Week 4 PAT 201 Pain PDF

Pain PAT 201 Fall 2024 Week 4 1 1 Pain “Pain is an unpleasant sensory and emotional Pain is a protective and experience associated with complex phenomenon made actual or potential tissue up of dynamic interactions damage or described in terms...

Pain PAT 201 Fall 2024 Week 4 1 1 Pain “Pain is an unpleasant sensory and emotional Pain is a protective and experience associated with complex phenomenon made actual or potential tissue up of dynamic interactions damage or described in terms among physical, cognitive, of such damage.”— spiritual, emotional, and International Association for environmental factors. the Study of Pain 2 2  Gate control theory Explains the complexities of the pain phenomenon Pain is modulated by a “gate” in the cells of the substantia gelatinosa in the spinal cord. Large myelinated A-delta fibers and small unmyelinated C fibers respond to a broad range of painful stimuli, such as mechanical, thermal, and chemical. These nociceptive transmissions “open” the gate. Stimuli from nonnociceptive transmissions, such as touch and larger A-beta fibers, “close” or partially close the gate. 3 3 Systems/Pathways Necessary for Pain Afferent pathways Begin in the peripheral nervous system (PNS), travel to the spinal gate in the dorsal horn, and then ascend to higher centers in the CNS Interpretive centers Located in the brainstem, midbrain, diencephalon (thalamus, epithalamus, and hypothalamus), and cerebral cortex Efferent pathways Descend from the CNS to the dorsal horn of the spinal cord 4 4 The Processing of Pain: Four Phases of Nociception 1. Transduction 2. Transmission 3. Perception 4. Modulation 5 5 4 Phases of Nociception 1. Transduction: begins when tissue is damaged by exposure to chemical, mechanical, or thermal noxious stimuli and is converted to electrophysiologic activity 2. Transmission: conduction of pain impulses along the A and C fibers into the dorsal horn of the spinal cord and eventually to the reticular formation, hypothalamus, thalamus, and limbic system 6 6 Transmission (cont’d) Primary-order neurons: nociceptors Stimulated by severe mechanical deformation, mechanical deformation, and/or temperature extremes. Myelinated Alfa-delta fibers: transmission is fast and causes reflex withdrawal of affected body part from stimulus before pain sensation is perceived. Pain sensations are sharp, well-localized, “fast” Unmyelinated C polymodal fibers (most numerous): stimulated by mechanical, thermal, and chemical nociceptors Transmission is slower and conveys dull, aching, or burning sensations. Alfa-beta fibers: large myelinated fibers that transmit touch and vibration sensations 7 7  Secondary- Are projection cells order neurons Are excitatory or inhibitory are interneurons interneurons in the dorsal horn of the spinal Cross over the cord and ascend column or descend Transmission (Cont.) Third-order Carry information to reticular neurons are formation, hypothalamus, afferent neurons thalamus, and limbic system to in the interpret pain location and spinothalamic intensity tract 8 8 Transmission (Cont.) Primary-, secondary-, and third-order neurons Figure 16.2 Rogers, 2023, p. 476 9 9 3. Perception: the conscious awareness of pain (occurs in reticular and limbic systems and cerebral cortex) Interpretation of pain can be influenced by genetics, cultural preferences, sex roles, age, level of health, and past pain experiences. Three systems interact to produce perception of pain: a) Sensory-discriminating system b) affective-motivational system c) cognitive-evaluative system 10 10 Perception (Cont.) Pain threshold Pain tolerance Is the lowest intensity of pain that Is the greatest intensity of pain a person can recognize that an individual can endure Intense pain at one location may Is very individualized; varies increase the threshold in another greatly among people and in the location. same person over time Decreases with repeated exposure to pain, fatigue, anger, boredom, apprehension, and sleep deprivation 11 11 Pediatrics and Perception of Pain Figure 16-7 Rogers, 2023, p. 476 12 12 Aging and Perception of Pain Research studies are conflicting. Pain threshold increases. Peripheral neuropathies Skin thickness changes Cognitive impairment Pain tolerance decreases. Alteration in the metabolism of drugs and metabolites occurs. 13 13 4. Modulation: the process of increasing or decreasing transmission of pain signals throughout the nervous system involves different mechanisms that facilitate and inhibit Excitatory and inhibitory neurotransmitters Endogenous opioids: 14 14 Pathways of Modulation Excitatory neurotransmitters: tissue injury and inflammation Inhibitory neurotransmitters: : gamma-aminobutyric acid (GABA) and glycine, norepinephrine and serotonin Endogenous opioids: morphine-like neuropeptides that inhibit transmission of pain impulses in the periphery, spinal cord, and brain by binding with specific opioid receptors on neurons. Are located throughout the body and are also responsible for feelings of well being. Endogenous opioids inhibit pain impulses in spinal cord, brain, and periphery Enkephalins - most prevalent of the natural opioids. Bind to δ opioid receptors. Endorphins – most substantial natural pain relief. Binds to μ receptors Dynorphins - most potent of the endogenous opioids, binding strongly with κ receptors Endomorphins - bind with μ receptors Nociceptin/orphanin FQ - an opioid that induces pain or hyperalgesia but does not interact with opioid receptors. 15 15 Pathways of Modulation Segmental Pain Inhibition: Diffuse Noxious Inhibitory Control: A-beta fibers (that transmit touch and Pain is relieved when two noxious or painful vibration sensations) are stimulated, and stimuli occur at the same time from different these impulses arrive at the same spinal sites (pain inhibiting pain). level or segment as impulses from A-delta or C fibers. Intense pain at one location may cause an increase in the pain threshold in another location. They stimulate an inhibitory interneuron and An individual with many painful sites may decrease pain transmission. E.G. rubbing an report only the most painful. injured area to relieve pain. After the dominant pain is diminished, the individual may then identify other painful areas. 16 16 The four phases allow for multiple targets for pharmacological intervention. Transduction Transmission Perception Modulation The two primary classes of analgesics act at different locations: the NSAIDs act at the peripheral level, whereas the opioids act on the CNS. Drugs that affect or mimic the inhibitory neurotransmitters are used as adjuvant analgesics Figure 23.1 Adams et al., 2025, p. 333 17 17 Figure 16.1 Rogers, 2023, p. 476 18 18 Clinical Description and Categories of Pain ✓ Neurophysiologic ✓ Neurogenic ✓ Temporal ✓ Regional ✓ Etiologic 19 19 Neurophysiologic A) Nociceptive pain 1. Somatic (e.g., skin, muscle, bone) 2. Visceral (e.g., intestine, liver, stomach) 3. Referred B). Neuropathic (non-nociceptive) 1. Central pain (lesion in brain or spinal cord) 2. Peripheral pain (lesion in peripheral nervous system) 20 20 Clinical Description of Pain Non- Classification Nociceptive nociceptive based on pain pain duration Pain with normal tissue Neuropathic Acute vs. injury from a pain chronic known cause Less than 3 Somatic and Peripheral months visceral and central versus more than 3 months 21 Neuropathic Pain Is the result of primary lesion or Burning, shooting, Is most often chronic dysfunction in shocklike, tingling nervous system Peripheral Central neuropathic neuropathic pain pain Hyperalgesia and allodynia Injured nerves become Is caused by a lesion or hyperexcitable. neuroplastic changes in the brain or spinal cord 22 22 Neuropathic Pain (Cont.) Phantom limb pain Central sensitization Pathologic changes in CNS that cause chronic pain 23 23  Acute Somatic Temporal Pain Visceral Referred Time/Duration related Chronic (longer than 3 months) 24  Is a protective mechanism Alerts an individual to a condition or experience that is immediately harmful to the body Acute Lasts less than 3 months (Nociceptive) Pain Clinical manifestations Tachycardia, hypertension, diaphoresis, dilated pupils Anxiety 25 25  Acute somatic Arises from joints, muscle, bone, and skin A-delta fibers: pain is sharp and well localized C fibers: pain is dull, aching, throbbing, and poorly Acute Pain localized (Cont.) Acute Visceral Pain arises from the internal organs and lining of body cavities - transmitted by C fibers Pain is poorly localized (aching, gnawing, throbbing, or intermittent cramping) as a result of the fewer number of nociceptors 26 26 Acute Pain (Cont.) Acute referred pain Pain in an area is removed or distant from its point of origin. Area of referred pain is supplied by the same spinal segment as the actual site. Can be acute or chronic 27 27 Acute Pain (Cont.) Sites of referred pain Figure 16.5 Rogers, 2023, p. 481 28 Chronic Pain Lasts at least 3 months; is poorly understood Does not respond to usual therapy Serves no protective purpose Thought to be caused by dysregulation of nociception and pain modulation processes (peripheral and central sensitization) Neuroplasticity: maintenance of pain May cause behavioral and psychologic changes, such as depression and anxiety 29 29 Chronic Pain Syndromes Specific or nonspecific spinal pain Many individuals of all ages have chronic recurrent back pain. Myofascial pain syndrome (MPS) Injury to the muscle, fascia, and tendons has occurred. Deep, aching, localized to generalized Chronic postoperative pain Plastic changes in the PNS and CNS contribute to allodynia and hypersensitivity. Cancer pain 30 30 Chronic Pain Syndromes (Cont.) Central poststroke pain Hypersensitivity on one half of body Phantom limb pain Regeneration/hyperactivity of injured/cut peripheral nerves Complex regional pain syndrome (CRPS) Types I and II Associated with limb injury 31 31  Pain Location E.g.; abdomen, chest, back, pelvic Categories of etc. Pain (cont’d) Etiologic Pain E.g.; cancer, dental, inflammatory, ischemic, vascular 32  Pain Management 3 The primary goal of pain management is 3 to reduce pain to a level that allows the client to continue normal daily activities. 33 Non-pharmacology & Pharmacology of Pain 34 34 Non-pharmacological pain management Acupressure and Biofeedback Massage Heat or cold acupuncture therapy Distraction, Relaxation Meditation including art or Imagery therapy music therapy Chiropractic Therapeutic Hypnosis Physical therapy manipulation touch Transcutaneous Energy therapies electrical nerve such as reiki and Yoga stimulation qigong (TENS) 35 35  Age-related considerations Knowledge of developmental theories, the aging process, behavioural cues, subtle signs of discomfort, and verbal and nonverbal responses to pain are a must when it comes to effective pain management. Can you think of some examples of what should be considered? 36 36  Opioids Non-opioids Categories of Adjuvant analgesics Analgesics Can you name a few examples for each? When do you use which? 37 37 What are analgesics? Medications used to relieve pain Two basic categories Opioid analgesic Non-opioid analgesic 38 Basis of analgesics The fact that the pain signal begins at nociceptors located within peripheral tissues and proceeds through the CNS provides several targets for the pharmacological intervention of pain transmission. Figure 23.3 Adams et al., 2025, p. 336 39 39  Pharmacotherapy of Pain Classification Drug Antidepressants Amitriptyline Antiepileptics Gabapentin Opioid Analgesics Morphine (see week 2) Hydromorphone Oxycodone Non-opioid Analgesics Acetaminophen Opioid Antagonists Naloxone (see week 2) Cannabinoids Cannabis 40 40 Mechanism of action of antidepressants Note our discussion in this lecture is for treating pain Antidepressants enhance the action of certain neurotransmitters in the brain (e.g., norepinephrine and serotonin) The two basic mechanisms of action are blocking the enzymatic breakdown of norepinephrine and slowing the reuptake of serotonin Four primary classes: 1. Tricyclic antidepressants (TCAs) 2. Selective serotonin reuptake inhibitors (SSRIs) 3. Monoamine oxidase (MAO) inhibitors 4. Atypical antidepressants 41 41  Amitriptyline Tricyclic antidepressant Indication for use: Neuropathic pain (in addition to depression etc) Mechanisms of action: Inhibits the reuptake of norepinephrine and serotonin, and to a lesser extent dopamine, into presynaptic nerve terminals Desired effects: Decrease in Neuropathic Pain Adverse effects: Drowsiness, sedation, orthostatic hypotension, urinary retention Serious interactions: MAO inhibitors Nursing Implications: Look at the adverse effects. What does that mean for the nurse caring for clients taking amitriptyline? What should the nurse think about? What should the nurse monitor for? What type of assessments are important? Figure 17.12Adams et al., 2025, p. 228 42  Gabapentin Anti-epileptic, GABA analogue Indications for use: Adjunct treatment of partial seizures, with or without generalization in patients >12 yr; adjunct in partial seizures in children 3-12 yr, postherpetic neuralgia, primary restless leg syndrome (RLS) in adults. Unlabeled uses: Neuropathic pain, bipolar disorder, migraine prophylaxis, fibromyalgia, anxiety Mechanisms of action: Stimulates an influx of chloride ions that interact with the GABA receptor-chloride channel complex → more GABA in synapse Desired effect: Decreased seizure activity, decreased pain Adverse effects: somnolence, sedation, confusion, Figure 21.3 Adams et al., 2025, p. 304 dizziness, ataxia Nursing Implications: Consider the adverse effects. What should nurses be assessing, monitoring and 43 43 considering?  Opioids (review) A natural or synthetic morphine-like substance capable of reducing severe pain Opioids are narcotic substances → produce numbness and stupor-like symptoms Narcotic is a general term used to describe morphine-like drugs that produce analgesia and CNS depression Natural or synthetic substances extracted from the poppy plant that exert their effects through interaction with mu and kappa receptors (most common) Opioids neither lower the threshold for pain at the nociceptor level nor slow or block the transmission of the pain impulse. It is the perception and emotional response to pain that is altered by these medications. Figure 23.3 Adams et al., 2025, p. 337 44 44 Pharmacotherapy with Opioids Drugs of choice for moderate to severe pain >20 different opioids are available as medications, classified by efficacy (strong or moderate narcotic activity) Opiates produce many important effects other than analgesia: Suppressing the cough reflex, slowing the motility of the GI tract (severe diarrhea), sedation, euphoria and intense relaxation, respiratory depression, sedation, nausea, and vomiting Note the potential to cause physical and psychological dependence 45 45  Different types of opioids exist (e.g.; oxycodone is synthetic) Each type is often combined with non-narcotic analgesics into a single tablet or capsule `For example: Percocet, Percodan, AC&C, Atasol, Tylenol #2 When combined, the two classes of analgesics work synergistically to relieve pain Keeps dose of narcotic small to avoid dependence and opioid-related side effects 46 46 https://www.swrwoundcareprogram.ca/uploads/contentdocuments/whopainladder.pdf 47 47 Morphine (see week 2) 48 48 Oxycodone Classification: Synthetic opioid Indications for use: Relief of moderate and severe pain Mechanisms of action: Inhibits ascending pain pathways in CNS, increases pain threshold, alters pain perception Desired effects: Pain reduction Adverse effects (common): Drowsiness, dizziness, confusion, sedation, euphoria, anorexia, constipation, respiratory depression Nursing Implications: Which vital sign should the nurse monitor closely? What education should the nurse provide clients who are taking this drug? What baseline assessments are important to perform so that the nurse can determine if there is a change? Can you think of a chronic condition that, when present in clients, would cause concern if oxycodone was prescribed? 49 Hydromorphone Classification: Opioid Indications for use: moderate to severe pain; antitussive to suppress cough Mechanisms of action: Inhibits ascending pain pathways in CNS, increases pain threshold, alters pain perception Desired effects: Pain reduction Adverse effects (common): sedation, drowsiness, dizziness, nausea, pruritic, hypotension, bradycardia, respiratory depression Nursing Implications: What would happen if the client was consuming alcohol with hydromorphone? What are all the important nursing assessments? Are there other chronic conditions that would lead to increased risk? 50 Nursing Implications for Opioids Assessment: Presence or history of severe respiratory disorders, increased intracranial pressure (ICP), seizures, and liver or renal disease, blood work (CBC, liver and renal functions), pain characteristics, current medication usage, allergy, respiratory distress (or low RR) Monitor for: Respiratory depression, LOC, fall risks, CIP increase, orthostatic hypotension, urine output, N&V, constipation Education: Pain management goals, reasons for obtaining baseline data, possible side effects 51 51 Opioid Antagonist : Naloxone (review Week 2) Opioid antagonists may be used to reverse the symptoms of opioid toxicity or overdose, such as sedation and respiratory depression 52 52 Non- Opioid Acetaminophen Analgesics NSAIDs And… a few centrally 53 Acetaminophen Action (unclear): Inhibits the synthesis of prostaglandins in the central nervous system; direct action at the level of the hypothalamus and causes dilation of peripheral blood vessels, enabling sweating and dissipation of heat. No anti-inflammatory action. Is completely metabolized by the liver. Indications for use: Treatment of fever, relief of mild to moderate pain Desired effect: Reduces fever and pain Adverse effects (rare at therapeutic dose): Acetaminophen inhibits warfarin (blood thinner) metabolism, causing warfarin to accumulate to toxic levels. High-dose or long-term acetaminophen usage may result in elevated warfarin levels and bleeding. Signs of acute toxicity includes nausea, vomiting, chills, and abdominal discomfort. Can lead to kidney and liver failure. Nursing Implications: What should nurses teach clients about taking acetaminophen? What is important about the fact that acetaminophen is completely metabolized by the liver? 54 54  Cannabis A plant: The buds contain over 100 substances called “cannabinoids” 🡪 it is the cannabinoids that cause its effects. THC gives psychoactive properties (feeling high) CBD is a non psychotropic chemical THC and CBD (cannabidiol) are currently the most well-understood of all cannabinoids Synthetic cannabinoids are produced in the lab to mimicking endocannabinoids Indications: Acute pain, chronic pain and other conditions and symptoms such as migraine, fibromyalgia, diabetic neuropathy, multiple sclerosis, Parkinson disease Mechanism of Action: Stimulate cannabinoid receptor type 1 (CB1) and type 2 (CB2) within the endocannabinoid system. Interacts with the body’s own endogenous cannabinoid system (endogenous cannabinoid receptors). Both THC and CBD bind with cannabinoid receptors CB1 and CB2 of endocannabinoids in the body. These endocannabinoids are found throughout the brain and nervous system, but also in the immune system and in the cardiovascular system. Desired effects: Reduction of pain, muscle spasms, nausea & vomiting related to cancer drugs Adverse effects: palpitations, anxiety, paranoia, confusion, poor coordination, seizures Nursing Implications: What should nurses teach clients using cannabis? What types of assessments should nurses perform? 55 https://globalnews.ca/news/7081677/cannabis-companies-proposed-lawsuit-potency/ https://physicianslab.com/cbd-and-the-endocannabinoid-system/ 56  How Cannabinoids Work https://www.mayoclinicproceedings.org/article/S0025-6196(19)30007-2/fulltext Figure 1 Health Canada (2018) 57 Cannabis and acute pain Evidence from human studies are limited and mixed and suggest a dose- dependent effect in some cases, with lower doses of THC having an analgesic effect and higher doses having a hyperalgesic effect. Clinical studies of certain cannabinoids (nabilone, oral THC, levonontradol, AZD1940, GW842166) for post-operative pain suggest a lack of efficacy. 58 Cannabis and chronic pain Neuropathic pain and chronic non-cancer pain in humans Cancer pain: The limited available clinical evidence with certain cannabinoids (dronabinol, nabiximols) suggests a modest analgesic effect of dronabinol and a modest and mixed analgesic effect of nabiximols on cancer pain. “Opioid-sparing” effects and cannabinoid-opioid synergy: While pre-clinical and case studies suggest an “opioid-sparing” effect of certain cannabinoids, epidemiological and clinical studies with oral THC and nabiximols are mixed. Headache and migraine: The evidence supporting using cannabis/certain cannabinoids to treat headache and migraine is very limited and mixed. 59 Other uses for symptoms other than pain Chemotherapy Wasting induced Multiple Palliative care Quality of life syndrome (e.g., nausea and sclerosis cachexia) vomiting Movement Psychiatric Epilepsy Glaucoma Asthma disorder disorder Alzheimer’s Gastrointestinal disease and Inflammation system dementia disorders 60 https://www.rxfiles.ca/RxFiles/uploads/documents/Cannabis-Medical-Patient-Booklet.pdf 61