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: 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 activates a tyrosine kinase receptor?

Insulin. **Explanation:** The mechanism of hormone action is a high-yield topic for NEET-PG. Hormones act via specific receptors categorized by their signaling pathways. **1. Why Insulin is Correct:** Insulin binds to a **Receptor Tyrosine Kinase (RTK)**, which is a transmembrane protein consisting of two alpha and two beta subunits. Upon insulin binding to the alpha subunits, the beta subunits undergo **autophosphorylation**. This activates the catalytic domain, leading to the recruitment and phosphorylation of **Insulin Receptor Substrates (IRS-1 to 4)**, eventually triggering the MAP kinase and PI3K pathways. **2. Analysis of Incorrect Options:** * **Growth Hormone (GH):** GH does not have intrinsic tyrosine kinase activity. Instead, it uses the **JAK-STAT pathway** (Non-receptor tyrosine kinase). When GH binds, it recruits Janus Kinase (JAK2) to phosphorylate the receptor. * **TSH & Glucagon:** Both of these hormones act via **G-Protein Coupled Receptors (GPCR)**. Specifically, they activate the **Gs-adenylyl cyclase-cAMP** second messenger system. **High-Yield Clinical Pearls for NEET-PG:** * **Intrinsic Tyrosine Kinase (RTK):** Insulin, IGF-1, EGF, PDGF, and FGF. * **JAK-STAT Pathway (Non-receptor TK):** Growth Hormone, Prolactin, Erythropoietin, and Leptin. * **cGMP Pathway:** ANP, BNP, and Nitric Oxide. * **IP3/DAG Pathway:** Oxytocin, GnRH, TRH, and Vasopressin (V1 receptor). * **Nuclear/Cytoplasmic Receptors:** Steroids, Thyroid hormones (T3/T4), and Vitamin D.

Q: Which of the following organs is not involved in calcium metabolism?

Spleen. **Explanation:** Calcium metabolism is a complex physiological process primarily regulated by the interplay between the skin, liver, kidneys, and bones, under the influence of Vitamin D, Parathyroid Hormone (PTH), and Calcitonin. **Why Spleen is the Correct Answer:** The **Spleen** is primarily a lymphoid organ involved in hemopoiesis (during fetal life), red blood cell sequestration, and immune surveillance. It plays no physiological role in the synthesis of Vitamin D, the regulation of serum calcium levels, or the storage of calcium ions. **Why the other options are involved:** * **Skin:** It is the site of the initial step in Vitamin D synthesis. Under the influence of UV-B radiation, **7-dehydrocholesterol** in the skin is converted into **Cholecalciferol (Vitamin D3)**. * **Liver:** This is the site of the first hydroxylation step. The enzyme **25-hydroxylase** converts Vitamin D3 into **25-hydroxycholecalciferol [25(OH)D3]**, which is the major circulating form of Vitamin D. * **Lung (and Kidneys):** While the **Kidney** is the primary site for the final activation (via 1-alpha-hydroxylase), the **Lungs** are involved in calcium metabolism in specific contexts. Alveolar macrophages possess 1-alpha-hydroxylase activity, allowing for extra-renal conversion of Vitamin D. Furthermore, the lungs are a common site for metastatic calcification in hypercalcemic states. **NEET-PG High-Yield Pearls:** 1. **Active Form:** 1,25-dihydroxycholecalciferol (Calcitriol) is the most active form of Vitamin D. 2. **Rate-limiting Step:** The 1-alpha-hydroxylation in the kidney (stimulated by PTH) is the regulatory bottleneck. 3. **Clinical Correlation:** In granulomatous diseases like **Sarcoidosis**, macrophages in the lungs produce excess Calcitriol, leading to hypercalcemia.

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: Which hormone is responsible for increased blood glucose levels?

Glucagon. **Explanation:** **Glucagon** is the correct answer because it is the primary counter-regulatory hormone secreted by the **alpha cells** of the pancreas in response to low blood glucose levels. It increases blood glucose primarily through two hepatic mechanisms: 1. **Glycogenolysis:** The breakdown of stored glycogen into glucose. 2. **Gluconeogenesis:** The synthesis of glucose from non-carbohydrate sources (like amino acids and glycerol). **Analysis of Incorrect Options:** * **Insulin:** Secreted by the **beta cells** of the pancreas, insulin is the only anabolic hormone that *decreases* blood glucose by promoting glucose uptake into skeletal muscle and adipose tissue via GLUT-4 transporters. * **Secretin:** This is a gastrointestinal hormone secreted by **S-cells** of the duodenum. Its primary role is to stimulate the secretion of bicarbonate-rich pancreatic juice and inhibit gastric acid secretion; it has no direct role in elevating blood glucose. **High-Yield NEET-PG Pearls:** * **The "Insulin-Glucagon Ratio":** The metabolic state of the body is determined by the ratio of these two hormones rather than their absolute levels. * **Somatostatin:** Secreted by **delta cells**, it inhibits the secretion of both insulin and glucagon (paracrine action). * **Other Hyperglycemic Hormones:** Besides glucagon, "stress hormones" like **Epinephrine, Cortisol, and Growth Hormone** also increase blood glucose levels. * **Glucagon Stimulus:** High amino acid levels (especially Arginine and Alanine) stimulate glucagon secretion to prevent hypoglycemia during a protein-rich, low-carb meal.

Q: Exercise is prescribed as an adjuvant treatment for depression. What is the most probable mechanism of action?

Raising endorphin levels. **Explanation:** **Mechanism of the Correct Answer (C):** The antidepressant effect of exercise is primarily attributed to the **"Endorphin Hypothesis."** During vigorous physical activity, the pituitary gland and hypothalamus increase the synthesis and release of **beta-endorphins**. These endogenous opioid peptides bind to mu-opioid receptors in the brain, leading to analgesia and a state of euphoria (often termed the "runner's high"). Furthermore, exercise stimulates **neurogenesis** and increases levels of **Brain-Derived Neurotrophic Factor (BDNF)**, which helps reverse the hippocampal atrophy often seen in chronic depression. **Analysis of Incorrect Options:** * **A & B (Pulse Pressure and Hemodynamics):** While exercise improves cardiovascular efficiency and stroke volume, these are physiological adaptations of the circulatory system. They do not have a direct, evidence-based neurochemical link to the pathophysiology of mood disorders. * **D (Inducing Good Sleep):** Although exercise improves sleep hygiene and circadian rhythms (which is beneficial for mental health), it is considered a secondary effect rather than the primary biochemical mechanism for treating depression. **NEET-PG High-Yield Pearls:** * **Neurotransmitters:** Exercise also increases the availability of serotonin, dopamine, and norepinephrine in the synaptic cleft, mimicking the action of traditional antidepressants. * **HPA Axis:** Regular exercise helps regulate the Hypothalamic-Pituitary-Adrenal (HPA) axis, reducing the baseline levels of **cortisol**, which is typically elevated in depressed patients. * **BDNF:** Remember that BDNF is the key molecule for **synaptic plasticity**; its deficiency is a core feature of the "Neurotrophic Hypothesis of Depression."

Question 1

All of the following developmental events are dependent on the production of maternal or fetal glucocorticoids, except?

Accepted Answer

Functional hypothalamic pituitary axis

Answer

Induction of thymic involution

Answer

Production of surfactant by type II alveolar cells

Answer

Functional thyroid

Question 2

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

Accepted Answer

Aldosterone

Answer

Cortisol

Answer

Testosterone

Answer

Catecholamines

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 activates a tyrosine kinase receptor?

Accepted Answer

Insulin

Answer

Growth hormone

Answer

TSH

Answer

Glucagon

Question 7

Which of the following organs is not involved in calcium metabolism?

Accepted Answer

Spleen

Answer

Lung

Answer

Liver

Answer

Skin

Question 8

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 9

Which hormone is responsible for increased blood glucose levels?

Accepted Answer

Glucagon

Answer

Insulin

Answer

Secretin

Answer

None of the above

Question 10

Exercise is prescribed as an adjuvant treatment for depression. What is the most probable mechanism of action?

Accepted Answer

Raising endorphin levels

Answer

Increasing pulse pressure

Answer

Improving hemodynamics

Answer

Inducing good sleep

Endocrinology — MCQs

Endocrinology — MCQs

On this page

Practice by Chapter

Want unlimited practice?