Sensitisation of nociceptive pathways 1 Flashcards
Q: What is peripheral sensitization?
A: A process where nociceptors (pain receptors) become more responsive to stimuli due to tissue injury or inflammation, leading to increased pain sensitivity in the affected area.
Q: What causes peripheral sensitization?
A: Tissue damage or inflammation that releases pro-inflammatory mediators such as bradykinin, prostaglandins, and histamine, which enhance nociceptor excitability.
Q: Name key mediators involved in peripheral sensitization.
A: Prostaglandins, bradykinin, ATP, histamine, cytokines (e.g., TNF-α, IL-1β), and nerve growth factor (NGF).
Q: How do prostaglandins contribute to peripheral sensitization?
A: Prostaglandins reduce the activation threshold of nociceptors by phosphorylating ion channels (such as Nav1.8 sodium channels) and making them more likely to open in response to stimuli.
Q: What role do ion channels play in peripheral sensitization?
A: Sensitizing agents (like prostaglandins) modulate ion channels (e.g., TRPV1, Nav1.8) to lower the activation threshold, making nociceptors more excitable and responsive to stimuli.
Q: How does nerve growth factor (NGF) affect nociceptors in peripheral sensitization?
A: NGF binds to its receptor TrkA on nociceptors, leading to increased expression of ion channels and growth of nociceptor terminals, enhancing pain sensitivity.
Q: What is hyperalgesia?
A: An increased sensitivity to painful stimuli, often a result of peripheral sensitization.
Q: What is allodynia?
A: A condition where non-painful stimuli, such as light touch, are perceived as painful, often due to sensitization of nociceptive pathways.
Q: Describe the role of bradykinin in peripheral sensitization.
A: Bradykinin binds to B2 receptors on nociceptors, activating intracellular signaling pathways (e.g., PKC) that increase ion channel activity, thus lowering the pain threshold.
Q: What is the impact of cytokines like TNF-α and IL-1β in peripheral sensitization?
A: These cytokines promote the release of other sensitizing factors and directly sensitize nociceptors by increasing the expression of pain-related ion channels and receptors.
Q: How does ATP contribute to peripheral sensitization?
A: ATP, released during tissue damage, activates purinergic receptors (P2X3) on nociceptors, leading to depolarization and heightened sensitivity to pain.
Q: What are the clinical implications of peripheral sensitization?
A: Peripheral sensitization can lead to chronic pain conditions, as heightened nociceptor sensitivity persists even after tissue healing, requiring targeted pain management strategies.
Q: What happens to the resting membrane potential of nociceptors during peripheral sensitization?
A: The resting membrane potential of nociceptors becomes less negative, making it easier for the nociceptor to reach the threshold for activation and transmit pain signals.
Q: How does peripheral sensitization differ from central sensitization?
A: Peripheral sensitization occurs at the level of the nociceptors in the periphery (at the site of injury), while central sensitization happens in the central nervous system (spinal cord and brain), involving changes in synaptic transmission.
Q: What is the role of TRPV1 channels in peripheral sensitization?
A: TRPV1 channels, also known as capsaicin receptors, become more sensitive to heat and protons in inflammatory conditions, contributing to heightened thermal pain sensitivity.
