Endocrinology Practice Questions

Q: Excessive production of aldosterone results in:

Depressed plasma renin. ***Depressed plasma renin*** - **Excessive aldosterone production** (primary hyperaldosteronism) independently leads to **sodium and water retention**, expanding extracellular fluid volume and consequently **suppressing renin secretion** via negative feedback. - While secondary hyperaldosteronism (e.g., due to renal artery stenosis) can involve high renin, primary aldosteronism is characterized by **low renin levels** because the adrenal glands are overproducing aldosterone autonomously. *Potassium retention* - Aldosterone's primary role in the kidney is to promote **sodium reabsorption** and **potassium excretion** in the principal cells of the collecting duct. - Therefore, excessive aldosterone typically leads to **hypokalemia** (low potassium levels) due to increased potassium loss, not retention. *Metabolic acidosis* - Aldosterone enhances the secretion of **hydrogen ions (H+)** in the intercalated cells of the collecting duct, helping to regulate acid-base balance. - Excessive aldosterone consequently leads to increased H+ excretion, which can result in **metabolic alkalosis**, not acidosis. *Severe hypotension* - Aldosterone promotes **sodium and water reabsorption**, leading to an increase in **blood volume** and **blood pressure**. - Therefore, excessive aldosterone production typically results in **hypertension** (high blood pressure), not hypotension.

Q: The arterial blood glucose concentration in normal humans after a meal is in the range of:

120 to 140 mg/dL. ***120 to 140 mg/dL*** - After a meal, **carbohydrates** are digested into glucose, which is absorbed into the bloodstream, causing a physiological rise in blood glucose levels. - This range represents the normal **postprandial (after meal)** peak glucose concentration in healthy individuals before insulin brings it back down. *30 to 50 mg/dL* - This range is significantly **lower than normal** and indicates severe **hypoglycemia**, which can lead to symptoms like confusion, seizures, and loss of consciousness. - Such low levels are not seen in healthy individuals after a meal. *50 to 70 mg/dL* - This range represents **mild to moderate hypoglycemia**, which can cause symptoms such as sweating, tremors, and hunger. - While lower than normal, it is still not the typical post-meal glucose level in healthy individuals. *220 to 250 mg/dL* - This range is significantly **higher than normal** and indicates **hyperglycemia**, suggesting impaired glucose regulation. - Such levels after a meal are often seen in individuals with **diabetes mellitus** or impaired glucose tolerance.

Q: Iodine uptake is seen in the following organ:

Thyroid. ***Thyroid*** - The **thyroid gland** actively traps **iodine** from the bloodstream using the **sodium-iodide symporter (NIS)** to synthesize thyroid hormones, **T3** and **T4**. - This high affinity for iodine is exploited in diagnostic imaging (e.g., **radioactive iodine uptake test**) and therapeutic applications (e.g., **radioactive iodine ablation** for thyroid cancer). *Parathyroid* - The **parathyroid glands** are primarily involved in regulating **calcium** and **phosphate** metabolism, producing **parathyroid hormone (PTH)**. - They do not have a significant mechanism for **iodine uptake** or utilization. *Ovary* - The **ovaries** are endocrine glands responsible for producing **estrogen** and **progesterone** and are involved in female reproduction. - They do not exhibit significant **iodine uptake** as they do not use iodine for their primary hormonal functions. *All of the options* - This option is incorrect because while the **thyroid** actively takes up iodine, the **parathyroid glands** and **ovaries** do not. - Only organs involved in **thyroid hormone synthesis** or with specific iodine-transporting mechanisms show significant iodine uptake.

Q: If blood supply to hypothalamus is interrupted through median eminence which hormone will have normal secretion?

Vasopressin. ***Vasopressin (ADH)*** - Vasopressin is synthesized in the **supraoptic and paraventricular nuclei** of the hypothalamus - It travels down **axons** (hypothalamic-hypophyseal tract) to the **posterior pituitary** where it is stored and released - Its secretion is **NOT dependent on the hypophyseal portal system** that passes through the median eminence - Interruption of the portal blood supply through the median eminence affects only the **anterior pituitary hormones** - Vasopressin secretion would remain **completely normal** as it bypasses the portal system entirely *Prolactin* - Prolactin is an anterior pituitary hormone under **tonic inhibition** by dopamine from the hypothalamus - Dopamine reaches the anterior pituitary via the **portal system through the median eminence** - Interruption of this blood supply would **block dopamine delivery**, resulting in **increased prolactin secretion** (not normal) - This is the classic "stalk effect" seen in pituitary stalk lesions *GH* - Growth Hormone requires **GHRH (Growth Hormone-Releasing Hormone)** stimulation from the hypothalamus - GHRH travels via the **portal system** to stimulate the anterior pituitary - Portal disruption prevents GHRH delivery → **Decreased GH secretion** *TSH* - Thyroid-Stimulating Hormone requires **TRH (Thyrotropin-Releasing Hormone)** stimulation - TRH travels via the **portal system** to the anterior pituitary - Portal disruption prevents TRH delivery → **Decreased TSH secretion**

Q: A 35 year old female presents to the OPD with headaches and high blood pressure. On investigations, increased aldosterone levels with low renin levels are seen and a diagnosis of Conn's syndrome is made. Excess secretion of aldosterone can cause all except

Slight increase in ECF volume. Slight increase in ECF volume - While aldosterone increases sodium reabsorption, the resulting ECF expansion is usually more than 'slight' and contributes significantly to hypertension [1]. - A significant increase in ECF volume is a hallmark of aldosterone excess due to its role in sodium and water retention [3]. *Hypertension* - Aldosterone causes sodium and water retention, leading to an increase in extracellular fluid volume and subsequently blood pressure [3]. - This is a primary clinical manifestation of Conn's syndrome. *Hypokalemia* - Aldosterone promotes the secretion of potassium into the renal tubules, leading to increased urinary excretion of potassium [2]. - Excessive aldosterone levels therefore result in hypokalemia, which is a classic feature of primary hyperaldosteronism [2]. *Increase in plasma Na+ > 7 meq/L* - While aldosterone increases sodium reabsorption, the increase in plasma sodium concentration is typically mild and rarely exceeds a few mEq/L [1]. - The elevated ECF volume triggers mechanisms that prevent severe hypernatremia, making a rise of more than 7 mEq/L unlikely [1].

Q: Which is not an action of cortisol?

Increases the number of eosinophils. ***Increases the number of eosinophils*** - Cortisol and other glucocorticoids actually cause a **decrease in the number of eosinophils** in circulation. - This effect is due to increased destruction of eosinophils and decreased production, contributing to their **immunosuppressive** actions. *Mobilization of fatty acids* - Cortisol plays a role in **lipid metabolism**, promoting the breakdown of fats from adipose tissue. - This leads to the **release of fatty acids** into the bloodstream for energy utilization, especially during stress or fasting. *Increases liver and plasma proteins* - Cortisol has an **anabolic effect on the liver**, promoting the synthesis of various proteins, including plasma proteins. - This contributes to maintaining protein levels in the body, although its overall effect on protein metabolism can be catabolic in muscle. *Stimulation of gluconeogenesis* - Cortisol is a major **glucocorticoid**, meaning it increases blood glucose levels. - It achieves this by stimulating the liver to produce glucose from non-carbohydrate sources like amino acids and glycerol, a process known as **gluconeogenesis**.

Q: All of the following act on cell membrane receptors except:

Cortisol. ***Cortisol*** - **Cortisol** is a **steroid hormone** which is **lipophilic** and can freely diffuse across the cell membrane to bind to **intracellular receptors** in the cytoplasm or nucleus. - Its mechanism of action involves altering gene transcription and protein synthesis, which is characteristic of steroid hormones acting on intracellular receptors. *TSH* - **Thyroid-stimulating hormone (TSH)** is a **glycoprotein hormone** that binds to specific **G protein-coupled receptors** on the surface of thyroid follicular cells. - This binding initiates a signaling cascade that stimulates thyroid hormone production and release. *Insulin* - **Insulin** is a **peptide hormone** that primarily acts by binding to and activating **tyrosine kinase receptors** on the cell surface of target cells like muscle, adipose, and liver cells. - This binding triggers a phosphorylation cascade leading to glucose uptake and metabolic regulation. *FSH* - **Follicle-stimulating hormone (FSH)** is a **glycoprotein hormone** that acts by binding to **G protein-coupled receptors** located on the surface of target cells in the gonads (granulosa cells in females, Sertoli cells in males). - Its binding activates intracellular signaling pathways that regulate reproductive functions, such as follicular development and spermatogenesis.

Q: Which of the following is the principal steroid secreted by the fetal adrenal cortex?

Dehydroepiandrosterone. ***Dehydroepiandrosterone*** - The **fetal adrenal cortex**, particularly the **fetal zone**, is highly active in synthesizing **steroid hormones**, with **dehydroepiandrosterone (DHEA)** being its principal secretion. - **DHEA** serves as a crucial precursor for **estrogen synthesis** in the placenta, which is essential for maintaining pregnancy. *Progesterone* - **Progesterone** is primarily synthesized by the **placenta** during pregnancy and by the **corpus luteum** in the early stages; it is not the main steroid secreted by the fetal adrenal cortex. - While progesterone is important for maintaining uterine quiescence, its production by the fetal adrenal gland is minimal compared to its placental synthesis. *Corticosterone* - **Corticosterone** is a glucocorticoid mainly produced by the adult adrenal cortex, and its synthesis in the fetal adrenal gland is less significant compared to DHEA. - In humans, **cortisol** is the primary glucocorticoid, while corticosterone is more prominent in rodents. *Cortisol* - **Cortisol** is the main glucocorticoid produced by the adult adrenal cortex, playing roles in stress response and metabolism, but it is not the principal steroid secreted by the fetal adrenal cortex. - While the fetal adrenal gland does produce some cortisol, its primary function is **DHEA** production for placental estrogen synthesis.

Q: Prolactin inhibiting substance is:

Dopamine. ***Dopamine*** - **Dopamine** acts as the primary **prolactin-inhibiting hormone (PIH)**, tonically suppressing prolactin release from the anterior pituitary. - It binds to **D2 receptors** on lactotroph cells, reducing prolactin synthesis and secretion. *Adrenaline* - **Adrenaline** (epinephrine) is primarily involved in the "fight or flight" response, affecting heart rate, blood pressure, and metabolism. - While it can indirectly influence pituitary hormones, it is not considered the primary prolactin-inhibiting substance. *Thyroxine* - **Thyroxine (T4)** is a thyroid hormone that regulates metabolism, growth, and development. - There is no direct role of thyroxine as a prolactin-inhibiting substance. *ACTH* - **Adrenocorticotropic hormone (ACTH)** stimulates the adrenal glands to produce cortisol. - It does not directly inhibit prolactin secretion.

Q: The suckling reflex:

Has afferent neuronal and efferent hormonal components. ***Correct: Has afferent neuronal and efferent hormonal components*** - The **suckling reflex** is a classic **neuroendocrine reflex** with both neural and hormonal components. - **Afferent pathway**: Mechanoreceptors in the nipple send sensory signals via **spinal nerves** to the hypothalamus. - **Efferent pathway**: Hormonal responses include **oxytocin release** (milk ejection) and **prolactin release** (milk production). - This represents the complete physiological description of the suckling reflex mechanism. *Incorrect: Triggers the release of oxytocin by stimulating the supraoptic nuclei* - While partially true, this is **anatomically imprecise**. - Oxytocin for milk ejection is primarily synthesized in the **paraventricular nuclei**, not the supraoptic nuclei. - The **supraoptic nucleus** primarily produces **vasopressin (ADH)**, though both nuclei produce some oxytocin. - This option is too specific and emphasizes the wrong nucleus. *Incorrect: Increases the release of dopamine from the arcuate nucleus* - The suckling reflex **decreases dopamine release** from the arcuate nucleus (tuberoinfundibular neurons). - Since dopamine acts as **prolactin-inhibiting factor (PIF)**, decreased dopamine leads to **increased prolactin secretion**. - This disinhibition mechanism is essential for milk production during lactation. *Incorrect: Increases placental lactogen secretion* - **Human placental lactogen (hPL)** is secreted by the **placenta during pregnancy**, not postpartum. - It prepares mammary glands during pregnancy but does not respond to suckling. - After delivery, the placenta is expelled and hPL secretion ceases.

Question 1

Excessive production of aldosterone results in:

Accepted Answer

Depressed plasma renin

Answer

Potassium retention

Answer

Metabolic acidosis

Answer

Severe hypotension

Question 2

The arterial blood glucose concentration in normal humans after a meal is in the range of:

Accepted Answer

120 to 140 mg/dL

Answer

30 to 50 mg/dL

Answer

50 to 70 mg/dL

Answer

220 to 250 mg/dL

Question 3

Iodine uptake is seen in the following organ:

Accepted Answer

Thyroid

Answer

Parathyroid

Answer

Ovary

Answer

All of the options

Question 4

If blood supply to hypothalamus is interrupted through median eminence which hormone will have normal secretion?

Accepted Answer

Vasopressin

Answer

GH

Answer

TSH

Answer

Prolactin

Question 5

A 35 year old female presents to the OPD with headaches and high blood pressure. On investigations, increased aldosterone levels with low renin levels are seen and a diagnosis of Conn's syndrome is made. Excess secretion of aldosterone can cause all except

Accepted Answer

Slight increase in ECF volume

Answer

Hypertension

Answer

Hypokalemia

Answer

Increase in plasma Na+ > 7 meq/L

Question 6

Which is not an action of cortisol?

Accepted Answer

Increases the number of eosinophils

Answer

Mobilization of fatty acids

Answer

Increases liver and plasma proteins

Answer

Stimulation of gluconeogenesis

Question 7

All of the following act on cell membrane receptors except:

Accepted Answer

Cortisol

Answer

TSH

Answer

Insulin

Answer

FSH

Question 8

Which of the following is the principal steroid secreted by the fetal adrenal cortex?

Accepted Answer

Dehydroepiandrosterone

Answer

Progesterone

Answer

Corticosterone

Answer

Cortisol

Question 9

Prolactin inhibiting substance is:

Accepted Answer

Dopamine

Answer

Adrenaline

Answer

Thyroxine

Answer

ACTH

Question 10

The suckling reflex:

Accepted Answer

Has afferent neuronal and efferent hormonal components

Answer

Increases the release of dopamine from the arcuate nucleus

Answer

Increases placental lactogen secretion

Answer

Triggers the release of oxytocin by stimulating the supraoptic nuclei

Endocrinology — MCQs

Endocrinology — MCQs

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