L14. Pain Flashcards
Pain?
Nociceptors are free nerve endings without obvious anatomical specialisations, found everywhere in the body, except brain neural tissue
Respond to noxious or potentially damaging stimuli
- Strong mechanical stimuli (piezo channels)
- Extreme temperatures (TRP channels)
- Chemicals released by damaged tissue (inflammatory signals)
Pain is useful to avoid injury, alert us to local infection, or aid recovery
C fibres?
- Smallest diameter, unmyelinated axons
- Slow conduction velocity
- Signal ongoing damage (or potential damage)
- Large receptive field
- Dull throbbing pain
A delta fibres?
- Small diameter myelinated axons
- Faster conduction velocity
- Signal acute onset of painful stimulus
- Small receptive field
- Sharp pain
A beta fibres (touch)?
- Largest diameter myelinated axons
- Fastest conduction velocity
- Mechanoreceptor fibres
Hyperalgesia?
Pain pathways become more sensitive following injury
- Injury site and area around injury become tender
Due to:
- Sensitisation of sensory endings by locally released factors (peripheral sensitisation) and Piezo channel sensitisation
- Changes at CNS synapses (neurons become more excitable along the anterolateral pathway)
Peripheral sensitisation?
Substance P and CGRP act on neighbouring mast cells and in response, the mast cells release histamine
Substance P and CGRP act on neighbouring blood vessels causing vasodilation and so the area of tissue that is damaged will become red and swollen which aids with healing
Essentially it’s making the damaged area more obvious to you
Gate control theory 1?
Inhibition of pain pathways
“Gating” of pain impulses by non-painful stimuli of nearby nerves
Inputs from nearby non-pain nerves inhibits responses of ascending pain fibres
TENS inhibition?
*trans-epidermal nerve stimulation
Inhibition of pain pathways
“Gating” of pain impulses by non-painful stimuli of nearby nerves
Inputs from nearby non-pain nerves inhibits responses of ascending pain fibres
Sodium channels inhibition?
Inhibition of pain pathways
All hijack the voltage-gated channels to stop action potentials going up/from firing
Done by local anaesthetics:
- Lidocaine
- Articain
- Marcaine (bupivacaine)
Local pain?
Experienced at the site of the origin
e.g. arm hurts because you got an injection at that point
Referred pain?
Felt in a region other than the site of origin
- Usually visceral pain felt at the body surface
- Presumed due to convergence of visceral and somatic pain pathways
e.g. cardiac arrest and could get sharp shooting pain on left side of arm and shoulder
‘Two axons, one sending to heart and one to skin, but they converge onto one interneuron in the spinal cord, but brain is so used to getting pain signals from skin so when it comes from heart it thinks it’s a mistake and will send information to somatosensory cortex representing the arm and shoulder instead’
Neurogenic pain?
Pain felt along distribution of a nerve
Muscle pain?
- Can be neurogenic
- Can be referred from joints, ligaments, tendons
- Can be due to blood supply
Phantom limb pain?
- Can be caused by the reorganisation of the sensory cortex
- The brain’s representation of the missing limb can become reorganised with neighbouring regions (i.e. face or hand), causing abnormal sensory activity in response to sensory inputs from the face or hand
- Could also be caused by ongoing/abnormal activity from the severed nerve, which would classify as neurogenic pain
What is diabetic neuropathy?
Nerve damage that can occur in people with diabetes, often affecting the legs and feet
It is caused by high blood sugar levels damaging the nerves
