Pain and Inflammation

pain

a defense mechanism signaling actual or potential tissue damage

subjective (whatever pt says it is)

nociceptors

specialized pain receptors located in tissues that detect noxious stimuli and send pain signals to the CNS

acute pain

sudden onset

lasts less than 6 months

usually resolves after healing

surgery, trauma, burns

chronic pain

persistent pain

greater than 6 months

may continue after healing

associated with psychosocial factors 

often resistant to tx

nociceptive pain

normal pain from tissue injury

involves nociceptors

treated with nonopioids, opioids, and local anesthetics 

neuropathic pain

abnormal pain from nerve or CNS injury

diabetic neuropathy

shooting, burning, stabbing

treated with analgesics 

somatic pain

originates in skin, bone, muscle, or soft tissue

sharp, localized, and intermittent/constant 

visceral pain

diffuse pain from organs

dull, aching, cramping

may be referred pain

inflammatory pain

caused by tissue inflammation

treated with NSAIDs or corticosteroids

neuropathic pain transmission

results from damaged or hyper excitable nerve endings

pain can occur without actual tissue injury 

transduction

conversion of noxious stimuli into a nerve impulse

depolarization of nociceptors 

transmission

propagation of the AP to the spinal cord and brain

via A-delta (fast) and C fibers (slow)

perception

pain is recognized in brain

awareness, emotion, and subjective response occur 

modulation

descending pathways (serotonin, norepinephrine, endorphins)

inhibit pain transmission 

endogenous analgesia system

body’s internal pain control system

releases endorphins and enkephalins that inhibit substance P and reduce pain perception 

Mu receptor

analgesia, euphoria, respiratory depression, miosis, decreased GI motility

kappa receptors

analgesia, sedation, dysphoria

delta receptors

analgesia

inflammation

localized protective responses to tissue injury that eliminates the cause and prepares tissue for repair 

5 cardinal signs of inflammation

redness

warmth

swelling

pain 

loss of function

vascular changes in inflammation

vasodilation leads to increased blood flow

increased blood flow causes redness and warmth

increased capillary permeability leads to swelling and pain

cellular changes in inflammation

WBC migration

increased neutrophils and macrophages

increased phagocytosis

tissue repair

key inflammatory mediators

bradykinin

histamine

prostaglandins

bradykinin

vasodilation

increased permeability

pain

histamine

vasodilation

increased capillary permeability 

prostaglandins

chemical mediators formed from arachidonic acid by COX enzymes

regulate inflammation, pain, fever, and platelet aggregation 

COX 1

enzyme continuously active in platelets, GI tract, and kidneys

produces protective prostaglandins that maintain mucosa, renal flow, and platelet function

COX 2

induced by inflammation

produce prostaglandins responsible for pain and inflammation

inhibition provides analgesia and anti inflammatory effects

COX 1 inhibition

gastric irritation

ulcers

bleeding

renal impairment

protects against MI and stroke by inhibiting platelet aggregation 

COX 2 inhibition

decreased pain and inflammation

increased risk of MI and stroke due to vasoconstriction 

lidocaine patch education

apply to painful area

remove after 12 hrs

fold to discard 

don’t apply to broken skin

no heat use over patch 

opioid toxicity triad

coma

respiratory depression

pinpoint pupils

opioid withdrawal s/s

anxiety

restlessness

n/v/d

sweating

pupil dilation

muscle cramps 

equianalgesic dosing

chart used to convert equivalent opioid doses

PCA pump

patient controlled analgesia

preset bolus

lockout interval 

a - delta fibers

release glutamate

sharp pain, temperature

c fibers

release substance P

dull and burning pain