Pain Pathophysiology & Pharmacology Flashcards

Vocabulary practice cards covering pain pathophysiology, opioid/non-opioid mechanisms, and adjuvant analgesics based on lecture notes.

Non-opioids

A class of analgesics including paracetamol and NSAIDs used for acute and chronic pain types such as trauma, post-op, cancer, arthritis, and somatic pain.

Phospholipase A2

The enzyme responsible for producing arachidonic acid (AA) from cell membrane lipids.

Cyclooxygenase (COX-1 and COX-2)

Enzymes that mediate the conversion of arachidonic acid into prostaglandin $G2$.

POX

The enzyme that converts prostaglandin $G2$ into prostaglandin $H2$, leading to the production of prostanoids like prostaglandins, prostacyclin ($PGI2$), and thromboxane ($TXA2$).

Mechanism of NSAIDs

Inhibition of COX enzymes to stop the production of prostaglandins, thereby reducing pain.

Mechanism of paracetamol

Inhibition of POX enzymes to stop the production of prostaglandins, thereby reducing pain.

Opioids

A class of drugs including morphine, fentanyl, and oxycodone; synthetic versions are often combined with non-opioids for an opioid-sparing effect.

Methadone

A synthetic opioid that provides an added effect by acting as a NMDA antagonist to block pain pathways.

Excitatory neurotransmitters (Pain)

Glutamate, CGRP, and substance P, which are released from DRG axons to depolarize DR neurons.

Endogenous opioids

Naturally occurring substances such as enkephalins, dynorphins, and endorphins that bind to mu opioid receptors.

Pre-synaptic opioid mechanism

Activation of mu receptors inhibits calcium ($Ca^{++}$) channels from moving into the cell, which blocks the release of neurotransmitters.

Post-synaptic opioid mechanism

Activation of mu receptors affects potassium ($K^+$) ion channels, causing potassium to leave the neuron and leading to hyperpolarization.

Antiepileptic Adjuvants

Drugs like gabapentin and pregabalin used to suppress neuronal hyperexcitability by reducing $Na^+$ and $Ca^{++}$ influx or enhancing GABA effects.

Topical Adjuvants

Agents such as Lidocaine or capsaicin that block sodium channel generation of abnormal impulses or cause the depletion of substance P in sensory nerve endings.