Endocrinology — MCQs

A 20-year-old college student has elevated stress levels due to her rigorous academic schedule, social commitments, and family pressures. She complains of never having enough time for all her responsibilities. Which of the following hormones acts by intracellular receptors to exert the physiologic effects of her stress?

Q609

Which of the following hormones regulates blood levels of 1,25-OH-cholecalciferol positively?

Q610

Testosterone is secreted by:

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 601: Which of the following mechanisms is used by the marked structure to influence neighboring cells?

A. Nerve mediated
B. Vein mediated
C. Paracrine (Correct Answer)
D. Autocrine

Explanation: ### **Explanation** The correct answer is **Paracrine (Option C)**. **1. Why Paracrine is Correct:** The question refers to the mechanism of **local cell-to-cell communication**. In the endocrine system, **paracrine signaling** occurs when a cell secretes chemical messengers (hormones or regulatory peptides) into the interstitial fluid to influence **neighboring cells** of a different type. * **Classic Example:** In the **Islets of Langerhans**, Somatostatin secreted by **Delta (δ) cells** inhibits the secretion of Insulin from **Beta (β) cells** and Glucagon from **Alpha (α) cells** via local diffusion. **2. Why Other Options are Incorrect:** * **Nerve mediated (A):** This refers to **neurotransmission**, where signals travel via axons and cross a synapse. While rapid, it is not the primary mechanism for "neighboring cell" regulation in glandular tissue. * **Vein mediated (B):** This describes **endocrine signaling**. Hormones are secreted into the bloodstream (veins) to act on **distant target organs**, not just immediate neighbors. * **Autocrine (D):** This occurs when a cell secretes a hormone or chemical messenger that binds to receptors on the **same cell** that secreted it, leading to self-regulation. --- ### **High-Yield Clinical Pearls for INI-CET** * **Juxtacrine Signaling:** A variation where the signaling molecule remains attached to the cell membrane and requires **direct physical contact** with the neighbor (e.g., Notch signaling). * **Intracrine Signaling:** When a hormone acts **inside the cell** without ever being secreted (e.g., Steroid hormones or Calcitriol). * **The "Islet" Hierarchy:** Within the pancreas, blood flows from the center (Beta cells) to the periphery (Alpha cells). This creates a **micro-portal system** where insulin can paracrinely inhibit glucagon release. * **Somatostatin:** Known as the "universal inhibitor," it acts primarily via paracrine pathways in both the pancreas and the GI tract (inhibiting Gastrin).

Question 602: Which of the following tissues will not be able to take up glucose in insulin resistance/insulin absence/diabetes mellitus?

A. Kidney
B. Skeletal muscle (Correct Answer)
C. Brain
D. Red blood cells

Explanation: ### **Explanation** The uptake of glucose into cells is mediated by **Glucose Transporters (GLUT)**. The fundamental concept here is the distinction between **Insulin-Dependent** and **Insulin-Independent** glucose uptake. **1. Why Skeletal Muscle is Correct:** * **Skeletal muscle** (and adipose tissue) primarily utilizes **GLUT-4**, which is the only **insulin-dependent** glucose transporter. * In the absence of insulin or in states of insulin resistance, GLUT-4 remains sequestered in intracellular vesicles and cannot translocate to the cell membrane. Consequently, these tissues cannot take up glucose effectively, leading to post-prandial hyperglycemia. **2. Why the Other Options are Incorrect:** * **Kidney (Option A):** Uses **GLUT-2** (basolateral membrane) and **SGLT-1/2** (apical membrane) for glucose reabsorption. These are insulin-independent. * **Brain (Option C):** Relies on **GLUT-1** and **GLUT-3**. The brain requires a continuous supply of glucose regardless of insulin levels to maintain metabolic function. * **Red Blood Cells (Option D):** Utilize **GLUT-1** for constitutive glucose uptake, which does not require insulin. --- ### **High-Yield Clinical Pearls for INI-CET** * **GLUT-4 Locations:** Remember the "Big Three": **Skeletal muscle**, **Cardiac muscle**, and **Adipose tissue**. * **Exercise Exception:** During exercise, skeletal muscle can take up glucose **independently of insulin** because muscle contraction triggers GLUT-4 translocation via the **AMPK pathway**. This is why exercise is a key management strategy for Type 2 Diabetes. * **GLUT-2:** Found in the **Liver, Pancreatic beta cells, and Small Intestine**. It acts as a "glucose sensor" due to its high $K_m$ (low affinity). * **SGLT:** These are **Secondary Active Transporters** (Sodium-Glucose Linked Transporters) found in the kidneys and small intestine, not to be confused with the facilitated diffusion of GLUTs.

Question 603: Which of the following is correct about the feedback hormone marked as $X$ ?

A. Inhibin A
B. Inhibin B (Correct Answer)
C. Progesterone
D. Estrone

Explanation: **Correct: Inhibin B** - The diagram shows a feedback loop where "X" is produced downstream and inhibits the anterior pituitary. This fits the role of **Inhibin B**, which is primarily secreted by the **granulosa cells** of the ovary and **Sertoli cells** of the testis. - **Inhibin B** selectively inhibits the secretion of **FSH** from the anterior pituitary, as indicated by the negative feedback arrow pointing towards the pituitary. - Inhibin B is the key hormone in the follicular phase that provides selective FSH feedback control. *Incorrect: Inhibin A* - **Inhibin A** is predominantly secreted by the **corpus luteum** during the luteal phase of the menstrual cycle and is involved in placental function during pregnancy. - Its levels peak later in the cycle compared to Inhibin B during the follicular phase, and its primary role is not the selective inhibition of FSH shown in this diagram's context for follicular development. *Incorrect: Progesterone* - **Progesterone** is a steroid hormone primarily involved in preparing the uterus for pregnancy and maintaining it during early pregnancy. - While it exerts negative feedback on GnRH and LH/FSH, it is typically secreted by the corpus luteum after ovulation, and the diagram appears to depict a more general inhibitory feedback on FSH. *Incorrect: Estrone* - **Estrone** is one of the three major naturally occurring estrogens but is less potent than estradiol. - While estrogens provide feedback on the hypothalamus and pituitary, the diagram specifically labels "Estrogen" separately, and "X" represents a distinct feedback hormone, making estrone an unlikely specific fit for "X."

Question 604: Which of the following represents a normal response to an OGTT?

A. Graph A
B. Graph B
C. Graph D (Correct Answer)
D. Graph C

Explanation: ***Graph D*** - Graph D shows a **fasting glucose level** below 100 mg/dL, a peak below the renal threshold around 1 hour, and a return to baseline or below within 2-2.5 hours. This pattern is characteristic of normal glucose regulation. - A healthy individual can efficiently clear the glucose load from circulation, preventing sustained hyperglycemia. *Graph A* - Graph A shows significantly **elevated fasting glucose levels** (above 200 mg/dL) and a sustained, very high blood glucose response, peaking above 350 mg/dL and remaining well above the renal threshold. - This pattern is indicative of **diabetes mellitus**, where insulin production or sensitivity is severely impaired. *Graph B* - Graph B displays a high fasting glucose level (above 125 mg/dL) and a blood glucose curve that peaks very high (above 250 mg/dL), staying significantly above the renal threshold even at 2.5 hours. - This profile is suggestive of **impaired glucose tolerance** or **diabetes mellitus**, as the body struggles to effectively lower blood glucose after the glucose load. *Graph C* - Graph C shows a normal fasting glucose level but an **extremely rapid and high peak** much earlier than usual, followed by a precipitous drop below normal fasting levels after 1.5 hours, indicating **reactive hypoglycemia**. - This rapid rise and fall, with a nadir below fasting levels, is not a normal response and may be seen in conditions like **dumping syndrome** or early-stage diabetes with a delayed insulin response.

Question 605: Which of the following is the primary tissue dependent on insulin for glucose uptake?

A. Adipose tissue
B. Brain
C. Muscle (Correct Answer)
D. Pancreas

Explanation: ***Muscle (Correct Answer)*** - **Skeletal muscle** is the **primary insulin-dependent tissue** for glucose uptake, accounting for approximately **80-90% of insulin-stimulated glucose disposal** in the postprandial state. - Insulin promotes the translocation of **GLUT4 transporters** to the cell membrane in muscle cells, enabling rapid and substantial glucose uptake. - This makes muscle the most quantitatively significant site for insulin-mediated glucose clearance from the bloodstream. *Adipose tissue (Incorrect)* - While **adipose tissue** does exhibit insulin-dependent glucose uptake via **GLUT4 transporters**, its contribution to overall glucose disposal is **much smaller** compared to skeletal muscle. - Glucose uptake in adipocytes is important for **lipogenesis** and triglyceride storage, but represents only a minor fraction of total body insulin-stimulated glucose uptake. *Brain (Incorrect)* - The **brain** has a constant, high glucose requirement but utilizes **insulin-independent** glucose uptake mechanisms, primarily through **GLUT1 and GLUT3 transporters**. - Glucose uptake in the brain is regulated by **blood glucose concentration gradients**, not by insulin signaling. - This ensures continuous glucose supply to the brain regardless of insulin levels. *Pancreas (Incorrect)* - The **pancreas**, particularly beta cells, employs **insulin-independent** glucose uptake via **GLUT1 and GLUT2 transporters**. - These transporters function as **glucose sensors**, allowing beta cells to detect blood glucose levels and regulate insulin secretion accordingly. - The pancreas produces insulin but does not depend on insulin for its own glucose uptake.

Question 606: Which hormone most strongly stimulates gluconeogenesis during prolonged fasting?

A. Insulin
B. Epinephrine
C. Cortisol
D. Glucagon (Correct Answer)

Explanation: ***Glucagon*** - **Glucagon** is the primary hormone that promotes **gluconeogenesis** and glycogenolysis to maintain blood glucose during fasting. - Its secretion is strongly stimulated by **low blood glucose levels**, making it critical throughout fasting states. - Glucagon directly stimulates hepatic gluconeogenic enzymes and increases the availability of gluconeogenic substrates. *Insulin* - **Insulin** is an **anabolic hormone** that promotes glucose uptake and storage, thereby decreasing blood glucose levels. - Its levels decrease during fasting, *suppressing* rather than stimulating gluconeogenesis. - Insulin inhibits gluconeogenic enzyme expression and promotes glycolysis instead. *Epinephrine* - **Epinephrine** (adrenaline) is a stress hormone that rapidly increases blood glucose through both **glycogenolysis** and gluconeogenesis. - Its effects are more prominent during **acute stress** or immediate energy demands (fight-or-flight response), rather than sustained fasting. - Its action is rapid but transient compared to glucagon's sustained effect during fasting. *Cortisol* - **Cortisol** is a glucocorticoid that promotes **gluconeogenesis** by providing amino acid substrates through protein catabolysis and inducing gluconeogenic enzymes. - While cortisol becomes increasingly important in **prolonged fasting** (>24-48 hours), **glucagon remains the primary and most potent direct stimulator** of hepatic gluconeogenesis throughout all phases of fasting. - Cortisol's effects are slower in onset but more sustained, working synergistically with glucagon during extended fasting periods.

Question 607: Which hormone is primarily responsible for initiating milk production postpartum?

A. Prolactin (Correct Answer)
B. Estrogen
C. Oxytocin
D. Progesterone

Explanation: ***Prolactin*** - **Prolactin** is the primary hormone responsible for **milk production (lactogenesis)** by stimulating alveolar epithelial cells in the mammary glands. - Its levels rise significantly after childbirth, especially after the expulsion of the placenta, which leads to a drop in inhibitory hormones like progesterone. *Estrogen* - **Estrogen** plays a role in the **growth and development of the mammary glands** during pregnancy but inhibits milk production during gestation. - High estrogen levels during pregnancy prevent prolactin from fully initiating lactation, and their sharp drop postpartum helps trigger milk synthesis. *Oxytocin* - **Oxytocin** is crucial for **milk ejection (let-down reflex)**, causing myoepithelial cells around the alveoli to contract and release milk. - It does not directly cause milk production but rather aids in the release of milk that has already been synthesized. *Progesterone* - **Progesterone** is essential for the **development of the mammary glands** during pregnancy, contributing to alveolar growth. - High levels of progesterone during pregnancy, along with estrogen, actually **inhibit** the full effect of prolactin, preventing milk production until after birth when these hormone levels drop.

Question 608: A 20-year-old college student has elevated stress levels due to her rigorous academic schedule, social commitments, and family pressures. She complains of never having enough time for all her responsibilities. Which of the following hormones acts by intracellular receptors to exert the physiologic effects of her stress?

A. Norepinephrine
B. Glucagon
C. Cortisol (Correct Answer)
D. Growth hormone

Explanation: ***Cortisol*** - **Cortisol** is a **steroid hormone** that, due to its **lipophilic nature**, can easily pass through the cell membrane and bind to **intracellular receptors** in the cytoplasm or nucleus [1]. - As the primary **stress hormone**, cortisol's effects are mediated through these receptors, influencing gene expression and various metabolic processes in response to stress [1], [2]. *Norepinephrine* - **Norepinephrine** is a **catecholamine** that acts on **G protein-coupled receptors** (adrenergic receptors) located on the **cell surface** [2]. - It plays a crucial role in the **"fight or flight" response** but does not exert its effects via intracellular receptors [2]. *Glucagon* - **Glucagon** is a **peptide hormone** primarily involved in glucose regulation, acting on **G protein-coupled receptors** on the **cell surface**. - It increases blood glucose levels by promoting **glycogenolysis** and **gluconeogenesis** and does not use intracellular receptors. *Growth hormone* - **Growth hormone** is a **peptide hormone** that acts through **cell surface receptors** (specifically, receptor tyrosine kinases) and the **JAK-STAT signaling pathway**. - Its primary functions are in **growth**, metabolism, and cell reproduction, not mediating stress responses via intracellular receptors.

Question 609: Which of the following hormones regulates blood levels of 1,25-OH-cholecalciferol positively?

A. Thyroxine
B. Parathormone (Correct Answer)
C. Calcitonin
D. Insulin

Explanation: ***Parathormone*** - **Parathormone (PTH)** directly stimulates the **renal 1-alpha-hydroxylase** enzyme, which converts 25-hydroxycholecalciferol to its active form, **1,25-dihydroxycholecalciferol (calcitriol)**. - This activation is crucial for increasing **calcium absorption** from the gut and maintaining calcium homeostasis. *Thyroxine* - **Thyroxine** (thyroid hormone) primarily regulates **metabolism**, growth, and development. - It does not have a direct positive regulatory effect on the synthesis or blood levels of **1,25-OH-cholecalciferol**. *Calcitonin* - **Calcitonin** is a hormone that **lowers blood calcium levels** by inhibiting osteoclast activity and decreasing renal calcium reabsorption. - It does not positively regulate the production of **1,25-OH-cholecalciferol**; in fact, its actions are generally antagonistic to those influenced by active vitamin D. *Insulin* - **Insulin** is a key hormone in **glucose metabolism**, facilitating glucose uptake by cells and promoting glycogen synthesis. - It plays no direct role in the regulation or synthesis of **1,25-OH-cholecalciferol**.

Question 610: Testosterone is secreted by:

A. Leydig cell (Correct Answer)
B. Granulosa cell
C. Theca cells
D. Sertoli cell

Explanation: ***Leydig cell*** - **Leydig cells** are located in the **interstitial tissue** of the testes and are responsible for producing **testosterone** in response to **luteinizing hormone (LH)** stimulation. - They are the primary source of androgens in males, crucial for the development of male secondary sexual characteristics and spermatogenesis. *Granulosa cell* - **Granulosa cells** are found in the **ovarian follicles** and are primarily involved in the production of **estrogen** and **progesterone** in females. - They surround the oocyte and convert androgens (produced by theca cells) into estrogens. *Theca cells* - **Theca cells** are found in the **ovarian follicles** and produce **androgens** (mainly androstenedione) in response to **LH** stimulation. - These androgens are then converted to estrogens by the adjacent granulosa cells through aromatization. - While they produce androgens, they are not the primary source of testosterone in the body. *Sertoli cell* - **Sertoli cells** are located in the **seminiferous tubules** of the testes and provide structural and metabolic support for **spermatogenesis**. - They produce substances like **androgen-binding protein**, inhibin, and Müllerian inhibiting factor, but they do not secrete testosterone.

Practice by Chapter

Principles of Endocrine Regulation

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Hypothalamus and Pituitary Gland

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Thyroid Physiology

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Adrenal Cortex and Medulla

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Pancreatic Hormones and Glucose Metabolism

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Calcium and Phosphate Homeostasis

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Growth Hormone and Growth Factors

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Endocrine Regulation of Metabolism

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Hormone Receptors and Signaling

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Assessment of Endocrine Function

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