Pain management involves understanding how pain signals are created, transmitted, and perceived by the body. Pain signals start at nociceptors and travel through fiber axons to the cerebral cortex.
-Paracetamol acts a reducing co-substrate to POX
-Works well in low arachidonic acid levels to inhibit POX
-In high levels it weakly inhibits POX
-Slows the prostaglandin formation
-Inhibits cyclooxygenase (COX)
-Blocks nociceptor activation
-Work by bonding to the opioid receptors
-Mimic endorphins
-Aid with opening of potassium channels
-Block the opening of calcium channels
-End result is inhibiting the ability to transmit the pain signal
-Signal travels to the cerebral cortex
-Travels via Fiber axons
-2 kinds of axons
-Type A
-Type C
- Release of prostaglandin
Paracetamol
-Work similar to NSAIDs by blocking prostaglandin formation
-Lack of strong anti-inflammatory effect
-2 step process to form prostaglandin
-COX produces prostaglandin G2 from arachidonic acid
-Peroxidase (POX) converts to prostaglandin H2
NSAIDs
Opioids
Nociceptors
-Nociceptors releases a signal in the form of action potienal
Modulation
- Where the body interacts with nerves to deal with the pain
-Releases endorphins or serotonin
