Respiratory System Drugs Practice Questions

Q: Zileuton is:

A 5 lipooxygenase inhibitor. **Explanation:** **1. Why Option A is Correct:** Zileuton is a specific inhibitor of **5-lipoxygenase (5-LOX)**, the enzyme responsible for converting arachidonic acid into leukotrienes (LTB4, LTC4, LTD4, and LTE4). By inhibiting this enzyme, Zileuton prevents the synthesis of all leukotrienes, which are potent mediators of bronchoconstriction, airway edema, and mucus secretion in asthma. **2. Why Other Options are Incorrect:** * **Option B (TXA2 inhibitor):** Thromboxane A2 (TXA2) inhibitors (like Dazoxiben) or synthesis inhibitors (like Aspirin, which inhibits COX-1) affect platelet aggregation and vascular tone, not the 5-LOX pathway. * **Option C (Leukotriene receptor antagonist):** These drugs (e.g., **Montelukast, Zafirlukast**) do not stop the production of leukotrienes; instead, they block the **CysLT1 receptor**. Zileuton acts upstream by preventing production entirely. * **Option D (Prostaglandin synthesis inhibitor):** These are **NSAIDs** (e.g., Ibuprofen, Indomethacin) which inhibit the Cyclooxygenase (COX) enzymes. **3. NEET-PG Clinical Pearls:** * **Metabolism:** Zileuton is metabolized by Cytochrome P450 (CYP1A2) and can increase the levels of **Theophylline** and **Warfarin**. * **Adverse Effect:** A high-yield side effect is **hepatotoxicity**; therefore, liver function tests (LFTs) must be monitored. * **Indication:** It is used for the prophylactic treatment of asthma, not for acute attacks. * **Mnemonic:** **Z**ileuton stops the **S**ynthesis (**Z**-**S**), while **M**ontelukast blocks the **R**eceptor (**M**-**R**).

Q: The mechanism of action of aspirin as an antiplatelet drug is its inhibitory action on which of the following?

Thromboxane A2. ### Explanation **Mechanism of Action:** Aspirin (Acetylsalicylic acid) acts as an antiplatelet agent by **irreversibly inhibiting the enzyme Cyclooxygenase-1 (COX-1)**. This inhibition occurs via the acetylation of a serine residue at the active site of the enzyme. In platelets, COX-1 is responsible for converting arachidonic acid into Prostaglandin H2, which is then converted into **Thromboxane A2 (TXA2)**. TXA2 is a potent vasoconstrictor and a powerful inducer of platelet aggregation. By blocking TXA2 synthesis for the entire lifespan of the platelet (7–10 days), aspirin effectively prevents clot formation. **Analysis of Options:** * **Option A (Prostacyclins/PGI2):** These are produced by vascular endothelial cells and inhibit platelet aggregation. While high doses of aspirin can inhibit PGI2, the antiplatelet effect is specifically due to the suppression of TXA2. * **Option B (PGF-2 alpha):** This prostaglandin is involved in uterine contraction and bronchoconstriction; it does not play a primary role in platelet aggregation. * **Option D (Phospholipase C):** This is an enzyme involved in the inositol trisphosphate (IP3) signaling pathway. Aspirin does not inhibit this enzyme; it targets the cyclooxygenase pathway downstream of phospholipase activity. **High-Yield Clinical Pearls for NEET-PG:** * **Low-dose Aspirin (75–150 mg):** Selectively inhibits TXA2 without significantly affecting PGI2, making it ideal for cardioprotection. * **Irreversible Inhibition:** Because platelets are anuclear and cannot synthesize new COX enzymes, the effect lasts the lifetime of the platelet. * **Primary/Secondary Prevention:** Aspirin is the drug of choice for secondary prevention of Myocardial Infarction (MI) and Ischemic Stroke. * **Side Effect:** Watch for **Reye’s Syndrome** in children with viral infections and **Aspirin-exacerbated respiratory disease (AERD)** in patients with nasal polyps and asthma.

Q: Which of the following should be avoided in a patient with asthma?

NSAID. **Explanation:** The correct answer is **NSAIDs**. This is a high-yield concept in respiratory pharmacology known as **Aspirin-Exacerbated Respiratory Disease (AERD)** or Samter’s Triad (asthma, nasal polyps, and aspirin sensitivity). **Mechanism of Action:** NSAIDs inhibit the enzyme **Cyclooxygenase (COX)**. In susceptible asthmatic patients, blocking the COX pathway causes the metabolism of Arachidonic acid to shift toward the **Lipoxygenase (LOX) pathway**. This results in the overproduction of **Cysteinyl Leukotrienes (LTC4, LTD4, LTE4)**, which are potent bronchoconstrictors, leading to life-threatening bronchospasm. **Analysis of Incorrect Options:** * **B. Terbutaline:** This is a short-acting **$\beta_2$-agonist (SABA)**. It causes bronchodilation by increasing cAMP in bronchial smooth muscle and is a first-line treatment for acute asthma attacks. * **C. Theophylline:** A **Methylxanthine** that acts by inhibiting phosphodiesterase (PDE), leading to increased cAMP and bronchodilation. It is used as an add-on therapy in chronic asthma. * **D. Steroids:** Corticosteroids (e.g., Fluticasone, Prednisolone) are the **mainstay of asthma treatment**. They reduce airway inflammation and hyper-responsiveness. **NEET-PG High-Yield Pearls:** 1. **Safe Alternative:** If an asthmatic patient requires an analgesic, **Acetaminophen (Paracetamol)** is generally considered safe at low doses. 2. **Other Drugs to Avoid:** **Non-selective $\beta$-blockers** (e.g., Propranolol) are strictly contraindicated as they block $\beta_2$ receptors, causing bronchoconstriction. 3. **Leukotriene Antagonists:** Drugs like **Montelukast** and **Zafirlukast** work by blocking leukotriene receptors and are particularly effective in treating aspirin-induced asthma.

Q: Which of the following drugs inhibits histamine release?

Ketotifen. The correct answer is **Ketotifen**. **1. Why Ketotifen is correct:** Ketotifen is a second-generation H1-antihistamine [1] that possesses unique **mast cell stabilizing** properties. It acts by inhibiting the degranulation of mast cells, thereby preventing the release of histamine and other inflammatory mediators (like leukotrienes). It is primarily used in the prophylactic treatment of bronchial asthma and allergic rhinitis [1], [2]. Unlike acute bronchodilators, it does not reverse an ongoing attack but reduces airway hyperreactivity over time [1]. **2. Why the other options are incorrect:** * **D-tubocurarine, Morphine, and Suxamethonium:** These drugs are well-known **histamine liberators**. Instead of inhibiting release, they displace histamine from mast cells via a non-immunologic mechanism (direct action). * **D-tubocurarine:** A skeletal muscle relaxant that frequently causes hypotension and bronchospasm due to significant histamine release. * **Morphine:** An opioid analgesic that can cause itching, urticaria, and vasodilation through direct histamine release. * **Suxamethonium (Succinylcholine):** A depolarizing neuromuscular blocker that can also trigger histamine release, though usually to a lesser extent than tubocurarine. **3. NEET-PG High-Yield Pearls:** * **Mast Cell Stabilizers:** Other examples include **Sodium Cromoglycate** and **Nedocromil**. They are "preventers," not "relievers." * **Dual Action:** Ketotifen is unique because it is both a potent H1-receptor antagonist and a mast cell stabilizer. * **Drug of Choice (DOC):** For an acute anaphylactic reaction, the drug of choice is **Epinephrine (Adrenaline) 1:1000 IM**, not antihistamines, as it physiologically opposes histamine. * **Histamine Liberators Mnemonic:** "Many Drugs Can Release Histamine" (**M**orphine, **D**-tubocurarine, **C**hymotrypsin, **R**adiocontrast media, **H**ydralazine).

Q: A patient presents with dyspnea and bilateral diffuse wheezing on lung auscultation. Which medication would provide the fastest relief?

Salbutamol. **Explanation:** The clinical presentation of dyspnea and bilateral diffuse wheezing is characteristic of an acute bronchospasm (e.g., Asthma or COPD exacerbation). In such scenarios, the priority is a **Short-Acting Beta-2 Agonist (SABA)** to achieve rapid bronchodilation. **Why Salbutamol is correct:** Salbutamol (Albuterol) is the drug of choice for acute attacks. It acts by stimulating $\beta_2$ receptors in the bronchial smooth muscle, leading to increased cAMP and rapid relaxation. Its onset of action is **3–5 minutes**, making it the fastest-acting rescue medication among the options provided. **Analysis of Incorrect Options:** * **Salmeterol:** This is a **Long-Acting Beta-2 Agonist (LABA)**. While it has high affinity for $\beta_2$ receptors, it has a slow onset of action (approx. 15–20 minutes) and is used for maintenance therapy, not acute relief. * **Ipratropium Bromide:** An anticholinergic (SAMA) that blocks M3 receptors. While used in acute asthma/COPD, its onset is slower (15–30 minutes) than Salbutamol. It is typically used as an add-on therapy. * **Montelukast:** A Leukotriene Receptor Antagonist (LTRA). It is an oral medication used for **prophylaxis** and chronic management of asthma; it has no role in the immediate reversal of acute bronchospasm. **NEET-PG High-Yield Pearls:** * **Drug of Choice (DOC)** for acute asthma: Inhaled Salbutamol. * **DOC for Exercise-Induced Asthma:** Salbutamol (taken 15 mins prior). * **Side effects of SABAs:** Muscle tremors (most common), tachycardia, and hypokalemia (due to stimulation of Na+/K+ ATPase pump). * **Formoterol** is a unique LABA because it has a **fast onset** of action, similar to Salbutamol, but a long duration of action.

Q: Which of the following second-generation antihistamines is used in allergic rhinitis?

All of these. **Explanation:** The correct answer is **D (All of these)** because all three drugs are second-generation H1-receptor antagonists commonly used in the management of allergic rhinitis. **Underlying Medical Concept:** Second-generation antihistamines are preferred over first-generation drugs (like Diphenhydramine) for allergic rhinitis because they are **highly selective for peripheral H1 receptors** and have **poor blood-brain barrier penetration**. This results in minimal sedation and fewer anticholinergic side effects (dry mouth, urinary retention). * **Azelastine:** This is a second-generation antihistamine available as a **nasal spray**. It is unique because it provides rapid relief of nasal symptoms and also possesses mast-cell stabilizing properties. * **Fexofenadine:** This is the active metabolite of Terfenadine. It is considered a "non-sedating" antihistamine because it does not cross the blood-brain barrier at all. Unlike its parent drug, it does not cause QT prolongation. * **Desloratadine:** This is the active metabolite of Loratadine. It has a long half-life, allowing for once-daily dosing, and is highly effective in reducing sneezing, rhinorrhea, and ocular itching. **High-Yield NEET-PG Pearls:** 1. **Non-sedating Antihistamines:** Fexofenadine, Loratadine, and Desloratadine are the least sedating. Cetirizine may cause mild sedation in some patients. 2. **Active Metabolites:** * Fexofenadine is the metabolite of Terfenadine. * Desloratadine is the metabolite of Loratadine. * Cetirizine is the metabolite of Hydroxyzine. 3. **Cardiac Safety:** Terfenadine and Astemizole were withdrawn from the market due to **Torsades de Pointes** (QT prolongation) caused by interaction with Ketoconazole/Erythromycin. Fexofenadine is the safe alternative. 4. **Topical H1 Blockers:** Azelastine and Olopatadine are used topically (nasal/ophthalmic) for rapid action.

Q: Which of the following is a 5-lipoxygenase synthesis inhibitor?

Zileuton. ### Explanation The question tests your knowledge of the **Leukotriene Pathway**, a critical target in the management of bronchial asthma. **1. Why Zileuton is Correct:** Leukotrienes are inflammatory mediators synthesized from arachidonic acid via the **5-lipoxygenase (5-LOX)** enzyme. **Zileuton** is a specific inhibitor of the 5-LOX enzyme. By blocking this enzyme, it prevents the synthesis of all leukotrienes (LTB4, LTC4, LTD4, and LTE4), thereby reducing bronchoconstriction and airway inflammation. **2. Why the Other Options are Incorrect:** * **Zafirlukast & Montelukast (Options B & C):** These drugs are **CysLT1 receptor antagonists**. They do not stop the production of leukotrienes; instead, they block the action of cysteinyl leukotrienes (LTC4, LTD4, LTE4) at the receptor level. They are the most commonly used "leukotriene modifiers" in clinical practice. * **Omalizumab (Option D):** This is a **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. **3. NEET-PG High-Yield Pearls:** * **Metabolism:** Zileuton is metabolized by the liver and can cause a rise in liver enzymes; therefore, **periodic LFT monitoring** is required (unlike Montelukast). * **Drug Interactions:** Zileuton inhibits CYP1A2 and can increase the levels of **Theophylline** and **Warfarin**. * **Aspirin-Induced Asthma:** Leukotriene modifiers (both synthesis inhibitors and receptor antagonists) are the drugs of choice for Aspirin-Exacerbated Respiratory Disease (AERD). * **Montelukast Side Effect:** Watch for **Churg-Strauss syndrome** (eosinophilic granulomatosis with polyangiitis) and neuropsychiatric symptoms (FDA boxed warning).

Q: Which of the following is classified as a "soft steroid" used in the management of bronchial asthma?

Ciclesonide. ### Explanation **Correct Option: C. Ciclesonide** **Why it is correct:** A **"soft steroid"** (or prodrug steroid) is a drug that is topically active but undergoes rapid metabolic inactivation into non-toxic metabolites once it reaches the systemic circulation. **Ciclesonide** is a unique inhaled corticosteroid (ICS) administered as an inactive prodrug. It is activated by **esterases** specifically in the bronchial epithelium to its active metabolite, **des-ciclesonide**. Because it is not active in the oropharynx and has high plasma protein binding with rapid hepatic clearance, it significantly reduces the risk of local side effects (like oral candidiasis) and systemic toxicity (like HPA axis suppression). **Analysis of Incorrect Options:** * **A. Budesonide:** A potent, non-halogenated ICS. While it has high first-pass metabolism, it is administered in its **active form**, not as a soft steroid/prodrug. * **B. Dexamethasone:** A systemic, long-acting glucocorticoid. It lacks the selective topical activation required to be classified as a soft steroid and has a high potential for systemic side effects. * **D. Flunisolide:** An older ICS used for asthma and rhinitis. Like Budesonide, it is an active compound upon inhalation and does not require local enzymatic activation. **NEET-PG High-Yield Pearls:** * **Ciclesonide Advantages:** Lowest incidence of **oral thrush (candidiasis)** and dysphonia among ICS due to its prodrug nature. * **Mometasone & Fluticasone:** These are highly potent ICS with very low oral bioavailability (<1%), making them preferred for minimizing systemic absorption, though they are not "soft steroids" in the same metabolic sense as Ciclesonide. * **Mechanism of ICS:** They do not cause direct bronchodilation; they work by reducing airway inflammation and **upregulating β₂ receptors**, making them the "controller" drugs of choice in chronic asthma.

Q: Cough syrup acts by inhibiting which of the following?

Cough center. **Cough suppressants (Antitussives)**, such as Codeine and Dextromethorphan, primarily act by raising the threshold of the **cough center** located in the **medulla oblongata** [1, 2]. By inhibiting this specific neurological pathway, these drugs reduce the frequency and intensity of the cough reflex. Antitussives are clinically indicated only for dry, non-productive coughs where the goal is to provide symptomatic relief without compromising airway clearance. Analysis of Incorrect Options: * **B. Respiratory Center:** While also located in the medulla, the respiratory center controls the rhythmic cycle of inspiration and expiration. Inhibiting this center would lead to respiratory depression (a dangerous side effect of opioids) rather than a targeted suppression of the cough reflex. * **C. Breathing Center:** This is a general term often used interchangeably with the respiratory center. It is not the specific physiological target for antitussive action. * **D. Pulmonary Secretion Center:** There is no anatomical "center" by this name. Drugs that affect secretions are classified as **Expectorants** (increase volume/reduce viscosity) or **Mucolytics** (break chemical bonds in mucus), which act peripherally rather than centrally. NEET-PG High-Yield Pearls: * **Dextromethorphan:** A centrally acting NMDA receptor antagonist [2]; it is the preferred antitussive because it lacks the addictive potential and constipating effects of Codeine. * **Noscapine:** An opium alkaloid used as an antitussive; it does not cause narcosis or analgesia but can release histamine, causing bronchoconstriction in asthmatics. * **Benzonatate:** A peripheral antitussive that acts by anesthetizing the stretch receptors in the lungs [2]. * **Contraindication:** Antitussives should be avoided in productive (wet) coughs, as suppressing the cough can lead to sputum retention and secondary infections.

Q: All of the following are true about theophylline except?

It is the drug of choice for exercise-induced asthma.. Theophylline is a methylxanthine derivative once widely used for asthma but now relegated to a second or third-line role due to its narrow therapeutic index and side effect profile. **Explanation of the Correct Answer (Option B):** Theophylline is **not** the drug of choice for exercise-induced asthma. The preferred treatment for preventing exercise-induced bronchospasm is the use of **Short-Acting Beta-2 Agonists (SABA)** like Salbutamol, taken 15–30 minutes before exercise. Alternatively, Mast Cell Stabilizers (Cromolyn) or Leukotriene Receptor Antagonists (Montelukast) can be used. Theophylline has a slow onset of action and is unsuitable for the acute prevention or rescue required in exercise-induced symptoms. **Analysis of Other Options:** * **Option A:** Theophylline primarily works by **inhibiting Phosphodiesterase (PDE 3 and 4)**, leading to increased intracellular cAMP, which results in bronchodilation. It also acts as an **Adenosine receptor antagonist**. * **Option C:** It has a **narrow therapeutic index** (10–20 µg/ml). Levels above 20 µg/ml cause toxicity, necessitating **Therapeutic Drug Monitoring (TDM)** to ensure safety and efficacy. * **Option D:** As a methylxanthine (related to caffeine), it is a potent **CNS stimulant**. Toxic doses can lead to severe adverse effects, including intractable **seizures** and cardiac arrhythmias. **High-Yield Clinical Pearls for NEET-PG:** * **Metabolism:** It follows first-order kinetics at therapeutic doses but shifts to **zero-order kinetics** in overdose. * **Drug Interactions:** Its metabolism is **increased** by smoking and Phenytoin (enzyme inducers) and **decreased** by Erythromycin and Ciprofloxacin (enzyme inhibitors). * **Other uses:** Aminophylline (a soluble salt of theophylline) is sometimes used in apnea of prematurity.

Question 1

Zileuton is:

Accepted Answer

A 5 lipooxygenase inhibitor

Answer

A TXA2 inhibitor

Answer

A leukotriene receptor antagonist

Answer

A prostaglandins synthesis inhibitor

Question 2

The mechanism of action of aspirin as an antiplatelet drug is its inhibitory action on which of the following?

Accepted Answer

Thromboxane A2

Answer

Prostacyclins

Answer

PGF-2 alpha

Answer

Phospholipase C

Question 3

Which of the following should be avoided in a patient with asthma?

Accepted Answer

NSAID

Answer

Terbutaline

Answer

Theophylline

Answer

Steroids

Question 4

Which of the following drugs inhibits histamine release?

Accepted Answer

Ketotifen

Answer

D-tubocurarine

Answer

Morphine

Answer

Suxamethonium

Question 5

A patient presents with dyspnea and bilateral diffuse wheezing on lung auscultation. Which medication would provide the fastest relief?

Accepted Answer

Salbutamol

Answer

Salmeterol

Answer

Ipratropium Bromide

Answer

Montelukast

Question 6

Which of the following second-generation antihistamines is used in allergic rhinitis?

Accepted Answer

All of these

Answer

Azelastine

Answer

Fexofenadine

Answer

Desloratadine

Question 7

Which of the following is a 5-lipoxygenase synthesis inhibitor?

Accepted Answer

Zileuton

Answer

Zafirlukast

Answer

Montelukast

Answer

Omalizumab

Question 8

Which of the following is classified as a "soft steroid" used in the management of bronchial asthma?

Accepted Answer

Ciclesonide

Answer

Budesonide

Answer

Dexamethasone

Answer

Flunisolide

Question 9

Cough syrup acts by inhibiting which of the following?

Accepted Answer

Cough center

Answer

Respiratory center

Answer

Breathing center

Answer

Pulmonary secretion center

Question 10

All of the following are true about theophylline except?

Accepted Answer

It is the drug of choice for exercise-induced asthma.

Answer

It acts by inhibiting phosphodiesterase enzyme.

Answer

Therapeutic drug monitoring is needed for theophylline.

Answer

It is a central nervous system stimulant and can lead to seizures.

Respiratory System Drugs — MCQs

Respiratory System Drugs — MCQs

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