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 diuretic is known to cause the maximum potassium loss?
Which of the following is a PGE1 analogue used in medical treatments?
Most common renal sequela of lithium toxicity is?
Which triptan is available in nasal spray form?
Acetaminophen [Paracetamol] induced liver toxicity is due to which metabolite?
Which of the following is the most characteristic sexual side effect of SSRIs?
NEET-PG 2015 - Pharmacology NEET-PG Practice Questions and MCQs
Question 41: 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 42: 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 43: 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 44: 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 45: Which diuretic is known to cause the maximum potassium loss?
- A. Spironolactone
- B. Furosemide (Correct Answer)
- C. Thiazide diuretics
- D. Acetazolamide
Explanation: ***Furosemide*** - Furosemide is a **loop diuretic** that inhibits the Na-K-2Cl cotransporter in the **thick ascending limb of the loop of Henle**, leading to significant excretion of sodium, chloride, potassium, and water. - Its potent diuresis and impact on potassium reabsorption result in a **high risk of hypokalemia**. *Thiazide* - Thiazide diuretics inhibit the **Na-Cl cotransporter** in the **distal convoluted tubule**, causing moderate sodium and water excretion, and some potassium loss. - While they can cause hypokalemia, their effect on potassium excretion is generally **less pronounced than loop diuretics**. *Acetazolamide* - Acetazolamide is a **carbonic anhydrase inhibitor** that acts primarily in the **proximal tubule**, inhibiting bicarbonate reabsorption and leading to increased excretion of bicarbonate, sodium, potassium, and water. - The potassium loss is due to increased delivery of sodium to the collecting duct, leading to enhanced potassium secretion, but it is typically **less severe than with loop diuretics**. *Spironolactone* - Spironolactone is a **potassium-sparing diuretic** that acts as an **aldosterone antagonist** in the collecting duct, inhibiting sodium reabsorption and potassium secretion. - Instead of causing potassium loss, spironolactone actually **conserves potassium** and can lead to hyperkalemia.
Question 46: 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 47: Most common renal sequela of lithium toxicity is?
- A. Renal tubular acidosis
- B. Glycosuria
- C. MPGN
- D. Nephrogenic Diabetes Insipidus (Correct Answer)
Explanation: ***Nephrogenic Diabetes Insipidus*** - **Lithium** interferes with the action of **ADH** on the renal tubules, specifically at the **collecting ducts**, leading to an inability to concentrate urine. - This results in **polyuria** (excessive urination) and **polydipsia** (excessive thirst), characteristic symptoms of **nephrogenic diabetes insipidus**. *Renal tubular acidosis* - While lithium can affect tubular function, **renal tubular acidosis** is less common than nephrogenic diabetes insipidus. - RTA involves impaired acid excretion or bicarbonate reabsorption, leading to **metabolic acidosis**. *Glycosuria* - **Glycosuria** (glucose in urine) is primarily associated with **diabetes mellitus** or other conditions affecting glucose reabsorption in the proximal tubule. - Lithium toxicity does not typically cause glycosuria. *MPGN* - **Membranoproliferative glomerulonephritis (MPGN)** is a type of glomerular injury characterized by specific changes in the glomerulus. - MPGN is not directly caused by **lithium toxicity**; lithium primarily affects tubular function rather than glomerular structure.
Question 48: 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 49: 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.
Question 50: Which of the following is the most characteristic sexual side effect of SSRIs?
- A. Retrograde ejaculation
- B. Erectile dysfunction
- C. Delayed ejaculation (Correct Answer)
- D. Anxiety
Explanation: ***Delayed ejaculation*** - **Delayed ejaculation** is a common and characteristic sexual side effect of SSRIs due to their impact on serotonin pathways involved in sexual response. - This effect can lead to significant distress and non-adherence to treatment, and often requires dose adjustment or switching to an alternative antidepressant. *Erectile dysfunction* - While **erectile dysfunction** can occur with SSRIs, it is a less specific and less consistently reported sexual side effect compared to ejaculatory dysfunction. - Many factors, including underlying mood disorder and comorbidities, can contribute to erectile dysfunction, making it less characteristic of SSRI use alone. *Retrograde ejaculation* - **Retrograde ejaculation** is a condition where semen enters the bladder during orgasm, and while it can be a side effect of some medications (e.g., alpha-blockers), it is not a hallmark sexual side effect of SSRIs. - SSRIs primarily affect the process of emission and expulsion, leading more commonly to delayed or absent ejaculation rather than retrograde flow. *Anxiety* - **Anxiety** is generally a *primary symptom* of the conditions SSRIs are prescribed to treat, such as depression or anxiety disorders, not a sexual side effect of the medication itself. - Although SSRIs can initially cause or worsen anxiety in some patients before therapeutic effects are seen, this is a systemic side effect, not a sexual one.