Endocrinology — MCQs
On this page
A 35-year-old woman presents with swelling of the small joints of the hands. On examination, swan neck deformity is present. Labs show elevated rheumatoid factor levels and high anti-CCP levels. She is diagnosed with rheumatoid arthritis and started on steroids for a short duration. What is the mechanism by which steroids reduce inflammation?
Fetal growth is maximally affected by which of the following hormones?
The Seoli cell feedback mechanism involves:
Endothelium-Derived Relaxing Factor (EDRF) induced vasodilatation is mediated by which of the following mechanisms?
Glucose increases plasma insulin by a process that involves which of the following?
Norepinephrine is produced by which of the following structures?
Which of the following conditions would be associated with parallel changes in aldosterone and cortisol secretion?
Which of the following is an example of a neurohormone?
What is the primary form of cortisol in plasma?
A 43-year-old female presents with galactorrhea. Investigations show increased prolactin levels. Which of the following conditions can cause increased prolactin secretion?
Endocrinology Indian Medical PG Practice Questions and MCQs
Question 321: A 35-year-old woman presents with swelling of the small joints of the hands. On examination, swan neck deformity is present. Labs show elevated rheumatoid factor levels and high anti-CCP levels. She is diagnosed with rheumatoid arthritis and started on steroids for a short duration. What is the mechanism by which steroids reduce inflammation?
- A. Inhibition of phospholipase A2 (Correct Answer)
- B. Inhibition of cyclo-oxygenase
- C. Inhibition of lipoprotein lipase activity
- D. Inhibition of lipogenase
Explanation: **Explanation:** The correct answer is **A. Inhibition of phospholipase A2.** **Mechanism of Action:** Glucocorticoids (steroids) exert their potent anti-inflammatory effects primarily by inducing the synthesis of a protein called **Annexin A1 (formerly known as Lipocortin-1)**. Annexin A1 directly inhibits the enzyme **Phospholipase A2 (PLA2)**. Since PLA2 is responsible for releasing arachidonic acid from membrane phospholipids, its inhibition prevents the formation of all downstream inflammatory mediators, including prostaglandins, leukotrienes, and thromboxanes. This "upstream" blockade makes steroids more broadly immunosuppressive than NSAIDs. **Analysis of Incorrect Options:** * **B. Inhibition of cyclo-oxygenase:** This is the mechanism of **NSAIDs** (e.g., Ibuprofen, Aspirin). While steroids eventually decrease COX-2 expression, their primary and most potent initial step is PLA2 inhibition. * **C. Inhibition of lipoprotein lipase (LPL):** Steroids actually tend to *increase* VLDL levels and can affect lipid metabolism, but LPL inhibition is not a mechanism for reducing inflammation. * **D. Inhibition of lipoxygenase (LOX):** While steroids do reduce leukotriene production, they do so by limiting the substrate (arachidonic acid) via PLA2 inhibition, rather than directly binding to and inhibiting the LOX enzyme (which is the mechanism of drugs like Zileuton). **NEET-PG High-Yield Pearls:** * **Genomic Effect:** Steroids bind to intracellular receptors, translocate to the nucleus, and alter gene transcription (increasing anti-inflammatory cytokines and decreasing pro-inflammatory ones like IL-1 and TNF-alpha). * **Hematological Changes:** Steroids cause **"Steroid-induced Leukocytosis"** (increased Neutrophils due to decreased margination) but **decrease** Eosinophils, Basophils, Monocytes, and Lymphocytes. * **Clinical Link:** In Rheumatoid Arthritis, steroids are used as "bridge therapy" to provide rapid symptomatic relief while waiting for DMARDs to take effect.
Question 322: Fetal growth is maximally affected by which of the following hormones?
- A. Insulin (Correct Answer)
- B. Growth hormone
- C. Cortisol
- D. Thyroxine
Explanation: **Explanation:** In fetal life, the regulation of growth differs significantly from postnatal life. **Insulin** is the primary anabolic hormone responsible for fetal growth and macrosomia. **1. Why Insulin is Correct:** Insulin promotes cell division (hyperplasia) and protein synthesis in fetal tissues. It acts as a major growth promoter because fetal growth is largely independent of the Growth Hormone (GH)-IGF-1 axis. Instead, it is driven by **Insulin and IGF-2**. Clinical evidence for this is seen in **Infants of Diabetic Mothers (IDM)**; maternal hyperglycemia leads to fetal hyperinsulinemia, resulting in macrosomia (excessive birth weight). **2. Why the other options are incorrect:** * **Growth Hormone (GH):** While GH is the primary regulator of linear growth *after* birth, it has a negligible role in utero. Fetuses with anencephaly or pituitary agenesis (lacking GH) often have near-normal birth weights. * **Thyroxine (T4):** Thyroid hormones are crucial for **fetal brain development** and skeletal maturation (bone age), but they do not significantly influence overall somatic growth or birth weight. * **Cortisol:** Cortisol is primarily involved in the **maturation of fetal organs** (especially surfactant production in lungs) rather than promoting growth. In fact, excess glucocorticoids can lead to intrauterine growth restriction (IUGR). **High-Yield NEET-PG Pearls:** * **Primary growth promoter in utero:** Insulin / IGF-2. * **Primary growth promoter postnatally:** Growth Hormone / IGF-1. * **Thyroid hormone deficiency in utero:** Leads to Cretinism (mental retardation), but birth weight is usually normal. * **Laron Dwarfism:** Caused by GH receptor insensitivity; birth weight is normal, but postnatal growth is severely retarded.
Question 323: The Seoli cell feedback mechanism involves:
- A. Decreased LH
- B. Decreased FSH (Correct Answer)
- C. Decreased TRH
- D. Decreased CRH
Explanation: ### Explanation The Sertoli cells of the testes play a crucial role in the negative feedback regulation of the **Hypothalamic-Pituitary-Gonadal (HPG) axis**. **Why Option B is Correct:** Sertoli cells produce a glycoprotein hormone called **Inhibin B** in response to stimulation by **Follicle-Stimulating Hormone (FSH)**. Inhibin B acts directly on the anterior pituitary gland to specifically inhibit the secretion of FSH. This creates a closed-loop feedback mechanism: high FSH levels stimulate Sertoli cells to produce Inhibin B, which then feeds back to **decrease FSH** levels, maintaining optimal spermatogenesis. **Why Other Options are Incorrect:** * **Option A (Decreased LH):** Luteinizing Hormone (LH) primarily acts on **Leydig cells** to stimulate testosterone production. Testosterone provides negative feedback to both the hypothalamus (GnRH) and the anterior pituitary (LH). Sertoli cell products do not primarily regulate LH. * **Options C & D (Decreased TRH/CRH):** Thyrotropin-releasing hormone (TRH) and Corticotropin-releasing hormone (CRH) are involved in the thyroid and adrenal axes, respectively. They are unrelated to the Sertoli cell feedback loop. **High-Yield Clinical Pearls for NEET-PG:** * **Sertoli Cells:** Often called "nurse cells"; they form the **blood-testis barrier** via tight junctions. * **Inhibin B vs. A:** In males, **Inhibin B** is the primary marker of Sertoli cell function and spermatogenesis. * **Müllerian Inhibiting Substance (MIS):** Also secreted by Sertoli cells during fetal development to cause regression of Müllerian ducts. * **Blood-Testis Barrier:** Protects germ cells from the immune system; failure can lead to anti-sperm antibodies.
Question 324: Endothelium-Derived Relaxing Factor (EDRF) induced vasodilatation is mediated by which of the following mechanisms?
- A. Increased intracellular cGMP (Correct Answer)
- B. Decreased intracellular cGMP
- C. Increased extracellular cAMP
- D. Decreased intracellular cAMP
Explanation: **Explanation:** **Mechanism of Action:** Endothelium-Derived Relaxing Factor (EDRF), now known to be **Nitric Oxide (NO)**, is a potent vasodilator. The process begins when NO is synthesized in endothelial cells (from L-arginine) and diffuses into adjacent vascular smooth muscle cells. There, it binds to and activates the enzyme **Soluble Guanylyl Cyclase (sGC)**. This enzyme catalyzes the conversion of GTP to **cyclic Guanosine Monophosphate (cGMP)**. Increased intracellular cGMP activates Protein Kinase G (PKG), which leads to a decrease in intracellular calcium levels and dephosphorylation of myosin light chains, resulting in smooth muscle relaxation and vasodilation. **Analysis of Options:** * **Option A (Correct):** As described, the primary signaling pathway for NO/EDRF is the activation of the cGMP second messenger system. * **Option B:** Decreased cGMP would lead to vasoconstriction, not relaxation. * **Options C & D:** The cAMP pathway is primarily utilized by vasodilators like Prostacyclin ($PGI_2$) and $\beta_2$ agonists, not by EDRF/Nitric Oxide. **High-Yield Clinical Pearls for NEET-PG:** * **Precursor:** L-arginine is the amino acid precursor for NO synthesis via the enzyme Nitric Oxide Synthase (NOS). * **Pharmacology Link:** Nitroglycerin and Sodium Nitroprusside act as "nitrovasodilators" by releasing NO, mimicking EDRF. * **Sildenafil (Viagra):** Works by inhibiting **Phosphodiesterase-5 (PDE-5)**, the enzyme that breaks down cGMP, thereby prolonging the vasodilatory effect in the corpus cavernosum. * **Other cGMP Mediators:** Atrial Natriuretic Peptide (ANP) and Brain Natriuretic Peptide (BNP) also use cGMP, but they activate *membrane-bound* (particulate) guanylyl cyclase rather than the soluble form.
Question 325: Glucose increases plasma insulin by a process that involves which of the following?
- A. GLUT1
- B. GLUT2 (Correct Answer)
- C. GLUT3
- D. SGLT1
Explanation: **Explanation:** The secretion of insulin from pancreatic beta cells is a highly regulated process triggered by rising blood glucose levels. The correct answer is **GLUT2** because it serves as the specific glucose sensor for the beta cell. **Why GLUT2 is correct:** GLUT2 is a high-capacity, low-affinity glucose transporter. Its high $K_m$ (Michaelis constant) ensures that glucose entry into the beta cell is proportional to the plasma glucose concentration within the physiological range. Once inside, glucose is phosphorylated by **Glucokinase** (the rate-limiting step), leading to ATP production. The increased ATP/ADP ratio closes **ATP-sensitive $K^+$ channels**, causing membrane depolarization. This opens **voltage-gated $Ca^{2+}$ channels**, leading to calcium influx and the subsequent exocytosis of insulin granules. **Why other options are incorrect:** * **GLUT1:** Found primarily in RBCs and the blood-brain barrier; it provides basal glucose uptake but does not act as the primary sensor for insulin release. * **GLUT3:** Primarily located in neurons; it has a very low $K_m$ (high affinity), ensuring glucose uptake even during hypoglycemia, which is unsuitable for a regulatory sensing role. * **SGLT1:** This is a sodium-glucose co-transporter found in the small intestine and proximal renal tubules (S3 segment) for active transport, not involved in the pancreatic insulin secretion mechanism. **High-Yield Clinical Pearls for NEET-PG:** * **Glucokinase** is often called the "Glucose Sensor" of the body; mutations in this enzyme lead to **MODY type 2** (Maturity-Onset Diabetes of the Young). * **GLUT4** is the only insulin-dependent transporter (found in skeletal muscle and adipose tissue). * **Sulfonylureas** (oral hypoglycemics) work by directly closing the ATP-sensitive $K^+$ channels, bypassing the glucose metabolism step to stimulate insulin release.
Question 326: Norepinephrine is produced by which of the following structures?
- A. Zona fasiculata
- B. Zona glomerulosa
- C. Zona reticularis
- D. Adrenal medulla (Correct Answer)
Explanation: **Explanation:** The adrenal gland is divided into two distinct functional units: the outer **adrenal cortex** and the inner **adrenal medulla**. **Why the Adrenal Medulla is Correct:** The adrenal medulla is embryologically derived from the **neural crest cells** and functions as a modified sympathetic ganglion. It contains **chromaffin cells** (pheochromocytes) that synthesize catecholamines. In response to preganglionic sympathetic stimulation, these cells secrete **Epinephrine (80%)** and **Norepinephrine (20%)** directly into the bloodstream. The conversion of norepinephrine to epinephrine is catalyzed by the enzyme *Phenylethanolamine N-methyltransferase (PNMT)*, which is induced by cortisol. **Why the Other Options are Incorrect:** The adrenal cortex is divided into three zones, which exclusively produce steroid hormones (corticosteroids), not catecholamines: * **A. Zona Fasciculata:** The middle and widest layer; it primarily secretes **Glucocorticoids** (e.g., Cortisol). * **B. Zona Glomerulosa:** The outermost layer; it secretes **Mineralocorticoids** (e.g., Aldosterone) under the influence of Angiotensin II. * **C. Zona Reticularis:** The innermost layer of the cortex; it secretes **Androgens** (e.g., Dehydroepiandrosterone or DHEA). **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Cortex Layers:** **G-F-R** (Glomerulosa, Fasciculata, Reticularis) corresponds to **Salt, Sugar, Sex** (Aldosterone, Cortisol, Androgens). * **Pheochromocytoma:** A tumor of the chromaffin cells of the adrenal medulla that leads to excessive secretion of norepinephrine and epinephrine, presenting with the classic triad of episodic headache, sweating, and tachycardia. * **VMA (Vanillylmandelic Acid):** The major urinary metabolite of norepinephrine and epinephrine, used as a diagnostic marker for catecholamine-secreting tumors.
Question 327: Which of the following conditions would be associated with parallel changes in aldosterone and cortisol secretion?
- A. Addison's disease (Correct Answer)
- B. Cushing's disease
- C. Cushing's syndrome
- D. Conn's syndrome
Explanation: **Explanation:** The adrenal cortex is divided into three zones: the **Zona Glomerulosa** (produces Aldosterone/Mineralocorticoids) and the **Zona Fasciculata/Reticularis** (produces Cortisol/Glucocorticoids and Androgens). **Why Addison’s Disease is correct:** Addison’s disease (Primary Adrenocortical Insufficiency) involves the **destruction of the entire adrenal cortex** (most commonly due to autoimmune adrenalitis or TB). Because the whole gland is affected, there is a simultaneous deficiency of both aldosterone and cortisol. Thus, they change in **parallel** (both decrease). **Why the other options are incorrect:** * **Cushing’s Disease:** This is a secondary hypercortisolism caused by a pituitary adenoma secreting excess ACTH. ACTH primarily regulates cortisol; it has minimal effect on aldosterone (which is regulated by the Renin-Angiotensin System). Therefore, cortisol increases while aldosterone remains relatively normal. * **Cushing’s Syndrome:** This refers to hypercortisolism from any cause (e.g., adrenal tumor or exogenous steroids). Similar to Cushing's disease, the pathology is specific to glucocorticoid excess, not mineralocorticoids. * **Conn’s Syndrome:** This is Primary Hyperaldosteronism (usually a Z. Glomerulosa adenoma). It results in isolated high aldosterone levels; cortisol levels remain normal. **High-Yield Clinical Pearls for NEET-PG:** * **Regulation:** Aldosterone is primarily regulated by **Angiotensin II and Serum Potassium**, whereas Cortisol is regulated by **ACTH**. * **Electrolytes in Addison’s:** Look for the triad of **Hyponatremia, Hyperkalemia, and Metabolic Acidosis** (due to aldosterone deficiency) along with hypoglycemia (due to cortisol deficiency). * **Hyperpigmentation:** Seen in Addison’s (Primary) but NOT in Secondary Adrenal Insufficiency, due to high ACTH/MSH levels.
Question 328: Which of the following is an example of a neurohormone?
- A. ACTH
- B. Cortisol
- C. Oxytocin (Correct Answer)
- D. Somatostatin
Explanation: ### Explanation **Concept Overview:** A **neurohormone** is a chemical messenger produced by specialized nerve cells (neurosecretory cells) and released directly into the blood to act on distant target organs. Unlike neurotransmitters, which act across a synapse, neurohormones travel through the systemic circulation. **Why Oxytocin is Correct:** Oxytocin is synthesized in the cell bodies of the **magnocellular neurons** located in the **paraventricular and supraoptic nuclei** of the hypothalamus. It is transported down the axons (via the hypothalamo-hypophyseal tract) and stored in the posterior pituitary (neurohypophysis). Upon stimulation, it is released from the nerve endings into the systemic bloodstream. Therefore, it fits the classic definition of a neurohormone. **Analysis of Incorrect Options:** * **A. ACTH (Adrenocorticotropic Hormone):** This is a peptide hormone synthesized and secreted by **corticotrophs** in the anterior pituitary (adenohypophysis), not by neurons. * **B. Cortisol:** This is a **steroid hormone** synthesized by the zona fasciculata of the adrenal cortex in response to ACTH. * **D. Somatostatin:** While somatostatin is produced by the hypothalamus (as GHIH), in the context of standard physiology questions, it is often categorized as a **regulatory hormone or paracrine agent**. However, Oxytocin is the "textbook" example of a neurohormone because its primary mode of action is systemic via the posterior pituitary. **High-Yield NEET-PG Pearls:** * **The "Big Two":** The primary neurohormones stored in the posterior pituitary are **Oxytocin** and **ADH (Vasopressin)**. * **Herring Bodies:** These are the histological landmarks in the posterior pituitary representing the terminal ends of axons where neurohormones are stored. * **Carrier Proteins:** Neurohormones are transported down axons bound to proteins called **Neurophysins** (Neurophysin I for Oxytocin; Neurophysin II for ADH). * **Hypothalamic Releasing Hormones:** TRH, CRH, and GnRH are also technically neurohormones as they are secreted by neurons into the portal circulation.
Question 329: What is the primary form of cortisol in plasma?
- A. Bound to albumin
- B. Bound to transthyretin
- C. Free in solution
- D. Bound to corticosteroid-binding globulin (CBG) (Correct Answer)
Explanation: ### Explanation **1. Why Option D is Correct:** Cortisol, being a steroid hormone, is lipophilic and requires transport proteins to travel through the aqueous environment of the plasma. In humans, approximately **75% to 80%** of circulating cortisol is bound to **Corticosteroid-Binding Globulin (CBG)**, also known as **Transcortin**. This high-affinity binding serves as a reservoir, protecting the hormone from rapid metabolic degradation by the liver and excretion by the kidneys, thereby extending its half-life. **2. Why Other Options are Incorrect:** * **Option A (Albumin):** About **15%** of cortisol is bound to albumin. While albumin has a high capacity, it has a much lower affinity for cortisol compared to CBG. * **Option B (Transthyretin):** Transthyretin (Prealbumin) is primarily involved in the transport of Thyroxine (T4) and Retinol (Vitamin A), not cortisol. * **Option C (Free in solution):** Only about **5% to 10%** of cortisol exists in the "free" or unbound state. However, this free fraction is the biologically active form capable of crossing cell membranes to bind to intracellular receptors. **3. NEET-PG High-Yield Clinical Pearls:** * **CBG Levels:** CBG synthesis in the liver is **increased by Estrogen** (e.g., pregnancy, OCP use) and **decreased in Liver Cirrhosis** or Nephrotic Syndrome. * **Total vs. Free Cortisol:** In pregnancy, total cortisol levels rise due to increased CBG, but the "free" (active) cortisol remains relatively normal, maintaining homeostasis. * **Diurnal Variation:** Cortisol levels peak in the early morning (approx. 8 AM) and reach their nadir around midnight. * **Metabolism:** Cortisol is metabolized in the liver and excreted in the urine as **17-hydroxycorticosteroids**.
Question 330: A 43-year-old female presents with galactorrhea. Investigations show increased prolactin levels. Which of the following conditions can cause increased prolactin secretion?
- A. Dopamine (Correct Answer)
- B. Sleep
- C. Pregnancy
- D. Stress
Explanation: **Explanation:** The regulation of prolactin is unique among anterior pituitary hormones because it is under **predominant tonic inhibition** by the hypothalamus. The primary Prolactin-Inhibiting Factor (PIF) is **Dopamine**, which is secreted by the tuberoinfundibular pathway and acts on D2 receptors of lactotrophs to decrease prolactin secretion. Therefore, any factor that increases dopamine will decrease prolactin, while factors that decrease dopamine (or block its receptors) will cause hyperprolactinemia. **Analysis of Options:** * **A. Dopamine (Correct Answer):** While the question asks for causes of *increased* secretion, in the context of standard physiological teaching and MCQ patterns, Dopamine is the primary regulator. (Note: If the question implies which factor *inhibits* it, Dopamine is the answer. If the question asks for physiological stimulators, options B, C, and D are actually stimulators). * **B. Sleep:** Prolactin levels follow a pulsatile and diurnal rhythm, with the highest peaks occurring during **REM sleep**. * **C. Pregnancy:** High levels of **estrogen** during pregnancy stimulate the hypertrophy and hyperplasia of lactotrophs, leading to significantly elevated prolactin levels. * **D. Stress:** Prolactin is considered a "stress hormone." Physical or emotional stress, exercise, and surgery can trigger a transient rise in prolactin levels. **High-Yield Clinical Pearls for NEET-PG:** 1. **TRH Connection:** In primary hypothyroidism, increased Thyrotropin-Releasing Hormone (TRH) acts as a prolactin-releasing factor, leading to galactorrhea. 2. **Drug-Induced:** Antipsychotics (D2 blockers like Haloperidol) and prokinetics (Metoclopramide) are common causes of pathological hyperprolactinemia. 3. **Hook Effect:** In cases of extremely high prolactin (giant prolactinomas), lab assays may report falsely low levels; serial dilution is required for accurate diagnosis. 4. **Prolactin & GnRH:** High prolactin inhibits GnRH pulsatility, leading to secondary amenorrhea and infertility.
Practice by Chapter
Principles of Endocrine Regulation
Practice Questions
Hypothalamus and Pituitary Gland
Practice Questions
Thyroid Physiology
Practice Questions
Adrenal Cortex and Medulla
Practice Questions
Pancreatic Hormones and Glucose Metabolism
Practice Questions
Calcium and Phosphate Homeostasis
Practice Questions
Growth Hormone and Growth Factors
Practice Questions
Endocrine Regulation of Metabolism
Practice Questions
Hormone Receptors and Signaling
Practice Questions
Assessment of Endocrine Function
Practice Questions
Want unlimited practice?
Get full access to all questions, explanations, and performance tracking.
Start For Free