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PAIN CH 6.pptx

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PAIN CHAPTER 6 EPIDEMIOLOGY OF PAIN Protective mechanism Most common symptom for seeking medical treatment Optimal pain management Quicker rate of recovery Better functioning Fewer postoperative complications PAIN: ASCENDING SIGNALS OVERVIEW Structure...

PAIN CHAPTER 6 EPIDEMIOLOGY OF PAIN Protective mechanism Most common symptom for seeking medical treatment Optimal pain management Quicker rate of recovery Better functioning Fewer postoperative complications PAIN: ASCENDING SIGNALS OVERVIEW Structure Role Nociceptors Pain receptors A-delta fibers: large and myelinated C fibers: smaller and unmyelinated Spinothalamic tract Ascending pathway Carry pain signals to brain Brain Perception of pain PAIN: DESCENDING SIGNAL OVERVIEW Structure Role Brain Interpret pain sensory signal Sends outgoing signals Endogenous Natural analgesic neurochemicals opioids Endorphins, enkephalins, dynorphins Receptors on pain Opioids bind to receptors fibers Block signaling from pain fibers SIMPLE REFLEX ARC Protective responses that do not involve brain input Example: patellar reflex Afferent neuron Incoming signal to dorsal horn of spinal cord Interneuron Connector Efferent neuron Outgoing signal from anterior spinal cord SIMPLE REFLEX ARC (CONTINUED_2) SPINAL CORD—BRAIN CONNECTION Brain: interprets pain signals Signals to and from brain Spinothalamic tract Primary ascending tract for pain signals Corticospinal tract Outgoing signals from the brain SPINAL TRACTS NEUROTRANSMITTERS AND PAIN Excitatory or inhibitory >50 neurotransmitters involved with pain Pharmacological manipulation of neurotransmitters for pain management Example: medications increase the level of the neurotransmitter, serotonin, to treat migraines NEUROTRANSMITTERS AND PAIN (CONTINUED_2) Neurochemicals Action Prostaglandins (from Enhances inflammation, pain, edema COX 1 enzymatic pathway) Interleukins Enhances inflammation, pain, edema Tumor necrosis factor Enhances inflammation, edema, and pain and decreases appetite Leukotrienes Enhances inflammation, edema, and bronchospasm, particularly in asthma and allergy Bradykinins Enhances inflammation Glutamate Amplifies pain signal Substance P Amplifies pain signal Enkephalins, Inhibitory influence on pain; natural opioid endorphins NEUROTRANSMITTERS AND PAIN (CONTINUED_3) Neurochemicals Action Acetylcholine Inhibitory action on pain in the spinal cord Gamma- Inhibitory action on pain in the spinal aminobutyric acid cord and brain Norepinephrine Inhibitory action on pain in the spinal cord Dopamine Inhibitory action on pain in the spinal cord and brain Serotonin Conveys analgesic signals from the PAG area to the NRM of the brain Diminished in migraine headache ENDOGENOUS OPIOID RELEASE Periaqueductal gray matter (PAG) Activates enkephalin-releasing neurons Project to nucleus rapine magnus (NRM) NRM Serotonin-releasing neurons Descend to dorsal horn of spinal cord Interneurons spinal cord Release endogenous opioids Opioids block incoming pain signals ENDOGENOUS OPIOID RELEASE (CONTINUED_2) SENSITIZATION Exaggerates excitement of pain nerve fibers Decreases pain inhibitory signals Pain mechanism Altered in some individuals Altered in some disease states DERMATOMES AND MYOTOMES Spinal nerves Innervate body in specific patterns “Map” Alterations in sensation or motor control Specific spinal nerve location GATE CONTROL PAIN THEORY Pain signals Travel to and from brain Pain Not necessarily proportional to injury Phantom pain Does not adequately explain STEPS OF GATE CONTROL THEORY Transduction Painful stimuli into neuronal signals Transmission Traveling of neuronal signal Modulation Influence of other neurons on the pain signal: GATE Perception Conscious awareness of the pain NEUROMATRIX PAIN THEORY Explains phantom pain Body-self neuromatrix located in brain Pain generated from nerve impulses of this matrxi Develops from sensory input throughout a person’s life Brain can generate painful stimuli apart from nociceptive stimulation TYPES OF PAIN Acute Lasts hours or days and resolves with healing Chronic Beyond expected time Can be due to persistent inflammation Does not serve a biological or protective function May profoundly affect quality of life Neuropathic Injury or malfunction of nervous tissue Burning, tingling, paresthesia (pins and needles) SOURCES OF PAIN Cutaneous Deep somatic Ligament, tendons Dull, poorly localized pain Visceral Deep organs Referred Pain occurs at a distance from actual pathology Phantom Amputated part of body PAIN ASSESSMENT 5th vital sign Pain is subjective Variability among patients Nonverbal and verbal expressions may vary Distinguishing features of pain Can aid in diagnosis Example: peripheral arterial disease causes leg cramps OLDCART PAIN ASSESSMENT Characteristic Example question Onset When did the pain begin? Location Where does it hurt? Can you point to where it hurts? Duration How long does it last? Characteristi What does it feel like? cs Aggravating Does anything make it worse? Relieving Does anything make it better? Factors Treatment Did anything make it better (pain medication, ice, heat)? DIAGNOSIS Pain severity Assessed using reliable scale May also use: Blood tests Nerve conduction studies Electromyography Nerve injection Imaging tools PAIN SCALES TREATMENT: WHO STEP ANALGESIC LADDER If multiple pain relievers used, should have different mechanisms of action Ladder used in bidirectional fashion TREATMENT: MODIFIED WHO ANALGESIC LADDER Includes non-pharmacological modalities THREE MAJOR CLASSES FOR PHARMACOLOGICAL PAIN RELIEVERS Opioids Nonopioids Adjuvant medications OPIOIDS Considered a controlled substance Morphine is prototypical opioid Produces analgesia, euphoria, and sedation Most effective when given before pain onset Can cause respiratory depression Additional side effects of opioids Constipation, nausea, dizziness, physical dependence COMMON OPIOIDS SCHEDULE II SCHEDULE III Morphine (MS Contin®, Roxanol®) Buprenorphine (Suboxone®, Codeine (Vicodin®) Subutex®) Hydromorphone (Dilaudid®) Meperidine (Demerol®) SCHEDULE IV Methadone (Dolophine®, Tramadol Methadose®) Oxycodone (Oxycontin®, Percocet®, Endocet®, Roxicodone®, Roxicet®) Fentanyl (Duragesic, Oralet®, Actiq®, Sublimaze®, Innovar®) Tapentadol COMPLICATIONS OF OPIOID USE Substance abuse Screener opioid assessment for patients with pain Addiction Tolerance Withdrawal Buprenorphine Used to wean patients from opioids Naloxone Helps counter the effects of opioid overdose NONOPIOID ANALGESICS Acetaminophen (Tylenol) NSAIDs ’ Aspirin, ibuprofen, naproxen, celecoxib Block prostaglandin (PG) synthesis by inhibiting cyclooxygenase (COX) enzymes COX-1: gastric mucus production, platelet adhesion  Use of medications that inhibit COX-1 can affect GI mucosa COX-2: inflammation  Celecoxib is selective for COX-2 CYCLOOXYGENASE PATHWAY ADJUVANT MEDICATIONS Adjuvant Medications Effect Antidepressants Can increase serotonin, norepinephrine, dopamine Local anesthetics Prevent nerve depolarization Peripheral-nerve Mainly used for post-operative pain blockade Injected Anti-inflammatory corticosteroids Anticonvulsants Help with neuropathic pain Topical pain relievers Lidocaine, capsaicin, NSAIDs Cannabinoids Potential to help manage pain in some disorders NONPHARMACOLOGICAL PAIN MANAGEMENT Nursing interventions Guided imagery Physiotherapy Intradiscal electrochemical Occupational therapy therapy Acupuncture Virtual reality Transcutaneous electrical Ultrasound-guided nerve stimulation (TENS) peripheral nerve Peripheral nerve stimulation cryoanalgesia Botulinum neurotoxin Psychological counseling CANCER PAIN Common May be intermittent or chronic Tumors: place pressure on adjacent structures Inflammatory mediators and enzymatic destruction of tissues Chemotherapy and radiation therapy Bone pain: metastatic cancers SPINAL NERVE RADICULOPATHY Spinal nerve impingement Lumbosacral area May lead to “sciatica” Pain radiates down the leg with numbness and tingling of foot Cervical radiculopathy Spinal nerve impingement in neck area Numbness in hand and fingers DIABETIC PERIPHERAL NEUROPATHY Both sensory and motor nerves affected High glucose levels cause cellular damage Structural breakdown of nerves Loss of pain sensation Further wounding undetected by patient Assessment of extremity health COMPLEX REGIONAL PAIN SYNDROME (CRPS) Chronic, progressive disorder Severe pain, edema, discoloration of injured area Unknown cause Autonomic nervous system dysfunction Treatment: Combination: Physical therapy, pain medications, occupational therapy POSTHERPETIC NEURALGIA Varicella zoster “chickenpox” Remains dormant along nerves after infection Reemerges as “shingles” Renamed “herpes zoster” when in an adult Commonly produces acute, vesicular, and linear rash along specific nerve Painful FIBROMYALGIA Pain presents at specific, exact tender points Diagnosis requires pain in 11 of 18 specific sites Linked to depression, fatigue, headaches, anxiety More common in women Joints are not affected TRIGEMINAL NEURALGIA Stabbing pain in facial area, arising from trigeminal nerve Very severe Lasts few seconds to minutes Triggered by touch, sounds, brushing teeth, eating, drinking Treatment Anticonvulsants and muscle relaxers POST-OPERATIVE PAIN Some agents can be used preoperatively or during surgery Experts recommend that health-care providers employ multimodal analgesia Includes pharmacological and nonpharmacological therapies Demonstrated better pain control and fewer adverse effects CLINICAL CONCEPT EXAMPLES Clinical Example Concept Sciatica Pain radiates down leg Impingement in the L4-S1 region Morphine Can cause respiratory depression, especially in patients with lung disease Back pain Epidural administration of local anesthetic and corticosteroids ALERT! Opioids High abuse potential Naloxone Rapid onset of opioid withdrawal symptoms Tricyclic antidepressants Overdose is often fatal

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