Endocrinology — MCQs

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 641: Increased ratio of insulin to glucagon causes

A. Decreased amino acid synthesis
B. Decreased levels of lipoprotein lipase
C. Hypoglycemia (Correct Answer)
D. Enhanced lipolysis in adipose tissue

Explanation: ***Hypoglycemia*** - An increased insulin-to-glucagon ratio indicates **high insulin levels**, promoting glucose uptake and utilization by cells, which can lead to a drop in blood glucose below normal levels. - High insulin suppresses **hepatic glucose production** (gluconeogenesis and glycogenolysis) and stimulates **glycogenesis**, further lowering blood glucose. *Decreased amino acid synthesis* - **Insulin** is an **anabolic hormone** that promotes protein synthesis, including amino acid incorporation into proteins. - Therefore, an increased insulin-to-glucagon ratio would generally **increase**, not decrease, amino acid synthesis. *Decreased levels of lipoprotein lipase* - **Insulin enhances the activity and synthesis of lipoprotein lipase (LPL)**, particularly in adipose tissue. - This promotes the uptake of fatty acids from circulating lipoproteins into fat cells for storage. *Enhanced lipolysis in adipose tissue* - **Insulin inhibits lipolysis**, the breakdown of triglycerides into fatty acids and glycerol, in adipose tissue. - An increased insulin-to-glucagon ratio would therefore **suppress**, rather than enhance, lipolysis.

Question 642: Menopausal hot flushes occur due to

A. Decrease in estrogen (Correct Answer)
B. FSH secretion
C. Increase in progesterone
D. Increase in estrogen

Explanation: ***Decrease in estrogen*** - **Decreased estrogen** levels in menopause lead to a narrowing of the **thermo-neutral zone**, causing the body to be more sensitive to small changes in core body temperature. - This hormonal withdrawal results in **vasodilation** and a sensation of heat, culminating in a hot flush. *FSH secretion* - While **FSH (Follicle-Stimulating Hormone)** levels do increase significantly during menopause due to reduced negative feedback from estrogen, FSH itself does not directly cause hot flushes. - The elevated FSH is a consequence of ovarian failure and is a marker of menopause, but the primary cause of hot flashes is the estrogen withdrawal. *Increase in progesterone* - **Progesterone levels actually decline** during menopause as ovulation ceases. - An increase in progesterone is not associated with hot flushes; rather, cyclical progesterone therapy can sometimes mitigate symptoms in certain hormonal contexts. *Increase in estrogen* - Hot flushes are a hallmark symptom of **estrogen deficiency**, not an increase in estrogen. - Conditions involving increased estrogen (e.g., pregnancy or certain tumors) would not typically present with menopausal hot flushes.

Question 643: Which of the following hormones will be affected most after the change in sex hormone binding globulin?

A. Testosterone (Correct Answer)
B. Progesterone
C. DHEA
D. Estrogen

Explanation: ***Testosterone*** - **Sex hormone-binding globulin (SHBG)** binds primarily to **testosterone** (and dihydrotestosterone) with **high affinity**. - SHBG has approximately **5 times greater affinity** for testosterone compared to estradiol. - A change in SHBG levels will significantly impact the proportion of **free (biologically active) testosterone** available in the circulation, thus affecting its overall function and measurement. - This makes testosterone the hormone **most affected** by changes in SHBG levels. *Progesterone* - **Progesterone** is primarily bound to **albumin** and **corticosteroid-binding globulin (CBG)**, not SHBG. - Therefore, changes in SHBG would have minimal direct impact on progesterone levels or its bioavailability. *DHEA* - **Dehydroepiandrosterone (DHEA)** is mostly bound to **albumin** in the blood. - Its binding to SHBG is negligible, making changes in SHBG irrelevant to its overall circulating levels or activity. *Estrogen* - **Estrogen (estradiol)** also binds to SHBG, but with **significantly lower affinity** than testosterone (approximately 5-fold less). - While affected by SHBG changes, the impact is less pronounced than on testosterone due to the lower binding affinity and its additional binding to albumin.

Question 644: A patient is on a low calcium diet for 8 weeks. Which of the following increases to maintain serum calcium levels?

A. Active 24,25 dihydroxy cholecalciferol
B. PTH (Correct Answer)
C. Serum phosphate level
D. Calcitonin

Explanation: ***PTH*** - **Parathyroid hormone (PTH)** is the primary regulator of calcium homeostasis and the key hormone that **increases in response to hypocalcemia** (low serum calcium). - In a patient on a low calcium diet for 8 weeks, **PTH secretion increases** to maintain normal serum calcium levels. - PTH acts through three main mechanisms: increasing **bone resorption** (releasing calcium from bone), enhancing renal **calcium reabsorption** in the distal tubule, and stimulating the production of **active vitamin D (1,25-dihydroxycholecalciferol)** which increases intestinal calcium absorption. *Active 24,25 dihydroxy cholecalciferol* - **24,25-dihydroxycholecalciferol** is a relatively **inactive metabolite** of vitamin D and represents a pathway of vitamin D catabolism, not activation. - The **active form** of vitamin D that increases calcium absorption is **1,25-dihydroxycholecalciferol (calcitriol)**, whose production is stimulated by PTH. - This metabolite does **not increase** in response to hypocalcemia as a compensatory mechanism. *Serum phosphate level* - A low calcium diet would **not directly lead to an increase in serum phosphate levels**. - In fact, PTH (which increases in response to low calcium) typically causes a **decrease in serum phosphate** by promoting renal phosphate excretion (phosphaturic effect). - High phosphate levels can actually exacerbate hypocalcemia by forming insoluble calcium-phosphate complexes. *Calcitonin* - **Calcitonin** is released from the thyroid parafollicular cells (C cells) in response to **high serum calcium levels** (hypercalcemia). - It acts to **lower** calcium by inhibiting osteoclast activity and reducing renal calcium reabsorption. - In hypocalcemia (low calcium diet), calcitonin secretion would **decrease, not increase**, making this the opposite of what occurs to maintain calcium homeostasis.

Question 645: If iodine supplementation in the diet was completely stopped today, thyroid hormone levels in blood will be severely depleted after:

A. 7 days
B. 30 days
C. 360 days
D. 90 days (Correct Answer)

Explanation: *7 days* - A 7-day period is too short for thyroid hormone levels to be severely depleted, given the **large iodine reserve** in the thyroid gland. - While daily iodine intake is essential, the body's stores provide a **buffer against acute deficiencies**. *30 days* - While some changes might begin to occur after 30 days, severe depletion of **thyroid hormone levels** is unlikely as the iodine stores are still substantial. - The body's homeostatic mechanisms would continue to draw upon the **thyroid's iodine reserve** during this period. *360 days* - A 360-day period is *too long*; severe depletion of **thyroid hormone levels** would have occurred much earlier. - By this point, the individual would likely be experiencing significant symptoms of **hypothyroidism** due to chronic iodine deficiency. ***90 days*** - The human body has a **significant reserve of iodine** stored in the thyroid gland, primarily within **colloid**. - This stored iodine is sufficient to maintain normal thyroid hormone production for approximately **2 to 4 months** in the absence of dietary intake. - Therefore, **90 days (approximately 3 months)** is when thyroid hormone levels would be severely depleted after complete cessation of iodine supplementation.

Question 646: Adrenal medulla secretes all EXCEPT:

A. Epinephrine
B. Norepinephrine
C. Dopamine
D. Cortisol (Correct Answer)

Explanation: ***Cortisol*** - **Cortisol** is a **glucocorticoid** hormone primarily secreted by the **adrenal cortex**, not the adrenal medulla. - Its main functions include regulating metabolism, suppressing the immune system, and aiding in stress response. *Epinephrine* - **Epinephrine** (adrenaline) is the primary hormone secreted by the **adrenal medulla**, constituting about 80% of its output. - It plays a crucial role in the **"fight-or-flight" response**, increasing heart rate, blood pressure, and glucose levels. *Norepinephrine* - **Norepinephrine** (noradrenaline) is also secreted by the **adrenal medulla**, making up about 20% of its secretion. - It works alongside epinephrine in the **sympathetic nervous system** to constrict blood vessels and increase alertness. - Norepinephrine also serves as a precursor in the biosynthesis of epinephrine. *Dopamine* - **Dopamine** is an important **neurotransmitter** that also serves as a precursor in the synthesis of norepinephrine and epinephrine. - While dopamine itself is secreted in small amounts by the adrenal medulla, its primary role is generally considered in the central nervous system and as an intermediate in catecholamine synthesis.

Question 647: Which of the following is true regarding parathormone (PTH)?

A. 90% calcium excreted by the glomerulus
B. Parathormone (PTH) promotes absorption of Ca++ from the intestine (Correct Answer)
C. PTH primarily acts on proximal tubule for calcium reabsorption
D. PTH promotes action of calcitonin

Explanation: ***Parathormone (PTH) promotes absorption of Ca++ from intestine*** - PTH **indirectly increases intestinal calcium absorption** by stimulating the renal synthesis of **1,25-dihydroxycholecalciferol (calcitriol)**, the active form of vitamin D. - Calcitriol then acts on the intestine to **enhance calcium absorption**. *PTH promote action of calcitonin* - **PTH and calcitonin** have **opposing effects** on calcium metabolism; PTH increases blood calcium, while calcitonin decreases it. - PTH directly stimulates bone resorption and renal calcium reabsorption, actions that would counteract rather than promote calcitonin's effects. *90% calcium excreted by glomerulus* - The **glomerulus filters approximately 99% of plasma calcium**, but the vast majority of this filtered calcium is subsequently reabsorbed in the renal tubules. - Only a **small percentage (typically less than 1-2%)** of filtered calcium is ultimately excreted in the urine under normal conditions. *PTH primarily acts on proximal tubule for calcium reabsorption* - While PTH does affect renal calcium reabsorption, its primary site of action for **increasing calcium reabsorption is the distal convoluted tubule and collecting ducts**. - In the **proximal tubule**, calcium reabsorption is largely unregulated and occurs passively along with sodium and water, with PTH having a less direct or significant role there.

Question 648: Which of the following statements is not true?

A. Mg2+ deficiency impairs PTH secretion and can lead to hypocalcemia
B. Parathyroid hormone-related protein is responsible for causing hypercalcemia in cancer patients
C. Ca2+ influences PTH secretion by acting on a calcium sensor G-protein coupled receptor located in the parathyroid gland
D. The unionized fraction of calcium in the plasma is an important determinant of PTH secretion (Correct Answer)

Explanation: ***The unionized fraction of calcium in the plasma is an important determinant of PTH secretion*** - The **ionized (free)** fraction of calcium, not the unionized fraction, is the physiologically active form that is critical for regulating **PTH secretion** and other cellular processes. - The parathyroid glands respond to the level of ionized calcium in the extracellular fluid to maintain **calcium homeostasis**. - This is the **FALSE statement** because unionized calcium is not the active determinant. *Mg2+ deficiency impairs PTH secretion and can lead to hypocalcemia* - **Hypomagnesemia** impairs PTH secretion and also causes target tissue resistance to PTH. - This leads to **hypocalcemia** that is difficult to correct until magnesium levels are restored. - Magnesium is a necessary cofactor for normal parathyroid function. *Parathyroid hormone-related protein is responsible for causing hypercalcemia in cancer patients* - **Parathyroid hormone-related protein (PTHrP)** is indeed a common cause of **humoral hypercalcemia of malignancy (HHM)**, mimicking the actions of PTH and leading to high calcium levels in cancer patients. - Many tumors, particularly squamous cell carcinomas, produce PTHrP, which binds to **PTH receptors** in bone and kidneys, resulting in increased bone resorption and renal calcium reabsorption. *Ca2+ influences PTH secretion by acting on a calcium sensor G-protein coupled receptor located in the parathyroid gland* - **Calcium (Ca2+)** directly regulates PTH secretion via the **calcium-sensing receptor (CaSR)**, which is a G-protein coupled receptor located on the chief cells of the parathyroid glands. - When **extracellular ionized calcium levels** are high, CaSR is activated, leading to inhibition of PTH secretion; conversely, low calcium levels reduce CaSR activation, stimulating PTH release.

Question 649: Which of the following inhibits appetite by counteracting the effects of neuropeptide Y?

A. Orexins
B. Leptin (Correct Answer)
C. Neuropeptide Y
D. Ghrelin

Explanation: ***Leptin*** - **Leptin** is a hormone primarily produced by **adipose tissue** that signals satiety to the brain, effectively counteracting the appetite-stimulating effects of neuropeptide Y. - It acts on receptors in the **hypothalamus** to reduce food intake and increase energy expenditure, thereby inhibiting appetite. *Orexins* - **Orexins** (also known as hypocretins) are **neurotransmitters** involved in regulating **wakefulness** and appetite. - Their primary role related to appetite is typically to **stimulate hunger** and food seeking behavior, rather than inhibiting it. *Neuropeptide Y* - **Neuropeptide Y (NPY)** is a potent **orexigenic peptide**, meaning it **stimulates appetite** and food intake. - It promotes the consumption of carbohydrates and is a key mediator of hunger signals in the brain through its action on the **hypothalamus**. *Ghrelin* - **Ghrelin** is a hormone produced mainly in the **stomach** that acts as a strong **appetite stimulant**. - It is often referred to as the "**hunger hormone**" and its levels rise before meals, signaling the brain to initiate food seeking.

Question 650: Stress induced hyperglycemia is mediated through which hormone:

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

Explanation: ***Cortisol*** - **Cortisol** is the **primary mediator** of stress-induced hyperglycemia among the counter-regulatory hormones - It promotes **gluconeogenesis** (formation of new glucose from amino acids and glycerol) in the liver - Stimulates **protein catabolism** in muscles, providing substrates for gluconeogenesis - Induces **insulin resistance** in peripheral tissues, reducing glucose uptake - Released as part of the **HPA axis response** to stress, with sustained elevation during prolonged stress - This is the **correct answer** for stress-induced hyperglycemia mediation *Epinephrine* - **Epinephrine** (adrenaline) is a potent hyperglycemic hormone but acts as an **acute, immediate response** to stress - Rapidly increases blood glucose through **glycogenolysis** (breakdown of glycogen) in liver and muscles - Stimulates **gluconeogenesis** and inhibits insulin secretion - Effects are **rapid but short-lived**, making it more of an emergency response rather than the sustained mediator - Works synergistically with cortisol but is not the primary sustained mediator *Growth hormone* - **Growth hormone** does contribute to hyperglycemia through **anti-insulin effects** and promoting lipolysis - Its hyperglycemic effects are **slower and less pronounced** compared to cortisol and epinephrine - Plays a role in **chronic stress** but is not the primary acute mediator - More important for **long-term metabolic adaptation** rather than immediate stress response *Insulin* - **Insulin** is a **glucose-lowering hormone** that facilitates glucose uptake into cells - During stress, insulin secretion is **suppressed** and tissues become **insulin-resistant** due to counter-regulatory hormones - It does **not mediate** stress-induced hyperglycemia; rather, its action is **opposed** by stress hormones - Decreased insulin action contributes to hyperglycemia but insulin itself is not the mediator

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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