Endocrinology Practice Questions

Q: Prolactin secretion is stimulated by:

TRH. **Explanation:** Prolactin (PRL) is unique among anterior pituitary hormones because its primary regulation is **inhibitory** rather than stimulatory. Under normal physiological conditions, the hypothalamus exerts a tonic inhibitory influence on prolactin via dopamine. **Why TRH is the correct answer:** Thyrotropin-Releasing Hormone (TRH), primarily known for stimulating TSH, also acts as a potent **prolactin-releasing factor**. In states of primary hypothyroidism, the lack of negative feedback leads to elevated TRH levels. This excess TRH stimulates lactotrophs in the anterior pituitary, leading to hyperprolactinemia. This explains why patients with hypothyroidism may present with galactorrhea or menstrual irregularities. **Analysis of Incorrect Options:** * **ACTH (Adrenocorticotropic Hormone):** This is a hormone secreted *by* the anterior pituitary to stimulate the adrenal cortex; it does not regulate prolactin secretion. * **GnRH (Gonadotropin-Releasing Hormone):** This stimulates the release of LH and FSH. Interestingly, high levels of prolactin actually *inhibit* GnRH secretion, leading to hypogonadism. * **Dopamine:** This is the primary **inhibitor** of prolactin (secreted via the tuberoinfundibular pathway). Drugs that block dopamine (antipsychotics) lead to increased prolactin levels. **NEET-PG High-Yield Pearls:** * **Prolactin Inhibitory Factor (PIF):** Dopamine. * **Prolactin Releasing Factors (PRF):** TRH, VIP (Vasoactive Intestinal Peptide), and Oxytocin. * **Physiological Stimuli:** Suckling (strongest), sleep, stress, and pregnancy (estrogen). * **Clinical Correlation:** Always check TSH levels in a patient with hyperprolactinemia to rule out primary hypothyroidism before considering a prolactinoma.

Q: FSH is secreted by which of the following cells?

Basophils. **Explanation:** The anterior pituitary (adenohypophysis) contains cells classified based on their staining properties with hematoxylin and eosin (H&E). **Basophils** are cells that stain with basic dyes and are responsible for secreting the "B-FLAT" hormones: **B**asophils produce **F**SH, **L**H, **A**CTH, and **T**SH. Specifically, FSH (Follicle-Stimulating Hormone) is secreted by **gonadotrophs**, which are a subtype of basophils. **Analysis of Options:** * **Option A (Chromophobes):** These are "color-hating" cells that do not pick up significant stain. They are generally considered to be either resting/degranulated acidophils/basophils or stem cells; they do not actively secrete FSH. * **Option C (Acidophils):** These stain with acidic dyes (eosin) and secrete Growth Hormone (Somatotrophs) and Prolactin (Lactotrophs). A common mnemonic is **"GPA"** (**G**rowth hormone, **P**rolactin are **A**cidophils). * **Option D (Theca interna cells):** These are ovarian cells, not pituitary cells. While they are involved in the reproductive axis, their role is to produce androgens (androstenedione) under the influence of LH, not to secrete FSH. **High-Yield Facts for NEET-PG:** * **Mnemonic for Pituitary Staining:** **"GPA"** (Acidophils: GH, Prolactin) and **"B-FLAT"** (Basophils: FSH, LH, ACTH, TSH). * **PAS Stain:** Basophils are PAS (Periodic Acid-Schiff) positive because the hormones they secrete (FSH, LH, TSH) are glycoproteins. * **Most Numerous Cell Type:** Somatotrophs (Acidophils) are the most abundant cells in the anterior pituitary. * **FSH Function:** In females, it stimulates follicular growth; in males, it acts on Sertoli cells to support spermatogenesis.

Q: Regarding the action of insulin, which of the following is true?

Decreased ketogenesis in the liver. **Explanation:** Insulin is the body’s primary **anabolic hormone**, secreted by the beta cells of the pancreas. Its overarching function is to promote energy storage and inhibit the mobilization of fuel reserves. **Why Option D is Correct:** Insulin **decreases ketogenesis** in the liver through two main mechanisms: 1. It inhibits **Hormone-Sensitive Lipase (HSL)** in adipose tissue, reducing the supply of free fatty acids (FFAs) to the liver. 2. It inhibits **Carnitine Palmitoyltransferase-1 (CPT-1)**, the rate-limiting enzyme for beta-oxidation, thereby preventing the conversion of fatty acids into ketone bodies. This is why insulin deficiency leads to Diabetic Ketoacidosis (DKA). **Analysis of Incorrect Options:** * **Option A:** Insulin **increases K+ uptake** into cells (muscle and adipose) by stimulating the Na+/K+ ATPase pump. This is why insulin/glucose infusion is a standard treatment for hyperkalemia. * **Option B:** Insulin is anabolic; it **increases protein synthesis** and **decreases protein catabolism** in muscle. * **Option C:** Insulin **inhibits Hormone-Sensitive Lipase (HSL)** to prevent lipolysis and instead activates **Lipoprotein Lipase (LPL)** to promote triglyceride storage in adipocytes. **High-Yield Clinical Pearls for NEET-PG:** * **GLUT-4:** The only insulin-dependent glucose transporter, found in skeletal muscle and adipose tissue. * **Enzyme Regulation:** Insulin dephosphorylates enzymes (usually activating them, except for HSL and Glycogen Phosphorylase, which are inactivated). * **Antagonism:** Glucagon, Epinephrine, Cortisol, and Growth Hormone are "counter-regulatory" hormones that oppose insulin's actions.

Q: Insulin secretion is inhibited by all of the following, EXCEPT:

Beta-ketoacids. **Explanation:** Insulin secretion from the pancreatic beta cells is a highly regulated process. To answer this question, one must distinguish between factors that inhibit insulin release and those that stimulate it. **Why Beta-ketoacids is the correct answer:** Beta-ketoacids (such as acetoacetate and beta-hydroxybutyrate) actually **stimulate** insulin secretion. This serves as a crucial physiological negative feedback loop: as ketone bodies rise (e.g., during fasting or starvation), they trigger a modest release of insulin to prevent runaway ketogenesis and the development of ketoacidosis. Therefore, they do not inhibit insulin; they promote it. **Analysis of incorrect options (Inhibitors of Insulin):** * **Somatostatin:** Known as the "universal endocrine off-switch," paracrine secretion of somatostatin from delta cells directly inhibits both insulin and glucagon release. * **Beta-adrenergic blockers:** Beta-2 receptors on pancreatic beta cells stimulate insulin release. Therefore, blocking these receptors (or alpha-adrenergic stimulation) results in the **inhibition** of insulin secretion. * **Diazoxide:** This drug is a potassium channel opener. By keeping the ATP-sensitive $K^+$ channels open, it hyperpolarizes the beta cell membrane, preventing calcium influx and thereby **inhibiting** insulin release. It is clinically used to treat hyperinsulinism. **NEET-PG High-Yield Pearls:** * **The "Incretin Effect":** Oral glucose stimulates more insulin than IV glucose due to GIP and GLP-1. * **Rate-limiting step:** The phosphorylation of glucose by **Glukokinase** is the glucose-sensor in beta cells. * **Alpha vs. Beta:** Alpha-2 adrenergic stimulation **inhibits** insulin, while Beta-2 stimulation **increases** it. In a "fight or flight" response, alpha-dominance ensures insulin is suppressed to keep blood glucose high for the brain and muscles.

Q: Which of the following statements can be regarded as the primary action of inhibin?

It inhibits the secretion of FSH.. ### Explanation **Correct Answer: D. It inhibits the secretion of FSH.** **Mechanism of Action:** Inhibin is a glycoprotein hormone belonging to the **transforming growth factor-beta (TGF-β) superfamily**. It is produced primarily by the **Sertoli cells** in males and the **Granulosa cells** in females. Its primary physiological role is the **selective negative feedback inhibition** of Follicle-Stimulating Hormone (FSH) secretion from the anterior pituitary. Unlike GnRH or sex steroids, inhibin does not significantly affect the secretion of Luteinizing Hormone (LH), making it a specific regulator of the FSH axis. **Analysis of Incorrect Options:** * **A & C (Prolactin and TSH):** Inhibin has no physiological role in regulating the secretion of Prolactin or Thyroid-Stimulating Hormone (TSH). These are regulated by Dopamine/TRH and TRH/Somatostatin, respectively. * **B (Estradiol Synthesis):** Inhibin does not stimulate estradiol synthesis. In fact, **Activin** (another member of the TGF-β family) is the hormone that stimulates FSH secretion and promotes granulosa cell aromatase activity, leading to increased estradiol. **High-Yield Clinical Pearls for NEET-PG:** * **Inhibin B vs. Inhibin A:** Inhibin B is the primary form in males (marker of spermatogenesis) and the early follicular phase in females. Inhibin A is dominant in the luteal phase and during pregnancy (produced by the corpus luteum and placenta). * **Clinical Marker:** Inhibin B levels are used as a clinical marker for **ovarian reserve** and **Sertoli cell function**. * **Tumor Marker:** Elevated Inhibin levels are a highly specific marker for **Granulosa Cell Tumors** of the ovary. * **The "Counter-Hormone":** Remember **Activin** as the functional antagonist to Inhibin; it stimulates FSH release.

Q: Bone resorption is enhanced by:

PGE2. ### Explanation **Correct Option: C (PGE2)** Prostaglandin E2 (PGE2) is a potent stimulator of bone resorption. It acts primarily by increasing the expression of **RANKL** (Receptor Activator of Nuclear Factor kappa-B Ligand) on osteoblasts and marrow stromal cells. RANKL then binds to its receptor, RANK, on osteoclast precursors, leading to their differentiation and activation. Additionally, PGE2 inhibits the production of **Osteoprotegerin (OPG)**, a decoy receptor that normally blocks RANKL, further shifting the balance toward bone breakdown. **Analysis of Incorrect Options:** * **A (PGD2):** Primarily involved in allergic and inflammatory responses, smooth muscle contraction, and sleep regulation. It does not play a significant role in bone remodeling. * **B (PGF2α):** Known for its role in luteolysis and uterine contraction. While it may have minor effects on bone cells, it is not the primary prostaglandin associated with bone resorption. * **D (PGI2 - Prostacyclin):** Produced by vascular endothelium, it is a potent vasodilator and inhibitor of platelet aggregation. It generally has an inhibitory effect on osteoclast activity, the opposite of PGE2. **High-Yield Facts for NEET-PG:** * **Mechanism:** PGE2 acts via G-protein coupled receptors (EP receptors), mainly increasing intracellular cAMP. * **Clinical Correlation:** Chronic inflammation (like Periodontitis or Rheumatoid Arthritis) leads to high local PGE2 levels, resulting in localized bone loss. * **NSAIDs Connection:** Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit COX enzymes, reducing PGE2 levels, which is why they can sometimes delay bone healing or be used to manage heterotopic ossification. * **Osteoblast Paradox:** While PGE2 stimulates resorption via RANKL, in certain pulsatile or low-dose conditions, it can also have anabolic (bone-forming) effects. However, in the context of standard physiology and exams, it is the classic mediator of **resorption**.

Q: All of the following cross the plasma membrane except?

Epinephrine. The core concept behind this question is the **solubility of hormones** and the location of their receptors. To cross the lipid bilayer of the plasma membrane, a molecule must be **lipophilic (lipid-soluble)**. ### **Explanation of the Correct Answer** * **A. Epinephrine:** This is a catecholamine derived from the amino acid tyrosine [1]. Epinephrine is **water-soluble (hydrophilic)** and cannot diffuse through the lipid-rich plasma membrane. Therefore, it binds to **G-protein coupled receptors (GPCRs)** located on the cell surface (extracellular receptors) to trigger a second messenger cascade (cAMP) [1]. ### **Why the Other Options are Incorrect** * **B. Thyroxine (T4):** Although derived from tyrosine like epinephrine, thyroid hormones are unique because they are highly lipophilic. They cross the plasma membrane via specific transporters to bind to **intranuclear receptors**. * **C & D. Androstenedione and Estrogen:** These are **steroid hormones** derived from cholesterol [1]. All steroid hormones (including glucocorticoids, mineralocorticoids, and sex steroids) are lipid-soluble and easily diffuse across the plasma membrane to bind to **cytoplasmic or nuclear receptors** [2]. ### **NEET-PG High-Yield Pearls** 1. **Receptor Locations:** * **Cell Surface:** Catecholamines (Epi/NE), Peptides (Insulin, Glucagon), and PTH [1]. * **Cytoplasmic:** Glucocorticoids, Mineralocorticoids, Progesterone. * **Nuclear:** Thyroid hormones (T3/T4), Estrogen, Vitamin D, Retinoic acid. 2. **Mnemonic for Nuclear Receptors:** "**T**ry **V**itamins **A**nd **RE**st" (**T**hroid, **V**itamin D, **A**ldosterone/Steroids, **RE**tinoic acid). 3. **Exception Note:** While thyroid hormones are lipophilic, they primarily use carrier-mediated transport (like MCT8) rather than simple diffusion to enter cells rapidly.

Q: Aldosterone secretion is increased when there is a fall in:

Plasma Na+. **Explanation:** Aldosterone, the primary mineralocorticoid secreted by the **Zona Glomerulosa** of the adrenal cortex, plays a crucial role in maintaining electrolyte balance and blood pressure. **Why Plasma Na+ is correct:** A fall in plasma sodium (**Hyponatremia**) acts as a direct stimulus for aldosterone secretion. More importantly, low sodium levels (often associated with low blood volume) trigger the **Renin-Angiotensin-Aldosterone System (RAAS)**. Decreased sodium delivery to the *macula densa* in the kidney stimulates renin release, leading to increased Angiotensin II, which is the most potent stimulator of aldosterone. Aldosterone then acts on the distal convoluted tubule and collecting ducts to promote **Na+ reabsorption** and water retention. **Analysis of Incorrect Options:** * **A. Plasma K+:** Aldosterone secretion is increased by a **rise** in plasma potassium (Hyperkalemia), not a fall. It functions to excrete excess K+ into the urine. * **C. pH of the plasma:** While aldosterone promotes H+ secretion (acid excretion), plasma pH is not a primary direct regulator of its secretion compared to electrolytes and the RAAS. * **D. Angiotensin II levels:** Aldosterone secretion increases when Angiotensin II levels **rise**, as it is the primary hormonal mediator of the RAAS. **High-Yield Clinical Pearls for NEET-PG:** * **Primary Stimuli:** The two most important direct stimuli for aldosterone are **Hyperkalemia** and **Angiotensin II**. * **ACTH Role:** ACTH is necessary for aldosterone secretion (permissive action) but plays a minor role in its daily regulation compared to K+ and Angiotensin II. * **Conn’s Syndrome:** Primary hyperaldosteronism characterized by the triad of Hypertension, Hypokalemia, and Metabolic Alkalosis. * **Atrial Natriuretic Peptide (ANP):** The only major hormone that **inhibits** aldosterone secretion.

Q: All of the following hormones bind to cell surface receptors of the target tissues EXCEPT?

Estrogen. ### Explanation The mechanism of hormone action is determined by the chemical nature of the hormone (solubility). Hormones are broadly classified into **Lipid-soluble** and **Water-soluble** groups. **1. Why Estrogen is the correct answer:** Estrogen is a **steroid hormone** derived from cholesterol. Being lipophilic (lipid-soluble), it easily diffuses through the lipid bilayer of the cell membrane. Therefore, it does not require a cell surface receptor; instead, it binds to **intracellular receptors** (specifically nuclear receptors). The hormone-receptor complex then acts as a transcription factor, binding to DNA to regulate gene expression. **2. Why the other options are incorrect:** * **Thyroid Stimulating Hormone (TSH):** This is a large glycoprotein hormone. Due to its size and water-soluble nature, it cannot cross the cell membrane and must bind to **G-protein coupled receptors (GPCR)** on the cell surface. * **Glucagon:** This is a peptide hormone. Like TSH, it is water-soluble and binds to cell surface **GPCRs**, primarily activating the Adenylyl Cyclase-cAMP pathway. * **Epinephrine:** This is a catecholamine (amino acid derivative). Although small, it is polar and cannot diffuse through the membrane, thus binding to **alpha or beta-adrenergic receptors** on the cell surface. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Intracellular Receptors:** *"PET CAT"* – **P**rogesterone, **E**strogen, **T**estosterone, **C**ortisol, **A**ldosterone, **T**hyroid hormones (T3/T4), and Vitamin D. * **Exception Note:** Although **Thyroid hormones (T3/T4)** are amino acid derivatives, they are lipophilic and use **intracellular (nuclear) receptors**, unlike Epinephrine. * **Fast vs. Slow:** Cell surface receptors (e.g., Epinephrine) usually trigger rapid enzymatic changes, while intracellular receptors (e.g., Estrogen) cause slower, genomic effects.

Question 1

Prolactin secretion is stimulated by:

Accepted Answer

TRH

Answer

ACTH

Answer

GnRH

Answer

Dopamine

Question 2

FSH is secreted by which of the following cells?

Accepted Answer

Basophils

Answer

Chromophobes

Answer

Acidophils

Answer

Theca interna cells

Question 3

All of the following short stature cases are caused by mechanisms independent of specific defects in the growth hormone axis, except?

Accepted Answer

Laron dwarfism

Answer

Gonadal dysgenesis

Answer

Kasper - Hauser syndrome

Answer

Achondroplasia

Question 4

Regarding the action of insulin, which of the following is true?

Accepted Answer

Decreased ketogenesis in the liver

Answer

Decreased K+ uptake in adipose tissue

Answer

Increased protein catabolism in muscle

Answer

Activation of hormone-sensitive lipase

Question 5

Insulin secretion is inhibited by all of the following, EXCEPT:

Accepted Answer

Beta-ketoacids

Answer

Somatostatin

Answer

Beta-adrenergic blockers

Answer

Diazoxide

Question 6

Which of the following statements can be regarded as the primary action of inhibin?

Accepted Answer

It inhibits the secretion of FSH.

Answer

It inhibits the secretion of prolactin.

Answer

It stimulates the synthesis of estradiol.

Answer

It stimulates the secretion of TSH.

Question 7

Bone resorption is enhanced by:

Accepted Answer

PGE2

Answer

PGD2

Answer

PGF2

Answer

PGI2

Question 8

All of the following cross the plasma membrane except?

Accepted Answer

Epinephrine

Answer

Thyroxine

Answer

Androstenedione

Answer

Estrogen

Question 9

Aldosterone secretion is increased when there is a fall in:

Accepted Answer

Plasma Na+

Answer

Plasma K+

Answer

pH of the plasma

Answer

Angiotensin II levels

Question 10

All of the following hormones bind to cell surface receptors of the target tissues EXCEPT?

Accepted Answer

Estrogen

Answer

Thyroid stimulating hormone

Answer

Glucagon

Answer

Epinephrine

Endocrinology — MCQs

Endocrinology — MCQs

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