Lecture 14 - Pain Flashcards
what are pain receptors?
receptors with axon endings without obvious anatomical specialisations
where are pain receptors found?
found everywhere in the body except the brain
what do pain receptors respond to?
respond to strong mechanical stimuli and/or high temperatures and chemicals released in damaged tissues
what are the exogenous chemicals released that pain receptors respond to?
capsaicin and menthol
how do capsaicin and menthol chemicals activate pain receptors?
activate receptors directly by internalising receptors by over activating pain fibres till the receptors eventually stop responding
what are the 4 things pain is useful for?
to avoid injury
alert us to local infection
aid in recovery
indicate further disease
what are the 2 types of nerve fibres that carry pain?
“c” fibres and “A-delta” fibres
what are “c” pain nerve fibres?
smallest diameter fibres (in relation to A-delta fibres) myelinated axons
what is the conduction velocity of “c” pain nerve fibres?
slow conduction velocity
what do “c” pain nerve fibres signal to?
signal to sustained and ongoing damage (or potential damage)
what are “A-delta” pain nerve fibres?
a subtype of A fibres that are small diameter myelinated axons
what is the conduction velocity of “A-delta” pain nerve fibres?
fast conduction velocity
what do “A-delta”pain nerve fibres signal to?
signal the acute onset of a painful stimulus
what is hyperalgesia?
increasing sensitivity of pain pathways following an injury or an inflammatory disease (e.g arthritis)
–> the tenderness of an area
how does hyperalgesia occur?
occurs as the injury site and area around the injury become ‘tender’
why does the injury site and area around the injury become ‘tender’?
this is due to the sensation of sensory endings by locally released factors and changes at the CNS synapses
what are the local factors that might be released if we damage an area of the skin?
K+
bradykinins
5-HT (serotonin)
prostaglandins
what is the effect of the release of K+ in a damaged area of the skin?
an increase of K+ from the high concentration of K+ inside the cell will generate more AP’s in response to tissue damage
what is the function of prostaglandins?
platelet aggregation for cloating
activation of pain fibres
what is the relationship between increasing sensitivity of a damaged area and the anterolateral pathway?
another way to increase sensitivity is to increase synapse efficiency in the anterolateral pathway in the spinal cord to the CNS
what do pain fibres release once activated?
release substance P and CGRP
what is the effect of the release of local factors?
local factors will activate mast cells to release histamine which will give positive feedback on to nerve terminals
what is the effect of histamine?
histamine spreading out from mast cells recruits neighbouring axons to bring them closer to threshold
what is the hyperalgesic area?
the area sensitised by neighbouring axons
what causes the itch sensation?
histamine
what is the function of asprin?
inhibitor of prostaglandin synthesis which are involved in blood clotting
what is asprin?
both an anti-blood clotting agent and a pain reliever
what is sensation in pain pathways modulated by?
modulated by descending pathways
what is the inhibition of pain pathways?
the “gating” of pain impulses by non-painful stimuli of nearby nerves. Inputs from nearby non-pain nerves inhibits the response of ascending pain fibres which is a non-chemical innervation to pain relief)
what are the methods of non-chemical innervation to pain relief?
methods include rubbing the affected area or trans-epidermal nerve stimulation (TENS) through an electronic skin rubber
what is the function of endogenous opiates?
decrease the post synaptic excitability of axons taking pain information to the CNS
where are endogenous opiates released?
released at synapses on pain-pathway neurons
what are endogenous opiates?
the site of action to ‘centrally acting’ painkillers of morphine and codeine
what is the function of endocannabinoids?
decrease long-term sensitivity to pain. They are involved in
- arousal
- placebo
- anxiety
- association
- suggestion
what is atonic modulation?
long term retrograde signalling thats released by the post synaptic neuron to effect the amount of neurotransmitter that the terminal releases on to it
what is the relationship between the level of arousal and pain?
the level of arousal tunes out pain fibre sensation level of conciousness
what are the symptoms of diabetic neuropathy?
- tingling or burning (in toes, legs, fingers, hands or arms)
- “pins and needles”
- pain/cramping
- loss of sensation
- insensitivity to heat/cold
- extreme sensitivity to light touch
- muscle weakness in hands or feet
- loss of coordination
- multiple autonomic dysfunctions
what do all of the symptoms of diabetic neuropathy result in?
result in loss of sensation, including loss of pain and this leads to tissue damage
why does tingling occur?
because AP’s are not occurring in the correct sequence to be interpreted
where does loss of sensation start?
starts way out in the periphery where the nerve endings are further away from the cell body in the spinal cord that is providing them their metabolic support
why is dental pain poorly localised?
dental pain could be located in the mouth but could also be referred pain from a sinus/ear infection or migraine
what is pulpitis?
a cavity in the tooth
what is referred pain?
pain feelings from the viscera referred to a body surface
e.g heart pain to the neck and arm
what causes referred pain?
the presumed “cross-talk” of visceral and somatic sensory pathways that is activated by stretch and ischemia
what is neurogenic pain?
nerve compression that can cause pain to be felt in the region of nerve termination
e.g pain in the leg from the compression of a nerve in the back by a slipped disc (herniated intervertebral disc)
what are the 2 causes of phantom limb pain?
1) ongoing activity in nerves that used to come from that limb
2) invasion of corticol representation for that part of intact body regions that cause spare neurons to invade regions that no longer exist
e. g cortex representation of amputated hand may become activated by inputs from the face
