Respiratory System Drugs — MCQs
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Which of the following is a leukotriene antagonist?
What adverse effect is commonly seen in theophylline overdose?
Which component of the management protocol of status asthmaticus has now been shown to be useless?
Compared to unfractionated heparin, low molecular weight heparins:
Which H1 receptor blocker has the least sedative action?
Which of the following drugs is not used in the treatment of bronchial asthma?
Omalizumab is:
Which of the following drugs used in asthma is not a bronchodilator?
Disodium cromoglycate is used by which of the following routes?
Which of the following is NOT an adverse effect of salbutamol?
Respiratory System Drugs Indian Medical PG Practice Questions and MCQs
Question 131: Which of the following is a leukotriene antagonist?
- A. Montelukast (Correct Answer)
- B. Zileuton
- C. Omalizumab
- D. Nedocromil
Explanation: ### Explanation **Correct Option: A. Montelukast** Montelukast and Zafirlukast are selective and competitive **CysLT₁ receptor antagonists**. In the pathophysiology of asthma, cysteinyl leukotrienes (LTC₄, LTD₄, and LTE₄) are potent bronchoconstrictors that also increase mucus secretion and vascular permeability. By blocking the CysLT₁ receptor, Montelukast effectively inhibits these actions. It is particularly useful for prophylaxis in chronic asthma, aspirin-induced asthma, and exercise-induced bronchospasm. **Analysis of Incorrect Options:** * **B. Zileuton:** While it acts on the leukotriene pathway, it is not an *antagonist*. It is a **5-Lipoxygenase (5-LOX) inhibitor**, preventing the synthesis of leukotrienes from arachidonic acid. * **C. Omalizumab:** This is a **humanized monoclonal antibody against IgE**. It binds to free IgE in the blood, preventing it from attaching to mast cells, and is used in severe, refractory allergic asthma. * **D. Nedocromil:** This is a **Mast Cell Stabilizer**. It prevents the degranulation of mast cells and the subsequent release of inflammatory mediators like histamine and leukotrienes. **High-Yield Clinical Pearls for NEET-PG:** * **Churg-Strauss Syndrome:** Rare association with leukotriene antagonists (often due to tapering of systemic steroids). * **Neuropsychiatric Events:** Montelukast has a FDA boxed warning for serious side effects like agitation, aggression, and suicidal ideation. * **Aspirin-Exacerbated Respiratory Disease (AERD):** Leukotriene antagonists are the preferred add-on therapy for patients with the "Samter’s Triad" (Asthma, Nasal Polyps, and Aspirin sensitivity). * **Administration:** Montelukast is typically given once daily in the evening.
Question 132: What adverse effect is commonly seen in theophylline overdose?
- A. Bradycardia
- B. Seizures (Correct Answer)
- C. Drowsiness
- D. Bronchospasm
Explanation: **Explanation:** Theophylline is a methylxanthine derivative with a **narrow therapeutic index** (10–20 µg/mL). Its mechanism involves non-selective inhibition of phosphodiesterase (PDE) and antagonism of adenosine receptors. **Why Seizures are the Correct Answer:** In cases of overdose (toxicity), theophylline acts as a potent Central Nervous System (CNS) stimulant. By antagonizing adenosine receptors—which normally act as inhibitory neuromodulators in the brain—theophylline lowers the seizure threshold. **Seizures** are a hallmark of severe toxicity and are often refractory to standard anticonvulsants. They can occur suddenly without premonitory symptoms when serum levels exceed 40–60 µg/mL. **Analysis of Incorrect Options:** * **A. Bradycardia:** Theophylline causes **tachycardia** and arrhythmias (e.g., SVT, PVCs) due to increased cAMP in cardiac tissue and catecholamine release. * **C. Drowsiness:** As a stimulant related to caffeine, theophylline causes **insomnia, restlessness, and agitation**, rather than sedation or drowsiness. * **D. Bronchospasm:** Theophylline is a **bronchodilator** used to treat asthma and COPD; it does not cause bronchospasm. **High-Yield Clinical Pearls for NEET-PG:** * **Metabolism:** It follows zero-order kinetics in overdose. * **Drug Interactions:** Levels are **increased** by Enzyme Inhibitors (Cimetidine, Erythromycin, Ciprofloxacin) and **decreased** by Enzyme Inducers (Rifampicin, Phenytoin) and smoking. * **Management:** For severe toxicity (seizures/arrhythmias), **Hemoperfusion** is the treatment of choice to rapidly clear the drug from the blood.
Question 133: Which component of the management protocol of status asthmaticus has now been shown to be useless?
- A. Intravenous aminophylline (Correct Answer)
- B. Intravenous hydrocortisone
- C. Nebulized ipratropium bromide
- D. Nebulized salbutamol
Explanation: **Explanation:** The management of status asthmaticus (Acute Severe Asthma) has evolved significantly. **Intravenous Aminophylline** was once a mainstay of treatment, but current guidelines (GINA and British Thoracic Society) have largely relegated it to a "last-resort" status or labeled it as **useless/obsolete** in the initial emergency protocol. **Why Aminophylline is considered "useless" in this context:** 1. **Narrow Therapeutic Index:** It requires frequent blood monitoring to avoid life-threatening toxicity (arrhythmias and seizures). 2. **Lack of Added Benefit:** Clinical trials have shown that IV aminophylline does not provide additional bronchodilation when added to optimal doses of inhaled $\beta_2$-agonists, but it significantly increases the risk of adverse effects. 3. **Superior Alternatives:** Inhaled SABA and systemic steroids are more effective and safer. **Analysis of Incorrect Options:** * **B. IV Hydrocortisone:** Systemic corticosteroids are **mandatory** in status asthmaticus. They reduce airway inflammation and upregulate $\beta_2$-receptors, though they take 4–6 hours to act. * **C. Nebulized Ipratropium Bromide:** Adding an anticholinergic to a SABA (like Salbutamol) produces a synergistic effect, further improving FEV1 and reducing hospitalization rates in severe attacks. * **D. Nebulized Salbutamol:** This is the **first-line treatment** (Short-Acting $\beta_2$ Agonist) for rapid bronchodilation. **High-Yield Clinical Pearls for NEET-PG:** * **Drug of Choice (Acute Attack):** Inhaled Salbutamol (SABA). * **Most Important Life-Saving Drug:** Systemic Corticosteroids. * **Magnesium Sulfate (IV):** Used in severe cases not responding to initial therapy (acts by inhibiting calcium influx into smooth muscles). * **Aminophylline Toxicity:** Characterized by persistent vomiting, cardiac arrhythmias, and intractable seizures.
Question 134: Compared to unfractionated heparin, low molecular weight heparins:
- A. Are absorbed more uniformly when given subcutaneously. (Correct Answer)
- B. Require more frequent laboratory monitoring.
- C. Can be given to patients with heparin-induced thrombocytopenia.
- D. Predispose to a higher risk of osteopenia.
Explanation: **Explanation:** Low Molecular Weight Heparins (LMWHs), such as Enoxaparin and Dalteparin, are derived from the fractionation of Unfractionated Heparin (UFH). Their pharmacological profile offers several advantages over UFH: **1. Why Option A is Correct:** LMWHs have **superior and more predictable bioavailability** (~90%) when administered subcutaneously compared to UFH (~20-30%). This is because LMWHs have lower non-specific binding to plasma proteins, macrophages, and endothelial cells. This uniform absorption allows for **fixed weight-based dosing** without the need for constant titration. **2. Why the other options are incorrect:** * **Option B:** LMWHs have a predictable dose-response relationship; therefore, **routine laboratory monitoring (aPTT) is not required**. Monitoring (Anti-Xa levels) is only reserved for special cases like renal failure or pregnancy. * **Option C:** LMWHs exhibit **high cross-reactivity** with UFH antibodies. Therefore, they are strictly contraindicated in patients with Heparin-Induced Thrombocytopenia (HIT). Alternatives like Fondaparinux or Argatroban should be used instead. * **Option D:** LMWHs have a **lower risk of osteopenia** and osteoporosis compared to UFH, as they have less effect on osteoblast activity and bone resorption. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** LMWHs mainly inhibit **Factor Xa** (Ratio of Xa:IIa activity is 3:1), whereas UFH inhibits both Xa and IIa equally (1:1). * **Elimination:** LMWHs are primarily **renally excreted**. They are contraindicated in chronic kidney disease (CrCl <30 ml/min); UFH is preferred in such patients. * **Antidote:** Protamine sulfate completely neutralizes UFH but only **partially neutralizes** LMWH. * **Half-life:** LMWHs have a longer half-life (4–6 hours) compared to UFH (1–2 hours).
Question 135: Which H1 receptor blocker has the least sedative action?
- A. Terfenadine (Correct Answer)
- B. Promethazine
- C. Astemizole
- D. Chlorpheniramine
Explanation: **Explanation:** The sedative potential of H1 antihistamines is primarily determined by their ability to cross the **blood-brain barrier (BBB)** and their affinity for central H1 receptors. **Why Terfenadine is correct:** Terfenadine is a **second-generation antihistamine**. Unlike first-generation drugs, second-generation agents have high molecular weights, are substrates for the P-glycoprotein efflux pump, and possess low lipid solubility. This prevents them from crossing the BBB in significant quantities, resulting in minimal to no sedative effects. Among the options provided, Terfenadine has the least central nervous system penetration. **Analysis of Incorrect Options:** * **Promethazine:** A first-generation antihistamine with high lipid solubility. It crosses the BBB easily and is highly sedative. It is often used clinically for its sedative and anti-emetic properties. * **Chlorpheniramine:** A potent first-generation antihistamine. While less sedative than Promethazine, it still causes significant drowsiness and is a common component of "night-time" cough syrups. * **Astemizole:** Like Terfenadine, this is a second-generation antihistamine. However, in comparative pharmacological profiles, Terfenadine is traditionally cited as having the least sedative potential among these specific choices. (Note: Both Terfenadine and Astemizole are now largely withdrawn due to cardiotoxicity). **High-Yield NEET-PG Pearls:** * **Cardiotoxicity:** Both Terfenadine and Astemizole were withdrawn from many markets because they block delayed rectifier K+ channels in the heart, leading to **QT interval prolongation** and **Torsades de Pointes**, especially when co-administered with CYP3A4 inhibitors (e.g., Ketoconazole, Erythromycin). * **Active Metabolites:** To avoid cardiotoxicity, their active metabolites were developed: **Fexofenadine** (from Terfenadine) and **Desloratadine** (from Loratadine). These are the preferred non-sedating agents today. * **P-glycoprotein:** This is the key efflux transporter that keeps second-generation antihistamines out of the brain.
Question 136: Which of the following drugs is not used in the treatment of bronchial asthma?
- A. Beta2 agonists
- B. Corticosteroids
- C. Cholinesterase inhibitors (Correct Answer)
- D. Phosphodiesterase inhibitors
Explanation: **Explanation:** The correct answer is **Cholinesterase inhibitors**. **1. Why Cholinesterase inhibitors are NOT used:** Bronchial asthma is characterized by reversible airway obstruction and hyper-responsiveness. Airway tone is regulated by the parasympathetic nervous system via acetylcholine acting on **M3 receptors**, which causes **bronchoconstriction** and increased mucus secretion. Cholinesterase inhibitors (e.g., Neostigmine, Physostigmine) prevent the breakdown of acetylcholine, leading to its accumulation. This exacerbates bronchospasm, making these drugs **contraindicated** in asthma. Conversely, *Anticholinergics* (like Ipratropium) are used to promote bronchodilation. **2. Analysis of Incorrect Options:** * **Beta2 agonists (e.g., Salbutamol, Salmeterol):** These are the mainstay of treatment. They stimulate Gs-coupled receptors, increasing intracellular cAMP, which leads to potent bronchodilation. * **Corticosteroids (e.g., Fluticasone, Prednisolone):** These are the most effective anti-inflammatory agents for asthma. They reduce mucosal edema and bronchial hyper-reactivity by inhibiting cytokine production. * **Phosphodiesterase (PDE) inhibitors (e.g., Theophylline):** These inhibit the enzyme PDE (mainly PDE3 and PDE4), preventing the breakdown of cAMP. Higher cAMP levels result in bronchodilation and anti-inflammatory effects. **3. NEET-PG High-Yield Pearls:** * **Drug of Choice (Acute Attack):** Inhaled short-acting beta2 agonists (SABA) like Salbutamol. * **Drug of Choice (Prophylaxis/Maintenance):** Inhaled Corticosteroids (ICS). * **Zileuton:** A 5-Lipoxygenase inhibitor used in asthma. * **Montelukast:** A Leukotriene receptor antagonist (CysLT1), particularly useful in aspirin-induced and exercise-induced asthma. * **Omalizumab:** An anti-IgE monoclonal antibody used in severe extrinsic asthma.
Question 137: Omalizumab is:
- A. Anti-IgM antibody
- B. Anti-IgG antibody
- C. Anti-IgE antibody (Correct Answer)
- D. Anti-IgD antibody
Explanation: <h3>Explanation</h3><p><strong>Correct Option: C. Anti-IgE antibody</strong></p><p><strong>Mechanism of Action:</strong> Omalizumab is a <strong>recombinant DNA-derived humanized monoclonal antibody</strong> that selectively binds to free human <strong>Immunoglobulin E (IgE)</strong> in the blood and interstitial fluid [1]. By binding to the Fc region of IgE, it prevents IgE from attaching to the high-affinity IgE receptors (<strong>FcεRI</strong>) on the surface of <strong>mast cells and basophils</strong>. This prevents the subsequent degranulation and release of inflammatory mediators (like histamine and leukotrienes) that trigger an asthma attack [2].</p><p><strong>Why Other Options are Incorrect:</strong></p><ul><li><strong>Option A (Anti-IgM):</strong> IgM is the first antibody produced in an immune response; it is not the primary mediator of Type I hypersensitivity (allergic) reactions.</li><li><strong>Option B (Anti-IgG):</strong> IgG is the most abundant circulating antibody. While involved in various immune responses, it is not the target for treating allergic asthma.</li><li><strong>Option D (Anti-IgD):</strong> IgD functions primarily as an antigen receptor on B cells; it has no established role in the pathogenesis of asthma.</li></ul><p><strong>High-Yield Clinical Pearls for NEET-PG:</strong></p><ul><li><strong>Indications:</strong> Used in <strong>moderate-to-severe persistent allergic asthma</strong> that is inadequately controlled by inhaled corticosteroids (Step 5 of GINA guidelines). It is also approved for <strong>Chronic Spontaneous Urticaria (CSU)</strong> [3].</li><li><strong>Route of Administration:</strong> Subcutaneous (S.C.) injection every 2–4 weeks.</li><li><strong>Key Side Effect:</strong> The most serious (though rare) side effect is <strong>anaphylaxis</strong>; patients must be monitored after injection.</li><li><strong>Diagnostic Requirement:</strong> Before starting Omalizumab, a patient must have a <strong>positive skin test</strong> or <em>in vitro</em> reactivity to a perennial aeroallergen and a specific range of <strong>total serum IgE levels</strong>.</li></ul>
Question 138: Which of the following drugs used in asthma is not a bronchodilator?
- A. Salbutamol
- B. Beclomethasone (Correct Answer)
- C. Theophylline
- D. Ipratropium
Explanation: **Explanation:** The management of bronchial asthma involves two main categories of drugs: **Bronchodilators** (relievers) and **Anti-inflammatory agents** (controllers). **Why Beclomethasone is the correct answer:** Beclomethasone is an **Inhaled Corticosteroid (ICS)**. Its primary mechanism of action is to reduce airway inflammation, mucosal edema, and bronchial hyper-responsiveness by inhibiting the release of inflammatory mediators (cytokines, leukotrienes). It does **not** cause direct relaxation of the bronchial smooth muscle; therefore, it is not a bronchodilator. It is used as a long-term "controller" medication to prevent attacks rather than treating acute bronchospasm. **Analysis of Incorrect Options:** * **Salbutamol:** A Short-Acting Beta-2 Agonist (SABA). It stimulates $\beta_2$ receptors in the lungs, increasing cAMP and leading to rapid relaxation of bronchial smooth muscle. It is the drug of choice for acute asthma attacks. * **Theophylline:** A Methylxanthine. It acts by inhibiting the enzyme phosphodiesterase (PDE), leading to increased cAMP levels, and by antagonizing adenosine receptors, resulting in bronchodilation. * **Ipratropium:** An Anticholinergic (LAMA/SAMA). It blocks M3 muscarinic receptors in the bronchial smooth muscle, inhibiting vagally-mediated bronchoconstriction. **NEET-PG High-Yield Pearls:** * **Drug of Choice (DOC) for Acute Asthma:** Inhaled SABA (Salbutamol). * **DOC for Chronic Maintenance:** Inhaled Corticosteroids (e.g., Beclomethasone, Budesonide). * **Steroid Sparing Effect:** Corticosteroids upregulate $\beta_2$ receptors, preventing the tachyphylaxis (tolerance) often seen with chronic SABA use. * **Side Effect:** A common side effect of inhaled beclomethasone is **oropharyngeal candidiasis** (thrush); patients are advised to rinse their mouths after use.
Question 139: Disodium cromoglycate is used by which of the following routes?
- A. Inhalation (Correct Answer)
- B. Oral
- C. Intravenous
- D. Intramuscular
Explanation: **Explanation:** **Disodium cromoglycate (DSCG)** is a **mast cell stabilizer** used primarily in the prophylactic management of bronchial asthma. 1. **Why Inhalation is Correct:** Disodium cromoglycate is highly polar and poorly absorbed from the gastrointestinal tract (less than 1%). To achieve therapeutic concentrations at the target site—the bronchial mucosa—it must be administered directly via **inhalation**. It works by stabilizing the membrane of sensitized mast cells, preventing the degranulation and release of inflammatory mediators like histamine and leukotrienes (LTC4, LTD4) triggered by allergens. It is available as a pressurized metered-dose inhaler (pMDI) or as a fine powder via a Spinhaler. 2. **Why Other Options are Incorrect:** * **Oral:** Due to its highly ionized nature, oral bioavailability is negligible (<1%), making it ineffective for systemic or respiratory action via this route. * **Intravenous/Intramuscular:** Injectable formulations are not used because the drug's primary utility is local mucosal stabilization. Furthermore, its short half-life would require frequent dosing if given systemically. **High-Yield Clinical Pearls for NEET-PG:** * **Prophylaxis Only:** DSCG is **not a bronchodilator**; it is useless in acute attacks of asthma (Status Asthmaticus). * **Mechanism:** It inhibits "Cl⁻ channels" in mast cells, preventing the calcium influx necessary for degranulation. * **Other Uses:** It is used topically for allergic rhinitis (nasal spray) and allergic conjunctivitis (eye drops). * **Side Effects:** The most common side effect is local irritation, cough, or bronchospasm caused by the inhalation of the dry powder itself.
Question 140: Which of the following is NOT an adverse effect of salbutamol?
- A. Tachycardia
- B. Tolerance
- C. Hypokalemia
- D. Hypoglycemia (Correct Answer)
Explanation: Salbutamol is a short-acting **eta_2$-selective agonist** primarily used as a bronchodilator [1, 2]. To understand its adverse effects, one must look at the systemic distribution of eta_2 receptors. **Why Hypoglycemia is the Correct Answer:** Salbutamol actually causes **Hyperglycemia**, not hypoglycemia. Stimulation of eta_2 receptors in the liver promotes **glycogenolysis** (breakdown of glycogen to glucose) and **gluconeogenesis**. It also stimulates the release of glucagon. Therefore, hypoglycemia is not an adverse effect of this drug. **Analysis of Incorrect Options:** * **Tachycardia:** Although selective for eta_2, high doses of salbutamol cause "cross-reactivity" with eta_1 receptors in the heart. Additionally, eta_2 stimulation causes peripheral vasodilation, leading to **reflex tachycardia**. * **Tolerance:** Prolonged or excessive use of eta_2 agonists leads to **downregulation (internalization)** of the receptors, resulting in tachyphylaxis or decreased clinical responsiveness. * **Hypokalemia:** eta_2 stimulation activates the **Na+/K+ ATPase pump**, driving potassium from the extracellular fluid into the skeletal muscles. This effect is actually utilized clinically to treat hyperkalemia. **NEET-PG High-Yield Pearls:** * **Muscle Tremors:** The most common side effect of salbutamol (due to eta_2 stimulation in skeletal muscles). * **Drug of Choice:** Salbutamol is the DOC for **acute asthma exacerbations** (rescue inhaler) [1]. * **Metabolic Effects:** Expect hyperglycemia, hypokalemia, and hypomagnesemia. * **Safety:** It is considered safe in pregnancy for treating asthma.
Practice by Chapter
Bronchodilators
Practice Questions
Corticosteroids in Respiratory Disorders
Practice Questions
Anti-inflammatory Respiratory Agents
Practice Questions
Mast Cell Stabilizers
Practice Questions
Leukotriene Modifiers
Practice Questions
Antitussives and Expectorants
Practice Questions
Nasal Decongestants
Practice Questions
Pulmonary Surfactants
Practice Questions
Drugs for Pulmonary Hypertension
Practice Questions
Oxygen Therapy
Practice Questions
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