Endocrine Pharmacology — MCQs

Endocrine Pharmacology Indian Medical PG Practice Questions and MCQs

Question 661: The amount of Ethinyl Estradiol in third generation combined oral contraceptive pills is:

A. 35–50 mcg
B. 10–20 mcg
C. 20–30 mcg
D. 30–35 mcg (Correct Answer)

Explanation: ***30–35 mcg*** - **Third-generation combined oral contraceptive pills (COCs)** typically contain **30-35 mcg of Ethinyl Estradiol**. - Third generation is defined by the type of **progestin used** (desogestrel, gestodene, or norgestimate), not the estrogen dose. - This dosage provides effective contraception while minimizing estrogen-related side effects compared to first-generation pills. - Common formulations include **30 mcg or 35 mcg** of ethinyl estradiol. *20–30 mcg* - While some third-generation formulations may contain doses at the lower end (20 mcg), this range overlaps with **ultra-low dose formulations**. - The typical and most common dosage for third-generation COCs is **30-35 mcg**, not this lower range. *10–20 mcg* - This represents **ultra-low dose COCs**, which aim to further reduce estrogen exposure. - These formulations may be associated with **breakthrough bleeding** and reduced cycle control. - Not the standard dose for third-generation COCs. *35–50 mcg* - These higher doses are characteristic of **first-generation COCs** from the 1960s-1970s. - Associated with higher rates of **thromboembolic events** and estrogen-related side effects. - Modern COCs use lower doses for improved safety profiles.

Question 662: Consider the following in respect of Ormeloxifene : 1. It is a research product of Central Drug Research Institute, Lucknow 2. It is a steroidal compound 3. It is a potent antiestrogen with weak estrogenic properties 4. It does not inhibit ovulation Which of the above are correct ?

A. 1, 2 and 3
B. 2, 3 and 4
C. 1, 3 and 4 (Correct Answer)
D. 1 and 3 only

Explanation: ***1, 3 and 4*** - Ormeloxifene, also known as **Centchroman**, was developed by the **Central Drug Research Institute (CDRI), Lucknow**, making statement 1 **correct**. - It is a **selective estrogen receptor modulator (SERM)** that acts as a **potent antiestrogen** in the uterus and breast, with **weak estrogenic activity** in other tissues like bone, thus statement 3 is **correct**. - Ormeloxifene has a **unique mechanism** among contraceptives: it **does not inhibit ovulation**. Instead, it works by **preventing implantation** through endometrial changes and altering cervical mucus, making statement 4 **correct**. - Statement 2 is **incorrect** because Ormeloxifene is a **non-steroidal compound**, not a steroidal one. *1, 2 and 3* - This option is incorrect because statement 2, claiming Ormeloxifene is a **steroidal compound**, is false. Ormeloxifene is a **non-steroidal SERM**. - While statements 1 and 3 are correct, the inclusion of incorrect statement 2 makes this option wrong. *1 and 3 only* - While statements 1 and 3 are indeed correct, this option is **incomplete** as it excludes statement 4. - Statement 4 is also correct—Ormeloxifene **does not inhibit ovulation**, which is a key distinguishing feature of this contraceptive. *2, 3 and 4* - This option is incorrect because statement 2 is false—Ormeloxifene is **non-steroidal**, not steroidal. - Although statements 3 and 4 are correct, the inclusion of the false statement 2 makes this entire option incorrect.

Question 663: Which one of the following is not a contraindication for prescribing combined oral contraceptive pills?

A. Viral hepatitis
B. Pelvic inflammatory disease (Correct Answer)
C. Well-controlled hypertension
D. Thromboembolic disease

Explanation: ***Pelvic inflammatory disease*** - **Pelvic inflammatory disease (PID)** is NOT a contraindication for combined oral contraceptive pills (COCs). - According to **WHO Medical Eligibility Criteria**, PID is classified as **Category 1** (no restriction) for COC use. - COCs do not worsen PID and may actually provide some **protective effect** against ascending genital tract infections. - PID concerns are primarily relevant for **IUD insertion**, not oral contraceptive use. *Viral hepatitis* - **Active viral hepatitis** is a contraindication (WHO Category 3-4) for COCs. - COCs are metabolized in the **liver**, and use during active hepatitis can exacerbate liver damage. - **Severe or acute liver disease** impairs hormone metabolism, increasing risks of adverse effects. *Well-controlled hypertension* - **Hypertension** is generally a contraindication for COCs depending on severity and vascular complications. - **Well-controlled hypertension without vascular disease** is WHO Category 3 (risks usually outweigh benefits). - **Uncontrolled hypertension** (≥160/100 mmHg) or hypertension with vascular disease is **Category 4** (absolute contraindication). - Estrogen in COCs can further elevate blood pressure and increase cardiovascular risks. *Thromboembolic disease* - History of **thromboembolic disease** (DVT, PE, stroke) is an **absolute contraindication** (WHO Category 4) for COCs. - Estrogen in COCs increases synthesis of **clotting factors** (I, VII, X) and decreases anticoagulant proteins, significantly raising **venous thromboembolism risk**.

Question 664: A female patient presented with vulvovaginal pruritus. On detailed history taking, it was found that she was on some antidiabetic drugs. Which antidiabetic drug can cause the above-mentioned side effect?

A. Metformin
B. Canagliflozin (Correct Answer)
C. Linagliptin
D. Liraglutide

Explanation: ***Canagliflozin*** - Canagliflozin is a **sodium-glucose co-transporter 2 (SGLT2) inhibitor**. These drugs work by increasing **urinary glucose excretion**. - The increased glucose in the urine (glycosuria) creates a favorable environment for fungal and bacterial growth, leading to common side effects such as **vulvovaginal candidiasis** (yeast infections) and urinary tract infections, which manifest as pruritus. *Metformin* - Metformin is a **biguanide** that primarily reduces hepatic glucose production and increases insulin sensitivity. - Its common side effects are gastrointestinal, such as **diarrhea, nausea, and abdominal discomfort**, but it does not typically cause genitourinary infections or pruritus. *Linagliptin* - Linagliptin is a **dipeptidyl peptidase-4 (DPP-4) inhibitor** that increases endogenous GLP-1 and GIP levels, enhancing glucose-dependent insulin secretion. - Common side effects include **nasopharyngitis** and **headache**, but it is not associated with vulvovaginal pruritus. *Liraglutide* - Liraglutide is a **glucagon-like peptide-1 (GLP-1) receptor agonist** that increases glucose-dependent insulin secretion, suppresses glucagon secretion, and slows gastric emptying. - Its most common side effects are **gastrointestinal (nausea, vomiting), decreased appetite, and pancreatitis (rare)**, but it generally does not cause vulvovaginal pruritus.

Question 665: Which of the following is not used to treat PCOD?

A. Tamoxifen (Correct Answer)
B. OCP
C. Metformin
D. Clomiphene citrate

Explanation: ***Tamoxifen*** - **Tamoxifen** is a selective estrogen receptor modulator (SERM) primarily used in the treatment of **estrogen receptor-positive breast cancer**. - While other SERMs like clomiphene citrate are used in PCOD for ovulation induction, tamoxifen is not a standard treatment for **PCOD** itself. *OCP* - **Oral contraceptive pills (OCPs)** are a common first-line treatment for managing various symptoms of PCOD, such as **menstrual irregularities** and **hirsutism**. - They work by suppressing ovarian androgen production and providing regular withdrawal bleeds. *Metformin* - **Metformin** is an insulin-sensitizing agent often used in PCOD, especially in women with **insulin resistance** or impaired glucose tolerance. - It helps improve **menstrual regularity** and can facilitate ovulation in some patients by reducing insulin levels. *Clomiphene citrate* - **Clomiphene citrate** is a selective estrogen receptor modulator (SERM) commonly used as an **ovulation induction agent** in women with PCOD who are trying to conceive. - It works by blocking estrogen receptors in the hypothalamus, leading to increased release of **gonadotropins** (FSH and LH).

Question 666: Mechanism of action of exenatide in diabetes mellitus is

A. It is DPP-4 inhibitor and results in decreased breakdown of GLP
B. It is amylin analogue and decreases glucagon
C. It is analogue of GLP released from gut and increases glucose dependent insulin secretion (Correct Answer)
D. It inhibits SGLT-2 and causes glucosuria

Explanation: ***It is analogue of GLP released from gut and increase glucose dependant insulin secretion*** - **Exenatide** is a **glucagon-like peptide-1 (GLP-1) receptor agonist**, mimicking the action of naturally occurring GLP-1 [1]. - It stimulates **glucose-dependent insulin secretion**, suppresses glucagon release, slows gastric emptying, and promotes satiety, all contributing to improved glycemic control [2]. *It inhibits SGLT-2 and cause glucosuria* - This describes the mechanism of **sodium-glucose co-transporter 2 (SGLT-2) inhibitors**, such as empagliflozin or canagliflozin, which promote glucose excretion in urine. - **Exenatide** does not directly affect renal glucose reabsorption. *It is DPP-4 inhibitor and result in decreased breakdown of GLP* - This mechanism belongs to **dipeptidyl peptidase-4 (DPP-4) inhibitors** (e.g., sitagliptin, saxagliptin), which prevent the rapid degradation of endogenous GLP-1, thus prolonging its action [1]. - **Exenatide** directly activates GLP-1 receptors rather than modulating the enzyme that breaks down endogenous GLP-1 [1]. *It is amylin analogue and decrease glucagon* - This describes **pramlintide**, an amylin analogue used in diabetes management, which primarily suppresses postprandial glucagon secretion, slows gastric emptying, and promotes satiety. - While **exenatide** also decreases glucagon, its primary mechanism is via GLP-1 receptor agonism [2].

Question 667: Insulin of choice for the treatment of diabetic ketoacidosis is:

A. Insulin lispro
B. Insulin glargine
C. NPH insulin
D. Regular Insulin (Correct Answer)

Explanation: ***Regular Insulin*** - **Regular insulin** is the insulin of choice for treating **diabetic ketoacidosis (DKA)** because it can be administered intravenously. - Its **short onset of action** and predictable duration allow for rapid and precise titration in a critical care setting. *Insulin lispro* - **Insulin lispro** is a **rapid-acting insulin analog** typically used for mealtime coverage, which has a very quick onset and short duration. - While it acts quickly, its primary use is not for the continuous intravenous infusion required in DKA management. *Insulin glargine* - **Insulin glargine** is a **long-acting insulin analog** designed to provide basal insulin replacement. - It has a prolonged duration of action and a slow, sustained release profile, making it unsuitable for the rapid correction needed in DKA. *NPH insulin* - **NPH insulin** is an **intermediate-acting insulin** that has a delayed onset and peak effect. - Its insoluble nature and variable absorption make it inappropriate for the acute, immediate intravenous insulin therapy required in DKA.

Question 668: In the management of diabetes mellitus, lactic acidosis is caused by which of the following?

A. Pioglitazone
B. Metformin (Correct Answer)
C. Glipizide
D. Tolbutamide

Explanation: ***Metformin*** - Metformin can cause **lactic acidosis**, especially in patients with **renal impairment**, as it inhibits hepatic gluconeogenesis and lactate clearance [1]. - The risk is increased in conditions leading to **tissue hypoperfusion** or **hypoxemia**, where lactate production is elevated. *Pioglitazone* - **Pioglitazone** is a thiazolidinedione that improves insulin sensitivity but is not associated with lactic acidosis [1]. - Its main risks include **fluid retention**, **heart failure**, and increased risk of **bladder cancer**. *Glipizide* - **Glipizide** is a sulfonylurea that stimulates insulin secretion from beta cells but does not cause lactic acidosis [2]. - The primary adverse effect is **hypoglycemia** [2]. *Tolbutamide* - **Tolbutamide** is an older generation sulfonylurea, similar to glipizide, and also acts by stimulating insulin release [2]. - Its main risk is **hypoglycemia**, and it is not associated with lactic acidosis [2].

Question 669: Exenatide is a new drug used in diabetes mellitus. Mechanism of action of this drug is:-

A. Inhibiting intestinal absorption of carbohydrates
B. Release of insulin acting as agonist of GLP-1 receptors (Correct Answer)
C. Stimulation of PPAR-gamma
D. Inhibition of DPP-4

Explanation: ***Release of insulin acting as agonist of GLP-1 receptors*** - **Exenatide** is a **glucagon-like peptide-1 (GLP-1) receptor agonist**, mimicking the action of endogenous GLP-1. - This leads to glucose-dependent **insulin release**, suppression of **glucagon secretion**, delayed **gastric emptying**, and increased **satiety**, all contributing to improved glycemic control. *Inhibition of DPP-4* - This mechanism describes the action of **DPP-4 inhibitors** (e.g., sitagliptin, saxagliptin), which prevent the breakdown of endogenous GLP-1 and other **incretin hormones**. - While both GLP-1 agonists and DPP-4 inhibitors target the incretin system, exenatide directly acts as an agonist, rather than preventing breakdown. *Inhibiting intestinal absorption of carbohydrates* - This mechanism describes drugs like **alpha-glucosidase inhibitors** (e.g., acarbose, miglitol), which delay carbohydrate absorption from the gut. - Exenatide's primary action is not on carbohydrate absorption but rather on pancreatic hormone secretion and gastric emptying. *Stimulation of PPAR-gamma* - This mechanism describes **thiazolidinediones** (TZDs) like pioglitazone and rosiglitazone, which enhance **insulin sensitivity** by acting on **peroxisome proliferator-activated receptor-gamma (PPAR-gamma)** in adipose tissue. - Exenatide belongs to a different class of antidiabetic drugs with a distinct mechanism of action.

Question 670: All of the following can result in gynecomastia except:

A. Spironolactone
B. Digoxin
C. Aromatase inhibitors (Correct Answer)
D. Sulphonamides

Explanation: ***Aromatase inhibitors*** - **Aromatase inhibitors** block the conversion of androgens to estrogens, thereby **decreasing estrogen levels** which would prevent rather than cause gynecomastia. - They are used in estrogen-sensitive breast cancers to reduce estrogen-dependent growth. *Spironolactone* - **Spironolactone** is an aldosterone antagonist that also possesses anti-androgenic effects and can inhibit androgen synthesis, leading to an **increased estrogen-to-androgen ratio** and gynecomastia. - It can also directly stimulate the estrogen receptor in male breast tissue. *Sulphonamides* - Certain **sulphonamides**, particularly sulfasalazine, have been associated with gynecomastia, possibly due to direct toxic effects on testicular function leading to a **relative increase in estrogen activity**. - While less common than with some other drugs, it can alter the estrogen-androgen balance. *Digoxin* - **Digoxin** can cause gynecomastia by mimicking estrogen physiologically or by inhibiting androgen production, leading to an **alteration in the estrogen-to-androgen ratio**. - The risk of gynecomastia is especially noted with prolonged use and higher doses of digoxin.

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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