Autonomic Nervous System Drugs Practice Questions

Q: All of the following can aggravate Myasthenia gravis except :

Azathioprine. ***Azathioprine*** - **Azathioprine** is an **immunosuppressant** used to *treat* Myasthenia Gravis, meaning it *alleviates* symptoms rather than aggravating them. - It works by suppressing the immune system, thereby reducing the production of **acetylcholine receptor antibodies** that cause muscle weakness in Myasthenia Gravis. *Aminoglycoside* - **Aminoglycosides** can worsen Myasthenia Gravis by blocking **acetylcholine release** from nerve terminals and by stabilizing the **postsynaptic membrane**, further impairing neuromuscular transmission. - This effect is due to their structural similarities to **magnesium**, which can interfere with calcium-dependent acetylcholine release. *d–Tubocurarine* - **d-Tubocurarine** is a **non-depolarizing neuromuscular blocker** that acts by competing with **acetylcholine** for binding to its receptors on the muscle endplate. - Patients with Myasthenia Gravis have fewer functional acetylcholine receptors, making them highly susceptible to the effects of **neuromuscular blockers** and easily aggravated by them. *Tetracycline* - **Tetracyclines** can exacerbate Myasthenia Gravis by inhibiting **presynaptic acetylcholine release** and hindering the actions of **acetylcholine** on the postsynaptic membrane. - While less potent than aminoglycosides, they can still significantly worsen **muscle weakness** in affected individuals.

Q: Fastest acting non-depolarizing neuromuscular blocker currently available in clinical practice:

Rocuronium. ***Rocuronium*** - **Rocuronium** has the most rapid onset among all currently available **non-depolarizing neuromuscular blockers**, making it clinically advantageous for rapid sequence intubation (RSI) when **succinylcholine** is contraindicated [1]. - Its rapid onset is due to its relatively **low potency**, meaning that a higher dose is typically administered, which hastens receptor binding and the establishment of neuromuscular blockade [1]. *Rapacuronium* - **Rapacuronium** was developed as an ultra-short-acting agent with rapid onset, but it was withdrawn from the market due to concerns about its association with **bronchospasm** and other serious adverse effects. - Therefore, it is no longer available in clinical practice. *Mivacurium* - **Mivacurium** is an intermediate-acting non-depolarizing neuromuscular blocker, but its onset of action is significantly **slower than rocuronium** and it is rarely used for rapid intubation. - Its metabolism by **plasma cholinesterase** allows for a relatively quick recovery, but this does not translate to a rapid onset. *Succinylcholine* - **Succinylcholine** is a **depolarizing neuromuscular blocker** with the fastest onset of action of ALL neuromuscular blockers (depolarizing and non-depolarizing) [1]. - However, the question specifically asks for a **non-depolarizing** agent, and succinylcholine's mechanism of action and side effect profile are distinct from non-depolarizing agents [1].

Q: Injection of muscarinic agonist in conjunctival sac will lead to all of the following except

Decreased secretion from ciliary epithelium. ***Decreased secretion from ciliary epithelium*** - Muscarinic agonists **do NOT significantly decrease** aqueous humor secretion from the ciliary epithelium. - The primary mechanism for reducing intraocular pressure with drugs like **pilocarpine** is by **increasing outflow** of aqueous humor through the trabecular meshwork via contraction of the ciliary muscle, NOT by decreasing production. - Therefore, "decreased secretion from ciliary epithelium" is the correct answer to this "EXCEPT" question—it does NOT occur with muscarinic agonists. *Miosis* - Muscarinic agonists cause the **pupillary sphincter muscle** (which has M3 receptors) to contract, leading to **pupil constriction** (miosis). - This effect opens the trabecular meshwork and facilitates aqueous humor drainage. *Conjunctival and uveal hyperemia* - Muscarinic agonists cause **vasodilation** in the conjunctival and uveal blood vessels, leading to increased blood flow and **redness** (hyperemia). - This is a common side effect associated with topical application of cholinergic drugs to the eye. *Ciliary spasm* - Muscarinic agonists stimulate the **ciliary muscle** (which has M3 receptors), causing it to contract. - This contraction leads to **accommodation spasm**, resulting in blurred distance vision and brow ache, which is a common adverse effect in younger patients.

Q: Effect of dopamine on renal vessels?

Vasodilatation. ***Vasodilatation*** - Dopamine, at **low doses**, acts on D1 receptors in the renal vasculature, leading to **renal vasodilation**. - This effect increases **renal blood flow** and **glomerular filtration rate**, improving kidney perfusion. *Increased permeability* - **Increased permeability** of renal vessels is not a primary direct effect of dopamine but rather a feature of inflammatory processes or damage. - This typically leads to protein leakage, which is distinct from dopamine's hemodynamic actions. *No effect* - This option is incorrect because dopamine has distinct and well-documented effects on renal vessels. - Dopamine is commonly used in clinical practice for its **pharmacological effects** on the kidneys, such as increasing urine output and renal blood flow. *Vasoconstriction* - While dopamine can cause vasoconstriction at **high doses** by activating alpha-1 adrenergic receptors, its primary and most significant effect on renal vessels at **lower, therapeutic doses** is vasodilation. - **Vasoconstriction** would decrease renal blood flow, which is contrary to the desired effect of dopamine in renal support.

Q: Which drug is used for Myasthenia Gravis testing?

Edrophonium. ***Edrophonium*** - **Edrophonium** is an **ultrashort-acting acetylcholinesterase inhibitor** that temporarily increases acetylcholine at the neuromuscular junction, improving muscle weakness in myasthenia gravis patients. - The **Tensilon test** (using edrophonium) is performed by injecting the drug and observing for rapid, transient improvement in muscle strength, such as in eyelid ptosis or extraocular muscle weakness. *Acetylcholine* - **Acetylcholine** is the neurotransmitter responsible for muscle contraction; however, direct administration is not used for diagnosing myasthenia gravis. - In myasthenia gravis, the problem is with **acetylcholine receptors** being blocked or destroyed, not a lack of acetylcholine production itself. *Phycostigmine* - **Physostigmine** is an **acetylcholinesterase inhibitor** but has a longer duration of action and crosses the blood-brain barrier, making it less suitable for rapid diagnostic testing of myasthenia gravis compared to edrophonium. - It is sometimes used for treating **anticholinergic toxicity**, not for diagnosing myasthenia gravis. *Adrenaline* - **Adrenaline (epinephrine)** is a **catecholamine** and a neurotransmitter primarily involved in the fight-or-flight response, mainly acting on adrenergic receptors. - It has no direct role in the *diagnosis* or *pathophysiology* of myasthenia gravis, which involves cholinergic transmission.

Q: Anticholinergic which can be used as sedative and antiemetic premedication is

Hyoscine. ***Hyoscine*** - **Hyoscine** (scopolamine) is a muscarinic antagonist that readily crosses the **blood-brain barrier**, allowing it to exert central effects such as **sedation** and potent **antiemetic** actions. - Its ability to reduce secretions and prevent **nausea and vomiting** makes it a suitable anticholinergic for premedication. *Atropine* - **Atropine** is primarily used to increase **heart rate**, reduce **salivary and bronchial secretions**, and as an antidote for cholinesterase inhibitors. - While it is an anticholinergic, its central effects are less pronounced at clinical doses compared to hyoscine, making it less suitable as a sole sedative or antiemetic. *Promethazine* - **Promethazine** is an antihistamine with significant **anticholinergic, sedative**, and **antiemetic** properties. - However, it is primarily classified as an **H1-receptor antagonist** rather than a pure anticholinergic for premedication, although it is often used for these effects. *Glycopyrrolate* - **Glycopyrrolate** is a quaternary ammonium anticholinergic that does not readily cross the **blood-brain barrier**. - Its action is largely peripheral, making it effective for reducing secretions but without significant **sedative** or **antiemetic** effects.

Q: Cisatracurium is better than atracurium because:-

Less histamine release. ***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]

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

Edrophonium. ***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

Q: Anti-glaucoma drug that acts by increasing uveoscleral outflow is

Latanoprost. ***Latanoprost*** - **Latanoprost** is a **prostaglandin F2α analog** that effectively lowers intraocular pressure by significantly increasing **uveoscleral outflow**. - It works by remodeling the extracellular matrix in the ciliary body and sclera, which facilitates the drainage of aqueous humor through the uveoscleral pathway. *Dorzolamide* - **Dorzolamide** is a **topical carbonic anhydrase inhibitor** that reduces the production of aqueous humor, thus lowering intraocular pressure. - It does not directly affect the uveoscleral outflow pathway. *Pilocarpine* - **Pilocarpine** is a **cholinergic agonist** that primarily works by increasing the **trabecular outflow** of aqueous humor through contraction of the ciliary muscle [1]. - It does not significantly influence the uveoscleral outflow pathway. *Timolol* - **Timolol** is a **beta-adrenergic blocker** that reduces aqueous humor production by the ciliary body [1]. - Its mechanism of action involves decreasing the formation, rather than increasing the outflow, of aqueous humor [1].

Question 1

All of the following can aggravate Myasthenia gravis except :

Accepted Answer

Azathioprine

Answer

Aminoglycoside

Answer

d–Tubocurarine

Answer

Tetracycline

Question 2

Fastest acting non-depolarizing neuromuscular blocker currently available in clinical practice:

Accepted Answer

Rocuronium

Answer

Rapacuronium

Answer

Mivacurium

Answer

Succinylcholine

Question 3

Injection of muscarinic agonist in conjunctival sac will lead to all of the following except

Accepted Answer

Decreased secretion from ciliary epithelium

Answer

Miosis

Answer

Conjunctival and uveal hyperemia

Answer

Ciliary spasm

Question 4

Effect of dopamine on renal vessels?

Accepted Answer

Vasodilatation

Answer

Increased permeability

Answer

No effect

Answer

Vasoconstriction

Question 5

Which drug is used for Myasthenia Gravis testing?

Accepted Answer

Edrophonium

Answer

Acetylcholine

Answer

Physostigmine

Answer

Adrenaline

Question 6

Anticholinergic which can be used as sedative and antiemetic premedication is

Accepted Answer

Hyoscine

Answer

Atropine

Answer

Promethazine

Answer

Glycopyrrolate

Question 7

Cisatracurium is better than atracurium because:-

Accepted Answer

Less histamine release

Answer

No active metabolites

Answer

Shorter half-life

Answer

Better neuromuscular blockade

Question 8

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

Accepted Answer

Edrophonium

Answer

Neostigmine

Answer

Ecothiophate

Answer

Ambenonium

Question 9

Anti-glaucoma drug that acts by increasing uveoscleral outflow is

Accepted Answer

Latanoprost

Answer

Dorzolamide

Answer

Pilocarpine

Answer

Timolol

Question 10

Mechanism of action of d-tubocurarine is:

Accepted Answer

Competitive, nondepolarizing block at the Nm cholinergic receptor

Answer

Noncompetitive, depolarizing block at the Nm cholinergic receptor

Answer

Non-competitive, nondepolarizing block at the Nm cholinergic receptor

Answer

Competitive, depolarizing block at the Nm cholinergic receptor

Autonomic Nervous System Drugs — MCQs

Autonomic Nervous System Drugs — MCQs

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