Pain Experience: Peripheral Mechanisms Flashcards
Why types of pain are there?
- Acute: fast, sharp/slow, burning
- Chronic: long term
Dimensions
- sensory - quality, intensity of pain, location
- affective: emotional aspects
What does sensory nervous system do?
- informs CNS of the internal and external environment
- role of nociceptive system is to signal the threat or occurence of injury
nociceptors present throughout the body:
- especially: cornea and tooth pulp where pain is predominant sensation
- lacking: brain, liver, lung
What are nociceptors?
Briefly discuss the anatomy of nociceptors:
- receptors that respond to noxious (hot water)/nociceptive stimuli
- classified by:
Parent axon
Stimulus
Anatomy: free nerve endings, axon is usually a c-fibre or A-delta fibre
What type of pain are A-delta fibres associated with?
What are their types?
- fast, sharp pain
A-delta mechanical nociceptors - respond to strong mechanical stimuli
A-delta polymodal nociceptors - respond to all types of noxious stimuli
What type of pain is associated with c fibres?
What type of fibres do they have?
What nerves are found in tooth pulp?
- slow burning pain
- polymodal - respond to all types of noxious/nociceptive stimuli
Tooth pulp afferent nerves:
- A-delta myelinated afferents
- C-fibres unmyelinated afferents
- A-beta myelinated afferents - associated with mechanoreception (touch), but likely to be involved in nociception in pulp
What are the two factors involved in nociceptor transduction?
What happens when you eat capsaisin?
Direct: stimulus acts directly - mechanical, chemical, thermal
Indirect: tissue injury/inflammation, effect of substances released from a nerve ending
Capsaisan - activates TRPV1 receptors in c-fibre terminals inducing pain/heat
What substances activate nociceptive nerve endings in local tissue damage (algogenic substances)?
Activate or sensitise nociceptive nerve endings?
Sensitise nociceptive nerve endings?
Activate:
- ATP, H and K
Activate or Sensitise:
- histamine, serotonin, bradykinin
Sensitise:
- prostaglandins
How may ATP be released and what is the effect of this?
H ions?
K?
Damage to cells release ATP into cell, which activates P2X3 channels, permeable to sodium, causing depolarisation and an action potential.
H ions are present in low pH conditions, and release due to lactic acid accumulation. This activates TRPV1 receptors and ASIC, sodium rushes in and depolarisation occurs
K ions released due to mechanical cell damage, leads to depolarisation as local K ion concentration is changed
How does histamine work?
Serotonin and bradykinin?
Histamine released by mast cells and works through an intracellular pathway making some ions more responsive, so at low concentrations - sensitise, at high cncentrations - activate
Serotonin and bradykinin: low concentrations sensitise, high concentrations activate
Prostaglandins: can sensitise receptors making channels more responsive so a gentle stimulus may be able to respond
Why do nerves fire back up another branch?
Axon reflexes - within an axon branch in the periphery
AP come back and arrive at the nerve ending, triggering nerve ending to release substance P
What does substance P release cause?
Neurotransmitter, present in fine peripheral fibres
Substance P release causes:
- vasodilation
- increase in vascular permeability
- mast cell degranulation
Makes nerve more sensitive to stimuli due to release of histamine, serotonin etc.
Define hyperalgesia?
Define allodynia?
What are both these things due to?
Hyperanalgesia: exaggerated response to a noxious/nociceptive stimulus
Allodynia: pain produced by a stimulus that would not normally produce pain e.g. sunburn/tender tooth
Because of a sensitised system, inflammatory soup, lowering threshold
What are cox inhibitors?
What is the ideal drug?
- NSAIDs e.g. aspirin, ibuprofen: non-selective COX inhibitors
Ideally just need an analgesic to block COX-2 enzyme that causes pain and inflammation, bit aspirin is non-selective and blocks COX-1 aswell, which affects haemostasis, vasodilation and gastric protection
