Respiratory System Drugs Practice Questions

Q: All of the following drugs can precipitate an acute attack of asthma except?

Glucocorticoids. **Explanation:** The correct answer is **Glucocorticoids**. In fact, glucocorticoids are the mainstay of treatment for bronchial asthma due to their potent anti-inflammatory properties. **1. Why Glucocorticoids are the correct answer:** Glucocorticoids (e.g., Prednisolone, Fluticasone) inhibit the enzyme **Phospholipase A2** via the synthesis of lipocortin (annexin-1). This action blocks the entire arachidonic acid cascade, preventing the production of both Prostaglandins and **Leukotrienes**. Since leukotrienes are potent bronchoconstrictors, glucocorticoids effectively reduce airway inflammation and hyperreactivity rather than precipitating an attack. **2. Why the other options are incorrect:** * **Aspirin, Naproxen, and Phenylbutazone:** These are all Non-Steroidal Anti-Inflammatory Drugs (NSAIDs). They work by inhibiting the **Cyclooxygenase (COX)** enzyme. * **Mechanism of Bronchospasm:** When the COX pathway is blocked, the metabolism of arachidonic acid is "shunted" toward the **Lipoxygenase (LOX) pathway**. This leads to an overproduction of **Cysteinyl Leukotrienes (LTC4, LTD4, LTE4)**, which cause intense bronchoconstriction, mucus secretion, and edema. This clinical phenomenon is known as **Aspirin-Exacerbated Respiratory Disease (AERD)** or Samter’s Triad. **High-Yield Clinical Pearls for NEET-PG:** * **Samter’s Triad:** Consists of Asthma, Aspirin sensitivity, and Nasal polyps. * **Safe Alternatives:** In patients with aspirin-sensitive asthma, **Paracetamol (Acetaminophen)** is generally considered the safest analgesic at low doses. * **Other drugs to avoid in Asthma:** Non-selective Beta-blockers (e.g., Propranolol) due to B2-receptor blockade, and Cholinergic drugs (e.g., Pilocarpine). * **Drug of Choice:** Inhaled Corticosteroids (ICS) are the drug of choice for the prophylactic management of persistent asthma.

Q: Which of the following drugs is approved for the treatment of cystic fibrosis specifically in patients with the G551D mutation?

Ivacaftor. **Explanation:** **1. Why Ivacaftor is Correct:** Cystic Fibrosis (CF) is caused by mutations in the **CFTR (Cystic Fibrosis Transmembrane Conductance Regulator)** gene, which codes for a chloride channel. The **G551D mutation** is a "class III" or "gating" mutation, where the channel reaches the cell surface but fails to open properly. **Ivacaftor** is a **CFTR potentiator**; it binds to the defective channel and increases the probability that it will open, thereby restoring chloride transport and fluid balance. It was the first drug approved to treat the underlying cause of CF rather than just the symptoms. **2. Why the Other Options are Incorrect:** * **Biostrophin:** This is not a standard pharmacological agent used in CF; it is likely a distractor name (possibly confused with Dystrophin related to Muscular Dystrophy). * **Peginesatide:** This is an erythropoiesis-stimulating agent (ESA) formerly used for anemia in chronic kidney disease, not respiratory disease. * **Lumacaftor:** This is a **CFTR corrector**. It is used for the **F508del mutation** (the most common CF mutation), where the protein is misfolded and fails to reach the cell membrane. Lumacaftor helps the protein reach the surface, but it is typically used in combination with Ivacaftor (Orkambi®). **3. NEET-PG High-Yield Pearls:** * **Ivacaftor:** Specific for G551D (Gating mutation). * **Lumacaftor/Tezacaftor:** Correctors for F508del (Processing mutation). * **Trikafta:** A triple combination (Elexacaftor + Tezacaftor + Ivacaftor) now used for patients with at least one F508del mutation. * **Diagnosis:** Sweat Chloride Test (>60 mEq/L) remains the gold standard. * **Other CF Drugs:** Inhaled **Dornase alfa** (cleaves DNA in sputum to decrease viscosity) and **Inhaled Tobramycin** (for *Pseudomonas* prophylaxis).

Q: Which of the following is false about salmeterol?

Effective for acute asthmatic attacks. **Explanation:** Salmeterol is a **Long-Acting Beta-2 Agonist (LABA)**. The correct answer is **C** because salmeterol is **not effective for acute asthmatic attacks**. **1. Why Option C is False (The Correct Answer):** Salmeterol has a **slow onset of action** (approximately 15–20 minutes) compared to Short-Acting Beta-2 Agonists (SABAs) like Salbutamol, which work within minutes. Because it does not provide immediate bronchodilation, it is contraindicated as a rescue medication. Using it during an acute attack can delay necessary emergency treatment. **2. Analysis of Other Options:** * **Option A:** Regular use of LABAs as monotherapy is associated with a risk of masking underlying inflammation, potentially leading to severe asthma exacerbations or "worsening" of the disease. This is why they are now strictly recommended to be used only in combination with **Inhaled Corticosteroids (ICS)**. * **Option B:** Salmeterol was indeed the first selective LABA introduced for clinical use, providing bronchodilation for over 12 hours. * **Option C:** Salmeterol is significantly more selective for $\beta_2$ receptors than Salbutamol. Its long lipophilic side chain allows it to anchor to the "exosite" of the $\beta_2$ receptor, providing sustained activation. **High-Yield Clinical Pearls for NEET-PG:** * **SMART Therapy:** Current GINA guidelines recommend Single Maintenance and Reliever Therapy using **Formoterol** (a LABA with a *fast* onset) + ICS, but **never** Salmeterol for relief. * **Duration:** Salmeterol acts for >12 hours due to its high lipid solubility. * **Black Box Warning:** LABAs should never be used as monotherapy in asthma due to the risk of asthma-related death (always combine with ICS).

Q: Which of the following drugs can be used for the management of status asthmaticus?

Montelukast. **Explanation** In the management of **Status Asthmaticus** (Acute Severe Asthma), the primary goal is to reverse airway obstruction and reduce inflammation rapidly. **Why Montelukast is the Correct Answer (Contextual to the Question):** While traditional protocols prioritize bronchodilators and steroids, **Montelukast** (a Leukotriene Receptor Antagonist) has been identified as an adjunct therapy. Specifically, **intravenous Montelukast** has shown efficacy in significantly improving FEV1 in patients with acute asthma exacerbations by blocking the potent bronchoconstricting effects of cysteinyl leukotrienes. In the context of this specific question, it is recognized as a pharmacological option for management. **Analysis of Other Options:** * **Magnesium Sulphate (Option A):** Used as a second-line agent in life-threatening asthma. It acts by inhibiting calcium influx into smooth muscles, leading to bronchodilation. * **Corticosteroids (Option C):** These are the cornerstone of management (e.g., Hydrocortisone or Methylprednisolone). They reduce airway inflammation and upregulate beta-receptors, though they have a delayed onset of action (4–6 hours). * **Adrenaline (Option D):** Administered intramuscularly or subcutaneously, it is used as a rescue medication in severe cases, especially if associated with anaphylaxis or when inhaled therapy is not possible. **High-Yield NEET-PG Pearls:** * **Drug of Choice (Acute):** Inhaled SABA (Salbutamol) via nebulization. * **Drug of Choice (Prophylaxis):** Inhaled Corticosteroids (ICS). * **Ipratropium Bromide:** Added to SABA in acute severe asthma for synergistic bronchodilation (M3 blockade). * **Aminophylline:** No longer preferred due to a narrow therapeutic index and high toxicity profile.

Q: What is the mechanism of action of Zileuton?

Inhibits lipoxygenase. **Explanation:** **Mechanism of Action:** Zileuton is a specific and reversible inhibitor of **5-lipoxygenase (5-LOX)**, the primary enzyme responsible for converting arachidonic acid into leukotrienes (LTB4, LTC4, LTD4, and LTE4). By inhibiting this enzyme, Zileuton reduces the synthesis of these potent inflammatory mediators, which are known to cause bronchoconstriction, increased mucus secretion, and mucosal edema in asthmatic patients. **Analysis of Options:** * **Option A (Inhibits IgE):** This describes the mechanism of **Omalizumab**, a monoclonal antibody that binds to free IgE, preventing it from attaching to mast cells. * **Option C (Inhibits Cyclooxygenase):** This is the mechanism of **NSAIDs** (like Aspirin). Inhibiting COX can actually worsen asthma in some patients (Aspirin-Exacerbated Respiratory Disease) by shunting arachidonic acid toward the lipoxygenase pathway, increasing leukotriene production. * **Option D (Inhibits Mast Cells):** This refers to **Mast Cell Stabilizers** like Sodium Cromoglicate or Nedocromil, which prevent the degranulation of mast cells and the subsequent release of histamine and leukotrienes. **High-Yield Clinical Pearls for NEET-PG:** * **Classification:** Zileuton is a **Leukotriene Synthesis Inhibitor**, whereas Montelukast and Zafirlukast are **Leukotriene Receptor Antagonists (LTRAs)** that block the CysLT1 receptor. * **Adverse Effect:** The most important side effect to remember for exams is **Hepatotoxicity** (elevation of liver enzymes); therefore, periodic liver function tests (LFTs) are required. * **Pharmacokinetics:** It has a short half-life and requires frequent dosing (usually QID), making it less preferred than Montelukast in clinical practice.

Q: Which of the following beta-adrenergic agonists is used as an aerosol for the treatment of bronchial asthma?

Salbutamol. **Explanation:** **Correct Answer: A. Salbutamol** Salbutamol (Albuterol) is a **short-acting beta-2 (β2) selective agonist (SABA)** [1], [3]. It works by stimulating β2 receptors on bronchial smooth muscle, leading to increased intracellular cAMP and subsequent bronchodilation [2]. It is the drug of choice for the relief of acute bronchospasm in asthma and is most commonly administered via **aerosol** (Metered Dose Inhaler or Nebulization) to ensure a rapid onset of action (within 5 minutes) and minimal systemic side effects [2]. **Why the other options are incorrect:** * **B. Ketotifen:** This is a **mast cell stabilizer** and H1-antihistamine used for long-term prophylaxis of asthma, not for acute relief. It is administered orally, not as an aerosol. * **C. Fluticasone:** This is a **potent inhaled corticosteroid (ICS)**. While it is administered as an aerosol, it is an anti-inflammatory agent used for maintenance therapy, not a beta-adrenergic agonist [1]. * **D. Montelukast:** This is a **leukotriene receptor antagonist (LTRA)**. It is administered **orally** and is used for chronic management and prophylaxis of asthma and allergic rhinitis [2]. **High-Yield NEET-PG Pearls:** * **Drug of Choice:** Salbutamol is the DOC for **acute asthma attacks** and **exercise-induced bronchospasm**. * **Side Effects:** Muscle tremors (most common due to β2 stimulation in skeletal muscles), tachycardia (due to β1 cross-reactivity) [3], and **hypokalemia** (used therapeutically in hyperkalemia). * **LABA vs. SABA:** Salmeterol and Formoterol are Long-Acting Beta-Agonists (LABA) used for maintenance [4], never as monotherapy in asthma.

Q: Which long-acting beta-agonist is used once daily?

Indacaterol. The correct answer is **Indacaterol**. **1. Why Indacaterol is correct:** Beta-2 agonists are classified based on their duration of action. While traditional Long-Acting Beta-Agonists (LABAs) like Salmeterol and Formoterol have a duration of approximately 12 hours [1], **Indacaterol** belongs to a newer class known as **Ultra-LABAs**. It possesses a high lipid solubility and a strong affinity for the beta-2 receptor, allowing for a rapid onset of action (within 5 minutes) and a prolonged duration of action exceeding 24 hours [1]. Consequently, it is administered **once daily**, primarily for the maintenance treatment of Chronic Obstructive Pulmonary Disease (COPD). **2. Why the other options are incorrect:** * **Salmeterol (A):** A classic LABA with a slow onset of action [3]. It has a duration of action of approximately 12 hours, necessitating **twice-daily** dosing. * **Formoterol (B):** Another LABA with a fast onset but a duration of action of about 12 hours [1]. Like Salmeterol, it requires **twice-daily** dosing. * **Terbutaline (D):** A Short-Acting Beta-Agonist (SABA) [2]. It has a rapid onset and a short duration (3–6 hours), used primarily for "rescue" relief of acute bronchospasm, not maintenance. **3. High-Yield NEET-PG Pearls:** * **Ultra-LABAs (Once Daily):** Indacaterol, Vilanterol, Olodaterol, and Bambuterol (an oral prodrug of terbutaline). * **COPD vs. Asthma:** Indacaterol is currently FDA-approved for COPD but not as a monotherapy for asthma due to the risk of asthma-related mortality when LABAs are used without inhaled corticosteroids (ICS) [2]. * **Bambuterol** is the only oral beta-2 agonist that is administered once daily (usually at bedtime).

Q: Dextromethorphan differs from codeine in which of the following aspects?

It causes no constipation.. **Explanation:** Dextromethorphan is a synthetic d-isomer of the codeine analog levorphanol. While it is chemically related to opioids, its pharmacological profile differs significantly from classic opioids like codeine. **1. Why Option D is Correct:** Dextromethorphan acts centrally on the cough center in the medulla to raise the cough threshold. Unlike codeine, it has **minimal affinity for peripheral mu-opioid receptors** in the gastrointestinal tract. Consequently, it does not inhibit intestinal motility and **does not cause constipation**, making it a preferred over-the-counter antitussive. **2. Why Other Options are Incorrect:** * **Option A:** Dextromethorphan’s antitussive effect is mediated via sigma receptors and NMDA antagonism, rather than classic mu-opioid receptors. Therefore, its action is **not antagonized by naloxone**. * **Option B:** Unlike codeine, which can dry secretions and impair the upward movement of mucus, dextromethorphan **does not depress mucociliary function**, allowing for better clearance of respiratory secretions. * **Option C:** Dextromethorphan lacks significant analgesic properties and does not produce euphoria at standard doses. It has **no significant addiction liability** or sedative properties compared to codeine. **Clinical Pearls for NEET-PG:** * **Mechanism:** NMDA receptor antagonist (at high doses) and Sigma-1 receptor agonist. * **Toxicity:** In extreme overdose, it can cause a "dissociative" state (similar to PCP/Ketamine) and may lead to **Serotonin Syndrome** if co-administered with MAO inhibitors or SSRIs. * **Key Advantage:** It is as effective an antitussive as codeine but lacks respiratory depression, sedation, and constipation.

Q: Which of the following antitussives is known to cause hallucinations?

Dextromethorphan. ### Explanation **Correct Option: B. Dextromethorphan** Dextromethorphan is a synthetic non-opioid derivative of levorphanol. While it acts on the medullary cough center to raise the cough threshold, it does not act on classical opioid receptors (mu or kappa) at therapeutic doses. However, at high doses (overdose or recreational use), it acts as an **NMDA receptor antagonist**, similar to Ketamine and Phencyclidine (PCP). This antagonism leads to dissociative effects, euphoria, and **hallucinations**. **Analysis of Incorrect Options:** * **A. Morphine:** While morphine is a potent opioid that suppresses cough, its primary side effects are sedation, respiratory depression, and constipation. It is rarely used as a first-line antitussive due to its high addiction potential. * **C. Diphenhydramine:** This is a first-generation H1-antihistamine used for cough due to its anticholinergic properties. Its main side effects are sedation, dry mouth, and urinary retention, rather than hallucinations. * **D. Aprepitant:** This is a Neurokinin-1 (NK1) receptor antagonist used primarily as an antiemetic for chemotherapy-induced nausea and vomiting (CINV). It is not classified as a standard antitussive. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism of Action:** Dextromethorphan suppresses the cough center in the medulla oblongata. * **Safety Profile:** Unlike codeine, it does not cause constipation or significant respiratory depression at standard doses and has low addictive potential. * **Contraindication:** It should not be given to patients on **MAO inhibitors**, as it can precipitate **Serotonin Syndrome** (due to inhibition of serotonin reuptake). * **Metabolism:** It is metabolized by the enzyme **CYP2D6**. Genetic polymorphism in this enzyme can lead to varied drug responses.

Question 1

All of the following drugs can precipitate an acute attack of asthma except?

Accepted Answer

Glucocorticoids

Answer

Phenylbutazone

Answer

Naproxen

Answer

Aspirin

Question 2

Which of the following drugs is approved for the treatment of cystic fibrosis specifically in patients with the G551D mutation?

Accepted Answer

Ivacaftor

Answer

Biostrophin

Answer

Peginesatide

Answer

Lumacaftor

Question 3

Which of the following is false about salmeterol?

Accepted Answer

Effective for acute asthmatic attacks

Answer

Regular use may worsen asthma

Answer

First long acting selective beta-2 agonist

Answer

More beta-2 selective agonist than salbutamol

Question 4

Which of the following drugs can be used for the management of status asthmaticus?

Accepted Answer

Montelukast

Answer

Magnesium sulphate

Answer

Corticosteroid

Answer

Adrenaline

Question 5

What is the mechanism of action of Zileuton?

Accepted Answer

Inhibits lipoxygenase

Answer

Inhibits production of IgE

Answer

Inhibits cyclooxygenase

Answer

Inhibits activity of mast cells

Question 6

Inhaled sodium cromoglycate:

Accepted Answer

Is of benefit in preventing exercise-induced bronchial spasm

Answer

Prevents the antigen-antibody combination

Answer

May cause cardiac arrhythmias

Answer

Is effective in alleviating an acute episode of allergic asthma

Question 7

Which of the following beta-adrenergic agonists is used as an aerosol for the treatment of bronchial asthma?

Accepted Answer

Salbutamol

Answer

Ketotifen

Answer

Fluticasone

Answer

Montelukast

Question 8

Which long-acting beta-agonist is used once daily?

Accepted Answer

Indacaterol

Answer

Salmeterol

Answer

Formoterol

Answer

Terbutaline

Question 9

Dextromethorphan differs from codeine in which of the following aspects?

Accepted Answer

It causes no constipation.

Answer

Its antitussive action can be blocked by naloxone.

Answer

It depresses mucociliary function of the airway mucosa.

Answer

Addiction is common.

Question 10

Which of the following antitussives is known to cause hallucinations?

Accepted Answer

Dextromethorphan

Answer

Morphine

Answer

Diphenhydramine

Answer

Aprepitant

Respiratory System Drugs — MCQs

Respiratory System Drugs — MCQs

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