Autonomic Nervous System Drugs — MCQs

Autonomic Nervous System Drugs Indian Medical PG Practice Questions and MCQs

Question 551: All are true about atropine poisoning, except

A. Decreased temperature (Correct Answer)
B. Dysarthria
C. Dysphagia
D. Dilated pupils

Explanation: ***Decreased temperature*** - Atropine is an **anticholinergic** agent that blocks muscarinic receptors, leading to decreased sweating and **hyperthermia** (increased temperature) in poisoning. - The phrase **"hot as a hare"** is a classic mnemonic for atropine poisoning, referring to this elevated body temperature. *Dysarthria* - **Dysarthria** (slurred or difficult speech) can be a symptom of atropine poisoning due to the **CNS effects** of anticholinergic toxicity. - Atropine crosses the blood-brain barrier and can cause a range of neurological symptoms including agitation, delirium, and impaired speech. *Dysphagia* - **Dysphagia** (difficulty swallowing) is a common symptom in atropine poisoning, related to the **drying of oral and pharyngeal secretions** due to anticholinergic effects. - The mouth becomes very dry, making it difficult to form a food bolus and swallow effectively. *Dilated pupils* - **Dilated pupils (mydriasis)** unresponsive to light are a hallmark sign of atropine poisoning, as atropine blocks parasympathetic innervation to the iris sphincter muscle. - This symptom is often described in the mnemonic as **"blind as a bat"** due to the associated blurred vision and photophobia.

Question 552: Mechanism of action of atropine in treatment of organophosphate poisoning is?

A. It inhibits secretion of acetylcholine
B. It has antimuscarinic activity (Correct Answer)
C. It is reactivator of acetylcholine esterase enzyme
D. It is agonist of acetylcholine receptors

Explanation: ***It has antimuscarinic activity*** - **Organophosphate poisoning** leads to **excessive acetylcholine** at muscarinic receptors, causing symptoms like miosis, bradycardia, and increased secretions. - **Atropine** is a **competitive antagonist** at these muscarinic receptors, thereby blocking the effects of excess acetylcholine. *It inhibits secretion of acetylcholine* - Atropine does not directly inhibit the secretion of **acetylcholine** from nerve terminals. - Its action is postsynaptic, specifically at the **receptor level**. *It is reactivator of acetylcholine esterase enzyme* - **Pralidoxime (2-PAM)** and other **oximes** are the drugs that reactivate **acetylcholinesterase**. - Atropine does not reactivate the enzyme; it only blocks the effects of acetylcholine. *It is agonist of acetylcholine receptors* - An **agonist** would mimic the effects of acetylcholine, which would worsen the symptoms of organophosphate poisoning. - Atropine is an **antagonist**, meaning it blocks the receptors.

Question 553: All of the following drugs are used for the treatment of urinary incontinence except:

A. Ipratropium (Correct Answer)
B. Oxybutynin
C. Tolterodine
D. Darifenacin

Explanation: ***Ipratropium*** - **Ipratropium** is a short-acting muscarinic antagonist primarily used as a **bronchodilator** in obstructive lung diseases. - While it has anticholinergic properties, it is not typically used for **urinary incontinence** due to its limited systemic absorption and short duration of action, making it less effective for bladder control compared to other agents. *Oxybutynin* - **Oxybutynin** is a commonly prescribed **muscarinic antagonist** that acts by relaxing the bladder detrusor muscle, increasing bladder capacity and reducing involuntary contractions. - It is effective in treating **overactive bladder** and urge incontinence. *Tolterodine* - **Tolterodine** is a **muscarinic receptor antagonist** that specifically targets M2 and M3 receptors in the bladder, reducing bladder hyperreactivity. - It is used for the symptomatic treatment of **urge incontinence** and overactive bladder. *Darifenacin* - **Darifenacin** is a highly M3-selective muscarinic receptor antagonist, which means it primarily blocks the M3 receptors responsible for **detrusor muscle contraction**. - Its selectivity helps minimize side effects common to less selective anticholinergics and is used for the treatment of **overactive bladder** with symptoms of urgency, frequency, and urge incontinence.

Question 554: All of the following functions of vasopressin are mediated by V1 receptors, except

A. Vasoconstriction
B. Smooth muscle contraction
C. Water reabsorption (Correct Answer)
D. None of the options

Explanation: ***Water reabsorption*** - Vasopressin's effect on **water reabsorption** in the kidney collecting ducts is primarily mediated by **V2 receptors**. - **V2 receptors** activate a G protein-coupled signaling pathway leading to the insertion of **aquaporin-2 channels** into the apical membrane, increasing water permeability. *Vasoconstriction* - **Vasoconstriction** is a well-known function of vasopressin, mediated by its binding to **V1a receptors** (a subtype of V1 receptors) on vascular smooth muscle cells. - This activation leads to an increase in **intracellular calcium**, causing the muscle cells to contract and the blood vessels to narrow. *Smooth muscle contraction* - Vasopressin can induce **smooth muscle contraction** in various tissues, including the gastrointestinal tract and uterus, primarily through **V1 receptors**. - This effect is similar to its vasoconstrictor action, involving **calcium mobilization** and muscle fiber shortening. *None of the options* - This option is incorrect because **water reabsorption** is indeed mediated by V2 receptors, not V1 receptors. - The other functions listed (vasoconstriction and smooth muscle contraction) are correctly attributed to **V1 receptors**.

Question 555: All of the following are cycloplegics except :

A. Phenylephrine (Correct Answer)
B. Atropine
C. Cocaine
D. Homatropine

Explanation: ***Phenylephrine*** - **Phenylephrine** is a **sympathomimetic** agent that primarily acts as a **mydriatic** (dilates the pupil) by stimulating the **alpha-1 adrenergic receptors** in the iris dilator muscle [1], [2]. - It has **absolutely no cycloplegic effect**, meaning it does not paralyze the ciliary muscle or affect accommodation at all [1]. - This makes it the **only pure mydriatic** among the options, with zero cycloplegic action [3]. *Atropine* - **Atropine** is a potent **anticholinergic** agent that blocks **muscarinic receptors** in the ciliary body, causing **strong cycloplegia** (paralysis of accommodation) [1], [4]. - Duration of cycloplegia: **7-14 days**, making it the longest-acting cycloplegic. - Also causes mydriasis by paralyzing the iris sphincter muscle. *Cocaine* - **Cocaine** is a **local anesthetic** and **sympathomimetic** that inhibits norepinephrine reuptake, causing **mydriasis** [2]. - Unlike phenylephrine, cocaine can produce **weak cycloplegic effects** through its local anesthetic action and sympathetic stimulation, though much less than anticholinergics. - Primarily used diagnostically in ophthalmology (e.g., Horner's syndrome testing) [2]. - Since it does have some cycloplegic effect (albeit minimal), it is technically a cycloplegic, making **phenylephrine the correct answer** as the only drug with no cycloplegia at all. *Homatropine* - **Homatropine** is an **anticholinergic** agent with **moderate cycloplegic** potency. - Duration: **1-3 days** (shorter than atropine, longer than tropicamide). - Blocks **muscarinic receptors** in the ciliary body, causing cycloplegia and mydriasis.

Question 556: Which of the following would increase the levels of acetylcholine in the synaptic cleft?

A. Administration of glucose
B. Activation of nicotinic receptors
C. Inhibition of acetylcholinesterase (Correct Answer)
D. Activation of muscarinic receptors

Explanation: ***Inhibition of acetylcholinesterase*** - **Acetylcholinesterase** is the enzyme responsible for breaking down acetylcholine in the synaptic cleft. - By **inhibiting** this enzyme, acetylcholine persists longer in the cleft, leading to increased levels and prolonged effects. *Administration of glucose* - **Glucose** is the primary energy source for cellular function, including neurotransmitter synthesis and release. - While essential for overall neuronal health, directly administering glucose does not specifically increase acetylcholine levels in the synaptic cleft. *Activation of nicotinic receptors* - **Nicotinic receptors** are postsynaptic receptors that bind acetylcholine, causing neuronal depolarization and muscle contraction. - Their activation mediates the effects of acetylcholine but does not influence the amount of acetylcholine present in the synaptic cleft. *Activation of muscarinic receptors* - **Muscarinic receptors** are another class of acetylcholine receptors, often found on target organs of the parasympathetic nervous system. - Like nicotinic receptors, their activation responds to acetylcholine but does not directly increase its concentration in the synaptic cleft.

Question 557: M2 cholinergic receptor is located at

A. Glands
B. Heart (Correct Answer)
C. Lungs
D. Skeletal muscle

Explanation: ***Heart*** - The **M2 muscarinic acetylcholine receptor** is predominantly located in the **heart**, where its activation mediates parasympathetic effects. - Activation of M2 receptors in the heart leads to a **decrease in heart rate** and force of contraction. *Glands* - **Glandular secretions**, such as saliva, tears, and sweat, are primarily mediated by **M3 muscarinic receptors**. - While M2 receptors may have some minor presence, M3 is the dominant subtype for secretory functions. *Lungs* - **Bronchoconstriction** and increased **mucus secretion** in the lungs are primarily mediated by **M3 muscarinic receptors**. - M2 receptors are present, but their role is often considered to be inhibitory to other M3 effects or to modulate neurotransmitter release. *Skeletal muscle* - **Skeletal muscle contraction** is mediated by **nicotinic acetylcholine receptors (Nm)** at the neuromuscular junction. - Muscarinic receptors, including M2, are not directly involved in skeletal muscle contraction.

Question 558: Non-depolarizing neuromuscular blocker is characterized by

A. Non competitive neuromuscular blocker
B. Reversed by neostigmine (Correct Answer)
C. Induces fasciculations
D. Persistent stimulator of nicotinic cholinergic receptors

Explanation: ***Reversed by neostigmine*** - **Non-depolarizing neuromuscular blockers** are **competitive antagonists** at the **nicotinic acetylcholine receptors** at the neuromuscular junction. - **Neostigmine** is an **acetylcholinesterase inhibitor** that increases the concentration of acetylcholine in the synaptic cleft, thereby overcoming the competitive blockade. *Non competitive neuromuscular blocker* - Non-depolarizing neuromuscular blockers are, by definition, **competitive antagonists** at the **nicotinic acetylcholine receptors**. - A non-competitive blocker would bind to a different site on the receptor or an allosteric site to produce its effect. *Induces fasciculations* - **Fasciculations** (visible muscle twitching) are characteristic of **depolarizing neuromuscular blockers** like **succinylcholine**, as they initially activate the receptors before causing prolonged depolarization and paralysis. - Non-depolarizing blockers do not typically cause fasciculations because they prevent acetylcholine from binding and activating the receptors. *Persistent stimulator of nicotinic cholinergic receptors* - This describes the mechanism of action of **depolarizing neuromuscular blockers** like **succinylcholine**, which persistently activate the receptor, leading to initial fasciculations followed by sustained depolarization and paralysis. - **Non-depolarizing blockers** act as **antagonists**, preventing activation of the receptors.

Question 559: Drug used for d-TC reversal is

A. Diazepam
B. Neostigmine (Correct Answer)
C. Atropine
D. Atracurium

Explanation: ***Neostigmine*** - **Neostigmine** is an **acetylcholinesterase inhibitor** that increases the concentration of **acetylcholine** at the neuromuscular junction, effectively reversing the effects of competitive (d-TC) neuromuscular blockers. - It is commonly administered with an **anticholinergic agent** like atropine or glycopyrrolate to prevent undesired muscarinic side effects. *Diazepam* - **Diazepam** is a **benzodiazepine** primarily used as an **anxiolytic**, sedative, anticonvulsant, and muscle relaxant (central action), not for reversing neuromuscular blockade. - It potentiates the effect of **GABA**, leading to central nervous system depression. *Atropine* - **Atropine** is an **anticholinergic agent** that blocks muscarinic acetylcholine receptors. - While it is often co-administered with neostigmine to counteract its muscarinic side effects (e.g., bradycardia, salivation), it does not directly reverse the neuromuscular blockade caused by d-TC. *Atracurium* - **Atracurium** is an **intermediate-duration, non-depolarizing neuromuscular blocking agent** itself, similar in action to d-tubocurarine (d-TC). - Therefore, it would worsen, rather than reverse, the neuromuscular blockade.

Question 560: To which muscle relaxant are patients with myasthenia gravis (MG) most sensitive?

A. Gallamine (Correct Answer)
B. Atracurium
C. Scoline
D. Decamethonium

Explanation: ***Gallamine*** - Patients with **myasthenia gravis (MG)** have fewer functional **acetylcholine receptors** at the neuromuscular junction, making them **extremely sensitive** to **non-depolarizing neuromuscular blockers** [1]. - Gallamine is a **long-acting non-depolarizing agent** with **no spontaneous degradation pathway**, relying entirely on renal elimination, which makes the **prolonged neuromuscular blockade particularly dangerous** in MG patients. - MG patients require **markedly reduced doses** (up to 50% reduction) of non-depolarizing agents, and standard doses can lead to **severe, prolonged paralysis** and respiratory failure. - Among non-depolarizing agents, **longer-acting drugs like gallamine** pose the greatest clinical risk due to extended blockade duration [2]. *Atracurium* - While atracurium is also a **non-depolarizing blocker** and MG patients are sensitive to it, it has a **more predictable, shorter duration** due to its unique **Hofmann elimination** (spontaneous degradation at physiological pH and temperature). - This spontaneous breakdown makes it **relatively safer** in MG patients compared to longer-acting agents that depend on hepatic or renal elimination. - Still requires dose reduction in MG, but with better safety profile. *Scoline (Succinylcholine)* - Scoline is a **depolarizing neuromuscular blocker** that acts differently from non-depolarizing agents [3]. - MG patients typically show **resistance** to succinylcholine initially (require **larger doses**) because they have fewer receptors to depolarize. - This is **opposite to the hypersensitivity** seen with non-depolarizing blockers, making this option incorrect for "most sensitive." *Decamethonium* - Decamethonium is another **depolarizing blocker**, now obsolete in clinical practice. - Like succinylcholine, MG patients show **initial resistance** rather than hypersensitivity, requiring higher doses for effect [4]. - This contradicts the concept of increased sensitivity.

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

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