Endocrinology Practice Questions

Q: Which of the following receptors mediate the release of ACTH by Vasopressin?

V3. **Explanation:** The release of Adrenocorticotropic Hormone (ACTH) from the anterior pituitary is primarily regulated by Corticotropin-Releasing Hormone (CRH). However, **Arginine Vasopressin (AVP)** acts as a potent synergistic secretagogue for ACTH. 1. **Why V3 is correct:** Vasopressin acts on the **V3 receptors** (also known as **V1b receptors**) located on the corticotroph cells of the anterior pituitary. These are G-protein coupled receptors (Gq) that activate the Phospholipase C pathway, leading to an increase in intracellular calcium and the subsequent release of ACTH. 2. **Why other options are incorrect:** * **V1a:** These receptors are primarily found on **vascular smooth muscle**, mediating vasoconstriction, and in the liver, mediating glycogenolysis. * **V2:** These receptors are located in the **principal cells of the renal collecting ducts**. They act via the Gs-cAMP pathway to insert Aquaporin-2 channels, mediating the antidiuretic effect. * **V4:** There is no clinically significant V4 receptor in human physiology; this is often used as a distractor in exams. **High-Yield Clinical Pearls for NEET-PG:** * **Synergy:** While CRH is the main stimulant, AVP (via V3) is crucial during the chronic stress response to sustain ACTH levels. * **Location Summary:** V1a (Vessels), V2 (Kidney), V3/V1b (Pituitary). * **Ectopic ACTH:** Some tumors (e.g., Small Cell Carcinoma of the Lung) may express V3 receptors, leading to paraneoplastic Cushing Syndrome. * **Desmopressin (dDAVP):** It is a selective V2 agonist, which is why it is used for Diabetes Insipidus without causing significant vasoconstriction (V1a) or ACTH release (V3).

Q: Natural light causes all except?

Destruction of the organ of Corti. **Explanation:** The question asks for the physiological effect that is **NOT** caused by natural light. **1. Why "Destruction of the organ of Corti" is the correct answer:** The **organ of Corti** is the sensory organ for hearing located within the inner ear (cochlea). It is stimulated by mechanical sound waves, not electromagnetic radiation (light). Destruction of the organ of Corti is typically caused by chronic exposure to loud noise (noise-induced hearing loss), ototoxic drugs (e.g., aminoglycosides), or aging—not by exposure to natural light. **2. Analysis of Incorrect Options:** * **Vitamin D synthesis:** Ultraviolet B (UVB) radiation from natural sunlight triggers the conversion of 7-dehydrocholesterol in the skin into cholecalciferol (Vitamin D3). * **Decrease in bilirubin level:** Blue-green light (wavelength 460–490 nm) helps decompose bilirubin into water-soluble isomers (lumirubin) that can be excreted without conjugation. This is the physiological basis for **phototherapy** used in neonatal jaundice. * **Melanin synthesis:** Exposure to UV light stimulates melanocytes in the basal layer of the epidermis to produce melanin (melanogenesis), which acts as a protective pigment against DNA damage. **High-Yield Clinical Pearls for NEET-PG:** * **Pineal Gland Connection:** Natural light inhibits the secretion of **Melatonin** from the pineal gland via the suprachiasmatic nucleus (SCN), regulating the circadian rhythm. * **Phototherapy:** The most effective wavelength for treating neonatal hyperbilirubinemia is approximately **450 nm**. * **Vitamin D:** The skin is the primary source of Vitamin D; deficiency leads to Rickets in children and Osteomalacia in adults. * **Retinal Damage:** While light doesn't affect the ear, excessive UV/blue light can cause **photoretinitis** or damage to the macula.

Q: What is the storage form of thyroid hormone?

Thyroglobulin. **Explanation:** The thyroid gland is unique among endocrine glands because it stores large quantities of hormone in an extracellular space. The correct answer is **Thyroglobulin (Tg)**. 1. **Why Thyroglobulin is Correct:** Thyroglobulin is a large glycoprotein synthesized by follicular cells and secreted into the follicular lumen (colloid). It contains numerous tyrosine residues. During thyroid hormone synthesis, iodine attaches to these residues. The iodinated thyroglobulin molecule acts as a **pro-hormone storage form**, containing enough T3 and T4 to supply the body for 2–3 months. When the body needs thyroid hormone, Tg is reabsorbed into the follicular cells and proteolyzed to release active hormones. 2. **Why Other Options are Incorrect:** * **A & B (MIT and DIT):** Monoiodotyrosine (MIT) and Diiodotyrosine (DIT) are intermediate precursors formed during the organification of iodine. They remain attached to the thyroglobulin backbone and are not the primary storage form themselves. * **D (Triiodothyronine/T3):** T3 is the most metabolically active form of the hormone, but it is stored *within* the thyroglobulin molecule in the colloid, not as a free hormone. **High-Yield NEET-PG Pearls:** * **Colloid:** The follicular lumen containing thyroglobulin is known as the colloid. * **Wolff-Chaikoff Effect:** An autoregulatory phenomenon where high levels of circulating iodide inhibit the organification of iodine, temporarily reducing thyroid hormone synthesis. * **Pendrin:** The transport protein responsible for chloride-iodide exchange across the apical membrane into the follicle. * **Clinical Marker:** Serum thyroglobulin levels are used as a tumor marker to monitor for recurrence in patients with differentiated thyroid cancer after total thyroidectomy.

Q: All of the following have a stimulatory action on glucagon secretion, EXCEPT:

Secretin. **Explanation:** Glucagon is a catabolic hormone secreted by the **alpha cells** of the pancreas. Its primary role is to increase blood glucose levels during states of energy deficiency or stress. **1. Why Secretin is the Correct Answer:** **Secretin** is a gastrointestinal hormone that primarily stimulates the secretion of bicarbonate-rich pancreatic juice. In the context of islet cell function, secretin (along with Somatostatin and Insulin) actually **inhibits** glucagon secretion. This is a physiological mechanism to prevent excessive glucose elevation during certain phases of digestion. **2. Analysis of Incorrect Options (Stimulators of Glucagon):** * **Beta-agonists (Option B):** Sympathetic stimulation via **Beta-2 adrenergic receptors** strongly stimulates glucagon release. This ensures adequate glucose availability for the "fight or flight" response. * **Exercise (Option C):** Exercise increases glucagon levels due to increased sympathetic activity and the body's demand for circulating glucose to fuel skeletal muscles. * **Amino Acids (Option D):** High levels of amino acids (especially Arginine and Alanine) stimulate glucagon. This is a protective mechanism: when a person eats a high-protein, low-carb meal, the insulin released (due to amino acids) could cause hypoglycemia. Glucagon is secreted simultaneously to maintain stable blood glucose. **High-Yield Clinical Pearls for NEET-PG:** * **Major Inhibitors:** Glucose, Insulin, Somatostatin, Secretin, and Free Fatty Acids (FFA). * **Major Stimulators:** Hypoglycemia, Amino acids (Arginine), Acetylcholine, Epinephrine (Beta-receptors), and CCK. * **The "Incretin" Distinction:** While **GLP-1** (Glucagon-like peptide-1) inhibits glucagon, **GIP** (Gastric Inhibitory Peptide) can actually stimulate it under certain conditions. * **Glucagonoma Clinical Triad:** Necrolytic migratory erythema (NME), Diabetes mellitus, and Anemia.

Q: Which of the following is NOT a function of angiotensin II?

Increases anger.. **Explanation:** Angiotensin II (AT-II) is a potent octapeptide and a key component of the **Renin-Angiotensin-Aldosterone System (RAAS)**, primarily responsible for maintaining blood pressure and fluid-electrolyte balance. **Why "Increases Anger" is the correct answer:** Angiotensin II acts on the central nervous system to modulate autonomic functions and thirst, but it has **no established physiological role in inducing anger** or specific emotional outbursts. While chronic RAAS activation is linked to stress and anxiety, "anger" is not a direct physiological function of the hormone. **Analysis of Incorrect Options:** * **A. Increases Thirst:** AT-II acts on the **subfornical organ (SFO)** and the organum vasculosum of the lamina terminalis (OVLT) in the brain to stimulate the dipsogenic (thirst) center, encouraging water intake to increase blood volume. * **B. Increases ADH secretion:** It stimulates the hypothalamus to release Antidiuretic Hormone (Vasopressin) from the posterior pituitary, which increases water reabsorption in the renal collecting ducts. * **C. Increases Aldosterone secretion:** AT-II acts directly on the **zona glomerulosa** of the adrenal cortex to stimulate the synthesis and release of aldosterone, leading to sodium and water retention. **High-Yield Clinical Pearls for NEET-PG:** * **Potency:** AT-II is a powerful direct vasoconstrictor (40 times more potent than norepinephrine). * **Renal Effect:** It preferentially constricts the **efferent arteriole**, maintaining the Glomerular Filtration Rate (GFR) when renal perfusion pressure is low. * **Receptors:** Most physiological effects are mediated via **AT1 receptors** (Gq protein-coupled). AT2 receptors generally oppose these actions (vasodilation). * **ACE Inhibitors/ARBs:** These are first-line drugs for hypertension and heart failure because they block these systemic effects.

Q: Decreased plasma renin activity is seen in which of the following conditions?

Primary hyperaldosteronism. **Explanation:** The key to answering this question lies in understanding the **negative feedback loop** of the Renin-Angiotensin-Aldosterone System (RAAS). **1. Why Primary Hyperaldosteronism is correct:** In Primary Hyperaldosteronism (e.g., Conn’s Syndrome), there is autonomous secretion of aldosterone from the adrenal cortex. This excess aldosterone causes sodium and water retention, leading to ECF volume expansion and hypertension. This increased blood pressure and volume are sensed by the juxtaglomerular apparatus, which **suppresses** the release of renin. Therefore, the hallmark of primary hyperaldosteronism is **High Aldosterone with Low Plasma Renin Activity (PRA).** **2. Why the other options are incorrect:** * **Secondary Aldosteronism:** Here, the primary pathology is an overactive RAAS (e.g., renal artery stenosis or congestive heart failure). Increased renin leads to increased aldosterone; thus, **both Renin and Aldosterone are high.** * **Bartter Syndrome:** This is a renal tubular defect (NKCC2 transporter) mimicking chronic loop diuretic use. It leads to salt wasting, volume depletion, and subsequent **activation** of the RAAS, resulting in high renin levels. * **Preeclampsia:** While the pathophysiology is complex, it is generally associated with **increased** renin activity and sensitivity, unlike the suppression seen in primary mineralocorticoid excess. **Clinical Pearls for NEET-PG:** * **Aldosterone-to-Renin Ratio (ARR):** This is the best screening test for Primary Hyperaldosteronism. An **elevated ARR** (High Aldosterone/Low Renin) is diagnostic. * **Liddle’s Syndrome:** This also presents with low renin and hypertension (pseudohyperaldosteronism) but, unlike Conn’s, it features **low aldosterone** levels due to constitutive activation of ENaC channels. * **Hypokalemia and Metabolic Alkalosis** are common laboratory findings in states of mineralocorticoid excess.

Q: Angiotensinogen is secreted by which organ?

Liver. **Explanation:** The correct answer is **Liver**. Angiotensinogen is a large $\alpha_2$-globulin protein (a type of non-specific transport protein) that is constitutively synthesized and secreted into the plasma by the **liver**. It serves as the essential precursor substrate in the Renin-Angiotensin-Aldosterone System (RAAS). **Why other options are incorrect:** * **Kidney:** The kidney (specifically the Juxtaglomerular cells) secretes **Renin**, which is the enzyme that cleaves Angiotensinogen into Angiotensin I. It does not produce the substrate itself. * **Lung:** The lungs are the primary site for **Angiotensin-Converting Enzyme (ACE)**, located on the surface of pulmonary capillary endothelial cells. ACE converts Angiotensin I into the active vasoconstrictor Angiotensin II. * **Brain:** While some local RAAS components exist in the brain for blood pressure regulation, it is not the primary source of circulating Angiotensinogen. **High-Yield NEET-PG Pearls:** 1. **Rate-Limiting Step:** The reaction between Renin and Angiotensinogen is the rate-limiting step of the RAAS cascade. 2. **Hormonal Regulation:** Angiotensinogen levels are increased by **estrogens, glucocorticoids, thyroid hormones, and Angiotensin II**. This explains why oral contraceptive pills (containing estrogen) can sometimes cause secondary hypertension. 3. **Site Summary:** * **Liver:** Angiotensinogen * **Kidney (JG cells):** Renin * **Lungs:** ACE * **Adrenal Cortex (Zona Glomerulosa):** Aldosterone (stimulated by Angiotensin II)

Q: All of the following hormones are secreted by the adrenal cortex EXCEPT:

Estriol. **Explanation:** The adrenal cortex is organized into three distinct zones, each responsible for secreting specific steroid hormones derived from cholesterol (the "GFR" mnemonic): 1. **Zona Glomerulosa:** Secretes Mineralocorticoids (e.g., **Aldosterone**). 2. **Zona Fasciculata:** Secretes Glucocorticoids (e.g., **Cortisol** and **Corticosterone**). 3. **Zona Reticularis:** Secretes Androgens (e.g., Dehydroepiandrosterone/DHEA and Androstenedione). **Why Estriol is the correct answer:** While the adrenal cortex produces weak androgens (DHEA) which can be peripherally converted into estrogens (estrone/estradiol), it does **not** directly secrete **Estriol**. Estriol (E3) is primarily a product of the **placenta** during pregnancy, requiring precursors from both the fetal liver and the adrenal glands. In non-pregnant states, it is a metabolic byproduct of estradiol and estrone. **Analysis of Incorrect Options:** * **Cortisol:** The primary glucocorticoid in humans, synthesized in the Zona Fasciculata. * **Corticosterone:** A glucocorticoid precursor and a minor glucocorticoid secreted by the Zona Fasciculata. In some species, it is the primary glucocorticoid. * **Aldosterone:** The main mineralocorticoid responsible for sodium retention and potassium excretion, synthesized in the Zona Glomerulosa. **High-Yield NEET-PG Pearls:** * **Rate-limiting step:** The conversion of cholesterol to pregnenolone by the enzyme **Desmolase** (stimulated by ACTH). * **Enzyme Deficiency:** 21-Hydroxylase deficiency is the most common cause of Congenital Adrenal Hyperplasia (CAH), leading to decreased cortisol/aldosterone and increased androgens. * **Estrogen Potency:** Estradiol (E2) > Estrone (E1) > Estriol (E3). Estriol is the hallmark of fetal well-being during pregnancy.

Q: Parathyroid hormone is responsible for all actions except:

Increase in phosphorous absorption. **Explanation:** The primary function of **Parathyroid Hormone (PTH)** is to maintain serum ionized calcium levels. It achieves this through direct actions on the bone and kidneys, and indirect actions on the intestine [1]. **Why Option A is correct:** PTH actually **decreases** serum phosphorus levels [2]. While PTH increases phosphorus mobilization from the bone, its most potent effect occurs in the **proximal convoluted tubule (PCT)** of the kidney, where it inhibits the Na⁺-K⁺-phosphorus cotransporter [1]. This leads to **phosphaturia** (increased excretion of phosphorus in urine) [4]. Therefore, PTH is a phosphaturic hormone, not one that increases its net absorption/retention. **Analysis of incorrect options:** * **Option B & D:** PTH stimulates the enzyme **1-alpha-hydroxylase** in the kidneys, which converts inactive Vitamin D to its active form, **Calcitriol (1,25-DHCC)** [1]. Calcitriol then acts on the intestines to increase the absorption of both Calcium and Vitamin D (via feedback) and Phosphorus [3]. Thus, PTH increases intestinal calcium absorption *indirectly*. * **Option C:** PTH stimulates osteoclasts (via RANKL signaling on osteoblasts) to resorb bone matrix, releasing calcium into the bloodstream [1]. **NEET-PG High-Yield Pearls:** * **Mnemonic for PTH:** "P" stands for **P**hosphaturic (it "Pees" out Phosphate). * **Site of Action:** PTH acts on the **PCT** to inhibit phosphate reabsorption and on the **DCT (Distal Convoluted Tubule)** to increase calcium reabsorption [1]. * **Secondary Hyperparathyroidism:** Commonly seen in Chronic Kidney Disease (CKD) due to phosphate retention and failure of Vitamin D activation [2].

Q: Acromegaly results from excessive release of which hormone?

Growth hormone. **Explanation:** **Acromegaly** is a clinical syndrome caused by the excessive secretion of **Growth Hormone (GH)**, typically due to a somatotroph adenoma of the anterior pituitary gland. The key pathophysiological feature is that this excess occurs **after the fusion of epiphyseal plates** (post-puberty). Because the long bones can no longer grow in length, the hormone stimulates the overgrowth of cancellous bones, soft tissues, and viscera, leading to characteristic features like frontal bossing, macroglossia, and enlargement of hands and feet (spade-like hands). **Analysis of Options:** * **Growth Hormone (Correct):** GH stimulates the liver to produce **IGF-1** (Insulin-like Growth Factor 1), which mediates most of its growth-promoting effects. Excess GH before epiphyseal closure leads to *Gigantism*. * **Thyroxine (Incorrect):** Excess thyroxine causes Hyperthyroidism (Grave’s disease), characterized by weight loss, tachycardia, and heat intolerance, not bony overgrowth. * **Insulin (Incorrect):** Excess insulin leads to hypoglycemia. While it is an anabolic hormone, it does not cause the skeletal changes seen in acromegaly. * **Glucagon (Incorrect):** Excess glucagon (Glucagonoma) leads to hyperglycemia and a characteristic skin rash called Necrolytic Migratory Erythema. **High-Yield Clinical Pearls for NEET-PG:** * **Best Screening Test:** Serum IGF-1 levels (due to its long half-life and stable levels). * **Gold Standard Diagnostic Test:** Glucose Suppression Test (Failure to suppress GH <1 ng/mL after 75g oral glucose). * **Most Common Cause of Death:** Cardiovascular disease (Cardiomyopathy/Hypertension). * **Associated Condition:** Increased risk of **Colonic Polyps** and Adenocarcinoma. * **Drug of Choice:** Somatostatin analogues (e.g., Octreotide).

Question 1

Which of the following receptors mediate the release of ACTH by Vasopressin?

Accepted Answer

V3

Answer

V1a

Answer

V2

Answer

V4

Question 2

Natural light causes all except?

Accepted Answer

Destruction of the organ of Corti

Answer

Vitamin D synthesis

Answer

Decrease in bilirubin level

Answer

Melanin synthesis

Question 3

What is the storage form of thyroid hormone?

Accepted Answer

Thyroglobulin

Answer

Monoiodotyrosine

Answer

Diiodotyrosine

Answer

Triiodothyronine

Question 4

All of the following have a stimulatory action on glucagon secretion, EXCEPT:

Accepted Answer

Secretin

Answer

Beta agonist

Answer

Exercise

Answer

Amino acids

Question 5

Which of the following is NOT a function of angiotensin II?

Accepted Answer

Increases anger.

Answer

Increases thirst.

Answer

Increases ADH secretion.

Answer

Increases aldosterone secretion.

Question 6

Decreased plasma renin activity is seen in which of the following conditions?

Accepted Answer

Primary hyperaldosteronism

Answer

Bartter syndrome

Answer

Preeclampsia

Answer

Secondary aldosteronism

Question 7

Angiotensinogen is secreted by which organ?

Accepted Answer

Liver

Answer

Kidney

Answer

Lung

Answer

Brain

Question 8

All of the following hormones are secreted by the adrenal cortex EXCEPT:

Accepted Answer

Estriol

Answer

Cortisol

Answer

Corticosterone

Answer

Aldosterone

Question 9

Parathyroid hormone is responsible for all actions except:

Accepted Answer

Increase in phosphorous absorption

Answer

Increase in Vitamin D absorption

Answer

Mobilization of calcium from bone

Answer

Increase in intestinal absorption of calcium

Question 10

Acromegaly results from excessive release of which hormone?

Accepted Answer

Growth hormone

Answer

Thyroxine

Answer

Insulin

Answer

Glucagon

Endocrinology — MCQs

Endocrinology — MCQs

On this page

Practice by Chapter

Want unlimited practice?