Endocrinology — MCQs

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 511: What is true about the function of Angiotensin II?

A. Constriction of afferent arteriole (Correct Answer)
B. Autoregulation of GFR
C. Secretion from endothelium
D. Release of aldosterone

Explanation: **Explanation:** **1. Why Option A is correct:** Angiotensin II (AT-II) is a potent vasoconstrictor. While its primary physiological role at low concentrations is to maintain GFR by preferentially constricting the **efferent arteriole**, at higher concentrations (as often tested in physiological stressors), it causes significant constriction of **both** afferent and efferent arterioles. This increases systemic blood pressure and renal vascular resistance. **2. Why other options are incorrect:** * **Option B:** Autoregulation of GFR is primarily mediated by the **Myogenic mechanism** and **Tubuloglomerular feedback (TGF)**. While AT-II helps maintain GFR during hypotension, it is a mediator of the Renin-Angiotensin-Aldosterone System (RAAS), which is an extrinsic hormonal control rather than the intrinsic autoregulatory process itself. * **Option C:** Angiotensin II is not secreted by the endothelium. It is produced in the circulation (primarily in the lungs) by the action of **Angiotensin-Converting Enzyme (ACE)** on Angiotensin I. * **Option D:** This is a common distractor. Angiotensin II **stimulates** the adrenal cortex (Zona Glomerulosa) to release aldosterone; it does not "release" it directly in the sense of a storage product, nor is it the primary function described in the context of renal hemodynamics often tested in this question format. **High-Yield Clinical Pearls for NEET-PG:** * **Preferential Action:** At low/normal levels, AT-II constricts the **Efferent Arteriole** > Afferent Arteriole (to maintain GFR). * **ACE Inhibitors:** They block AT-II production, leading to efferent vasodilation. This is why they are contraindicated in **Bilateral Renal Artery Stenosis** (can cause acute renal failure due to a sudden drop in GFR). * **Other Actions:** AT-II stimulates thirst (hypothalamus), increases ADH secretion, and promotes proximal tubule Na+/H+ exchange (increasing Na+ reabsorption).

Question 512: All of the following are true about neuropeptide Y EXCEPT:

A. It consists of 36 amino acids.
B. It causes vasodilatation.
C. It acts as a neurotransmitter.
D. It decreases food intake. (Correct Answer)

Explanation: **Explanation:** Neuropeptide Y (NPY) is a 36-amino acid peptide widely distributed in the central and peripheral nervous systems. It is one of the most potent **orexigenic** (appetite-stimulating) peptides known. **Why Option D is the Correct Answer (The Exception):** NPY **increases** food intake; it does not decrease it. It is synthesized in the arcuate nucleus of the hypothalamus and acts on the paraventricular nucleus to stimulate hunger and promote weight gain. Substances that decrease food intake are called anorexigenic (e.g., Leptin, POMC, and CART). **Analysis of Other Options:** * **Option A:** NPY is indeed a polypeptide consisting of **36 amino acids**. It belongs to the same family as Peptide YY (PYY) and Pancreatic Polypeptide (PP). * **Option B:** While NPY is a potent vasoconstrictor in many vascular beds, it is known to cause **vasodilation** in specific tissues (like the heart and brain) under certain physiological conditions, often through the release of nitric oxide or by modulating sympathetic tone. (Note: In many textbooks, it is primarily highlighted as a co-transmitter with norepinephrine causing vasoconstriction, but its multifaceted role includes complex vascular regulation). * **Option C:** NPY acts as a **neurotransmitter** and neuromodulator. It is often co-stored and co-released with Norepinephrine in postganglionic sympathetic neurons. **High-Yield Clinical Pearls for NEET-PG:** * **Hypothalamic Control:** NPY/AgRP neurons are inhibited by **Leptin** and **Insulin** (satiety signals) and stimulated by **Ghrelin** (the hunger hormone). * **Location:** Highest concentrations are found in the **Arcuate Nucleus** of the Hypothalamus. * **Functions:** Beyond appetite, NPY is involved in regulating circadian rhythms, reducing anxiety (anxiolytic), and modulating cardiovascular function.

Question 513: Which of the following hormones is not secreted by the kidney?

A. Renin
B. Angiotensin I (Correct Answer)
C. Erythropoietin
D. 1, 25-dihydroxycholecalciferol

Explanation: **Explanation:** The kidney functions as both an excretory and an endocrine organ. The correct answer is **Angiotensin I** because it is not secreted by the kidney; rather, it is **produced in the circulating blood.** 1. **Why Angiotensin I is the correct answer:** The kidney secretes the enzyme **Renin**. Renin acts on **Angiotensinogen** (a plasma protein synthesized by the liver) to cleave it into **Angiotensin I**. Therefore, Angiotensin I is a product of an enzymatic reaction occurring in the plasma, not a direct secretion from renal cells. 2. **Analysis of incorrect options:** * **Renin:** Secreted by the **Juxtaglomerular (JG) cells** of the afferent arteriole in response to low blood pressure or low chloride delivery to the macula densa. * **Erythropoietin (EPO):** Produced by **interstitial cells (peritubular capillaries)** in the renal cortex. it stimulates RBC production in the bone marrow in response to hypoxia. * **1, 25-dihydroxycholecalciferol (Calcitriol):** The kidney contains the enzyme **1-alpha-hydroxylase** (in the proximal convoluted tubule), which converts inactive 25-hydroxyvitamin D into the active form, Calcitriol. **High-Yield NEET-PG Pearls:** * **Site of ACE:** Angiotensin I is converted to Angiotensin II primarily in the **lungs** by Angiotensin-Converting Enzyme (ACE) located on the vascular endothelium. * **Thrombopoietin:** While primarily produced in the liver, a small amount is also synthesized in the kidney. * **Prostaglandins:** The kidney also produces PGE2 and PGI2 (vasodilators) which help maintain renal blood flow.

Question 514: 17-alpha hydroxylase is not involved in the pathway for synthesis of?

A. Cortisol
B. Aldosterone (Correct Answer)
C. Androstenedione
D. Testosterone

Explanation: **Explanation:** The adrenal cortex is divided into three zones, each producing specific steroid hormones based on the presence or absence of specific enzymes. The enzyme **17-alpha hydroxylase** is the key "branch point" enzyme that diverts precursors away from the mineralocorticoid pathway. **1. Why Aldosterone is the correct answer:** Aldosterone is synthesized in the **Zona Glomerulosa**. This zone lacks the enzyme 17-alpha hydroxylase. Therefore, Pregnenolone is converted to Progesterone and then eventually to Aldosterone via 21-hydroxylase and 11-beta hydroxylase. Because 17-alpha hydroxylase is absent here, the mineralocorticoid pathway remains "17-deoxy." **2. Why the other options are incorrect:** * **Cortisol (Option A):** Synthesized in the **Zona Fasciculata**. This zone requires 17-alpha hydroxylase to convert Progesterone into 17-OH Progesterone, the essential precursor for cortisol. * **Androstenedione & Testosterone (Options C & D):** Synthesized in the **Zona Reticularis** (and gonads). 17-alpha hydroxylase is mandatory to convert C21 steroids into C19 androgenic precursors (via its 17,20-lyase activity). **Clinical Pearls for NEET-PG:** * **17-alpha Hydroxylase Deficiency:** Results in a "shunting" of precursors toward the Mineralocorticoid pathway. Clinical presentation includes **Hypertension** and **Hypokalemia** (due to excess 11-deoxycorticosterone) and **Delayed Puberty/Sexual Infantilism** (due to lack of sex steroids). * **Mnemonic:** "The deeper you go, the sweeter it gets" (Salt → Sugar → Sex). * *Glomerulosa:* Salt (Aldosterone) - No 17-α hydroxylase. * *Fasciculata:* Sugar (Cortisol) - Has 17-α hydroxylase. * *Reticularis:* Sex (Androgens) - Has 17-α hydroxylase.

Question 515: Which of the following hormones increases during sleep?

A. Insulin
B. ACTH
C. GH (Correct Answer)
D. Glucocorticoid

Explanation: **Explanation:** The correct answer is **GH (Growth Hormone)**. Growth hormone secretion follows a distinct pulsatile and circadian rhythm, with its most significant peak occurring during sleep. **1. Why GH is correct:** GH secretion is maximal during **Slow-Wave Sleep (Stage N3/Deep Sleep)**, typically occurring within the first 90 minutes after sleep onset. This surge is mediated by an increase in GHRH (Growth Hormone Releasing Hormone) and a decrease in Somatostatin. In children and adolescents, this sleep-associated peak is crucial for linear growth and metabolic repair. **2. Why other options are incorrect:** * **ACTH and Glucocorticoids (Cortisol):** These follow a diurnal rhythm but are at their **lowest** levels during the early part of the night (around midnight). Their levels begin to rise in the early morning hours (3 AM – 4 AM) and peak just before awakening (the "dawn phenomenon"). * **Insulin:** Insulin levels are primarily regulated by blood glucose levels (post-prandial). During sleep (a fasting state), insulin levels generally decrease to allow for glucagon-mediated glycogenolysis and gluconeogenesis to maintain basal glucose levels. **High-Yield Clinical Pearls for NEET-PG:** * **Sleep Stages:** GH peaks specifically during **Stage 3 (N3) NREM sleep**. If sleep is deprived or fragmented, GH secretion is significantly blunted. * **Other Hormones that increase during sleep:** Prolactin, Melatonin, and TSH (TSH peaks just before sleep onset). * **Somatomedins:** While GH is pulsatile, IGF-1 (Somatomedin C) levels remain stable throughout the day and are used for the clinical screening of Acromegaly. * **Inhibitors of GH:** Hyperglycemia, Free Fatty Acids, and Somatostatin.

Question 516: Selenocysteine residues are present in which of the following enzymes?

A. Pyruvate carboxylase
B. Xanthine oxidase
C. Deiodinase (Correct Answer)
D. Lysyl oxidase

Explanation: **Explanation:** The correct answer is **Deiodinase**. Selenocysteine is often referred to as the "21st amino acid" and is unique because it contains selenium instead of the sulfur found in cysteine. **1. Why Deiodinase is Correct:** The conversion of the prohormone Thyroxine (T4) to the active Triiodothyronine (T3) is catalyzed by **Iodothyronine Deiodinases** (Types 1, 2, and 3). These enzymes are **selenoproteins**, meaning they require selenocysteine at their active site for catalytic activity. Selenium deficiency can lead to impaired thyroid hormone metabolism, mimicking symptoms of hypothyroidism despite normal T4 levels. Other notable selenoproteins include **Glutathione peroxidase** (an antioxidant) and **Thioredoxin reductase**. **2. Why the Other Options are Incorrect:** * **Pyruvate carboxylase:** This enzyme, involved in gluconeogenesis, requires **Biotin (Vitamin B7)** as a cofactor and Manganese/Magnesium for activation. * **Xanthine oxidase:** This enzyme, crucial for purine catabolism (converting hypoxanthine to uric acid), requires **Molybdenum**, Iron, and FAD. * **Lysyl oxidase:** Essential for cross-linking collagen and elastin fibers, this enzyme is a **Copper-dependent** metalloenzyme. Deficiency leads to Menkes disease or Ehlers-Danlos syndrome. **Clinical Pearls for NEET-PG:** * **Codon:** Selenocysteine is encoded by the **UGA** codon, which usually acts as a "stop" codon. A specific mRNA sequence (SECIS element) directs the ribosome to insert selenocysteine instead. * **Antioxidant link:** Glutathione peroxidase (containing selenium) protects cells from oxidative damage by reducing hydrogen peroxide to water. * **Deficiency:** Selenium deficiency is linked to **Keshan disease** (cardiomyopathy) and **Kashin-Beck disease** (osteoarthropathy).

Question 517: What is the effect of cortisol on metabolism?

A. Gluconeogenesis (Correct Answer)
B. Lipogenesis
C. Proteolysis
D. Proteolysis

Explanation: **Explanation:** Cortisol, the primary glucocorticoid secreted by the adrenal cortex, is often referred to as the "stress hormone." Its primary metabolic goal is to increase blood glucose levels to ensure the brain and heart have adequate fuel during periods of stress. **1. Why Gluconeogenesis is Correct:** Cortisol promotes **gluconeogenesis** (the synthesis of glucose from non-carbohydrate sources) primarily in the liver. It achieves this by increasing the expression of key enzymes like PEPCK (Phosphoenolpyruvate carboxykinase) and by mobilizing substrates (amino acids and glycerol) from peripheral tissues. **2. Analysis of Incorrect Options:** * **Lipogenesis:** This is incorrect. Cortisol is primarily **lipolytic** (breaks down fats) in the extremities to provide free fatty acids for energy. While chronic high levels cause "central obesity" (re-deposition of fat in the face and trunk), its direct metabolic action is the mobilization of lipids. * **Proteolysis:** While cortisol *does* cause proteolysis (breakdown of proteins in muscle and lymphoid tissue) to provide amino acids for gluconeogenesis, the question asks for the primary metabolic effect on glucose homeostasis. In the context of NEET-PG, if "Gluconeogenesis" is an option, it is the most definitive "anabolic" effect in the liver, whereas proteolysis is a catabolic process used to fuel it. *(Note: If the options provided were identical for C and D, it suggests a focus on the liver's synthetic role).* **Clinical Pearls for NEET-PG:** * **Permissive Action:** Cortisol is required for glucagon and catecholamines to exert their maximal calorigenic and lipolytic effects. * **Anti-Insulin Effect:** Cortisol decreases GLUT-4 mediated glucose uptake in peripheral tissues (muscle and adipose), leading to "adrenal diabetes" in states of excess (Cushing’s Syndrome). * **Bone Metabolism:** Cortisol inhibits osteoblast activity and decreases calcium absorption, leading to osteoporosis.

Question 518: Which of the following inhibits the secretion of Growth Hormone (GH)?

A. Bromocriptine
B. Hyperglycemia (Correct Answer)
C. Vigorous exercise
D. Deep sleep

Explanation: **Explanation:** Growth Hormone (GH) secretion is regulated by a complex interplay of hypothalamic factors and metabolic signals. **Why Hyperglycemia is Correct:** GH is a **diabetogenic hormone**; it increases blood glucose levels by stimulating gluconeogenesis and antagonizing insulin action. According to the negative feedback principle, **Hyperglycemia** (high blood glucose) inhibits GH secretion to prevent further glucose elevation. This occurs via the stimulation of hypothalamic **Somatostatin** (Growth Hormone Inhibiting Hormone - GHIH) and the direct inhibition of the anterior pituitary. **Why Other Options are Incorrect:** * **Bromocriptine:** In healthy individuals, dopamine agonists like Bromocriptine actually *stimulate* GH release. (Note: Paradoxically, it inhibits GH in patients with Acromegaly, which is a common clinical confusion). * **Vigorous Exercise:** Physical stress and exercise are potent physiological *stimulators* of GH secretion, mediated via increased sympathetic tone and GHRH release. * **Deep Sleep:** GH is secreted in pulsatile bursts, with the largest peak occurring during **Stage 3 and 4 (NREM) deep sleep**. Sleep deprivation significantly suppresses GH levels. **High-Yield NEET-PG Pearls:** 1. **Stimulators of GH:** Hypoglycemia (most potent metabolic stimulus), fasting/starvation, Ghrelin, Arginine (amino acids), and Sleep. 2. **Inhibitors of GH:** Hyperglycemia, Free Fatty Acids (FFA), Somatostatin, and IGF-1 (via negative feedback). 3. **Clinical Correlation:** The **Oral Glucose Tolerance Test (OGTT)** is the gold standard for diagnosing Acromegaly. In a healthy person, a glucose load suppresses GH to <1 ng/mL; failure to suppress confirms the diagnosis.

Question 519: Excessive secretion of ACTH causes which of the following conditions?

A. Cushing's syndrome (Correct Answer)
B. Addison's disease
C. Myxoedema
D. Thyrotoxicosis

Explanation: **Explanation:** **1. Why Cushing’s Syndrome is Correct:** Adrenocorticotropic hormone (ACTH), secreted by the anterior pituitary, stimulates the adrenal cortex to produce cortisol. Excessive secretion of ACTH (most commonly due to a pituitary adenoma, known specifically as **Cushing’s Disease**) leads to chronic hypercortisolism. This clinical state is characterized by the classic symptoms of **Cushing’s Syndrome**, including "moon facies," "buffalo hump," central obesity, purple striae, and hypertension. **2. Why Other Options are Incorrect:** * **Addison’s Disease:** This is primary adrenocortical insufficiency (low cortisol and aldosterone). In this condition, ACTH levels are actually **elevated** as a compensatory mechanism (negative feedback), but the primary pathology is the *lack* of adrenal response, not the *excess* of ACTH itself. * **Myxoedema:** This refers to severe **hypothyroidism** in adults, caused by a deficiency of thyroid hormones (T3/T4), not ACTH. * **Thyrotoxicosis:** This is a clinical state resulting from excessive circulating **thyroid hormones**, usually associated with Grave’s disease or toxic nodular goiter. **3. NEET-PG High-Yield Pearls:** * **Cushing’s Disease vs. Syndrome:** "Cushing’s Disease" specifically refers to a pituitary tumor secreting ACTH. "Cushing’s Syndrome" is the broad term for hypercortisolism from any cause (iatrogenic, adrenal tumor, or ectopic ACTH). * **Hyperpigmentation:** Excessive ACTH causes skin hyperpigmentation because ACTH is derived from **POMC (Pro-opiomelanocortin)**, which also produces Melanocyte-Stimulating Hormone (MSH). * **Dexamethasone Suppression Test (DST):** High-dose DST is used to differentiate Cushing’s Disease (suppresses) from ectopic ACTH production (does not suppress).

Question 520: Plasma of a hyperthyroid patient contains excess of which substance?

A. T3
B. Free thyroxine (Correct Answer)
C. Protein bound thyroxine
D. Reverse T3 (RT3)

Explanation: **Explanation:** In hyperthyroidism, the thyroid gland overproduces thyroid hormones, leading to an elevation in both total and free fractions. However, **Free Thyroxine (fT4)** is the most clinically significant substance found in excess because it represents the biologically active form of the hormone. **Why Free Thyroxine is the correct answer:** While total T4 increases, it is the **unbound (free) fraction** that is responsible for the clinical manifestations of thyrotoxicosis. Free T4 is independent of changes in thyroid-binding globulin (TBG) levels, making it the gold-standard diagnostic marker for confirming hyperthyroidism (alongside suppressed TSH). In almost all cases of hyperthyroidism (Graves' disease, toxic multinodular goiter), fT4 is significantly elevated. **Analysis of Incorrect Options:** * **T3:** While T3 is often elevated (and is the primary hormone in "T3 toxicosis"), T4 is the major secretory product of the thyroid gland. In standard hyperthyroidism, the rise in T4 is more characteristic and serves as the primary screening parameter. * **Protein-bound thyroxine:** Over 99% of T4 is bound to proteins (TBG, transthyretin). While this level rises in hyperthyroidism, it can also rise due to non-thyroidal factors like pregnancy or OCP use (which increase TBG). Therefore, it is not as definitive a marker of the hyperthyroid state as fT4. * **Reverse T3 (rT3):** This is a biologically inactive isomer. While it may increase in hyperthyroidism, it is most notably elevated in **Euthyroid Sick Syndrome** due to decreased peripheral conversion of T4 to T3. **High-Yield Clinical Pearls for NEET-PG:** * **Best Screening Test:** Serum TSH (it is the most sensitive). * **Best Confirmatory Test:** Free T4. * **T3 Toxicosis:** High T3, Low TSH, but **Normal T4**. Suspect this if clinical features of hyperthyroidism exist but T4 is normal. * **Wolff-Chaikoff Effect:** Transient inhibition of thyroid hormone synthesis due to high iodine intake.

Practice by Chapter

Principles of Endocrine Regulation

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Hypothalamus and Pituitary Gland

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Thyroid Physiology

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Adrenal Cortex and Medulla

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Pancreatic Hormones and Glucose Metabolism

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Calcium and Phosphate Homeostasis

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Growth Hormone and Growth Factors

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Endocrine Regulation of Metabolism

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Hormone Receptors and Signaling

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Assessment of Endocrine Function

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