Endocrinology — MCQs

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 381: Which of the following statements is true regarding calcium and phosphorus metabolism?

A. Parathormone increases phosphate reabsorption in the proximal convoluted tubule.
B. Parathormone increases calcium reabsorption in the proximal convoluted tubule.
C. Calcitriol increases phosphate reabsorption in the proximal convoluted tubule. (Correct Answer)
D. Calcitriol decreases phosphate absorption in the intestine.

Explanation: **Explanation:** The regulation of calcium and phosphorus is a tightly controlled process involving Parathyroid Hormone (PTH), Calcitriol (Active Vitamin D), and Calcitonin. **Why Option C is correct:** Calcitriol ($1,25-dihydroxycholecalciferol$) acts to increase the plasma levels of both calcium and phosphate. In the kidneys, it promotes the reabsorption of both ions in the proximal convoluted tubule (PCT). It achieves this by increasing the expression of sodium-dependent phosphate co-transporters (NaPi), thereby ensuring that the body retains phosphate for bone mineralization. **Analysis of Incorrect Options:** * **Option A:** PTH is the most potent **phosphaturic** hormone. It *decreases* phosphate reabsorption in the PCT by internalizing and degrading NaPi transporters. This prevents calcium-phosphate precipitation when PTH raises serum calcium. * **Option B:** While PTH increases calcium reabsorption, it does so primarily in the **Distal Convoluted Tubule (DCT)** and the thick ascending limb. In the PCT, PTH actually *decreases* the reabsorption of calcium (though its net effect on the kidney is calcium retention). * **Option D:** Calcitriol *increases* phosphate (and calcium) absorption in the intestine by upregulating transport proteins. **High-Yield Clinical Pearls for NEET-PG:** * **PTH Effect:** "Phosphate Trashing Hormone" (increases urinary $PO_4^{3-}$). * **FGF-23:** Another key phosphaturic hormone; it decreases phosphate reabsorption and inhibits calcitriol synthesis. * **Vitamin D Paradox:** While Calcitriol increases renal reabsorption of phosphate, its primary role in phosphate homeostasis is increasing intestinal absorption. * **PTH vs. Calcitriol:** PTH increases serum $Ca^{2+}$ but decreases $PO_4^{3-}$; Calcitriol increases both $Ca^{2+}$ and $PO_4^{3-}$.

Question 382: Which of the following receptors is NOT found in the nucleus?

A. Estrogen receptor
B. Androgen receptor (Correct Answer)
C. Thyroxine receptor
D. Vitamin D receptor

Explanation: To answer this question correctly, it is essential to distinguish between the two types of intracellular receptors: **Cytoplasmic** and **Nuclear**. ### **Why Androgen Receptor is the Correct Answer** The **Androgen receptor (Option B)**, along with Glucocorticoid, Mineralocorticoid, and Progesterone receptors, is primarily located in the **cytoplasm** in its inactive state. These receptors are bound to heat shock proteins (HSPs). Upon ligand binding, the receptor dissociates from the HSP, undergoes dimerization, and translocates into the nucleus to act as a transcription factor. ### **Analysis of Incorrect Options** * **Estrogen Receptor (Option A):** Unlike other steroid receptors, the Estrogen receptor is predominantly located **inside the nucleus**, even in its unbound state. * **Thyroxine (T3/T4) Receptor (Option C):** Thyroid hormone receptors are classic examples of **constitutive nuclear receptors**. They are always bound to DNA (Thyroid Response Elements), often acting as repressors until the hormone binds. * **Vitamin D Receptor (Option D):** Similar to Thyroid and Retinoic acid receptors, the Vitamin D receptor (VDR) is located **within the nucleus**. ### **High-Yield NEET-PG Pearls** * **Mnemonic for Cytoplasmic Receptors:** **"M-A-G-P"** (Mineralocorticoid, Androgen, Glucocorticoid, Progesterone). * **Nuclear Receptors:** Remember **"T-E-V-R"** (Thyroid, Estrogen, Vitamin D, Retinoic Acid). * **Mechanism:** All these receptors belong to the **Steroid Hormone Receptor Superfamily** and regulate gene expression by binding to specific DNA sequences called Hormone Response Elements (HREs). * **Exception:** While Estrogen is a steroid, its receptor is a notable exception as it resides in the nucleus, not the cytoplasm.

Question 383: Constriction of efferent arteriole produces which of the following effects?

A. Biphasic response on GFR
B. Increased peritubular oncotic pressure
C. Increased peritubular absorption
D. All of the above (Correct Answer)

Explanation: **Explanation:** The constriction of the efferent arteriole is a key physiological mechanism for regulating the Glomerular Filtration Rate (GFR) and tubular reabsorption. 1. **Biphasic response on GFR:** At low to moderate levels of constriction, GFR increases because the outflow resistance raises the glomerular hydrostatic pressure ($P_{GC}$). However, at high levels of constriction, the GFR actually decreases. This is because severe constriction significantly reduces Renal Plasma Flow (RPF), causing the filtration fraction to rise so sharply that the plasma oncotic pressure ($π_{GC}$) increases rapidly along the capillary, eventually opposing filtration. 2. **Increased peritubular oncotic pressure:** As blood passes through the glomerulus, fluid is filtered out, leaving behind concentrated plasma proteins. Efferent constriction increases the filtration fraction, meaning a higher proportion of plasma is filtered. Consequently, the blood entering the peritubular capillaries has a significantly higher colloid osmotic (oncotic) pressure. 3. **Increased peritubular absorption:** Tubular reabsorption is governed by Starling forces in the peritubular capillaries. The increased oncotic pressure (noted above) combined with a *decreased* peritubular hydrostatic pressure (due to the resistance at the efferent arteriole) creates a powerful pressure gradient that favors the movement of fluid from the interstitium back into the capillaries. **High-Yield Facts for NEET-PG:** * **Angiotensin II** preferentially constricts the efferent arteriole to maintain GFR during states of low renal perfusion (e.g., dehydration). * **ACE Inhibitors** block this mechanism, leading to efferent vasodilation, which can cause a precipitous drop in GFR in patients with renal artery stenosis. * **Filtration Fraction (FF) = GFR / RPF.** Efferent constriction always increases FF because it decreases RPF more than it affects GFR.

Question 384: All of the following hormones are secreted by the islet cells in the pancreas, EXCEPT:

A. Insulin
B. Somatostatin
C. Glucagon
D. Triacylglycerol hydrolase (Correct Answer)

Explanation: **Explanation:** The islets of Langerhans are the endocrine components of the pancreas, consisting of several distinct cell types that secrete hormones directly into the bloodstream. **Why Triacylglycerol hydrolase is the correct answer:** Triacylglycerol hydrolase (also known as **pancreatic lipase**) is an **exocrine enzyme**, not an endocrine hormone. It is synthesized and secreted by the **pancreatic acinar cells** into the pancreatic duct to aid in the digestion of dietary fats in the small intestine. It is not secreted by the islet cells. **Analysis of incorrect options:** * **Insulin:** Secreted by **Beta (β) cells** (approx. 60-70% of islet mass). it is the primary anabolic hormone responsible for lowering blood glucose. * **Glucagon:** Secreted by **Alpha (α) cells** (approx. 20-25% of islet mass). It is a catabolic hormone that increases blood glucose via glycogenolysis and gluconeogenesis. * **Somatostatin:** Secreted by **Delta (δ) cells** (approx. 5-10% of islet mass). It acts locally (paracrine) to inhibit the secretion of both insulin and glucagon. **High-Yield NEET-PG Pearls:** 1. **Other Islet Cells:** Don't forget **F cells (or PP cells)** which secrete Pancreatic Polypeptide, and **Epsilon (ε) cells** which secrete Ghrelin. 2. **Blood Flow Pattern:** Blood in the islets generally flows from the center (Beta cells) to the periphery (Alpha/Delta cells), allowing insulin to inhibit glucagon secretion directly. 3. **Marker for Insulin:** **C-peptide** is secreted in equimolar amounts with insulin and is a key clinical marker to distinguish endogenous insulin production from exogenous insulin administration.

Question 385: Oxytocin causes all except:

A. Lactogenesis (Correct Answer)
B. Milk ejection
C. Contraction of uterine muscle
D. Myoepithelial cell contraction

Explanation: **Explanation:** The correct answer is **A. Lactogenesis**. In endocrinology, it is crucial to distinguish between milk **production** and milk **ejection**. 1. **Why Lactogenesis is the correct answer:** Lactogenesis (the initiation of milk secretion) and Galactopoiesis (maintenance of milk production) are primarily functions of **Prolactin**, secreted by the anterior pituitary. Oxytocin has no role in the synthesis of milk; it only facilitates its release. 2. **Why other options are incorrect:** * **Milk ejection (B) & Myoepithelial cell contraction (D):** These are the same physiological process. Oxytocin causes the contraction of myoepithelial cells surrounding the mammary alveoli. This creates the "Milk Ejection Reflex" (or Let-down reflex) in response to suckling. * **Contraction of uterine muscle (C):** Oxytocin acts on the G-protein coupled receptors of the myometrium to increase intracellular calcium, causing powerful uterine contractions. This is essential for parturition (labor) and postpartum hemostasis. **NEET-PG High-Yield Pearls:** * **Site of Synthesis:** Oxytocin is synthesized in the **Paraventricular nucleus** (primarily) and Supraoptic nucleus of the **Hypothalamus**, then stored/released by the Posterior Pituitary (Neurohypophysis). * **Ferguson Reflex:** This is the positive feedback loop where uterine cervical stretching triggers more oxytocin release. * **Clinical Use:** Synthetic oxytocin (**Pitocin**) is the drug of choice for induction of labor and prevention of Postpartum Hemorrhage (PPH). * **Mnemonic:** **P**rolactin **P**roduces milk; **O**xyto**C**in **C**ontracts (myoepithelium/uterus).

Question 386: Which hormone is secreted by the posterior pituitary gland?

A. Growth Hormone (GH)
B. Thyroid Stimulating Hormone (TSH)
C. Antidiuretic Hormone (ADH) (Correct Answer)
D. Follicle Stimulating Hormone (FSH)

Explanation: **Explanation:** The posterior pituitary gland (neurohypophysis) does not synthesize hormones; instead, it stores and releases two hormones produced by the hypothalamus: **Antidiuretic Hormone (ADH/Vasopressin)** and **Oxytocin**. ADH is synthesized primarily in the **supraoptic nucleus**, while Oxytocin is synthesized in the **paraventricular nucleus**. They travel down the hypothalamo-hypophyseal tract and are released into the systemic circulation from the posterior pituitary in response to physiological triggers like increased plasma osmolarity. **Analysis of Incorrect Options:** * **A, B, and D (GH, TSH, FSH):** These are all synthesized and secreted by the **Anterior Pituitary (Adenohypophysis)**. The anterior pituitary contains specialized glandular cells (Somatotrophs for GH, Thyrotrophs for TSH, and Gonadotrophs for FSH/LH) regulated by hypothalamic releasing hormones. **NEET-PG High-Yield Pearls:** * **Storage Site:** Hormones in the posterior pituitary are stored in terminal nerve endings called **Herring Bodies**. * **ADH Receptors:** * **V1 receptors:** Located on vascular smooth muscle (cause vasoconstriction). * **V2 receptors:** Located in the late distal tubule and collecting ducts (increase water reabsorption via **Aquaporin-2** channels). * **Clinical Correlation:** A deficiency in ADH secretion or action leads to **Diabetes Insipidus**, characterized by polyuria and polydipsia. * **Mnemonic:** Remember **"FLAT PIG"** for Anterior Pituitary hormones (FSH, LH, ACTH, TSH, Prolactin, GH). If it’s not on this list, it’s likely Posterior Pituitary.

Question 387: Which one of the following androgens is not produced by Leydig cells of the testis?

A. Testosterone
B. Androstenedione
C. Dihydrotestosterone (Correct Answer)
D. Dehydroepiandrosterone

Explanation: ### Explanation **1. Why Dihydrotestosterone (DHT) is the Correct Answer:** The Leydig cells of the testis are the primary site for the synthesis of androgens from cholesterol. However, they lack significant amounts of the enzyme **5α-reductase**. Dihydrotestosterone (DHT) is a potent metabolite of testosterone produced primarily in **peripheral tissues** (such as the prostate, skin, and hair follicles) through the action of 5α-reductase on testosterone. Therefore, while the testis produces the precursors, DHT itself is not a direct secretory product of Leydig cells. **2. Analysis of Incorrect Options:** * **Testosterone (A):** This is the principal androgen secreted by Leydig cells (approx. 95% of circulating testosterone). Its production is stimulated by Luteinizing Hormone (LH). * **Androstenedione (B) and Dehydroepiandrosterone (DHEA) (D):** These are intermediate weak androgens in the steroidogenic pathway. Leydig cells contain the necessary enzymes (like 3β-HSD and 17β-HSD) to synthesize these precursors before they are converted into testosterone. Small amounts of these are secreted directly into the bloodstream. **3. Clinical Pearls & High-Yield Facts for NEET-PG:** * **Potency:** DHT is the most potent natural androgen; it has a higher affinity for the androgen receptor than testosterone. * **Embryology:** Testosterone is responsible for the development of internal male genitalia (Wolffian duct derivatives), whereas **DHT** is essential for the development of **external male genitalia** and the prostate. * **Clinical Correlation:** 5α-reductase inhibitors (e.g., **Finasteride**) are used to treat Benign Prostatic Hyperplasia (BPH) and male pattern baldness by blocking the peripheral conversion of testosterone to DHT. * **Rate-limiting step:** The conversion of cholesterol to pregnenolone by the enzyme **Desmolase** (stimulated by LH) is the rate-limiting step in Leydig cell steroidogenesis.

Question 388: Which one of the following is a precursor of both gonadal and adrenocortical hormones?

A. Progesterone (Correct Answer)
B. Cortisol
C. Testosterone
D. Corticosterone

Explanation: ### Explanation **1. Why Progesterone is the Correct Answer:** All steroid hormones are derived from **cholesterol**. The first step in steroidogenesis is the conversion of cholesterol to Pregnenolone. Pregnenolone is then converted into **Progesterone**. Progesterone serves as a critical "branching point" or common precursor in the steroidogenic pathway: * **Adrenocortical Hormones:** Progesterone is hydroxylated to form 11-deoxycorticosterone (leading to **Mineralocorticoids** like Aldosterone) and 17-hydroxyprogesterone (leading to **Glucocorticoids** like Cortisol). * **Gonadal Hormones:** Through the action of 17,20-lyase, 17-hydroxyprogesterone is converted into androstenedione, which serves as the precursor for **Androgens** (Testosterone) and **Estrogens**. **2. Why Other Options are Incorrect:** * **B. Cortisol:** This is an end-product of the glucocorticoid pathway in the adrenal cortex. It does not convert back into sex steroids or mineralocorticoids. * **C. Testosterone:** This is a terminal androgen produced primarily in the gonads. While it can be converted to Dihydrotestosterone (DHT) or Estradiol, it is not a precursor for adrenocortical hormones like cortisol or aldosterone. * **D. Corticosterone:** This is an intermediate in the mineralocorticoid pathway (precursor to aldosterone). It is "downstream" from progesterone and cannot be converted into gonadal steroids. **3. High-Yield Clinical Pearls for NEET-PG:** * **Rate-limiting step:** The conversion of Cholesterol to Pregnenolone by the enzyme **Desmolase** (Cholesterol side-chain cleavage enzyme), stimulated by ACTH. * **21-Hydroxylase Deficiency:** The most common cause of Congenital Adrenal Hyperplasia (CAH). It results in the shunting of precursors (like Progesterone and 17-OHP) away from cortisol/aldosterone synthesis toward androgen synthesis, leading to virilization. * **Mnemonic:** "Progesterone is the Pro-genitor" of the three major steroid pathways (Mineralocorticoids, Glucocorticoids, and Sex steroids).

Question 389: Glucose-mediated insulin release is primarily mediated through which mechanism?

A. ATP-dependent potassium channels (Correct Answer)
B. Cyclic adenosine monophosphate (cAMP)
C. Carrier modulators
D. Receptor phosphorylation

Explanation: ### Explanation The release of insulin from pancreatic beta cells is a sophisticated process of **stimulus-secretion coupling**. **Why Option A is Correct:** When blood glucose levels rise, glucose enters the beta cell via **GLUT-2** transporters. It undergoes glycolysis and oxidative phosphorylation, leading to an increase in the **ATP/ADP ratio** within the cytoplasm. This rise in ATP triggers the closure of **ATP-sensitive Potassium ($K_{ATP}$) channels**. The resulting decrease in $K^+$ efflux causes **depolarization** of the cell membrane. This depolarization opens **Voltage-Gated Calcium Channels (VGCC)**, allowing an influx of $Ca^{2+}$, which ultimately triggers the exocytosis of insulin granules. **Why Other Options are Incorrect:** * **Option B (cAMP):** While cAMP acts as a secondary messenger that *potentiates* insulin secretion (e.g., via Incretins like GLP-1), it is not the primary mediator of glucose-induced release. * **Option C (Carrier modulators):** This is a vague term; while GLUT-2 is a carrier, the "mediation" of release refers to the signaling cascade, not just entry. * **Option D (Receptor phosphorylation):** This describes the **mechanism of action** of insulin at the target cell (Tyrosine Kinase receptor), not the mechanism of its release. **NEET-PG High-Yield Pearls:** * **Sulfonylureas** (e.g., Gliclazide) work by directly closing these $K_{ATP}$ channels, bypassing glucose metabolism to treat Type 2 Diabetes. * **Diazoxide**, used in hyperinsulinism, keeps these channels *open*, inhibiting insulin release. * The $K_{ATP}$ channel is a complex of four **Kir6.2** subunits and four **SUR1** (Sulfonylurea Receptor) subunits. * **Rate-limiting step** of glucose sensing in the beta cell: **Glucokinase** enzyme activity.

Question 390: Which of the anterior pituitary hormones is under tonic inhibitory control from the hypothalamus, rather than hypothalamic releasing factors?

A. Luteinizing hormone (LH)
B. Follicle-stimulating hormone (FSH)
C. Thyroid-stimulating hormone (TSH)
D. Prolactin (PRL) (Correct Answer)

Explanation: **Explanation:** The secretion of most anterior pituitary hormones is primarily regulated by **hypothalamic releasing factors** (stimulatory control). However, **Prolactin (PRL)** is the unique exception as it is under **tonic inhibitory control** by the hypothalamus. **Why Prolactin is the correct answer:** The primary regulator of prolactin is **Dopamine**, which is secreted by the tuberoinfundibular neurons of the hypothalamus. Dopamine acts on **D2 receptors** on the lactotrophs of the anterior pituitary to inhibit prolactin release. If the pituitary stalk is severed (stalk effect), the levels of all other anterior pituitary hormones decrease, but **prolactin levels rise** because it has been released from this tonic inhibition. **Why the other options are incorrect:** * **LH and FSH (Options A & B):** These gonadotropins are under the positive, pulsatile control of **Gonadotropin-Releasing Hormone (GnRH)**. * **TSH (Option C):** Its secretion is primarily stimulated by **Thyrotropin-Releasing Hormone (TRH)**. While Somatostatin can inhibit TSH, the primary regulatory mode is stimulatory. **High-Yield Clinical Pearls for NEET-PG:** * **The "Stalk Effect":** Any lesion compressing the pituitary stalk (e.g., Craniopharyngioma) leads to **Hyperprolactinemia** due to the loss of dopamine delivery. * **Drug-Induced Hyperprolactinemia:** Antipsychotics (D2 antagonists) block dopamine's inhibitory effect, leading to galactorrhea and amenorrhea. * **TRH Influence:** In primary hypothyroidism, elevated TRH levels can stimulate lactotrophs, leading to secondary hyperprolactinemia. * **Prolactinoma:** The most common functioning pituitary adenoma; treated primarily with dopamine agonists like **Cabergoline** or Bromocriptine.

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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