Endocrinology Practice Questions

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.

Q: Which of the following is not seen after removal of testis in an adult?

Decrease FSH. ***Decrease FSH*** - Removal of the testes (orchiectomy) in an adult leads to a **decrease in testosterone production** and the **loss of inhibin B**, which normally suppress FSH secretion. - This reduction in negative feedback on the pituitary gland results in a **marked rise in FSH and LH levels**, not a decrease. - Therefore, "decrease FSH" is **NOT seen** after testicular removal - FSH actually **increases**. *Impotence* - The testes are the primary site of **testosterone production**, which is crucial for erectile function. - Their removal substantially reduces testosterone, leading to **erectile dysfunction (impotence)**. *Loss of libido* - **Testosterone** plays a vital role in maintaining sexual desire and libido in males. - Orchiectomy causes a significant drop in testosterone, leading to a **marked decrease or loss of libido**. *Muscle weakness* - **Testosterone** has anabolic effects, promoting muscle growth and strength. - Its removal leads to a chronic state of **hypogonadism**, often resulting in **muscle atrophy and weakness** over time.

Q: Which of the following is the primary physiological stimulus for prolactin release?

Nipple stimulation. ***Nipple stimulation*** - **Nipple stimulation** (e.g., during breastfeeding or suckling) is the **primary physiological stimulus** for prolactin release. - It activates neural pathways from the nipple to the hypothalamus, which **inhibit dopamine release**. - Since dopamine acts as **prolactin-inhibiting hormone (PIH)**, reduced dopamine leads to **disinhibition** of prolactin secretion from the anterior pituitary lactotroph cells. - This is the most clinically important mechanism for maintaining lactation. *Increased sleep duration* - Prolactin levels do exhibit a **circadian rhythm** with elevated levels during sleep (nocturnal surge). - However, sleep is not considered a primary or acute stimulus for prolactin release. - **Suckling/nipple stimulation** and **stress** are much more potent stimuli. *Reduction in dopamine levels* - This represents the **biochemical mechanism** underlying prolactin release rather than a physiological stimulus. - Dopamine from the hypothalamus tonically **inhibits** prolactin secretion. - Various physiological stimuli (like nipple stimulation, stress, or pregnancy) work by reducing dopamine tone. - When asking for a "stimulus," we refer to the **initiating event** (e.g., suckling), not the intermediate biochemical step. *Elevated blood glucose levels* - **Elevated blood glucose** primarily stimulates **insulin release** from pancreatic beta cells. - There is no direct physiological link between blood glucose and prolactin secretion. - Prolactin is not involved in glucose homeostasis.

Q: Appetite is stimulated by all except

Melanocyte stimulating hormone. ***Melanocyte stimulating hormone*** - **Alpha-melanocyte stimulating hormone (α-MSH)** is a catabolic hormone that acts to reduce appetite and increase energy expenditure. - It is an **anorexigenic peptide** that suppresses feeding by binding to central melanocortin receptors, primarily MC4R. *Neuropeptide Y* - **Neuropeptide Y (NPY)** is a potent **orexigenic peptide** that stimulates appetite and food intake. - It plays a crucial role in regulating energy balance and is increased during fasting states. *Agouti related peptide* - **Agouti-related peptide (AgRP)** is a strong **orexigenic peptide** that increases food intake. - It acts as an **antagonist** at the MC3R and MC4R melanocortin receptors, counteracting the appetite-suppressing effects of α-MSH. *Melanocyte concentrating hormone* - **Melanin-concentrating hormone (MCH)** is an **orexigenic neuropeptide** that stimulates feeding behavior. - It is primarily expressed in the lateral hypothalamus and plays a significant role in promoting appetite and weight gain.

Q: Systemic factor which is responsible for bone remodeling :

PTH. ***PTH*** - **Parathyroid hormone (PTH)** is a major systemic regulator of bone remodeling, primarily influencing **calcium and phosphate homeostasis**. - High levels of PTH, particularly prolonged or continuous elevation, stimulate **osteoclasts** directly or indirectly, leading to increased **bone resorption**. *Cytokines (e.g., IL-1, IL-6)* - These are primarily **local humoral factors** that regulate bone remodeling in a specific area, often in response to inflammation or injury. - While they can influence bone metabolism, their action is generally more localized, unlike the widespread systemic effects of PTH. *Prostaglandin E2 (PGE2)* - **PGE2** is another **local mediator** involved in bone remodeling, produced by various cells including osteoblasts and osteocytes. - It plays a role in both bone formation and resorption depending on concentration and context, but its effects are typically paracrine or autocrine rather than systemic endocrine control. *Transforming Growth Factor-beta (TGF-β)* - **TGF-β** is a potent **local growth factor** stored within the bone matrix and released during bone resorption. - It regulates proliferation and differentiation of osteoblasts and osteoclasts, primarily acting as a local regulator of bone formation and repair rather than a systemic hormone.

Question 1

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 2

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 3

All of the following act on cell membrane receptors except:

Accepted Answer

Cortisol

Answer

TSH

Answer

Insulin

Answer

FSH

Question 4

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

Accepted Answer

Dehydroepiandrosterone

Answer

Progesterone

Answer

Corticosterone

Answer

Cortisol

Question 5

Prolactin inhibiting substance is:

Accepted Answer

Dopamine

Answer

Adrenaline

Answer

Thyroxine

Answer

ACTH

Question 6

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

Question 7

Which of the following is not seen after removal of testis in an adult?

Accepted Answer

Decrease FSH

Answer

Impotence

Answer

Loss of libido

Answer

Muscle weakness

Question 8

Which of the following is the primary physiological stimulus for prolactin release?

Accepted Answer

Nipple stimulation

Answer

Increased sleep duration

Answer

Reduction in dopamine levels

Answer

Elevated blood glucose levels

Question 9

Appetite is stimulated by all except

Accepted Answer

Melanocyte stimulating hormone

Answer

Neuropeptide Y

Answer

Agouti related peptide

Answer

Melanocyte concentrating hormone

Question 10

Systemic factor which is responsible for bone remodeling :

Accepted Answer

PTH

Answer

Cytokines (e.g., IL-1, IL-6)

Answer

Prostaglandin E2 (PGE2)

Answer

Transforming Growth Factor-beta (TGF-β)

Endocrinology — MCQs

Endocrinology — MCQs

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