Endocrine Pharmacology — MCQs

Endocrine Pharmacology Indian Medical PG Practice Questions and MCQs

Question 731: Which of the following drugs does not cause adrenocortical suppression?

A. Prednisone
B. Ketoconazole
C. Mitotane
D. Spironolactone (Correct Answer)

Explanation: ***Spironolactone*** - This drug is an **aldosterone antagonist** and a **potassium-sparing diuretic**. While it can interfere with androgen synthesis and bind to androgen and progesterone receptors, it does not directly cause generalized adrenocortical suppression of cortisol or other adrenal hormones. - Its primary actions are on the **renal tubules** to increase sodium and water excretion while retaining potassium. *Prednisone* - Prednisone is a **synthetic glucocorticoid** that, when administered exogenously, suppresses the body's natural production of cortisol by inhibiting the HPA axis (hypothalamic-pituitary-adrenal axis). - Chronic use leads to **adrenal atrophy** and decreased endogenous cortisol secretion, requiring gradual tapering to allow adrenal recovery. *Ketoconazole* - Ketoconazole is an antifungal agent that also inhibits several **cytochrome P450 enzymes** involved in steroid biosynthesis, including 11β-hydroxylase and 17α-hydroxylase. - This inhibition directly reduces the production of **cortisol** and other adrenal steroids, making it useful in conditions like Cushing's syndrome but also causing adrenocortical suppression as a side effect. *Mitotane* - Mitotane is an **adrenolytic agent** specifically used in the treatment of adrenocortical carcinoma. - It causes **selective atrophy and necrosis** of the adrenal cortex, leading to a significant reduction in cortisol and other adrenal steroid production.

Question 732: A middle-aged male patient presents with protrusion of the chin, excessive sweating, impaired glucose tolerance, and enlargement of hands and feet. Which of the following is a growth hormone receptor antagonist used to treat this condition?

A. Pegvisomant (Correct Answer)
B. Olcegepant
C. Cabergoline
D. Octreotide

Explanation: ***Pegvisomant*** - **Pegvisomant** is a **growth hormone receptor antagonist** that binds to growth hormone receptors, preventing endogenous growth hormone from signaling and reducing IGF-1 levels. - It is specifically used in the treatment of **acromegaly**, a condition characterized by excessive growth hormone secretion, which aligns with the patient's symptoms of chin protrusion, excessive sweating, impaired glucose tolerance, and enlarged hands and feet. *Octreotide* - **Octreotide** is a **somatostatin analog** that works by inhibiting growth hormone secretion from the pituitary gland. - While used in acromegaly, it is not a growth hormone receptor antagonist, but rather reduces the production of growth hormone itself. *Cabergoline* - **Cabergoline** is a **dopamine agonist** primarily used to treat hyperprolactinemia by inhibiting prolactin secretion. - It can sometimes be used in acromegaly for patients with co-secretion of prolactin or those who are sensitive to its effects on growth hormone, but it is not a direct growth hormone receptor antagonist. *Olcegepant* - **Olcegepant** is a **calcitonin gene-related peptide (CGRP) receptor antagonist** developed for the treatment of migraine. - It has no known therapeutic role in the management of acromegaly or growth hormone-related disorders.

Question 733: Misoprostol used in the induction of labour is an analogue of which of the following type of prostaglandin?

A. PG E1 (Correct Answer)
B. PG E2
C. PG I2
D. PG F2alpha

Explanation: ***PG E1*** - **Misoprostol** is a synthetic analogue of **prostaglandin E1 (PGE1)**, which is used for cervical ripening and uterine contractions in labor induction. - PGE1 analogues help to soften the cervix, increase its compliance, and stimulate uterine smooth muscle contraction. *PG E2* - **Dinoprostone** is a synthetic analogue of **prostaglandin E2 (PGE2)**, commonly used for cervical ripening and induction of labor. - While PGE2 also induces labor, misoprostol specifically mimics the actions of PGE1. *PG I2* - **Prostacyclin (PGI2)** is primarily known for its role in inhibiting platelet aggregation and causing vasodilation. - It is not routinely used for labor induction due to its primary vascular effects and lack of direct uterine contractile properties at relevant doses. *PG F2alpha* - **Prostaglandin F2-alpha (PGF2α)**, such as **carboprost**, is used for postpartum hemorrhage to cause strong uterine contractions. - While it causes uterine contractions, its primary obstetric use is not for labor induction but rather for stimulating aggressive uterine contraction to stop bleeding.

Question 734: What is the first-line drug for osteoporosis in postmenopausal women?

A. Bisphosphonates (Correct Answer)
B. Strontium
C. Oral Contraceptive Pills
D. Selective Estrogen Receptor Modulator (SERM)

Explanation: ***Bisphosphonates*** - **Bisphosphonates** are the **first-line treatment** for osteoporosis in postmenopausal women due to their proven efficacy in reducing the risk of fragility fractures. - They work by **inhibiting osteoclast activity**, thereby decreasing bone turnover and increasing bone mineral density. *Oral Contraceptive Pills* - **Oral contraceptive pills** are primarily used for contraception and managing menstrual irregularities; they are **not a treatment for established osteoporosis**. - While estrogen plays a role in bone health, the focus for osteoporosis treatment is on anti-resorptive or anabolic agents. *Strontium* - **Strontium ranelate** has been used in some countries for osteoporosis, but its use is **limited due to concerns about cardiovascular adverse events** and is not typically a first-line drug. - It has a dual mechanism of action, both decreasing bone resorption and increasing bone formation. *Selective Estrogen Receptor Modulator (SERM)* - **SERMs**, such as **raloxifene**, are indicated for the prevention and treatment of osteoporosis, particularly in women with a high risk of **breast cancer**, but they are **not considered first-line** for all postmenopausal women compared to bisphosphonates. - They act as estrogen agonists in bone but are antagonists in breast and uterine tissue.

Question 735: Niacin therapy is contraindicated in diabetes because it

A. Increases the blood sugar levels (Correct Answer)
B. Causes scleroderma
C. Difficult to give injection
D. Increases the metabolism of oral hypoglycemic drugs

Explanation: ***Increases the blood sugar levels*** - **Niacin** can cause an increase in **insulin resistance** and glucose production, leading to elevated **blood sugar levels**. - This effect makes it contraindicated or used with extreme caution in patients with **diabetes mellitus**, as it can exacerbate **hyperglycemia**. *Causes scleroderma* - **Scleroderma** is a **chronic autoimmune** disorder characterized by widespread **fibrosis** and vascular dysfunction; it is not typically caused by niacin. - While niacin can have various side effects, **scleroderma** is not a known adverse reaction of this medication. *Difficult to give injection* - **Niacin** is available in various formulations, including **oral tablets** and **extended-release preparations**, which are easy to administer. - The mode of administration (injectable difficulty) is not a primary reason for its **contraindication in diabetes**. *Increases the metabolism of oral hypoglycemic drugs* - **Niacin** does not typically increase the **metabolism of oral hypoglycemic drugs**; rather, its primary concern in diabetes is its direct impact on **glucose metabolism**. - The interaction of niacin with **antidiabetic medications** is mainly related to its effect on **blood glucose levels**, requiring dose adjustments.

Question 736: What is the physiological dose of hydrocortisone (mg/m2/day)?

A. 20-25 mg/m²/day
B. 15-18 mg/m²/day
C. 10-12 mg/m²/day (Correct Answer)
D. 8-10 mg/m²/day

Explanation: ***10-12 mg/m²/day*** - This range represents the typical **physiological replacement dose** of hydrocortisone, mimicking the body's natural cortisol production. - This dose is used for patients with **adrenal insufficiency** to maintain normal metabolic functions without causing significant side effects. *8-10 mg/m²/day* - This dose is slightly on the lower side of the accepted physiological range and might not be sufficient for complete replacement in all individuals. - While close, it is not the most commonly cited optimal physiological dose for hydrocortisone replacement. *15-18 mg/m²/day* - This dose is typically considered above the physiological replacement level and may begin to cause **mild corticosteroid side effects** with prolonged use. - It might be used for short periods or in specific conditions, but not as a standard physiological replacement. *20-25 mg/m²/day* - This dose is well above the physiological range and would be considered a **pharmacological dose** often used for its anti-inflammatory or immunosuppressive effects. - Prolonged use at this dose would likely lead to significant **corticosteroid side effects** such as Cushingoid features, osteoporosis, and hyperglycemia.

Question 737: Which of the following drugs is used in SIADH?

A. Desmopressin
B. Terlipressin
C. Tolvaptan (Correct Answer)
D. Von Willebrand factor

Explanation: ***Tolvaptan*** - **Tolvaptan** is a **vasopressin receptor antagonist** that blocks the action of **antidiuretic hormone (ADH)** at the **V2 receptors** in the kidneys [1]. - This action promotes **water excretion (aquaresis)** without significantly affecting electrolyte balance, thereby increasing serum sodium levels in patients with **SIADH** [1]. *Desmopressin* - **Desmopressin** is a synthetic analog of **ADH** that primarily acts on **V2 receptors**, promoting water reabsorption [3], [4]. - It is used in conditions like **diabetes insipidus** [3], [4] or **hemophilia** [2] to increase ADH activity or clotting factors, which is contrary to the goal in SIADH. *Von Willebrand factor* - **Von Willebrand factor** is a **glycoprotein** involved in **hemostasis**, promoting platelet adhesion and carrying **factor VIII**. - It plays no role in the direct management of **SIADH** or fluid balance disorders. *Terlipressin* - **Terlipressin** is an analog of **vasopressin** that primarily acts on **V1 receptors**, causing vasoconstriction [5]. - It is used in conditions like **hepatorenal syndrome** or **esophageal variceal bleeding**, not for treating **SIADH**.

Question 738: Which of the following is glucocorticoid synthesis inhibitor?

A. Mifepristone
B. Flutamide
C. Finasteride
D. Metyrapone (Correct Answer)

Explanation: ***Metyrapone*** - **Metyrapone** inhibits **11-beta-hydroxylase**, an enzyme essential for the final step in cortisol and corticosterone synthesis in the adrenal cortex [2]. - This inhibition leads to a decrease in **cortisol production** and an increase in upstream steroid precursors like 11-deoxycortisol [2]. *Mifepristone* - **Mifepristone** is a **progesterone receptor antagonist** and, at higher doses, a **glucocorticoid receptor antagonist** [1]. - It does not inhibit the synthesis of glucocorticoids but rather blocks their action at the receptor level [1]. *Flutamide* - **Flutamide** is an **androgen receptor antagonist** used primarily in the treatment of prostate cancer. - It works by blocking the binding of androgens to their receptors, thereby inhibiting androgen-mediated effects. *Finasteride* - **Finasteride** is a **5-alpha-reductase inhibitor**, preventing the conversion of testosterone to the more potent dihydrotestosterone (DHT) [3]. - It is used to treat benign prostatic hyperplasia (BPH) and male-pattern baldness, and does not affect glucocorticoid synthesis [3].

Question 739: Which of the following oral antidiabetic drugs is an insulin secretagogue?

A. Metformin
B. Pioglitazone
C. Nateglinide (Correct Answer)
D. Acarbose

Explanation: **Nateglinide** - **Nateglinide** is a **meglitinide**, which is a type of **insulin secretagogue**. - It stimulates **insulin release** from pancreatic beta cells by blocking ATP-sensitive potassium channels. *Metformin* - **Metformin** is a **biguanide** that primarily works by **decreasing hepatic glucose production** and increasing insulin sensitivity in peripheral tissues. - It does not directly stimulate insulin secretion. *Pioglitazone* - **Pioglitazone** is a **thiazolidinedione** (TZD) that improves insulin sensitivity by activating **PPAR-gamma receptors**. - It does not directly affect insulin secretion but rather enhances the body's response to existing insulin. *Acarbose* - **Acarbose** is an **alpha-glucosidase inhibitor** that delays the digestion and absorption of carbohydrates in the small intestine. - This reduces postprandial glucose excursions and does not directly stimulate insulin secretion.

Question 740: Which of the following antidiabetic drugs is a GLP-1 receptor agonist?

A. Pramlintide
B. Glucomannan
C. Exenatide (Correct Answer)
D. Sitagliptin

Explanation: ***Exenatide*** - **Exenatide** is a synthetic analog of **glucagon-like peptide-1 (GLP-1)**, acting as a GLP-1 receptor agonist [1]. - It works by stimulating **insulin secretion** in a glucose-dependent manner, suppressing glucagon release, slowing gastric emptying, and promoting satiety [2], [3]. - Other GLP-1 agonists include liraglutide, dulaglutide, and semaglutide [1]. *Pramlintide* - **Pramlintide** is an **amylin analog**, not a GLP-1 receptor agonist. - It is used in both type 1 and type 2 diabetes to slow gastric emptying, suppress glucagon secretion, and promote satiety, but it acts via **amylin receptors**. *Glucomannan* - **Glucomannan** is a **dietary fiber** derived from the konjac plant, used as a food additive and supplement for weight loss and constipation. - It does not directly affect GLP-1 receptors or regulate insulin or glucagon secretion as a pharmacological agent. *Sitagliptin* - **Sitagliptin** is a **DPP-4 inhibitor** (dipeptidyl peptidase-4 inhibitor), not a GLP-1 receptor agonist [2]. - While it enhances endogenous GLP-1 activity by preventing its degradation, it does not directly stimulate GLP-1 receptors like exenatide does [4].

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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