Pathophysiology of Pain PAINPAIN “…is whatever a person says it is and exists whenever the...
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Transcript of Pathophysiology of Pain PAINPAIN “…is whatever a person says it is and exists whenever the...
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Pathophysiology of PainPathophysiology of Pain
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PAINPAINPAINPAIN
“…is whatever a person says it is and exists whenever the person says it does.”
(McCaffery)
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PainPainPainPain
5th Vital Sign
Should be recorded along with temperature, pulse, respiration, & blood pressure
(American Pain Society)
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Multidimensional Experience
Physical– Medical-Surgical conditions
(special standards for acute post-operative pain)
Social– Support system & societal response
Psychological– Coping abilities, internal locus of control vs. external
locus of control
Cultural– Emotionally expressive, introverted, stoic
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Why it is necessary to study pain
• Pain is the primary symptom that motivates people to seek medical treatment
• Pain is subjective and therefore can only be measured indirectly
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The Economic Cost of Pain in AmericaThe Economic Cost of Pain in America
$100 billion/year related to chronic pain
* includes healthcare expenses * compensation * litigation
Pain accounts for approximately:
* 25% all sick days taken in US * 21% of emergency room visits (NIH, 2002)
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Physiological Componentsof Pain
Physiological Componentsof Pain
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TransductionTransduction
Noxious substance changes to an electrical stimulus by activating nociceptors
(afferent nerve fibers that initiate the pain experience).
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Pain Receptors and Periferal Afferent Pathways
Pain Receptors and Periferal Afferent Pathways
Stimulus impulse Information about possible tissue damage.
Specific theory (von Frey):– Distinctive end organs on the skin, each stimulus has
specific end organ
Intensity theory:– Pattern or Summation Theory (Goldscheider):
• Any sensory stimulus is sufficiently intense could produce pain.
Afferent fibers:– C fiber (0.4-1.1 mm)
– A-delta fiber (1-5 mm)
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Types of NociceptorsTypes of Nociceptors
C-nociceptors– Polymodal nociceptors (C-MH, mechano-heat sensors)
• Loc.: skin 50-70%
• Stim.: >50 oC, mechanical (biting, twinging), endogen substances (bradikinin, serotonin, acidic pH), exogen substances (capsaicin etc.)
• Function: inflamatory pain and heat sensing. PGE2 and PGI2 potentiate the effect of bradikinin COX inhibitors
• Signal transduction: VR-1 cation (Na+/Ca2+ chanell) capsaicin and heat
• Mediators: Substance P, CGRP and somatostatin
• Substance P: neurogenic inflammation extravasation, leukocytosis, Ig secretion of B lymphocytes, TNF production of hystiocytes
• CGRP: enhance microcirculation, potentiate neurogenic inflamation
• Somatostatin: possible inhibits the inflammatory reactions
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Types of NociceptorsTypes of Nociceptors
C-nociceptors– Heat receptors
• Loc: skin 4%, (pig 30%)
• Stim: heat, capsaicin and chemicals but mechanical stimuli not!
– Chemoreceptors• Stim: electrical but heat and mechanical not. However they
respond to repeated stimuli. (sleeping or silent receptors)
– Others• High-Treshhold-Mechanociceptors (C-HTM): heat, capsaicin
• C-Mechano-Cold (C-MC): Cold sensitive HTM receptors
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Types of NociceptorsTypes of NociceptorsTypes of NociceptorsTypes of Nociceptors
A-delta Nociceptors– A-delta Mechano-Nociceptors
• Loc: basal part of the epidermis and between of collagen fibers of joints
• Stim: Hight-Treshhold-Mechanoreceptors sensing the pricking, cutting. Heat, capsaicin and irritants do not stimulate
– A-delta Polynodal Nociceptors (AHH)• Loc: palm and hairless areas (Type I.)
Hairy areas (Type II.)• Stim: mechanical• Function: Sensing of the first pain
– Visceral Receptors
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TransmissionTransmission
Passage of electrical impulse from the site of injury through the dorsal horn of spinal nerves & up the spinalthalmic tract to the brain.
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Figure 10-9: Sensory pathways cross the body’s midline
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Substances That Stimulate Nociceptors:Substances That Stimulate Nociceptors:
Bradykinin: a powerful vasodilator that increases capillary permeability and constricts smooth muscle. Plays a role in chemistry of pain at site of injury.
Postaglandins: hormone-like substances that send additional pain stimuli to CNS
Substance P: believed to act as a stimulant at pain receptor sites and may influence inflammatory response
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Neuromodulators:Neuromodulators:
EndorphinsEnkephalinsDynorphin
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Theories of pain
• Specificity model
• Patterning theory
• Gate control theory
• Multidimensional model
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Hereditary Sensory and Autonomic Neuropathy (HSAN)
5 Types
HSAN4 neurotroph tirozin-kináz receptor1 (NTRK1) mutation
Autosomal reseccive
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Patterning Theory
• Multiple neural pathways cause pain
• Nociceptors plus other receptors
• Cannot fully account for subjective nature pain
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If you hurt yourself, you often rub the affected area to make it
feel better. Why does this work?
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Counter Irritant TheoryCounter Irritant Theory
Gate Control Theory– Gate Cells
– Tract Cells
Touch Input– Ab Fibers
Local Inhibition– GABA and Enkephalin
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Gate Control Theory(Melzack & Wall 1960’s)
Gating Mechanism
Transmission cells
Spinal cord
From pain fibres
From other peripheral fibres
Modulation of pain information by a gate mechanism
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Cingulate Cortex Periaqueductal Gray
– Opiod Receptors– Projects to Raphe Nuclei
Raphe Nuclei– Project down to dorsal horn and Spinal
5 Nucleus– Serotonin (5-HT)– Inhibits Ascending Systems
• Substance P release by Primary Afferents
Locus Coeruleus– Norepinephrine
Hormonal Analgesia
Descending Pain ControlDescending Pain Control
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Gate Control Theory
• Accounts for high pain perception with
Low damage (e.g. back ache)
• Accounts for low pain perception with high damage (e.g. sport, bed of nails)
• Does not fully account for reinforcement/ learning and environmental influences
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Multidimensional model
This model is consistent with Gate Control
Theory and distinguishes four dimensions of
pain: • Nociception - neural detection
• Sensation - experience of pain (e.g. intensity)
• Emotion - emotional response (e.g. anxiety)
• Behaviour - e.g. withdrawal
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Multidimensional model
Physiological
Sensation
Behavioural response
e.g limping
Emotional response
e.g. tension
Learning Environment
??
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Psychosocial Determinants of Pain
• Emotional response
• Cognition
• Conditioning
• Cultural/social context
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Emotional response
• Stress/Anxiety: Associated with pain
• Motivation reduces pain, e.g sport. Possible opioid mechanism.
• Depression: associated with increased pain.
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Cognitive response
• Appraisal e.g. pain is perceived as greater when it is life threatening
• Higher self-efficacy = less pain
• Expectations e.g. anxious dental patients expect more pain and therefore experience more pain
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Conditioning
• Reinforcement e.g. children with eczema who receive more attention in response to their pain behaviour are likely to increase their pain behaviour
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Culture
• e.g Bedouin women report less pain during child birth than in other cultures because it is not culturally acceptable to report pain
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Types of PainTypes of PainTypes of PainTypes of Pain
Somatic– Smooth muscle walls,
receptors in abdominal cavity, cranium, & thorax
Visceral– Arises from ligaments,
tendons, bones
Referred– Pain experienced from a site
distant from injury
Phantom– Sensations of burning, tingling
felt in absent limb
Neuropathic– Pain signal from injury to
higher centers of brain
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Acute Pain Acute Pain vs.vs. Chronic Pain Chronic Pain Acute Pain Acute Pain vs.vs. Chronic Pain Chronic Pain
Usually sudden, self-limiting < 6 months
Precipitating event Resolves with treatment Restless, anxious, crying
May be sudden or gradual with periods of remission & exacerbation > 6 mo.
May not be associated with injury
Difficult to treatment Depressed, withdrawn
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Classification of AnalgesicsClassification of AnalgesicsClassification of AnalgesicsClassification of Analgesics
Non-opiod (non-narcotic)– Acetaminophen
- NSAIDS:
ASA, Advil, Motrin, Naprosyn, Feldene
Toradol (Ketorolac)
Cox – 2 Inhibitors (Vioxx & Celebrex)
- Side Effects:
Gastric erosion, GI bleeding, fluid retention, Platelet dysfunction, & renal insufficiencies
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Classification of AnalgesicsClassification of AnalgesicsClassification of AnalgesicsClassification of Analgesics
Opiod Analgesics: Synthetic NarcoticsCommonly Used:
- Morphine Sulfate, Oxycontin- Dilaudid (hydromorphone)- Oxycodone (Percodan, Percocet, Oxycontin SR- Demerol (Meperidine)- Fentanyl- Codeine Plain
- Tylenol 300 mg - # 2 (15 mg), # 3, (30 mg) # 4 (60mg)- Vicodin (Hydrocodone 5/500, 7.5/750, 10/660
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Non-pharmacological InterventionsNon-pharmacological InterventionsNon-pharmacological InterventionsNon-pharmacological Interventions
Heat & cold Progressive relaxation Massage Meditation, Guided Imagery Music Biofeedback Transcutaneous Electric Nerve Stimulation Therapeutic Touch Yoga
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Invasive Pain ManagementInvasive Pain ManagementInvasive Pain ManagementInvasive Pain Management
Epidural Intrathecal Nerve Blocks
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