Endocrinology — MCQs

Endocrinology Indian Medical PG Practice Questions and MCQs

Question 571: Insulin decreases:

A. Glucose uptake
B. Glycogen synthesis
C. Protein synthesis
D. Lipolysis (Correct Answer)

Explanation: **Explanation:** Insulin is the body’s primary **anabolic hormone**, secreted by the beta cells of the Islets of Langerhans. Its fundamental role is to promote energy storage and inhibit the breakdown of stored fuels (catabolism). **Why Lipolysis is the correct answer:** Insulin is a potent **anti-lipolytic** hormone. It inhibits the enzyme **Hormone-Sensitive Lipase (HSL)** in adipose tissue. HSL is responsible for breaking down stored triglycerides into free fatty acids and glycerol. By inhibiting HSL, insulin decreases the concentration of circulating free fatty acids, thereby promoting fat storage and preventing ketogenesis. **Analysis of Incorrect Options:** * **A. Glucose uptake:** Insulin **increases** glucose uptake in peripheral tissues (skeletal muscle and adipose tissue) by inducing the translocation of **GLUT-4** transporters to the cell membrane. * **B. Glycogen synthesis:** Insulin **increases** glycogenesis by activating the enzyme **Glycogen Synthase**, ensuring excess glucose is stored in the liver and muscles. * **C. Protein synthesis:** Insulin is anabolic for proteins; it **increases** amino acid uptake and protein synthesis while inhibiting proteolysis. **NEET-PG High-Yield Pearls:** * **GLUT-4** is the only insulin-dependent glucose transporter (found in heart, skeletal muscle, and adipose tissue). * Insulin stimulates **Lipoprotein Lipase (LPL)** in capillary walls to clear chylomicrons from the blood, but inhibits **Hormone-Sensitive Lipase (HSL)** inside adipocytes. * **Key Enzyme Regulation:** Insulin activates Phosphofructokinase (Glycolysis) and Glycogen Synthase (Glycogenesis), while inhibiting Fructose-1,6-bisphosphatase (Gluconeogenesis).

Question 572: What is the half-life of T3?

A. 10 hours
B. 2 days (Correct Answer)
C. 6 days
D. 10 days

Explanation: The half-life of thyroid hormones is primarily determined by their affinity for plasma proteins, specifically **Thyroxine-Binding Globulin (TBG)**. ### **Explanation of the Correct Answer** **Option B (2 days)** is correct. Triiodothyronine (T3) has a significantly lower affinity for TBG compared to T4. Because less T3 is protein-bound (~99.7%) and more exists in the free, metabolically active form, it is cleared from the circulation much faster. Its half-life is approximately **1 to 2 days** (24–48 hours). ### **Analysis of Incorrect Options** * **Option A (10 hours):** This is too short for thyroid hormones. While T3 is "fast-acting," its protein binding still allows it to persist longer than catecholamines or peptide hormones. * **Option C (6 days):** This is the approximate half-life of **Thyroxine (T4)**. T4 is >99.9% protein-bound and has a much higher affinity for TBG, which acts as a reservoir, slowing its clearance. * **Option D (10 days):** This exceeds the physiological half-life of any thyroid hormone. ### **NEET-PG High-Yield Pearls** * **Potency vs. Half-life:** T3 is **4 times more potent** than T4 but has a shorter half-life. * **The "Pro-hormone":** T4 is considered a pro-hormone; most T3 in the body (80%) is produced by the peripheral deiodination of T4 by the enzyme **5'-deiodinase**. * **Reverse T3 (rT3):** Formed by the action of 5-deiodinase; it is metabolically inactive. * **Clinical Correlation:** Due to the long half-life of T4 (6–7 days), it takes about 4–6 weeks to reach a new steady state after initiating Levothyroxine therapy. This is why TSH is not rechecked sooner than 6 weeks.

Question 573: All of the following are known effects of corticosteroids on the skin and connective tissue except?

A. Antiproliferative effect on fibroblasts
B. Antiproliferative effect on keratinocytes
C. Loss of collagen
D. Hyperpigmentation (Correct Answer)

Explanation: **Explanation:** The correct answer is **Hyperpigmentation**. Corticosteroids actually cause **hypopigmentation** (skin lightening) by inhibiting the activity of melanocytes and reducing the production of melanocyte-stimulating hormone (MSH). Hyperpigmentation is typically seen in conditions of corticosteroid *deficiency* (like Addison’s disease) due to the compensatory increase in ACTH, which shares a precursor with MSH. **Analysis of Options:** * **A & B (Antiproliferative effects):** Glucocorticoids inhibit the mitotic activity of both **keratinocytes** (epidermis) and **fibroblasts** (dermis). This is the pharmacological basis for using topical steroids in hyperproliferative skin disorders like psoriasis. * **C (Loss of collagen):** By inhibiting fibroblasts, steroids decrease the synthesis of Type I and III collagen and glycosaminoglycans. This leads to the hallmark clinical features of steroid excess: skin thinning (atrophy), easy bruising, and the formation of wide, purple **striae**. **High-Yield Clinical Pearls for NEET-PG:** * **Iatrogenic Cushing Syndrome:** Prolonged steroid use leads to a "moon face," "buffalo hump," and truncal obesity, but the skin remains thin and fragile. * **Wound Healing:** Corticosteroids **delay wound healing** because they inhibit the inflammatory phase and reduce the fibroblastic repair required for wound contraction. * **Topical Potency:** Fluorinated steroids are more potent but carry a higher risk of causing irreversible skin atrophy and telangiectasia.

Question 574: What is the recommended daily intake of Vitamin A for adults?

A. 1000 IU
B. 2000 IU
C. 3000 IU
D. 4000 IU (Correct Answer)

Explanation: **Explanation:** The recommended dietary allowance (RDA) for Vitamin A is essential for maintaining normal vision, epithelial integrity, and immune function. According to the **ICMR (Indian Council of Medical Research)** and standard physiological guidelines, the daily requirement for a healthy adult is approximately **600–1000 µg of Retinol**, which translates to roughly **2000–4000 International Units (IU)** depending on the specific population group (gender and activity level). In the context of standard medical examinations, **4000 IU** is considered the upper threshold of the normal daily requirement for adults to maintain adequate hepatic stores. **Analysis of Options:** * **A & B (1000–2000 IU):** These values are generally considered inadequate for adults. 1000 IU is closer to the requirement for infants, while 2000 IU may be the bare minimum to prevent deficiency but does not meet the optimal RDA for an active adult. * **C (3000 IU):** While closer to the requirement for adult females, it is often superseded by the 4000 IU recommendation in competitive exams to cover the broader adult population (including males). * **D (4000 IU):** This is the standard high-yield value for adult RDA, ensuring sufficient Retinol Binding Protein (RBP) saturation. **Clinical Pearls for NEET-PG:** * **Storage:** Vitamin A is stored in the **Ito cells (Stellate cells)** of the liver. * **Earliest Sign of Deficiency:** Conjunctival xerosis (though **Night Blindness/Nyctalopia** is the earliest *symptom*). * **Bitot’s Spots:** Triangular, pearly-white foamy patches on the bulbar conjunctiva (pathognomonic for deficiency). * **Toxicity:** Chronic ingestion of >25,000 IU/day can lead to **Pseudotumor Cerebri** (idiopathic intracranial hypertension) and hepatotoxicity.

Question 575: Inhibition of prolactin is caused by:

A. Dopamine (Correct Answer)
B. Dobutamine
C. TRH
D. AT-II

Explanation: **Explanation:** The secretion of Prolactin from the anterior pituitary is unique because it is under **tonic inhibitory control** by the hypothalamus. **A. Dopamine (Correct):** Dopamine is the primary **Prolactin-Inhibiting Factor (PIF)**. It is secreted by the tuberoinfundibular dopaminergic (TIDA) neurons of the hypothalamus into the hypophyseal portal system. It binds to **D2 receptors** on the lactotrophs in the anterior pituitary, inhibiting the synthesis and release of prolactin [1]. **B. Dobutamine:** This is a synthetic catecholamine that acts primarily as a $\beta_1$-adrenergic agonist used in cardiac failure. It does not play a physiological role in pituitary hormone regulation. **C. TRH (Thyrotropin-Releasing Hormone):** TRH is a potent **stimulator** of prolactin release [1]. In patients with primary hypothyroidism (where TRH levels are elevated), hyperprolactinemia is a common clinical finding [2]. **D. AT-II (Angiotensin II):** While AT-II has various systemic effects on blood pressure and aldosterone, it is generally considered a weak stimulator of prolactin release in certain physiological contexts, not an inhibitor. **High-Yield Clinical Pearls for NEET-PG:** * **The "Stalk Effect":** Any compression of the pituitary stalk (e.g., by a craniopharyngioma) prevents dopamine from reaching the pituitary, leading to **increased** prolactin levels (disinhibition) [2]. * **Drug-Induced Hyperprolactinemia:** Antipsychotics (D2 antagonists like Haloperidol or Risperidone) and Metoclopramide block dopamine's inhibitory effect, leading to galactorrhea and amenorrhea [2]. * **Prolactinoma Treatment:** Dopamine agonists (Cabergoline, Bromocriptine) are the first-line treatment to shrink the tumor and normalize prolactin levels [3].

Question 576: Axillary hair growth is stimulated by which hormone?

A. Testosterone (Correct Answer)
B. Estrogen
C. Prolactin
D. Androgens

Explanation: **Explanation:** The growth of axillary and pubic hair is primarily regulated by **androgens**. While both adrenal androgens (DHEA, DHEAS, and Androstenedione) and gonadal androgens play a role, **Testosterone** is the potent androgen responsible for the terminal hair transformation in these regions during puberty. 1. **Why Testosterone is Correct:** Axillary hair is a secondary sexual characteristic. In both males and females, the rise in circulating androgens (adrenarche and gonadal maturation) triggers the transition of fine vellus hair into thick, pigmented terminal hair. Testosterone acts on the hair follicles in the axilla, where it is often converted to Dihydrotestosterone (DHT) by the enzyme 5-alpha-reductase to stimulate growth. 2. **Why Other Options are Incorrect:** * **Estrogen:** This hormone is responsible for female fat distribution, breast development, and bone maturation, but it does not stimulate body hair growth; in fact, high levels can sometimes oppose androgenic hair effects. * **Prolactin:** Primarily involved in lactation and reproductive inhibition. Excess prolactin (prolactinoma) can cause hirsutism indirectly by increasing adrenal androgen production, but it is not the primary physiological stimulator. * **Androgens:** While technically correct as a category, in medical entrance exams, if a specific potent hormone like **Testosterone** is listed alongside a general category, the specific hormone is often the preferred answer. (Note: In some contexts, "Adrenal Androgens" are cited for females, but Testosterone remains the definitive physiological driver). **High-Yield NEET-PG Pearls:** * **Adrenarche:** The increase in adrenal androgen secretion (DHEA) around age 6–8, which precedes puberty and initiates axillary/pubic hair growth. * **Ferriman-Gallwey Score:** Used clinically to quantify hirsutism (excess androgen-dependent hair) in women. * **Sequence in Females:** The typical order of puberty is Thelarche (breast) → Pubarche (hair) → Growth Spurt → Menarche (menses).

Question 577: ACTH levels are increased in all of the following conditions except:

A. Exercise
B. Emotions
C. Evening (Correct Answer)
D. Tumors

Explanation: The regulation of Adrenocorticotropic Hormone (ACTH) is governed by the hypothalamic-pituitary-adrenal (HPA) axis and is highly sensitive to stress and circadian rhythms. **Explanation of the Correct Answer:** **C. Evening:** ACTH secretion follows a distinct **diurnal (circadian) rhythm**. Levels are highest in the early morning (around 6:00 AM to 8:00 AM) and gradually decline throughout the day, reaching their **nadir (lowest point) in the evening** and early hours of sleep (around midnight). Therefore, ACTH levels are decreased, not increased, in the evening compared to morning levels. **Explanation of Incorrect Options:** * **A. Exercise:** Physical exertion is a potent physiological stressor that activates the HPA axis, leading to a significant increase in CRH and subsequent ACTH release to mobilize energy stores. * **B. Emotions:** Psychological stress (anxiety, fear, or emotional trauma) triggers the amygdala to stimulate the hypothalamus, resulting in elevated ACTH levels. * **C. Tumors:** Pathological increases occur in **Cushing’s Disease** (pituitary adenoma secreting ACTH) or **Ectopic ACTH Syndrome** (e.g., Small Cell Carcinoma of the lung). **High-Yield Clinical Pearls for NEET-PG:** * **Diurnal Variation:** To diagnose Cushing’s syndrome, the loss of this diurnal rhythm (elevated late-night cortisol/ACTH) is a key diagnostic finding. * **Primary vs. Secondary:** ACTH is **increased** in Addison’s disease (Primary Adrenal Insufficiency) due to loss of negative feedback, but **decreased** in Secondary Adrenal Insufficiency (Pituitary failure). * **Nelson’s Syndrome:** Rapid increase in ACTH levels and skin hyperpigmentation following bilateral adrenalectomy due to the growth of a pre-existing pituitary adenoma.

Question 578: Which of the following hormones exhibits genomic action?

A. Thyroid hormone
B. 1,25-dihydroxycholecalciferol
C. Cortisol
D. All of these (Correct Answer)

Explanation: ### Explanation The correct answer is **D. All of these**. **1. Underlying Medical Concept: Mechanism of Hormone Action** Hormones are generally classified into two groups based on their solubility and receptor location. **Genomic action** refers to the process where a hormone binds to an intracellular receptor (either in the cytoplasm or nucleus), acts as a ligand-activated transcription factor, and directly influences gene expression (mRNA synthesis). Lipid-soluble hormones can easily cross the cell membrane to exert these effects. These include: * **Steroid Hormones:** Cortisol, Aldosterone, Estrogen, Progesterone, Testosterone. * **Thyroid Hormones:** $T_3$ and $T_4$. * **Vitamin D:** 1,25-dihydroxycholecalciferol (Calcitriol). * **Retinoids:** Vitamin A. **2. Analysis of Options** * **Thyroid Hormone (A):** Binds to receptors already attached to DNA in the nucleus (TR-RXR complex). It is a classic example of genomic action. * **1,25-dihydroxycholecalciferol (B):** As a steroid-like hormone, it binds to the Vitamin D Receptor (VDR) in the nucleus to regulate calcium-binding protein synthesis. * **Cortisol (C):** A glucocorticoid that binds to cytoplasmic receptors, translocates to the nucleus, and binds to Glucocorticoid Response Elements (GRE) on DNA. **3. High-Yield Clinical Pearls for NEET-PG** * **Speed of Action:** Genomic actions are **slow** (minutes to hours) because they require protein synthesis. In contrast, peptide hormones (like Insulin or Epinephrine) use second messengers (cAMP, $IP_3/DAG$) for **fast** non-genomic actions. * **Exception:** Thyroid hormones are amino-acid derivatives but behave like steroids (intracellular receptors). * **Receptor Location:** * **Cytoplasmic:** Glucocorticoids, Mineralocorticoids. * **Nuclear:** Thyroid hormones, Retinoic acid, Estrogen, Vitamin D.

Question 579: Chvostek’s sign is elicited by:

A. Inflating a blood pressure cuff in the arm for 5 minutes
B. Stimulating the facial nerve by tapping over the parotid gland (Correct Answer)
C. Tapping over the extensor pollicis brevis tendon
D. Tapping over the flexor retinaculum

Explanation: **Explanation:** **Chvostek’s sign** is a clinical indicator of **latent tetany**, most commonly caused by **hypocalcemia**. Low serum ionized calcium levels increase the permeability of neuronal membranes to sodium ions, leading to progressive depolarization and neuromuscular irritability (hyperexcitability). * **Why Option B is Correct:** The sign is elicited by tapping the **facial nerve (CN VII)** as it passes over the **parotid gland**, just anterior to the external auditory meatus. In a hypocalcemic state, this mechanical stimulation triggers an abnormal twitching or contraction of the ipsilateral facial muscles (typically the corner of the mouth or nose). **Analysis of Incorrect Options:** * **Option A:** Inflating a blood pressure cuff above systolic pressure for 3 minutes to induce carpal spasm is the procedure for **Trousseau’s sign**. This is considered more sensitive and specific for hypocalcemia than Chvostek’s sign. * **Option C:** Tapping over tendons is used to elicit Deep Tendon Reflexes (DTRs), but tapping the extensor pollicis brevis is not a standard clinical test for tetany. * **Option D:** Tapping over the flexor retinaculum (specifically the median nerve) is known as **Tinel’s sign**, used to diagnose Carpal Tunnel Syndrome. **High-Yield NEET-PG Pearls:** 1. **Hypocalcemia Etiology:** Often seen post-thyroidectomy (accidental removal of parathyroid glands) or in Vitamin D deficiency. 2. **Sensitivity:** Chvostek’s sign can be absent in 30% of patients with hypocalcemia and present in 10% of healthy individuals (false positives). 3. **Other Signs of Tetany:** Look for **Erb’s sign** (increased electrical irritability) and **Hoffman’s sign** (digital hyperreflexia). 4. **Management:** Acute symptomatic hypocalcemia is treated with **IV Calcium Gluconate**.

Question 580: Corticosteroids suppress:

A. Growth Hormone (GH)
B. Adrenocorticotropic Hormone (ACTH) (Correct Answer)
C. Follicle-Stimulating Hormone (FSH)
D. Luteinizing Hormone (LH)

Explanation: ### Explanation **1. Why Option B is Correct:** The regulation of the adrenal cortex occurs via the **Hypothalamic-Pituitary-Adrenal (HPA) axis**. Corticosteroids (specifically glucocorticoids like cortisol) exert a powerful **negative feedback** effect. When systemic levels of corticosteroids rise, they act on: * **The Anterior Pituitary:** To directly inhibit the secretion of **ACTH**. * **The Hypothalamus:** To inhibit the release of Corticotropin-Releasing Hormone (CRH). This feedback loop ensures hormonal homeostasis. Clinically, exogenous steroid administration mimics this effect, leading to the suppression of endogenous ACTH. **2. Why Other Options are Incorrect:** * **Option A (GH):** While chronic, high-dose glucocorticoids can interfere with growth in children by inhibiting IGF-1 and affecting growth plates, they are not the primary physiological suppressors of GH. GH is primarily regulated by GHRH and Somatostatin. * **Options C & D (FSH & LH):** These gonadotropins are regulated by the Hypothalamic-Pituitary-Gonadal (HPG) axis via GnRH. While extreme stress (high cortisol) can indirectly disrupt the menstrual cycle, corticosteroids do not directly suppress FSH and LH as their primary mechanism of action. **3. High-Yield Clinical Pearls for NEET-PG:** * **Adrenal Atrophy:** Prolonged exogenous steroid use leads to chronic ACTH suppression. Without ACTH (the trophic hormone), the adrenal cortex undergoes **disuse atrophy**. * **Steroid Tapering:** This is why steroids must be tapered slowly; sudden withdrawal can lead to **Acute Adrenal Insufficiency** because the atrophied adrenals cannot immediately resume cortisol production. * **Cushing’s Disease vs. Syndrome:** In Cushing’s *Disease* (pituitary adenoma), ACTH is high. In Cushing’s *Syndrome* due to an adrenal tumor, ACTH is suppressed due to the negative feedback of excess cortisol.

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

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