Physiology · MU Sofia

84. Physiology of pain. Primary and secondary pain. Visceral pain. Antinociceptive system.

Explains pain as a protective sensation, then contrasts fast, sharp primary pain carried by Aδ fibres with slower, dull secondary pain carried by C fibres. Covers inflammatory mediators, the triple response and hyperalgesia, the pathway and referred pain of visceral pain, and the descending antinociceptive system with its opioid peptides.

Inside: 5 sections · 7 labelled pictures · 10 flashcards · 6 min

Topic 83 of 104 in the MU Sofia syllabus for Physiology (Dental Medicine, Year 2). The free AceMed note covers it in 5 sections, about 904 words (6 min of reading), with 10 flashcards.

In this note

  1. Physiology of pain. Primary and secondary pain. Visceral pain. Antinociceptive system.
  2. Visceral Pain
  3. Antinociceptive System
  4. Enkephalins and Endorphins: The Body’s Natural Painkillers
  5. Recap Questions

Physiology of pain. Primary and secondary pain. Visceral pain. Antinociceptive system.

Pain is a complex physiological and emotional experience that serves as a protective mechanism, alerting us to potential or actual tissue damage. It involves the activation of specialized sensory receptors called nociceptors, which detect noxious stimuli and transmit signals to the brain via afferent pathways.

Primary pain is the initial sharp, well-localized pain that occurs immediately after a noxious stimulus. It is transmitted by fast-conducting Aδ fibers.

Secondary pain develops later and is characterized by a dull, aching, poorly localized sensation. This type of pain is transmitted by slower-conducting C fibers.

The inflammatory response contributes to both primary and secondary pain. When tissues are injured, they release inflammatory mediators such as:

  • Bradykinin
  • Histamine
  • Serotonin
  • Prostaglandins
  • Leukotrienes

These mediators sensitize nociceptors, lowering their activation threshold and increasing their responsiveness, leading to hyperalgesia (increased sensitivity to pain).

Example: When you touch a hot stove, you experience immediate sharp pain (primary pain) due to the activation of thermal nociceptors. This is followed by a lingering, throbbing pain (secondary pain) as inflammation develops in the injured area.

  • Triple Response of Injury:
  • Injury leads to vasodilation, resulting in redness and swelling at the affected site.
  • This inflammation causes pain and increases sensitivity to painful stimuli.
  • The heightened sensitivity is classified into:
  • Primary pain (hyperalgesia): Increased pain sensitivity in the damaged tissue.
  • Secondary pain (hyperalgesia): Increased pain sensitivity in the surrounding undamaged tissue.
  • Mechanism of Pain and Inflammation:
  1. 1. Tissue damage occurs, leading to the release of intracellular substances.
  2. 2. Damaged cells release chemical mediators (e.g., bradykinin, prostaglandins) that activate and sensitize nociceptors.
  3. 3. Activated nociceptors send pain signals to the brain and release Substance P:
  • Promotes vasodilation in local blood vessels.
  • Stimulates histamine release from mast cells, further amplifying inflammation.
  1. 4. Increased blood flow to the area enhances the inflammatory response, resulting in swelling, heat, and further sensitization.

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