Endocrinology Practice Questions

Q: Inactivation of cortisol into cortisone occurs mainly in which organ?

Kidney. ### Explanation The conversion of active **cortisol** to inactive **cortisone** is a protective mechanism primarily occurring in the **Kidney**. **1. Why Kidney is the Correct Answer:** The kidney expresses high levels of the enzyme **11β-hydroxysteroid dehydrogenase type 2 (11β-HSD2)**. This enzyme inactivates cortisol into cortisone. This is crucial because cortisol has a high affinity for **Mineralocorticoid Receptors (MR)** in the distal nephron. Without this inactivation, the high circulating levels of cortisol would overwhelm the MR, leading to excessive sodium retention and potassium loss (mimicking hyperaldosteronism). **2. Why Other Options are Incorrect:** * **Liver:** The liver primarily performs the **reverse** reaction. It contains **11β-HSD type 1**, which converts inactive cortisone back into active cortisol (activation). * **Adrenals:** The adrenal cortex is the site of cortisol **synthesis** (specifically the Zona Fasciculata), not its primary site of inactivation. * **Lungs:** While the lungs possess some metabolic activity, they are not the principal site for the systemic inactivation of cortisol via the 11β-HSD2 pathway. **3. Clinical Pearls for NEET-PG:** * **Apparent Mineralocorticoid Excess (AME):** A genetic deficiency of 11β-HSD2 (or inhibition by **Glycyrrhizic acid** found in **Licorice**) prevents cortisol inactivation. This leads to hypertension, hypokalemia, and metabolic alkalosis despite low aldosterone levels. * **11β-HSD1 (Liver):** Bidirectional but mainly acts as a **reductase** (Cortisone → Cortisol). * **11β-HSD2 (Kidney):** Unidirectional **dehydrogenase** (Cortisol → Cortisone). * **Cortisol vs. Aldosterone:** Cortisol circulates at concentrations ~1000 times higher than aldosterone; hence, 11β-HSD2 is the "gatekeeper" of the mineralocorticoid receptor.

Q: Which hormone causes increased food intake?

Ghrelin. **Explanation:** The regulation of food intake is controlled by the hypothalamus, specifically through the interplay of **orexigenic** (appetite-stimulating) and **anorexigenic** (appetite-suppressing) signals. **Why Ghrelin is Correct:** Ghrelin is a peptide hormone secreted primarily by the **P/D1 cells of the stomach fundus**. It is known as the "hunger hormone" because it is the only peripheral hormone that stimulates food intake (orexigenic). It acts on the **Arcuate Nucleus** of the hypothalamus to stimulate **NPY (Neuropeptide Y)** and **AgRP (Agouti-related peptide)** neurons, which increase appetite and growth hormone secretion. Ghrelin levels rise sharply before meals and fall immediately after eating. **Why Other Options are Incorrect:** * **Leptin:** Produced by adipocytes, it is a long-term satiety signal. It inhibits NPY/AgRP neurons and stimulates POMC neurons, thereby **decreasing** food intake. * **CART (Cocaine-and-Amphetamine-Regulated Transcript):** This is a potent **anorexigenic** neurotransmitter found in the hypothalamus that decreases appetite. * **Serotonin (5-HT):** In the CNS, serotonin acts as a **satiety signal**. Drugs that increase serotonin levels (like fenfluramine) were historically used to suppress appetite. **High-Yield Clinical Pearls for NEET-PG:** * **Prader-Willi Syndrome:** Characterized by hyperphagia and obesity due to pathologically **elevated Ghrelin levels**. * **Sleep Deprivation:** Increases Ghrelin and decreases Leptin, leading to weight gain. * **Vagus Nerve:** Ghrelin signals are also transmitted via the vagus nerve to the brainstem. * **Post-Gastric Bypass:** Weight loss is partly attributed to a significant **reduction in Ghrelin** levels due to the bypass of the stomach fundus.

Q: Which hormone acts on intracellular receptors?

Thyroid-stimulating hormone (TSH). **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).

Q: Vasopressin is secreted by which nucleus?

Supraoptic nucleus. **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.

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

Decreases phosphate excretion. **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.**

Q: What is true about insulin?

It promotes the synthesis of triglycerides.. ### 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.

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

Adiponectin. **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.

Question 1

Most peptide and protein hormones are synthesized as what?

Accepted Answer

A preprohormone

Answer

A secretagogue

Answer

A pleiotropic hormone

Answer

Proopiomelanocortin (POMC)

Question 2

Inactivation of cortisol into cortisone occurs mainly in which organ?

Accepted Answer

Kidney

Answer

Lungs

Answer

Liver

Answer

Adrenals

Question 3

Which hormone causes increased food intake?

Accepted Answer

Ghrelin

Answer

Leptin

Answer

Cart

Answer

Serotonin

Question 4

Which of the following sources of cholesterol is most important for sustaining adrenal steroidogenesis when it occurs at a high rate for a long time?

Accepted Answer

Cholesterol in LDL particles

Answer

De novo synthesis of cholesterol from acetate

Answer

Cholesterol in the plasma membrane

Answer

Cholesterol in lipid droplets within adrenal cortical cells

Question 5

Which hormone acts on intracellular receptors?

Accepted Answer

Thyroid-stimulating hormone (TSH)

Answer

Follicle-stimulating hormone (FSH)

Answer

Glucagon

Answer

Epinephrine

Question 6

Vasopressin is secreted by which nucleus?

Accepted Answer

Supraoptic nucleus

Answer

Preoptic nucleus

Answer

Paraventricular nucleus

Answer

Posterior nucleus

Question 7

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

Accepted Answer

Decreases phosphate excretion

Answer

Maintains serum calcium levels

Answer

Promotes calcium retention

Answer

May cause osteolysis

Question 8

What is true about insulin?

Accepted Answer

It promotes the synthesis of triglycerides.

Answer

Its release is enhanced by somatostatin.

Answer

It has an identical chemical structure in all species.

Answer

It is released from the pancreas only in the postprandial state.

Question 9

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

Accepted Answer

Adiponectin

Answer

Catecholamines

Answer

Insulin

Answer

Copeptin

Question 10

A 16-year-old girl diagnosed with anorexia nervosa presents with light-headedness, diaphoresis, and palpitations during exercise. Her serum glucose is 40 mg/dL. She improves after consuming a soft drink. Which of the following hormones most likely triggered the sweating and palpitations?

Accepted Answer

Epinephrine

Answer

ACTH

Answer

Calcitonin

Answer

Insulin

Endocrinology — MCQs

Endocrinology — MCQs

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