Module 3 - Post op Pain Flashcards
Pain description
unpleasant sensory/emotional experience assoc with actual or potential tissue damage
Pain transmission stages
Transduction
Transmission
Perception
Modulation
Transduction
somatic & visceral receptors are stimulated by external stimuli –> convert stimulus into an electrochemical signal
Transmission
a-delta & c-fibers generate action potentials that are transmitted towards the CNS
Perception
cortex, limbic system, hypothalamus, reticular system involved in processing & sensation of pain
Modulation
descending pathway
release of neurotransmitters at the dorsal horn to modulate pain sensation
Complications of pain
PSR
shallow breathing, atelectasis, pneumonia
chronic pain
sleep disturbance
decreased appetite
impaired mobility & ADLs –> increased risk of pressure ulcers, DVT, PE
Acute pain
<3-6 months
resolves with healing/removal of stimuli
protective purpose
activates SNS
Chronic pain
> 3-6 months
pain lasts longer than recovery period
pathological
no SNS activation. psychosocial damages
Types of pain
nociceptive
neuropathic
Chemical mediators causing pain
prostaglandins
kinins
intracellular contents (potassium & hydrogen)
Substance P
neuropeptide released by C-fibers
sensitize pain receptors –> decrease pain threshold
Hyperalgesia
increased sensitivity to pain
Neurogenic inflammation
substance p released by C-fibers
activates mast cells to rls histamine
histamine –> vasodilation increasing inflammation
Allodynia
pain perceived in response to a non-painful stimulus
Excitatory neurotransmitters
glutamate
substance P
norepinephrine
dopamine
Inhibitory interneurons
loc near the dorsal horn
release GABA to inhibit 2nd order neurons
Gate control theory
the dorsal horn acts as pain gate where incoming nerve impulses COMPETE to get through
increasing non-painful sensation can decrease pain by activating inhibitory interneurons
Gate control pathway
nociceptors stimulated –> pain sensation
glutamate & substance P are released from axon terminal of nociceptors
2nd order neurons @ the dorsal horn excited & generate AP
pain gate is opened –> impulse proceeds to thalamus
A-beta fibers
another type of sensory fiber that responds to non-painful stimuli
Gate control modulation
A-beta fibers stimulate inhibitory interneurons at the dorsal horn –> release GABA –> hyperpolarizes 2nd order neuron (takes longer for 2nd order neuron to depolarize)
A-beta fibers travel via the MCL pathway. A-delta ascends the spinothalamic tract
Serotonergic pathways
descending neurons rls serotonin
serotonin activate opioid-releasing interneurons
Endogenous opioids
enkephalins
endorphins
dynorphin
Modulation phsyiology
rls of serotonin activates opioid interneurons loc near the dorsal horn
opioids bind to receptors on the 2nd order neuron hyperpolarizing them & bind to nociceptors inhibiting rls of glutamate & substance p (excitatory neurotransmitters)
Where are opioid receptors most concentrated?
brainstem
regulate descending pathways
Opioids MOA
act at all steps of pain pathway
transmission, transduction, perception, modulation
Local anesthesia MOA
block Na+ channels –> inhibit production of APs blocking pain sensation
(transduction & transmission)
NSAID MOA
inhibit production of PGs that sensitize nociceptors (transduction)
4 P’s of pain management
Prevention
Psychological
Physical
Pharmaceutical
Breakthrough pain
transient increase in pain
Multi-modal analgesia
combines analgesics from 2+ drug classes to act on different parts of the pain pathway
increased therapeutic fx, decreased risk
Non-opioid analgesia
NSAIDs
acetaminophen
adjuvants (antidepressants, anticonvulsants)
Mild opioids
codeine
tramadol
Where are opioid receptors located
brain
spinal cord
GI tract plexus
periphery
Therapeutic fx of opioids
analgesia
sedation
euphoria
Types of opioid receptors
mu (main)
kappa
delta
PK of opioids
IV = most reliable IM/SC = variable absorption metabolized by liver excreted by kidneys/bile teratogenic
Common adverse fx of opioids
nausea/vomiting sedation (happens before respiratory depression) constipation pruritus urinary retention respiratory depression hypotension (vasodilation)
PCA assessments
drug concentration dose (loading, bolus) delay interval 4-hr dose limit attempts successful attempts total injections
Epidural assessment
sensory dermatome
motor score
Withdrawal
body develops a physical dependence on a drug –> withdrawal symptoms occur when drug is stopped/decreased
Tolerance
body develops increased tolerance for drug requiring higher amounts for same therapeutic fx
Addiction
physiologic compulsion to take a drug for its euphoric/psychic fx
S/S of overdose
choking cyanosis dizziness/disorientation cold/clammy skin slow/absent breathing somnolence pinpoint pupils
Adverse fx of opioid antagonists
headache
tachycardia
hypertension
+w/drawal symptoms
S/S of withdrawal
increased HR & BP vomiting diarrhea anxiety shivering tremors yawning body aches sweating sneezing/runny nose abdominal cramps
Inhibitory neurotransmitters
serotonin
gaba
dopamine
Opioid neurons
release endogenous opioids that act on presynaptic and postsynaptic neurons
Opioids & presynaptic neuron
binds to receptors inhibiting the opening of calcium channel gates –> inhibits release of neurotransmitters
Opioids & postsynaptic neuron
hyperpolarizes postsynaptic neuron –> decreased nerve transmission
What # on the pain scale are pts comfortable at
0-3
Location of opioid receptors
brainstem
spinal cord
peripheral nerves
GI tract
Methadone
opioid agonist
long acting
higher risk of overdose
similar adverse fx as opioids
Suboxone
buprenorphine + naloxone
partial opioid agonist
less likely to cause overdose (d/t naloxone)
preferred agonist
