Week 6 Lecture 1 PDF

Lecture Material is adapted from © 2022 Wolters Kluwer Health, Lippincott Williams & Wilkins Applied Pathophysiology: A Conceptual Approach to the Mechanisms of Disease Chapter 12: Altered Somatic and Special Sensory Function Module 1: Pain Dr. Romeo Batacan Jr. MPAT12001 Medical Pathophysiology...

Lecture Material is adapted from © 2022 Wolters Kluwer Health, Lippincott Williams & Wilkins Applied Pathophysiology: A Conceptual Approach to the Mechanisms of Disease Chapter 12: Altered Somatic and Special Sensory Function Module 1: Pain Dr. Romeo Batacan Jr. MPAT12001 Medical Pathophysiology Lecture Series Copyright © 2017 Wolters Kluwer Health | Lippincott Williams &Wilkins Why do we have pain? Warns of actual or impending tissue damage  protective action Motivates people to seek help for medical problems Encourages the adoption of behaviours to enhance healing ‘Pain is an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage’ — International Association for the Study of Pain  Mechanism of acute pain Tissue injury leads to release of inflammatory mediators Inflammatory mediators will stimulate nociceptor Pain impulses are then transmitted to the dorsal horn of the spinal cord (first order neurons) Contact with second‐order neurons that cross to the opposite side of the cord Impulse ascend by the spinothalamic tract to the reticular activating system (RAS) and thalamus The localization and meaning of pain occur at the level of the somatosensory cortex Conduction of Pain sensation (Nociception) ‐ involves stimulation of free nerve endings inducing autonomic and motor reflexes which result in the interpretation of stimuli as pain Processes: Transduction Transmission Modulation Perception Transduction Transduction of noxious stimuli into a nerve impulse and depolarization of the nerve stimulate the conduction of the sensory impulse The electrical impulses promote the release of algesic (causing pain) substances e.g. substance P, H+ and K+ ions, serotonin, histamine, prostaglandins, bradykinin Transmission of nerve impulses from tissues to the CNS Occurs along type A ( delta) and type C fibers Rapidly conducting type A fibers Produce sensations of sharp, stinging, or pin‐prick type local sensations Induced by mechanical or thermal stimuli Impulses along type C fibers Produce a dull ache or burning general response Induced by mechanical, thermal, chemical stimuli Responses of the brain resulting from the transmission of impulses must be delivered back to the original site of stimulation. Modulation of the pain Occurs during transmission of the impulse Substances released in response to pain stimuli result from activation of inhibitory processes Serotonin, norepinephrine, endorphins Inhibit the transmission of the pain impulse by slowing the release of nociceptive neurotransmitters McCance KL, Huether S. Pathophysiology. 7th ed. N.S.W, Mosby; 2015 Perception of the pain response Involves the sensory (somatosensory cortex), emotional (limbic system), and subjective reactions to the stimuli Perception is varied among individuals because of the influence of Pain threshold: the intensity of the pain required to achieve a response Perceptual dominance: the existence of pain at another location which is given more attention Pain tolerance: the degree to which pain is endured (duration or intensity) before initiating a response  Pain Theories Two established theory Pattern theory Specificity theory Do not fully explain origin, transmission, perception of pain Phantom pain? Chronic pain? Two complex theory Gate control theory: builds upon other theories to explain pain perception and pain modulation Neuromatrix theory: builds upon gate control theory to explain phantom pain, chronic pain  Pain Theories: Pattern theory Nerves transmitting pain impulse are shared with other senses Pain Other somatosensory modalities Shared pathways influence perception Each type of sensation occurs through a specific and particular pattern of nerve impulses Does not account for all types of pain experience  Pain Theories: Specificity theory Various sensations involve distinct receptors and pathways Impulse generation begins in specific pain receptor Signal is sent along specific pathways to pain centers in brain Pain is perceived Pain intensity Depends on the amount of tissue injured or damaged Needle: minimal pain Cutting hand with a knife: more pain  Pain Theories: Gate control theory Implies a non‐painful stimulus can block the transmission of a noxious stimulus. Is based on the premise that the gate, located in the dorsal horn of the spinal cord (substantia gelatinosa), modulates the afferent nerve impulses. http://physrev.physiology.org/content/92/1/193 Stimulation of large type A beta and alpha inhibitory fibers close the gate at the substantia gelatinosa preventing crossover and inhibiting pain impulse conduction along type A delta and type C fibers Stimuli which close the gate: electrical stimulation, massage, scratching, rubbing of skin, mother strokes  Pain Theories: Neuromatrix theory Expounds on gate control theory Pain is multidimensional experience Pain perception: result of impulses generated along a widely distributed network in the brain Trigger: Sensory input Independent of identified stimulation Pain can be felt in absence of input (phantom pain) Multiple sources of inputs Multiple perceptions of pain: cognitive, affective, sensory Phantom pain and chronic pain Pain Classification Nociceptive: stimulus initiated outside of the nervous system Involves specific receptors and pathways Non‐nociceptive: originating within the nervous system Neuropathic Does not activate these receptors Does not follow a typical transmission pattern McCance KL, Huether S. Pathophysiology. 7th ed. N.S.W, Mosby; 2015  Pain Classification: Temporal Acute pain Self‐limiting (lasting less than 3 months) Results from disease, inflammation, or injury to tissue Sudden onset Responsive to treatment Associated with autonomic responses Chronic pain Persistent (lasting longer than 3 months) Resistant to treatment Associated with anorexia, insomnia, and depression McCance KL, Huether S. Pathophysiology. 7th ed. N.S.W, Mosby; 2015 Somatic Pain Occurs when pain receptors in tissues (skin, muscles, bones, joints and connective tissues) are activated Superficial Either sharp and well localized or dull, aching, throbbing Poorly localized Visceral pain Stimulation of visceral organ receptors Felt as vague aching, gnawing, burning Associated with nausea, vomiting, hypotension, restlessness, shock Radiates OR referred Activated by tissue stretching, ischemia, chemicals, muscle spasms Referred pain Pain from one body region perceived from different region Visceral and somatic pain fibers travel in same nerves Brain cannot distinguish between the sources Brain assumes stimulus from common (somatic) region Number of receptors is greater superficially (skin) For example left arm pain during heart attack Can become chronic Marieb EN, Hoehn KN. Human Anatomy & Physiology. 9th ed. Boston, Pearson Education; 2013 Porth C. Pathophysiology : concepts of altered health states. 7th ed. Philadelphia, Lippincott Williams & Wilkins; 2005.  What is your pain level? Wong‐Baker FACES Pain Rating Scale From Wong, DL, Hockenberry‐Eaton M, Wilson D, Winkelstein ML, Ahmann E, DiVito‐Thomas PA: Whaley and Wong's Nursing Care of Infants and Children, ed. 6, St. Louis, 1999, Mosby, p. 1153. Copyrighted by Mosby‐Year Book, Inc. Reprinted by permission. Tool for Characterization of Pain Nonpharmacologic: Cognitive behavior interventions Pain control Action Relaxation Focus on lessening muscle tension Distraction Focus attention on stimuli not associated with pain Cognitive Self‐distraction reappraisal Focus on the positive aspects of the experience Imagery Use of imagination to develop a soothing mental picture Biofeedback Awareness of bodily function on a cognitive level Biofeedback Voluntary cortical control of visceral activities is possible Awareness of physiological conditions with goal of consciously influencing them Biofeedback training allows some to control migraines and manage stress Nonpharmacologic: Physical agents Pain Action control Heat Increase in local circulation, reducing local ischemia, and nociceptive stimulation Modulation of pain Release of endogenous opioids Cold Vasoconstriction to decrease swelling and stimulation of nociceptive pain fibers Reduced afferent activity Nonpharmacologic: Other Pain control Action Transcutaneous Transmission of electrical impulses across the skin electrical nerve to peripheral nerve fibers stimulation Stimulation of large fibers to modulate pain transmission Acupuncture Insertion of needles at specific points on the body surface Stimulate secretion of endorphins Stimulate large fibers to modulate pain transmission Neurostimulation Deliver low‐voltage electrical stimulation to spinal cord or peripheral nerve to block sensation of pain Pharmacologic Pain control Action Nonnarcotic (e.g., aspirin [acetylsalicylic acid], NSAIDs, or acetaminophen) analgesia Central and peripheral blockade of nerve impulses Inhibition of cyclooxygenase enzymes (COX), decreasing production of prostaglandins Decreased sensitivity to bradykinin and histamine Opioid (e.g., morphine, codeine) analgesics Bind to mu, delta, and kappa receptors, modulating pain at the level of the spinal cord Stimulate release of endogenous opioids, including enkephalins, endorphins, and dynorphins Adjuvant (tricyclic antidepressants) analgesics Block reuptake of serotonin from the synaptic cleft Particularly useful in chronic pain Pharmacologic treatment Craft AJ, Gordon C, Tiziani A. Understanding pathophysiology. 1st ed. Chatswood, Mosby; 2011 Surgical intervention Craft AJ, Gordon C, Tiziani A. Understanding pathophysiology. 1st ed. Chatswood, Mosby; 2011 Severe chronic pain Inadequately controlled Cut axons of the spinothalamic tract as they course through the anterolateral funiculus As they cross the midline in front of the central canal