Endocrine Pharmacology — MCQs

Endocrine Pharmacology Indian Medical PG Practice Questions and MCQs

Question 631: Which of the following is NOT an anti-androgenic drug?

A. Flutamide
B. Spironolactone
C. Finasteride
D. Cypionate (Correct Answer)

Explanation: **Explanation:** The correct answer is **Cypionate**. To answer this question correctly, one must distinguish between anti-androgens (which inhibit androgen action or synthesis) and androgen esters (which act as pro-drugs for testosterone). **Why Cypionate is the correct answer:** **Testosterone Cypionate** is a long-acting ester of testosterone. It is an **androgen agonist**, not an antagonist. It is administered intramuscularly to treat male hypogonadism and delayed puberty. The suffix "-ate" (like cypionate, enanthate, or propionate) typically denotes an esterified form of the hormone used for replacement therapy. **Why the other options are incorrect:** * **Flutamide:** A potent **competitive antagonist** at the androgen receptor. It is primarily used in the management of prostatic carcinoma. * **Spironolactone:** Primarily an aldosterone antagonist (potassium-sparing diuretic), but it also possesses significant **anti-androgenic activity** by displacing testosterone from its receptor and inhibiting androgen synthesis. It is used clinically for hirsutism in females. * **Finasteride:** A **5-alpha reductase inhibitor** that prevents the conversion of testosterone to the more potent dihydrotestosterone (DHT). It is used for Benign Prostatic Hyperplasia (BPH) and male pattern baldness. **High-Yield NEET-PG Pearls:** 1. **Bicalutamide** is preferred over Flutamide for prostate cancer due to less hepatotoxicity and once-daily dosing. 2. **Cyproterone acetate** is another anti-androgen used for severe acne and precocious puberty. 3. **Abiraterone** inhibits CYP17, blocking the synthesis of androgens in both the testes and adrenal glands; it is used in castration-resistant prostate cancer. 4. **Finasteride vs. Dutasteride:** Finasteride inhibits Type II 5-alpha reductase, while Dutasteride inhibits both Type I and Type II.

Question 632: Which 5α reductase inhibitor is effective for both benign prostatic hypertrophy and male pattern baldness?

A. Flutamide
B. Finasteride (Correct Answer)
C. Prazosin
D. Minoxidil

Explanation: **Explanation:** **Finasteride** is the correct answer because it is a selective inhibitor of the **Type II 5α-reductase enzyme**. This enzyme is responsible for converting testosterone into the more potent androgen, **Dihydrotestosterone (DHT)**. * **In BPH:** DHT is the primary mediator of prostatic growth. By lowering intraprostatic DHT levels, Finasteride reduces prostate volume, improves urinary flow, and prevents disease progression. * **In Male Pattern Baldness (Androgenetic Alopecia):** DHT causes miniaturization of hair follicles. Finasteride (at a lower dose of 1mg) prevents this process, promoting hair regrowth and preventing further loss. **Analysis of Incorrect Options:** * **Flutamide:** This is a competitive **Androgen Receptor Antagonist** (not an enzyme inhibitor). It is primarily used in the treatment of metastatic prostate cancer, not BPH or baldness. * **Prazosin:** This is a non-selective **α1-blocker**. While it is used for BPH, it works by relaxing the smooth muscle of the bladder neck (dynamic component) and has no effect on hormone levels or hair growth. * **Minoxidil:** While used for baldness, it is a **K+ channel opener** (vasodilator). It works by increasing blood flow to follicles, not by inhibiting 5α-reductase. **High-Yield Clinical Pearls for NEET-PG:** * **Dutasteride:** A non-selective inhibitor of **both Type I and Type II** 5α-reductase; it is more potent and has a longer half-life than Finasteride. * **Teratogenicity:** 5α-reductase inhibitors are Category X; pregnant women should not even handle crushed tablets due to the risk of feminization of a male fetus. * **PSA Levels:** Finasteride can decrease PSA levels by approximately 50%; this must be accounted for when screening for prostate cancer.

Question 633: Which of the following hormones is orally active?

A. TSH
B. Thyroxine (Correct Answer)
C. GH
D. Prolactin

Explanation: Explanation: The oral bioavailability of a hormone is primarily determined by its chemical structure. Hormones that are **proteins or peptides** are susceptible to degradation by gastric acid and proteolytic enzymes (like pepsin and trypsin) in the gastrointestinal tract, rendering them inactive if swallowed. Why Thyroxine (T4) is correct: Thyroxine is an amino acid derivative (iodinated tyrosine). Unlike large proteins, it is a small, relatively stable molecule that is well-absorbed from the small intestine (primarily the jejunum and ileum). This stability allows it to be administered orally, which is the standard route for long-term replacement therapy in hypothyroidism. Why the other options are incorrect: * **TSH (Thyroid Stimulating Hormone):** This is a large glycoprotein. If taken orally, it would be digested into its constituent amino acids and lose all biological activity. * **GH (Growth Hormone):** This is a 191-amino acid polypeptide. It must be administered parenterally (subcutaneously) because it is rapidly proteolyzed in the stomach. * **Prolactin:** Similar to GH, prolactin is a protein hormone. It lacks oral activity due to enzymatic degradation in the gut. High-Yield Clinical Pearls for NEET-PG: * **Absorption Fact:** Oral absorption of Thyroxine is decreased by food, calcium carbonate, ferrous sulfate, and proton pump inhibitors (PPIs). It should be taken on an empty stomach [1]. * **Steroid Hormones:** Like Thyroxine, steroid hormones (e.g., Estrogen, Testosterone derivatives) are also orally active because they are lipophilic and resistant to gastric digestion. * **Exceptions:** Insulin and Oxytocin are classic examples of peptide hormones that **cannot** be given orally.

Question 634: Calcitonin is used in all of the following conditions, EXCEPT:

A. Hypervitaminosis D
B. Postmenopausal osteoporosis
C. Paget's disease
D. Fanconi syndrome (Correct Answer)

Explanation: **Explanation:** Calcitonin is a hormone secreted by the parafollicular (C-cells) of the thyroid gland. Its primary physiological role is to **lower serum calcium levels** by inhibiting osteoclast-mediated bone resorption and increasing renal calcium excretion. **Why Fanconi Syndrome is the Correct Answer:** Fanconi syndrome is a generalized dysfunction of the proximal renal tubule leading to the loss of glucose, amino acids, uric acid, phosphate, and bicarbonates in the urine. It is often associated with **hypocalcemia** and vitamin D deficiency (leading to rickets or osteomalacia). Since calcitonin further lowers serum calcium and promotes phosphate excretion, it has no therapeutic role here and could potentially worsen the electrolyte imbalance. **Analysis of Other Options:** * **Hypervitaminosis D:** This condition leads to severe hypercalcemia. Calcitonin is used as an adjunctive treatment to rapidly lower serum calcium levels by inhibiting bone resorption. * **Postmenopausal Osteoporosis:** Calcitonin (specifically the nasal spray formulation) inhibits osteoclasts, thereby reducing bone loss and providing an analgesic effect on bone pain associated with vertebral fractures. * **Paget’s Disease:** This is a condition of disordered bone remodeling. Calcitonin is used to suppress the overactive osteoclasts, reducing bone turnover and relieving associated bone pain. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice:** While calcitonin is used in Paget’s and Osteoporosis, **Bisphosphonates** are currently the first-line treatment for both. * **Salmon Calcitonin:** It is preferred over human calcitonin because it is more potent and has a longer duration of action. * **Tachyphylaxis:** A unique feature of calcitonin is the rapid development of tolerance (tachyphylaxis) with repeated use, likely due to the downregulation of receptors. * **Marker:** Serum calcitonin levels are used as a tumor marker for **Medullary Carcinoma of the Thyroid**.

Question 635: Which of the following medications can be safely used in pregnancy?

A. ACE inhibitors
B. Aldosterone
C. AT receptor antagonist
D. Propylthiouracil (Correct Answer)

Explanation: **Explanation:** **Propylthiouracil (PTU)** is the drug of choice for managing hyperthyroidism during the **first trimester** of pregnancy. While both PTU and Methimazole cross the placenta, PTU is more extensively protein-bound, leading to less placental transfer. More importantly, Methimazole is avoided in early pregnancy due to its association with **choanal atresia** and **aplasia cutis** (Methimazole embryopathy). PTU is preferred initially, though many clinicians switch to Methimazole in the second and third trimesters to avoid PTU-induced maternal hepatotoxicity. **Incorrect Options:** * **ACE Inhibitors (e.g., Enalapril) & AT Receptor Antagonists (ARBs, e.g., Losartan):** Both are strictly contraindicated (Category X/D) throughout pregnancy, especially in the 2nd and 3rd trimesters. They interfere with fetal renal development, leading to **oligohydramnios**, fetal renal failure, hypocalvaria (skull defects), and pulmonary hypoplasia. * **Aldosterone:** While not a standard medication, mineralocorticoid antagonists (like Spironolactone) are generally avoided due to potential anti-androgenic effects on the developing male fetus. **NEET-PG High-Yield Pearls:** * **Safe Antihypertensives in Pregnancy:** Remember the mnemonic **"Better Mother Care During Hypertensive"** (B-Blockers/Labetalol, Methyldopa, Calcium Channel Blockers/Nifedipine, Hydralazine). * **Methyldopa** is the traditional drug of choice for chronic hypertension in pregnancy. * **Labetalol** is currently preferred for acute management of hypertensive emergencies in pregnancy. * **Teratogenic effect of Methimazole:** Aplasia cutis (congenital focal absence of skin).

Question 636: Which of the following is a long-acting glucocorticoid?

A. Dexamethasone (Correct Answer)
B. Triamcinolone
C. Prednisolone
D. Hydrocortisone

Explanation: **Explanation:** Glucocorticoids are classified based on their duration of action (biological half-life), which correlates with their anti-inflammatory potency and mineralocorticoid (salt-retaining) activity. **1. Why Dexamethasone is Correct:** **Dexamethasone** is a **long-acting** glucocorticoid with a biological half-life of **36–54 hours**. It is highly potent (about 25–30 times more potent than hydrocortisone) and possesses negligible mineralocorticoid activity. This makes it ideal for conditions requiring sustained suppression of inflammation or the immune system, such as cerebral edema or as a diagnostic tool in the Dexamethasone Suppression Test (DST). **2. Why the Other Options are Incorrect:** * **Hydrocortisone (Option D):** This is a **short-acting** glucocorticoid (half-life 8–12 hours). It is the pharmaceutical form of cortisol and has significant mineralocorticoid activity, making it the drug of choice for replacement therapy in adrenal insufficiency. * **Prednisolone (Option C):** This is an **intermediate-acting** glucocorticoid (half-life 18–36 hours). It is commonly used for chronic inflammatory and autoimmune conditions. * **Triamcinolone (Option B):** Also an **intermediate-acting** steroid. It is notable for having zero mineralocorticoid activity and is frequently used in topical or intra-articular preparations. **NEET-PG High-Yield Pearls:** * **Potency Rule:** As the duration of action increases, anti-inflammatory potency increases, while mineralocorticoid activity decreases. * **Betamethasone:** Another long-acting steroid; it is specifically used to accelerate **fetal lung maturity** in preterm labor because it crosses the placental barrier and has low protein binding. * **Mnemonic for Duration:** * **Short:** Hydrocortisone, Cortisone. * **Intermediate:** Prednisolone, Triamcinolone, Methylprednisolone. * **Long:** Dexamethasone, Betamethasone.

Question 637: All of the following increase insulin release except?

A. Rosiglitazone (Correct Answer)
B. Nateglinide
C. Glipizide
D. Exenatide

Explanation: ### Explanation The core concept in this question is distinguishing between **insulin secretagogues** (drugs that stimulate the release of insulin from pancreatic beta cells) and **insulin sensitizers** (drugs that improve the body's response to existing insulin). **Why Rosiglitazone is the correct answer:** Rosiglitazone belongs to the **Thiazolidinedione (TZD)** class. Its primary mechanism of action is as a ligand for the **PPAR-γ** (Peroxisome Proliferator-Activated Receptor gamma) nuclear receptor. It works by increasing the expression of glucose transporters (GLUT-4) in peripheral tissues (adipose and muscle) and decreasing hepatic glucose production. **It does not stimulate the pancreas to release insulin**; rather, it makes the body more sensitive to the insulin already present. **Analysis of incorrect options:** * **Glipizide:** A second-generation **Sulfonylurea**. It closes ATP-sensitive K⁺ channels in the pancreatic beta-cell membrane, leading to depolarization, calcium influx, and subsequent insulin exocytosis. * **Nateglinide:** A **Meglitinide** (Glinide) derivative. Like sulfonylureas, it acts on the K⁺-ATP channel to stimulate rapid, short-acting insulin release, specifically targeting postprandial glucose. * **Exenatide:** A **GLP-1 Receptor Agonist** (Incretin mimetic). It stimulates glucose-dependent insulin secretion from the pancreas and suppresses glucagon release. **High-Yield Clinical Pearls for NEET-PG:** * **Secretagogues (Increase release):** Sulfonylureas, Meglitinides, GLP-1 Agonists, and DPP-4 Inhibitors. * **Sensitizers (Do not increase release):** Biguanides (Metformin) and TZDs (Pioglitazone/Rosiglitazone). * **Side Effect Note:** Because TZDs and Metformin do not increase insulin release, they have a much lower risk of causing **hypoglycemia** when used as monotherapy compared to secretagogues. * **Adverse Effect of TZDs:** Weight gain, edema, and a potential risk of congestive heart failure (due to fluid retention).

Question 638: A 55-year-old diabetic man presents to the emergency room in an unresponsive state. His laboratory values show PCO2 19 mm Hg, HCO3 11 mEq/L, and pH 6.9. What is the most appropriate immediate treatment for this patient?

A. Administration of an oral hypoglycemic agent
B. Administration of bicarbonate
C. Administration of insulin (Correct Answer)
D. Close observation only

Explanation: ### Explanation **Diagnosis: Diabetic Ketoacidosis (DKA)** The patient presents with the classic triad of DKA: hyperglycemia (implied by diabetic status and coma), metabolic acidosis (pH 6.9, low $HCO_3$), and respiratory compensation (low $PCO_2$). A pH of 6.9 indicates severe, life-threatening acidosis. **Why Option C is Correct:** The cornerstone of DKA management is **Intravenous Regular Insulin**. Insulin is essential because it: 1. Suppresses lipolysis and the delivery of free fatty acids to the liver. 2. Inhibits ketogenesis, thereby stopping the production of acidic ketone bodies (beta-hydroxybutyrate and acetoacetate). 3. Promotes glucose utilization, correcting the underlying metabolic derangement. **Why Other Options are Incorrect:** * **Option A:** Oral hypoglycemic agents are contraindicated in acute emergencies and comatose patients due to slow onset and aspiration risk. * **Option B:** While the pH is very low, **bicarbonate administration is controversial** and generally reserved only if pH < 6.9 after initial hydration. The primary treatment for the acidosis in DKA is insulin, which stops ketone production; the body then metabolizes existing ketones back into bicarbonate. * **Option D:** DKA is a medical emergency with high mortality if left untreated; close observation without intervention is inappropriate. **NEET-PG High-Yield Pearls:** * **Initial Step:** The very first step in DKA management is actually **aggressive fluid resuscitation** (Normal Saline) to restore perfusion. * **Insulin Protocol:** Use **Regular Insulin** (IV infusion). Do not use long-acting analogs in the acute phase. * **Potassium Warning:** Insulin shifts $K^+$ into cells. Always check potassium levels before starting insulin; if $K^+ < 3.3$ mEq/L, replace potassium first to avoid fatal arrhythmias. * **Resolution Marker:** DKA resolution is defined by the **closure of the anion gap**, not just the normalization of blood glucose.

Question 639: Which of the following drugs is used to treat both diabetes mellitus and diabetes insipidus?

A. Chlorpropamide (Correct Answer)
B. Glibenclamide
C. Glicazide
D. Glipizide

Explanation: **Explanation:** **Chlorpropamide** is a first-generation sulfonylurea that is unique because it possesses clinical utility in both Diabetes Mellitus (DM) and Central Diabetes Insipidus (DI). 1. **Mechanism in Diabetes Mellitus:** Like other sulfonylureas, it stimulates insulin release from pancreatic beta cells by blocking ATP-sensitive potassium channels ($K_{ATP}$), leading to depolarization and calcium influx. 2. **Mechanism in Diabetes Insipidus:** Chlorpropamide treats Central DI through two mechanisms: * It sensitizes the renal collecting ducts to the action of endogenous Antidiuretic Hormone (ADH/Vasopressin). * It may stimulate a modest increase in the release of ADH from the posterior pituitary. * *Note:* It is ineffective in Nephrogenic DI because the renal receptors are non-functional. **Why other options are incorrect:** * **Glibenclamide, Gliclazide, and Glipizide:** These are second-generation sulfonylureas. While they are significantly more potent than chlorpropamide for treating Type 2 DM, they lack the ADH-sensitizing effect required to treat Diabetes Insipidus. **High-Yield Clinical Pearls for NEET-PG:** * **Disulfiram-like reaction:** Chlorpropamide is notorious for causing a disulfiram-like reaction when consumed with alcohol. * **Dilutional Hyponatremia:** Due to its ADH-potentiating effect (SIADH-like picture), chlorpropamide can cause significant hyponatremia, especially in elderly patients. * **Longest Half-life:** It has the longest duration of action among sulfonylureas, increasing the risk of prolonged hypoglycemia. * **Other drugs for DI:** Thiazides (Paradoxical effect in Nephrogenic DI), Amiloride (Lithium-induced DI), and Desmopressin (Drug of choice for Central DI).

Question 640: Which oral hypoglycemic drug is least likely to cause hypoglycemia?

A. Repaglinide
B. Gliclazide
C. Rosiglitazone (Correct Answer)
D. Glimipiride

Explanation: ### Explanation The risk of hypoglycemia with oral hypoglycemic agents (OHAs) depends primarily on whether the drug’s mechanism is **insulin-independent** or **insulin-secretagogue** based. **1. Why Rosiglitazone is the Correct Answer:** Rosiglitazone belongs to the **Thiazolidinedione (TZD)** class. These drugs act as agonists for the **PPAR-γ receptor**, which increases peripheral insulin sensitivity (primarily in adipose tissue, muscle, and liver). Because TZDs do not stimulate the pancreas to release more insulin but rather make existing insulin work more efficiently, they are considered **"euglycemic"** agents. They do not cause hypoglycemia when used as monotherapy. **2. Why the Other Options are Incorrect:** * **Gliclazide & Glimepiride (Options B & D):** These are **Sulfonylureas**. They act by closing ATP-sensitive K⁺ channels in pancreatic beta cells, leading to depolarization and forced insulin secretion regardless of blood glucose levels. Hypoglycemia is their most common and significant side effect. * **Repaglinide (Option A):** This is a **Meglitinide** (Glinide). Like sulfonylureas, it is an insulin secretagogue. Although it has a shorter duration of action and is taken pre-prandially, it still carries a distinct risk of hypoglycemia if a meal is delayed or skipped. **3. NEET-PG High-Yield Pearls:** * **Weight Gain:** Both TZDs and Sulfonylureas cause weight gain, but via different mechanisms (TZDs cause fluid retention and fat redistribution; Sulfonylureas are anabolic due to high insulin). * **TZD Side Effects:** Watch for **fluid retention/edema** (contraindicated in CHF), **bone fractures** (osteoporosis risk), and bladder cancer (specifically associated with Pioglitazone). * **Drug of Choice:** Metformin (a Biguanide) is also an insulin sensitizer and, like TZDs, has a very low risk of hypoglycemia, making it the first-line treatment for Type 2 Diabetes.

Practice by Chapter

Hypothalamic and Pituitary Hormones

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Thyroid Drugs and Antithyroid Agents

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Insulin and Oral Hypoglycemic Agents

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Adrenocorticosteroids

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Sex Hormones: Estrogens and Progestins

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Androgens and Anabolic Steroids

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Hormonal Contraceptives

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Drugs Affecting Calcium Metabolism

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Drugs for Osteoporosis

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Pharmacological Management of Obesity

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