Endocrinology Practice Questions

Q: Where are steroid receptors primarily located?

All of the above. **Explanation:** Steroid hormones are lipophilic (lipid-soluble) molecules derived from cholesterol. Because they can easily cross the lipid bilayer of the cell membrane, their receptors are not limited to a single location. 1. **Why "All of the above" is correct:** While classic textbooks often emphasize intracellular receptors, modern physiology recognizes that steroid receptors exist in three primary locations: * **Cytoplasm:** Classically, **Glucocorticoid** and **Mineralocorticoid** receptors are found in the cytoplasm. Upon binding, they translocate into the nucleus. * **Nucleus:** Receptors for **Estrogen, Progesterone, and Androgens** are primarily located within the nucleus even before the hormone binds. * **Cell Membrane:** Steroids can also bind to membrane-bound receptors to trigger "non-genomic" effects (rapid actions that do not involve gene transcription), such as the rapid effect of aldosterone on vascular tone. 2. **Analysis of Options:** * **Option A:** Incorrect as a sole answer because membrane receptors represent only the rapid-action pathway. * **Option B & C:** Incorrect as sole answers because different steroid classes favor different intracellular compartments. **High-Yield NEET-PG Pearls:** * **Mnemonic for Receptor Location:** * **C**ytoplasmic: **C**ortisol (Glucocorticoids) and Aldosterone. * **N**uclear: **E**strogen, **P**rogesterone, **T**estosterone (Androgens), and **T**hyroid hormone (though Thyroid hormone is not a steroid, it shares the nuclear receptor mechanism). * **Mechanism of Action:** Most steroids act as **transcription factors**, binding to Hormone Response Elements (HRE) on DNA to regulate mRNA synthesis. * **Exception:** Vitamin D (a steroid derivative) has receptors primarily in the **nucleus**.

Q: Sertoli cells have receptors for which hormone?

Follicle-stimulating hormone (FSH). **Explanation:** The correct answer is **Follicle-stimulating hormone (FSH)**. This is a fundamental concept in the hypothalamic-pituitary-gonadal axis. **1. Why FSH is correct:** Sertoli cells, often called "nurse cells," are located within the seminiferous tubules. They possess specific G-protein coupled receptors for **FSH**. When FSH binds to these receptors, it stimulates the Sertoli cells to facilitate spermatogenesis, produce **Androgen Binding Protein (ABP)** to maintain high local testosterone levels, and secrete **Inhibin B**. A helpful mnemonic is **"S for S"**: **S**ertoli cells are stimulated by **S**-FSH. **2. Why the other options are incorrect:** * **Luteinizing hormone (LH):** LH receptors are located on the **Leydig cells** (interstitial cells). LH stimulates Leydig cells to produce testosterone. (Mnemonic: **L for L**). * **Inhibin:** Inhibin is a *product* of the Sertoli cells, not a hormone for which they have primary receptors. It acts via negative feedback on the anterior pituitary to inhibit FSH secretion. * **Progesterone:** While steroid precursors exist in the testes, Sertoli cells are not the primary target for progesterone in the male reproductive axis. **3. NEET-PG High-Yield Pearls:** * **Blood-Testis Barrier:** Formed by tight junctions between adjacent Sertoli cells. * **Müllerian Inhibiting Substance (MIS):** Also secreted by Sertoli cells during fetal development to cause regression of paramesonephric ducts. * **Spermiation:** The process of releasing mature spermatozoa from Sertoli cells into the lumen of seminiferous tubules. * **Blood-Testis Barrier:** Protects germ cells from the immune system; Sertoli cells are the only non-germinal cells inside the seminiferous tubules.

Q: How many hormones are produced by the anterior pituitary gland?

5. **Explanation:** The anterior pituitary gland (adenohypophysis) is composed of distinct cell types that synthesize and secrete specific hormones. While many textbooks list six primary hormones, they are categorized into **five functional groups** based on the hormones produced: 1. **Growth Hormone (GH):** Produced by Somatotrophs. 2. **Prolactin (PRL):** Produced by Lactotrophs. 3. **Adrenocorticotropic Hormone (ACTH):** Produced by Corticotrophs. 4. **Thyroid-Stimulating Hormone (TSH):** Produced by Thyrotrophs. 5. **Gonadotropins (LH & FSH):** Produced by Gonadotrophs. *Note: Although LH and FSH are two different molecules, they are produced by the same cell type (Gonadotrophs) and act on the same target system, representing one functional hormonal axis.* **Why other options are incorrect:** * **Options A, B, and C:** These underestimate the complex endocrine function of the adenohypophysis, which regulates multiple peripheral glands (thyroid, adrenal, gonads) and somatic growth. * **Posterior Pituitary Note:** It is crucial to remember that the posterior pituitary (neurohypophysis) produces **zero** hormones; it only stores and releases ADH and Oxytocin, which are synthesized in the hypothalamus. **High-Yield NEET-PG Pearls:** * **Acidophils:** Somatotrophs (GH) and Lactotrophs (PRL). (Mnemonic: **GPA** - **G**rowth hormone, **P**rolactin are **A**cidophils). * **Basophils:** Corticotrophs, Thyrotrophs, and Gonadotrophs. (Mnemonic: **B-FLAT** - **B**asophils: **F**SH, **L**H, **A**CTH, **T**SH). * **Chromophobes:** These are cells that have depleted their hormone granules. * **Most abundant cell type:** Somatotrophs (approx. 50%).

Q: Which of the following is NOT seen in Growth Hormone (GH) deficiency?

Hyperglycemia. **Explanation:** The correct answer is **A. Hyperglycemia**. Growth Hormone (GH) is a potent **diabetogenic hormone**. It antagonizes the action of insulin, decreases glucose uptake by peripheral tissues (anti-insulin effect), and increases hepatic gluconeogenesis. Therefore, GH deficiency leads to **hypoglycemia** (especially fasting hypoglycemia), not hyperglycemia. **Analysis of other options:** * **B. Stunting:** GH is essential for linear bone growth via the production of IGF-1 (Somatomedin C). Deficiency results in proportionate short stature or stunting. * **C. Delayed bone age:** In GH deficiency, the maturation of the skeletal system is slowed. On X-ray, the bone age is significantly lagging behind the chronological age. * **D. High-pitched voice:** GH is responsible for the growth of the larynx. Deficiency leads to a small larynx, resulting in a characteristic high-pitched or "cherubic" voice. **High-Yield Clinical Pearls for NEET-PG:** * **Laron Syndrome:** A condition of GH insensitivity due to GH receptor mutations. Features include high GH levels but low IGF-1 levels. * **Micropenis:** A common clinical sign of congenital GH deficiency in male neonates due to lack of synergistic action with androgens. * **Metabolic Effects:** GH increases lipolysis (increasing free fatty acids) and promotes protein anabolism (positive nitrogen balance). * **Screening Test:** Insulin-induced hypoglycemia is the gold standard provocative test for GH deficiency (GH levels fail to rise).

Q: Which of the following secretes Testosterone in a normal male?

Leydig cells. **Explanation:** The primary source of testosterone in males is the **Leydig cells** (also known as interstitial cells), located in the connective tissue between the seminiferous tubules of the testes. This process is regulated by the Hypothalamic-Pituitary-Gonadal (HPG) axis. Luteinizing Hormone (LH) from the anterior pituitary binds to specific receptors on Leydig cells, stimulating the conversion of cholesterol into testosterone via the enzyme cholesterol desmolase. **Analysis of Options:** * **Leydig cells (Correct):** They secrete approximately 95% of circulating testosterone in males. The remaining 5% is produced by the adrenal cortex. * **Pituitary:** The anterior pituitary secretes **LH** (which stimulates testosterone production) and **FSH** (which stimulates spermatogenesis), but it does not produce steroid hormones like testosterone itself. * **Sertoli cells:** Located within the seminiferous tubules, these "nurse cells" support spermatogenesis. They secrete **Inhibin B** (which inhibits FSH) and **Androgen Binding Protein (ABP)**, which helps maintain high local concentrations of testosterone, but they do not synthesize testosterone. * **Liver:** The liver is the primary site for the **metabolism and conjugation** of testosterone into 17-ketosteroids for excretion; it is not a secretory organ for this hormone. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic:** **L**H acts on **L**eydig cells; **F**SH acts on **S**ertoli cells. * **Blood-Testis Barrier:** Formed by tight junctions between Sertoli cells. * **Testosterone Derivatives:** In peripheral tissues, testosterone is converted to the more potent **Dihydrotestosterone (DHT)** by the enzyme **5-alpha reductase**. * **Rate-limiting step:** The transport of cholesterol into the mitochondria by the **StAR protein** (Steroidogenic Acute Regulatory protein) is the rate-limiting step in testosterone synthesis.

Q: Which of the following statements is incorrect regarding melatonin?

It is secreted by the pituitary gland.. **Explanation:** The correct answer is **C**, as melatonin is **not** secreted by the pituitary gland; it is synthesized and secreted by the **pineal gland** (epiphysis cerebri). **1. Why Option C is the correct (incorrect statement) answer:** Melatonin is a derivative of the amino acid **Tryptophan**. It is produced by the pinealocytes of the pineal gland. The secretion is regulated by the suprachiasmatic nucleus (SCN) of the hypothalamus, which acts as the body's master biological clock. The pituitary gland, conversely, secretes hormones like GH, TSH, ACTH, and LH/FSH, but not melatonin. **2. Analysis of other options:** * **Option A & B:** Melatonin is known as the "hormone of darkness." Its levels rise in the evening, promoting sleep onset and regulating the sleep-wake cycle. Clinically, exogenous melatonin is used to treat **circadian rhythm disorders**, such as insomnia and **jet lag syndrome**, to help reset the internal clock. * **Option D:** This is a factual statement. The pineal gland is the primary anatomical source of melatonin in the body. **High-Yield NEET-PG Pearls:** * **Precursor:** Tryptophan → Serotonin → Melatonin. * **Rate-limiting enzyme:** N-acetyltransferase (activity increases at night). * **Light Inhibition:** Light exposure to the retina inhibits melatonin secretion via the retinohypothalamic tract. * **Other Functions:** It is a potent antioxidant and plays a role in inhibiting reproductive function (antigonadotropic effect) in certain species by inhibiting GnRH release. * **Tumor Association:** Pineal tumors can lead to precocious puberty if they destroy the gland (removing the inhibitory effect of melatonin on gonadotropins).

Q: Which of the following findings shall be seen in a patient with hyperparathyroidism?

Hypophosphatemia. **Explanation:** The primary function of **Parathyroid Hormone (PTH)** is to maintain calcium homeostasis by increasing serum calcium levels. In **Hyperparathyroidism**, the excess secretion of PTH acts on three main target organs: the bones, the kidneys, and the intestines (indirectly). **Why Hypophosphatemia is correct:** PTH has a potent **phosphaturic effect**. It acts on the proximal convoluted tubules (PCT) of the kidney to inhibit the sodium-phosphate cotransporter (NaPi-IIa). This leads to a decrease in the reabsorption of phosphate, causing increased urinary excretion of phosphate (**phosphaturia**) and a subsequent decrease in serum phosphate levels (**Hypophosphatemia**). **Analysis of Incorrect Options:** * **B. Hyperphosphatemia:** This is typically seen in *Hypoparathyroidism* or Chronic Kidney Disease (CKD). In hyperparathyroidism, the kidney is actively "wasting" phosphate. * **C & D. Magnesium levels:** While PTH can slightly increase magnesium reabsorption in the distal tubule, magnesium levels are not a primary diagnostic hallmark of hyperparathyroidism. In fact, chronic hyperparathyroidism can sometimes lead to mild *hypomagnesemia* due to associated hypercalciuria, but **Hypophosphatemia** is the classic, high-yield biochemical finding. **NEET-PG High-Yield Pearls:** 1. **Biochemical Triad:** Hypercalcemia + Hypophosphatemia + Hypercalciuria (the latter occurs because the filtered load of calcium exceeds the kidney's reabsorptive capacity). 2. **Bone Finding:** *Osteitis fibrosa cystica* (subperiosteal bone resorption, especially in phalanges). 3. **Renal Finding:** PTH stimulates **1-alpha-hydroxylase** in the kidneys, increasing the production of active Vitamin D [1,25(OH)₂D]. 4. **Mnemonic:** "Stones, bones, abdominal groans, and psychic overtones."

Q: Which of the following steroid hormones is a C-21 steroid?

Progesterone. **Explanation:** Steroid hormones are derivatives of cholesterol and are classified based on the number of carbon atoms in their structure. Understanding these carbon counts is a high-yield topic for NEET-PG. **1. Why Progesterone is Correct:** Progesterone belongs to the **Pregnane** group. All hormones in this group, including **Progesterone**, **Aldosterone**, and **Cortisol**, contain **21 carbon atoms (C-21)**. These are synthesized from pregnenolone, which is the immediate 21-carbon derivative of cholesterol (C-27). **2. Analysis of Incorrect Options:** * **A & C. Testosterone and Androgens:** These belong to the **Androstane** group. Androgens (like Testosterone and Dehydroepiandrosterone/DHEA) contain **19 carbon atoms (C-19)**. They are formed by the cleavage of the side chain of C-21 steroids. * **B. Estrogen:** Estrogens (like Estradiol, Estrone, and Estriol) belong to the **Estrane** group. They contain **18 carbon atoms (C-18)**. They are formed via the aromatization of C-19 androgens, a process that involves the loss of the C-19 methyl group. **High-Yield NEET-PG Pearls:** * **Carbon Count Summary:** * **C-27:** Cholesterol (Precursor) * **C-21:** Progestogens, Glucocorticoids, Mineralocorticoids (Pregnane series) * **C-19:** Androgens (Androstane series) * **C-18:** Estrogens (Estrane series) * **Rate-limiting step:** The conversion of Cholesterol (C-27) to Pregnenolone (C-21) by the enzyme **Desmolase** (CYP11A1) in the mitochondria. * **Aromatase:** The enzyme responsible for converting C-19 androgens to C-18 estrogens.

Question 1

Where are steroid receptors primarily located?

Accepted Answer

All of the above

Answer

Cellular membrane

Answer

Cytoplasm

Answer

Nucleus

Question 2

Sertoli cells have receptors for which hormone?

Accepted Answer

Follicle-stimulating hormone (FSH)

Answer

Luteinizing hormone (LH)

Answer

Inhibin

Answer

Progesterone

Question 3

How many hormones are produced by the anterior pituitary gland?

Accepted Answer

5

Answer

1

Answer

2

Answer

3

Question 4

Which of the following is NOT seen in Growth Hormone (GH) deficiency?

Accepted Answer

Hyperglycemia

Answer

Stunting

Answer

Delayed bone age

Answer

High pitched voice

Question 5

Which of the following secretes Testosterone in a normal male?

Accepted Answer

Leydig cells

Answer

Pituitary

Answer

Liver

Answer

Sertoli cells

Question 6

Which of the following statements is incorrect regarding melatonin?

Accepted Answer

It is secreted by the pituitary gland.

Answer

It induces sleep.

Answer

It is used in the treatment of jet lag syndrome.

Answer

It is a pineal hormone.

Question 7

Which of the following findings shall be seen in a patient with hyperparathyroidism?

Accepted Answer

Hypophosphatemia

Answer

Hyperphosphatemia

Answer

Hypermagnesemia

Answer

Hypomagnesemia

Question 8

What is the primary action of estrogen on bone?

Accepted Answer

Acts as an antiresorptive agent on trabecular bone

Answer

Stimulates bone matrix deposition

Answer

Has an anti-osteoblastic effect on compact bone

Answer

Acts as a resorptive agent on compact bone

Question 9

Estrogen receptors are typically located in which cellular compartment?

Accepted Answer

Nucleus

Answer

Microsomes

Answer

Membrane-bound organelles

Answer

Mitochondria

Question 10

Which of the following steroid hormones is a C-21 steroid?

Accepted Answer

Progesterone

Answer

Testosterone

Answer

Estrogen

Answer

Androgen

Endocrinology — MCQs

Endocrinology — MCQs

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