Autonomic Nervous System Drugs — MCQs
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Which of the following is the site of action of botulinum toxin? (Recent NEET Pattern 2016-17)
A 20-year-old woman is admitted with the following presentation. 1% pilocarpine is not showing any response on the side of mydriasis. What is the diagnosis? (Recent NEET Pattern 2016-17)
A 35-year-old farmer consumed a pesticide due to inability to repay loans. On examination he is having increased sweating, salivation and muscle fasciculations. The family members have also brought the empty canister of insecticide. All are correct about the condition except: (Recent NEET Pattem 2016-17)
Which of the following statement is correct regarding the graph shown? (AllMS Nov 2016)
A man was brought to the emergency room after poisoning with an unknown substance. Muscarinic poisoning was suspected and he was treated for the same. What is the possible presenting feature which led to the diagnosis?
Match the following: Column A: a. Beta 1 b. Beta 2 c. Beta 3 Column B: 1. Mirabegron 2. Betaxolol 3. Salbutamol
A kid went to a temple with his grandmother and was constantly crying. On examination he had excruciating pain, hypertension, increased heart rate, sweating profusely, priapism and cold clammy skin. What should be the treatment given to the patient?
An investigator is developing a new intravenous medication that acts as a selective agonist at β-2 receptors. In addition to causing bronchodilation, this drug is most likely to have which of the following effects?
A 61-year-old woman comes to the emergency department because of a 2-hour history of headache, nausea, blurred vision, and pain in the left eye. She has had similar symptoms in the past. Her vital signs are within normal limits. The left eye is red and is hard on palpation. The left pupil is mid-dilated and nonreactive to light. Administration of which of the following drugs should be avoided in this patient?
Ritodrine is a:-
Autonomic Nervous System Drugs Indian Medical PG Practice Questions and MCQs
Question 541: Which of the following is the site of action of botulinum toxin? (Recent NEET Pattern 2016-17)
- A. Synaptobrevin and SNAP-25 (Correct Answer)
- B. Syntaxin and Synaptotagmin
- C. Synaptic cleft
- D. Synaptic vesicle
Explanation: ***Synaptobrevin and SNAP-25*** - Botulinum toxin (BoNT) is a neurotoxin that cleaves **SNARE proteins** involved in neurotransmitter release. - Specifically, BoNT A, C, and E target **SNAP-25**, while BoNT B, D, F, and G target **synaptobrevin (VAMP)**. *Syntaxin and Synaptotagmin* - **Syntaxin** is part of the SNARE complex, however, synaptotagmin is primarily involved in **calcium sensing** and triggering vesicle fusion, not a direct cleavage target of common botulinum toxins. - While syntaxin is part of the overall fusion machinery, other SNARE proteins are the primary targets for cleavage. *Synaptic cleft* - The **synaptic cleft** is the space between the presynaptic and postsynaptic neurons where neurotransmitters are released, but it is not a direct site of action for botulinum toxin which works intracellularly. - Botulinum toxin acts *inside* the presynaptic neuron, preventing the release of neurotransmitters into the cleft. *Synaptic vesicle* - The **synaptic vesicle** contains neurotransmitters, and its fusion with the presynaptic membrane is inhibited by botulinum toxin. - However, the toxin's action is on the **proteins** associated with the vesicle and the presynaptic membrane, specifically those involved in docking and fusion, rather than on the vesicle itself.
Question 542: A 20-year-old woman is admitted with the following presentation. 1% pilocarpine is not showing any response on the side of mydriasis. What is the diagnosis? (Recent NEET Pattern 2016-17)
- A. Pharmacological block (Correct Answer)
- B. Diabetic neuropathy
- C. Uncal herniation
- D. Adie tonic pupil
Explanation: ***Pharmacological block*** - A **dilated pupil** that shows **no response to 1% pilocarpine** is characteristic of **pharmacological mydriasis** caused by anticholinergic agents (atropine, scopolamine, tropicamide, homatropine). - The muscarinic receptors on the iris sphincter muscle are **competitively blocked** by these agents, preventing acetylcholine and even exogenous pilocarpine from causing pupillary constriction. - This is the **key distinguishing feature** from other causes of mydriasis: the pupil remains dilated despite administration of cholinergic agonists. - Common scenarios include **accidental exposure** to belladonna alkaloids, intentional cosmetic use, or contamination from medications. *Adie tonic pupil* - Adie's tonic pupil presents with a **dilated pupil with sluggish or absent light reflex**, but it shows **positive response to dilute pilocarpine (0.125%)** due to **denervation supersensitivity**. - This supersensitivity is the hallmark diagnostic feature distinguishing Adie's from other causes. - Since this patient shows **no response to 1% pilocarpine** (a much higher concentration), Adie's pupil is ruled out. - Typically seen in young women with **vermicular iris movements** on slit-lamp examination. *Diabetic neuropathy* - Diabetic autonomic neuropathy may affect pupillary responses, but typically causes **smaller pupils** with impaired dilation rather than fixed mydriasis. - Would be associated with other signs of diabetic neuropathy: **peripheral neuropathy, gastroparesis, orthostatic hypotension**. - Does not present as isolated, fixed mydriasis unresponsive to pilocarpine. *Uncal herniation* - Results from **compression of CN III (oculomotor nerve)** due to increased intracranial pressure. - Causes a **"blown pupil"** (dilated and fixed) with associated **ptosis and eye positioned "down and out"**. - This is a **neurosurgical emergency** with altered consciousness, not consistent with a stable outpatient presentation in a young woman. - The pupil may show minimal response to strong pilocarpine, but the clinical context is entirely different.
Question 543: A 35-year-old farmer consumed a pesticide due to inability to repay loans. On examination he is having increased sweating, salivation and muscle fasciculations. The family members have also brought the empty canister of insecticide. All are correct about the condition except: (Recent NEET Pattem 2016-17)
- A. Ach excess at neuromuscular junction leads to hypersalivation (Correct Answer)
- B. ECG shows 2nd degree heart block
- C. Atropine will reverse peripheral muscular paralysis
- D. RBC cholinesterase level decreases by >50% in organophosphate poisoning
Explanation: ***Ach excess at neuromuscular junction leads to hypersalivation*** - This statement is **INCORRECT** and is the answer to this EXCEPT question. - **Hypersalivation** is a **muscarinic effect** caused by excessive ACh stimulation of **salivary gland receptors**, not from ACh at the neuromuscular junction. - ACh excess at the **neuromuscular junction** (NMJ) causes **nicotinic effects** like muscle fasciculations, weakness, and eventually paralysis, NOT hypersalivation. - The two receptor systems are distinct: muscarinic receptors (glands, smooth muscle, heart) vs nicotinic receptors (NMJ, autonomic ganglia). *Atropine will reverse peripheral muscular paralysis* - This statement is also incorrect, but not the best answer. - Atropine blocks **muscarinic receptors** and reverses symptoms like salivation, sweating, and bradycardia. - Atropine **does NOT reverse nicotinic effects** like muscle fasciculations and paralysis at the NMJ. - **Pralidoxime (2-PAM)** is needed to reactivate cholinesterase and reverse nicotinic effects. *ECG shows 2nd degree heart block* - This statement is partially correct. - OP poisoning typically causes **bradycardia** due to excessive muscarinic stimulation of the heart. - While 2nd degree heart block can occur, bradycardia and other conduction abnormalities are more characteristic findings. *RBC cholinesterase level decreases by >50% in organophosphate poisoning* - This statement is **CORRECT**. - A significant decrease (>50%) in **RBC/plasma cholinesterase activity** is a diagnostic hallmark of OP poisoning. - This reduction reflects enzyme inhibition and correlates with severity of poisoning.
Question 544: Which of the following statement is correct regarding the graph shown? (AllMS Nov 2016)
- A. Drug in graph A is epinephrine
- B. Effect on heart in graph A can be overcome by antimuscarinic
- C. Drug acting on graph C is nor-epinephrine
- D. Drug acting on graph B is isoproterenol (Correct Answer)
Explanation: ***Drug acting on graph B is isoproterenol*** - Graph B shows a definite **increase in pulse rate** and a **decrease in peripheral resistance**, while blood pressure remains largely unchanged due to the combined effects. - **Isoproterenol** is a non-selective β-adrenergic agonist that causes increased heart rate (β1 effect) and vasodilation leading to decreased peripheral resistance (β2 effect). - This unique hemodynamic profile is characteristic of isoproterenol and distinguishes it from other catecholamines. *Drug in graph A is epinephrine* - Graph A shows a **decrease in pulse rate**, which is **not characteristic** of epinephrine at the dose shown (10 μg/min). - Epinephrine typically causes **tachycardia** due to β1-adrenergic stimulation, not bradycardia. - The cardiovascular profile in graph A does not match epinephrine's expected effects. *Effect on heart in graph A can be overcome by antimuscarinic* - The decreased pulse rate in graph A suggests **reflex bradycardia** or parasympathetic stimulation. - However, without knowing the actual drug, we cannot definitively state whether antimuscarinic agents would reverse this effect. - This option makes assumptions that cannot be verified from the graph alone. *Drug acting on graph C is nor-epinephrine* - Graph C shows **increased pulse rate** and **decreased peripheral resistance** with slight drop in blood pressure. - **Norepinephrine** primarily acts on α1-receptors, causing **vasoconstriction and increased peripheral resistance**, not decreased. - Norepinephrine would also increase blood pressure significantly, which contradicts the graph. - This cardiovascular profile does not match norepinephrine.
Question 545: A man was brought to the emergency room after poisoning with an unknown substance. Muscarinic poisoning was suspected and he was treated for the same. What is the possible presenting feature which led to the diagnosis?
- A. Diuresis
- B. Bradycardia (Correct Answer)
- C. Mydriasis
- D. Muscle fasciculations
Explanation: ***Bradycardia*** - Muscarinic poisoning stimulates **parasympathetic nervous system** activity, leading to a decrease in heart rate. - This **bradycardia** is a classic sign of excessive muscarinic receptor activation, as seen with organophosphate or carbamate poisoning [1, 2].*Diuresis* - While muscarinic receptor activation can increase bladder detrusor contraction (leading to urinary urgency and frequency) [1, 2], **diuresis** (increased urine production) is not a primary or direct presenting feature of muscarinic poisoning. - Instead, the focus is on incontinence rather than simply increased urine output.*Mydriasis* - **Mydriasis** (pupil dilation) is associated with **anticholinergic poisoning**, which blocks muscarinic receptors. - Muscarinic poisoning, conversely, causes **miosis** (pupil constriction) due to excessive stimulation of muscarinic receptors in the iris sphincter muscle.*Muscle fasciculations* - **Muscle fasciculations** are a characteristic sign of **nicotinic receptor overstimulation**, not muscarinic [1, 3]. - While both nicotinic and muscarinic receptors are activated in organophosphate poisoning, fasciculations point to the **nicotinic effects** at the neuromuscular junction [1, 3].
Question 546: Match the following: Column A: a. Beta 1 b. Beta 2 c. Beta 3 Column B: 1. Mirabegron 2. Betaxolol 3. Salbutamol
- A. a-2, b-3 ,c-1 (Correct Answer)
- B. a-2, b-1, c-3
- C. a-3, b-2, c-1
- D. a-3, b-1, c-2
Explanation: ***a-2, b-3, c-1*** - This pairing correctly matches **Betaxolol** with **Beta 1 selective** antagonism, **Salbutamol** with **Beta 2 selective** agonism, and **Mirabegron** with **Beta 3 selective** agonism. - **Betaxolol** is a beta-1 selective adrenergic receptor antagonist, primarily used in ophthalmology to reduce intraocular pressure and as an antihypertensive. **Salbutamol** is a selective beta-2 adrenergic agonist used as a bronchodilator in asthma and COPD, causing relaxation of bronchial smooth muscle. **Mirabegron** is a selective beta-3 adrenergic agonist used to treat overactive bladder by relaxing the detrusor muscle. *a-2, b-1, c-3* - This option incorrectly assigns **Mirabegron** to Beta 2. Mirabegron is a **Beta 3 selective agonist**. - It also incorrectly assigns **Salbutamol** to Beta 3. Salbutamol is a **Beta 2 selective agonist**. *a-3, b-2, c-1* - This option incorrectly assigns **Salbutamol** to Beta 1. Salbutamol is a **Beta 2 selective agonist**. - It also incorrectly assigns **Betaxolol** to Beta 2. Betaxolol is a **Beta 1 selective antagonist**. *a-3, b-1, c-2* - This option incorrectly assigns **Salbutamol** to Beta 1 and **Betaxolol** to Beta 3. - **Salbutamol** is a Beta 2 selective agonist, and **Betaxolol** is a Beta 1 selective antagonist.
Question 547: A kid went to a temple with his grandmother and was constantly crying. On examination he had excruciating pain, hypertension, increased heart rate, sweating profusely, priapism and cold clammy skin. What should be the treatment given to the patient?
- A. Atropine
- B. Phentolamine (Correct Answer)
- C. Pralidoxime
- D. Naloxone
Explanation: ***Phentolamine*** - The symptoms described (hypertension, tachycardia, sweating, priapism, cold clammy skin) are indicative of an **alpha-adrenergic crisis** or **pheochromocytoma crisis**, which results from excessive release of catecholamines (e.g., norepinephrine) [1]. - **Phentolamine** is a **non-selective alpha-adrenergic antagonist** that effectively blocks the effects of excessive catecholamines, thereby reducing blood pressure and heart rate and relieving other alpha-mediated symptoms like priapism [1]. *Atropine* - **Atropine** is an **anticholinergic drug** used to treat **bradycardia** or **organophosphate poisoning**. - It would worsen the patient's condition by potentially increasing heart rate further and would not address the underlying alpha-adrenergic overstimulation. *Pralidoxime* - **Pralidoxime** is an **acetylcholinesterase reactivator** used specifically for **organophosphate poisoning**. - It works by restoring the function of acetylcholinesterase, which is inhibited by organophosphates, and is not indicated for an adrenergic crisis. *Naloxone* - **Naloxone** is an **opioid receptor antagonist** used to reverse the effects of **opioid overdose**. - This patient's symptoms are not consistent with opioid toxicity, and naloxone would have no therapeutic benefit.
Question 548: An investigator is developing a new intravenous medication that acts as a selective agonist at β-2 receptors. In addition to causing bronchodilation, this drug is most likely to have which of the following effects?
- A. Peripheral vasoconstriction
- B. Increased uterine tone
- C. Increased gastrointestinal peristalsis
- D. Bladder detrusor relaxation (Correct Answer)
Explanation: ***Bladder detrusor relaxation*** - **β2-adrenergic receptors** are located in the detrusor muscle of the bladder, and their activation leads to **relaxation** of this smooth muscle. - This effect is mediated by the **sympathetic nervous system**, which generally promotes storage of urine. *Peripheral vasoconstriction* - **Vasoconstriction** in peripheral arteries is primarily mediated by **α1-adrenergic receptors**, not β2-receptors, which generally cause vasodilation in skeletal muscle. - Activation of β2-receptors typically leads to **vasodilation** in certain vascular beds to increase blood flow during fight-or-flight responses. *Increased uterine tone* - **β2-adrenergic receptor activation** in the uterus causes **relaxation** of the uterine smooth muscle, not increased tone. - This property is exploited therapeutically with **tocolytic agents** (e.g., terbutaline) to prevent premature labor. *Increased gastrointestinal peristalsis* - **Peristalsis** in the gastrointestinal tract is primarily regulated by the **parasympathetic nervous system** and local enteric reflexes. - **β2-receptor activation** [3] generally leads to **decreased gastrointestinal motility** and relaxation of smooth muscles in the GI tract. *General β2-Selective Agonist Properties* - β2-selective agonists are designed to minimize cardiac side effects mediated by β1-receptors [1], although this selectivity is relative [1]. They are primarily used as bronchodilators [3], acting to relax airway smooth muscle [2].
Question 549: A 61-year-old woman comes to the emergency department because of a 2-hour history of headache, nausea, blurred vision, and pain in the left eye. She has had similar symptoms in the past. Her vital signs are within normal limits. The left eye is red and is hard on palpation. The left pupil is mid-dilated and nonreactive to light. Administration of which of the following drugs should be avoided in this patient?
- A. Pilocarpine
- B. Timolol
- C. Acetazolamide
- D. Epinephrine (Correct Answer)
Explanation: ***Epinephrine*** - Epinephrine is a **sympathomimetic** agent [1] that can cause **mydriasis** (pupil dilation) [1], [2] by activating alpha-1 receptors on the iris dilator muscle. - In a patient with **angle-closure glaucoma**, mydriasis can further narrow the anterior chamber angle, worsening the blockage of aqueous humor outflow and exacerbating the **intraocular pressure** (IOP) elevation [2], [3]. *Pilocarpine* - Pilocarpine is a **muscarinic agonist** that causes **miosis** (pupil constriction) and contraction of the ciliary muscle. - Miosis pulls the iris away from the trabecular meshwork, opening the anterior chamber angle and facilitating aqueous outflow, thereby **reducing IOP** [3]. *Timolol* - Timolol is a **beta-blocker** that reduces the production of aqueous humor by the ciliary body. - It is often used as a first-line treatment for glaucoma to **lower IOP** without significantly affecting pupil size. *Acetazolamide* - Acetazolamide is a **carbonic anhydrase inhibitor** that decreases aqueous humor production. - It is an effective systemic medication for rapidly **reducing IOP** in acute angle-closure glaucoma.
Question 550: Ritodrine is a:-
- A. β antagonist
- B. α agonist
- C. β2 agonist (Correct Answer)
- D. α1 antagonist
Explanation: ***β2 agonist*** - Ritodrine is a **selective beta-2 adrenergic receptor agonist** primarily used as a **tocolytic agent** to relax the uterus and stop premature labor. - Its action involves stimulating **beta-2 receptors** in the myometrium, leading to decreased intracellular calcium and uterine smooth muscle relaxation. *α1 antagonist* - Alpha-1 antagonists block **alpha-1 adrenergic receptors**, causing vasodilation and are used to treat conditions like **hypertension** or **benign prostatic hyperplasia**. - Ritodrine's mechanism is distinct, as it targets beta-2 receptors, not alpha-1. *β antagonist* - Beta antagonists (beta-blockers) block **beta adrenergic receptors** (beta-1, beta-2, or both) and are used for conditions like **hypertension**, **angina**, or **arrhythmias**. - Ritodrine is an agonist, meaning it activates receptors, rather than blocking them. *α agonist* - Alpha agonists stimulate **alpha adrenergic receptors**, causing vasoconstriction and increased blood pressure, as seen with agents like **phenylephrine**. - Ritodrine specifically targets beta-2 receptors, leading to opposite effects like smooth muscle relaxation in the uterus and bronchi.
Practice by Chapter
Cholinergic Agonists
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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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