Antitussives and Expectorants — MCQs
Which opioid analgesic is used in the treatment of cough?
A female was given morphine sulphate during labour for pain but she developed respiratory distress. Which of the following will be the correct antidote?
Acetaminophen [Paracetamol] induced liver toxicity is due to which metabolite?
Which of the following is a centrally acting non-opioid antitussive?
Which of the following is an antitussive opioid?
What mechanism primarily leads to cough in patients with congestive heart failure?
Cough reflex on scratching the floor of external auditory meatus is due to which nerve?
All of the following are expectorants except:
Which drug is used for long-term maintenance in opioid addiction?
What is the drug of choice for acute severe asthma?
Antitussives and Expectorants Indian Medical PG Practice Questions and MCQs
Question 1: Which opioid analgesic is used in the treatment of cough?
- A. Loperamide
- B. Diphenoxylate
- C. Codeine (Correct Answer)
- D. Meperidine
Explanation: ***Codeine*** - **Codeine** is a commonly used **opioid antitussive** that acts directly on the **cough center** in the medulla to suppress the cough reflex [2], [3]. - It is often found in combination with other medications in prescription and over-the-counter cough syrups [4]. *Loperamide* - **Loperamide** is an **opioid derivative** primarily used as an **antidiarrheal** agent. - It works by decreasing gut motility and fluid secretion, with minimal central nervous system penetration at therapeutic doses. *Diphenoxylate* - **Diphenoxylate** is an **opioid agonist** used in combination with atropine (as Lomotil) to treat **diarrhea**. - Its antidiarrheal action is due to decreased gastrointestinal motility and fluid secretion, and it is not primarily used for cough. *Meperidine* - **Meperidine** (also known as Pethidine) is a **synthetic opioid analgesic** primarily used for the treatment of **moderate to severe pain** [1]. - It has significant euphoric and addictive potential and is not typically used as an antitussive due to its stronger analgesic effects and side effect profile [3].
Question 2: A female was given morphine sulphate during labour for pain but she developed respiratory distress. Which of the following will be the correct antidote?
- A. Naloxone (Correct Answer)
- B. Epinephrine
- C. Pralidoxime
- D. Atropine
Explanation: ***Naloxone*** - **Naloxone** is a pure opioid antagonist that rapidly reverses the effects of **opioid overdose** [1, 3], including **respiratory depression** [2], by competitively binding to opioid receptors [1]. - Its short half-life may necessitate repeated doses, especially with longer-acting opioids like morphine, to prevent recurrence of respiratory depression [1]. *Epinephrine* - **Epinephrine** is an adrenergic agonist used to treat **anaphylaxis** and severe allergic reactions, as it causes **vasoconstriction** and **bronchodilation**. - It is not an antidote for opioid-induced respiratory depression, which primarily results from central nervous system effects rather than allergic reactions. *Pralidoxime* - **Pralidoxime** is a **cholinesterase reactivator** used to treat poisoning by **organophosphates**, which inhibit acetylcholinesterase, leading to cholinergic crisis. - It works by restoring the function of the enzyme, thereby breaking down excess acetylcholine, and is not indicated for opioid overdose. *Atropine* - **Atropine** is an **anticholinergic agent** that blocks muscarinic acetylcholine receptors, used to treat **bradycardia** and **organophosphate poisoning**. - It would not reverse opioid-induced respiratory depression, as it primarily affects the parasympathetic nervous system and does not antagonize opioid receptor effects.
Question 3: 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 4: Which of the following is a centrally acting non-opioid antitussive?
- A. Ambroxol
- B. Guaifenesin
- C. Diphenhydramine
- D. Dextromethorphan (Correct Answer)
Explanation: ***Dextromethorphan*** - **Dextromethorphan** is a **centrally acting non-opioid antitussive** that suppresses the cough reflex by acting on the cough center in the medulla oblongata [1], [2]. - It is an **NMDA receptor antagonist** and a **sigma-1 receptor agonist**, which are the primary mechanisms responsible for its antitussive effects [2]. - Unlike opioid antitussives (codeine, hydrocodone), it does **not bind significantly to opioid receptors** at therapeutic doses and therefore lacks addiction potential, respiratory depression, and other opioid side effects [1], [3]. - It is a synthetic morphine analog (dextro-isomer) but is pharmacologically distinct from opioids [1]. *Ambroxol* - **Ambroxol** is a **mucolytic agent** that helps to thin and clear mucus from the respiratory tract. - It works by stimulating serous gland secretion and breaking down mucopolysaccharide fibers, which is different from suppressing the cough reflex centrally. *Guaifenesin* - **Guaifenesin** is an **expectorant** that increases the volume and reduces the viscosity of respiratory tract secretions. - This action helps to make coughs more productive, rather than directly suppressing the cough reflex. *Diphenhydramine* - **Diphenhydramine** is a first-generation **antihistamine** with significant sedative and anticholinergic properties. - While it has some antitussive effects, these are primarily due to its anticholinergic actions causing drying of respiratory secretions and its sedative properties, rather than direct central action on the cough center.
Question 5: Which of the following is an antitussive opioid?
- A. Pethidine
- B. Methadone
- C. Buprenorphine
- D. Ethylmorphine (Correct Answer)
Explanation: ***Ethylmorphine*** - **Ethylmorphine** (also known as dionin) is an opioid derivative with significant **antitussive properties**, meaning it suppresses coughing. - It works by acting on opioid receptors in the **medulla oblongata**, reducing the cough reflex. *Pethidine* - **Pethidine** (also known as meperidine) is a synthetic opioid primarily used for **moderate to severe pain relief**. - While it has some central nervous system effects, its main therapeutic use is as an **analgesic**, not an antitussive. *Methadone* - **Methadone** is a synthetic opioid used for treating **opioid dependence** and for **chronic severe pain**. - Its main application is in addiction treatment and pain management, not specifically as a cough suppressant. *Buprenorphine* - **Buprenorphine** is a **partial opioid agonist** used for pain management and **opioid dependence**. - It has a high affinity for opioid receptors but produces a limited effect, making it less likely to be used solely as an antitussive and more for its analgesic or anti-addictive properties.
Question 6: What mechanism primarily leads to cough in patients with congestive heart failure?
- A. Fluid accumulation in alveoli (Correct Answer)
- B. Stimulation of pulmonary J-receptors
- C. Upper airway obstruction due to edema
- D. Increased airway resistance
Explanation: ***Fluid accumulation in alveoli*** - In **congestive heart failure (CHF)**, the heart's pumping efficiency decreases, leading to **pulmonary venous congestion** and increased hydrostatic pressure [1]. - This pressure forces fluid from the capillaries into the **interstitial space** and subsequently into the alveoli, triggering a cough reflex to clear the airways [1]. *Stimulation of pulmonary J-receptors* - While J-receptors can be stimulated by **interstitial edema** and distension, this stimulation primarily contributes to **dyspnea** (shortness of breath) and shallow, rapid breathing rather than directly initiating a productive cough [1]. - The cough in CHF is more directly related to the physical presence of fluid within the alveolar spaces [1]. *Upper airway obstruction due to edema* - **Upper airway obstruction** from edema is less common as a primary cause of cough in CHF and is more characteristic of conditions like **angioedema** or **laryngitis** [2]. - The edema in CHF predominantly affects the lower respiratory tract, specifically the **pulmonary parenchyma**. *Increased airway resistance* - **Increased airway resistance** is typically associated with conditions like **asthma** or **chronic obstructive pulmonary disease (COPD)** where there is **bronchoconstriction** or inflammation of the bronchioles [3]. - Although some degree of bronchoconstriction can occur due to congestion, the primary mechanism for cough in CHF is not airway resistance but alveolar fluid filling.
Question 7: Cough reflex on scratching the floor of external auditory meatus is due to which nerve?
- A. Greater auricular nerve
- B. Auriculo temporal
- C. Facial nerve
- D. Auricular branch of vagus (Correct Answer)
Explanation: ***Auricular branch of vagus*** - The **auricular branch of the vagus nerve (cranial nerve X)**, also known as Arnold's nerve, innervates the posterior and inferior walls of the external auditory meatus. - Stimulation of this nerve in some individuals can trigger a vagal reflex, leading to coughing, gagging, or even syncope, known as **Arnold's reflex**. *Greater auricular nerve* - This nerve is a branch of the **cervical plexus** and primarily supplies sensation to the skin over the mastoid process, auricle (excluding the concha and tragus), and angle of the mandible. - It does not innervate the deep parts of the external auditory meatus responsible for the cough reflex. *Auriculo temporal* - The **auriculotemporal nerve** is a branch of the mandibular division of the trigeminal nerve (cranial nerve V3). - It supplies sensory innervation to the anterior part of the external ear, temporal region, and glandular innervation to the parotid gland, but is not primarily involved in the cough reflex from the ear canal. *Facial nerve* - The **facial nerve (cranial nerve VII)** supplies motor innervation to the muscles of facial expression and sensory innervation to a small area around the concha of the external ear. - While it has sensory branches in the ear, it is not the primary mediator of the cough reflex stimulated by the external auditory meatus.
Question 8: All of the following are expectorants except:
- A. Guaifenesin
- B. Ammonium chloride
- C. Noscapine (Correct Answer)
- D. Hypertonic saline
Explanation: ***Noscapine*** - **Noscapine** is an **antitussive** (cough suppressant) that works by suppressing the **cough reflex** in the brainstem, with no expectorant properties. - It is an **opium alkaloid** derivative but lacks significant analgesic or addictive effects. *Hypertonic saline* - **Hypertonic saline** is used as an **expectorant** to induce sputum production by drawing water into the airways through osmosis, thinning mucus. - It works by irritating the airways, leading to a reflexive increase in mucus secretion and clearance. *Guaifenesin* - **Guaifenesin** is a well-known **expectorant** that works by increasing the volume and reducing the viscosity of respiratory tract secretions. - This helps to facilitate the removal of mucus from the airways by making coughs more productive. *Ammonium chloride* - **Ammonium chloride** acts as a **systemic expectorant** by irritating the bronchial mucosa, which reflexively increases the secretion of respiratory fluids. - It is thought to thin the mucus, making it easier to expel.
Question 9: Which drug is used for long-term maintenance in opioid addiction?
- A. Naloxone
- B. Nalorphine
- C. Methadone (Correct Answer)
- D. Butorphanol
Explanation: ***Methadone*** - **Methadone** is a long-acting opioid agonist used daily for **maintenance therapy** in opioid addiction, preventing withdrawal symptoms and reducing cravings. - Its long half-life allows for once-daily dosing, which helps in stabilizing patients and reducing illicit opioid use. - Along with **buprenorphine** (a partial agonist), methadone is one of the two primary medications used for opioid maintenance therapy. *Naloxone* - **Naloxone** is an **opioid antagonist** used to rapidly reverse opioid overdose by competitively binding to opioid receptors. - It is not used for long-term maintenance but rather as an emergency intervention to counteract life-threatening respiratory depression. *Nalorphine* - **Nalorphine** is an older, mixed opioid agonist-antagonist that was once used for opioid overdose but has largely been replaced by naloxone due to its own opioid agonistic effects. - It does not have a role in current long-term maintenance treatment for opioid addiction. *Butorphanol* - **Butorphanol** is a mixed opioid agonist-antagonist primarily used as an analgesic, particularly for pain management. - It can precipitate withdrawal in opioid-dependent individuals and is not indicated for the treatment or maintenance of opioid addiction.
Question 10: What is the drug of choice for acute severe asthma?
- A. Short-acting beta-2 agonists (Correct Answer)
- B. Long-acting beta-2 agonists
- C. Oral theophylline
- D. Inhaled ipratropium bromide
Explanation: **Explanation:** **Short-acting beta-2 agonists (SABA)**, such as Salbutamol (Albuterol) or Terbutaline, are the drugs of choice for acute severe asthma because they provide rapid bronchodilation. They act by stimulating $\beta_2$ receptors on bronchial smooth muscle, increasing intracellular cAMP, which leads to immediate muscle relaxation. In acute settings, they are typically administered via nebulization or a metered-dose inhaler (MDI) with a spacer to ensure quick onset of action (within 5 minutes). **Why other options are incorrect:** * **Long-acting beta-2 agonists (LABA):** Drugs like Salmeterol have a slow onset of action and are used for maintenance therapy, not acute relief. (Note: Formoterol has a fast onset but is generally used in combination with ICS for maintenance and reliever therapy, not as monotherapy for acute severe attacks). * **Oral theophylline:** This has a narrow therapeutic index and a slow onset of action. It is much less effective than SABAs and carries a high risk of toxicity (arrhythmias, seizures). * **Inhaled ipratropium bromide:** This is an anticholinergic used as an *add-on* therapy to SABAs in acute severe asthma to provide synergistic bronchodilation, but it is not the first-line drug of choice. **Clinical Pearls for NEET-PG:** * **Route of choice:** Inhalation is preferred over parenteral routes due to faster action and fewer systemic side effects (like tremors and tachycardia). * **Management of Acute Severe Asthma:** The standard protocol includes high-flow oxygen, frequent SABA nebulization, and **systemic corticosteroids** (to reduce airway inflammation). * **Magnesium Sulfate:** Used intravenously in life-threatening cases that are refractory to initial treatment. * **Drug of choice for Exercise-Induced Asthma:** SABA (taken 15–20 minutes before exercise).
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