Lecture 14 - Pain Flashcards
pain =
nociception
Pain receptors
Receptors are axon endings without obvious anatomical specialisations, found everywhere in the body - except brain.
Broad receptive fields, bare nerve endings, multiple branches spreading out in the skin - does not give precise location of pain, use other sensory modalities to tell us precisely where the injury has occurred
Different endings respond to strong mechanical stimuli, and/or high temperatures, chemicals (that are released in damaged tissue)
[some exogenous chemicals activate receptors directly, e.g. capsaicin, menthol]
Things that have the potential to cause injury are responded to
When you overactive pain fibres they stop responding
Pain is used to
Pain is useful to avoid injury, alert us to local infection, or aid recovery, but can become chronic or spontaneous, and can indicate disease elsewhere in the body.
No pain would not be ideal
Pain is carried by
two types of nerve fibres - C fibres and A delta fibres
“C”- fibres
“C”- fibres
Smallest diameter, unmyelinated axons
Slow conduction velocity (they do not need to be as efficient in bringing information into the nervous system
Signal ongoing damage (or potential damage) (longer duration of pain)
“A𝜹”-fibres (A delta fibres)
“A𝜹”-fibres (A delta fibres)
Small diameter myelinated axons
Faster conduction velocity
Signal acute onset of painful stimulus
Sensation in pain pathways
Sensation can change over time
Pain pathways become more sensitive (hyperalgesia - increased pain sensitivity locally) following injury, or inflammatory disease (e.g. arthritis).
Injury site and area around injury become ‘tender’
Pain pathway sensation can change due to
Sensitisation of sensory endings by locally released factors (become more sensitive to changes in the environment, fire more action potentials, easier to get to threshold from smaller inputs because of factors released by the tissue locally
Changes at CNS synapses
Hyperalgesic area
enderness, sensitised neighbouring axons are present here
K+ in pain perception
K+ - cell breaks, intracellular contents comes out, potassium levels rise and axons locally will get close to threshold because the equilibrium potential of K+ changes therefore more likely to generate action potentials i.e. more action potentials in pain fibres due to local tissue damage
Bradykinin, 5-HT (serotonin) and prostaglandins in pain perception
Bradykinin, 5-HT (serotonin) and prostaglandins - all of these molecules especially prostaglandins are associated with the clotting mechanism (participate in platelet aggregation for clotting) but they are also involved in activating pain fibres, these local factors are released by damaged tissue that can increase the sensitivity of pain fibres locally
Mast cells in pain perception
Mast cells = filled with granules that contain histamines, histamines spreadings out from the mast cells recruits neighbouring axons to bring them closer to threshold. Now in a situation where there has been a local injury, local doctors released that activate pain fibres that feedback into the system’s chemistry that activates surrounding pain fibres that makes them more likely to be activated by any other inputs so the injury may initially have been very small but now the surrounding areas are sensing painful signals to the brain
Substance P, CGRP in pain perceptions
Substance P, CGRP - released from pain fibres to activate other cells like mast cells which release histamines which in turn gives positive feedback on to the nerve terminals themselves (local inflammatory changes feeding into increased pain sensation)
Histamines in pain perception
Histamines are also involved in the allergic reaction
Give the itch sensation
Aspirin in pain perception
Aspirin = inhibitor of prostaglandin synthesis which are involved in clotting therefore it is a anticlotting agent and a analgesic (pain reliving medication)