Exam 3 - acute pain Flashcards
Definition of pain
An unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage
a physiological, emotional and behavioral experience
algesia
Increased sensitivity to pain
algogenic
pain producing
allodynia
a normally nonharmful stimuli is perceived as painful
analgesia
absence of pain in presence of normally painful stimuli
dysesthesia
unpleasant painful abnormal sensation, whether evoked or spontaneous
hyperalgesia
a heightened response to a normally painful stimulus
Neuralgia
pain in distribution of a peripheral nerve
Neuropathy
Abnormal disturbance in the function of nerves
Paresthesia
abnormal sensation whether spontaneous or evoked
fibromyalgia has
allodynia
herpes zoster has
neuralgia
surgical incision has
algogenic
Nociceptive is
tissue injury
non nociceptive neuropathic is
nerve injury
nociceptors detect
acute pain to tissue injury and chronic pain from swelling or injury
temp, pressure, stretch
Nociceptive pain can be (3)
- somatic
- visceral
- radicular
Somatic pain
identifiable location as a result of tissue causing release of chemicals from injured cells
localized, sharp in nature
Visceral pain definition and associations
diffuse, can be referred
dull cramping/squeezing or vague
associated with autonomic reflexes (nausea, vomiting, diarrhea)
Radicular pain description and cause
irritation of the nerve root
numbness, weakness, tingling, pins and needles
Neuropathic pain description and cause
caused by damage to peripheral or central neural structures
burning, tingling or shocl like
Non-nociceptive pain
Chronic - neuropathic or idopathic
Idiopathic pain description
Psychogenic pain associated with chronic pain
No apparent cause
Phases of Nociceptive pain (4)
- Transduction
- transmission
- Perception
- Modulation
transduction
Transmission of noxious stimuli into action potential
transmission
Pain message moves to spine and on to brain (signal enters brainstem or thalmus and extends to cerebral cortex)
A-delta and C fibers are
noxious stimulus pathways to the brain
A-gamma and C fiber are (afferent or efferent)
afferent
A-delta and C fiber pathway:
found in dorsal root ganglion –> dorsal cord –>divide and ascend in the tract of Lissauer
A-delta and C fibers decend:
1-3segmetns of tract of Lissauer
Perception includes (3)
- attention
- expectation
- interpretation
Modulation roles (4)
- Brain interacts with nerves to modulate or alter pain experience
- adjust the intensity and duration
- involves release of chemicals (i.e. endorphins and serotonin
- decrease transmission of pain signals
Modulation stages
- Periphery
2.Dorsal horn - Descending inhibitory pathway
- Cortical
Periphery stage of modulation
descending dorsolateral efferent pathway is activated
Primary afferent fibers:
A-delta and C fibers
A delta fiber pathway: Speed, characteristics and pain type
fast-sharp,peircing pain
large myelinated
(fast bunny)
A delta fibers terminate in
Rexed’s lamina I, V
C fibers pathway: speed, characteristics, pain type
Dull, chronic pain. Dull, aching, burning
small unmyelinated
slow turtle
C fibers terminate in
lamina II and III
Dorsal horn modulation stage
nural impulses modulated in spinal cord (dorsal horn) by “gatelike” process before traveling to CNS
Gate theory
APs are transmitted that inhibit inhibitory neuron
projection neuron is activated opening the gate
*think of pressure before IV stick
Modulation stage 3: Descending inhibitory pathway controls the
ascending pathway
Modulation stage 3: Descending inhibitory pathway releases _____ and inhibits ____
releases serotonin and noradrenergic neuron and inhibits substance P
Inhibitory nerotransmitters in descending pathway:
-enkephalin
-glycine
-norepinephrine
-serotonin
-GABA
Enkephalin
binds to opiate receptors on pre-synaptic first order neurons and post-synaptic second order afferent fibers
=decrease substance P release = suppress ascending pain transmission
Stage 4 modulation: Cortical
role
Pain learning and memory
remembers “that hurt”
central sensitization
neural plasticity that occurs in CNS
central sensitization occurs by
Repetitive stimulation of injury and repetitive firing in dorsal horn nociceptorsce
central sensitization can cause
activation of lower non-nociceptive mechanoreceptors to trigger a pain response - chronic pain
Two major ascending pain pathways:
- Direct lateral spinothalmic
- Indirect medial spinoreticulothalmic
Indirect medial spinoreticulothalamic pathway pain
deep somatic and visceral (dull)
Lateral spinothalmic pathway pain
sharp
Second order neuron location
dorsal horn - cross midline of spinal cord –>thalmus
Third order neuron location
Thalmus –>specific area of somatosensory cortex
mediators are
released from inflammatory cells/injured tissue
Mediator categories:
- vasoactive amines
- peptides
- Eicosanoids
Vasoactive amiens:
- HIstamine
- Serotonin
Peptide amines:
- bradykinen
Eicosanoids:
- Thromboxane
- Leukotrienes
- Prostaglandins
Bradykinen role and cause
stimulates peripheral nociceptors
causes algesia (increased sensitivity to pain)
Histamine role and cause
maintain acute-phase response
vasodilation and edama
Arachidonic acid role and examples
important substrate in synthesis of active mediators of inflammation (such as cox 1 and 2)
ex: prostiglandins and thromboxanes
Cyclooxygenase (aka cox 1) is secreted in
vascular endothelium, stomach, forbrain, uterine epithelium, kidney
cox two is stimulated at
site of inflammation
primary periphery
Cox 2 is responsible for
pain and fever
IP receptor biological effects
Vasodilator
antiaggregant
Endorphins (peptide NTs) role and example
attatches to endorphin (opiate) receptors of axon terminals of pain afferents –> inhibits release of substance P –>limits sensation of pain
(mediated by descending projections)
ex. enkephalin
TP receptor biological effects
Vasoconstrictor
Proaggregant
EP receptor biological effects
Vasodilator
Neuroprotective
Neurodestructive
DP receptor biological effects
Vasodilator
antiinflammatory
proapoptotic
FP receptor biological effects
vasodilator
antiaggregant
Substance P is a _____ released from _______
Neurotransmitter released from afferent nociceptor C fibers
Substance P is involved with
slow chronic pain, systemic
Substance P action
- vasodilation
- extravasation of plasma proteins (edema)
- degranulation of mast cells
- sensitization of stimulated sensory nerve
Glutamate
major excitatory neurotransmitter
glutamate is released in
- CNS
- A-delta afferent nerve fibers
- C primary afferent nerve fibers
glutamate is involved with what type of pain?
fast and sharp
Serotonin location and release
descending pathway, released from platelets after tissue injury
Serotonin role
algesic effect of peripheral nociceptors
Prostaglandins (PGs) are synthesized from
cox 1 and cox 2
Prostaglandins role
sensitize peripheral nociceptors, cause hyperalgesia
Prolonged pain, keeps going
Cytokines: what are they and what to they cause
released in response to tissue injury
Increasein PGs –>cause excitation and sensitization of nociceptive fibers
CGRP released from _____ and cause ____ effects
(calcitonin gene related peptide)
released from peripheral C fibers and cause LOCAL vasodilation, plasma extravasation, sensitization of sensory nerve
Major neurotransmitter released from A-delta fibers is
glutamate
glutamate binds to
AMPA and NMDA receptors on postsynaptic membrane
Major neurotransmitter that is released from C fibers
Substance P
substance P binds to
NK-1 neurokinen-1 receptors on postsynaptic membrane
Endorphine MOA and result
binds to pre-synaptic neuron (from descending pathway) to prevent substance P secretion
Substance P does not bind to norciceptive neuron
How does acute pain activate SNS?
Increases released catecholamines and adrenal glands, increased cortisol release
Pain effects on respiratory system (3)
- decreased vital capacity (VC)
-decreased inspiratory capacity (IC)
-decreased functional residual capacity (FRC)
decreased VS can cause
V/Q mismatch
NSAID MOA
inhibits cox-2 = prevents PG formation = less substance P and glutamate
Ketorolac MOA
nonselective COX inhibitor
Ketorlac contraindication
GI bleeding, renal impairment, asthma, possible impairment in bone healing
Celbrex class and MOA
NSAID inhibitor of Cox-2
Fentanyl vs morphine
fentanyl is 80-100 x more potent than morphine
Fentanyl onset and duration
short
2-5 min onset
30 min duration
most widely used narcotic for acute and chronic pain
morphine
Hydromorphone vs morphine
Hydromorphone 7-8 times more potent
Dependence can be
physiologic or psychologic
physiologic dependence
Withdrawal
psychological dependence
need for a specific substance either for positive effect or avoidance of negative
Addiction
cravings, obsessive thinking, impaired behavior control, compulsive drug taking, inability to recognize problem
Pseudoaddiction
origin in inadequate analgesia - actually have a pain problem. Not drug seeking
NOT psychological dependence
Opioid tolerance
repeated exposure to a drug = need higher dose for analgesia
opioid tolerance mechanisms (4)
- enzyme induction or down regulation of opioid receptors
2.drug-receptor interaction
- cellular alteration
- long term adaptations in gene expression
If opioid tolerance is suspected:
opioid rotation
Opioid-induced hyperalgesia
worsening pain/spreading pain/pain in different location
hard to differentiate from tolerance
Ketamine MOA
NMDA antagonist
Clonidine MOA
Centrally acting selective partial alpha-2 agonist (and some alpha 1)
Acute pain adjucts
- ketamine
- clonidine
- dexmedetomidine
- local anesthestics
- PCA
- Epidural
- Spinal
Dexmedetomidine MOA
highly selective alpha-2 agonist
activation of alpha 2 receptor results in
inhibition of adenylate cyclase and decreased cAMP levels = reduced neurotransmitter release
Local anesthetics MOA
inhibit conduction of action potentials in ascending pathway
common PCA drugs (3)
- morphine
- hydromophone
- fentanyl
Epidurals are a combination of
local anesthetic and narcotic (synergy)
Spinal MOA
Hydrophillic opioids surround spinal cord and bind to specific pre and post synaptic receptors within the dorsal horn
McLott mix is for _____ and includes _____ (4)
opioid free anestheisla
- lidocaine
- ketamine
- magnesium
- dex
