Endocrine Pharmacology — MCQs

Endocrine Pharmacology Indian Medical PG Practice Questions and MCQs

Question 721: Which of the following is/are side effect(s) of growth hormone administration?

A. All of the above (Correct Answer)
B. Hypothyroidism
C. Pain at injection site
D. Glucose intolerance

Explanation: ***All of the above*** - **Growth hormone (GH)** administration can lead to a variety of side effects, including **pain at the injection site**, **glucose intolerance**, and **hypothyroidism**. - These side effects are important considerations when managing patients receiving GH therapy. *Pain at injection site* - This is a common local side effect due to the injection method itself and the substance being administered. - It is typically mild and transient but can affect patient adherence to treatment. *Glucose intolerance* - Growth hormone has **anti-insulin effects**, which can lead to **insulin resistance** and increased blood glucose levels. - This can worsen pre-existing diabetes or induce **glucose intolerance** in susceptible individuals. *Hypothyroidism* - Growth hormone can influence thyroid function, sometimes reducing the conversion of **thyroxine (T4)** to **triiodothyronine (T3)**. - This may lead to **central hypothyroidism** or exacerbate subclinical hypothyroidism, requiring thyroid hormone supplementation.

Question 722: What is the mechanism of action of Pegvisomant?

A. Somatostatin antagonist
B. Somatotropin antagonist
C. GH receptor antagonist (Correct Answer)
D. GH receptor agonist

Explanation: ***GH receptor antagonist*** - Pegvisomant is a **growth hormone (GH) receptor antagonist** that binds to GH receptors but does not activate them. - This action blocks the binding of endogenous GH to its receptors, thereby inhibiting the downstream production of **insulin-like growth factor 1 (IGF-1)** and reducing the symptoms of **acromegaly**. *Somatostatin antagonist* - **Somatostatin analogues** (e.g., octreotide, lanreotide) are used to treat acromegaly by inhibiting the release of growth hormone from the pituitary gland. - Pegvisomant does not act on somatostatin receptors; it functions at the level of the **GH receptor**. *Somatotropin antagonist* - **Somatotropin** is another name for **growth hormone (GH)**. - While Pegvisomant opposes the action of somatotropin, its mechanism is specifically at the receptor level, making "GH receptor antagonist" a more precise description. *GH receptor agonist* - A **GH receptor agonist** would stimulate the growth hormone receptor, leading to increased IGF-1 production and exacerbating conditions like acromegaly. - Pegvisomant has the opposite effect, blocking GH action rather than promoting it, making it an **antagonist**.

Question 723: Which of the following is not a component of Mala D?

A. 0.03 mg Ethinyl estradiol
B. 0.15 mg levonorgestrel
C. Iron tablets
D. 0.15 mg desogestrel (Correct Answer)

Explanation: ***0.15 mg desogestrel*** - **Mala D** is a combined oral contraceptive pill that does not contain **desogestrel**. - **Desogestrel** is a progestin primarily found in some *third-generation combined oral contraceptives* or *progestin-only pills*, not Mala D. *0.03 mg Ethinyl estradiol* - **Mala D** contains **0.03 mg of Ethinyl estradiol**, which is the estrogen component of this combined oral contraceptive. - This dosage of estrogen helps to suppress ovulation and stabilize the endometrial lining. *0.15 mg levonorgestrel* - **Mala D** contains **0.15 mg of levonorgestrel**, which is the progestin component of this combined oral contraceptive. - **Levonorgestrel** works by thickening cervical mucus, inhibiting ovulation, and altering the endometrial lining. *Iron tablets* - **Mala D** packs typically include **iron tablets** (usually 75 mg of ferrous fumarate equivalent to 60 mg elemental iron) to be taken during the placebo week. - These iron tablets are included to help prevent or treat **iron-deficiency anemia**, which can occur with menstrual blood loss.

Question 724: Which of the following statements about tamoxifen is false?

A. It increases the risk of venous thromboembolism.
B. It is a competitive inhibitor of estrogen at receptor site
C. It cannot be used for induction of ovulation. (Correct Answer)
D. It is a selective estrogen receptor modulator

Explanation: ***It cannot be used for induction of ovulation.*** - Tamoxifen, as a **selective estrogen receptor modulator (SERM)** with anti-estrogenic effects on the hypothalamus and pituitary, can in fact be used off-label for **ovulation induction** by increasing gonadotropin secretion. - Its anti-estrogenic action at the hypothalamus removes negative feedback, leading to increased **follicle-stimulating hormone (FSH)** release, which stimulates ovarian follicle development. *It increases the risk of venous thromboembolism.* - Tamoxifen exerts **estrogenic effects** on the coagulation system, which can lead to an increased risk of **venous thromboembolism (VTE)**, including deep vein thrombosis and pulmonary embolism. - This side effect is a significant concern, particularly in patients with other risk factors for clotting. *It is a competitive inhibitor of estrogen at receptor site* - Tamoxifen acts as a **selective estrogen receptor modulator (SERM)** by competitively binding to estrogen receptors in target tissues. - This binding prevents **endogenous estrogen** from activating the receptors, thereby exerting its anti-estrogenic effects, particularly in breast tissue. *It is a selective estrogen receptor modulator* - Tamoxifen is indeed classified as a **SERM**, meaning it has both estrogenic and anti-estrogenic effects depending on the target tissue. - It acts as an **estrogen antagonist** in breast tissue, making it effective in treating estrogen receptor-positive breast cancer, and an **estrogen agonist** in other tissues like bone and the endometrium.

Question 725: Which drug is preferred for the treatment of a 21-hydroxylase deficient female fetus to prevent genital virilization?

A. Maternal dexamethasone (Correct Answer)
B. Maternal hydrocortisone
C. Maternal methylprednisolone
D. Maternal cortisol

Explanation: ***Maternal dexamethasone*** - **Dexamethasone** is the preferred corticosteroid because it is not significantly metabolized by the placenta and can effectively reach the fetus to suppress adrenal androgen production. [2] - Its potent **glucocorticoid activity** helps to reduce the overproduction of androgens, preventing the virilization of external genitalia in affected female fetuses. [2] *Maternal cortisol* - **Cortisol** is rapidly metabolized by the placenta via **11β-hydroxysteroid dehydrogenase 2**, making it ineffective in reaching the fetal circulation in sufficient concentrations. - Therefore, it cannot adequately suppress the fetal adrenal gland's androgen production to prevent virilization. *Maternal hydrocortisone* - Similar to cortisol, **hydrocortisone** is also extensively metabolized by the placenta, reducing its bioavailability to the fetus. - It would not achieve the necessary fetal adrenal suppression to prevent **genital virilization**. [1] *Maternal methylprednisolone* - While **methylprednisolone** can cross the placenta, it is less potent than dexamethasone and may not provide sufficient suppression of fetal adrenal androgen synthesis. - **Dexamethasone** is generally considered more effective for this specific indication due to its superior placental transfer and potency.

Question 726: HbA1C is decreased most by?

A. Thiazolidinediones
B. Sulfonylureas
C. Acarbose
D. Biguanides (Correct Answer)

Explanation: ***Biguanides***- **Metformin**, the primary biguanide, is considered a first-line agent for type 2 diabetes and can significantly lower **HbA1c** by 1.0-2.0% [1].- It primarily works by decreasing hepatic **glucose production** and increasing **insulin sensitivity** in peripheral tissues [1].*Sulfonylureas*- Sulfonylureas stimulate **insulin release** from pancreatic beta cells, thereby lowering blood glucose.- They typically decrease **HbA1c** by 1.0-2.0%, similar to biguanides, but are associated with a higher risk of **hypoglycemia** and weight gain.*Thiazolidinediones*- Thiazolidinediones (TZDs) improve **insulin sensitivity** in peripheral tissues and reduce hepatic glucose production [1].- They reduce **HbA1c** by approximately 0.5-1.5% but have a slower onset of action and are associated with side effects like **fluid retention** and weight gain [1].*Acarbose*- Acarbose is an **alpha-glucosidase inhibitor** that delays the absorption of carbohydrates in the small intestine, primarily reducing postprandial glucose excursions [2].- Its effect on **HbA1c** is more modest, typically lowering it by 0.5-0.8%, making it less potent for overall long-term glucose control compared to other agents.

Question 727: Which of the following statements about GnRH agonists is false?

A. Long acting preparations can be used as nasal spray.
B. Used in cases of precocious puberty.
C. Ganirelix is a GnRH agonist. (Correct Answer)
D. They have action similar to gonadotropin releasing hormone.

Explanation: ***Ganirelix is a GnRH agonist.*** - **Ganirelix** is a **GnRH antagonist**, meaning it blocks the GnRH receptor and immediately suppresses gonadotropin release. - GnRH agonists initially stimulate the receptor, leading to a surge, before causing downregulation and desensitization. *Used in cases of precocious puberty.* - **GnRH agonists** are indeed used to treat **precocious puberty** by downregulating the GnRH receptors and suppressing endogenous gonadotropin-releasing hormone activity, which halts pubertal progression. - This therapy induces a temporary, reversible **hypogonadotropic hypogonadism**, effectively pausing inappropriate early puberty. *Long acting preparations can be used as nasal spray.* - Some **GnRH agonists**, like **buserelin**, are available as **nasal sprays** for long-term administration. - This route of administration allows for convenience and consistent delivery, particularly in conditions requiring chronic suppression. *They have action similar to gonadotropin releasing hormone.* - **GnRH agonists** are synthetic analogs of natural **gonadotropin-releasing hormone (GnRH)**, sharing a similar molecular structure. - They bind to and stimulate the GnRH receptors in the pituitary, initially causing increased **gonadotropin** release, followed by receptor desensitization and downregulation.

Question 728: 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 729: Which of the following drugs can prevent the peripheral conversion of T4 to T3?

A. Propranolol
B. Iodides
C. a and b both
D. Propylthiouracil (Correct Answer)

Explanation: ***Propylthiouracil*** - Propylthiouracil (PTU) is a **thionamide drug** that inhibits thyroid peroxidase, thereby blocking the synthesis of thyroid hormones. - Additionally, PTU specifically inhibits the **5'-deiodinase enzyme**, which is responsible for the peripheral conversion of **thyroxine (T4)** to the more active **triiodothyronine (T3)**. - This is a **unique property** of PTU that distinguishes it from methimazole, making it preferred in thyrotoxic storm. *Propranolol* - Propranolol is a **beta-blocker** primarily used to alleviate the **symptomatic effects** of hyperthyroidism, such as palpitations, tremor, and anxiety. - Although high doses may have a minor effect on T4 to T3 conversion, this is **not clinically significant** and not the reason for its use in thyroid disorders. *Iodides* - High doses of iodides, such as **potassium iodide**, can acutely inhibit thyroid hormone release (the **Wolff-Chaikoff effect**) and decrease thyroid gland vascularity. - Iodides do **not prevent the peripheral conversion of T4 to T3**; their main action is on hormone synthesis and release from the thyroid gland itself. *a and b both* - This option is incorrect because neither propranolol nor iodides have a clinically significant effect on inhibiting peripheral 5'-deiodinase enzyme. - Only **propylthiouracil** has this specific and therapeutically relevant action.

Question 730: What is a special feature of glargine insulin?

A. It is suitable for once daily administration.
B. It is stable at physiological pH.
C. It is primarily used for basal insulin control.
D. It provides a long duration of action with a smooth, peakless effect. (Correct Answer)

Explanation: ***It provides a long duration of action with a smooth, peakless effect.*** - **Insulin glargine** is a **long-acting insulin analog** designed to provide a steady, basal insulin level over an extended period. - Its **peakless profile** minimizes the risk of hypoglycemia and offers continuous glycemic control for up to 24 hours. *It is suitable for once daily administration.* - While glargine is often administered once daily due to its **long duration of action**, this is a consequence of its pharmacological properties rather than its defining special feature. - Other long-acting insulins or even some intermediate-acting insulins can be given once daily, but glargine's strength lies in its **smooth, peakless profile**. *It is stable at physiological pH.* - **Insulin glargine** is formulated to be soluble in an acidic solution but precipitates into micro-precipitates at the **physiological pH** of subcutaneous tissue. - This precipitation allows for slow and sustained release, unlike the implication of direct stability at physiological pH. *It is primarily used for basal insulin control.* - **Basal insulin control** is indeed the primary purpose of glargine, providing a consistent background insulin level. - However, the 'special feature' is *how* it achieves this, which is through its **long duration** and **peakless profile**, making this option a consequence rather than the most distinct characteristic.

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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