Which of the following statements about glucocorticoids is true?
A 47-year-old woman presents with complaints of nervousness and increased sensitivity to hot weather. She is diagnosed with hyperthyroidism and prescribed propylthiouracil. What is the principal mechanism by which this drug acts?
Which of the following is an aromatase inhibitor?
Which antithyroid drug is preferred during the first trimester of pregnancy due to relatively lower placental transfer?
Which of the following oral antidiabetic drugs is an insulin secretagogue?
Which non-selective beta-blocker has sympathomimetic activity?
Which of the following is a PGE1 analogue used in medical treatments?
Which of the following is a long-acting beta-2 agonist?
Which triptan is available in nasal spray form?
Acetaminophen [Paracetamol] induced liver toxicity is due to which metabolite?
NEET-PG 2015 - Pharmacology NEET-PG Practice Questions and MCQs
Question 51: Which of the following statements about glucocorticoids is true?
- A. Glucocorticoids directly activate T-helper cells.
- B. Glucocorticoids have no effect on immune cells.
- C. Glucocorticoids downregulate MHC class II expression. (Correct Answer)
- D. Glucocorticoids enhance the activity of cytotoxic T cells.
Explanation: ***Glucocorticoids downregulate MHC class II expression.*** - Glucocorticoids exert **immunosuppressive effects** by reducing the expression of **MHC class II molecules** on antigen-presenting cells. - This downregulation impairs the ability of antigen-presenting cells to activate **CD4+ T-helper cells**, thereby suppressing adaptive immune responses. *Glucocorticoids directly activate T-helper cells.* - Glucocorticoids do not directly activate T-helper cells; rather, they have an **inhibitory effect** on T-cell function and proliferation. - They tend to promote **T-cell apoptosis** and reduce cytokine production, thus dampening T-helper cell responses. *Glucocorticoids have no effect on immune cells.* - This statement is incorrect as glucocorticoids have profound and widespread **immunosuppressive and anti-inflammatory effects** on various immune cells. - They influence the function, proliferation, and survival of **lymphocytes, macrophages, and granulocytes**. *Glucocorticoids enhance the activity of cytotoxic T cells.* - Glucocorticoids generally **suppress immune responses**, including the activity of **cytotoxic T cells (CTLs)**, rather than enhancing it. - They tend to inhibit the production of **interleukins** necessary for CTL activation and proliferation.
Question 52: A 47-year-old woman presents with complaints of nervousness and increased sensitivity to hot weather. She is diagnosed with hyperthyroidism and prescribed propylthiouracil. What is the principal mechanism by which this drug acts?
- A. Reducing the proteolysis of thyroglobulin.
- B. Inhibiting the binding of TSH to its receptor.
- C. Inhibiting the enzyme thyroid peroxidase, which reduces the synthesis of thyroid hormones. (Correct Answer)
- D. Altering the levels of reverse T3 (rT3) in the body.
Explanation: ***Inhibiting the enzyme thyroid peroxidase, which reduces the synthesis of thyroid hormones.*** - **Propylthiouracil (PTU)** is a **thionamide** drug that primarily acts by inhibiting the enzyme **thyroid peroxidase**. - Thyroid peroxidase is crucial for the **organification of iodide** and the **coupling of iodotyrosines** (MIT and DIT) to form T3 and T4, thus reducing the synthesis of thyroid hormones. *Inhibiting the binding of TSH to its receptor.* - This mechanism is characteristic of **TSH receptor antibodies**, which are a cause of hyperthyroidism (e.g., in Graves' disease), rather than the action of an antithyroid drug like PTU. - PTU works at the level of hormone synthesis within the thyroid gland, not at the receptor level for TSH. *Reducing the proteolysis of thyroglobulin.* - While thyroid hormones are stored as part of thyroglobulin, and their release involves proteolysis, this is not the **principal mechanism of action** for PTU. - The main effect of PTU is upstream, preventing the formation of the hormones themselves. *Altering the levels of reverse T3 (rT3) in the body.* - PTU does inhibit the **peripheral conversion of T4 to T3**, which can reduce overall T3 levels and increase rT3, but this is a **secondary mechanism**. - The primary and most significant action for reducing hyperthyroid symptoms is the direct inhibition of thyroid hormone synthesis within the gland.
Question 53: 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 54: Which antithyroid drug is preferred during the first trimester of pregnancy due to relatively lower placental transfer?
- A. Carbimazole
- B. Propylthiouracil (Correct Answer)
- C. Both
- D. None of the options
Explanation: ***Propylthiouracil*** - **Propylthiouracil (PTU)** is the preferred antithyroid drug during the **first trimester** of pregnancy because it crosses the placenta less readily than methimazole/carbimazole. - While it still crosses the placenta, its lower placental transfer and association with fewer fetal anomalies in early pregnancy make it a safer initial choice, especially to minimize the risk of **fetal embryopathy** associated with methimazole. *Carbimazole* - **Carbimazole** (which is metabolized to methimazole) can cross the placenta more easily than PTU and has been associated with **fetal anomalies**, particularly in the first trimester. - Its use is generally avoided during the first trimester due to concerns about congenital malformations such as **aplasia cutis** and **esophageal atresia**. *Both* - While both drugs can cross the placenta to some extent, their safety profiles and recommended use during pregnancy differ significantly. - Carbimazole (methimazole) has a higher risk of teratogenicity in the first trimester compared to PTU. *None of the options* - This option is incorrect because propylthiouracil is indeed known to cross the placenta and is commonly used in pregnancy, especially during the first trimester. - The choice of antithyroid drug is a critical consideration in managing hyperthyroidism in pregnancy.
Question 55: 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 56: Which non-selective beta-blocker has sympathomimetic activity?
- A. Nadolol
- B. Pindolol (Correct Answer)
- C. Acebutalol
- D. Metoprolol
Explanation: ***Pindolol*** - **Pindolol** is a **non-selective beta-blocker** that exhibits **intrinsic sympathomimetic activity (ISA)**, meaning it acts as a partial agonist at beta-adrenergic receptors. - Due to ISA, it causes less reduction in resting heart rate and cardiac output compared to beta-blockers without ISA. *Acebutalol* - **Acebutalol** is a **beta-1 selective blocker** (cardioselective) that possesses **intrinsic sympathomimetic activity (ISA)**. - While it has ISA, it is not a non-selective beta-blocker, making it an incorrect answer for this question. *Nadolol* - **Nadolol** is a **non-selective beta-blocker** that does **not** have intrinsic sympathomimetic activity (ISA). - It primarily acts as a pure antagonist at both beta-1 and beta-2 adrenergic receptors. *Metoprolol* - **Metoprolol** is a **beta-1 selective blocker** (cardioselective) and does **not** possess intrinsic sympathomimetic activity (ISA). - Its primary action is blockade of cardiac beta-1 receptors.
Question 57: Which of the following is a PGE1 analogue used in medical treatments?
- A. Carboprost
- B. Alprostadil (Correct Answer)
- C. Epoprostenol
- D. Dinoprostone
Explanation: ***Alprostadil*** - **Alprostadil** is a synthetic **prostaglandin E1 (PGE1)** analogue. - It is used in neonates to maintain the **patency of the patent ductus arteriosus** and in adults for the treatment of **erectile dysfunction**. *Carboprost* - **Carboprost** is a synthetic analogue of **prostaglandin F2 alpha (PGF2α)**. - It is primarily used to manage **postpartum hemorrhage** due to its potent uterotonic effects. *Epoprostenol* - **Epoprostenol** is a synthetic analogue of **prostacyclin (PGI2)**. - It is known for its potent **vasodilatory** and **antiplatelet** properties, making it useful in treating **pulmonary arterial hypertension**. *Dinoprostone* - **Dinoprostone** is a synthetic form of **prostaglandin E2 (PGE2)**. - It is used to **induce labor** or **cervical ripening** due to its role in uterine contractions and cervical dilation.
Question 58: Which of the following is a long-acting beta-2 agonist?
- A. Isoprenaline
- B. Ephedrine
- C. Salbutamol
- D. Formoterol (Correct Answer)
Explanation: ***Formoterol*** - **Formoterol** is a **long-acting beta-2 agonist (LABA)** commonly used in the treatment of asthma and COPD. - It provides **bronchodilation** for up to 12 hours due to its high lipophilicity, allowing it to remain in the cell membrane and continuously activate beta-2 receptors. *Isoprenaline (non-selective adrenergic agonist)* - **Isoprenaline** is a **non-selective beta-adrenergic agonist**, meaning it activates both beta-1 and beta-2 receptors. - It is **short-acting** and primarily used as a vasodilator or to stimulate heart rate, not as a long-acting bronchodilator. *Ephedrine (non-selective adrenergic agonist)* - **Ephedrine** is a **mixed-acting sympathomimetic amine** that increases the release of norepinephrine and directly stimulates alpha and beta receptors. - It has a short duration of action and is primarily used as a decongestant or bronchodilator in emergency situations, not as a long-acting agent. *Salbutamol (short-acting beta-2 agonist)* - **Salbutamol** is a **short-acting beta-2 agonist (SABA)**, providing rapid onset but a short duration of action (typically 4-6 hours). - It is used for **relieving acute bronchospasm** and is not considered a long-acting medication for maintenance therapy.
Question 59: Which triptan is available in nasal spray form?
- A. Sumatriptan (Correct Answer)
- B. Rizatriptan
- C. Naratriptan
- D. Frovatriptan
Explanation: ***Sumatriptan*** - **Sumatriptan** is available in multiple formulations, including **oral, subcutaneous injection, and nasal spray**, making it versatile for migraine treatment [1], [2]. - The nasal spray formulation allows for **faster absorption** and onset of action, which can be beneficial for patients with nausea or vomiting during migraine attacks [1]. *Rizatriptan* - **Rizatriptan** is primarily available in **oral tablet** and **orally disintegrating tablet** (ODT) forms [2]. - It does not have a commonly available nasal spray formulation for migraine treatment [2]. *Naratriptan* - **Naratriptan** is available as an **oral tablet** and is known for its **longer half-life** and generally milder side effect profile compared to sumatriptan [2]. - It is not available in a nasal spray formulation [2]. *Frovatriptan* - **Frovatriptan** is available exclusively as an **oral tablet** and is notable for having the **longest half-life** among triptans, making it useful for preventing recurring migraines [2]. - There is no nasal spray formulation for frovatriptan [2].
Question 60: Acetaminophen [Paracetamol] induced liver toxicity is due to which metabolite?
- A. Co-Q
- B. Cytochrome 'C'
- C. NAPQI (Correct Answer)
- D. N-acetylcysteine
Explanation: ***NAPQI*** - **N-acetyl-p-benzoquinone imine (NAPQI)** is a highly reactive and toxic metabolite produced during acetaminophen metabolism, especially in overdose situations [1, 3]. - When glutathione stores are depleted due to excessive NAPQI formation, this metabolite covalently binds to hepatic macromolecules, causing **hepatocellular damage and necrosis** [1, 3].*N-acetylcysteine* - **N-acetylcysteine (NAC)** is the antidote for acetaminophen overdose, not the toxic metabolite itself [2, 3]. - NAC works by replenishing hepatic **glutathione stores**, which helps detoxify NAPQI and prevent liver injury [2, 3].*Co-Q* - **Coenzyme Q10 (CoQ10)** is an endogenous antioxidant and electron carrier in the mitochondrial respiratory chain. - It is not a metabolite of acetaminophen and plays no direct role in acetaminophen-induced liver toxicity.*Cytochrome 'C'* - **Cytochrome c** is a protein involved in the electron transport chain in mitochondria and plays a critical role in apoptosis. - While cellular damage from NAPQI can eventually lead to cytochrome c release and apoptosis, cytochrome c itself is not a metabolite of acetaminophen or the direct cause of toxicity.