Anesth Lec 01 - Pain Basic Mechanisms

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Anesth Lec 01 - Pain Basic Mechanisms

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<ul><li><p>PAIN BASIC MECHANISMSBy: Annie Yu-Soliven,Md, DpbaProfessor Department Of Anesthesiology____________________________________________Transcribed by: Thea C. Marcelo Section C</p><p>Pain is what the patient says hurts- McCaffery 1968 </p><p>Pain is perfect misery, the worst of evils, and excessive, overturns all patience.</p><p>- John Milton</p><p>PAIN An unpleasant sensory and emotional experience </p><p>associated with actual or potential tissue damage, or described in terms of such damage</p><p>(Merskey, 1979, International Association for the Study of Pain Ready &amp; Edwards 1992)</p><p>DEFINITIONS OF PAIN TERMINOLOGY Allodynia perception of non-noxious stimulus as </p><p>pain Analgesia absence of pain perception Anesthesia absence of all sensations Dysesthesia - unpleasant sensation with or without </p><p>stimulus Hypoalgesia diminished response to noxious </p><p>stimulus Hyperalgesia - increased response to noxious </p><p>stimulus Hyperesthesia increased response to mild stimulus Hypoesthesia - reduced cutaneous sensation Neuralgia pain in the distribution of a nerve Neuritis inflammation of a nerve or nerves Neuropathy - disturbance of function or pathologic </p><p>change in a nerve Pain perception point which the person becomes </p><p>aware of pain Pain threshold least experience of pain that a </p><p>patient can recognize Pain tolerance greatest level of pain a patient can </p><p>tolerate Paresthesia abnormal sensation whether </p><p>spontaneous/evoked</p><p>PHYSIOLOGY OF PAINMajor Mechanisms: Nociceptive (sensory) - inflammatory pain due to </p><p>chemical, mechanical and thermal stimuli at the nociceptors</p><p> Neuropathic - initiated or caused by a primary lesion or dysfunction in the nervous system (Merskey 1994);acutely occurs after trauma and surgery.</p><p>TRIAD OF PAIN PERCEPTION Pain receptors nociceptors; free nerve endings that </p><p>respond to intense, potentially damaging stimuli Pain stimuli mechanical; thermal; chemical</p><p>o Mechanical pressure, squeeze, pin pricko Thermal heat/freezingo Chemical P factors- bradykinin, serotonin, </p><p>histamine, prostaglandin, substance P Pain fibers</p><p>o Myelinated A-delta small diameter rapidly transmit (fast pain); initial pain sharp pain sensation</p><p>o Unmyelinated C very small diameter slower (slow pain); delayed pain diffuse burning/aching sensation deep throbbing pain, visceral, chronic </p><p>pain</p><p>NOCICEPTION ability to detect noxious and potentially tissue-</p><p>damaging stimuli protective mechanism involves multiple interacting peripheral &amp; central</p><p>mechanisms multifactorial influenced by psychological &amp; </p><p>environmental factors</p><p>PHASES OF NOCICEPTION Transduction - translation of noxious stimuli into </p><p>electrical energy at peripheral nociceptors. Transmission - propagation of impulse from </p><p>nociceptors to the dorsal spinal cord Modulation - alteration of nociceptive information to </p><p>attenuate/amplify the signal Perception - sensory discrimination /localization of </p><p>nociceptive information in the thalamus and cortex resulting into the emotional and physical pain experience</p></li><li><p>GATE CONTROL THEORY Ronald Melzack &amp; Patrick Wall peripheral</p><p>nerve fibers carrying pain to the spinal cordcan have their input modified at the spinalcord level before transmission to the brain</p><p> Concept: a non-painful stimulus can block thetransmission of a noxious stimulus; based onthe premise that the gate located in the dorsalhorn modulates afferent nerve impulses</p><p> Small diameter nerve fibers carry pain stimulithrough same gate</p><p> Large diameter fibers that carry non-painimpulses go through same gate and inhibittransmission of pain impulses, that is, closethe gate</p><p>Example:o Bumping the heado Initial trauma activates A-delta and C</p><p>fiberso Rubbing traumatized area stimulates A-</p><p>beta fibers which activate the SG to closethe spinal gate</p><p>o Inhibiting transmission of painful stimulus</p><p> The theory led to recognition that PAIN can bereduced or modulated at 4 points:1. Peripheral site2. Spinal cord3. Brainstem4. Cerebral cortex</p><p> Electrical stimulation of skins sensory nerve fibersinhibits pain</p><p> Release of endogenous opioids from the CNS(enkephalins, endorphins,dynorphins) havemorphine-like actions</p><p> Pain gate at the substancia gelatinosa in the dorsalhorn of the spinal cord can be shut by stimulation oftouch-fibers (rubbing, stroking, massage, vibration,liniments)</p><p> Normal/excessive sensory stimuli may relieve painby competing with pain stimuli (music, heat/cold,imagery, video games) can close the pain gate</p><p>TYPES OF PAIN According to location/origin</p><p>o Superficial cutaneous body surface or skin segments</p><p>o Deep somatic- ligaments, tendons, bones, blood vessels, nerves</p><p>o Visceral abdominal cavity, thorax, cranium</p><p> According to duration/intensity</p><p> Surgical trauma - produces an initial afferent barrage of pain signals and subsequently generate a secondary inflammatory response releasing inflammatory mediators (sensitizing soup) at the site of injury and surrounding uninjured tissue. </p><p> These signals initiate changes in the peripheral and CNS that amplify and prolong pain. </p><p> Peripheral sensitization results due to reduction in the threshold of nociceptor afferent terminals brought by inflammation at the site of injury. </p></li><li><p> Central sensitization/spinal wind-up - activity-dependent increase in the excitability of spinal neurons due to persistent exposure to afferent input from peripheral neurons. </p><p> Combined, the pain signals and inflammation contribute to the hypersensitivity state responsible for a decrease in pain threshold, at the site of injury as primary hyperalgesia and in the surrounding uninjured tissue as secondary hyperalgesia; and explains why pain may be prolonged beyond the duration normally expected with an acute insult like surgery. </p><p> The prolonged central sensitization can result to permanent alterations in the CNS including death of inhibitory neurons, replacement with new afferent excitatory neurons, and the establishment of aberrant excitatory synaptic connections. </p><p> This is the reason for the intractable post-surgical pain unresponsive to many analgesics.</p><p>PAIN SENSITIZATIONThe impact of acute postoperative pain can therefore extend beyond the time of surgical injury and healing and imprint indelibly on the nervous system amplifying the response to subsequent noxious stimuli. </p><p>PSYCHOSOCIAL FACTORS IN PAIN STRESSo Perception influenced by stresso Stress leads to behaviors (teeth grinding, muscle </p><p>tensing)o Stress-induced analgesia (increased tolerance via </p><p>endogenous opioids) LEARNINGo Modelingo Secondary gain/reinforcemento Culturally learned</p><p> COGNITIONo Anticipation is worse than pain itselfo Expectations of ability to cope</p><p>ASSESSMENT TOOLS Self-Report The Gold Standard Unidimensional Pain Scales </p><p>o Wong-Baker FACES Pain Rating Scaleo Verbal Rating Scale (VRS)o Numerical Rating Scale (NRS)o Visual Analogue Scale (VAS)</p><p> Multidimensional Pain Scales o Brief Pain Inventoryo McGill Pain Questionnaireo Memorial pain Assessment Cardo Neuropathic Pain Scaleo Leeds Assessment of Neuropathic </p><p>Symptoms and Signs (LANSS) Physiologic/Biologic Parameters Behavioral Observations SELECTION OF SUITABLE ASSESSMENT TOOL</p></li></ul>