Endocrinology Practice Questions

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: What is the primary source of progesterone during a normal menstrual cycle?

Corpus luteum. **Explanation:** The correct answer is **Corpus luteum**. **1. Why Corpus Luteum is Correct:** During the luteal phase of the menstrual cycle (post-ovulation), the remnants of the Graafian follicle undergo **luteinization** under the influence of Luteinizing Hormone (LH). The granulosa and theca cells transform into granulosa-lutein and theca-lutein cells, forming the corpus luteum. This temporary endocrine gland is the primary source of **progesterone**, which is essential for preparing the endometrium for implantation (secretory phase). **2. Why Other Options are Incorrect:** * **Stroma:** The ovarian stroma provides structural support and contains theca cells which primarily produce androgens (androstenedione) under LH stimulation, rather than progesterone. * **Surface Epithelium:** This is a single layer of cuboidal cells covering the ovary. It is involved in repair after ovulation but does not have an endocrine function. * **Sertoli Cells:** These are found in the **male** testes (seminiferous tubules). They support spermatogenesis and secrete Inhibin B and Anti-Müllerian Hormone (AMH), not progesterone. **High-Yield Clinical Pearls for NEET-PG:** * **Source Transition:** In the first 8–10 weeks of pregnancy, the corpus luteum is the main source of progesterone (maintained by hCG). After this, the **placenta** takes over (the "luteal-placental shift"). * **Hormonal Trigger:** Progesterone levels peak approximately 7 days after ovulation (Day 21 of a 28-day cycle). * **Thermoregulation:** Progesterone acts on the hypothalamus to increase basal body temperature by 0.5°F–1.0°F after ovulation.

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: About ADH secretion all are true except?

Level increased by low plasma osmolality.. **Explanation:** The correct answer is **D** because it is a false statement. Antidiuretic Hormone (ADH), also known as Vasopressin, is primarily regulated by plasma osmolality. Secretion is **stimulated by high plasma osmolality** (detected by osmoreceptors in the hypothalamus) and inhibited by low plasma osmolality. When osmolality is low (dilute blood), ADH levels drop to allow the excretion of excess water. **Analysis of other options:** * **Option A:** ADH secretion increases during the **early postoperative period** as part of the body's surgical stress response. Factors like pain, anxiety, and blood loss (hypovolemia) are potent non-osmotic stimuli for ADH release. * **Option B:** ADH acts on the V2 receptors in the **Distal Convoluted Tubule (DCT)** and collecting ducts. It facilitates the insertion of Aquaporin-2 channels, thereby increasing water permeability and reabsorption. * **Option C:** ADH is a classic example of **neurosecretion**. It is synthesized in the supraoptic and paraventricular nuclei of the hypothalamus and transported axonally to the posterior pituitary (neurohypophysis) for storage and release. **High-Yield Clinical Pearls for NEET-PG:** * **Most sensitive stimulus:** A change in plasma osmolality as small as 1%. * **Most potent stimulus:** Severe hypovolemia/hypotension (though it requires a >10% change in volume). * **SIADH:** Characterized by inappropriately high ADH despite low plasma osmolality, leading to dilutional hyponatremia. * **Diabetes Insipidus:** Central (lack of ADH) or Nephrogenic (resistance to ADH), resulting in polyuria and high plasma osmolality.

Q: Excess of cortisol causes which of the following conditions?

Cushing's syndrome. **Explanation:** **Cushing’s syndrome** is the clinical state resulting from chronic exposure to excessive levels of glucocorticoids (primarily **cortisol**). Cortisol is a steroid hormone produced by the *zona fasciculata* of the adrenal cortex. Excess cortisol leads to a multisystem disorder characterized by protein catabolism, gluconeogenesis, and fat redistribution. **Analysis of Options:** * **Cushing’s syndrome (Correct):** Caused by hypercortisolism. It can be ACTH-dependent (e.g., Pituitary adenoma, known as Cushing’s Disease) or ACTH-independent (e.g., Adrenal adenoma or exogenous steroid use). * **Conn’s syndrome:** This refers to primary hyperaldosteronism, usually due to an aldosterone-secreting adrenal adenoma. It presents with hypertension and hypokalemia, not cortisol excess. * **Acromegaly:** Caused by the excessive secretion of **Growth Hormone (GH)**, usually from a pituitary adenoma after the closure of epiphyseal plates. * **Diabetes insipidus:** A disorder of water metabolism caused by a deficiency of **Antidiuretic Hormone (ADH)** or resistance to its action, leading to polyuria and polydipsia. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Features:** "Moon face," "Buffalo hump" (supraclavicular fat pads), "Lemon on a stick" appearance (truncal obesity with thin extremities), and purple striae. * **Screening Tests:** 24-hour urinary free cortisol, Low-dose dexamethasone suppression test (LDDST), or late-night salivary cortisol. * **Metabolic Effects:** Cortisol excess causes hyperglycemia (adrenal diabetes), osteoporosis, and impaired wound healing. * **Differentiating Feature:** **Cushing’s Disease** specifically refers to a pituitary cause of Cushing’s syndrome.

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 of the following hormones stimulates gluconeogenesis?

Glucagon. **Explanation:** The correct answer is **Glucagon**. **Why Glucagon is correct:** Glucagon is a potent catabolic hormone secreted by the alpha cells of the pancreas. Its primary role is to increase blood glucose levels during fasting states. It stimulates **gluconeogenesis** (the synthesis of glucose from non-carbohydrate sources like amino acids and glycerol) and **glycogenolysis** (breakdown of glycogen) in the liver. It achieves this by increasing the activity of key enzymes like PEPCK (Phosphoenolpyruvate carboxykinase) and Fructose-1,6-bisphosphatase. **Why the other options are incorrect:** * **Progesterone:** This is a steroid hormone involved in the menstrual cycle and pregnancy maintenance; it does not have a primary role in stimulating hepatic gluconeogenesis. * **Aldosterone:** A mineralocorticoid secreted by the adrenal cortex, its primary function is sodium reabsorption and potassium excretion in the distal nephron to regulate blood pressure and volume. * **Epinephrine:** While epinephrine increases blood glucose, its primary mechanism in the liver is **glycogenolysis** (rapid breakdown of existing glycogen) rather than being the primary stimulator of gluconeogenesis compared to glucagon. **High-Yield NEET-PG Pearls:** * **The "Big Four" Hyperglycemic Hormones:** Glucagon, Epinephrine, Cortisol, and Growth Hormone. * **Cortisol vs. Glucagon:** While both stimulate gluconeogenesis, Glucagon acts rapidly (minutes), whereas Cortisol acts slowly (hours) by increasing the synthesis of gluconeogenic enzymes. * **Insulin:** The only major hormone that **inhibits** gluconeogenesis and promotes glycogenesis. * **Key Enzyme:** Glucagon increases **cAMP**, which activates Protein Kinase A, leading to the phosphorylation and inactivation of Pyruvate Kinase, thereby favoring gluconeogenesis.

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: What is the definition of hyperthermia?

Temperature between 37.5°C and 38.3°C. **Explanation:** The core concept in thermoregulation is the distinction between **fever (pyrexia)** and **hyperthermia**. While both involve an elevated body temperature, their pathophysiology differs significantly. **1. Why Option C is Correct:** In clinical physiology, **hyperthermia** is defined as a core body temperature exceeding the normal range, typically cited between **37.5°C and 38.3°C (99.5°F–101.0°F)**, occurring **without a change in the hypothalamic set-point**. Unlike fever, where cytokines raise the "thermostat," hyperthermia results from failed thermoregulation (e.g., excessive heat production or decreased heat dissipation). **2. Analysis of Incorrect Options:** * **Option A (> 41.5°C):** This defines **Hyperpyrexia**, an extreme elevation of body temperature (often seen in severe infections or CNS hemorrhages). * **Option B (> 40°C with autonomic dysfunction):** This describes **Heat Stroke**, a medical emergency characterized by severe hyperthermia, CNS dysfunction (confusion/coma), and anhidrosis. * **Option D (36.5°C to 37.5°C):** This is the **Normothermic** range (the "Goldilocks zone") for a healthy adult. **High-Yield NEET-PG Pearls:** * **Fever vs. Hyperthermia:** Antipyretics (like Paracetamol) work in fever by lowering the hypothalamic set-point; they are **ineffective** in hyperthermia because the set-point is already normal. * **Malignant Hyperthermia:** A life-threatening condition triggered by volatile anesthetics (e.g., Halothane) or Succinylcholine due to a mutation in the **RYR1 receptor** (Ryanodine receptor). Treatment of choice: **Dantrolene**. * **Thermoregulatory Center:** Located in the **Preoptic nucleus of the Anterior Hypothalamus**.

Q: Diuresis produced by alcohol is due to which of the following mechanisms?

Inhibition of ADH secretion. **Explanation:** The correct answer is **D. Inhibition of ADH secretion.** **Mechanism of Action:** Alcohol (ethanol) acts as a potent diuretic primarily by inhibiting the release of **Antidiuretic Hormone (ADH)**, also known as Vasopressin, from the posterior pituitary gland. Under normal physiological conditions, ADH acts on the V2 receptors in the late distal convoluted tubules and collecting ducts of the kidney to increase water reabsorption via aquaporin-2 channels. By suppressing ADH secretion, alcohol prevents this reabsorption, leading to the excretion of a large volume of dilute urine (diuresis). **Analysis of Incorrect Options:** * **A. Decreased tubular reabsorption:** While alcohol does lead to decreased water reabsorption, this is a *secondary effect* of the lack of ADH, not a direct primary action on the tubular transport mechanisms themselves. * **B. Increased glomerular filtration rate (GFR):** Alcohol does not significantly or consistently increase GFR to a degree that would explain its potent diuretic effect. * **C. Osmotic diuresis:** This occurs when non-reabsorbable solutes (like glucose in diabetes or mannitol) pull water into the tubule. Alcohol does not act as an osmotic agent in the renal filtrate. **High-Yield Clinical Pearls for NEET-PG:** * **Central vs. Nephrogenic:** Alcohol causes a temporary "central" suppression of ADH. In contrast, Lithium causes nephrogenic diabetes insipidus by making the kidneys resistant to ADH. * **The "Hangover" Connection:** The dehydration resulting from alcohol-induced diuresis is a major contributor to the symptoms of a hangover. * **Cold Diuresis:** Similar to alcohol, exposure to cold also inhibits ADH secretion (and causes peripheral vasoconstriction), leading to increased urine output. * **ADH Stimulants:** Conversely, pain, stress, and nicotine are potent stimulators of ADH secretion.

Question 1

Insulin secretion is increased by all except:

Accepted Answer

VIP

Answer

Gastrin

Answer

Secretin

Answer

G1P

Question 2

What is the primary source of progesterone during a normal menstrual cycle?

Accepted Answer

Corpus luteum

Answer

Stroma

Answer

Surface epithelium of the ovary

Answer

Sertoli cells

Question 3

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

Accepted Answer

Iodide

Answer

Radioiodine

Answer

Propylthiouracil

Answer

Thyroxine

Question 4

About ADH secretion all are true except?

Accepted Answer

Level increased by low plasma osmolality.

Answer

Secretion increased in early postoperative period.

Answer

Causes increased permeability of DCT.

Answer

Neurosecretion.

Question 5

Excess of cortisol causes which of the following conditions?

Accepted Answer

Cushing's syndrome

Answer

Conn's syndrome

Answer

Acromegaly

Answer

Diabetes insipidus

Question 6

How many parts are there in the insulin receptor?

Accepted Answer

4

Answer

1

Answer

2

Answer

3

Question 7

Which of the following hormones stimulates gluconeogenesis?

Accepted Answer

Glucagon

Answer

Progesterone

Answer

Aldosterone

Answer

Epinephrine

Question 8

Which hormone acts by genetic modification?

Accepted Answer

Thyroxine

Answer

Insulin

Answer

Growth Hormone (GH)

Answer

Adrenocorticotropic Hormone (ACTH)

Question 9

What is the definition of hyperthermia?

Accepted Answer

Temperature between 37.5°C and 38.3°C

Answer

Temperature > 41.5°C

Answer

Temperature > 40°C with autonomic dysfunction

Answer

Temperature between 36.5°C and 37.5°C

Question 10

Diuresis produced by alcohol is due to which of the following mechanisms?

Accepted Answer

Inhibition of ADH secretion

Answer

Decreased tubular reabsorption

Answer

Increased glomerular filtration rate

Answer

Osmotic diuresis

Endocrinology — MCQs

Endocrinology — MCQs

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