What is a common side effect of salmeterol?
Which of the following is NOT a function of Prostaglandin E1 (PGE1)?
Which second generation antihistaminic does not produce an active metabolite?
Which of the following is a metabolite of hydroxyzine?
Aminophylline inhibits which of the following enzymes?
Which of the following is NOT a beta-2 agonist?
Beta2-agonists cause all except:
What is the mechanism of action of Abatacept?
Why do NSAIDs cause gastric ulcers?
Which of the following is a mineralocorticoid antagonist?
NEET-PG 2013 - Pharmacology NEET-PG Practice Questions and MCQs
Question 61: What is a common side effect of salmeterol?
- A. Tremors (Correct Answer)
- B. Seizures
- C. Hypertension
- D. Hyperkalemia
Explanation: ***Tremors*** - **Salmeterol** is a **long-acting beta-2 adrenergic agonist (LABA)** that can stimulate beta-2 receptors in skeletal muscle, leading to **fine muscle tremors**. - This side effect is dose-dependent and more common with higher doses or in patients sensitive to sympathomimetic effects. *Seizures* - **Seizures** are a rare and atypical side effect of **salmeterol** and other beta-2 agonists; they are not considered a common adverse event. - While systemic absorption can occur, the central nervous system effects leading to seizures are not frequently observed. *Hypertension* - While beta-2 agonists can cause a slight increase in **heart rate** due to systemic absorption, **hypertension** is not a common side effect of inhaled salmeterol. - Other cardiovascular effects like palpitations can occur, but significant or sustained hypertension is rare. *Hyperkalemia* - **Hyperkalemia** (elevated potassium) is not a side effect of **salmeterol**; in fact, beta-2 agonists commonly cause the **opposite effect - hypokalemia** (decreased serum potassium). - Beta-2 receptor stimulation activates Na⁺-K⁺-ATPase pumps, driving potassium from serum into cells, causing transient hypokalemia. - This effect is clinically relevant and requires monitoring, especially when combined with other medications that lower potassium.
Question 62: Which of the following is NOT a function of Prostaglandin E1 (PGE1)?
- A. Plays a role in initiating puberty (Correct Answer)
- B. Modulates inflammatory responses
- C. Used in the management of erectile dysfunction
- D. Maintains the patency of the ductus arteriosus
Explanation: ***Plays a role in initiating puberty*** - **Prostaglandin E1 (PGE1)** is primarily involved in smooth muscle relaxation, vasodilation, and inflammation, and does not have a direct role in initiating **puberty**. - The initiation of puberty is mainly controlled by the **hypothalamic-pituitary-gonadal (HPG) axis** and surge of **gonadotropin-releasing hormone (GnRH)**. *Used in the management of erectile dysfunction* - **PGE1 formulations** (alprostadil) are used as a topical or intracavernosal injection to treat **erectile dysfunction** by inducing vasodilation in the penis. - Its vasodilatory effects increase blood flow to the corpora cavernosa, leading to **penile erection**. *Modulates inflammatory responses* - **PGE1** is involved in **inflammatory processes**, often exerting both pro- and anti-inflammatory effects depending on the context and specific receptors activated. - It can help to **reduce inflammation** and pain, as well as influencing immune cell function. *Maintains the patency of the ductus arteriosus* - In newborns with **congenital heart defects**, **PGE1** is administered to maintain the **patency of the ductus arteriosus**, allowing for blood flow between the aorta and pulmonary artery. - This is crucial for conditions where pulmonary or systemic blood flow is dependent on a patent ductus, bridging the infant to surgery or other interventions.
Question 63: Which second generation antihistaminic does not produce an active metabolite?
- A. Loratadine
- B. Terfenadine
- C. Cetirizine (Correct Answer)
- D. None of the options
Explanation: ***Cetirizine*** - Cetirizine is unique among second-generation antihistamines as it is an **active metabolite** of hydroxyzine and **does not undergo further significant metabolism** to an active compound. - This characteristic contributes to its relatively **predictable pharmacokinetics** and reduced potential for drug interactions related to metabolism. *Loratadine* - Loratadine is a **prodrug** that is extensively metabolized in the liver by **CYP3A4 and CYP2D6** to its active metabolite, **desloratadine**. - Desloratadine is responsible for most of the **antihistaminic effects** of loratadine. *Terfenadine* - Terfenadine is a **prodrug** that is extensively metabolized by **CYP3A4** to its active metabolite, **fexofenadine**. - Due to its **cardiotoxicity** (QT prolongation) when its metabolism was inhibited, terfenadine was withdrawn from the market, and fexofenadine was developed as a safer alternative. *None of the options* - This option is incorrect because **cetirizine** does not produce an active metabolite, making it a valid answer for the question.
Question 64: Which of the following is a metabolite of hydroxyzine?
- A. Fexofenadine
- B. Terfenadine
- C. Cetirizine (Correct Answer)
- D. Azelastine
Explanation: ***Cetirizine*** - **Cetirizine** is the principal active metabolite of **hydroxyzine**, formed through the oxidation of the primary alcohol group of hydroxyzine [2]. - Both hydroxyzine and cetirizine are **H1-receptor antagonists**, but cetirizine is a **second-generation antihistamine** known for being less sedating due to its limited ability to cross the blood-brain barrier [2]. *Fexofenadine* - **Fexofenadine** is an active metabolite of **terfenadine**, not hydroxyzine [2]. - **Fexofenadine** is a second-generation antihistamine used to treat allergies, known for its non-sedating properties [3]. *Terfenadine* - **Terfenadine** is a second-generation antihistamine that was withdrawn from the market due to its cardiotoxicity, particularly the risk of **QT prolongation** and **Torsades de Pointes**. - Its active metabolite is **fexofenadine**, which does not cause similar cardiac issues [2]. *Azelastine* - **Azelastine** is an antihistamine primarily available as a **nasal spray** for the treatment of allergic rhinitis and conjunctivitis [1], [3]. - It is not a metabolite of hydroxyzine but a distinct therapeutic compound.
Question 65: Aminophylline inhibits which of the following enzymes?
- A. MAO
- B. Alcohol dehydrogenase
- C. Cytochrome P450
- D. Phosphodiesterase (Correct Answer)
Explanation: ***Phosphodiesterase*** - **Aminophylline** is a methylxanthine derivative that primarily acts as a **phosphodiesterase (PDE) inhibitor** [1], [2]. - By inhibiting PDE, aminophylline increases intracellular levels of **cAMP** and **cGMP**, leading to **bronchodilation** and other effects [2], [3]. *MAO* - **MAO (monoamine oxidase)** inhibitors are antidepressants that prevent the breakdown of neurotransmitters like serotonin, norepinephrine, and dopamine. - Aminophylline does not significantly inhibit MAO. *Alcohol dehydrogenase* - **Alcohol dehydrogenase** is an enzyme responsible for metabolizing alcohol (ethanol) in the liver. - Aminophylline has no direct inhibitory effect on alcohol dehydrogenase. *Cytochrome P450* - **Cytochrome P450 (CYP450)** enzymes are a group of enzymes primarily involved in the metabolism of drugs and other xenobiotics in the liver [4]. - While aminophylline (and its active metabolite theophylline) can be metabolized by and *affect* certain **CYP450** isoenzymes (e.g., CYP1A2), it does not act as a general inhibitor of the entire CYP450 system; its primary therapeutic action is not through CYP450 inhibition.
Question 66: Which of the following is NOT a beta-2 agonist?
- A. Ketotifen (Correct Answer)
- B. Terbutaline
- C. Salbutamol
- D. Bambuterol
Explanation: ***Ketotifen*** - **Ketotifen** is an **oral anti-allergic drug** that acts as a **mast cell stabilizer** and **H1-antihistamine**, not a beta-2 agonist. - It is used for **prophylactic treatment** of asthma and allergic conditions, working through different mechanisms than bronchodilators. *Terbutaline* - **Terbutaline** is a **short-acting beta-2 agonist (SABA)** used for bronchodilation in asthma and COPD [2]. - Available in **oral, inhaled, and injectable forms** for rapid relief of bronchospasm. *Salbutamol* - **Salbutamol** (also known as albuterol) is a **short-acting beta-2 agonist (SABA)** and the most widely used rescue inhaler for asthma [1], [2]. - Provides **rapid bronchodilation** by stimulating beta-2 receptors in airway smooth muscles [3]. *Bambuterol* - **Bambuterol** is a **long-acting beta-2 agonist (LABA)** that is a prodrug of **terbutaline**. - It is slowly converted to the active form in the body, providing **sustained bronchodilation** for maintenance therapy.
Question 67: Beta2-agonists cause all except:
- A. Hyperkalemia (Correct Answer)
- B. Hyperglycemia
- C. Tremor
- D. Palpitation
Explanation: ***Hyperkalemia*** - Beta2-agonists actually cause **hypokalemia**, not hyperkalemia, by promoting the intracellular shift of potassium. - This effect is due to the stimulation of the **Na+/K+-ATPase pump** by beta-2 adrenergic receptors. *Hyperglycemia* - Beta2-agonists can lead to **hyperglycemia** by promoting glycogenolysis and gluconeogenesis in the liver. - They also decrease **insulin secretion** and increase insulin resistance. *Tremor* - **Tremor** is a common side effect of beta2-agonists, particularly in the hands, due to direct stimulation of beta2 receptors on skeletal muscle. - This muscle stimulation leads to increased muscle twitching and a fine tremor. *Palpitation* - **Palpitations** can occur due to the systemic absorption of beta2-agonists, leading to activation of beta1 receptors in the heart. - This can cause **tachycardia** and a sensation of a racing heart.
Question 68: What is the mechanism of action of Abatacept?
- A. Tumor necrosis factor (TNF) alpha inhibitor
- B. Monoclonal antibody against interleukin-6 (IL-6) receptor
- C. Interleukin-1 (IL-1) receptor antagonist
- D. Inhibitor of co-stimulation of T cells (Correct Answer)
Explanation: ***Inhibitor of co-stimulation of T cells*** - Abatacept is a **fusion protein** that blocks the **CD28-CD80/86 co-stimulatory pathway**, which is crucial for full T-cell activation. - By binding to **CD80** and **CD86** on antigen-presenting cells, it prevents their interaction with **CD28** on T cells, thus inhibiting T-cell proliferation and cytokine production. *Tumor necrosis factor (TNF) alpha inhibitor* - TNF alpha inhibitors (e.g., **adalimumab**, **infliximab**, **etanercept**) bind to and neutralize **TNF alpha**, a pro-inflammatory cytokine. - While used in similar conditions, their mechanism is distinct from Abatacept's T-cell co-stimulation blockade. *Monoclonal antibody against interleukin-6 (IL-6) receptor* - Drugs like **tocilizumab** target the **IL-6 receptor**, blocking the signaling of **IL-6**, another important inflammatory cytokine. - This mechanism primarily affects cytokine signaling rather than directly inhibiting T-cell activation in the same way as abatacept. *Interleukin-1 (IL-1) receptor antagonist* - **Anakinra** is an example of an **IL-1 receptor antagonist**, which competes with IL-1 for binding to its receptor, thereby blocking its pro-inflammatory effects. - This mechanism focuses on inhibiting the action of IL-1, unlike Abatacept's role in T-cell activation.
Question 69: Why do NSAIDs cause gastric ulcers?
- A. They increase gastric acid secretion
- B. They delay gastric emptying
- C. They inhibit the production of protective mucus
- D. They inhibit COX-1 and COX-2 enzymes (Correct Answer)
Explanation: ***They inhibit COX-1 and COX-2 enzymes*** - NSAIDs primarily exert their anti-inflammatory effects by inhibiting **cyclooxygenase (COX) enzymes**, specifically COX-1 and COX-2. - While COX-2 inhibition is responsible for anti-inflammatory action, **COX-1 inhibition** reduces the production of protective prostaglandins in the gastric mucosa, leading to a loss of mucosal integrity and an increased risk of ulceration. *They inhibit the production of protective mucus* - While NSAIDs do compromise the gastric mucosal barrier, their primary mechanism is not a direct inhibition of mucus production itself. - Instead, the reduced prostaglandin synthesis indirectly affects the quantity and quality of mucus and bicarbonate, which are crucial for mucosal defense. *They increase gastric acid secretion* - NSAIDs do not directly increase gastric acid secretion; in fact, some studies suggest a mild inhibitory effect. - The main problem is the diminished mucosal protection against the normal levels of gastric acid. *They delay gastric emptying* - Delaying gastric emptying is not a primary mechanism by which NSAIDs cause ulcers. - While some medications can affect gastric motility, this is not the key pathway for NSAID-induced gastropathy.
Question 70: Which of the following is a mineralocorticoid antagonist?
- A. Spironolactone (Correct Answer)
- B. Inamrinone
- C. Nicorandil
- D. Ketorolac
Explanation: ***Spironolactone*** - **Spironolactone** is a **potassium-sparing diuretic** that acts as a competitive antagonist of **aldosterone** at the mineralocorticoid receptors in the renal tubules [1], [2]. - Its primary use is in conditions like **heart failure**, **cirrhosis with ascites**, and **primary hyperaldosteronism** (Conn's syndrome) [2]. *Inamrinone* - **Inamrinone** is a **phosphodiesterase-3 inhibitor** (PDE3 inhibitor) and is classified as an **inotropic agent**. - It increases **intracellular cAMP** in cardiac cells, leading to increased **contractility** and **vasodilation**, and is used in severe heart failure. *Nicorandil* - **Nicorandil** is a **potassium channel opener** and a **nitrate-like drug** that causes both venous and arterial vasodilation. - It is primarily used as an **antianginal agent** due to its ability to reduce cardiac workload and improve coronary blood flow. *Ketorolac* - **Ketorolac** is a **nonsteroidal anti-inflammatory drug (NSAID)** that primarily inhibits **cyclooxygenase (COX) enzymes**. - It is used for **short-term management of acute moderate to severe pain** and has no direct activity on mineralocorticoid receptors.