by **Thyrotropin-Releasing Hormone (TRH)** from the hypothalamus. - The hypothalamus does not primarily inhibit TSH; rather, it promotes its release, which is then regulated by negative feedback from thyroid hormones. *FSH* - **Follicle-stimulating hormone (FSH)** is *stimulated* by **Gonadotropin-Releasing Hormone (GnRH)** from the hypothalamus. - The hypothalamus promotes FSH release, which is essential for gamete production and ovarian follicle development. *CRH* - **Corticotropin-Releasing Hormone (CRH)** is a hormone secreted by the **hypothalamus** itself. - CRH acts on the anterior pituitary to *stimulate* the release of **ACTH**, not inhibit another hormone.

Q: What is the major adrenal androgen produced by the adrenal glands?

Dehydroepiandrosterone (DHEA). ***Dehydroepiandrosterone (DHEA)*** - **Dehydroepiandrosterone (DHEA)**, or specifically **dehydroepiandrosterone sulfate (DHEA-S)**, is the major adrenal androgen produced by the adrenal cortex and is an important **17-ketosteroid** [1]. - Its production is controlled by **ACTH** and serves as a precursor for more potent androgens and estrogens in peripheral tissues. *Testosterone* - While testosterone is a potent androgen, the primary source in males is the **testes**, and in females, it's produced in smaller amounts by the **ovaries** and peripherally from adrenal androgens. - The adrenal glands produce only a **small fraction** of circulating testosterone directly; they primarily produce precursors like DHEA [1]. *11-hydroxy derivative of androstenedione* - **Androstenedione** is an adrenal androgen precursor, but its 11-hydroxy derivative is not typically referred to as the major adrenal androgen. - The most significant adrenal androgen is DHEA, which is then converted peripherally to other androgens including androstenedione [1]. *Cortisol* - **Cortisol** is the primary **glucocorticoid** produced by the adrenal glands, playing a critical role in stress response, metabolism, and immune function [2]. - While produced by the adrenal cortex, it is a **steroid hormone**, but its primary function is not androgenic; it is a glucocorticoid.

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.

Question 1

Which hormone increases with age?

Accepted Answer

Parathormone

Answer

GH

Answer

Prolactin

Answer

Insulin

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 of the following does not stimulate growth hormone (GH) release?

Accepted Answer

Free fatty acids

Answer

Exercise

Answer

Fasting

Answer

Stress

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

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 7

Which of the following hormones does not mediate its action through cAMP?

Accepted Answer

Estrogen

Answer

Glucagon

Answer

Follicle stimulating hormone

Answer

Luteinizing hormone

Question 8

Which hormone is primarily inhibited by the hypothalamus?

Accepted Answer

Prolactin

Answer

TSH

Answer

FSH

Answer

CRH

Question 9

What is the major adrenal androgen produced by the adrenal glands?

Accepted Answer

Dehydroepiandrosterone (DHEA)

Answer

Testosterone

Answer

11-hydroxy derivative of androstenedione

Answer

Cortisol

Question 10

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

Accepted Answer

Decreased insulin

Answer

Increased glucagon

Answer

Increased cortisol

Answer

Increased norepinephrine

Endocrinology — MCQs

Endocrinology — MCQs

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