Endocrinology Practice Questions

Q: Insulin acts through which receptor?

Enzyme-linked. ***Enzyme-linked*** - Insulin binds to an **enzyme-linked receptor**, specifically a **receptor tyrosine kinase**, to initiate its cellular effects. - Upon binding, the receptor undergoes **autophosphorylation** and then phosphorylates intracellular substrate proteins, leading to a cascade of metabolic actions. *GPCR* - **G protein-coupled receptors (GPCRs)** are integral membrane proteins that, upon ligand binding, activate intracellular G proteins, transmitting signals through second messengers. - Hormones like **glucagon** and **epinephrine** commonly act via GPCRs, not insulin. *Intracellular* - **Intracellular receptors** are typically found in the cytoplasm or nucleus and are activated by small, lipid-soluble ligands that can pass through the cell membrane, such as **steroid hormones**. - Insulin is a large peptide hormone and cannot readily cross the cell membrane to act on intracellular receptors. *Ion channel* - **Ion channel receptors** are transmembrane proteins that open or close an ion channel in response to ligand binding, leading to changes in membrane potential or ion concentration. - Neurotransmitters like **acetylcholine** often act on ligand-gated ion channels, which is not the mechanism of action for insulin.

Q: What is the primary form in which testosterone circulates in the plasma?

Testosterone bound to sex-hormone-binding globulin. ***Testosterone bound to sex-hormone-binding globulin*** - The majority of circulating **testosterone** (approximately **60-70%**) is bound to **sex-hormone-binding globulin (SHBG)**, making this the **primary specific form** in which testosterone circulates. - **SHBG** is a high-affinity binding protein that tightly regulates testosterone bioavailability and maintains a stable hormone reservoir. - This is the standard answer in medical physiology when asked about the primary circulating form of testosterone. *Bound testosterone* - While it is true that approximately **98%** of total testosterone is protein-bound (SHBG + albumin combined), this option is too **general** and lacks the specificity expected in medical examination questions. - When asking for the "primary form," medical education refers to the **single largest specific fraction**, which is SHBG-bound testosterone. *Free testosterone* - Only **1-2%** of circulating testosterone is in the **free** (unbound) form. - While this is the **biologically active** fraction that can enter cells and bind to androgen receptors, it represents only a small minority of circulating testosterone. *Dihydrotestosterone bound to sex-hormone-binding globulin* - **Dihydrotestosterone (DHT)** is a potent **metabolite** of testosterone formed by 5α-reductase in peripheral tissues. - DHT is not the primary circulating form of **testosterone** itself; it is a different, more potent androgen present in much smaller quantities in plasma.

Q: After pituitary stalk resection, all hormones are affected except.

Prolactin. ***Prolactin*** - After pituitary stalk resection, prolactin is the **only anterior pituitary hormone that increases** rather than decreases, making it the exception. - Prolactin secretion is normally under **tonic inhibition** by **dopamine** from the hypothalamus, which reaches the anterior pituitary via the hypophyseal portal system. - When the pituitary stalk is severed, this **dopaminergic inhibition is lost**, resulting in **disinhibition** and a marked **increase in prolactin levels** (hyperprolactinemia). - This is in contrast to all other pituitary hormones which decrease after stalk resection. *Follicle-stimulating hormone* - FSH is an **anterior pituitary hormone** stimulated by **GnRH** from the hypothalamus. - Stalk resection interrupts GnRH delivery via the portal system, leading to **decreased FSH secretion**. - This results in hypogonadism. *Adrenocorticotropic hormone* - ACTH is an **anterior pituitary hormone** stimulated by **CRH** from the hypothalamus. - Stalk resection prevents CRH from reaching the anterior pituitary, causing **decreased ACTH production**. - This leads to secondary adrenal insufficiency. *Antidiuretic hormone (ADH)* - ADH is synthesized in the **hypothalamus** (supraoptic and paraventricular nuclei) and transported down axons to the posterior pituitary for storage and release. - Pituitary stalk resection **interrupts these axons**, initially causing **diabetes insipidus** with decreased ADH release. - While the cell bodies remain intact in the hypothalamus and some recovery may occur over time, ADH secretion is still acutely affected (decreased) by stalk resection, following the same pattern as other hormones except prolactin.

Q: Conversion of chondrocytes into osteogenic cells is caused by

IGF-1. ***IGF-1*** - **Insulin-like Growth Factor 1 (IGF-1)** is the primary direct mediator in endochondral ossification, stimulating chondrocyte proliferation, differentiation, and hypertrophy in the growth plate. - IGF-1 acts directly on chondrocytes to promote their maturation and the subsequent invasion of osteoprogenitor cells that form bone. - It plays a crucial role in longitudinal bone growth by regulating various cellular processes in the growth plate and promoting the replacement of cartilage with bone tissue. *Insulin* - While insulin has anabolic effects on bone and can interact with IGF-1 receptors due to structural similarity, its primary role is in **glucose metabolism** rather than direct regulation of chondrocyte activity in endochondral ossification. - Insulin may have supportive effects on bone formation but is not the primary hormone driving growth plate chondrocyte function. *Growth hormone* - **Growth hormone (GH)** stimulates the production of IGF-1 both systemically (from the liver) and locally (from chondrocytes and other skeletal tissues). - GH acts upstream by increasing IGF-1 levels, which then directly mediates the effects on chondrocytes. - While GH is essential for normal bone growth, IGF-1 is considered the direct effector molecule on chondrocytes. *Thyroxine* - **Thyroxine (T4)** is essential for normal skeletal development and bone maturation, particularly in regulating the timing of growth plate fusion and overall metabolic support for bone growth. - However, it does not directly regulate chondrocyte proliferation and differentiation in the growth plate during endochondral ossification. - Thyroid hormone deficiency causes growth retardation, but thyroxine is not the primary hormonal driver of chondrocyte activity.

Q: In premenopausal obese patients, which hormone is primarily formed from the peripheral conversion of androgen precursors?

Estrone (E1). **Estrone (E1)** - **Estrone** is the primary estrogen produced by the peripheral conversion of **androstenedione** in the adipose tissue of premenopausal obese women. - This conversion is facilitated by the enzyme **aromatase**, which is abundant in fat cells. *Estriol (E3)* - **Estriol** is mainly produced by the **placenta** during pregnancy and is largely considered a marker of fetal well-being. - It is a weak estrogen and is not primarily formed from peripheral conversion in non-pregnant individuals. *Estradiol (E2)* - **Estradiol** is the most potent and abundant estrogen during the reproductive years, primarily produced by the **ovaries**. - While some peripheral conversion can occur, it is not the primary estrogen formed from precursors in obese premenopausal patients. *Androgen precursor* - **Androgen precursors** (like androstenedione) are the *substrates* for estrogen production, not the estrogen itself. - These precursors are converted into estrogens, particularly estrone, in peripheral tissues.

Q: Which of the following hormones in pregnancy is more associated with blood vessels and increased permeability?

Estrogen. ***Estrogen*** - **Estrogen** levels increase significantly during pregnancy and are known to cause **vasodilation** and increased vascular permeability. - This hormonal influence contributes to common pregnancy symptoms like **edema**, increased blood flow to various organs, and changes in vascular tone. - Estrogen is the primary hormone responsible for systemic vascular changes during pregnancy. *Prolactin* - **Prolactin** is primarily responsible for **milk production** (lactation) and breast development during pregnancy. - While it has various metabolic effects, it is not directly associated with increased vascular permeability in the way estrogen is during pregnancy. *Relaxin* - **Relaxin** is a pregnancy hormone that does affect blood vessels and connective tissue remodeling. - However, its primary vascular effects are on **increasing vascular compliance** and **remodeling of maternal tissues** to accommodate pregnancy, rather than directly increasing permeability. - While relaxin contributes to hemodynamic changes, estrogen has a more direct and prominent role in increasing vascular permeability. *Progesterone* - **Progesterone** is crucial for maintaining pregnancy, relaxing smooth muscles, and supporting the uterine lining. - While it can affect vascular tone and causes some vasodilation, its primary role is not to directly increase blood vessel permeability to the same extent as estrogen.

Q: In hypoglycemia, which hormone does not increase?

Insulin. ***Correct Answer: Insulin*** - In hypoglycemia (low blood glucose), the primary goal of the body is to **raise blood glucose levels** - **Insulin** acts to lower blood glucose by promoting glucose uptake into cells - Therefore, insulin secretion is **decreased, not increased**, during hypoglycemia - This makes insulin the hormone that does NOT increase in response to hypoglycemia *Incorrect: Cortisol* - **Cortisol** is a stress hormone released during hypoglycemia - Helps **increase glucose production** through gluconeogenesis - Decreases glucose utilization by peripheral tissues - Its levels **increase** during hypoglycemic events *Incorrect: Glucagon* - **Glucagon** is the primary counter-regulatory hormone for hypoglycemia - Stimulates the liver to release stored glucose through **glycogenolysis** and **gluconeogenesis** - Its secretion **markedly increases** in response to low blood glucose - Works opposite to insulin *Incorrect: Epinephrine* - **Epinephrine** (adrenaline) is released from the adrenal medulla during hypoglycemia - Key component of **glucose counterregulation** - Increases blood glucose by promoting **glycogenolysis** and **gluconeogenesis** - Also inhibits insulin secretion and glucose uptake by peripheral tissues

Q: Calcium levels in blood are increased by:

Parathormone. ***Parathormone*** - **Parathormone (PTH)** increases blood calcium levels by stimulating **osteoclast activity**, leading to bone resorption [1]. - It also enhances **calcium reabsorption** in the kidneys and promotes the production of **calcitriol** (active vitamin D), which increases intestinal calcium absorption [1], [2]. *Calcitonin* - **Calcitonin** is a hormone that **decreases blood calcium levels** by inhibiting osteoclast activity and promoting calcium deposition in bones. - It counteracts the effects of parathormone. *Insulin* - **Insulin** primarily regulates **blood glucose levels** by facilitating glucose uptake into cells. - It does not have a direct role in the regulation of blood calcium. *TNF alpha* - **TNF-alpha (Tumor Necrosis Factor-alpha)** is a **cytokine** involved in inflammation and immune responses. - While it can indirectly affect bone metabolism in chronic inflammatory conditions, it is not a primary regulator of acute blood calcium levels.

Q: During fetal life, maximum growth is caused by:

Insulin. ***Insulin*** - **Insulin** is a major anabolic hormone in fetal life, primarily responsible for regulating nutrient uptake and utilization, leading to **growth and deposition of fat and glycogen**. - High levels of available nutrients from the mother stimulate fetal insulin production, which then promotes **cellular proliferation and growth**. *Growth hormone* - While essential for postnatal growth, **growth hormone** plays a relatively minor role in **fetal growth and development**. - Its effects on growth become more prominent after birth, especially during childhood and adolescence. *Cortisol* - **Cortisol** is crucial for **fetal lung maturation** and the development of other organ systems, but it generally has an **inhibitory effect on growth** rather than promoting it. - Excessive cortisol exposure in utero can lead to intrauterine growth restriction. *Thyroxine* - **Thyroid hormones (thyroxine)** are vital for normal **fetal brain development** and skeletal maturation. - However, they are **not the primary driver of overall fetal growth** in terms of size and weight gain, unlike insulin.

Question 1

Insulin acts through which receptor?

Accepted Answer

Enzyme-linked

Answer

GPCR

Answer

Intracellular

Answer

Ion channel

Question 2

What is the primary form in which testosterone circulates in the plasma?

Accepted Answer

Testosterone bound to sex-hormone-binding globulin

Answer

Free testosterone

Answer

Bound testosterone

Answer

Dihydrotestosterone bound to sex-hormone-binding globulin

Question 3

After pituitary stalk resection, all hormones are affected except.

Accepted Answer

Prolactin

Answer

Follicle-stimulating hormone

Answer

Adrenocorticotropic hormone

Answer

Antidiuretic hormone (ADH)

Question 4

Conversion of chondrocytes into osteogenic cells is caused by

Accepted Answer

IGF-1

Answer

Insulin

Answer

Thyroxine

Answer

Growth hormone

Question 5

In premenopausal obese patients, which hormone is primarily formed from the peripheral conversion of androgen precursors?

Accepted Answer

Estrone (E1)

Answer

Estriol (E3)

Answer

Estradiol (E2)

Answer

Androgen precursor

Question 6

Which of the following hormones in pregnancy is more associated with blood vessels and increased permeability?

Accepted Answer

Estrogen

Answer

Prolactin

Answer

Relaxin

Answer

Progesterone

Question 7

Which of the following statements best describes the mechanism of action of insulin on target cells?

Accepted Answer

Insulin binds to a transmembrane receptor on the outer surface of the plasma membrane, activating the tyrosine kinase in the cytosolic domain of the receptor.

Answer

Insulin binds to a receptor on the outer surface of the plasma membrane, activating adenylate cyclase through the Gs protein.

Answer

Insulin binds to a cytoplasmic receptor and is transferred as a hormone receptor complex to the nucleus to modulate gene expression.

Answer

Insulin enters the cell and causes the release of calcium ions from intracellular stores.

Question 8

In hypoglycemia, which hormone does not increase?

Accepted Answer

Insulin

Answer

Glucagon

Answer

Epinephrine

Answer

Cortisol

Question 9

Calcium levels in blood are increased by:

Accepted Answer

Parathormone

Answer

Calcitonin

Answer

Insulin

Answer

TNF alpha

Question 10

During fetal life, maximum growth is caused by:

Accepted Answer

Insulin

Answer

Thyroxine

Answer

Growth hormone

Answer

Cortisol

Endocrinology — MCQs

Endocrinology — MCQs

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