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Dr tarek pain controle
1. Pain is defined as an unpleasant sensory and emotional experience associated with actual or potential tissue damage. It is subjective and based on expectations, past experience, and emotional factors. 2. Pain is transmitted via nociceptors that detect extreme mechanical, thermal, or chemical stimuli and transmit signals along nerve fibers to the spinal cord and brain. 3. Chronic pain lasts longer than 6 months and is more complex, often involving altered anatomy and neural pathways. It is a lasting condition compared to acute pain which subsides with healing.
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Dr tarek pain controle
- 1. PAIN Managing Pain Dr TAREKNASRALLAH RHEUMATOLOGY AL AZHAR
- 2. What is Pain? •“An unpleasant sensory & emotional experience associated with actual or potential tissue damage, or described in terms of such damage” – The International Association for the Study of Pain • Subjective sensation • Pain Perceptions – based on expectations, past experience, anxiety, suggestions – Affective – one’s emotional factors that can affect pain experience – Behavioral – how one expresses or controls pain – Cognitive – one’s beliefs (attitudes) about pain
- 3. What is Pain •Physiological response produced by activation of specific types of nerve fibers • Experienced because of nociceptors being sensitive to extreme mechanical, thermal, & chemical energy. • Composed of a variety of discomforts • One of the body’s defense mechanism (warns the brain that tissues may be in jeopardy) • Acute vs. Chronic – – The total person must be considered. It may be worse at night when the person is alone. They are more aware of the pain because of no external diversions.
- 4. Where Does PainCome From? • Cutaneous Pain – sharp, bright, burning; can have a fast or slow onset • Deep Somatic Pain – stems from tendons, muscles, joints, periosteum, & b. vessels • Visceral Pain – originates from internal organs; diffused @ 1st & later may be localized (i.e. appendicitis) • Psychogenic Pain – individual feels pain but cause is emotional rather than physical
- 5. Pain Sources • Fastvs. Slow Pain – – Fast – localized; carried through A-delta axons in skin – Slow – aching, throbbing, burning; carried by C fibers – Nociceptive neuron transmits pain information to spinal cord via unmyelinated C fibers & myelinated A-delta fibers. • The smaller C fibers carry impulses : rate 0.5 to 2.0 m/sec. • The larger A-delta fibers carry impulses : of 5 to 30 m/sec.
- 6. Acute pain: lasts lessthan 6 months, subsides once the healing process is accomplished.
- 7. • Chronic pain: •Complex processes & pathology. Usually altered anatomy & neural pathways. • Constant & prolonged, > 6 months, sometimes for life. • “Lasting longer than expected time frame”
- 8. Altered Neuronal Structure Chronicpain accompanied by cortical reorganization Chronic back pain is accompanied by brain atrophy
- 9. Most Common ChronicPain Syndromes • Low Back • Headaches • Neck • Facial • Arthritides • Fibromyalgia • Cancer
- 10. What is ReferredPain? • Occurs away from pain site • Examples: McBurney’s point • Types of referred pain: – Myofascial Pain – trigger points, small hyperirritable areas within a m. in which n. impulses bombard CNS & are expressed at referred pain – Sclerotomic & Dermatomic Pain – deep pain; may originate from sclerotomic, myotomic, or dermatomic n. irritation/injury • Sclerotome: area of bone/fascia that is supplied by a single n. root
- 11. Terminology • Noxious –harmful, injurious – Noxious stimuli – stimuli that activate nociceptors (pressure, cold/heat extremes, chemicals) • Nociceptor – nerve receptors that transmits pain impulses • Pain Threshold – level of noxious stimulus required to alert an individual of a potential threat to tissue • Hyperesthesia – abnormal acuteness of sensitivity to touch, pain, or other sensory stimuli • Paresthesia – abnormal sensation, such as burning, pricking, tingling • Inhibition – depression or arrest of a function – Inhibitor – an agent that restrains/retards physiologic, chemical, or enzymatic action • Analgesic – a neurologic or pharmacologic state in which painful stimuli are no longer painful
- 12. • Dysesthesia –An unpleasant abnormal sensation, whether spontaneous or evoked. • Allodynia – Pain due to a stimulus which does not normally provoke pain, such as pain caused by light touch to the skin • Hyperalgesia – An increased response to a stimulus which is normally painful • Hyperesthesia - Increased sensitivity to stimulation, excluding the special senses. Hyperesthesia includes both allodynia and hyperalgesia, but the more specific terms should be used wherever they are applicable.
- 13. Nerve Endings • “Anerve ending is the termination of a nerve fiber in a peripheral structure.” (Prentice, p. 37) • Nerve endings may be sensory (receptor) or motor (effector). • Nerve endings may be: – Respond to phasic activity - produce an impulse when the stimulus is ↓ or ↑, but not during sustained stimulus; adapt to a constant stimulus (Meissner’s corpuscles & Pacinian corpuscles) – Respond to tonic receptors produce impulses as long as the stimulus is present. (muscle spindles, free n. endings, Krause’s end bulbs)
- 14. Nerve Endings • Merkel’s corpuscles/disks- – Sensitive to touch & vibration – Slow adapting – Superficial location – Most sensitive • Meissner’s corpuscles – – Sensitive to light touch & vibrations – Rapid adapting – Superficial location • Krause’s end bulbs – – Thermoreceptor • Ruffini corpuscles/endings – Thermoreceptor – Sensitive to touch & tension – Slow adapting • Free nerve endings - – Afferent – Detects pain, touch, temperature, mechanical stimuli
- 15. Types of Nerves •Afferent (Ascending) – transmit impulses from the periphery to the brain – First Order neuron – Second Order neuron – Third Order neuron • Efferent (Descending) – transmit impulses from the brain to the periphery
- 16. Peripheral and CentralPathways for Pain Ascending TractsAscending Tracts Descending TractsDescending Tracts Cortex Midbrain Medulla Spinal Cord Thalamus Pons
- 17. First Order Neurons •Stimulated by sensory receptors • End in the dorsal horn of the spinal cord • Types – A-alpha – non-pain impulses – A-beta – non-pain impulses • Large, myelinated • Low threshold mechanoreceptor; respond to light touch & low-intensity mechanical info – A-delta – pain impulses due to mechanical pressure • Large diameter, thinly myelinated • Short duration, sharp, fast, bright, localized sensation (prickling, stinging, burning) – C – pain impulses due to chemicals or mechanical
- 18. Second Order Neurons •Receive impulses from the FON in the dorsal horn – Lamina II, Substantia Gelatinosa (SG) - determines the input sent to T cells from peripheral nerve • T Cells (transmission cells): transmission cell that connects sensory n. to CNS; neurons that organize stimulus input & transmit stimulus to the brain – Travel along the spinothalmic tract – Pass through Reticular Formation • Types – Wide range specific • Receive impulses from A-beta, A-delta, & C
- 19. Third Order Neurons •Begins in thalamus • Ends in specific brain centers (cerebral cortex) – Perceive location, quality, intensity – Allows to feel pain, integrate past experiences & emotions and determine reaction to stimulus
- 20. Descending Neurons • DescendingPain Modulation (Descending Pain Control Mechanism) • Transmit impulses from the brain (corticospinal tract in the cortex) to the spinal cord (lamina) – Periaquaductal Gray Area (PGA) – release enkephalins – Nucleus Raphe Magnus (NRM) – release serotonin – The release of these neurotransmitters inhibit ascending neurons • Stimulation of the PGA in the midbrain & NRM in the pons & medulla causes
- 21. Pain Process The neuralmechanisms by which pain is perceived involves a process that has four major steps: –Transduction –Transmission –Modulation –Perception
- 23. Facilitating Transduction • Biochemicalmediators: “Chemical Soup” Prostaglandins Bradykinins Serotonin Histamines Cytokines Leukotrienes Substance P Norepinephrine
- 25. Peripheral Excitatory MediatorsPeripheralExcitatory Mediators (Pain)(Pain) SubstanceSubstance ReceptorReceptor MechanismMechanism Substance PSubstance P (SP)(SP) NKNK11 ↑↑ neuronal excitability, edemaneuronal excitability, edema ProstaglandinProstaglandin (PG)(PG) ?? Sensitize nociceptors, inflammation,Sensitize nociceptors, inflammation, edemaedema BradykininBradykinin BB22 (normal)(normal) BB11 (inflammation)(inflammation) Sensitize nociceptorsSensitize nociceptors ↑↑ PG productionPG production HistamineHistamine HH11 C-fiber activation, edema,C-fiber activation, edema, VasodilatationVasodilatation SerotoninSerotonin 5-HT5-HT33 C-fiber activation, release SPC-fiber activation, release SP NorepinephrineNorepinephrine (NE)(NE) αα11 Sensitize nociceptorsSensitize nociceptors Activate nociceptorsActivate nociceptors
- 27. • NSAIDs (local & systemic ) • Antihistaminic drugs
- 28. Acetaminophen (paramol) • Analgesic,antipyretic • Inhibits prostaglandin synthetase in the CNS, weak peripheral anti-inflammatory activity • Serotonergic effect at descending pathway • Used to treat osteoarthritis
- 29. Acetaminophen (Tylenol) • AmericanPain Society: Maximum dose 4,000 mg/day, • American Liver Foundation: 3,000 mg/day • Risk of hepatotoxicity with higher doses • Antidote – acetylcysteine (Mucomyst, Acetadote)
- 30. Major Categories ofPain Classified by inferred pathophysiology: 1. Nociceptive pain (stimuli from somatic and visceral structures) 2. Neuropathic pain (stimuli abnormally processed by the nervous system)
- 31. Mixed Type Caused bya combination of both primary injury or secondary effects Nociceptive vs Neuropathic Pain Nociceptive Pain Caused by activity in neural pathways in response to potentially tissue-damaging stimuli Neuropathic Pain Initiated or caused by primary lesion or dysfunction in the nervous system Postoperative pain Mechanical low back pain Sickle cell crisis Arthritis Postherpetic neuralgia Neuropathic low back pain CRPS* Sports/exercise injuries *Complex regional pain syndrome Central post- stroke pain Trigeminal neuralgia Distal polyneuropathy (eg, diabetic, HIV)
- 32. COMPONENT DESCRIPTORS EXAMPLES Steady, Dysesthetic •Burning, Tingling • Constant, Aching • Squeezing, Itching • Allodynia • Hypersthesia • Diabetic neuropathy • Post-herpetic neuropathy Paroxysmal, Neuralgic • Stabbing • Shock-like, electric • Shooting • Lancinating • trigeminal neuralgia • may be a component of any neuropathic pain FEATURES OF NEUROPATHIC PAIN
- 33. Local Anesthetic Agents •Patch (topical) • Eml gel: Lidocaine (topical) • Oint. 4% lidocaine (topical)
- 34. Local Anesthetics Blocks conductionof nerve impulses by decreasing or preventing an increase in the permeability of excitable membranes to Na+. Inhibits depolarization of nerve Blocks neuronal firing
- 35.
- 38. Mentholatum Menthol generates analgesic activity through: •Ca2+ channel blocking activity • Binding to kappa opioid receptors
- 39. Methyl Salicylate Toxicity •Salicylic acid derivative • Lipid solubility increases toxicity –More toxic than aspirin –1 teaspoon (5ml) wintergreen oil contains 4,000 mg salicylate –30ml wintergreen oil is a fatal dose in adults • Risk of toxicity reduced with use for acute pain, limited to a small area of dermal application
- 40. Anticonvulsants 1)Inhibit sustained high-frequency neuronalfiring by blocking Na+ channels after an action potential, reducing excitability in sensitized C-nociceptors. 2)Blockade of Na+ channels and increase in synthesis and activity of GABA, in inhibitory neurotransmitter, in the brain. 3)Modulates Ca+ channel current and increases synthesis of GABA.
- 41. Antiepileptic Agents • Broadclinical actions in the CNS: – Reduce seizures – Neuropathic pain – Bipolar disorder – Anxiety – Schizophrenia – Agitation • Impulse dyscontrol • Dementia • Delirium • Three proposed mechanisms of action: – Blockade of voltage gated sodium channels (↓ glutamate release) – Blockade of voltage gated calcium channels – alpha 2 delta subunits (reduces excessive neurotransmitter release) – Enhancement of GABA actions
- 42.
- 43. Transmission of pain Defined as: Projectionof pain into the Central Nervous System
- 44. Transmission A synapse containsthree elements: the presynaptic terminal the synaptic cleft the receptive membrane
- 46. Transmission • The presynapticterminal is the axon terminal of the presynaptic neuron • Here that the presynaptic neuron releases neurotransmitters which are found in vesicles
- 49. Neurotransmitters Chemical substances thatallow nerve impulses to move from one neuron to another Found in synapses – Substance P - thought to be responsible for the transmission of pain-producing impulses – Acetylcholine – responsible for transmitting motor nerve impulses – Enkephalins – reduces pain perception by bonding to pain receptor sites – Norepinephrine – causes vasoconstriction – Endorphins - morphine-like neurohormone; thought to ↑ pain threshold by binding to receptor sites – Serotonin - substance that causes local vasodilation & ↑ permeability of capillaries
- 51. Capsaicin • Hot peppers •May deplete & prevent re-accumulation of substance P in primary afferent neurons responsible for transmitting painful impulses from peripheral sites to the CNS. • Absorption, distribution, metabolism & excretion, half life – unknown • May produce transient burning with application, usually disappears in 2-4 days, but may persist for several weeks.
- 53. Transmission • The synapticcleft is the narrow intercellular space between neurons. • Neurotransmitters cross the synaptic cleft and bind to specific receptors on the postsynaptic neurons • This will excite or inhibit the postsynaptic neurons.
- 56. Questions to Askabout Pain • P-Q-R-S-T format • Provocation – How the injury occurred & what activities ↓ ↑ the pain • Quality - characteristics of pain – Aching (impingement), Burning (n. irritation), Sharp (acute injury), Radiating within dermatome (pressure on n.)? • Referral/Radiation – – Referred – site distant to damaged tissue that does not follow the course of a peripheral n. – Radiating – follows peripheral n.; diffuse • Severity – How bad is it? Pain scale • Timing – When does it occur? p.m., a.m., before, during, after activity, all the time Pattern: onset & duration Area: location Intensity: level Nature: description
- 57. Pain Assessment Scales •McGill pain questionnaire – Evaluate sensory, evaluative, & affective components of pain – 20 subcategories, 78 words
- 58. Assessment of PainIntensity No Mild Moderate Severe Very Worst pain pain pain pain severe possible pain pain Verbal Pain Intensity Scale No pain Visual Analog Scale Faces Scale 0 1 2 3 4 5 0–10 Numeric Pain Intensity Scale No Moderate Worst pain pain possible pain 0 1 2 3 4 5 6 7 8 9 10 Worst possible pain 21
- 59. Smiling Faces Patients seldom rememberhow good a clinician your are. But they do remember how much they hurt when you were treating them.
- 60.
Editor's Notes
- #17 The physiology of normal pain transmission involves some basic concepts that are necessary to understand the pathophysiology of abnormal or nonphysiologic pain. These include the concept of transduction of the first-order afferent neuron nociceptors. The nociceptor neurons have specific receptors that respond to specific stimuli if a specific degree of amplitude of the stimulus is applied to the receptor in the periphery. If sufficient stimulation of the receptor occurs, then there is a depolarization of the nociceptor neuron. The nociceptive axon carries this impulse from the periphery into the dorsal horn of the spinal cord to make connections directly, and indirectly, through spinal interneurons, with second-order afferent neurons in the spinal cord. The second-order neurons can transmit these impulses from the spinal cord to the brain. Second-order neurons ascend mostly via the spinothalamic tract up the spinal cord and terminate in higher neural structures, including the thalamus of the brain. Third-order neurons originate from the thalamus and transmit their signals to the cerebral cortex. Evidence exists that numerous supraspinal control areas—including the reticular formation, midbrain, thalamus, hypothalamus, the limbic system of the amygdala and the cingulate cortex, basal ganglia, and cerebral cortex—modulate pain. Neurons originating from these cerebral areas synapse with the neuronal cells of the descending spinal pathways, which terminate in the dorsal horn of the spinal cord.
- #26 Reference: Polomano, R.C. (2010). Neurophysiology of Pain. In B. St. Marie (Ed.) Core Curriculum for Pain Management Nursing. Lenexa, KA: American Society for Pain Management Nursing, p. 68.
- #32 Nociceptive, or inflammatory, pain is pain resulting from activity in neural pathways caused by potentially tissue-damaging stimuli.1 Examples include postoperative pain, arthritis, mechanical low back pain, sickle cell crisis, and sports or exercise injuries. Neuropathic pain is pain caused by a primary lesion or dysfunction in the peripheral and/or central nervous systems.2 Examples of peripheral neuropathic pain syndromes include HIV sensory neuropathy, postherpetic neuralgia (PHN), and diabetic neuropathy. Examples of central neuropathic pain include central poststroke pain, spinal cord injury pain, trigeminal neuralgia, and multiple sclerosis pain. As indicated by the “mixed type” area on the slide, chronic pain can be of mixed etiology with both nociceptive and neuropathic characteristics. Two types of neuropathic pain—PHN and diabetic neuropathy—will be emphasized within this module. These types of pain are being stressed because the great majority of randomized controlled trials of treatments for neuropathic pain have examined these two disorders, and because our understanding of the mechanisms of neuropathic pain is largely derived from those studies. 1.Portenoy RK, Kanner RM. Definition and Assessment of Pain. In: Portenoy RK, Kanner RM, eds. Pain Management: Theory and Practice. Philadelphia, Pa: FA Davis Company; 1996:4. 2.Galer BS, Dworkin RH. A Clinical Guide to Neuropathic Pain. Minneapolis, Minn: The McGraw-Hill Companies Inc; 2000:8-9.
- #59 Addressing analgesia, the first of the “Four A’s of Pain,” requires an assessment of pain intensity to determine whether existing treatment is providing adequate relief. This slide depicts four of the pain scales that are used to assess a patient’s pain. The scales are considered simple for patients to use as well as being validated methods for measuring the severity of pain.1-3 These scales can be used at the patient’s bedside, and patients can be asked to respond to either a spoken or written a question. The 0-10 numeric scale can be administered over the phone. With some scales, especially the visual analog scale, the patient marks the line at the point that best indicates the pain’s intensity. Older patients may have difficulty using visual analog scales and it might be more appropriate to use a 0-10 numeric pain intensity scale.4 The Wong-Baker FACES Pain Rating Scale is validated and recommended for patients aged 3 years or older. On this scale, Face 0 indicates no pain at all, Face 1 feels mild pain, Face 2 feels moderate pain, Face 3 feels severe pain, Face 4 feels very severe pain, and Face 5 feels the worst possible pain. The original appears above, and can be used as is or with the brief word descriptions under each number. In a study of 148 children aged 4 to 5 years, there were no differences in pain scores when children used the original or brief word instructions.2 People with cognitive impairments and limited ability to communicate (eg, stroke patients) may have difficulty with the use of any self-report pain assessment scales. For these patients it will be necessary for the physician to rely on behavioral observation of patients' facial expressions, movement patterns (eg, bracing, guarding, distorted postures, avoidance of activity), and nonverbal sounds (eg, moans, winces) and reports of significant others (eg, partner, spouse, child) to make judgment of pain intensity.5 However, remember that patient pain is multidimensional and involves more than just assessment of pain intensity. 1.Portenoy RK, Kanner RM. Definition and Assessment of Pain. In: Portenoy RK, Kanner RM, eds. Pain Management: Theory and Practice. Philadelphia, Pa: FA Davis Company; 1996:8-10. 2. Wong DL. Waley and Wong’s Essentials of Pediatric Nursing. 5th ed. St. Louis, Missouri: Mosby, Inc.; 1997:1215-1216. 3. McCaffery M, Pasero C. Pain: Clinical Manual. St. Louis, Missouri: Mosby, Inc.;1999:16. 4. Jensen MP, Karoly P, Braver S. The measurement of Clinical pain intensity: a comparison of six methods. Pain. 1986;27:117-126. 5. Hadjistavropoulos T, von Baeyer C, Craig KD. Pain assessment in persons with limited ability to communicate. In: Turk DC, Melzack R, eds. Handbook of Pain Assessment. 2nd ed. New York, New York: Guilford; 2001:134-152.