12 OTC Analgesics
Public Lecture Overview
Title: The Art & Science of Brain Rhythms
Date & Time: February 6, 2025, at 6:00 PM
Location: Myer-Horowitz Theatre
Presenters:
Clayton Dickson (Scientist)
Kyle Mathewson (Scientist)
Janette Mailo (Neurologist)
Gary James Joynes (Sound Artist)
Host: Anna Taylor
Organized by: Neuroscience and Mental Health Institute, University of Alberta
Event Details:
Interactive discussion on how sound rhythms affect the mind and brain function.
Free tickets available.
Over-The-Counter (OTC) Drugs Overview
Focus of Study: Analgesics
Course Code: PMCOL 200
Instructor: Dr. Anna Taylor
Pain Management Content
Key Topics Covered
Review of peripheral pain circuitry.
Types of pain relief drugs:
NSAIDs: Treat inflammation and fever.
Topical Anesthetics: Block sensation.
Capsaicin Cream: Blocks pain.
Learning Objectives
Describe pathways of pain transduction.
Identify OTC drugs for pain and explain their mechanisms.
Peripheral Pain Circuitry
Neuron Types
Primary Afferents:
Detect sensory info from the periphery (skin, GI tract).
Transmit information to spinal cord.
Synapse with secondary afferents to relay data to the brain.
Motor Efferents:
Deliver motor commands from the brain to muscles.
Pain Detection Mechanism
Nociceptors:
Class of primary afferents that detect pain stimuli (thermal, mechanical, chemical, electrical).
Polymodal Nociceptors:
Detect multiple types of painful stimuli, densely innervate all body surfaces.
Pain Importance
Pain serves as a critical warning system for injury or potential harm.
Specific Pain Stimulus Detection
Receptors and Signaling
TRP Channels:
Temperature-sensitive, ligand-gated ion channels.
Specific types:
TRPM8: Activates below 10°C (cold).
TRPV1: Activates above 43°C (hot).
Activation by ligands:
TRPV1 → Capsaicin.
TRPM8 → Menthol.
Inflammatory Response
Receptors responsive to inflammatory molecules (bradykinin, cytokines, prostaglandins).
Inflammation triggered following tissue injury or infection leads to pain signaling.
Inflammation and Pain Modulation
Arachidonic Acid Pathway
Arachidonic acid derived from phospholipids in cell membranes.
Metabolized by enzymes COX1 and COX2 into prostaglandins and thromboxanes, influencing inflammation and pain responses.
Key Molecules in Inflammation
Prostaglandin E2 (PGE2):
Potent vasodilator, induces fever, attracts immune cells.
Thromboxane A2:
Promotes platelet aggregation and vasoconstriction.
Non-Steroidal Anti-Inflammatory Drugs (NSAIDs)
Mechanism of Action
NSAIDs block COX1 and COX2, decreasing prostaglandin production to reduce inflammation and pain.
Aspirin:
Irreversible inhibitor; long half-life due to binding to catalytic sites.
Side Effects
Gastric Toxicity:
Common with chronic NSAID use due to COX1 inhibition, can cause ulcers and bleeding.
Ketorolac: Highly effective but has associated risks.
COX2 Specific Inhibitors
Developed to reduce gastric toxicity, but may increase cardiovascular risk.
Acetaminophen
Profile and Mechanism
Used since the 1800s; identified as a weak COX1 and COX2 inhibitor.
Recent findings (2002) suggest inhibition of a third isoform (COX3) concentrated in the cerebral cortex.
Safety and Risks
Minimal toxicity at therapeutic doses; overdose can lead to severe liver damage.
Local Anesthetics
History and Development
Cocaine was the first local anesthetic identified; later substituted by synthetic alternatives due to addiction risks.
Examples: Procain, Lidocaine, Bupivicaine.
Mechanism of Action
Local anesthetics block sodium channels crucial for action potential propagation, potentially leading to motor paralysis.
Effective in blocking active nociceptors preferentially during pain.
Capsaicin and Pain Management
Capsaicin Cream Mechanism
Acts as a TRPV1 receptor agonist leading to initial burning sensation.
Continuous use induces desensitization of TRPV1+ nociceptors, leading to pain relief.
Sensory Pathway Overview
Review of Pain Modulation:
Various methodologies including NSAIDs, acetaminophen, topical anesthetics, and capsaicin for managing pain.
Pain as the primary reason for medical consultations, with ongoing research into mechanisms, especially for acetaminophen.