Introduction to Drugs Acting on Peripheral Nervous System
Moving from general principles to specific body systems, this unit focuses on the Peripheral Nervous System (PNS). It examines the pharmacology of the Autonomic Nervous System (ANS)—both sympathetic (fight or flight) and parasympathetic (rest and digest) drugs. Furthermore, it covers the Somatic nervous system, detailing the drugs used in the operating room to paralyze skeletal muscles (Neuromuscular blockers) to allow for intubation. Finally, it explores the mechanism of Local Anesthetics used in dentistry and minor surgeries to completely block pain signals in isolated areas.
Syllabus & Topics
- 1Organization and function of ANS.
- 2Parasympathomimetics and Parasympatholytics.
- 3Sympathomimetics and Sympatholytics.
- 4Neuromuscular blocking agents (Non-depolarizing and Depolarizing).
- 5Skeletal muscle relaxants (Centrally and peripherally acting).
- 6Local anesthetic agents: Chemistry, mechanism of action, and techniques.
- 7Drugs used in Myasthenia gravis and Glaucoma.
Learning Objectives
Frequently Asked Questions (FAQs)
Q1. How Do Local Anesthetics Work?
Local anesthetics such as Lidocaine and Bupivacaine block voltage-gated sodium channels on the axonal membrane of sensory neurons from the intracellular side. This prevents sodium influx, inhibits depolarization, and stops the conduction of pain action potentials to the brain.
Q2. Why is Adrenaline Often Combined with Local Anesthetics?
Adrenaline (epinephrine) produces local vasoconstriction at the injection site. This reduces blood flow, slows the removal of the anesthetic from the site, prolongs the duration of nerve block, and decreases systemic toxicity by limiting absorption into the circulation.
Q3. What are Depolarizing vs Non-Depolarizing Skeletal Muscle Relaxants?
Non-depolarizing agents such as Pancuronium act as competitive antagonists at nicotinic acetylcholine receptors at the neuromuscular junction, preventing acetylcholine from binding. Depolarizing agents such as Succinylcholine act as agonists that initially stimulate the receptor (causing fasciculations) but then remain bound, preventing repolarization and resulting in sustained muscle paralysis.
Q4. What Happens in Myasthenia Gravis?
Myasthenia gravis is an autoimmune condition in which antibodies destroy nicotinic acetylcholine receptors at the neuromuscular junction, leading to muscle weakness. It is treated with reversible cholinesterase inhibitors such as Neostigmine, which increase the concentration of acetylcholine at the synapse to stimulate the remaining functional receptors.