Autonomic Nervous System Drugs — MCQs
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Acetylcholine acting on nicotinic receptors produces:
Sympathomimetic causing an increase in mean blood pressure, heart rate, and cardiac output on intravenous infusion is:
Which of the following drugs is least likely to cause sicca syndrome?
Which drug is contraindicated in angle-closure glaucoma?
Suxamethonium acts on which type of receptors?
Cardioselective β-blocker used in glaucoma?
The activation of muscarinic receptors in bronchiolar smooth muscle is associated with:
Mirabegron is a:
Which of the following is a depolarizing muscle relaxant?
Which of the following effects of adrenaline would be blocked by phentolamine but not by propranolol?
Autonomic Nervous System Drugs Indian Medical PG Practice Questions and MCQs
Question 621: Acetylcholine acting on nicotinic receptors produces:
- A. Contraction of skeletal muscle (Correct Answer)
- B. Secretion of saliva
- C. Bradycardia
- D. Pupillary constriction
Explanation: ***Contraction of skeletal muscle*** - Acetylcholine (ACh) binds to **nicotinic acetylcholine receptors (nAChRs)** at the **neuromuscular junction**, leading to muscle fiber depolarization and contraction [2]. - These receptors are **ligand-gated ion channels** that allow sodium influx, crucial for initiating muscle action potentials [2]. *Secretion of saliva* - Saliva secretion is primarily mediated by **muscarinic acetylcholine receptors (mAChRs)**, not nicotinic receptors, on glandular cells. - Parasympathetic stimulation, leading to ACh release, increases both the volume and enzyme content of saliva. *Bradycardia* - Bradycardia (slowing of heart rate) is mediated by **muscarinic acetylcholine receptors (M2 receptors)** in the heart [1]. - ACh decreases heart rate by increasing potassium efflux and decreasing cAMP levels in cardiac pacemaker cells [1]. *Pupillary constriction* - Pupillary constriction (miosis) is predominantly controlled by **muscarinic acetylcholine receptors (M3 receptors)** on the pupillary constrictor muscle. - Activation of these receptors causes the circular muscle fibers to contract, reducing pupil size.
Question 622: Sympathomimetic causing an increase in mean blood pressure, heart rate, and cardiac output on intravenous infusion is:
- A. Adrenaline (Correct Answer)
- B. Isoprenaline
- C. Norepinephrine
- D. Phenylephrine
Explanation: ***Adrenaline*** - Adrenaline (epinephrine) acts on **α1, β1, and β2 receptors**. Stimulation of these receptors leads to **vasoconstriction (α1), increased heart rate and contractility (β1), and vasodilation in skeletal muscle (β2)**, resulting in an overall increase in mean blood pressure, heart rate, and cardiac output. - The combined effects on both heart and vasculature contribute to the observed **increase across all three hemodynamic parameters**: mean blood pressure, heart rate, and cardiac output. *Isoprenaline* - Isoprenaline primarily acts on **β1 and β2 receptors**, causing a significant increase in heart rate and contractility, but also leads to widespread **vasodilation** through β2 agonism. - While it increases heart rate and cardiac output, its potent vasodilatory effect often results in a **decrease or no significant change in mean blood pressure**. *Norepinephrine* - Norepinephrine (noradrenaline) mainly acts on **α1 and β1 receptors**, causing strong vasoconstriction and increased heart rate and contractility. - This typically results in a significant **increase in mean blood pressure** and cardiac output, but the reflex bradycardia due to unopposed α1 stimulation often leads to a **less pronounced increase or even a slight decrease in heart rate**. *Phenylephrine* - Phenylephrine is a selective **α1-receptor agonist**, causing potent **vasoconstriction** leading to a significant increase in mean blood pressure. - However, the marked increase in systemic vascular resistance often triggers a **reflex bradycardia**, causing a decrease in heart rate and potentially little change or even a decrease in cardiac output.
Question 623: Which of the following drugs is least likely to cause sicca syndrome?
- A. Atropine
- B. Nicotine (Correct Answer)
- C. Olanzapine
- D. Clonidine
Explanation: ***Nicotine*** - **Nicotine** is a **nicotinic cholinergic receptor agonist** that acts primarily at autonomic ganglia and the neuromuscular junction. - Unlike antimuscarinic drugs, nicotine **does NOT block parasympathetic glandular secretion** and is **not associated with causing sicca syndrome**. - While nicotine has complex autonomic effects, it does **not significantly reduce salivary or lacrimal gland secretion**, making it the **least likely** among these options to cause sicca syndrome. - The question asks for the drug *least likely* to cause sicca syndrome, and nicotine's mechanism of action does not involve blocking secretory glands. *Atropine* - **Atropine** is a potent **muscarinic acetylcholine receptor antagonist** with strong anticholinergic effects. - It directly **blocks parasympathetic stimulation** of salivary and lacrimal glands, leading to marked reduction in secretions. - **Dry mouth (xerostomia) and dry eyes (xerophthalmia)** are classic and prominent side effects, making atropine one of the **most likely drugs to cause sicca syndrome**. *Olanzapine* - **Olanzapine** is an atypical antipsychotic with **moderate anticholinergic properties** due to muscarinic M1 receptor blockade. - **Dry mouth is a common side effect** occurring in 20-30% of patients taking olanzapine. - While less potent than atropine, olanzapine's anticholinergic effects make it **likely to contribute to sicca symptoms**. *Clonidine* - **Clonidine** is an **alpha-2 adrenergic agonist** that reduces sympathetic outflow centrally. - **Dry mouth (xerostomia)** is one of the **most common side effects** of clonidine, occurring in up to 40% of patients. - The mechanism involves decreased salivary gland secretion, making clonidine **highly likely to cause sicca syndrome symptoms**.
Question 624: Which drug is contraindicated in angle-closure glaucoma?
- A. Atropine (Correct Answer)
- B. Pilocarpine
- C. Timolol
- D. Dorzolamide
Explanation: ***Atropine*** - **Atropine** is an **anticholinergic** agent that causes **mydriasis** (pupil dilation) by blocking muscarinic receptors in the iris sphincter muscle. - In angle-closure glaucoma, pupillary dilation can narrow the **anterior chamber angle**, preventing aqueous humor outflow and acutely increasing **intraocular pressure**. *Pilocarpine* - **Pilocarpine** is a **muscarinic agonist** that causes **miosis** (pupil constriction) and contraction of the ciliary muscle, widening the anterior chamber angle. - This action facilitates **aqueous humor outflow**, making it a treatment for, not contraindicated in, angle-closure glaucoma. *Timolol* - **Timolol** is a **beta-blocker** that reduces aqueous humor production, thereby lowering intraocular pressure. - It does not significantly affect pupil size or the anterior chamber angle, making it a safe and effective treatment for various forms of glaucoma, including open-angle. *Dorzolamide* - **Dorzolamide** is a **carbonic anhydrase inhibitor** that reduces aqueous humor production. - Like timolol, it primarily acts to lower intraocular pressure without affecting pupil size or the anterior chamber angle, making it suitable for glaucoma treatment.
Question 625: Suxamethonium acts on which type of receptors?
- A. Nicotinic acetylcholine receptors (Correct Answer)
- B. Muscarinic acetylcholine receptors
- C. Adrenergic receptors
- D. Dopaminergic receptors
Explanation: ***Nicotinic acetylcholine receptors*** - **Suxamethonium** is a depolarizing neuromuscular blocker that primarily acts as an **agonist** at the **nicotinic acetylcholine receptors** at the neuromuscular junction [1], [2]. - This initial activation leads to depolarization, followed by a persistent depolarization that prevents further muscle contraction, resulting in **flaccid paralysis** [1]. *Muscarinic acetylcholine receptors* - **Muscarinic receptors** are primarily found in the **autonomic nervous system** and target organs (e.g., heart, smooth muscle, glands), mediating parasympathetic effects [3]. - While acetylcholine does act on these receptors, **suxamethonium** has only weak and clinically insignificant effects here compared to its primary action at the neuromuscular junction. *Adrenergic receptors* - **Adrenergic receptors** (alpha and beta) are activated by **catecholamines** like adrenaline and noradrenaline, mediating effects of the sympathetic nervous system. - **Suxamethonium** does not bind to or exert its primary pharmacological action through these receptors. *Dopaminergic receptors* - **Dopaminergic receptors** are primarily involved in the central nervous system, mediating effects related to motor control, reward, and cognition. - **Suxamethonium** does not target these receptors; its action is peripheral at the **neuromuscular junction** [4].
Question 626: Cardioselective β-blocker used in glaucoma?
- A. Timolol
- B. Betaxolol (Correct Answer)
- C. Acebutalol
- D. Carvedilol
Explanation: ***Betaxolol*** - **Betaxolol** is a **cardioselective β1-adrenergic receptor blocker** that reduces aqueous humor production, making it suitable for glaucoma patients, especially those with pulmonary disease. - Its **selectivity for β1 receptors** minimizes systemic side effects on the lungs (bronchoconstriction) compared to non-selective β-blockers. *Timolol* - **Timolol** is a **non-selective β-blocker** commonly used in glaucoma to reduce intraocular pressure. - It blocks both **β1 and β2 receptors**, which can lead to systemic side effects like bronchoconstriction and bradycardia, making it less suitable for patients with **asthma or COPD**. *Acebutalol* - **Acebutalol** is a **cardioselective β1-blocker** with **intrinsic sympathomimetic activity (ISA)**, primarily used for hypertension and arrhythmias. - While cardioselective, it is **not commonly formulated or indicated for topical ocular use** in glaucoma. *Carvedilol* - **Carvedilol** is a **non-selective β-blocker** with **alpha-1 adrenergic blocking activity**, primarily used for heart failure and hypertension. - It is **not used for glaucoma** as it is not formulated for topical ophthalmic application and its systemic effects are not ideal for this purpose.
Question 627: The activation of muscarinic receptors in bronchiolar smooth muscle is associated with:
- A. Increase in IP3 and DAG (Correct Answer)
- B. Inhibition of protein kinase C
- C. Activation of adenylyl cyclase
- D. Opening of Na+/K+ cation channels
Explanation: ***Increase in IP3 and DAG*** - **Muscarinic receptors** on bronchial smooth muscle (M3 receptors) are **Gq protein-coupled receptors** [1]. - Activation of **Gq proteins** leads to the activation of **phospholipase C**, which hydrolyzes **PIP2** into **IP3** and **DAG** [1, 3]. *Inhibition of protein kinase C* - **DAG** (diacylglycerol), produced from the breakdown of PIP2, **activates protein kinase C (PKC)**, rather than inhibiting it [2]. - This activation of PKC contributes to downstream cellular responses, including smooth muscle contraction [1]. *Activation of adenylyl cyclase* - **Adenylyl cyclase** is typically activated by **Gs protein-coupled receptors**, leading to an increase in **cAMP**. - **Muscarinic (M3) receptors** are **Gq-coupled**, so they do not activate adenylyl cyclase; instead, they operate through the phospholipase C pathway [1, 3]. *Opening of Na+/K+ cation channels* - While some neurotransmitter receptors are **ligand-gated ion channels** (e.g., nicotinic receptors), muscarinic receptors are **G protein-coupled receptors** [1]. - Their activation does not directly lead to the opening of **Na+/K+ cation channels**; rather, they initiate intracellular signaling cascades.
Question 628: Mirabegron is a:
- A. Beta-3 antagonist
- B. Beta-3 adrenergic agonist (Correct Answer)
- C. Beta-1 agonist
- D. Beta-1 antagonist
Explanation: Mirabegron is a: ***Beta-3 adrenergic agonist*** - **Mirabegron** selectively stimulates **beta-3 adrenergic receptors** in the bladder [1]. - This activation leads to **relaxation of the detrusor muscle**, increasing bladder capacity and reducing urgency. *Beta-3 antagonist* - An **antagonist** would block the beta-3 receptors, which would constrict the detrusor muscle and worsen symptoms of overactive bladder. - This mechanism of action is opposite to the therapeutic effect of mirabegron. *Beta-1 agonist* - **Beta-1 agonists** primarily affect the heart, increasing heart rate and contractility. - Mirabegron has very low affinity for beta-1 receptors, making this an incorrect classification. *Beta-1 antagonist* - **Beta-1 antagonists** (beta-blockers) are used to decrease heart rate and blood pressure. - This is an entirely different pharmacological class with no direct relevance to mirabegron's mechanism of action on the bladder.
Question 629: Which of the following is a depolarizing muscle relaxant?
- A. Succinylcholine (Correct Answer)
- B. Rocuronium
- C. Vecuronium
- D. Atracurium
Explanation: ***Succinylcholine*** - **Succinylcholine** is the only **depolarizing neuromuscular blocker** used clinically [1], [2]. - It works by acting as an **acetylcholine receptor agonist**, causing initial muscle fasciculations followed by sustained depolarization and paralysis [3], [4]. - Characterized by Phase I block (not reversed by anticholinesterases) [4]. *Vecuronium* - **Vecuronium** is a **non-depolarizing neuromuscular blocker** (competitive antagonist). - It acts by competitively blocking acetylcholine at the neuromuscular junction without causing depolarization. - Can be reversed by anticholinesterases like neostigmine. *Rocuronium* - **Rocuronium** is a **non-depolarizing muscle relaxant** with rapid onset of action [1]. - It competitively blocks nicotinic receptors at the neuromuscular junction. - Can be reversed by sugammadex (specific reversal agent) or anticholinesterases. *Atracurium* - **Atracurium** is a **non-depolarizing neuromuscular blocker** with intermediate duration. - Undergoes Hofmann elimination and ester hydrolysis, making it useful in renal/hepatic failure. - Does not cause depolarization; acts as a competitive antagonist at the nicotinic receptor.
Question 630: Which of the following effects of adrenaline would be blocked by phentolamine but not by propranolol?
- A. Cardiac stimulation
- B. Relaxation of bronchial smooth muscle
- C. Relaxation of uterus
- D. Contraction of radial smooth muscle in the iris (Correct Answer)
Explanation: ***Contraction of radial smooth muscle in the iris*** - This effect is mediated by **α1-adrenergic receptors**. **Phentolamine** is a non-selective **α-blocker** and would block this effect. - **Propranolol** is a **non-selective β-blocker** and would not block α1-mediated effects. *Cardiac stimulation* - This effect is primarily mediated by **β1-adrenergic receptors** in the heart. - **Propranolol** is a non-selective **β-blocker** and would block this effect, while phentolamine (an **α-blocker**) would not. *Relaxation of bronchial smooth muscle* - This effect is mediated by **β2-adrenergic receptors** in the bronchi. - **Propranolol**, a non-selective **β-blocker**, would block this effect, potentially causing bronchoconstriction in susceptible individuals. Phentolamine would not. *Relaxation of uterus* - This effect is mediated by **β2-adrenergic receptors** in the uterus. - **Propranolol** would block this β2-mediated relaxation, while **phentolamine** (an α-blocker) would not.
Practice by Chapter
Cholinergic Agonists
Practice Questions
Cholinergic Antagonists
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Adrenergic Agonists
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Adrenergic Antagonists
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Ganglionic Agents
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Neuromuscular Blocking Agents
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Autonomic Drugs in Ophthalmology
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Autonomic Drugs in Cardiovascular Disease
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Autonomic Drugs in Respiratory Disease
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Autonomic Drugs in Urological Disorders
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