Tissue injury releases arachidonic acid (orange), which active cyclooxygenase (COX) enzymes convert into prostaglandins (red) — the molecules that drive swelling and sensitize nerve endings. Nerve impulses (cyan pulses) then carry the pain signal along the pathway to the brain.
AA release rate: R_AA = R0 · severity · (1 − 0.9·dose_gluco)
Active COX fraction: f_COX = 1 − dose_nsaid − 0.25·dose_paracetamol
Prostaglandin rate: R_PG = R_AA · f_COX
Inflammation (swelling): dI/dt = R_PG − I/τ τ ≈ 6 s
Peripheral pain input: P = baseline + k·I
Pain reaching brain: P_brain = P · (1 − dose_opioid) · (1 − 0.6·dose_paracetamol)
- NSAIDs (ibuprofen, diclofenac) block the COX active site directly — fewer active enzymes, less prostaglandin, less swelling and peripheral pain.
- Paracetamol only weakly inhibits peripheral COX, but dampens pain perception centrally — modest anti-inflammatory effect, useful analgesic/antipyretic effect.
- Glucocorticoids (prednisolone) block phospholipase A2 upstream, cutting off arachidonic acid release itself — the broadest anti-inflammatory action of the four.
- Opioids (morphine, fentanyl) do not touch the inflammatory pathway at all — they bind receptors along the nerve pathway and block pain-signal transmission to the brain directly.
Drag to orbit the scene; the swelling sphere at the injury site tracks inflammation, and the glow at the brain node tracks the pain signal actually arriving.