Androgens and Anabolic Steroids — MCQs
What is the primary mechanism of action of 5-α reductase?
Which of the following is an aromatase inhibitor?
Which of the following is not an androgen?
Dihydrotestosterone acts on
What is the most common gastrointestinal side effect of oral contraceptives?
Which medication is commonly used in heart failure that also has aldosterone antagonistic properties?
Long-term steroid ingestion leads to all of the following except:
Which of the following is least effective in the management of polycystic ovary syndrome?
Which of the following drugs does not cause pharmacological adrenalectomy?
The best drug to lower prolactin levels in a female with infertility is:
Androgens and Anabolic Steroids Indian Medical PG Practice Questions and MCQs
Question 1: What is the primary mechanism of action of 5-α reductase?
- A. Reduction of C4-C5 double bond (Correct Answer)
- B. Breakage of amide bond
- C. Breakage of C-N bond
- D. Breakage of N-N bond
Explanation: ***Reduction of C4-C5 double bond*** - 5-α reductase is a **NADPH-dependent reductase enzyme** that catalyzes the **reduction (saturation) of the C4-C5 double bond** in the A-ring of testosterone to form **dihydrotestosterone (DHT)**. - This reduction involves **adding two hydrogen atoms** across the double bond, converting it to a single bond with **5-α stereochemistry**. - DHT is a more potent androgen crucial for **prostate development, external genitalia formation, and male pattern baldness**, making 5-α reductase inhibitors (like finasteride) clinically important for treating benign prostatic hyperplasia and androgenetic alopecia. *Breakage of amide bond* - Breaking **amide bonds (C-N bonds with a carbonyl)** is the function of **proteases and amidases**, not reductases. - This process involves **hydrolysis** and is fundamental to protein degradation and peptide metabolism. *Breakage of C-N bond* - **Carbon-nitrogen bond cleavage** occurs in reactions like **deamination** (catalyzed by deaminases) or metabolism of nitrogenous compounds. - Reductases perform **electron transfer reactions**, not bond cleavage reactions. *Breakage of N-N bond* - **Nitrogen-nitrogen bond** cleavage is rare in human biochemistry and may occur in hydrazine metabolism or by specialized enzymes. - Steroid hormones do not contain N-N bonds, making this mechanism irrelevant to 5-α reductase function.
Question 2: Which of the following is an aromatase inhibitor?
- A. Letrozole (Correct Answer)
- B. Tamoxifen
- C. Danazol
- D. Taxane
Explanation: ***Letrozole*** - **Letrozole** is a commonly used **aromatase inhibitor**, which works by blocking the enzyme **aromatase** that converts androgens into estrogens [1]. - This reduction in estrogen levels is crucial in treating **hormone-sensitive breast cancers** [1]. *Tamoxifen* - **Tamoxifen** is a **selective estrogen receptor modulator (SERM)**, not an aromatase inhibitor [2]. - It acts by blocking estrogen receptors in breast tissue while potentially stimulating them in other tissues like bone and uterus [2]. *Danazol* - **Danazol** is a synthetic androgen that suppresses the hypothalamic-pituitary-gonadal axis, leading to **decreased estrogen production**. - It works by inhibiting gonadotropin release and directly inhibiting ovarian steroidogenesis, rather than blocking the aromatase enzyme directly. *Taxane* - **Taxanes** are a class of **chemotherapy drugs** that interfere with cell division by stabilizing microtubules. - They are used to treat various cancers, including breast cancer, but do not act as aromatase inhibitors.
Question 3: Which of the following is not an androgen?
- A. 17α-hydroxyprogesterone (Correct Answer)
- B. Testosterone
- C. Dihydrotestosterone
- D. Androstenedione
Explanation: ***17α-hydroxyprogesterone*** - This is a **progesterone derivative** and an intermediate in the synthesis of androgens and corticosteroids, but it does **not possess significant androgenic activity** itself. - Its primary role is as a precursor, rather than a direct androgen. *Testosterone* - **Testosterone** is the **primary male sex hormone** and a potent androgen, responsible for the development of male secondary sexual characteristics. - It plays crucial roles in muscle mass, bone density, libido, and erythropoiesis. *Dihydrotestosterone* - **Dihydrotestosterone (DHT)** is a potent androgen, formed from testosterone by the enzyme 5α-reductase. - DHT is responsible for the development of external male genitalia during fetal development and contributes to prostate growth and male pattern baldness in adults. *Androstenedione* - **Androstenedione** is a **weak androgen** and an important **precursor hormone** in the biosynthesis of testosterone and estrogens. - It is produced in the adrenal glands and gonads, serving as an intermediate step in steroidogenesis.
Question 4: Dihydrotestosterone acts on
- A. Pituitary
- B. External genitalia (Correct Answer)
- C. Internal genitalia
- D. Testis
Explanation: ***External genitalia*** - **Dihydrotestosterone (DHT)** is critical for the development of **male external genitalia** during fetal development. - In adulthood, **DHT** is responsible for the growth of the **prostate** and secondary male sexual characteristics like **facial hair** and **balding**. *Pituitary* - The **pituitary gland** is primarily regulated by **gonadotropin-releasing hormone (GnRH)** from the hypothalamus and feedback from **gonadal steroids** like **testosterone** and **estrogen**, not directly by **DHT**. - **DHT** does not exert significant direct action on the anterior pituitary to regulate gonadotropin release. *Internal genitalia* - The development of **internal male genitalia**, such as the **epididymis**, **vas deferens**, and **seminal vesicles**, is primarily mediated by **testosterone** directly, not **DHT**. - **Testosterone** acts on the **Wolffian ducts** to promote their differentiation into the internal male reproductive structures. *Testis* - The **testis** is the primary site of **testosterone production** and conversion to **DHT** by **5α-reductase**. - While **DHT** is produced within the testis, its main actions are on peripheral target tissues rather than directly regulating testicular function.
Question 5: What is the most common gastrointestinal side effect of oral contraceptives?
- A. Decreased appetite
- B. Weight loss
- C. Nausea (Correct Answer)
- D. Constipation
Explanation: ***Nausea*** - **Nausea** is a very common gastrointestinal side effect of oral contraceptives, especially during the initial weeks of use, due to the **estrogen component**. - This side effect often **improves over time** as the body adjusts, or can be managed by taking the pill with food or at bedtime. *Weight loss* - Oral contraceptives are **not typically associated with weight loss**; in fact, some users may experience slight weight gain, although studies show no consistent significant effect. - Changes in weight are more often due to **fluid retention** rather than true fat loss. *Decreased appetite* - **Decreased appetite** is not a common side effect of oral contraceptives; rather, some individuals might experience an increased appetite due to hormonal fluctuations. - The hormonal effects on metabolism and appetite are **varied and not consistently demonstrated** to lead to decreased appetite. *Constipation* - **Constipation** is not a frequent gastrointestinal side effect of oral contraceptives; rather, some users may experience changes in bowel habits, but **diarrhea is more commonly reported** than constipation when GI issues occur. - Hormonal contraceptives primarily affect the gut through **estrogen and progestin**, leading to various effects, but constipation is not a predominant one.
Question 6: Which medication is commonly used in heart failure that also has aldosterone antagonistic properties?
- A. Carvedilol
- B. Spironolactone (Correct Answer)
- C. Abiraterone
- D. Sacubitril/Valsartan
Explanation: ***Spironolactone*** - **Spironolactone** is a **potassium-sparing diuretic** that acts as a **competitive antagonist of aldosterone** receptors, primarily in the collecting ducts of the kidneys. - This action leads to increased excretion of sodium and water, and retention of potassium, which is beneficial in **heart failure** by reducing fluid overload and mitigating the detrimental effects of aldosterone on cardiac remodeling. *Carvedilol* - **Carvedilol** is a **beta-blocker** with additional **alpha-1 blocking** properties, commonly used in heart failure to reduce heart rate, blood pressure, and myocardial oxygen demand. - It does not possess significant aldosterone antagonistic properties. *Sacubitril/Valsartan* - **Sacubitril/Valsartan** is an **angiotensin receptor-neprilysin inhibitor (ARNI)**. Valsartan is an **angiotensin receptor blocker (ARB)**, and sacubitril inhibits neprilysin, an enzyme that degrades natriuretic peptides. - While it modulates the **renin-angiotensin-aldosterone system (RAAS)** and is highly effective in heart failure, it does not directly antagonize aldosterone receptors. *Abiraterone* - **Abiraterone** is an **androgen-biosynthesis inhibitor** used in the treatment of **prostate cancer**. - Its primary mechanism involves inhibiting **CYP17**, an enzyme critical for androgen production, and it has no role in the management of heart failure or aldosterone antagonism.
Question 7: Long-term steroid ingestion leads to all of the following except:
- A. Avascular necrosis of head of femur
- B. Growth retardation
- C. Hypoglycemia (Correct Answer)
- D. Cataract
Explanation: ***Hypoglycemia*** - Chronic steroid use primarily leads to **hyperglycemia** due to increased **gluconeogenesis** and **insulin resistance**, not hypoglycemia. - Steroids raise blood glucose levels, potentially inducing or worsening **diabetes mellitus**. *Avascular necrosis of head of femur* - Long-term steroid use is a well-established risk factor for **avascular necrosis**, particularly affecting the **femoral head**. - This occurs due to impaired blood supply to the bone, leading to its death. *Cataract* - **Posterior subcapsular cataracts** are a known ocular complication of prolonged systemic corticosteroid therapy. - The mechanism involves direct effects of steroids on lens metabolism and protein aggregation. *Growth retardation* - In children, chronic corticosteroid therapy can suppress growth, leading to **growth retardation**. - This is due to interference with **growth hormone secretion** and direct effects on bone formation.
Question 8: Which of the following is least effective in the management of polycystic ovary syndrome?
- A. OC pills
- B. Cyclical progesterones
- C. Myoinositol
- D. Danazol (Correct Answer)
Explanation: ***Danazol (Least Effective - Correct Answer)*** - **Danazol** is an attenuated androgen that suppresses ovarian function and is primarily used for the treatment of **endometriosis** and **fibrocystic breast disease**, not for PCOS. - Its **androgenic side effects**, such as hirsutism and acne, would **exacerbate symptoms already present in PCOS**, making it unsuitable and often contraindicated. - It does not address the underlying metabolic or hormonal derangements in PCOS and may worsen the clinical picture. *OC Pills (Effective Treatment)* - **Oral contraceptive pills** (OCPs) are a cornerstone in PCOS management, primarily by suppressing **androgen production** from the ovaries. - They help regulate menstrual cycles, reduce **hirsutism** and **acne**, and protect the endometrium from hyperplasia. - First-line therapy for women with PCOS not seeking pregnancy. *Cyclical Progesterones (Effective Treatment)* - **Cyclical progesterones** are used in PCOS to induce regular shedding of the **endometrial lining** in anovulatory women. - This prevents **endometrial hyperplasia** and reduces the risk of endometrial cancer, making them effective for endometrial protection. - Although they do not address hyperandrogenism, they serve an important role in preventing long-term complications. *Myoinositol (Effective Treatment)* - **Myoinositol** is a natural insulin sensitizer that can improve ovarian function, reduce **hyperandrogenism**, and improve **insulin resistance** in women with PCOS. - It plays a role in the **insulin signaling pathway**, improving follicular development and ovulation rates. - Increasingly recognized as an evidence-based supplement in PCOS management.
Question 9: Which of the following drugs does not cause pharmacological adrenalectomy?
- A. Mitotane
- B. Methotrexate (Correct Answer)
- C. Ketoconazole
- D. Aminoglutethimide
Explanation: ***Methotrexate*** - **Methotrexate** is an **antimetabolite** and **folate antagonist** primarily used in chemotherapy and for autoimmune diseases. It does not exert its primary action on the adrenal gland or steroid synthesis. - Its mechanism involves inhibiting **dihydrofolate reductase**, leading to reduced DNA synthesis and cell proliferation, which is unrelated to adrenal function. *Ketoconazole* - **Ketoconazole** is an antifungal agent that inhibits several **cytochrome P450 enzymes** involved in steroidogenesis, including 17α-hydroxylase and 11β-hydroxylase. - This inhibition leads to a decrease in **cortisol and androgen synthesis**, effectively causing a pharmacological adrenalectomy. *Mitotane* - **Mitotane** is a cytotoxic agent that causes **adrenocortical atrophy** and inhibits the synthesis of adrenal steroids. - It is specifically used in the treatment of **adrenocortical carcinoma** due to its direct destructive effect on adrenal cells. *Aminoglutethimide* - **Aminoglutethimide** inhibits the enzymatic conversion of **cholesterol to pregnenolone**, the rate-limiting step in steroid hormone synthesis. - This broad inhibition reduces the production of **all adrenal steroids**, including cortisol, thus inducing a pharmacological adrenalectomy.
Question 10: The best drug to lower prolactin levels in a female with infertility is:
- A. Bromocriptine (Correct Answer)
- B. GnRH
- C. Testosterone
- D. Corticosteroids
Explanation: ***Bromocriptine*** - **Bromocriptine** is a **dopamine agonist** that directly inhibits prolactin secretion from the pituitary gland [1]. - It is highly effective in lowering prolactin levels and restoring ovulatory function, making it the preferred treatment for **hyperprolactinemia-induced infertility** [1], [2]. *GnRH* - **Gonadotropin-releasing hormone (GnRH)** stimulates the release of LH and FSH, but it does not directly lower prolactin levels. - In cases of hyperprolactinemia, high prolactin can actually inhibit GnRH pulse frequency, so administering GnRH without addressing prolactin would be ineffective or counterproductive. *Testosterone* - **Testosterone** is a male androgen and has no direct role in lowering prolactin levels in women. - Administering testosterone to a female would likely cause virilizing effects and would not address the underlying cause of infertility. *Corticosteroids* - **Corticosteroids** are used to reduce inflammation and suppress the immune system, but they do not have a direct mechanism to lower prolactin levels. - While stress (which corticosteroids can sometimes help manage) can influence prolactin, corticosteroids are not a primary treatment for hyperprolactinemia.
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