Barbara St. Marie, MA, ANP, GNP PhD Candidate University of
Wisconsin Milwaukee Nurse Practitioner Supervisor Pain and
Palliative Care Fairview Ridges Hospital
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Objectives: Basic Neurophysiology of Pain Pathways
Pharmacological and Non-pharmacological Interventions of Pain
Pathways Matching neurophysiology with pharmacology Pathophysiology
of Pain When Pain becomes Chronic or Persistent Pain Interventions
of Chronic or Persistent Pain Nursing Contributions to Pain
Management
Pain Process The neural mechanisms by which pain is perceived
involves a process that has four major steps: Transduction
Transmission Modulation Perception
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Facilitating Transduction Biochemical mediators: Chemical Soup
Prostaglandins Bradykinins Serotonin Histamines Cytokines
Leukotrienes Substance P Norepinephrine
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Peripheral Excitatory Mediators (Pain)
SubstanceReceptorMechanism Substance P (SP) NK 1 neuronal
excitability, edema Prostaglandin(PG)? Sensitize nociceptors,
inflammation, edema Bradykinin B 2 (normal) B 1 (inflammation)
Sensitize nociceptors PG production Histamine H1H1H1H1 C-fiber
activation, edema, vasodilatation Serotonin 5-HT 3 C-fiber
activation, release SP Norepinephrine(NE) 1111 Sensitize
nociceptors Activate nociceptors
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Peripheral sensitization Peripheral opioid receptors Management
of histamine
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Diclofenac
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Acetaminophen (Tylenol) Analgesic, antipyretic Inhibits
prostaglandin synthetase in the CNS, weak peripheral
anti-inflammatory activity Serotonergic effect at descending
pathway Used to treat osteoarthritis
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Acetaminophen (Tylenol) American Pain Society: Maximum dose
4,000 mg/day, American Liver Foundation: 3,000 mg/day Risk of
hepatotoxicity with higher doses Antidote acetylcysteine (Mucomyst,
Acetadote)
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Transmission of pain Defined as: Projection of pain into the
Central Nervous System
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Transmission A synapse contains three elements: the presynaptic
terminal the synaptic cleft the receptive membrane
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Transmission The presynaptic terminal is the axon terminal of
the presynaptic neuron Here that the presynaptic neuron releases
neurotransmitters which are found in vesicles
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Capsaicin Hot peppers May deplete & prevent re-
accumulation of substance P in primary afferent neurons responsible
for transmitting painful impulses from peripheral sites to the CNS.
Absorption, distribution, metabolism & excretion, half life
unknown May produce transient burning with application, usually
disappears in 2-4 days, but may persist for several weeks.
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Transmission The synaptic cleft is the narrow intercellular
space between neurons. Neurotransmitters cross the synaptic cleft
and bind to specific receptors on the postsynaptic neurons This
will excite or inhibit the postsynaptic neurons.
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Muscle Pain Correlated with Lactic acid levels Lactic acid
levels in the blood vessels of the muscle influence neuronal
noxious stimuli What might that tell us about intervening with
muscle pain?
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Neuropathic Pain Features Burning, prickling, tingling
Shock-like May or may not be lancinating Paresthesia May be
associated with Allodynia Hyperalgesia Hyperethesia Referred Pain
More intense at noc
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Local Anesthetic Agents On-Q delivery Synera patch (topical)
Emla: Lidocaine and Prilocaine 1:1 (topical) LMX 4% lidocaine
(topical)
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Local Anesthetics Blocks conduction of nerve impulses by
decreasing or preventing an increase in the permeability of
excitable membranes to Na+. Inhibits depolarization of nerve Blocks
neuronal firing Challapalli, V., et. al., 2005
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Lidoderm 5% Patch
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Mentholatum Menthol generates analgesic activity through: Ca 2+
channel blocking activity Binding to kappa opioid receptors Stanos,
S.P., 2007
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Methyl Salicylate Toxicity Salicylic acid derivative (a.k.a.
wintergreen oil, sweet birch oil) Lipid solubility increases
toxicity More toxic than aspirin 1 teaspoon (5ml) wintergreen oil
contains 4,000 mg salicylate 30ml wintergreen oil is a fatal dose
in adults Risk of toxicity reduced with use for acute pain, limited
to a small area of dermal application Chyka, P.A., et al.,
2007
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Anticonvulsants 1) Inhibit sustained high-frequency neuronal
firing by blocking Na+ channels after an action potential, reducing
excitability in sensitized C-nociceptors. 2) Blockade of Na+
channels and increase in synthesis and activity of GABA, in
inhibitory neurotransmitter, in the brain. 3) Modulates Ca+ channel
current and increases synthesis of GABA. Deglin, J.H. &
Vallerand, A.H., 2001
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Antiepileptic Agents Broad clinical actions in the CNS: Reduce
seizures Neuropathic pain Bipolar disorder Anxiety Schizophrenia
Agitation Impulse dyscontrol Dementia Delirium Three proposed
mechanisms of action: Blockade of voltage gated sodium channels (
glutamate release) Blockade of voltage gated calcium channels alpha
2 delta subunits (reduces excessive neurotransmitter release)
Enhancement of GABA actions
Perception Review: Impulses go through the postsynaptic
junction Cross the dorsal horn To the spinothalamic tract
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Meperidine (Demerol) Duration 2-3 hrs PO doses 1/4 analgesic
effect Toxic metabolite - normeperidine dysphoria, irritability,
seizures t 1/2 =12-15 hrs; not reversible with Narcan Do not use
Demerol for more than 48 hrs or at doses >600 mg/24hr Only
indications: rigors, short term use, i.e. endoscopy.
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Reference: Am Family Physician, 71(7), 2005 Methadone FDA
Indications: Severe pain, narcotic detoxification, and temporary
maintenance of narcotic addiction
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Methadone Inexpensive Accumulates with repeated dosing 85%
protein bound Slowly released up to 10 days after dose increase
Available in 10 mg tablet or oral solution, use of 40 mg diskette
no longer available for pain mgt use Patient may be subjected to
scrutiny, stigma & misconceptions
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Federal Regulation Prevention of withdrawal in opioid addiction
Special annual registration with DEA Use only in an established
addiction treatment program Maintenance patients may continue tx
when admitted to acute care facility Treatment for pain Any
clinician licensed to prescribe Schedule II drugs may prescribe
methadone for pain
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Methadone Incomplete Cross-Tolerance Inverse relationship with
dosing Monitor ekg for QT prolongation
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Schmittner, J., 2006 Clinical Indications for Electrocardiogram
in Patients Receiving Methadone History of long-QT syndrome or
torsades de pointes Family history of long-QT syndrome or early
sudden cardiac death Cardiac arrhythmia and heart block (2 nd or 3
rd degree AV block) Anorexia nervosa Frequent electrolyte depletion
(K, Ca, Mg) HIV patients on multiple-antiretroviral therapy
Methadone dosages greater than 150mg/day Initiation of a P-450
inhibitor Initiation of medications associated with QTc
prolongation Presyncopal or syncope symptoms Unexplained
tonic-clonic seizures with abnormal electroencephalogram
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Routhier, D., et al., 2007
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Methadone Black Box Warning Deaths during initiation and
conversion from other opioids Respiratory depression chief hazard
Use of concomitant sedatives including alcohol Self-titration
iatrogenic overdose QTc prolongation
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Key Teaching Points Careful of mix up between long acting and
short acting with same mg amount (ex. MS Contin and MSIR) Remove
old patch before new one put on Safe disposal issues Drinking,
driving issues Tell all of your healthcare providers everything
that you take, always Careful about buying on the Intranet
Sleepers, sedatives Teach S & S of withdrawal
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Key Teaching Points Never take more or less than prescribed
without calling us Only you take your pain medication, do not
share! Never alter the medication, i.e. splitting sustained release
medications Keep in a safe place always! Medication parties Middle
& High School students; #1 medicine cabinet thefts Inciardi,
J.A., et al., 2007
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Some of our biggest safety issues Careful of look alike names
and sustained release versus immediate release Only witness waste
when you see it first, protect your hard earned license Careful of
which line is which PCA pumps; double check, double check and
double check-settings and syringe concentration, medication and
document Instruct patient only to press button ISMP, February
2007
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Descending Pathway Anatomic path From cerebral cortex Brain
stem To dorsal horn Pain inhibition Enkephalin excites inhibitory
interneurons in the dorsal horn
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Descending Pathway Mediates voluntary and involuntary motor
control Regulates somatic sensory processing Regulates the
autonomic nervous system
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Coexisting CD and Pain Unique experiences Anatomic paths of the
nervous system have commonalities Addictive responses are altered
by the physiological presence of pain Pain responses are altered by
the physiological presence of addiction.
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Endocannabinoids Research on the adaptations of cells continue
with the recent discover of the cannabinoid receptor and the
subsequent searching and findings of the endogenous cannabinoids.
Two endocannabinoids, anandamine and 2- arachidonyl glycerol or
2-AG.
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Endocannibinoids Found in most brain function Equal balance
between endocannibinoids and their receptors occur (Fride, 2005)
Role in brain plasticity leading to long term effects on movement
and coordination habit formation reward and addiction
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Opioid-Induced Pain Hypersensitivity Opioids may produce
abnormally heightened pain sensations May share mechanisms with
antinociceptive tolerance Possibly dose related? Observed both with
acute and chronic use Current research indicates potential for
targets for new therapies
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Questions
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Nursing Research in Pain Management Peggy Compton, PhD, RN Pain
and Addiction Christine Miaskowski, PhD, RN Gender and Pain
Christine Kovach, PhD, RN Elders and Pain Margo McCaffrey, MSN, RN
Pain is what the patient says it is Betty Morgan, PhD, RN Pain and
Addiction
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Nursing Research in Pain Management Rosemary Polomano, PhD, RN
Pain, Rat lab Keela Herr, PhD, RN Geriatric Pain Jo Eland, PhD, RN
Pediatric Pain Donna Wong, PhD, RN Smiley Faces, Faces Scale for
Pain assessment
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What is Flare of Pain? Same Pain as Chronic (Persistent) Pain
Same Location as Chronic (Persistent) Pain Different Pain Intensity
from Chronic (Persistent) Pain Temporary increase in pain intensity
from a more stable baseline pain with otherwise similar
characteristics.
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Pain Flare Study 2001-2002 Pain Flare Study Descriptive study
N= 67 Location: University of Minnesota Fairview Pain Management
Center Survey mailed to 75 patients, 67 responses IRB approval
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Pain Flare Study Purpose of study Describe the characteristics
of and factors contributing to pain flares in patients with chronic
pain who receive care from the nurse practitioner in Fairview Pain
Management Center
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Conclusions Pain Flare definition: Same Pain, same location,
different intensity This definition implies that Pain flare should
not represent new pathology Patient has an ongoing pain problem
that has been relatively stable No presumption of what baseline
pain intensity was
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Conclusions Studying flare gives meaning to the patients
experiences of flare of their pain Gave patients a voice Assurance
that it is not permanent condition Universality of flares in
chronic pain Pain intensity rating less important in chronic non-
malignant pain than changes in pain intensity Once contributing
factors to pain flares have been resolved, chronic pain returns to
baseline
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Envision the Future Better pain control with fewer side effects
Genome pain management Helping the brain erase persistent pain
Social Policy that enhances comprehensive approach to pain
management rather than reinforce procedures to get rid of pain
Abuse deterrent opioid formulations that significantly reduce
diversion and are available for those who need it.