Endocrinology Practice Questions

Q: Which of the following hormones is NOT released by the anterior pituitary gland?

Prolactin. **Explanation:** The anterior pituitary gland (adenohypophysis) synthesizes and secretes six major peptide hormones: Growth Hormone (GH), Thyroid-stimulating hormone (TSH), Adrenocorticotropic hormone (ACTH), Follicle-stimulating hormone (FSH), Luteinizing hormone (LH), and Prolactin. **Wait! Re-evaluating the Question and Key:** There appears to be a technical error in the provided key. **All four options (TSH, Prolactin, ACTH, and FSH) are indeed released by the anterior pituitary.** In the context of NEET-PG, this type of question usually aims to distinguish between the **Anterior Pituitary** (Adenohypophysis) and the **Posterior Pituitary** (Neurohypophysis). The posterior pituitary does not synthesize hormones; it only stores and releases **Oxytocin** and **Antidiuretic Hormone (ADH/Vasopressin)**, which are produced in the hypothalamus. **Analysis of Options:** * **TSH (Option A):** Secreted by thyrotrophs in the anterior pituitary to stimulate the thyroid gland. * **Prolactin (Option B):** Secreted by lactotrophs in the anterior pituitary to stimulate milk production. * **ACTH (Option C):** Secreted by corticotrophs in the anterior pituitary to stimulate the adrenal cortex. * **FSH (Option D):** Secreted by gonadotrophs in the anterior pituitary to regulate gametogenesis. **High-Yield Clinical Pearls for NEET-PG:** 1. **Hypothalamic Control:** All anterior pituitary hormones are regulated by hypothalamic "releasing" or "inhibiting" hormones. 2. **The Prolactin Exception:** Unlike other hormones, Prolactin is under **predominant inhibitory control** by Dopamine. Therefore, any stalk injury or dopamine antagonist (like antipsychotics) leads to *increased* prolactin levels (Hyperprolactinemia). 3. **Embryology:** The anterior pituitary develops from **Rathke’s pouch** (oral ectoderm), while the posterior pituitary develops from **neuroectoderm**.

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: 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: 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: Which of the following factors determines whether a patient develops acromegaly or gigantism?

Age at onset of the tumor. The clinical manifestation of growth hormone (GH) excess is primarily determined by the **status of the epiphyseal plates** at the time of onset [1]. ### Why the Correct Answer is Right: * **Gigantism:** Occurs when GH hypersecretion begins **before the fusion of the epiphyses** (pre-pubertal) [1]. Excessive GH stimulates the open growth plates of long bones, leading to dramatic longitudinal growth and tall stature [1]. * **Acromegaly:** Occurs when GH hypersecretion begins **after the fusion of the epiphyses** (post-pubertal) [1]. Since longitudinal growth is no longer possible, the excess GH causes appositional bone growth (thickening), leading to characteristic features like frontal bossing, enlarged hands/feet (acral enlargement), and macroglossia [1]. ### Why Other Options are Wrong: * **Sex:** GH excess affects both males and females similarly; gender does not dictate the clinical entity (gigantism vs. acromegaly). * **Amount of available calcium:** While GH affects bone metabolism, calcium levels do not determine the pattern of skeletal growth. * **Degree of function of the tumor:** The quantity of GH produced influences the severity of symptoms, but the *type* of skeletal deformity is strictly dependent on whether the bones are still capable of linear growth [1]. ### High-Yield Clinical Pearls for NEET-PG: * **Most common cause:** Somatotroph adenoma of the anterior pituitary. * **Best Screening Test:** Serum **IGF-1** levels (more stable than pulsatile GH) [2]. * **Confirmatory Test:** Oral Glucose Tolerance Test (**OGTT**) – failure to suppress GH below 1 ng/mL (or 0.4 ng/mL in newer assays) after 75g glucose [2]. * **Most common cause of death:** Cardiovascular disease (specifically cardiomyopathy). * **Associated condition:** Increased risk of **Colonic Polyps** and Adenocarcinoma [2].

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: Which hormone(s) utilize the cyclic adenosine monophosphate (cAMP) as a second messenger system?

Calcitonin. **Explanation:** The mechanism of hormone action is a high-yield topic for NEET-PG. Hormones that are water-soluble (peptides and catecholamines) cannot cross the lipid bilayer and must bind to cell surface receptors, triggering **second messenger systems**. **1. Why Calcitonin is Correct:** Calcitonin, secreted by the parafollicular (C-cells) of the thyroid, binds to G-protein coupled receptors (GPCRs). This activates the enzyme **Adenylate Cyclase**, which converts ATP into **cyclic AMP (cAMP)**. Other major hormones using this pathway include ACTH, Glucagon, TSH, PTH, and ADH (via V2 receptors). **2. Why Incorrect Options are Wrong:** * **Angiotensin-Converting Enzyme (ACE):** This is an **enzyme**, not a hormone. It converts Angiotensin I to Angiotensin II. While Angiotensin II is a hormone, it primarily utilizes the **IP3/DAG (Phospholipase C)** pathway, not cAMP. * **Prolactin:** Prolactin (along with Growth Hormone and Insulin) utilizes the **JAK-STAT pathway** (Enzyme-linked receptor). It does not use cAMP as a second messenger. **3. Clinical Pearls & High-Yield Facts:** * **cAMP Pathway Mnemonic (FLAT ChAMP):** **F**SH, **L**H, **A**CTH, **T**SH, **C**alcitonin, **h**CG, **A**DH (V2), **M**SH, **P**TH. * **IP3/DAG Mnemonic (GOAT):** **G**nRH, **O**xytocin, **A**ngiotensin II, **T**RH. * **ANP/NO:** Utilize **cyclic GMP (cGMP)**. * **Steroid/Thyroid Hormones:** These are lipid-soluble and act via **intracellular/nuclear receptors** to alter gene transcription directly.

Question 1

Which of the following hormones is NOT released by the anterior pituitary gland?

Accepted Answer

Prolactin

Answer

Thyroid-stimulating hormone (TSH)

Answer

Adrenocorticotropic hormone (ACTH)

Answer

Follicle-stimulating hormone (FSH)

Question 2

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

Accepted Answer

V3

Answer

V1a

Answer

V2

Answer

V4

Question 3

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

Accepted Answer

Secretin

Answer

Beta agonist

Answer

Exercise

Answer

Amino acids

Question 4

A 30-year-old pregnant woman and her 2-year-old child reside in a high-altitude area. The child presents with short stature, a potbelly, an enlarged protruding tongue, and developmental delay. Iodine supplementation is initiated for both mother and child to prevent mental retardation in the developing fetus. All statements regarding iodide oxidation are true EXCEPT:

Accepted Answer

Iodide transported to the follicular lumen by Na-I symporter

Answer

Conversion of iodide to iodine

Answer

Promoted by the enzyme peroxidase

Answer

Propylthiouracil blocks this step

Question 5

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 6

Angiotensinogen is secreted by which organ?

Accepted Answer

Liver

Answer

Kidney

Answer

Lung

Answer

Brain

Question 7

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

Accepted Answer

Estriol

Answer

Cortisol

Answer

Corticosterone

Answer

Aldosterone

Question 8

Which of the following factors determines whether a patient develops acromegaly or gigantism?

Accepted Answer

Age at onset of the tumor

Answer

Sex

Answer

Amount of available calcium

Answer

Degree of function of the tumor

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

Which hormone(s) utilize the cyclic adenosine monophosphate (cAMP) as a second messenger system?

Accepted Answer

Calcitonin

Answer

Angiotensin Converting Enzyme

Answer

Prolactin

Answer

All of the above

Endocrinology — MCQs

Endocrinology — MCQs

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