F24 PAT201 Week 4 Pain Voice Over Slides DONNA (1).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 centres 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 Neuroanatomy of Pain (Cont.) Nociception or the processing of pain involves Four phases Phases Transduction: begins when tissue is damaged by exposure to chemical, mechanical, or thermal noxious stimuli and is converted to electrophysiologic activity 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 Perception: is the conscious awareness of pain (reticular and limbic systems and the cerebral cortex) Sensory-discriminating system, affective-motivational system, cognitive-evaluative system Modulation: process of increasing or decreasing transmission of pain signals throughout the nervous system 5 5 Neuroanatomy of Pain (Cont.) 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 6 6  Secondary- order Are projection cells neurons: are Are excitatory or inhibitory interneurons in interneurons the dorsal horn Cross over the cord and of the spinal ascend or descend column Neuroanatomy of Pain (Cont.) Third-order Carry information to reticular neurons: are formation, hypothalamus, afferent thalamus, and limbic system neurons in the to interpret pain location and spinothalamic intensity tract 7 7 Neuroanatomy of Pain (Cont.) Primary-, secondary-, and third- order neurons Figure 16.2 Rogers, 2023, p. 476 8 8 Pain physiology Transduction Transmission Perception Modulation These four phases allow for multiple targets for pharmacological intervention. 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 Figure 23.1 Adams et al., 2021, p. 272 the inhibitory neurotransmitters are used as adjuvant analgesics 9 9 Neuroanatomy of Pain (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 10 10 Neuroanatomy of Pain (Cont.) Intense pain at one location may cause an increase in the pain threshold in another location. An individual with many painful sites may report only the most painful. After the dominant pain is diminished, the individual may then identify other painful areas. 11 11 Pathways of Modulation Expectancy- Segmental Conditioned pain related cortical inhibition modulation activation A-beta fibers stimulated Diffuse noxious inhibitory Cognitive expectations and impulses arrive at control (DNIC) can have an affect on same spinal level as A- Simultaneous pain pain (e.g., placebo) delta or C fiber impulses. stimulation and inhibition Inhibitory interneuron Decreases pain transmission (e.g., rubbing painful area) 12 12 Pathways of Modulation (Cont.) Excitatory neurotransmitters: tissue injury and inflammation Inhibitory neurotransmitters: GABA and glycine Endogenous opioids: inhibit pain impulses in spinal cord, brain, and periphery Enkephalins Endorphins Dynorphins Endomorphins Nociceptin/orphanin FQ 13 13 Pathways of Modulation (Cont.) Figure 16.1 Rogers, 2023, p. 476 14 14 Clinical description of pain 15 15 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 16  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 17 17  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 18 18 Acute Pain (Cont.) 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 19 19 Acute Pain (Cont.) Sites of referred pain Figure 16.5 Rogers, 2023, p. 481 20 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 21 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 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 24 24 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 25 25 Pediatrics and Perception of Pain Pathways associated with pain are functional in preterm and newborn infants. Nociceptor system is functional by 15-20 weeks’ gestation. Expressions of pain Facial expression Crying Body movements Lack of consolability Children, ages 5−18, have a lower pain threshold than adults. 26 26 Pediatrics and Perception Figure 16-7 Rogers, 2023, p. 476 of Pain (Cont.) Pediatric pain signs 27 27 Aging and Perception of Pain Research studies are conflicting. Pain threshold increases. Peripheral neuropathies Skin thickness changes Cognitive impairment Pain tolerance decreases. Pain sensitivity is affected by biological factors: Female sex shown to have a higher level of sensitivity of pain. Alteration in the metabolism of drugs and metabolites occurs. 28 28  2 9 Pain management The primary goal of pain management is to reduce pain to a level that allows the client to continue normal daily activities. 29  Opioids Non-opioids Categories of Adjuvant analgesics analgesics Can you name a few examples for each? When do you use which? 30 30 https://www.swrwoundcareprogram.ca/uploads/contentdocuments/whopainladder.pdf 31 31  Cancer pain Other Special Topics Patient- controlled analgesia (PCA) 32 32 Non-pharmacology & Pharmacology of Pain 33 33  Pharmacotherapy of Pain Classification Drug Antidepressants Amitriptyline Antiepileptics Gabapentin Morphine (see week 2) Opioid Analgesics Hydromorphone Oxycodone Non-opioid Analgesics Acetaminophen Opioid Antagonists Naloxone (see week 2) Cannabinoids Cannabis 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 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 23.2 Adams et al., 2021, p. 274 36 36 What are analgesics? Medications used to relieve pain Two basic categories Opioid analgesic Non-opioid analgesic 37  Opioids 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 Figure 23.3 Adams et al., 2021, p. 275 altered by these medications. 38 38 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 39 39 Morphine (see week 2) 40 40  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 Hydromorphone 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? 41 41 Oxycodone and Codeine Different types of opioid (Oxycodone is synthetic) Each type is often combined with non-narcotic analgesics into a single tablet or capsule When combined, the two classes of analgesics work synergistically to relieve pain Keep dose of narcotic small to avoid dependence and opioid-related side effects For example: Percocet, Percodan, AC&C, Atasol, Tylenol #2 Note: Codeine can also be used as a cough suppressant 42 42 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, headache, sedation, euphoria, nausea, vomiting, anorexia, constipation, cramps, rash, respiratory depression 43 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 46 46 Opioid Antagonist (see Week 2) Opioid antagonists may be used to reverse the symptoms of opioid toxicity or overdose, such as sedation and respiratory depression Example: Narcan (naloxone) 47 47  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? 48 48  Acetaminophen Non- opioid NSAIDs Analgesics And… a few centrally acting agents 49 NSAIDs NSAIDs inhibit cyclooxygenase, which is an enzyme responsible for the formation of prostaglandins. When cyclooxygenase is inhibited, inflammation and pain are reduced. Use: Relieve mild to moderate pain, especially for pain associated with inflammation Desired effects: Anti-pyretic, anti- inflammatory, analgesics OTC examples: Acetylsalicylic acid (ASA), ibuprofen (Advil, Motrin), naproxen (Aleve), and diclof-enac (Voltaren) gel Figure 23.4 Adams et al., 2021, p. 282 50 Treating inflammation with NSAID Please refer to week 3 Table 42.3 Adams et al., 2021, p. 526 51  Here we go Fever again… inflammation! fever is a natural mechanism in the body’s defence system to remove foreign organisms Many species of bacteria are killed by high fever The goal of antipyretic therapy: Lower body temperature while treating the underlying cause of the fever, usually an infection NSAIDs (ASA, ibuprofen) and acetaminophen are safe and effective anti-pyretic But NSAIDs are not recommended in children and teens 52 52 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. Indications for use: Treatment of fever, relief of mild to moderate pain Desired effect: Reduces fever and pain Adverse effects (very rare at therapeutic dose): Acetaminophen inhibits warfarin (Coumadin) metabolism, causing warfarin to accumulate to toxic levels. High-dose or long-term acetaminophen usage may result in elevated warfarin levels and bleeding. Acute toxicity include nausea, vomiting, chills, and abdominal discomfort. 53 53 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 54 54  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: Orthostatic hypotension, anticholinergic effects (dry mouth, blurred vision, urinary retention) Serious interactions: MAO inhibitors Figure 17.1 Adams et al., 2021, p. 186 55  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 Adverse effects: somnolence, dizziness, ataxia, Figure 21.4 Adams et al., 2021, p. 249 fatigue, nystagmus, weight gain, headache, and rhinitis 57 57  Cannabis (marijuana) A plant: The buds contain over 100 substances called “cannabinoids” 🡪 it is the cannabinoids that cause its effects. Psychoactive properties are primarily due to one cannabinoid: delta-9-tetrahydrocannabinol (THC) THC and CBD (cannabidiol) are currently the most well- understood of all cannabinoids; however, there is still much we do not understand. Indication: Acute pain, chronic pain and other conditions and symptoms https://globalnews.ca/news/7081677/cannabis- companies-proposed-lawsuit-potency/ 58 https://physicianslab.com/cbd-and-the-endocannabinoid-system/ 59 The Endocannabinoid System in the Nervous System Figure 1 Health Canada (2018) 60 How Cannabinoids Work https://www.mayoclinicproceedings.org 61 /article/S0025-6196(19)30007-2/fulltext Medical use of cannabis Forms: Smoked, vapourized, oral; Also synthetic vs. non-synthetic Indications for use: Pain and various conditions (see next slides) Mechanisms of actions: Stimulate cannabinoid receptor type 1 (CB1) and type 2 (CB2) within the endocannabinoid system Desired effects: Reduction of pain, muscle spasms, nausea & vomiting r/t cancer drugs Adverse effects: Somnolence, amnesia, cough, nausea, dizziness, euphoric mood, hyperhidrosis, and paranoia DOSING: Start low and go slow; Varies https://www.rxfiles.ca/RxFiles/uploads/documents/Cannabis-Medical-Patient-Booklet.pdf by forms and types 62 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. 63 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. 64 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 65 https://www.rxfiles.ca/RxFiles/uploads/doc uments/Cannabis-Medical-Patient- Booklet.pdf 66