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
Elimination of NSAIDs include
hepatic oxidation & conjugation
less than 10% renal elimination
some active metabolites
Examples of propionic acid include
Naproxen (aleve)- non-selective COX
ibuprofen- non-selective COX
Anthranilic acid includes
meloxicam (Mobic)- cox 2
-cox 2 selective at lower doses <15 mg
Acetic acid drugs include
diclofenic
indomethacin- non-selective- high GI side effects
toradol- non-selective- can impair renal function, limit doses to 3-5 days
Describe issues with diclofenic.
hepatic toxicity
transdermal use is effective without systemic toxicity
increased risk of thrombotic event
Pure cox 2 inhibitor includes
celecoxib (celebrex)
Celebrex may be used in treatment of
colon polyps, cancer, mental illness
IV tylenol may be used to
reduce post-operative narcotic consumption
Tylenol works by
inhibiting central prostaglandin synthesis
poor cox inhibition
no effect on platelet function or gastric mucosa
Salicylates include
aspirin
-nonselective cox inhibitor
long term antipyretic and anti-inflammatory properties
Long term effects of aspirin include
bleeding
ulcers
Reye’s syndrome (children)
NSAID side effects include
gastric mucosa
dyspepsia
decreased renal function
hepatic side effects
acetaminophen hepatotoxicity
increased platelet aggregation at high doses
decreased platelet aggregation at low doses (ASA)
Opioid receptors include
Mu, Kappa, & Delta
Effects of stimulating the Mu receptors include
analgesia respiratory depression euphoria sedation decreased GI motility dependence
Effects of stimulating the kappa receptors include
spinal analgesia sedation dyspnea dependence dysphoria respiratory depression
Effects of stimulating the delta receptors include
psychomimetic effects**
dysphoria
increased release of dopamine stimulating pleasure centers
insignificant analgesic effects
Most effects and side effects of opioids can be traced to
metabolites
higher metabolite activity usually means more side effects
Metabolites can produce
hyperalgesia
Opioid side effects include
constipation - does not resolve over time
nausea
pruritus
sedation- transient
respiratory depression- long term use leads to sleap apnea
endocrine- low testosterone, amenorrha, immunologic, inhibition of cellular response
The solution to opioid side effects is to
reduce opioid use
The primary action of oxycodone is
kappa (dysphoria)
metabolites have anti-sedative effects
