Autonomic Nervous System Drugs — MCQs

Autonomic Nervous System Drugs Indian Medical PG Practice Questions and MCQs

Question 571: Cisatracurium is better than atracurium because:-

A. No active metabolites
B. Shorter half-life
C. Less histamine release (Correct Answer)
D. Better neuromuscular blockade

Explanation: ***Less histamine release*** - **Cisatracurium** causes significantly less **histamine release** compared to atracurium, reducing the risk of **hypotension** and **bronchospasm**. [1] - This makes cisatracurium a safer choice for patients with **cardiovascular instability** or **asthma**. *No active metabolites* - While cisatracurium produces **laudanosine** as a metabolite, this is also true for **atracurium**. - The difference lies in the **concentration** of laudanosine and its potential for central nervous system toxicity, which is generally lower with cisatracurium. *Shorter half-life* - **Cisatracurium** generally has a **slightly longer half-life** than atracurium, but both are characterized by a relatively rapid onset and offset of action. - Their elimination primarily occurs via **Hoffman elimination** and **ester hydrolysis**, independent of renal or hepatic function. *Better neuromuscular blockade* - Both **cisatracurium** and **atracurium** are effective **neuromuscular blockers** when administered at appropriate doses. - The "better" aspect for cisatracurium relates more to its **improved safety profile** (less histamine release) rather than a significantly superior blockade efficacy. [1]

Question 572: Agent used for eliciting diagnostic differentiation of Myasthenia Gravis from Cholinergic crisis is:-

A. Edrophonium (Correct Answer)
B. Neostigmine
C. Ecothiophate
D. Ambenonium

Explanation: ***Edrophonium*** - **Edrophonium** is a **short-acting acetylcholinesterase inhibitor** (duration 5-10 minutes) used in the **Tensilon test** to differentiate myasthenic crisis from cholinergic crisis - In **myasthenic crisis**, edrophonium temporarily improves muscle strength due to increased acetylcholine at the neuromuscular junction - In **cholinergic crisis**, it worsens weakness or shows no improvement - The rapid onset and short duration allow clear observation of transient response, making it ideal for diagnostic differentiation *Neostigmine* - **Neostigmine** is a longer-acting acetylcholinesterase inhibitor (duration 2-4 hours) used for chronic management of myasthenia gravis - Its prolonged effect makes it unsuitable for rapid diagnostic differentiation in acute crisis situations - The extended duration would make it difficult to observe transient changes and could worsen a cholinergic crisis for a prolonged period *Ecothiophate* - **Ecothiophate** is an irreversible acetylcholinesterase inhibitor used primarily in ophthalmology for glaucoma - Its irreversible action and prolonged effect (days to weeks) make it completely inappropriate for crisis differentiation - Would severely exacerbate cholinergic symptoms with sustained effect that cannot be reversed *Ambenonium* - **Ambenonium** is another long-acting acetylcholinesterase inhibitor (duration 3-8 hours) used for chronic treatment of myasthenia gravis - Similar to neostigmine, its extended duration makes it unsuitable for acute diagnostic challenge - The rapid onset and offset required for the Tensilon test cannot be achieved with this agent

Question 573: Mechanism of action of d-tubocurarine is:

A. Competitive, nondepolarizing block at the Nm cholinergic receptor (Correct Answer)
B. Noncompetitive, depolarizing block at the Nm cholinergic receptor
C. Non-competitive, nondepolarizing block at the Nm cholinergic receptor
D. Competitive, depolarizing block at the Nm cholinergic receptor

Explanation: ***Competitive, nondepolarizing block at the Nm cholinergic receptor*** - **d-tubocurarine** acts as a **competitive antagonist** at the **nicotinic muscle (Nm) cholinergic receptors** on the motor endplate. - It competes with **acetylcholine (ACh)** for binding sites, preventing ACh from activating the receptor and causing **muscle paralysis** without depolarization. *Noncompetitive, depolarizing block at the Nm cholinergic receptor* - This describes the mechanism of action of **depolarizing neuromuscular blockers** like **succinylcholine**, which first *depolarize* the motor endplate before causing paralysis. - d-tubocurarine does not cause initial depolarization; it directly blocks the receptor. *Non-competitive, nondepolarizing block at the Nm cholinergic receptor* - While d-tubocurarine is **nondepolarizing**, it is a **competitive antagonist**, not a non-competitive one. - A non-competitive block would involve binding to a different site on the receptor or an associated ion channel, altering receptor function indirectly. *Competitive, depolarizing block at the Nm cholinergic receptor* - This option incorrectly combines the concepts, as **depolarizing blockers** like succinylcholine act initially by **depolarizing** the endplate, whereas d-tubocurarine is purely a **nondepolarizing** agent. - The "competitive" aspect would be true for the binding of ACh to its site on a depolarizing agent, but the effect of d-tubocurarine is simply to block, not depolarize.

Question 574: Which of the following is a uterine relaxant?

A. Salmeterol
B. Tiotropium
C. Tolterodine
D. Ritodrine (Correct Answer)

Explanation: ***Ritodrine*** **Ritodrine** is a **beta-2 adrenergic agonist** primarily used as a **tocolytic agent** to relax the uterus and prevent premature labor. It works by stimulating beta-2 receptors in the myometrium, leading to a decrease in intracellular calcium and subsequent **uterine smooth muscle relaxation** [1]. *Salmeterol* **Salmeterol** is a **long-acting beta-2 adrenergic agonist (LABA)** primarily used in the management of **asthma and COPD** to relax bronchial smooth muscle, not uterine muscle [2]. While it also stimulates beta-2 receptors, its primary clinical application is in the **airways**, not the uterus [2]. *Tiotropium* **Tiotropium** is a **long-acting anticholinergic (LAMA)** bronchodilator used for the maintenance treatment of **COPD and asthma** [2]. It functions by blocking muscarinic receptors in the bronchial smooth muscle, leading to **bronchodilation**, and has no significant effect on uterine muscle [2]. *Tolterodine* **Tolterodine** is an **antimuscarinic agent** used to treat **overactive bladder (OAB)** symptoms like urinary urgency, frequency, and urge incontinence. It works by blocking muscarinic receptors in the bladder smooth muscle, leading to **bladder relaxation**, but does not affect the uterus.

Question 575: Which agent stimulates both beta-1 and beta-2 receptors?

A. Dopamine
B. Dobutamine
C. Albuterol
D. Epinephrine (Correct Answer)

Explanation: ***Epinephrine*** - **Epinephrine** is a potent agonist at both **beta-1 (β1)** and **beta-2 (β2)** adrenergic receptors, leading to widespread sympathetic nervous system effects. - Its β1 stimulation increases **heart rate** and **contractility**, while β2 stimulation causes **bronchodilation** and vasodilation in certain vascular beds. *Dopamine* - **Dopamine** acts on different receptors depending on the dose: at low doses, it primarily activates **D1 receptors** (renal vasodilation), at intermediate doses, it activates **β1 receptors** (cardiac stimulation), and at high doses, it activates **α1 receptors** (vasoconstriction). - It does not significantly stimulate **beta-2 receptors** at therapeutic concentrations, distinguishing it from epinephrine. *Dobutamine* - **Dobutamine** is a synthetic catecholamine that acts primarily as a **β1-selective agonist**, significantly increasing **myocardial contractility** and heart rate. - While it has some weak β2 agonist activity, its predominant effect is on **β1 receptors**, making it less effective for widespread β2 stimulation compared to epinephrine. *Albuterol* - **Albuterol** is a **short-acting β2-adrenergic agonist** primarily used in the treatment of **asthma** to induce **bronchodilation**. - It has a high selectivity for **β2 receptors** in the lungs and has minimal effects on **β1 receptors** at therapeutic doses.

Question 576: How does botulinum toxin affect synaptic transmission?

A. Prevents ACh release (Correct Answer)
B. Inhibits Ca2+ release
C. Increases K+ influx
D. Blocks Na+ channels

Explanation: ***Prevents ACh release*** - Botulinum toxin acts by **cleaving SNARE proteins** (SNAP-25, synaptobrevin, syntaxin) which are essential for the fusion of acetylcholine (ACh) vesicles with the presynaptic membrane [2]. - By preventing vesicle fusion, it effectively **blocks the release of ACh** into the synaptic cleft, leading to muscle paralysis [1, 2]. *Inhibits Ca2+ release* - While **calcium influx** is crucial for neurotransmitter release, botulinum toxin's primary mechanism is not direct inhibition of calcium release from the sarcoplasmic reticulum or entry into the presynaptic terminal. - Its action is further downstream, targeting the machinery involved in **vesicle fusion** rather than the initial calcium signal. *Increases K+ influx* - An increase in **potassium (K+) influx** would typically cause hyperpolarization or counteract depolarization, which is not the direct action of botulinum toxin. - Botulinum toxin specifically targets the **release mechanism of neurotransmitters**, not the ion channels responsible for maintaining resting membrane potential or repolarization. *Blocks Na+ channels* - Blocking **sodium (Na+) channels** would prevent depolarization and action potential generation, similar to the mechanism of local anesthetics. - Botulinum toxin does not directly interfere with sodium channel function; its effect is focused on the **vesicular release process of acetylcholine**.

Question 577: Which drug is commonly used for pupil dilation during an eye exam?

A. Tropicamide (Correct Answer)
B. Latanoprost
C. Timolol
D. Prednisolone

Explanation: ***Tropicamide*** - **Tropicamide** is an **anticholinergic** agent that blocks **muscarinic receptors** in the iris **sphincter muscle**, causing **mydriasis** (pupil dilation) and also **cycloplegia** (paralysis of the ciliary muscle). - It has a rapid onset and relatively short duration of action, making it ideal for routine eye examinations. *Latanoprost* - **Latanoprost** is a **prostaglandin analog** primarily used to reduce intraocular pressure in **glaucoma**. - It increases **uveoscleral outflow** of aqueous humor and does not cause pupil dilation. *Timolol* - **Timolol** is a **beta-blocker** used to lower intraocular pressure in **glaucoma** by decreasing the production of aqueous humor. - It does not cause pupil dilation and is often used as a first-line treatment for open-angle glaucoma. *Prednisolone* - **Prednisolone** is a **corticosteroid** used to treat ocular inflammation. - It does not cause pupil dilation and, if used long-term, can actually lead to side effects such as increased intraocular pressure and cataract formation.

Question 578: A 65-year-old male with benign prostatic hyperplasia (BPH) is prescribed a drug that relaxes smooth muscle in the bladder neck and prostate. Which alpha-1 blocker is most likely to be prescribed?

A. Tamsulosin (Correct Answer)
B. Alfuzosin
C. Terazosin
D. Doxazosin

Explanation: ***Tamsulosin*** - **Tamsulosin** is a **selective alpha-1A blocker** that specifically targets alpha-1A receptors in the prostate and bladder neck, leading to smooth muscle relaxation and improved urine flow. - Its **uroSelectivity** minimizes cardiovascular side effects (orthostatic hypotension, dizziness), making it the **most commonly prescribed** alpha-1 blocker for **BPH**. - Preferred for patients who need symptomatic relief without significant blood pressure lowering effects. *Alfuzosin* - **Alfuzosin** is a **non-selective alpha-1 blocker** that acts on alpha-1A, 1B, and 1D receptors. - While effective for **BPH**, it has more cardiovascular effects than tamsulosin, including potential for orthostatic hypotension. - Often requires dose titration and may not be suitable for all patients. *Terazosin* - **Terazosin** is a **non-selective alpha-1 blocker** used for both **BPH** and hypertension. - Has significant blood pressure-lowering effects and is associated with **first-dose hypotension**. - Requires gradual dose titration starting from low doses, making it less convenient than tamsulosin. *Doxazosin* - **Doxazosin** is a **non-selective alpha-1 blocker** that relaxes smooth muscle in the prostate and also significantly affects systemic blood pressure. - While effective for **BPH**, its non-selectivity leads to orthostatic hypotension and dizziness, especially with the first dose (**first-dose phenomenon**). - Less preferred when BP control is not needed.

Question 579: A patient is diagnosed with benign prostatic hyperplasia (BPH) and is prescribed a selective alpha-1 receptor blocker. Which drug fits this description?

A. Propranolol
B. Tamsulosin (Correct Answer)
C. Labetalol
D. Clonidine

Explanation: ***Tamsulosin*** - **Tamsulosin** is a **selective alpha-1a receptor blocker** specifically approved for the treatment of **benign prostatic hyperplasia (BPH)** [1]. - It works by **relaxing the smooth muscle** in the prostate and bladder neck, improving urine flow without significantly affecting blood pressure [1], [2]. *Propranolol* - **Propranolol** is a **non-selective beta-blocker** used primarily for conditions like **hypertension**, angina, and arrhythmias. - It has no significant alpha-1 blocking activity and is not used in the treatment of BPH. *Labetalol* - **Labetalol** is an **alpha and beta-blocker**, used primarily for **hypertension**. - While it has some alpha-1 blocking effects, it is not selective for the alpha-1a receptors in the prostate and its beta-blocking effects make it inappropriate for BPH [2]. *Clonidine* - **Clonidine** is an **alpha-2 adrenergic agonist** that acts centrally to reduce sympathetic outflow. - It is used for **hypertension** and **ADHD**, and does not act as an alpha-1 blocker to relieve BPH symptoms.

Question 580: A patient is prescribed a topical prostaglandin analog for glaucoma. Which drug increases the outflow of aqueous humor and may cause iris pigmentation as a side effect?

A. Timolol
B. Latanoprost (Correct Answer)
C. Brimonidine
D. Acetazolamide

Explanation: ***Latanoprost*** - **Latanoprost** is a **prostaglandin F2α analog** that increases the outflow of aqueous humor through the **uveoscleral pathway**. - A common and unique side effect associated with latanoprost and other prostaglandin analogs is **increased iris pigmentation** (darkening of the iris) and eyelid skin, as well as increased eyelash growth. *Timolol* - **Timolol** is a **non-selective beta-blocker** that reduces aqueous humor production, thereby lowering intraocular pressure. - It does not significantly affect aqueous humor outflow and is not associated with iris pigmentation changes. *Brimonidine* - **Brimonidine** is an **alpha-2 adrenergic agonist** that reduces aqueous humor production and also slightly increases uveoscleral outflow. - While effective in lowering intraocular pressure, it is not primarily associated with iris pigmentation changes. *Acetazolamide* - **Acetazolamide** is a **carbonic anhydrase inhibitor** that decreases the production of aqueous humor. - It is often used systemically or topically (dorzolamide, brinzolamide) but does not impact aqueous humor outflow or cause iris pigmentation.

Practice by Chapter

Cholinergic Agonists

Practice Questions

Cholinergic Antagonists

Practice Questions

Adrenergic Agonists

Practice Questions

Adrenergic Antagonists

Practice Questions

Ganglionic Agents

Practice Questions

Neuromuscular Blocking Agents

Practice Questions

Autonomic Drugs in Ophthalmology

Practice Questions

Autonomic Drugs in Cardiovascular Disease

Practice Questions

Autonomic Drugs in Respiratory Disease

Practice Questions

Autonomic Drugs in Urological Disorders

Practice Questions

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free