PRIMARY CARE AND
CHRONIC PAIN
MANAGEMENT
Kristin L. Kuhlmann, Ph.D., APRN, FNP-BC
West Texas A & M University
Assistant Professor, Graduate Nursing Program
Director, WTAMU Health Partner’s Clinic
22nd Annual Panhandle Nurse Practitioner Association Symposium
Amarillo, TX
April 11, 2015
Objectives
1. Identify physiological differences between acute and
chronic, non-malignant pain.
2. Describe the important pharmacodynamic and
pharmacokinetic differences among opioids, and adjuvant
pain medications, with rationale for the
pharmacotherapeutic plan.
3. Describe other modalities for chronic pain management.
4. Discuss important inter-professional clinical
considerations related to chronic pain management.
5. Discuss the importance of a “healthy” patient/provider
relationship for effective pain management.
*No financial/non-financial conflicts of interest*
Controlled Substances Updates
Texas Board of Nursing
• In addition to the 20 contact hours of continuing nursing education
in the advanced practice role and population focus area or renewal of
the certification, an APRN who has Prescriptive Authority must also
complete a minimum of 5 additional contact hours in
pharmacotherapeutics within the preceding 2 years.
Texas Nurse Practitioners Association
• Controlled Substances CE
• A total of 3 hours is required for APRNs with prescriptive authority
who order/ prescribe controlled substances for every licensure cycle
after January 1, 2015. Those who renew this year do not need this CE,
but will need it in the next licensure cycle.
Reclassification of Medications by DEA
• August 18, 2014- Tramadol classified as Schedule IV
• October 6, 2014- Hydrocodone combination products (HCPs)
reclassified as Schedule II
*Only APRNs working in hospital-based practice or hospice-affiliated facilities
can prescribe Schedule II medications in Texas.*
Controlled Substances
• The U.S., Drug Enforcement Agency (DEA) have delineated
five categories, or schedules for controlled drugs:
• Based on accepted medical use
• Potential for dependency and abuse
• Health care providers are provided with both a DEA and
state license to prescribe, distribute, or administer
controlled substances.
• General Classes/Uses:
• Pain Management
• Anxiety
• Sleep Disorders
• ADHD
DEA Controlled
Substance
Schedules
Schedule I
No consensus- accepted medical use
High potential for abuse
Severe psychological or physical
dependence
heroin, LSD, marijuana,
methaqualone, peyote
Schedule II
High potential for abuse
Potentially severe psychological or
physical dependence
Considered “dangerous”
Schedule III
Moderate to low potential for
psychological/ physical dependence
Drug abuse potential lower than
Schedule II
Schedule IV
Low risk for potential abuse and
dependence
Schedule V
Lower potential for abuse or dependence
Opioids: hydrocodone,
morphine, methadone,
hydromorphone, meperidine,
oxycodone, fentanyl
Amphetamines:
methamphetamines, cocaine,
dexedrine, Adderall, Ritalin
Opioids: codeine
Anesthetic: Ketamine
Male sex hormones:
anabolic steroids,
testosterone
Opioids: Tramadol, Talwin,
Talwin Nx
Benzodiazepines: Xanax,
Ativan, Soma, Valium
Sedative: Ambien(zolpidem)
Anticonvulsant/neuropathy:
Lyrica (pregabalin)
Cough preparations: Less
than 200 mg of codeine
Antidiarrheals: Lomotil,
parapectolin, Motofen
 All scheduled
drugs/substances
have potential for
dependence and
abuse.
 Schedule I
substances are the
most “dangerous”;
Schedule V have
the lowest potential
for dependence and
abuse.
Opioid Agents/ Narcotics
OPIOID AGENTS (GENERIC NAMES)
OPIOID AGONISTS
PHENANTHRENES- SCHEDULE II
morphine sulfate (extended release)
morphine sulfate (short acting)
hydrocodone with acetaminophen
hydrocodone with ibuprofen
hydrocodone high dose
oxycodone
oxycodone with aspirin
oxycodone with acetaminophen
hydromorphone
codiene with acetaminophen- SCHEDULE III
PHENYLPIPERIDINES- SCHEDULE II
meperidine
fentanyl
DIPHENYLHEPTANES- SCHEDULE II
methadone
MU RECEPTOR AGONIST & NE REUPTAKE
INHIBITOR- SCHEDULE II
tapentadol, tapentadol ER
MIXED AGONIST/ANTAGONIST- SCHEDULE IV
pentazocine; pentzocine with nalaxone
PARTIAL AGONISTS- SCHEDULE IV
Tramadol; tramadol with acetaminophen
BRAND NAMES
MS Contin, Avinza, Kadian, Embeda,
Oramorph SR, generic
MS-IR, Kadian, MS
Lortab, Vicodin, Norco
Vicoprofen
Zohydro ER
Oxycontin, Oxy IR, Oxecta
Percodan
Endocet, Percocet, Roxicet, Tylox
Dilaudid, Exalgo ER
Tylenol #3, Tylenol #4
Demerol
Duragesic transdermal, Actiq
(transmucosal), Abstral, Fentora,
Onsolis, Lazanda
Dolophine
Nucynta; Nucynta ER
Talwin; Talwin Nx
Ultram; Ultracet
Neurobiology of Narcotic Use
• Like food and sex, opioids (narcotics) stimulate mu receptors of the
mesolimbic reward system in the midbrain:
• Generate signals to cells in the Ventricle tegmental area (VTA)
• Releases the neurotransmitter, dopamine, into the Nucleus accumbens
• Elicits feelings of pleasure/euphoria with pain relief
• This reward circuit includes areas of
motivation and memory, encouraging
repeated use or behavior.
• The Hippocampus stores memories
of rapid satisfaction induced by the drug.
• With repeated use, the Prefrontal cortex,
with normal functions of planning and
executing responsible actions, becomes
involved in craving activities:
• Override inhibitory signals in some
individuals, overuse and addictive behaviors begin.
Hippocampus
Tolerance
• Narcotics provide a shortcut to endorphin release
• Quickly flood the brain with dopamine and other neurotransmitters, at
2-10 times the amount of natural induction.
• With repeated use of narcotics, ventricle tegmental area (VTA)
receptors in the midbrain get overwhelmed
• Seeking homeostasis, the VTA:
• Produces less dopamine and some dopamine receptors are inactivated
• An increase in drug dosage is needed for the same effect over time
(tolerance)
• Repeated exposure to escalating doses of the narcotics alters brain
function:
• Functions “normally” when drug present, and abnormally when absent
• Drug dependence occurs
• Without the drug, withdrawal symptoms occur
Narcotic Withdrawal, Overuse, Addiction
 Orexin activates enzymes that convert ATP into another chemical, cAMP:
• Triggers the release of norepinephrine, stimulating normal functioning, such
as wakefulness, appetite, muscle tone, general feeling of well being.
 When a narcotic links to the mu opioid receptors:
• Enzymes are inhibited, less cAMP is produced,
• Less norepinephine is released:
• Opioid effects of sedation, shallow breathing,
incoordination, slurred speech occur
 With repeated opioid use, neurons produce
more cAMP to offset the inhibitory effect of drug:
• Clinical symptoms of withdrawal symptoms
occur:
• Jitters, anxiety, muscle cramps, insomnia,
dilated pupils, diarrhea, nausea and vomiting.
• These unpleasant symptoms play a part in the cycle of
overuse, physical and psychological addiction.
Narcotic Overdose Deaths
• In 2011, there were 1.5 million emergency room visits for
pharmaceutical overdoses.
• Annually, drug overdoses kill more people than motor vehicle
accidents.
• The drug overdose death rate has doubled since 1999, largely due to
the increased use of narcotics in the outpatient population.
Overdose Deaths
• In 2013, there were 23,000 deaths
from pharmaceutical overdoses.
• Every day in the U.S., 120 people
die and 6,750 people are treated for
drug overdose.
• Of pharmaceutical overdose deaths,
70% result from opioids and 30%
from benzodiazepines.
• 81% of pharmaceutical overdose
deaths are unintentional.
Pain- Definitions and Categories
• Definition of pain:
• Unpleasant sensory and emotional experience
• Bodily sensation of tissue damage occurring
• An experience of a threat is associated with the sensation,
prompting action to make it stop
• Two categories of pain:
• Adaptive (acute)- necessary for survival, protection from further
injury, body response to promote healing
• Maladaptive (chronic)- part of a disease process; pathologic
functioning of the nervous system (neuropathy)
• Lasts beyond the time necessary for injury of the body to heal
• Duration of 3 to 6 months, or longer
Transmission of Pain
• Transduction- conversion of thermal, mechanical, or chemical electrical activity at
peripheral sensory nerve endings (nocioceptors)
• Transmission- through laminae of dorsal horn of the spinal cord to the brain stem, and
through connections between the thalamus and brain cortex
• A-delta nerve fibers are myelinated, quick transmission of pain, intense sensation
• C-fibers are non-myelinated; delayed, throbbing, dull, longer-lasting pain; emotional
response elicited
• Modulation- In the spinal cord, the sensation is augmented by excitatory
neurotransmitters (ascending) and sent up to the brain;
• Brain sends down inhibitory neuropeptides (descending)
• Perception- Interpretation of input in brain gives rise to specific sensory consciousness,
a multidimensional experience of pain
Perception of Pain
Pain stimulates multiple areas of the brain; response is
elicited by three major areas:
1. Somatosensory cortex
• 3-neural relay system
• From peripheral sensory nocioceptors to dorsal root ganglia
(first order neuron cell bodies)
• Within spinal cord (second order neuron cell bodies)
• Sensation of pain, touch, temperature relayed to:
• Medulla evaluates stimuli- touch, vibratory sense, position
• Through brainstem to thalamus nucleus (third order neuron
cell bodies)
• Impulse then sent to anterior cingulate cortex:
• Intensity, type, and location of pain interpreted and analyzed
• Sensation related to memory of past experiences; formulate
cognitive assessment of level/ management of painful stimuli
Perception of Pain
2. Reticular activating system (RAS)- Located in
brainstem
• Part of the mammalian brain, responsible for sleep, waking, elimination
• Drive for sex, eating, breathing, and heart rate
• Ascending neural fibers connect with hypothalamus, thalamus, and
cortex
• Descending neural fibers connect with cerebellum and sensory nerves
• Motor response to pain
• e. g.: Moving the hand quickly away from a hot surface
• Affective-motivation response
• Assess the level of injury; limits or restriction of movement
3. Limbic system (Reward)- Thalamus
• Emotional and behavioral responses to pain
• Affects mood, responsible for perception and the motivation to respond
to the pain experience
Neural Pain Pathway
Adapted from: A. K. Srivastava. (2010). Pain: Physiological
considerations. Retrieved from HomeOrizon website:
http://www.homeorizon.com/homeopathic-articles/neurology/painphysiological-consideration
Pain Receptor Sites and Opioid Action
Receptor
Mu1
Mu2
Kappa1
Kappa2
Kappa3
Delta
Location/Function
Supraspinal, periphery
Analgesia
Spinal analgesia
Spinal, mediates visceral pain
Spinal, mediates visceral pain
Supraspinal analgesia
Supraspinal, Spinal
antagonist activity only, no
delta agonists developed yet
Side Effects
Euphoria, respiratory depression
Opioids
Morphine-like narcotics
Respiratory depression, physical dependence, (Table 1),
decreased GI motility, pruritus
endorphin neuropeptides
Spinal analgesia; sedation, miosis
See Table 1 below,
Dysphoria
morphine(slight),
Dynorphin neuropeptides
Antidepressant effect, convulsant effect,
Antagonists of delta receptortachycardia, tachypnea, hallucinations,
buprenorphine, trazodone
mydriasis, hypertonia
Enkephalin neuropeptides
Types of Pain
• Nocioceptive pain- pain along a nerve fiber, usually due
to tissue damage
• Somatic- caused by injury to body tissues
• Well localized, but variable in description and experience
• Musculoskeletal (fractures, sprain/strains)
• Inflammatory (arthritis, bursitis, infection, gout)
• Mechanical/compressive (low back pain, neck pain, crush injury)
• Visceral- caused by stretch receptors within or surrounding the
chest and abdominal (internal) organs
• Poorly localized- cramping, shooting, stabbing, aching, burning
• Inflammatory- (pneumonia, appendicitis, urinary tract infection)
• Mechanical/compressive -(tumors, growths, scarring, shifting/prolapse)
Treatment of Nocioceptive Pain
Identified Risks and Treatment Considerations
Chronic kidney disease, advanced age - avoid NSAIDs
and COX-2 inhibitors
Peptic ulcer disease, glucocorticoid use - avoid NSAIDs
Hepatic disease - avoid NSAIDs, COX-2 inhibitors, and
acetaminophen (APAP); use TCAs or duloxetine first line
Cardiovascular disease or risk - use lowest effective
dose of NSAIDs; in patients who require treatment, suggest
naproxen
Adapted from: T. M. Woo, & A. L. Wynne,
(Eds.). (2012). Pharmacotherapeutics for nurse
practitioner prescribers (3rd ed.). Philadelphia,
PA: F.A. Davis Company.
NSAID: nonsteroidal anti-inflammatory drug; COX-2 inhibitor:
cyclooxygenase 2 inhibitor; APAP: acetaminophen/paracetamol;
TCA: tricyclic antidepressant; PPI: proton pump inhibitor.
Types of Pain (cont.)
• Neuropathic- Abnormal neural activity due to disease,
injury, or dysfunction of the nervous system
• Sympathetically mediated pain (SMP)- complex regional pain
(reflex sympathetic dystrophy)- post-injury, triggering of immune
response
• Peripheral neuropathic pain – post herpetic neuralgia, neuroma
• Central nervous system pain- phantom limb pain, spinal cord
injury, post-stroke pain
• Classification of Neuropathy
• Mononeuropathy- one nerve affected (e.g. carpal tunnel syndrome)
• Mononeuropathy multiplex- several nerves affected, multifocal
• Numbness, tingling, abnormal sensation (e.g., diabetic neuropathy)
• Polyneuropathy- symptoms are diffuse and bilateral (e.g., fibromyalgia;
stocking/glove neuropathy)
Treatment of Neuropathic Pain
SNRI: serotonin-norepinephrine reuptake inhibitor; TCA: tricyclic
antidepressant; NMDA: N-methyl-D-aspartate.
Adapted from: T. M. Woo, & A. L. Wynne,
(Eds.). (2012). Pharmacotherapeutics for nurse
practitioner prescribers (3rd ed.). Philadelphia,
PA: F.A. Davis Company.
Acute and Chronic Pain
• Acute Pain
• Sudden onset
• Usually from a clearly identifiable cause
• Treatment is designed to prevent further injury and treat pain
• Pain totally resolves with healing of the injury
• Chronic Pain
• Persists for weeks to months
• Often associated with an underlying medical condition
• Treatment goal is to return the patient to optimal function
• Total eradication of pain may not be possible
• Treatment
• Pharmaceutical/Medications
• Other Treatment Modalities
•
•
•
•
•
Physical therapies
Psychological support
Multiprofessional health support
Family/Social support
Lifestyle modifications
Non-Pharmacologic Measures
• Physical measures
• Heat, ice, massage, splinting/support, manipulative therapies (e.g. chiropractic,
osteopathy), physiotherapy
• Treat primary cause
• Improve diabetic control, reduce weight if overweight/obese; moderate, regular
exercise; reduce/stop alcohol consumption, vitamin/mineral supplementation (thiamine,
niacin, Vitamin D, copper, selenium, magnesium).
• Surgical interventions to correct defect structural defects (e.g.: disc prolapse, spinal
stenosis, carpal tunnel syndrome)
• Inhibitory stimulation of the periphery/spinal cord
• Acupuncture/TENS
• Electrical peripheral nerve or dorsal column stimulation
• Central (deep-brain) stimulation
• Inhibition or prevention of ascending nerve transmission from
periphery/ spinal cord
• Nerve blocks
• Neurolysis or rhyzolysis
• Alter pain processing at the cortical level
• Cognitive therapies, biofeedback, hypnosis, meditation
• Improved effect on descending inhibition
• Decreased sensitivity to ascending painful stimuli
Acute Pain Management Algorithm
Chronic Pain
• Over 100 million Americans suffer chronic pain annually
• 1 in 3 people will experience chronic pain at some time
• 80-90% experience pain in their neck or lower back
• 20% of outpatient visits and 12% of all prescriptions written
in the U.S. are for chronic pain
• In 2010, 19% of adults reported constant or frequent pain,
with most stating pain is moderate or severe
• Cost of untreated/undertreated pain- $100B annually
• Overall, 35% of patients with chronic pain have PTSD
• PTSD-related neurohormones, neurotransmitters, and inflammatory
system factors transmit and/or amplify pain stimuli:
• 98% of persons with PTSD will experience chronic pain in their
lifetime
Chronic Pain Treatment Algorithm
Copyright 2012 F.A. Davis Company www.fadavis.com
Establishing/Maintaining a Healthy Relationship:
Chronic Pain Management
• Detailed history and physical to assess the pain condition
(biopsychosocial approach)
• Identify the specific context of how the patient’s pain interferes with
ADLs, including sleep, work, social events (family/friends/church),
emotions, coping, side effects of treatment
• Obtain records from pain management provider
• Collaborate to provide best care for patient
• Mutual establishment and understanding of realistic treatment
goals and expectations
• Pain may not be fully alleviated, but improvement in ADLs is goal
• Acknowledge and validate the patient’s pain symptoms
• Formulation of a meaningful treatment plan
• Input of patient’s specific needs
• Be clear about comfort level/agreement about prescribing medications
• Participatory decision making
• Modification of the treatment plan
• Re-assessment and communication with the patient on follow-up visits