Autonomic Nervous System Drugs Practice Questions

Q: Which of the following is the site of action of botulinum toxin? (Recent NEET Pattern 2016-17)

Synaptobrevin and SNAP-25. ***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.

Q: Which of the following statement is correct regarding the graph shown? (AllMS Nov 2016)

Drug acting on graph B is isoproterenol. ***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.

Q: 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?

Bradycardia. ***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].

Q: Match the following: Column A: a. Beta 1 b. Beta 2 c. Beta 3 Column B: 1. Mirabegron 2. Betaxolol 3. Salbutamol

a-2, b-3 ,c-1. ***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.

Q: 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?

Phentolamine. ***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.

Q: 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?

Bladder detrusor relaxation. ***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].

Q: 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?

Epinephrine. ***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.

Q: Ritodrine is a:-

β2 agonist. ***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.

Question 1

Which of the following is the site of action of botulinum toxin? (Recent NEET Pattern 2016-17)

Accepted Answer

Synaptobrevin and SNAP-25

Answer

Syntaxin and Synaptotagmin

Answer

Synaptic cleft

Answer

Synaptic vesicle

Question 2

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)

Accepted Answer

Pharmacological block

Answer

Diabetic neuropathy

Answer

Uncal herniation

Answer

Adie tonic pupil

Question 3

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)

Accepted Answer

Ach excess at neuromuscular junction leads to hypersalivation

Answer

ECG shows 2nd degree heart block

Answer

Atropine will reverse peripheral muscular paralysis

Answer

RBC cholinesterase level decreases by >50% in organophosphate poisoning

Question 4

Which of the following statement is correct regarding the graph shown? (AllMS Nov 2016)

Accepted Answer

Drug acting on graph B is isoproterenol

Answer

Drug in graph A is epinephrine

Answer

Effect on heart in graph A can be overcome by antimuscarinic

Answer

Drug acting on graph C is nor-epinephrine

Question 5

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?

Accepted Answer

Bradycardia

Answer

Diuresis

Answer

Mydriasis

Answer

Muscle fasciculations

Question 6

Match the following:

Column A:
a. Beta 1
b. Beta 2
c. Beta 3

Column B:
1. Mirabegron
2. Betaxolol
3. Salbutamol

Accepted Answer

a-2, b-3 ,c-1

Answer

a-2, b-1, c-3

Answer

a-3, b-2, c-1

Answer

a-3, b-1, c-2

Question 7

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?

Accepted Answer

Phentolamine

Answer

Atropine

Answer

Pralidoxime

Answer

Naloxone

Question 8

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?

Accepted Answer

Bladder detrusor relaxation

Answer

Peripheral vasoconstriction

Answer

Increased uterine tone

Answer

Increased gastrointestinal peristalsis

Question 9

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?

Accepted Answer

Epinephrine

Answer

Pilocarpine

Answer

Timolol

Answer

Acetazolamide

Question 10

Ritodrine is a:-

Accepted Answer

β2 agonist

Answer

β antagonist

Answer

α agonist

Answer

α1 antagonist

Autonomic Nervous System Drugs — MCQs

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