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

Objectives1. 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 UpdatesTexas 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 abuseSevere psychological or physical dependence

heroin, LSD, marijuana, methaqualone, peyote

Schedule II High potential for abusePotentially severe psychological or physical dependenceConsidered “dangerous”

Opioids: hydrocodone, morphine, methadone, hydromorphone, meperidine, oxycodone, fentanyl Amphetamines: methamphetamines, cocaine, dexedrine, Adderall, Ritalin

Schedule III Moderate to low potential for psychological/ physical dependenceDrug abuse potential lower than Schedule II

Opioids: codeineAnesthetic: Ketamine Male sex hormones: anabolic steroids, testosterone

Schedule IV Low risk for potential abuse and dependence

Opioids: Tramadol, Talwin, Talwin NxBenzodiazepines: Xanax, Ativan, Soma, ValiumSedative: Ambien(zolpidem)

Schedule V Lower potential for abuse or dependence Anticonvulsant/neuropathy: Lyrica (pregabalin)Cough preparations: Less than 200 mg of codeineAntidiarrheals: 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/ NarcoticsOPIOID AGENTS (GENERIC NAMES) BRAND NAMESOPIOID AGONISTS  PHENANTHRENES- SCHEDULE II  morphine sulfate (extended release) MS Contin, Avinza, Kadian, Embeda,

Oramorph SR, genericmorphine sulfate (short acting) MS-IR, Kadian, MShydrocodone with acetaminophen Lortab, Vicodin, Norcohydrocodone with ibuprofen Vicoprofenhydrocodone high dose Zohydro ERoxycodone Oxycontin, Oxy IR, Oxectaoxycodone with aspirin Percodanoxycodone with acetaminophen Endocet, Percocet, Roxicet, Tyloxhydromorphone Dilaudid, Exalgo ERcodiene with acetaminophen- SCHEDULE III

Tylenol #3, Tylenol #4

PHENYLPIPERIDINES- SCHEDULE II  meperidine Demerolfentanyl Duragesic transdermal, Actiq

(transmucosal), Abstral, Fentora, Onsolis, Lazanda

DIPHENYLHEPTANES- SCHEDULE II  methadone DolophineMU RECEPTOR AGONIST & NE REUPTAKE INHIBITOR- SCHEDULE II

 

tapentadol, tapentadol ER Nucynta; Nucynta ERMIXED AGONIST/ANTAGONIST- SCHEDULE IV

 

pentazocine; pentzocine with nalaxone Talwin; Talwin NxPARTIAL AGONISTS- SCHEDULE IV  Tramadol; tramadol with acetaminophen 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 PainPain 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/pain-physiological-consideration

Pain Receptor Sites and Opioid ActionReceptor Location/Function Side Effects Opioids Mu1 Supraspinal, periphery

Analgesia Euphoria, respiratory depression  

Morphine-like narcotics (Table 1), endorphin neuropeptides

Mu2 Spinal analgesia Respiratory depression, physical dependence, decreased GI motility, pruritus

Kappa1 Spinal, mediates visceral pain Spinal analgesia; sedation, miosis  See Table 1 below, morphine(slight), Dynorphin neuropeptides

Kappa2 Spinal, mediates visceral pain DysphoriaKappa3 Supraspinal analgesia  Delta Supraspinal, Spinal

antagonist activity only, no delta agonists developed yet

Antidepressant effect, convulsant effect, tachycardia, tachypnea, hallucinations, mydriasis, hypertonia

Antagonists of delta receptor- buprenorphine, trazodone 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 NSAID: nonsteroidal anti-inflammatory drug; COX-2 inhibitor: cyclooxygenase 2 inhibitor; APAP: acetaminophen/paracetamol; TCA: tricyclic antidepressant; PPI: proton pump inhibitor.

Adapted from: T. M. Woo, & A. L. Wynne, (Eds.). (2012). Pharmacotherapeutics for nurse practitioner prescribers (3rd ed.). Philadelphia, PA: F.A. Davis Company.

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