Test: Autonomic Nervous System - 1 - NEET PG MCQ

Cholinergic medications reduce the transmission from the atrium to the ventricle, so they should be avoided in cases of partial heart block.

• Cholinergic agents such as pilocarpine and physostigmine are employed in the management of angle-closure glaucoma.
• Neostigmine, which is an acetylcholinesterase inhibitor and a cholinergic drug, is utilised for treating myasthenia gravis.
• Additionally, neostigmine is used for post-operative paralytic ileus and urinary retention following surgery.

• Drug: Mechanism of action in glaucoma
• Apraclonidine/Brimonidine: Activate post-synaptic alpha 2 receptors, leading to a reduction in aqueous production.
• Latanoprost: Enhances uveoscleral outflow.
• Miotics (Pilocarpine): Promotes trabecular outflow.
• Beta blockers (Timolol/betaxolol): Lowers aqueous production.
• Carbonic anhydrase inhibitors (acetazolamide): Reduces aqueous secretion.

A cholinomimetic medication will lead to bradycardia as a side effect, making it unsuitable for treating this condition.

These are typical signs of anti-cholinesterase (organophosphate and carbamate) poisoning.

• Features of Organophosphate poisoning:
• Muscarinic symptoms: constricted pupils, increased salivation, tears, urination, defecation, gastrointestinal upset, vomiting, bronchospasm, slow heart rate.
• Nicotinic symptoms: muscle twitching and spasms, rapid heart rate, increased breathing rate.
• CNS symptoms: tremors, dizziness, loss of coordination, coma.
• Red tears: caused by the build-up of porphyrin in the tear glands.

Apraclonidine is a sympathomimetic drug employed in the treatment of open-angle glaucoma. It reduces aqueous secretion.

• It may lead to upper lid retraction as a side effect.
• Ocular allergy can also occur, although this is less common with brimonidine.

Both apraclonidine and brimonidine have the potential to induce CNS depression and apnea in neonates.

Additionally, they are contraindicated for use in children under the age of 2 years.

• Diabetic 3rd nerve palsy: Third nerve palsy caused by any factor leads to mydriasis (as the oculomotor nerve innervates the constrictor pupillae). However, since only the nerve supply is compromised while the receptors remain functional, they will respond to pilocarpine (1%), resulting in miosis.
• Adie’s tonic pupil: This condition is characterised by denervation supersensitivity. A normal pupil reacts to 1% pilocarpine but will not contract with a highly diluted solution (0.05-0.1%). In contrast, Adie’s pupil shows such supersensitivity that even this diluted solution can cause constriction.
• Uncal herniation: This condition exerts pressure on the third cranial nerve, leading to a dilated pupil; however, it will still respond to pilocarpine since the receptors are intact.
• Pharmacological block: Medications like atropine inhibit the muscarinic receptors located on the pupil. Because these receptors are nonfunctional, even substantial doses of pilocarpine cannot induce miosis.

The constrictor pupillae, a circular muscle of the iris, receives its innervation from postganglionic parasympathetic fibres originating from the Edinger-Westphal nucleus. In contrast, the dilator pupillae, which is the radial muscle of the iris, is innervated by sympathetic fibres from the cervical sympathetic chain.

The cranial nerves associated with the parasympathetic system include:

• III (oculomotor)
• VII (facial)
• IX (glossopharyngeal)
• X (vagus)

This is part of the Autonomic Nervous System.

Autonomic ganglia, including both sympathetic and parasympathetic types, secrete ACh, which activates the N_N nicotinic receptors found on the post-ganglionic fibres.

The parasympathetic system is characterised by its craniosacral outflow. The cranial component comprises:

• III (oculomotor)
• VII (facial)
• IX (glossopharyngeal)
• X (vagus) nerves

Meanwhile, the sacral section encompasses S₂ to S₄.

The neurotransmitter released at the terminal effectors of the sympathetic system is predominantly nor-adrenaline. This differs in sweat glands and hair follicles, where acetylcholine is the primary neurotransmitter. In contrast, acetylcholine is the neurotransmitter utilised in the parasympathetic system.

Metoprolol is a beta blocker that possesses local anaesthetic properties. However, these beta blockers are not suitable for treating glaucoma.

• Apraclonidine (an alpha 2 agonist),
• timolol (a beta blocker lacking local anaesthetic effects),
• and pilocarpine (a directly acting miotic) are employed in the treatment of glaucoma.

Apraclonidine and brimonidine are capable of crossing the blood-brain barrier, which may lead to central nervous system depression and apnea in neonates. Consequently, these medications are contraindicated for children under 2 years of age.

Pralidoxime and diacetylmonoxime are compounds that act as regenerator agents for cholinesterase, utilised in cases of organophosphate poisoning.

Myasthenia gravis can be distinguished from a cholinergic crisis using a short-acting anticholinesterase agent, edrophonium.

• It alleviates symptoms in myasthenia gravis.
• In contrast, it exacerbates the situation in cholinergic crisis.

Neostigmine is utilised for the management of myasthenia gravis.

Hemicholinium prevents the uptake of choline, which is the rate-limiting step in the synthesis of ACh.

• Vesamicol obstructs the transportation of ACh into synaptic vesicles.
• Botulinum toxin hampers the release of acetylcholine.
• Acetylcholine esterase is inhibited by organophosphates and carbamates.
• Pralidoxime reactivates ACh.

Neostigmine is a reversible inhibitor of cholinesterase. It is a quaternary ammonium compound, which is a lipid-insoluble agent, thus it cannot penetrate the blood-brain barrier. It undergoes partial hydrolysis by serum cholinesterase and is also partially eliminated unchanged by the kidneys. Additionally, it exhibits some agonistic effects on N_M receptors.

The activation of muscarinic (M₃) receptors leads to a reduction in blood pressure, while stimulation of the parasympathetic system does not influence blood pressure. This is due to the presence of M₃ receptors in blood vessels, despite the absence of parasympathetic innervation.

Pilocarpine is a cholinergic medication that acts directly. It induces miosis and cyclospasm (rather than cycloplegia). Additionally, it has the ability to enhance all bodily secretions.

Neostigmine is a quaternary ammonium compound and is not soluble in lipids. Its absorption from the gastrointestinal tract and its ability to penetrate the brain and cornea are significantly lower than that of physostigmine. It also exerts additional effects on N_M receptors.

Pyridostigmine has an effect that lasts 3-6 hours, while neostigmine's duration of action is 0.5-2 hours.

• Pyridostigmine is less potent than neostigmine.
• The remainder of the characteristics are comparable to those of neostigmine.

Activation of α₂ receptors found in the ciliary epithelium decreases the production of aqueous humour.