Endocrinology Practice Questions

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.

Q: Which hormone acts by genetic modification?

Thyroxine. **Explanation:** The mechanism of action of a hormone is determined by its chemical nature and the location of its receptors. Hormones that act via **genetic modification** (regulation of gene expression) are lipid-soluble, allowing them to cross the cell membrane and bind to intracellular receptors. **Why Thyroxine (T4) is correct:** Thyroxine is a derivative of tyrosine but behaves like a steroid hormone due to its lipophilic nature. It enters the cell and binds to **nuclear receptors** (TR-α and TR-β). The hormone-receptor complex then binds to specific DNA sequences called **Thyroid Response Elements (TREs)**. This directly stimulates or inhibits the transcription of specific genes, leading to the synthesis of new proteins (e.g., Na+/K+ ATPase, respiratory enzymes), which mediates the hormone's long-term effects. **Why other options are incorrect:** * **Insulin:** A peptide hormone that binds to a transmembrane **Tyrosine Kinase receptor**. It acts via a phosphorylation cascade (MAP kinase and PI-3 kinase pathways). * **Growth Hormone (GH):** A peptide hormone that binds to a cell surface receptor associated with the **JAK-STAT signaling pathway**. * **ACTH:** A peptide hormone that binds to G-protein coupled receptors (GPCR) on the adrenal cortex, activating the **adenylyl cyclase-cAMP** second messenger system. **High-Yield Clinical Pearls for NEET-PG:** * **Nuclear Receptors:** Remember the mnemonic **"KITE"** for hormones acting on nuclear receptors: **K**ortisol (Steroids), **I**odothyronines (T3/T4), **T**estosterone (Androgens), **E**strogen/Vitamin D/Retinoic acid. * **Speed of Action:** Hormones acting via genetic modification (Thyroid/Steroids) have a **slow onset** (hours to days) but **long duration** of action compared to peptide hormones. * **T3 vs. T4:** While T4 is secreted in higher quantities, **T3** is the active form that binds to the nuclear receptor with much higher affinity.

Q: Lesions of which of the hypothalamic nuclei cause diabetes insipidus?

Supraoptic and paraventricular nuclei. **Explanation:** **1. Why Option B is Correct:** The **Supraoptic (SON)** and **Paraventricular (PVN)** nuclei of the hypothalamus are responsible for the synthesis of **Antidiuretic Hormone (ADH)**, also known as vasopressin. ADH is synthesized in the cell bodies of these nuclei and transported via the hypothalamo-hypophyseal tract to the posterior pituitary for storage and release. * **Mechanism:** ADH acts on the V2 receptors in the collecting ducts of the kidney to increase water reabsorption. * **Lesion Effect:** Destruction of these nuclei (or the tract) leads to a deficiency of ADH, resulting in **Central Diabetes Insipidus**, characterized by polyuria (excessive dilute urine) and polydipsia. **2. Why Other Options are Incorrect:** * **A. Dorsomedial Nuclei:** Primarily involved in emotional behavior and GI stimulation (sham rage). * **C. Median Preoptic Nuclei:** Involved in thermoregulation (the "heat loss center") and bladder control. * **D. Ventromedial Nuclei:** Known as the **Satiety Center**. Lesions here lead to hyperphagia and obesity. **3. High-Yield Clinical Pearls for NEET-PG:** * **ADH vs. Oxytocin:** While both nuclei produce both hormones, the **Supraoptic** nucleus primarily produces **ADH**, while the **Paraventricular** nucleus primarily produces **Oxytocin**. * **Osmoreceptors:** These are located in the *organum vasculosum of the lamina terminalis* (OVLT), which sense plasma osmolality and signal the SON/PVN to release ADH. * **Triphasic Response:** Post-surgical trauma to this area can cause a "triphasic" response: initial DI, followed by a period of SIADH (due to leaking stored ADH), and finally permanent DI.

Q: Which of the following is a function of prolactin during lactation?

Decreased estrogen. **Explanation:** The correct answer is **D. Decreased estrogen**. **Mechanism:** Prolactin, primarily known for stimulating milk production (lactogenesis), exerts a potent inhibitory effect on the hypothalamic-pituitary-gonadal (HPG) axis. High levels of prolactin during lactation inhibit the pulsatile release of **Gonadotropin-Releasing Hormone (GnRH)** from the hypothalamus. This suppression leads to a decrease in the secretion of **FSH (Follicle-Stimulating Hormone)** and **LH (Luteinizing Hormone)** from the anterior pituitary. Consequently, the ovaries are not stimulated to produce **estrogen**, leading to a state of temporary hypogonadism known as **lactational amenorrhea**. **Analysis of Incorrect Options:** * **A. Increased FSH:** Prolactin suppresses GnRH, which leads to a *decrease* in FSH levels, not an increase. * **B. Increased libido:** Estrogen and testosterone are key drivers of libido. Since prolactin suppresses these sex steroids, it typically results in *decreased* libido. * **C. Increased testosterone:** In both males and females, hyperprolactinemia inhibits the HPG axis, leading to *decreased* production of testosterone. **Clinical Pearls for NEET-PG:** * **Lactational Amenorrhea Method (LAM):** This physiological suppression of ovulation serves as a natural (though not 100% reliable) form of contraception postpartum. * **Prolactinoma:** In non-lactating patients, a prolactin-secreting tumor presents with galactorrhea, infertility, and decreased bone density (due to chronic low estrogen). * **Dopamine Connection:** Dopamine is the primary "Prolactin-Inhibiting Factor." Drugs that block dopamine (like antipsychotics) can cause hyperprolactinemia.

Q: Pheochromocytoma predominantly secretes which hormone?

Norepinephrine. ### Explanation **Pheochromocytoma** is a catecholamine-secreting tumor derived from the chromaffin cells of the adrenal medulla. **Why Norepinephrine is Correct:** In the normal adrenal medulla, approximately 80% of the secretion is Epinephrine and 20% is Norepinephrine. This is because the enzyme **PNMT** (Phenylethanolamine N-methyltransferase), which converts norepinephrine to epinephrine, is induced by high concentrations of cortisol draining from the adrenal cortex. However, in a **Pheochromocytoma**, the tumor cells often lack sufficient contact with cortical cortisol or lose the ability to express PNMT efficiently. Consequently, the predominant hormone secreted into the circulation is **Norepinephrine**. **Analysis of Incorrect Options:** * **A. Serotonin:** This is primarily secreted by enterochromaffin cells of the GI tract and is the hallmark of Carcinoid Syndrome, not Pheochromocytoma. * **B. Epinephrine:** While secreted by the normal adrenal medulla and some specific pheochromocytomas (especially those associated with MEN 2 syndrome), it is not the *predominant* secretion in sporadic cases. * **D. Dopamine:** Though a precursor in the catecholamine pathway, it is rarely the primary secretion. High dopamine levels are more characteristic of neuroblastomas or extra-adrenal paragangliomas. **High-Yield Clinical Pearls for NEET-PG:** * **Rule of 10s:** 10% bilateral, 10% malignant, 10% pediatric, 10% extra-adrenal (Paraganglioma). * **Diagnosis:** Best initial screening test is **24-hour urinary fractionated metanephrines** and VMA. * **Management:** Always give **Alpha-blockers (Phenoxybenzamine)** before Beta-blockers to prevent a hypertensive crisis (unopposed alpha-1 stimulation). * **Associated Syndromes:** MEN 2A, MEN 2B, von Hippel-Lindau (VHL), and NF-1.

Question 1

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

Accepted Answer

GH

Answer

ACTH

Answer

Insulin

Answer

Somatostatin

Question 2

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 3

Insulin secretion is increased by all except:

Accepted Answer

VIP

Answer

Gastrin

Answer

Secretin

Answer

G1P

Question 4

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 5

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

Accepted Answer

Iodide

Answer

Radioiodine

Answer

Propylthiouracil

Answer

Thyroxine

Question 6

How many parts are there in the insulin receptor?

Accepted Answer

4

Answer

1

Answer

2

Answer

3

Question 7

Which hormone acts by genetic modification?

Accepted Answer

Thyroxine

Answer

Insulin

Answer

Growth Hormone (GH)

Answer

Adrenocorticotropic Hormone (ACTH)

Question 8

Lesions of which of the hypothalamic nuclei cause diabetes insipidus?

Accepted Answer

Supraoptic and paraventricular nuclei

Answer

Dorsomedial nuclei

Answer

Median preoptic nuclei

Answer

Ventromedial nuclei

Question 9

Which of the following is a function of prolactin during lactation?

Accepted Answer

Decreased estrogen

Answer

Increased FSH

Answer

Increased libido

Answer

Increased testosterone

Question 10

Pheochromocytoma predominantly secretes which hormone?

Accepted Answer

Norepinephrine

Answer

Serotonin

Answer

Epinephrine

Answer

Dopamine

Endocrinology — MCQs

Endocrinology — MCQs

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