pain physiology Flashcards
nociception of pain has 4 stages
transduction
transmission
perception
modulation
transduction
nociceptors convert painful stimuli to neuronal action potentials.
-physical and chemical mediators alter the membrane potential of the pain receptor
chemical mediators of transduction
K, H, lactate, histamine, serotonin, bradykinins, prostaglandins
Transduction and NSAIDS
cyclooxygenase is needed to convert arachidonic acid to prostaglandin form. Which can then be used as a chemical mediator for pain.
NSAIDs block cycloosygenase, unable to convert arachidonic acid
transmission
action potentials transmitted to the CNS by means of specialized sensory fibers
sensory fibers
a fibers
c fibers
a fibers
mylinated
10% of pain fibers
fast traveling
sharp, stinging, cutting, pinching
c fibers
unmyelinated
90% of pain fibers
slower traveling
dull, burning, aching
trasmission in spinal cord
enter through the dorsal horn, synapse on interneurones, cross the cord and project centrally in the anterolateral tract
anterolateral tract has 2 divisions
neospinothalmic tract
paleospinothalamic tract
neospinothalmic tract
carries A fiber input, projects to thalamus and then sensory cortex
paleospinothalmic tract
carries C fiber input, protects diffusely to the reticular formation, mesencephalon, and thalamus
sensory dermatome
brain can localize pain sensation to a particular part of the body because nociceptor pathways are kept in specific anatomic order in the cord and somatosensory cortex
perception
result of neural processing of pain sensations in the brain
pain threshold
level beyond which a pain stimulation causes pain:
-similar between people
pain tolerance
degree of pain an individual is willing to bear before seeking relief
- differs with people
modulation
alters synaptic transmission of pain signals
occurs within
- peripheral nociceptors
- spinal cord
- brain
– descending pathways from brain release neurotransmitters that can inhibit synaptic transmission of pain signals
endogenous opiods
enkephalins, endorphins
play important role in pain modulation
-have different effects depending on the types of receptors they activate
receptors with analgesic activities
mu (brain)
kappa (spinal cord)
gate control theory
rubbing, pressing, or shaking the painful area may reduce pain
-impulses carried by A fibers can close the gate on nociceptor impulses; pain signals would be blocked
types of pain
physiologic pain
pathologic pain
physiologic pain
when tissue injury has occured
pathologic pain
occurs after tissue injury, but longterm changes occur along sensory pathways
classification of pain
duration (acute, chronic)
source (cancer, neuropathic, ischemic)
location (referred pattern)
Acute pain
results from tissue injury and resolves when the injury heals
-less than 3 months
S/S acute pain
increase sympathetic activity
- increased HR
- increased RR
- HTN
- pallor
- sweating
- nausea
- grimacing
- crying or moaning
pain relief with acute pain
nonopiod and opiod medicatoins
- risk of becoming dependent minimal
- try to not use opiods
chronic pain
gradual in onset, persists beyond the time for normal healing: 3 months
allodynia
hyperalgesia
Examples of chronic pain
headaches
low back pain
osteoarthritis
fibromyalgia
tx of chronic pain
multimodal therapies
opiods are neither safe nor effective
fibromyalgia
chronic widespread pain affecting all four extremities
fibromyalgia s/s
sleep disturbance/insomnia difficulty concentrating fatigue depression irritable bowl syndrome
tx of fibromyalgia
antidepressant
restore sleep patterns
regular exercise
pregabalin to target pain pathways
cancer pain
infiltration of organs
compression of structures by an expanding tumor
cancer treatments
cancer pain s/s
mixture of sympathetic NS and behavioral changes
cancer pain tx
multifaceted approace and use of potent meds: opiods
neuropathic pain
results from nerve damage or dysfunction
constant aching with intermittent burning or shock-like pain
results from alteration in any of the stages of nociception
neuropathic pain s/s
allodynia hyperalgesia atrophy of affected extremity coldness in affected area dystrophic changes - hair loss, shiny skin
neuropathic pain tx
antidepressants
anticonvulsants
allodynia
hurts when it shouldn’t
- light touch
hyperalgesia
hurts more than it should
trigeminal neuralgia
sudden, momentary, excruciating sharp pains along the II and III divisions of the trigeminal nerve
compression of nerve causing demyelination and irritation
trigeminal neuralgia tx
anticonvulsants
surgical nerve decompression
gamma knife radiosurgery
postherpetic neuralgia
caused by peripheral nerve damage by the reactivation of the latent herpes zoster virus
- burning follows a dermatomal pathway
- pain lasts > 8 weeks
postherpetic neuralgia tx
early use of antiviral meds within 72 hours of rash can decrease risk for postherpetic neuralgia liodcain capsaicin crea anticonvulsants antidepressants vaccine
diabetic neuropathy
damage to the large peripheral nerves by inflammation and demyelination
diabetic neuropathy s/s
burning pain
numbness, tingling
weakness
loss of vibratory sense and proprioception
diabetic neuropathy tx
pt education for foot care and glucose control
antidepressants
anticonvulsants
ischemic pain
sudden or profound loss of blood flow
chronic ischemic pain associated with atherosclerosis; intermittent claudication
- pain with activity and alleviated with rest
activates inflammatory response
ischemic pain s/s
aching
burning
tingling
ischemic pain tx
improving blood flow and reducing tissue hypoxia wt loss smoking cessation exercise lipid-lowering meds surgical bypass vascular stents
referred pain
perceived in an area other than the site of injury
result of convergence of visceral nociceptor activity with primary somatic afferents in the posterior horn
physiologic responses to pain
sympathetic nervous system activation during acute pain leads to -dilated pupils perspiration pallor increased HR and BP increased blood sugar decreased GI motility hypomotility of the bladder increased RR
Pain in young and elderly
- pain perception doesn’t decrease with age, but communication and expression of main may vary
- infants have pain perception
- inadequate pain treatment in neonates and infants can result in persistent behavioral changes and physical changes in the CNS
pain tx modality points
nociception
spinal cord
brain
interrupting peripheral transmission of pain
NSAIDs: dec. prostaglandins
local anesthetic agents
- blocking sodium influx through fast channels
modulating at spinal cord
cutaneous stimulation activates large sensory fibers that block the central progression of nociceptive transmission at the interneurons
- TENS
- massage
- acupuncture
- heat/cold
- theraeutic touch
- epidural and intrathecal analgesia
- dorsal column stimulators
altering pain perception in brain
analgesics: NSAIDs opiods nonpharmacologic - distraction -guided imagery -relaxation -biofeedback -hypnosis
