Endocrinology — MCQs

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 161: A mutation in the gene coding for ryanodine receptors is associated with malignant hyperthermia. Which of the following statements best explains the increased heat production in malignant hyperthermia?

A. Increased muscle metabolism due to excess calcium ions (Correct Answer)
B. Thermic effect of food
C. Increased sympathetic discharge
D. Mitochondrial thermogenesis

Explanation: **Explanation** **Why Option A is correct:** Malignant Hyperthermia (MH) is a pharmacogenetic disorder triggered by volatile anesthetics (e.g., halothane) or succinylcholine. The underlying pathology involves a mutation in the **RYR1 gene**, which codes for the **Ryanodine Receptor** on the sarcoplasmic reticulum of skeletal muscle. In MH, the mutated receptor remains stuck in an open state, leading to a massive, uncontrolled release of **calcium ions (Ca²⁺)** into the cytosol. This excess calcium causes: 1. **Persistent muscle contraction (rigidity):** Continuous cross-bridge cycling. 2. **Hypermetabolism:** The plasma membrane and sarcoplasmic reticulum pumps (SERCA) work over-time to sequester the excess calcium, consuming massive amounts of **ATP**. This accelerated metabolic activity generates excessive heat, CO₂, and lactic acid, leading to hyperthermia and metabolic acidosis. **Why the other options are incorrect:** * **Option B:** The thermic effect of food refers to the energy expenditure required for digestion and absorption; it plays no role in anesthetic-induced hyperthermia. * **Option C:** While sympathetic overactivity (tachycardia, hypertension) occurs as a *secondary* response to the metabolic crisis in MH, it is not the primary source of heat production. * **Option D:** Mitochondrial thermogenesis (via uncoupling proteins) is the primary mechanism in **brown adipose tissue** (non-shivering thermogenesis), not the mechanism behind MH. **Clinical Pearls for NEET-PG:** * **Inheritance:** Autosomal Dominant. * **Earliest Sign:** Increase in end-tidal CO₂ (ETCO₂). * **Classic Sign:** Masseter muscle rigidity. * **Drug of Choice:** **Dantrolene** (acts by binding to the RYR1 receptor and inhibiting calcium release). * **Associated Conditions:** Central Core Disease and King-Denborough Syndrome.

Question 162: A 26-year-old woman with a 32-day menstrual cycle, who is planning for conception, regularly checks her body temperature orally each morning before rising. She observes an increase in her body temperature on the 18th day of her menstrual cycle. What hormone causes this temperature increase?

A. Estradiol
B. Progesterone (Correct Answer)
C. LH peak
D. FSH peak

Explanation: **Explanation:** The correct answer is **Progesterone**. **Underlying Medical Concept:** In a normal menstrual cycle, the Basal Body Temperature (BBT) follows a biphasic pattern. During the follicular phase, temperatures are lower. Following ovulation, the ruptured follicle transforms into the **corpus luteum**, which secretes high levels of **progesterone**. Progesterone acts directly on the **hypothalamic thermoregulatory center**, increasing the set-point and causing a rise in body temperature by approximately 0.5°F to 1.0°F (0.3°C to 0.6°C). In this patient with a 32-day cycle, ovulation typically occurs around Day 18 (32 minus 14 days of the fixed luteal phase), correlating with the observed temperature spike. **Analysis of Incorrect Options:** * **A. Estradiol:** Estrogen levels peak just before ovulation. Estrogen actually has a mild "thermolyitc" (cooling) effect and is responsible for the lower temperatures seen in the follicular phase. * **C & D. LH and FSH Peaks:** These gonadotropins peak approximately 10–12 hours before ovulation. While they trigger the process that leads to the formation of the corpus luteum, they do not have a direct pyrogenic effect on the hypothalamus. **High-Yield Clinical Pearls for NEET-PG:** * **Fixed Luteal Phase:** Regardless of cycle length, the luteal phase is almost always constant at **14 days**. To calculate the day of ovulation, subtract 14 from the total cycle length. * **Thermogenic Effect:** Progesterone is the only hormone responsible for the biphasic BBT curve. This is a retrospective indicator that ovulation has occurred. * **Pregnancy Indicator:** If the BBT remains elevated for more than 18 consecutive days after the shift, it is a highly specific early sign of pregnancy.

Question 163: Which hormone acts on intracellular receptors?

A. Thyroid-stimulating hormone (TSH) (Correct Answer)
B. Follicle-stimulating hormone (FSH)
C. Glucagon
D. Epinephrine

Explanation: **Explanation:** The mechanism of hormone action is determined by the chemical nature of the hormone. Hormones that are **lipid-soluble** (lipophilic) can cross the cell membrane and bind to **intracellular receptors** (cytoplasmic or nuclear), whereas water-soluble hormones bind to cell surface receptors. **Why Option A is Correct:** **Thyroid-stimulating hormone (TSH)** is a glycoprotein hormone. *Note: There appears to be a discrepancy in the provided key.* In standard physiology, TSH binds to G-protein coupled receptors (GPCR) on the **cell surface**. However, if the question intended to refer to **Thyroid Hormones (T3/T4)**, they are the classic examples of hormones acting on **intracellular (nuclear) receptors**. If this is a recall-based question where TSH is the keyed answer, it is often a common point of confusion with T3/T4; however, strictly speaking, Steroids, Vitamin D, and Thyroid hormones (T3/T4) are the primary groups using intracellular receptors. **Why Other Options are Incorrect:** * **B. FSH:** A glycoprotein hormone that acts via the **cAMP second messenger system** through cell surface GPCRs. * **C. Glucagon:** A peptide hormone that binds to Gs-coupled receptors on the cell membrane, activating adenylate cyclase. * **D. Epinephrine:** A catecholamine that acts on membrane-bound **α and β-adrenergic receptors**. **High-Yield NEET-PG Pearls:** 1. **Nuclear Receptors:** Remember the mnemonic **"PET TV"** (Progesterone, Estrogen, Testosterone, Thyroid hormones, Vitamin D/A). 2. **Cytoplasmic Receptors:** Primarily used by **Glucocorticoids** and **Mineralocorticoids**. 3. **Second Messengers:** Most peptide hormones use **cAMP** (e.g., ACTH, LH, FSH, PTH), while others like Oxytocin and GnRH use the **IP3/DAG** pathway. 4. **Insulin & Growth Factors:** Utilize **Tyrosine Kinase** activity (enzyme-linked receptors).

Question 164: Insulin acts through which transporter?

A. GLUT-1
B. GLUT-4 (Correct Answer)
C. SGLT-1
D. SGLT-2

Explanation: **Explanation:** The correct answer is **GLUT-4**. Insulin regulates glucose homeostasis primarily by stimulating the translocation of GLUT-4 from intracellular vesicles to the plasma membrane. **Why GLUT-4 is correct:** GLUT-4 is the only **insulin-dependent** glucose transporter. It is primarily expressed in **skeletal muscle** and **adipose tissue**. When insulin binds to its tyrosine kinase receptor, it triggers a signaling cascade (PI3K pathway) that causes GLUT-4 to move to the cell surface, allowing facilitated diffusion of glucose into the cell. This is the fundamental mechanism by which insulin lowers blood glucose levels. **Analysis of Incorrect Options:** * **GLUT-1:** This is an insulin-independent transporter found in most tissues, including RBCs and the Blood-Brain Barrier. It provides a basal level of glucose uptake required for cellular respiration. * **SGLT-1:** This is a Sodium-Glucose Linked Transporter (active transport) located in the **small intestine** (for glucose absorption) and the late proximal tubule of the kidney. * **SGLT-2:** Located in the early proximal tubule of the **kidney**, it is responsible for 90% of renal glucose reabsorption. (Note: SGLT-2 inhibitors like Dapagliflozin are key drugs in modern Diabetes management). **High-Yield Clinical Pearls for NEET-PG:** * **Exercise** can also trigger GLUT-4 translocation to the cell membrane in skeletal muscle, independent of insulin. This is why exercise helps manage blood sugar in Type 2 Diabetes. * **GLUT-2** is a bidirectional transporter found in the **Liver, Pancreatic Beta cells, and Kidney**. It acts as a "glucose sensor." * **GLUT-3** is the primary transporter in **Neurons** (high affinity). * **GLUT-5** is unique because it primarily transports **Fructose**, not glucose.

Question 165: Vasopressin is secreted by which nucleus?

A. Supraoptic nucleus (Correct Answer)
B. Preoptic nucleus
C. Paraventricular nucleus
D. Posterior nucleus

Explanation: **Explanation:** The posterior pituitary hormones, **Vasopressin (ADH)** and **Oxytocin**, are synthesized in the hypothalamus and transported via the hypothalamo-hypophyseal tract to the posterior pituitary for storage and release. 1. **Why Supraoptic Nucleus is Correct:** While both the Supraoptic Nucleus (SON) and the Paraventricular Nucleus (PVN) synthesize both hormones, they do so in different proportions. The **Supraoptic nucleus** is the primary site for **Vasopressin (ADH)** synthesis (roughly 5/6th of the total ADH), while the Paraventricular nucleus is primarily responsible for Oxytocin. 2. **Analysis of Incorrect Options:** * **Preoptic Nucleus:** This area is primarily involved in thermoregulation (the "heat loss center") and the release of Gonadotropin-Releasing Hormone (GnRH). * **Paraventricular Nucleus:** As mentioned, this is the primary site for **Oxytocin** synthesis. It also plays a role in secreting CRH and TRH. * **Posterior Nucleus:** This nucleus is part of the hypothalamus involved in "heat production" (shivering) and sympathetic nervous system activation. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic:** **S**-**O**-**V**-**A** (**S**upra**O**ptic = **V**asopressin; **P**ara**V**entricular = **O**xytocin). * **Precursor:** Vasopressin is synthesized as a preprohormone called **Prepro-pressophysin**. * **Carrier Protein:** Both hormones are transported down axons bound to proteins called **Neurophysins** (Neurophysin II for ADH). * **Lesion Site:** A lesion in the hypothalamus or the tract (above the median eminence) leads to **Central Diabetes Insipidus**, whereas a lesion of the posterior pituitary alone often results in only transient deficiency because the hypothalamus continues to secrete the hormone into the portal circulation.

Question 166: Which of the following is NOT a function of parathyroid hormone (PTH)?

A. Maintains serum calcium levels
B. Promotes calcium retention
C. Decreases phosphate excretion (Correct Answer)
D. May cause osteolysis

Explanation: **Explanation:** Parathyroid Hormone (PTH) is the primary regulator of calcium and phosphate homeostasis. Its overarching goal is to **increase serum calcium** and **decrease serum phosphate**. **Why Option C is the Correct Answer:** PTH **increases** phosphate excretion (phosphaturia), it does not decrease it. It acts on the proximal convoluted tubule (PCT) of the kidney to inhibit the sodium-phosphate cotransporter (NaPi-IIa), leading to decreased phosphate reabsorption. This is a physiological mechanism to prevent calcium-phosphate precipitation as serum calcium levels rise. **Analysis of Other Options:** * **A. Maintains serum calcium levels:** This is the primary function of PTH. It responds to hypocalcemia via calcium-sensing receptors (CaSR) to restore normalcy. * **B. Promotes calcium retention:** PTH increases calcium reabsorption in the distal convoluted tubule (DCT) and thick ascending limb of the loop of Henle, effectively "retaining" calcium in the body. * **D. May cause osteolysis:** In high concentrations (chronic elevation), PTH stimulates osteoclasts indirectly via the RANKL pathway, leading to bone resorption (osteolysis) to mobilize calcium into the blood. **NEET-PG High-Yield Pearls:** * **The "Phosphate Trashing" Hormone:** Remember the mnemonic: **"PTH: Phosphate Trashing Hormone"**—it dumps phosphate in the urine. * **Vitamin D Activation:** PTH stimulates **1-alpha-hydroxylase** in the kidney, converting 25-hydroxyvitamin D to its active form, 1,25-dihydroxyvitamin D (Calcitriol). * **Clinical Correlation:** In **Primary Hyperparathyroidism**, the classic biochemical profile is **Hypercalcemia + Hypophosphatemia + Hyperphosphaturia.**

Question 167: GnRH is a

A. Peptide (Correct Answer)
B. Amine
C. Steroid
D. Lipid

Explanation: **Explanation:** **1. Why Peptide is Correct:** Gonadotropin-Releasing Hormone (GnRH) is a **decapeptide** (composed of 10 amino acids) synthesized and released by the GnRH neurons in the hypothalamus. Like other hypothalamic releasing hormones (except Dopamine), it is proteinaceous in nature. It travels through the hypophyseal portal system to the anterior pituitary to stimulate the release of LH and FSH. **2. Why Other Options are Incorrect:** * **Amine:** Amine hormones are derived from the amino acids tyrosine or tryptophan. Examples include Catecholamines (Epinephrine, Norepinephrine), Thyroid hormones (T3, T4), and Melatonin. * **Steroid:** Steroid hormones are derived from cholesterol and are lipid-soluble. Examples include Glucocorticoids, Mineralocorticoids, and Sex steroids (Estrogen, Progesterone, Testosterone). * **Lipid:** While steroids are a subset of lipids, "Lipid" is a broad category. Other lipid-based signaling molecules include Eicosanoids (Prostaglandins), but GnRH does not fall into this structural class. **3. Clinical Pearls & High-Yield Facts for NEET-PG:** * **Pulsatile Secretion:** GnRH must be secreted in **pulses** to be physiological. Continuous (non-pulsatile) administration of GnRH or its long-acting analogs (e.g., Leuprolide) causes **downregulation/desensitization** of receptors, leading to a medical castration effect. This is used clinically to treat Prostate Cancer, Endometriosis, and Precocious Puberty. * **Location:** Primarily synthesized in the **Preoptic area** of the hypothalamus. * **Kallmann Syndrome:** A high-yield condition characterized by the failure of GnRH neurons to migrate from the olfactory placode to the hypothalamus, resulting in **hypogonadotropic hypogonadism** and **anosmia**.

Question 168: What is true about insulin?

A. Its release is enhanced by somatostatin.
B. It has an identical chemical structure in all species.
C. It is released from the pancreas only in the postprandial state.
D. It promotes the synthesis of triglycerides. (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. It promotes the synthesis of triglycerides.** Insulin is the primary **anabolic hormone** of the body. In adipose tissue, it promotes lipogenesis (the synthesis of triglycerides) by increasing the transport of glucose into adipocytes via GLUT-4 and activating **Lipoprotein Lipase (LPL)**, which breaks down circulating chylomicrons into free fatty acids for storage. Simultaneously, it inhibits **Hormone-Sensitive Lipase (HSL)**, thereby preventing lipolysis. **Analysis of Incorrect Options:** * **A. Its release is enhanced by somatostatin:** This is incorrect. Somatostatin (produced by delta cells of the pancreas) acts as a universal inhibitor; it **inhibits** the secretion of both insulin and glucagon via paracrine signaling. * **B. It has an identical chemical structure in all species:** This is incorrect. While the basic structure (A and B chains linked by disulfide bonds) is conserved, amino acid sequences vary. For example, **porcine insulin** differs from human insulin by one amino acid (Alanine instead of Threonine at position B30), while bovine insulin differs by three. * **C. It is released from the pancreas only in the postprandial state:** This is incorrect. Insulin secretion is continuous. There is a **basal secretion** (approx. 1 unit/hour) to maintain glucose homeostasis during fasting, which spikes significantly (bolus secretion) in response to meals (postprandial). **High-Yield Clinical Pearls for NEET-PG:** * **GLUT-4** is the only insulin-dependent glucose transporter, found primarily in skeletal muscle and adipose tissue. * **C-peptide** is secreted in equimolar amounts with insulin; it is a key marker to distinguish endogenous insulin production from exogenous insulin injection (Factitious Hypoglycemia). * Insulin causes an **intracellular shift of potassium**, making it a standard treatment for acute hyperkalemia.

Question 169: Thyroid-stimulating hormone (TSH) on its surface receptor uses which second messenger?

A. cAMP (Correct Answer)
B. cGMP
C. Ca2+
D. IP3

Explanation: **Explanation:** **1. Why cAMP is Correct:** Thyroid-stimulating hormone (TSH) is a glycoprotein hormone that binds to its specific G-protein coupled receptor (GPCR) on the follicular cells of the thyroid gland. This binding activates **Adenylate Cyclase**, which converts ATP into **cyclic AMP (cAMP)**. cAMP then activates Protein Kinase A (PKA), leading to the phosphorylation of proteins responsible for thyroid hormone synthesis (iodine trapping, thyroglobulin synthesis, and proteolysis). **2. Why the Other Options are Incorrect:** * **cGMP (Option B):** This second messenger is primarily used by Atrial Natriuretic Peptide (ANP), Brain Natriuretic Peptide (BNP), and Nitric Oxide (NO). * **Ca2+ and IP3 (Options C & D):** These are part of the Phospholipase C (PLC) pathway. While very high concentrations of TSH can minimally stimulate this pathway, the **primary and physiological** mechanism for TSH action is the cAMP pathway. Hormones using IP3/Ca2+ include GnRH, TRH, GHRH, and Oxytocin (the "G-Q" protein coupled receptors). **3. Clinical Pearls & High-Yield Facts for NEET-PG:** * **Mnemonic for cAMP:** "FLAT ChAMP" (FSH, LH, ACTH, TSH, CRH, hCG, ADH [V2 receptor], MSH, PTH, Glucagon). * **TSH Receptor Antibodies:** In Graves' disease, IgG antibodies (TSI) bind to the TSH receptor and mimic TSH, causing constitutive activation of the cAMP pathway, leading to hyperthyroidism. * **Dual Signaling:** Note that TSH is unique; while cAMP mediates growth and hormone secretion, the PLC pathway (IP3/DAG) is involved in iodine organification at higher TSH levels. However, for exam purposes, **cAMP** is the standard answer.

Question 170: In obesity, which of the following hormone levels is decreased?

A. Catecholamines
B. Insulin
C. Adiponectin (Correct Answer)
D. Copeptin

Explanation: **Explanation:** In obesity, the adipose tissue undergoes structural and functional changes that alter its endocrine profile. While most adipokines (like Leptin) increase with increasing fat mass, **Adiponectin** is a notable exception. **1. Why Adiponectin is the Correct Answer:** Adiponectin is a protective adipokine that enhances insulin sensitivity and exerts anti-inflammatory and anti-atherogenic effects. In obesity, specifically central/visceral obesity, the expansion of adipocytes leads to increased production of pro-inflammatory cytokines (like TNF-α and IL-6). These cytokines **downregulate** the expression and secretion of adiponectin. Therefore, adiponectin levels are **inversely correlated** with Body Mass Index (BMI) and fat mass. Low levels contribute to the development of insulin resistance and metabolic syndrome. **2. Analysis of Incorrect Options:** * **Catecholamines (A):** Obesity is generally associated with increased sympathetic nervous system activity, leading to normal or elevated levels of catecholamines, which contribute to obesity-related hypertension. * **Insulin (B):** Obesity is a primary cause of insulin resistance. To compensate, the pancreas secretes more insulin, leading to **hyperinsulinemia**. * **Copeptin (D):** Copeptin is a surrogate marker for Arginine Vasopressin (AVP). Studies show that copeptin levels are typically elevated in obesity and metabolic syndrome, correlating with water retention and increased stress response. **High-Yield Clinical Pearls for NEET-PG:** * **The "Adiponectin Paradox":** Despite being produced by adipose tissue, its levels decrease as adipose tissue increases. * **Leptin vs. Adiponectin:** In obesity, **Leptin increases** (leading to leptin resistance), while **Adiponectin decreases**. * **Thiazolidinediones (TZDs):** Drugs like Pioglitazone work partly by increasing the expression of Adiponectin, thereby improving insulin sensitivity.

Practice by Chapter

Principles of Endocrine Regulation

Practice Questions

Hypothalamus and Pituitary Gland

Practice Questions

Thyroid Physiology

Practice Questions

Adrenal Cortex and Medulla

Practice Questions

Pancreatic Hormones and Glucose Metabolism

Practice Questions

Calcium and Phosphate Homeostasis

Practice Questions

Growth Hormone and Growth Factors

Practice Questions

Endocrine Regulation of Metabolism

Practice Questions

Hormone Receptors and Signaling

Practice Questions

Assessment of Endocrine Function

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free