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Descending inhibitory pathways can reduce pain transmission. Drugs like serotonin-norepinephrine reuptake inhibitors (e.g., duloxetine) can enhance this modulation.

Suggests that non-painful input closes the 'gates' to painful input. Managed through physical therapy and electrical nerve stimulation.

CB1 and CB2 receptors are involved in pain regulation. Cannabinoids (e.g., THC) can provide analgesic effects.

Capsaicin binds to TRPV1 receptors, causing an initial excitation and subsequent desensitization of pain fibers. It is used topically for pain relief.

Prostaglandins sensitize nociceptors and enhance pain transmission. NSAIDs (e.g., aspirin) inhibit prostaglandin synthesis, offering pain relief.

Initiated by noxious stimuli, transmitted via Aδ and C fibers. Managed with NSAIDs (e.g., ibuprofen) and opioids (e.g., morphine).

Caused by nerve damage, involves central and peripheral sensitisations. Managed with anticonvulsants (e.g., gabapentin) and antidepressants (e.g., amitriptyline).

Opioid receptors (mu, delta, kappa) modulate pain. Agonists (e.g., fentanyl) provide profound analgesia but carry risk of dependence.

Endorphins, enkephalins, and dynorphins are natural pain modulators. They act on opioid receptors to provide pain relief.

GABA is an inhibitory neurotransmitter that can reduce pain sensation. Benzodiazepines (e.g., diazepam) enhance GABAergic activity for pain relief.

Glutamate is a major excitatory neurotransmitter in pain pathways. NMDA receptor antagonists (e.g., ketamine) can modulate pain.