Test: Autonomic Nervous System - 2 - NEET PG MCQ

• It has a longer duration of action compared to timolol.
• Levobunolol is another non-selective β-blocker applied topically for glaucoma treatment.

• Bronchospasm and diarrhoea are indicative of muscarinic stimulation.
• Muscle spasms can occur due to nicotinic stimulation.

Pilocarpine is a directly acting cholinomimetic, while physostigmine functions as an indirectly acting cholinomimetic, both of which are beneficial for treating glaucoma.

All symptoms are indicative of anticholinesterase poisoning, except for elevated blood pressure and heart rate.

• At elevated doses, ACh can activate both N_N and N_M receptors.
• These effects may arise from the nicotinic actions of ACh.

Atropine acts as a non-selective antagonist at muscarinic receptors.

• It is capable of crossing the blood-brain barrier and can counteract the muscarinic effects within the CNS.
• Additionally, it can reverse hypertension and bronchoconstriction that result from the stimulation of muscarinic receptors.

However, muscle paralysis is attributed to nicotinic (N_N) action, which atropine does not influence.

Postural hypotension results from the inhibition of the sympathetic system. Ganglion blockers prevent transmission across both sympathetic and parasympathetic ganglia, while muscarinic blockers solely inhibit parasympathetic function.

• diarrhoea
• increased secretions

Neostigmine functions by obstructing the enzyme acetylcholinesterase. This enzyme plays a role in the breakdown of ACh, thus neostigmine elevates the synaptic concentration of ACh.

• Muscle weakness may be alleviated by the activation of N_M receptors at the muscle end plate due to the heightened levels of ACh.

Medications that compete with acetylcholine at the neuromuscular junction are known as either competitive or non-depolarising neuromuscular blockers. These agents function as muscle relaxants. Unlike depolarising muscle relaxants, they do not induce initial fasciculations.

Donepezil, rivastigmine, galantamine, and tacrine are cholinergic medications that work by inhibiting the cholinesterase enzyme, making them beneficial for Alzheimer’s disease.

Memantine functions as an NMDA receptor antagonist and is also employed in the treatment of Alzheimer’s disease.

Most blood vessels have cholinergic M₃ receptors, yet lack a parasympathetic nerve supply. When ACh is administered externally, it can activate M₃ receptors, leading to vasodilation.

• Activation of M₃ receptors boosts the production of NO (endothelium-derived relaxing factor; EDRF), which causes smooth muscle relaxation and promotes vasodilation.
• Vasodilation may also occur indirectly through the inhibition of NA release from nerve endings by ACh.

If the endothelium is compromised, ACh can activate receptors on vascular smooth muscle cells, leading to vasoconstriction.

Pralidoxime is an ACh esterase reactivator employed in cases of organophosphate poisoning. Monitoring blood cholinesterase levels can assist in assessing therapy; however, RBC cholinesterase levels provide a more accurate indication of ACh esterase activity compared to serum or plasma levels. This is particularly true because, with prolonged exposure to organophosphates, serum levels may normalise while RBC levels continue to remain suppressed.

• Chlorinated pesticides, such as DDT, act as CNS stimulants.
• Overdoses of these substances are managed with diazepam-like medications.
• Pralidoxime does not play a role in treating chlorinated pesticide overdoses.

Nerve agents used in warfare function by inhibiting acetyl cholinesterase. Treatment for exposure includes atropine and oximes. When atropine is administered alongside pralidoxime, the symptoms of atropinisation may manifest sooner than anticipated compared to when atropine is used in isolation.

Due to its potential for hepatotoxicity and the need for frequent dosing, tacrine is not utilised as frequently as other medications.

• Poisoning caused by anticholinesterase agents, such as organophosphate compounds, attaches to the esteratic site of AChE.

The medication employed in the ameliorative test (tensilon test) for myasthenia gravis is edrophonium. It is classified as a cholinergic drug and is utilised for diagnosing myasthenia gravis due to its brief duration of action (10–30 minutes).

• It exhibits no activity on nicotinic receptors.
• Additionally, it does not affect the release of ACh.

Pralidoxime is a reactivator of cholinesterase that is beneficial in cases of poisoning caused by organophosphates, such as malathion and parathion.

• Causes of pinpoint pupils include:
• Opioid poisoning
• Organophosphate poisoning
• Carbamate poisoning
• Carbolic acid poisoning
• Pontine haemorrhage