Endocrinology Practice Questions

Q: Match List-I with List-II and select the correct answer using the code given below the Lists: **List-I** A. Pineal gland B. Testis C. Adrenal gland D. Ovary **List-II** 1. Testosterone 2. Estrogen 3. Cortisol 4. Melatonin

A→4 B→1 C→3 D→2. **A→4 B→1 C→3 D→2** - This option correctly matches each endocrine gland with its primary hormone: the **pineal gland** produces **melatonin**, the **testis** produces **testosterone**, the **adrenal gland** produces **cortisol**, and the **ovary** produces **estrogen**. - These pairings are fundamental to understanding the basic functions of the endocrine system. *A→4 B→3 C→1 D→2* - This option incorrectly matches the **testis** with **cortisol** (should be testosterone) and the **adrenal gland** with **melatonin** (should be cortisol). - Cortisol is a steroid hormone produced by the adrenal cortex, while melatonin from the pineal gland regulates sleep-wake cycles. *A→4 B→2 C→3 D→1* - This option incorrectly matches the **testis** with **estrogen** (should be testosterone) and the **ovary** with **melatonin** (should be estrogen). - Estrogen is the primary female sex hormone, while testosterone is the primary male sex hormone. *A→3 B→4 C→1 D→2* - This option incorrectly matches the **pineal gland** with **cortisol** (should be melatonin) and the **testis** with **estrogen** (should be testosterone). - The pineal gland is known for its role in circadian rhythms through melatonin production, not stress response hormones like cortisol.

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

Graph D. ***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.

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

Muscle. ***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.

Q: Which hormone most strongly stimulates gluconeogenesis during prolonged fasting?

Glucagon. ***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.

Q: A patient with a pituitary tumor demonstrates elevated prolactin levels. Which of the following changes in dopamine signaling best explains the hyperprolactinemia?

Decreased tuberoinfundibular dopamine release. ***Decreased tuberoinfundibular dopamine release*** - **Dopamine** acts as a **prolactin-inhibiting hormone (PIH)**, primarily through the **tuberoinfundibular pathway** from the hypothalamus to the pituitary [1]. - A **pituitary tumor** can compress or damage the pituitary stalk or the hypothalamus, leading to decreased dopamine delivery to the pituitary and thus **hyperprolactinemia** [1]. *Increased D1 receptor activation* - **D1 receptors** are generally associated with **excitatory effects** and are not the primary receptors mediating dopamine's inhibitory effect on prolactin. - **Dopamine's inhibitory action** on prolactin secretion is predominantly mediated by **D2 receptors**. *Enhanced dopamine reuptake* - Enhanced reuptake would lead to **less dopamine availability** at the receptor site, which would indeed cause hyperprolactinemia. - However, this is not the most direct or specific consequence of a **pituitary tumor's mechanical effects** on dopamine signaling [1]. *Increased dopamine synthesis* - **Increased dopamine synthesis** would lead to higher dopamine levels and thus **inhibit prolactin secretion**, which is contrary to the hyperprolactinemia observed in the patient. - This option would result in **hypoprolactinemia**. *Increased D2 receptor activation* - **D2 receptor activation** by dopamine **inhibits prolactin release** from lactotrophs in the pituitary [1]. - Therefore, increased D2 receptor activation would lead to **decreased prolactin levels**, not hyperprolactinemia.

Q: 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?

Cortisol. ***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.

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

Parathormone. ***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**.

Q: Secretion of prolactin is inhibited by?

Dopamine. ***Dopamine*** - **Dopamine**, produced by the **hypothalamus**, is the primary physiological inhibitor of **prolactin secretion** from the anterior pituitary gland. - It acts on **D2 receptors** on lactotrophs, leading to a decrease in prolactin synthesis and release. *Serotonin* - **Serotonin** generally has a stimulatory effect on **prolactin secretion**, rather than an inhibitory one. - Elevated serotonin levels can lead to **hyperprolactinemia**. *Noradrenaline* - While **noradrenaline** can have complex effects on pituitary hormones, it is not considered the primary direct inhibitor of **prolactin secretion**. - Its influence is often indirect or less potent than that of **dopamine**. *Adrenaline* - **Adrenaline** (epinephrine) is a neurotransmitter and hormone primarily involved in the **"fight or flight" response** and does not directly inhibit **prolactin secretion**. - Its effects on pituitary hormone release are typically less direct compared to **dopamine's** specific action on lactotrophs.

Q: Through which of the following does glucose mediated insulin release occur?

ATP sensitive K+ channels. ***ATP sensitive K+ channels*** - Glucose metabolism within pancreatic beta cells leads to an increase in **intracellular ATP**, which then binds to and closes **ATP-sensitive K+ channels**. - Closure of these channels causes **depolarization of the cell membrane**, triggering the opening of voltage-gated calcium channels, leading to insulin release. *cAMP* - While **cAMP** can **potentiate glucose-stimulated insulin secretion**, it is not the primary mechanism by which glucose directly mediates insulin release. - Its effects usually involve the activation of protein kinase A (PKA), which can influence the exocytosis of insulin granules. *Carrier-mediated glucose uptake (GLUT2)* - **GLUT2** is crucial for **glucose entry into pancreatic beta cells**, which is the initial step for glucose sensing. - However, it is the subsequent **metabolism of glucose** and its effect on ATP production, not the uptake itself, that directly mediates insulin release. *Receptor phosphorylation* - **Receptor phosphorylation** is a common mechanism in many signaling pathways, but it is not the direct mechanism by which glucose mediates insulin release in beta cells. - While insulin receptors themselves undergo phosphorylation, this refers to the action of insulin on target cells, not glucose-stimulated insulin secretion from beta cells.

Q: Which of the following would be least likely seen 14 days after a rat is injected with a drug that kills all of its pancreatic B cells?

A fall in the plasma amino acid concentration. ***A fall in the plasma amino acid concentration*** - Destruction of pancreatic **B cells** leads to a lack of **insulin**. Insulin promotes amino acid uptake and protein synthesis, so its absence would lead to a *rise*, not a *fall*, in plasma amino acids due to increased protein breakdown. - In **insulin deficiency**, the body shifts to catabolic states, breaking down proteins for energy and glucose production (gluconeogenesis), thus releasing amino acids into the plasma. *A rise in plasma osmolality* - The absence of insulin would lead to **hyperglycemia** (high blood sugar) as glucose cannot be efficiently taken up by cells. - **High plasma glucose** significantly increases plasma osmolality due to its osmotic activity. *A rise in the plasma H+ concentration* - Long-term **insulin deficiency** can lead to **diabetic ketoacidosis (DKA)**, where the body breaks down fats for energy, producing **ketone bodies**. - Ketone bodies are acids, and their accumulation increases the **plasma H+ concentration**, leading to **metabolic acidosis**. *A rise in the plasma amino acid concentration* - Without **insulin**, protein synthesis is inhibited, and protein breakdown (proteolysis) is enhanced to provide substrates for gluconeogenesis. - This results in a release of **amino acids** from muscle and other tissues into the bloodstream, increasing their plasma concentration.

Question 1

Match List-I with List-II and select the correct answer using the code given below the Lists:

**List-I**
A. Pineal gland
B. Testis
C. Adrenal gland
D. Ovary

**List-II**
1. Testosterone
2. Estrogen
3. Cortisol
4. Melatonin

Accepted Answer

A→4  B→1  C→3  D→2

Answer

A→4  B→3  C→1  D→2

Answer

A→4  B→2  C→3  D→1

Answer

A→3  B→4  C→1  D→2

Question 2

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

Accepted Answer

Graph D

Answer

Graph A

Answer

Graph B

Answer

Graph C

Question 3

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

Accepted Answer

Muscle

Answer

Adipose tissue

Answer

Brain

Answer

Pancreas

Question 4

Which hormone most strongly stimulates gluconeogenesis during prolonged fasting?

Accepted Answer

Glucagon

Answer

Insulin

Answer

Epinephrine

Answer

Cortisol

Question 5

A patient with a pituitary tumor demonstrates elevated prolactin levels. Which of the following changes in dopamine signaling best explains the hyperprolactinemia?

Accepted Answer

Decreased tuberoinfundibular dopamine release

Answer

Increased D1 receptor activation

Answer

Enhanced dopamine reuptake

Answer

Increased dopamine synthesis

Answer

Increased D2 receptor activation

Question 6

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?

Accepted Answer

Cortisol

Answer

Norepinephrine

Answer

Glucagon

Answer

Growth hormone

Question 7

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

Accepted Answer

Parathormone

Answer

Thyroxine

Answer

Calcitonin

Answer

Insulin

Question 8

Secretion of prolactin is inhibited by?

Accepted Answer

Dopamine

Answer

Serotonin

Answer

Noradrenaline

Answer

Adrenaline

Question 9

Through which of the following does glucose mediated insulin release occur?

Accepted Answer

ATP sensitive K+ channels

Answer

cAMP

Answer

Carrier-mediated glucose uptake (GLUT2)

Answer

Receptor phosphorylation

Question 10

Which of the following would be least likely seen 14 days after a rat is injected with a drug that kills all of its pancreatic B cells?

Accepted Answer

A fall in the plasma amino acid concentration

Answer

A rise in plasma osmolality

Answer

A rise in the plasma H+ concentration

Answer

A rise in the plasma amino acid concentration

Endocrinology — MCQs

Endocrinology — MCQs

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