Endocrinology Practice Questions

Q: Destruction of the zona glomerulosa will lead to a depletion of which hormone?

Aldosterone. **Explanation:** The adrenal gland is divided into an outer cortex and an inner medulla. The adrenal cortex consists of three distinct layers, often remembered by the mnemonic **"GFR"** (from superficial to deep), which correspond to the hormones they produce: **"Salt, Sugar, Sex."** 1. **Zona Glomerulosa (Outer):** Produces mineralocorticoids, primarily **Aldosterone**. This hormone regulates sodium and potassium balance. Therefore, destruction of this layer leads directly to a depletion of Aldosterone. 2. **Zona Fasciculata (Middle):** The thickest layer, responsible for producing glucocorticoids, mainly **Cortisol**. 3. **Zona Reticularis (Inner):** Produces adrenal androgens, such as **Dehydroepiandrosterone (DHEA)** and **Testosterone**. **Analysis of Incorrect Options:** * **B. Cortisol:** Produced by the Zona Fasciculata, not the Glomerulosa. * **C. Testosterone:** Produced by the Zona Reticularis (and primarily by the testes in males). * **D. Catecholamines:** These (Epinephrine and Norepinephrine) are produced by the **Adrenal Medulla** (chromaffin cells), which is embryologically derived from the neural crest, unlike the cortex. **High-Yield Clinical Pearls for NEET-PG:** * **Regulation:** The Zona Glomerulosa is primarily regulated by **Angiotensin II and Potassium levels**, whereas the Fasciculata and Reticularis are regulated by **ACTH**. * **Conn’s Syndrome:** Primary hyperaldosteronism usually caused by an adenoma in the Zona Glomerulosa. * **Addison’s Disease:** Primary adrenal insufficiency involving the destruction of all three cortical layers, leading to deficiencies in aldosterone, cortisol, and androgens.

Q: Which of the following hormones increases appetite?

Ghrelin. **Explanation:** The regulation of appetite is controlled by the arcuate nucleus of the hypothalamus, which balances **orexigenic** (appetite-stimulating) and **anorexigenic** (appetite-suppressing) signals. **Correct Option: D. Ghrelin** Ghrelin is the only major peripheral hormone that is **orexigenic**. It is secreted primarily by the P/D1 cells in the fundus of the stomach and epsilon cells of the pancreas. Ghrelin levels rise during fasting (pre-prandially) and stimulate the **NPY/AgRP neurons** in the hypothalamus to increase hunger and food intake. **Incorrect Options:** * **A. Leptin:** Produced by adipocytes, leptin is a long-term satiety signal. It inhibits NPY/AgRP neurons and stimulates POMC/CART neurons to **decrease** appetite. * **B. GLP-1:** Secreted by L-cells of the ileum and colon in response to food, it stimulates insulin secretion and acts as a potent **satiety** signal. * **C. Peptide YY (PYY):** Also secreted by L-cells of the distal small intestine and colon, it reduces appetite by inhibiting NPY release. **High-Yield Facts for NEET-PG:** * **"Hunger Hormone":** Ghrelin (G for "Growl" of the stomach). * **Sleep Deprivation:** Increases Ghrelin and decreases Leptin, leading to weight gain. * **Prader-Willi Syndrome:** Characterized by hyperphagia and obesity due to pathologically high Ghrelin levels. * **Vagus Nerve:** Ghrelin also acts via the vagal afferents to signal the brain. * **Bariatric Surgery:** Gastric bypass often leads to weight loss not just by restriction, but by significantly lowering Ghrelin production.

Q: The final cleavage products of proopiomelanocortin (POMC) are all of the following except?

Testosterone. **Explanation:** The correct answer is **Testosterone** because it is a steroid hormone synthesized from cholesterol in the Leydig cells of the testes, not a peptide derivative of Proopiomelanocortin (POMC). **Understanding POMC Cleavage:** Proopiomelanocortin (POMC) is a large precursor polypeptide synthesized primarily in the corticotrophs of the anterior pituitary and the intermediate lobe. It undergoes extensive post-translational proteolytic cleavage by enzymes called prohormone convertases to produce several biologically active peptides: * **ACTH (Adrenocorticotropic Hormone):** The primary product in the anterior pituitary. * **MSH (Melanocyte-Stimulating Hormone):** Derived from the cleavage of ACTH (α-MSH) and γ-LPH (β-MSH). This explains why hyperpigmentation occurs in Addison’s disease (high ACTH). * **Lipotropin (LPH):** Specifically β-LPH and γ-LPH, which are involved in lipid metabolism. * **Endorphins:** Specifically β-endorphin, which is derived from the cleavage of β-lipotropin and acts as an endogenous opioid. **Why other options are incorrect:** * **MSH, Lipotropin, and Endorphin** are all direct or indirect cleavage products of the POMC prohormone chain. **High-Yield Clinical Pearls for NEET-PG:** 1. **Hyperpigmentation Link:** In primary adrenal insufficiency, high levels of POMC/ACTH lead to increased α-MSH, causing characteristic skin darkening. 2. **Location Matters:** In the **Anterior Pituitary**, the main products are ACTH and β-LPH. In the **Intermediate Lobe** (and hypothalamus), these are further cleaved into MSH and Endorphins. 3. **MC4R Receptor:** α-MSH produced in the hypothalamus acts on MC4 receptors to inhibit appetite; mutations here are a common cause of monogenic obesity.

Q: TSH acts through which mechanism?

cAMP. **Explanation:** **Mechanism of Action:** Thyroid-Stimulating Hormone (TSH) is a glycoprotein hormone that acts via the **G-protein coupled receptor (GPCR)** pathway. Upon binding to its specific receptor on the thyroid follicular cell membrane, it activates the enzyme **Adenylate Cyclase**. This enzyme converts ATP into **cyclic AMP (cAMP)**, which serves as the second messenger. cAMP then activates Protein Kinase A (PKA), leading to the phosphorylation of proteins responsible for thyroid hormone synthesis (iodine trapping, thyroglobulin synthesis, and proteolysis). **Analysis of Options:** * **Option A (Ion channels):** This mechanism is typical for neurotransmitters (e.g., Acetylcholine at nicotinic receptors) or GABA, which produce rapid electrical changes, not for trophic hormones like TSH. * **Option B & D (Nuclear/Cytoplasmic receptors):** These are used by lipid-soluble hormones. **Thyroid hormones (T3/T4)** themselves act via nuclear receptors, but TSH (a peptide hormone) is water-soluble and cannot cross the lipid bilayer, necessitating a cell-surface receptor. **High-Yield Clinical Pearls for NEET-PG:** * **Second Messenger Mnemonic:** Most "stimulating" or "releasing" hormones from the pituitary (TSH, ACTH, FSH, LH, Glucagon, PTH, and V2 receptors of ADH) use the **cAMP** pathway. * **Exceptions:** Oxytocin, GnRH, and TRH use the **IP3/DAG** (Phospholipase C) pathway. * **Graves’ Disease:** This condition involves "Thyroid Stimulating Immunoglobulins" (TSI) that mimic TSH by binding to the TSH receptor and overactivating the cAMP pathway, leading to hyperthyroidism.

Q: All the following hormones can affect the growth of a child except?

GH. **Explanation:** The question asks which hormone **does not** affect growth. However, based on physiological principles, the provided key (A. GH) is technically incorrect as Growth Hormone is the primary driver of linear growth. In the context of standard medical examinations, **Somatostatin (Option D)** is the most logical "except" choice because its primary role is inhibitory, whereas GH, Insulin, and ACTH (via cortisol) all significantly modulate the growth process. **1. Why Somatostatin is the likely intended answer (Concept):** * **Somatostatin:** Known as Growth Hormone Inhibiting Hormone (GHIH), it inhibits the release of GH and TSH. While it regulates the *secretion* of growth-promoting hormones, it does not directly act on peripheral tissues to promote or modulate growth in the way the others do. **2. Why the other options affect growth:** * **GH (Growth Hormone):** The master regulator of postnatal growth. It acts directly on bones and indirectly via IGF-1 (Somatomedin C) to promote epiphyseal plate expansion. * **Insulin:** Crucial for fetal growth. It is structurally similar to IGF-1 and is required for protein synthesis. Children with uncontrolled Type 1 Diabetes often exhibit growth retardation (Mauriac Syndrome). * **ACTH:** Stimulates the release of Cortisol. In excess (Cushing’s syndrome), glucocorticoids are potent inhibitors of growth as they antagonize GH action and cause premature closure of epiphyses. **High-Yield Clinical Pearls for NEET-PG:** * **Thyroid Hormone:** Essential for GH secretion and skeletal maturation; deficiency leads to Cretinism (stunted growth). * **Androgens/Estrogens:** Cause the "pubertal growth spurt" but eventually lead to the closure of epiphyseal plates. * **Fetal Growth:** Primarily regulated by **Insulin and IGF-2**, not GH. * **Laron Dwarfism:** Characterized by GH resistance due to GH receptor mutations (High GH, Low IGF-1).

Q: Which of the following is NOT a function of corticosteroids?

Decreases the catabolism of immunoglobulins. ### Explanation Corticosteroids (specifically glucocorticoids like cortisol) are primarily **catabolic** hormones. They function to mobilize energy stores and suppress the immune system. **Why Option D is the Correct Answer:** Glucocorticoids **increase** the catabolism (breakdown) of proteins, including immunoglobulins (antibodies). By promoting the breakdown of existing antibodies and inhibiting the production of new B-cells and T-cells, they exert a potent immunosuppressive effect. Therefore, the statement that they "decrease" catabolism is incorrect. **Analysis of Incorrect Options:** * **Option A (Protein Breakdown):** Cortisols are catabolic in peripheral tissues (muscle, adipose, lymphoid). They promote the breakdown of proteins into amino acids to provide substrates for gluconeogenesis in the liver. * **Option B (Lymphatic Cells):** Glucocorticoids cause **lymphocytopenia** and eosinopenia. They induce apoptosis in lymphocytes and cause the sequestration of cells into the bone marrow, leading to a decrease in the size of the spleen and lymph nodes. * **Option C (Glucose Utilization):** Cortisol is "diabetogenic." It inhibits GLUT-4 mediated glucose uptake in peripheral tissues (muscle and fat) to ensure adequate glucose remains available for the brain during stress. **High-Yield NEET-PG Pearls:** * **Hematological Effects:** Cortisol increases "BBC" (**B**enign **B**ertie's **C**ounts): **B**lood pressure, **B**one loss, and **C**ounts of RBCs, Platelets, and Neutrophils (due to demargination). * **Immunosuppression:** They inhibit **Phospholipase A2**, thereby reducing the production of prostaglandins and leukotrienes. * **Metabolic Rule:** Cortisol is catabolic everywhere (muscle, bone, lymphoid) **except the liver**, where it is anabolic (increases gluconeogenesis and glycogen synthesis).

Q: Insulin secretion is increased by all except:

VIP. **Explanation:** Insulin secretion is regulated by a complex interplay of nutrients, hormones, and neural signals. The concept tested here is the **Incretin Effect**, where oral glucose triggers a higher insulin response than intravenous glucose due to the release of gastrointestinal hormones. **Why VIP is the Correct Answer:** **Vasoactive Intestinal Peptide (VIP)** primarily functions as a potent vasodilator and a stimulator of intestinal water and electrolyte secretion. While it belongs to the secretin family, it does **not** significantly stimulate insulin secretion under physiological conditions. In fact, in the context of the pancreas, VIP is more closely associated with stimulating the secretion of pancreatic juice rich in bicarbonate. **Analysis of Incorrect Options:** * **Gastrin:** This hormone, released from G-cells, is a known insulin secretagogue. It stimulates the beta cells of the pancreas to release insulin, especially during the cephalic and gastric phases of digestion. * **Secretin:** Secretin stimulates the exocrine pancreas to release bicarbonate and also acts as a mild stimulator of insulin release. * **GIP (Glucose-dependent Insulinotropic Peptide):** (Note: G1P in the question is a common typo for GIP in exams). GIP is a major **Incretin**. It is secreted by K-cells in the duodenum and directly stimulates insulin secretion in a glucose-dependent manner. **High-Yield NEET-PG Pearls:** 1. **Incretins:** The two primary incretins are **GIP** and **GLP-1** (Glucagon-like peptide-1). GLP-1 is currently a major pharmacological target (e.g., Semaglutide). 2. **Most Potent Stimulator:** Glucose is the most potent physiological stimulator of insulin. 3. **Inhibitors of Insulin:** Somatostatin, Alpha-adrenergic agonists (Norepinephrine), and fasting/starvation. 4. **Biphasic Release:** Insulin release is biphasic; the first phase is the release of stored insulin, and the second phase is the release of newly synthesized insulin.

Q: All of the following hormones act through cell surface receptors except?

Cortisol. **Explanation:** The mechanism of action of a hormone is primarily determined by its chemical nature (solubility). Hormones are broadly classified into **water-soluble** (lipophobic) and **lipid-soluble** (lipophilic). **1. Why Cortisol is the Correct Answer:** Cortisol is a **steroid hormone** derived from cholesterol. Being lipid-soluble, it easily diffuses across the phospholipid bilayer of the cell membrane. Therefore, it does not require a cell surface receptor; instead, it binds to **intracellular receptors** (specifically, Type 1 cytoplasmic receptors). The hormone-receptor complex then translocates to the nucleus to alter gene transcription. **2. Why the Other Options are Incorrect:** * **Insulin (Option B):** A peptide hormone that binds to a **Tyrosine Kinase receptor** (an enzyme-linked cell surface receptor). * **FSH and TSH (Options C & D):** Both are glycoprotein hormones. Being large and water-soluble, they cannot cross the cell membrane. They bind to **G-Protein Coupled Receptors (GPCRs)** on the cell surface and utilize the **cAMP** second messenger system. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Intracellular Receptors:** *"**VET** **T**v **C**hannels"* (**V**itamin D, **E**strogen, **T**estosterone, **T**hyroid hormones (T3/T4), **C**ortisol/Aldosterone). * **Exceptions:** While most lipid-soluble hormones use intracellular receptors, **Thyroid hormones** are unique because they bind directly to receptors already located on the **chromatin in the nucleus**. * **Second Messengers:** Remember that **ANP** and **Nitric Oxide** use **cGMP**, while **Catecholamines (α1)** and **Oxytocin** use the **IP3/DAG** pathway.

Q: Wolf-Chaikoff effect is due to excess of which substance?

Iodide. **Explanation:** The **Wolff-Chaikoff effect** is an autoregulatory phenomenon where the ingestion of a large amount of **Iodide (Option A)** leads to a transient inhibition of thyroid hormone synthesis. **Mechanism:** When plasma iodide levels are acutely elevated, the high concentration of intrathyroidal iodide inhibits the enzyme **thyroid peroxidase (TPO)**. This prevents the organification of iodine (binding of iodine to tyrosine) and the coupling reactions, effectively shutting down the production of T3 and T4. This serves as a protective mechanism to prevent the thyroid gland from producing excessive amounts of hormone in an iodine-rich environment. **Analysis of Incorrect Options:** * **Radioiodine (Option B):** Used for thyroid scanning (I-123) or ablation of thyroid tissue in hyperthyroidism/cancer (I-131) via radiation, not by inhibiting organification through autoregulation. * **Propylthiouracil (Option C):** An antithyroid drug that pharmacologically inhibits TPO and peripheral conversion of T4 to T3; it is not the substance that triggers the physiological Wolff-Chaikoff effect. * **Thyroxine (Option D):** This is the end-product (T4). High levels of T4 exert negative feedback on the pituitary/hypothalamus, but do not trigger the Wolff-Chaikoff effect. **High-Yield Facts for NEET-PG:** * **Escape Phenomenon:** The Wolff-Chaikoff effect is temporary. After about 10–14 days, the gland "escapes" this inhibition by downregulating the **Sodium-Iodide Symporter (NIS)**, reducing internal iodide levels. * **Clinical Application:** This effect is the rationale behind using **Lugol’s iodine** or Potassium Iodide (SSKI) pre-operatively in Graves' disease to decrease the vascularity and size of the thyroid gland. * **Jod-Basedow Phenomenon:** The opposite of Wolff-Chaikoff; it is iodine-induced hyperthyroidism occurring in patients with underlying thyroid autonomy (e.g., multinodular goiter).

Q: How many parts are there in the insulin receptor?

4. **Explanation:** The insulin receptor is a **heterotetrameric** glycoprotein complex, meaning it consists of **four subunits**: **two alpha (α) subunits** and **two beta (β) subunits**, linked together by disulfide bonds. 1. **Alpha (α) Subunits (2):** These are entirely extracellular and contain the insulin-binding domain. 2. **Beta (β) Subunits (2):** These are transmembrane proteins. The intracellular portion of the beta subunit possesses **intrinsic tyrosine kinase activity**, which is essential for signal transduction (MAP kinase and PI3K pathways). **Why the other options are incorrect:** * **Option A (1):** While the receptor is synthesized from a single mRNA transcript, it is proteolytically cleaved into distinct subunits before reaching the cell membrane. * **Option B (2):** This might refer to the types of subunits (α and β), but the functional receptor requires two of each, totaling four. * **Option C (3):** There is no physiological model of the insulin receptor consisting of three parts. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Insulin binding causes **autophosphorylation** of the beta subunits. * **Receptor Type:** It belongs to the **Enzyme-linked receptor** family (specifically, Receptor Tyrosine Kinase). * **Downregulation:** In states of chronic hyperinsulinemia (like Type 2 Diabetes or obesity), the number of insulin receptors decreases, contributing to **insulin resistance**. * **GLUT-4:** The activation of this receptor leads to the translocation of GLUT-4 vesicles to the cell membrane in skeletal muscle and adipose tissue, facilitating glucose uptake.

Question 1

Destruction of the zona glomerulosa will lead to a depletion of which hormone?

Accepted Answer

Aldosterone

Answer

Cortisol

Answer

Testosterone

Answer

Catecholamines

Question 2

Which of the following hormones increases appetite?

Accepted Answer

Ghrelin

Answer

Leptin

Answer

Glucagon-like peptide 1 (GLP-1)

Answer

Peptide YY (PYY)

Question 3

The final cleavage products of proopiomelanocortin (POMC) are all of the following except?

Accepted Answer

Testosterone

Answer

MSH

Answer

Lipotropin

Answer

Endorphin

Question 4

TSH acts through which mechanism?

Accepted Answer

cAMP

Answer

Ion channels

Answer

Nuclear receptors

Answer

Cytoplasmic receptors

Question 5

All the following hormones can affect the growth of a child except?

Accepted Answer

GH

Answer

ACTH

Answer

Insulin

Answer

Somatostatin

Question 6

Which of the following is NOT a function of corticosteroids?

Accepted Answer

Decreases the catabolism of immunoglobulins

Answer

Promotes the breakdown of proteins

Answer

Decreases the amount of lymphatic cells in the spleen and lymph nodes

Answer

Inhibits the peripheral utilization of glucose

Question 7

Insulin secretion is increased by all except:

Accepted Answer

VIP

Answer

Gastrin

Answer

Secretin

Answer

G1P

Question 8

All of the following hormones act through cell surface receptors except?

Accepted Answer

Cortisol

Answer

Insulin

Answer

Follicle-stimulating hormone (FSH)

Answer

Thyroid-stimulating hormone (TSH)

Question 9

Wolf-Chaikoff effect is due to excess of which substance?

Accepted Answer

Iodide

Answer

Radioiodine

Answer

Propylthiouracil

Answer

Thyroxine

Question 10

How many parts are there in the insulin receptor?

Accepted Answer

4

Answer

1

Answer

2

Answer

3

Endocrinology — MCQs

Endocrinology — MCQs

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