Lecture 17 acute pain Flashcards
Define pain
Unpleasant sensory and emotional experience associated with actual or potential tissue damage.
Lots of types/descriptions: aching, burning, throbbing, electric shock like, dull, sore, nagging, piercing etc.
Associated with crying, sympathetic activation, behavioural changes.
Describe the receptors and pathways through which pain signals reach the brain.
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How drugs/other factors can modulate the experience of pain.
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Describe the similarities between physical and emotional/social pain.
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Gate theory of pain
There is feedback loop in the spinal cord that determines which stimuli reach the brain.
Chronic stress opens gate
Adrenaline closes gate
Explains how pain can be ignored on battlefield but intensified when upset.
Rubbing sore limb/TENS may “close gate”.
Consult the slides for a graph
Describe the reciptors for pain
Nociceptors
sensory receptor capable of transducing noxious stimuli.
Free nerve endings
Several classes which respond to different stimuli
Stimuli
Mechanical
Temperature (extreme)
Electrical
Chemical (Capsaicin: Respond to heat/chilli/jalepenos)
Inflammation (mechanical and ↑nociceptor sensitivity)
Describe pain nerves
Aδ fibres: some myelin, faster for sharp pain.
C fibres: no myelin, slower, dull aching pain.
Synapse in the substantia gelatinosa in the dorsal horn of the spinal cord and use glutamate (and substance P).
Two sense pathways
Proprioceptors + mechanoreceptors - dorsal column at spinal cord - cross over at medulla - thalamus - primary somatosensory cortex
nociceptors + thermoreceptors - cross over at spinal cord - medulla - thalamus - primary somatosensory cortex
Ascending pain pathways
C & A fibre - cross over at spinal cord - medulla - midbrain - thalamus - insular, somatosensory cortex, anterior cingulate cortex
Primary somatosensory cortex.
Anterior cingulate – emotional aspects, sympathetic pain and social rejection.
Insular – modulate physical pain response.
Descending pain pathways
amygdala - PAG
hypothalamus - cross over at spinal cord
Amygdala (involved in emotions) and hypothalamus can modify pain responses by activating the periaqueductal gray (PAG).
PAG uses endorphins (“endogenous morphine”).
What happens when you have prolonged pain
Once pain alerts you to danger/potential danger continued pain is unnecessary.
Brain diminishes prolonged pain through endorphin release, which bind to opiate receptors in periaqueductal gray area.
Inescapable pain, exercise and sex all result in increased endorphin release and reduce pain sensitivity.
Drug treatments for pain
Opiates
Block the release of substance P in the periaqueductal gray.
Same mechanism as endogenous endorphins.
Mechanism of panadol and tylenol
Panadol (paracetamol)/Tylenol (acetaminophen)
Exact mechanism of analgesia unknown. (sounds like good science to me)
Both inhibit the synthesis of prostaglandins (pro inflammatory).
Analgesia is presumed central and related to reduced serotonin, opioids or through the endogenous cannabinoid system as blocking these systems reduce the analgesic effect.
placebo and acupuncture
Placebo
Placebo’s quite effective for pain.
Reduce the emotional aspects of pain via reducing activity in the cingulate (not somatosensory) cortex.
Also result in increased release of endorphins (placebo effect reduced with naloxone).
Acupuncture
Also results in release of endogenous opioids.
does social exclusion hurt
virtual ball toss game, same area as if physically hurting