Endocrinology Practice Questions

Q: Increased ratio of insulin to glucagon causes

Hypoglycemia. ***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.

Q: Menopausal hot flushes occur due to

Decrease in estrogen. ***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.

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

Testosterone. ***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.

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

PTH. ***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.

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

90 days. *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.

Q: Adrenal medulla secretes all EXCEPT:

Cortisol. ***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.

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

Leptin. ***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.

Q: Stress induced hyperglycemia is mediated through which hormone:

Cortisol. ***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

Question 1

Increased ratio of insulin to glucagon causes

Accepted Answer

Hypoglycemia

Answer

Decreased amino acid synthesis

Answer

Decreased levels of lipoprotein lipase

Answer

Enhanced lipolysis in adipose tissue

Question 2

Menopausal hot flushes occur due to

Accepted Answer

Decrease in estrogen

Answer

FSH secretion

Answer

Increase in progesterone

Answer

Increase in estrogen

Question 3

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

Accepted Answer

Testosterone

Answer

Progesterone

Answer

DHEA

Answer

Estrogen

Question 4

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

Accepted Answer

PTH

Answer

Active 24,25 dihydroxy cholecalciferol

Answer

Serum phosphate level

Answer

Calcitonin

Question 5

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

Accepted Answer

90 days

Answer

7 days

Answer

30 days

Answer

360 days

Question 6

Adrenal medulla secretes all EXCEPT:

Accepted Answer

Cortisol

Answer

Epinephrine

Answer

Norepinephrine

Answer

Dopamine

Question 7

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

Accepted Answer

Parathormone (PTH) promotes absorption of Ca++ from the intestine

Answer

90% calcium excreted by the glomerulus

Answer

PTH primarily acts on proximal tubule for calcium reabsorption

Answer

PTH promotes action of calcitonin

Question 8

Which of the following statements is not true?

Accepted Answer

The unionized fraction of calcium in the plasma is an important determinant of PTH secretion

Answer

Mg2+ deficiency impairs PTH secretion and can lead to hypocalcemia

Answer

Parathyroid hormone-related protein is responsible for causing hypercalcemia in cancer patients

Answer

Ca2+ influences PTH secretion by acting on a calcium sensor G-protein coupled receptor located in the parathyroid gland

Question 9

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

Accepted Answer

Leptin

Answer

Orexins

Answer

Neuropeptide Y

Answer

Ghrelin

Question 10

Stress induced hyperglycemia is mediated through which hormone:

Accepted Answer

Cortisol

Answer

Epinephrine

Answer

Insulin

Answer

Growth hormone

Endocrinology — MCQs

Endocrinology — MCQs

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