Inflammatory Pain and Sensitization
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Questions and Answers

What is the result of the release of inflammatory mediators such as prostaglandins and bradykinin in response to tissue damage?

  • Desensitization of the pain pathway
  • Activation of low-threshold mechanoreceptors and thermoreceptors
  • Reduced sensitivity of nociceptors to noxious stimuli
  • Increased sensitivity of nociceptors to noxious stimuli (correct)
  • What is the term for hypersensitivity to a noxious stimulus?

  • Allodynia
  • Analgesia
  • Hyperalgesia (correct)
  • Hypoalgesia
  • What is the effect of NSAIDs on prostaglandins?

  • Reduce production of prostaglandins (correct)
  • Have no effect on prostaglandins
  • Increase production of prostaglandins
  • Activate low-threshold mechanoreceptors and thermoreceptors
  • What is the term for pain that results from a non-noxious stimulus?

    <p>Allodynia</p> Signup and view all the answers

    What type of receptors are activated in response to a non-noxious stimulus, resulting in pain?

    <p>Low-threshold mechanoreceptors and thermoreceptors</p> Signup and view all the answers

    Study Notes

    Inflammatory Pain

    • Tissue damage releases inflammatory mediators, including prostaglandins and bradykinin, which increase the sensitivity of nociceptors to noxious stimuli.
    • This process leads to sensitization in the pain pathway, resulting in hyperalgesia (hypersensitivity to noxious stimuli).
    • Hyperalgesia is characterized by hypersensitive nociceptors.
    • In addition, inflammatory pain can cause allodynia, which is pain resulting from a non-noxious stimulus.
    • Allodynia is mediated by the activation of low-threshold mechanoreceptors and thermoreceptors.
    • NSAIDs (non-steroidal anti-inflammatory drugs) reduce the production of prostaglandins, which contributes to the alleviation of inflammatory pain.

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    Description

    This quiz assesses your understanding of inflammatory pain, including the role of prostaglandins and bradykinin in sensitizing nociceptors, and the effects of NSAIDs on prostaglandin production.

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