Endocrinology Practice Questions

Q: Hyperpigmentation in Addison's disease is due to increased secretion of:

B. ACTH. ***ACTH*** - In **primary adrenal insufficiency** (Addison's disease), low cortisol production results in loss of negative feedback to the pituitary gland, leading to massively increased secretion of **ACTH** (Adrenocorticotropic Hormone) [1]. - ACTH is synthesized from the precursor molecule **Pro-opiomelanocortin (POMC)**. Cleavage of POMC also generates Melanocyte-Stimulating Hormone (MSH) (or ACTH itself acts like MSH), which stimulates melanocytes, causing **hyperpigmentation** [1]. *Cortisol* - Cortisol levels are **low** in Addison's disease because of adrenal gland destruction, which is the underlying pathological issue [2]. - Cortisol is a glucocorticoid and its primary role is metabolic; it does not directly stimulate **melanogenesis**. *Aldosterone* - Aldosterone, a mineralocorticoid, is also deficient in primary Addison's disease, leading to **salt-wasting** and electrolyte disturbances (hyponatremia, hyperkalemia) [2]. - Aldosterone's synthesis pathway is distinct from that of the pituitary hormone ACTH and therefore does not influence **skin pigmentation**. *Renin* - Renin levels are often **elevated** in Addison's disease due to hypovolemia and hypotension resulting from aldosterone deficiency (activation of the **Renin-Angiotensin-Aldosterone System**) [3]. - Renin is an enzyme secreted by the kidney and has no direct mechanism or shared precursor pathway related to stimulating **melanocytes**.

Q: A woman is diagnosed with a pituitary microadenoma and has elevated serum prolactin levels. She presents with secondary amenorrhea and infertility. What is the most likely mechanism by which hyperprolactinemia causes these symptoms?

Decreased GnRH secretion from the hypothalamus. ***Decreased GnRH secretion from the hypothalamus*** - High levels of prolactin directly inhibit the pulsatile release of **Gonadotropin-Releasing Hormone (GnRH)** from the hypothalamus. - This inhibition leads to decreased pituitary secretion of **Luteinizing Hormone (LH)** and Follicle-Stimulating Hormone (FSH), causing **hypogonadotropic hypogonadism**, resulting in anovulation, amenorrhea, and infertility. *Antagonism of estrogen receptors* - Prolactin primarily exerts its reproductive effects centrally on the **hypothalamic-pituitary axis**, not by acting as a peripheral antagonist of estrogen receptors. - The resulting symptoms are due to **low estrogen production** secondary to inhibited gonadotropins, not receptor blockade. *Increased pulsatile FSH secretion* - Hyperprolactinemia actually causes **decreased** and non-pulsatile secretion of FSH and LH, rather than an increase. - If FSH were increased, it would stimulate follicular development and likely lead to ovarian hyperfunction, which is the opposite of the clinical presentation. *Increased LH secretion from the pituitary* - Prolactin actively inhibits LH release, causing **low plasma LH** levels and disrupting the mid-cycle LH surge necessary for ovulation. - The resulting state is one of inadequate follicular stimulation and anovulation, causing infertility and oligomenorrhea/amenorrhea.

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

Inhibin B. **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."

Q: The blood levels of hormones are elevated during exercise and sleep as shown. Which hormone would exhibit this diurnal pattern?

Growth hormone. ***Growth hormone*** - **Growth hormone (GH)** secretion is known to increase significantly during both **strenuous exercise** and **sleep**, particularly during deep sleep stages. - The elevated levels during exercise promote **lipolysis** and **glucose production**, while during sleep, it facilitates **tissue repair** and **growth**. *Insulin* - **Insulin** levels typically **decrease during exercise** to promote the utilization of fat as fuel and increase during sleep in response to reduced metabolic demand and preparation for morning. - Its primary role is to regulate blood glucose, and its secretion is mainly stimulated by **high blood glucose** rather than exercise or sleep directly in this pattern. *Cortisol* - **Cortisol** secretion follows a **circadian rhythm**, peaking in the early morning and gradually decreasing throughout the day, reaching its lowest point at night. - While exercise can acutely increase cortisol, its **sleep-related pattern** is the opposite of what is shown, typically decreasing during early sleep. *Thyroid* - **Thyroid hormones (T3 and T4)** maintain a relatively **stable level** throughout the day and night, with minor diurnal fluctuations. - Their primary function is to regulate **metabolism** and they do not exhibit sharp, distinct peaks in response to exercise or sleep in the manner depicted.

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.

Question 1

Hyperpigmentation in Addison's disease is due to increased secretion of:

Accepted Answer

B. ACTH

Answer

C. Aldosterone

Answer

D. Renin

Answer

A. Cortisol

Question 2

A woman is diagnosed with a pituitary microadenoma and has elevated serum prolactin levels. She presents with secondary amenorrhea and infertility. What is the most likely mechanism by which hyperprolactinemia causes these symptoms?

Accepted Answer

Decreased GnRH secretion from the hypothalamus

Answer

Increased LH secretion from the pituitary

Answer

Antagonism of estrogen receptors

Answer

Increased pulsatile FSH secretion

Question 3

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

Accepted Answer

Inhibin B

Answer

Inhibin A

Answer

Progesterone

Answer

Estrone

Question 4

The blood levels of hormones are elevated during exercise and sleep as shown. Which hormone would exhibit this diurnal pattern?

Accepted Answer

Growth hormone

Answer

Insulin

Answer

Cortisol

Answer

Thyroid hormones

Question 5

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 6

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 7

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 8

Which hormone most strongly stimulates gluconeogenesis during prolonged fasting?

Accepted Answer

Glucagon

Answer

Insulin

Answer

Epinephrine

Answer

Cortisol

Question 9

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 10

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

Endocrinology — MCQs

Endocrinology — MCQs

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