Pain lecture part 1 Flashcards
Common chronic pain conditions include
lumbar radiculopathy
facet arthropathy
SI joint dysfunction
occipital neuritis
The following material is released after trauma and is thought to enhance afferent transmission
potassium plasma red and white blood cells clotting factors peptides prostaglandins inflammatory cells
Release of substance P & calcitonin gene related peptide causes
vascular leaking leading to swelling
Release of materials enhance activation of
membrane channels (Na+, Ca++)
Pain response without tissue injury includes
“escape” response consistent with intensity of stimulation
removal of stimulation terminates the sensation & response
The sensation of a pain response without tissue injury is specific to
a site of potential injury
The initial sensation to pain response without tissue injury is
sharp, followed by dull sensation
Pain response with tissue injury includes
pain persists after removal of stimulus
stimulating injured tissue cause an intense response (hyperalgesia)
Pain response with tissue injury has both
localized sensation and referred sensation
______ of stimulation is required to elicit an adverse response in pain response with tissue injury
lower threshold
Allodynia is defined as
increased pain sensation with light touch
-pain that should not be
Pain response with nerve injury is an ongoing unpleasant pain sensation usually referred to
the dermatome innervated by the injured nerve (hyperalgesia)
-pain greater than expected)
The evolution of chronic pain is
associated with nerve injury response failure to treat nerve & tissue injury effectively occult inflammation failure of tissue healing persistent inflammation
Windup is defined as
when normal pain responses become abnormal
Chronic pain results in
despair, poverty, homelessness, divorce, suicide
The pathway to windup includes
repetitive stimulation releases glutamate, neurokinin, substance P** overwhelming the Mg block
channels are opened, proteins couple with receptors producing long lasting Ca++ release
glial cell dysfunction (dorsal horn)
loss of central inhibition mechanisms
Loss of central inhibition mechanisms include
increased intracellular Ca++ release of arachidonic acid (irritant) creation of cylooxygenase (Cox) Cox synthesizes prostaglandins which reduce glycine and GABA mediated inhibition negative impact on NMDA receptors promote dorsal horn excitability
Goals of pain treatment include
improve mobility and activities of daily living
ensure compliance with treatment plan
address emotional/social components
decrease pain sensation
Nonsteroidal anti-inflammatory drugs have the following activities:
antipyretic
anti-inflammatory
analgesia
acetaminophen has little anti-inflammatory activity
MOA of NSAIDS include
inhibits prostaglandin production from arachidonic acid by acetylation of COX
COX1 is responsible for
contributes to hemostasis & platelet aggregation
protects the gastric mucosa via prostacyclin production
Cox2 is responsible for
producing inflammation
contribute to fever
stimulates pain sensation
supports prostacyclin anti-coagulation activity
both are present peripherally and in the CNS
Absorption of NSAIDs includes
orally in the stomach and small intestines
peak concentration in 1-4 hours
food delays absorption
IV admin may not reduce negative gastric effects
topical absorption has advantages of local targeted effect
Distribution of NSAIDs include
weakly acidic
highly plasma bound
liphophilic
only unbound portion is effective