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PAIN: PHYSIOLOGY AND
TREATMENT
Definitions
• Pain
– “Unpleasant sensory and emotional experience
associated with actual or potential tissue
damage or des...
Transduction
Transmission
Modulation
Perception
Transduction
• Mechanical, chemical and thermal energy
are converted into electrical
energy/impulses by specialized nerve
...
Nociceptors
• A-fiber mechanoheat receptors
-signal “first” pain (sharp, stinging, pricking
sensation), well localized pai...
Nociceptors
• Repeated stimulation produces:
– reduction in receptor threshold
– an enhanced magnitude of response.
Transmission
• occurs along 2 different types of afferent
nerve fibers:
A-delta fibers
– large diameter
– myelinated
– rap...
Transmission
• C fibers
– small diameter
– unmyelinated
– slow conduction
• (0.5 – 2 m/sec)
– reinforces the immediate
res...
Transmission
• Spinothalamic tract
– Most important tract in
transmission of nociceptive
information
• Spinoreticular trac...
Perception-Supraspinal
Processing
• Reticular System
• Limbic System
• Thalamus
• Cortex
Transduction
Transmission
Modulation
Perception
Descending Modulation
• Inhibitory influences at the
cortical and spinal cord levels
• Inhibitory neurotransmitters
includ...
Peripheral Sensitization
• arises as a result of the exposure of
nociceptor to chemical mediators of
inflammation: substan...
Central Sensitization
• Produced by changes in the membrane
excitability of dorsal horn neurons.
– Increase in receptive f...
Types of Pain
• Physiologic pain
– transient stimulus, no tissue damage or
inflammation, neurophysiology associated with
s...
Types of Pain
• Pathologic pain
– pain that arises in the clinical setting
– involves dynamic changes in the processing of...
Acute Post-Operative Pain
• arises from soft tissue trauma or inflammation
• plays a biologically adaptive role by facilit...
Chronic Pain:
• pain that persists beyond the expected time frame
for a given disease, process or injury.
• may be associa...
Visceral Pain
• nature of pain originating from viscera versus
somatic tissues is significantly different.
• the viscera m...
Neuropathic Pain
• produced as a consequence of damage to the
nervous system.
• characterized by altered sensory processin...
Systemic Response to Pain and
Injury
• increased sympathetic tone
– vasoconstriction
– increased cardiac output through in...
Systemic Response to Pain and
Injury
• hormonal changes
– increased secretion of cortisol, ADH, catecholamines,
renin, ang...
Stress Response Markers/Pain
Assessment
• heart rate
• respiratory rate
• blood pressure
• posture
• attitude
• food and w...
Stress Response Markers/Pain
Assessment
• Change in activity levels
• Natural behaviors – inquisitive, grooming
• Provoked...
General Approaches to Pain
Management
• minimize debilitating pathologic pain while
maintaining the protective and adaptiv...
General Approaches to Pain
Management
• Pre-emptive analgesia
-initiating treatment prior to acute insult helps to
limit t...
General Approaches to Pain
Management
• Multimodal/balanced
analgesia:
– combining analgesic
drugs and techniques
to achie...
General Classes of Analgesic
Drugs
• 1. Opioids
• 2. Local Anesthetics
• 3. Non Steroidal Anti Inflammatory Drugs
• 4. Alp...
OPIOID ANALGESICS
USES
• 1. sedation
• 2. analgesia
• a. preoperatively
• b. intraoperatively
• c. postoperatively
• 3. neuroleptanalgesia
•...
Opioid Classification
• Agonists
– Stimulate receptor activity
– Mu agonists
• most common group of opioid agonists used
•...
Opioid Classification
• Agonists-Antagonists
– Stimulate activity at some receptors and
antagonize others
– Butorphanol – ...
Opioid Classification
• Partial Agonists
– Bind to receptor but only produce a partial
effect
• Buprenorphine – partial mu...
Opioid Classification
• Antagonists
– Primary activity is mu receptor antagonism
• Naloxone
• Naltrexone
• Nalmefene
• Dip...
• Classification:
– Traditional:
• μ, κ, δ, ε, σ
– New (?) Classification:
• OP1 (δ), OP2 (κ), OP3 (μ)
Opioid Receptor
Pha...
Opioid Receptor Pharmacology
• Mu
– Supraspinal, spinal, peripheral analgesia
– Respiratory depression
– Euphoria/Sedation...
Opioid Receptor Pharmacology
• Kappa
– Spinal analgesia
– Sedation
– Respiratory depression
• Sigma (opioid receptor?)
– D...
Opioid Effects
• Cardiovascular
– Bradycardia – vagally mediated
– Negligible effect on myocardial contractility
– Hypoten...
Opioid Effects
• Respiratory
– Decrease in frequency and tidal volume
– Blunts response to carbon dioxide
– Cough suppress...
Opioid Effects
• CNS
– Narcosis – sedation, euphoria, hypnosis, analgesia,
excitement, dysphoria
– Medullary depression
• ...
Opioid Effects
• Gastrointestinal
– Salivation
– Nausea
– Vomiting
– Nonpropulsive hypermotility
– Defecation
Opioid Effects
• Species Specific Effects
– Excitement in horses (u agonists;
agonists/antagonists)
– Excitement in cats (...
Opioid Pharmacology:
Distribution
Routes of Administration
• SC, IM, IV
• CRI
• Oral
• Epidural
• Transdermal
• Intra-articular
Epidural Catheter
Epidural Catheter
 
Commonly Used Opioids
Mu agonists 
DRUG DOSE (MG/KG)
ROUTE
DUR
ATIO
N
COST 
(20 
KG)
Morphine 0.5 – 1
IM/SC
4-6 0.27
Mep...
 
Commonly Used Opioids
Mixed agonists/antagonists 
DRUG DOSE (MG/KG)
ROUTE
DURA
TION
Butorphanol 0.2-0.4
IV/IM/SC
3-4
Bup...
Reversal of Opioid Effects
• Naloxone (1 ug/kg diluted in 5-10 ml
normal)
• Butorphanol (0.1-0.2 mg/kg)
Which Opioid?
Which Route of Administration?
• Nature of procedure – severity and
expected duration of pain.
• Nature of p...
Neuroleptanalgesia
• A state of quiescence, altered awareness and
analgesia produced by the administration of an
opioid an...
Neuroleptanalgesia
• Clinical Effects
– Narcosis without unconsciousness
– Hyper-responsive to auditory stimuli
– Defecati...
Neuroleptanalgesia
• Combinations:
Acepromazine
Midazolam
Diazepam
Oxymorphone
Hydromorphone
Butorphanol
Morphine
Buprenor...
Pain physiology and treatment
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Pain physiology and treatment

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Pain, physiology, treatment, Nociceptor, Unpleasant sensory and emotional experience associated with actual or potential tissue damage, Central Sensitization, pathologic pain, physiologic pain, chronic pain, visceral pain, neuropathic pain, Opioids
Local Anesthetics
Non Steroidal Anti Inflammatory Drugs
Alpha 2 adrenergic agonists NMDA Antagonists GABApentin Tramadol

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  • What’s New in Terms of a) drugs and b) novel forms of delivery The term opioid refers to a compound with morphine-like activities. It was derived from “opiate”, a substance extracted from opium, an exudate of the seed pod of Papver somniferum .
  • Opioid receptors classified 25 years ago Radioligand binding divides them into 3 distinct types But still controversila Mu, delta, kappa, epsilon, sigma New classification based on molecular cloning techniques Named in the order in which they were cloned There is controversy and the reclassification is being considered
  • Opioid receptors interfere with ascending pain transmission at various anatomic sites: Peripheral sites 2. The dorsal horn of the spinal cord 3. The thalamus Rostal Ventromedial medulla – 2 types of cells – the Primary Cells which contain serotonin and when activated are antinociceptive and secondary cells – GABA – which inhibit the action of the Primary cells; mu agonists inhibit the secondary cells so that the primary cells are disinhibited; kappa agonists can directly inhibit primary cells in the RVM thereby antagonizing the antinocipetive effects of mu opioid receptor agonists. Kappa agonistic effect is likely due to presynaptic inhibition of excitatory inputs to secondary cells, thereby resulting in a net disinhibition or excitation of primary cells. recent identification of opioid receptors on peripheral nerve endings of primary afferent neurons Opioids also activate descending pain-modulation pathways by inhibiting inhibitory neurons…so that these pathways are activated……and spinal pain transmission is inhibited.
  • Transcript of "Pain physiology and treatment"

    1. 1. PAIN: PHYSIOLOGY AND TREATMENT
    2. 2. Definitions • Pain – “Unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage”. • Nociceptor – is a receptor that is preferentially sensitive to a noxious (damaging to tissue) stimulus or to a stimulus that would become noxious if prolonged.
    3. 3. Transduction Transmission Modulation Perception
    4. 4. Transduction • Mechanical, chemical and thermal energy are converted into electrical energy/impulses by specialized nerve endings called “nociceptors” • Nociceptors – free nerve endings of primary afferent fibers. – have high stimulus thresholds for activation.
    5. 5. Nociceptors • A-fiber mechanoheat receptors -signal “first” pain (sharp, stinging, pricking sensation), well localized pain, transient, lasts only as long as the stimulus activates the nociceptors C-fiber mechanoheat (polymodal) receptors -mediate “second” or “slow” pain, a diffuse, persistent sensation that exists past the termination of an acute painful stimulus.
    6. 6. Nociceptors • Repeated stimulation produces: – reduction in receptor threshold – an enhanced magnitude of response.
    7. 7. Transmission • occurs along 2 different types of afferent nerve fibers: A-delta fibers – large diameter – myelinated – rapid impulse conduction (6-30 m/sec) – stimulates immediate reaction
    8. 8. Transmission • C fibers – small diameter – unmyelinated – slow conduction • (0.5 – 2 m/sec) – reinforces the immediate response that is signaled by A-delta fibers
    9. 9. Transmission • Spinothalamic tract – Most important tract in transmission of nociceptive information • Spinoreticular tract • Spinohypothalamic tract
    10. 10. Perception-Supraspinal Processing • Reticular System • Limbic System • Thalamus • Cortex
    11. 11. Transduction Transmission Modulation Perception
    12. 12. Descending Modulation • Inhibitory influences at the cortical and spinal cord levels • Inhibitory neurotransmitters include GABA, glycine, serotonin, dopamine, NE, endogenous opioids
    13. 13. Peripheral Sensitization • arises as a result of the exposure of nociceptor to chemical mediators of inflammation: substance P, hydrogen ions, norepinephrine, bradydkinin, histamine, potassium, cytokines, serotonin, nitric oxide • all of these mediators act together to lower the response threshold of both the A-delta and C fibers nociceptors
    14. 14. Central Sensitization • Produced by changes in the membrane excitability of dorsal horn neurons. – Increase in receptive field of dorsal horn neurons (zone of secondary hyperalgesia). – increased responsiveness to mechanical stimulation that is normally innocuous (allodynia). – Recruitment of non-nociceptive receptors (A- beta fibers)
    15. 15. Types of Pain • Physiologic pain – transient stimulus, no tissue damage or inflammation, neurophysiology associated with simple stimulus-response model.
    16. 16. Types of Pain • Pathologic pain – pain that arises in the clinical setting – involves dynamic changes in the processing of noxious input at both the peripheral and central levels – stimulus is not transient – usually associated with significant tissue inflammation. – can be associated with damage to nervous tissue (neuropathic pain). – recently occurring (acute) or long-lasting (chronic).
    17. 17. Acute Post-Operative Pain • arises from soft tissue trauma or inflammation • plays a biologically adaptive role by facilitating tissue repair – functions: -hypersensitizes injured area (primary hyperalgesia) -sensitizes surrounding tissues (secondary hyperalgesia) – serves to facilitate avoidance of external stimuli – doesn’t give license to allow pain to exist untreated
    18. 18. Chronic Pain: • pain that persists beyond the expected time frame for a given disease, process or injury. • may be associated with ongoing inflammation • may be autonomous with no temporal relation to the inciting cause. • Maladaptive, offers no biologic advantage • examples of chronic pain: – cancer pain – osteoarthritic pain – postamputation phantom limb pain
    19. 19. Visceral Pain • nature of pain originating from viscera versus somatic tissues is significantly different. • the viscera most sensitive to distention (hollow organs of GI tract), ischemia (myocardium) and inflammation (pancreatitis). • poorly localized. • referred – pain response is localized to distant structures
    20. 20. Neuropathic Pain • produced as a consequence of damage to the nervous system. • characterized by altered sensory processing of stimuli • several manifestations of hypersensitivity: – persistent burning sensations, partial or focal loss of sensitivity • allodynia (an increased responsiveness to mechanical stimulation that is normally innocuous). • may arise from an acute injury discharge in axotomized afferent fibers.
    21. 21. Systemic Response to Pain and Injury • increased sympathetic tone – vasoconstriction – increased cardiac output through increases in stroke volume and heart rate – decreased gastrointestinal and urinary tone – increased skeletal muscle tone
    22. 22. Systemic Response to Pain and Injury • hormonal changes – increased secretion of cortisol, ADH, catecholamines, renin, angiotensin II, aldosterone – decreases in insulin and testosterone • endocrine changes result in a catabolic state: – hyperglycemia – increased protein catabolism and lipolysis, – renal retention of water and sodium, – increased potassium excretion – decreased GFR.
    23. 23. Stress Response Markers/Pain Assessment • heart rate • respiratory rate • blood pressure • posture • attitude • food and water intake • patterns of defecation, urination
    24. 24. Stress Response Markers/Pain Assessment • Change in activity levels • Natural behaviors – inquisitive, grooming • Provoked behavior • Aggression • Gait-/posture • Vocalization • Appearance of stereotypical behaviors
    25. 25. General Approaches to Pain Management • minimize debilitating pathologic pain while maintaining the protective and adaptive aspects associated with physiologic pain. • a single drug administered at a standard dose for different pain syndromes is not an effective pain management strategy.
    26. 26. General Approaches to Pain Management • Pre-emptive analgesia -initiating treatment prior to acute insult helps to limit the development of peripheral and central sensitization.
    27. 27. General Approaches to Pain Management • Multimodal/balanced analgesia: – combining analgesic drugs and techniques to achieve beneficial additive or synergistic analgesic effects. – can use lower doses, fewer side effects.
    28. 28. General Classes of Analgesic Drugs • 1. Opioids • 2. Local Anesthetics • 3. Non Steroidal Anti Inflammatory Drugs • 4. Alpha 2 adrenergic agonists • 5. NMDA Antagonists • 6. Others • GABApentin • Tramadol
    29. 29. OPIOID ANALGESICS
    30. 30. USES • 1. sedation • 2. analgesia • a. preoperatively • b. intraoperatively • c. postoperatively • 3. neuroleptanalgesia • a. in combination with a tranquilizer/sedative • b. useful for minor procedures that do not require general anesthesia
    31. 31. Opioid Classification • Agonists – Stimulate receptor activity – Mu agonists • most common group of opioid agonists used • Include morphine, meperidine, oxymorphone, hydromorphone, fentanyl, carfentanil
    32. 32. Opioid Classification • Agonists-Antagonists – Stimulate activity at some receptors and antagonize others – Butorphanol – kappa agonist, mu antagonist
    33. 33. Opioid Classification • Partial Agonists – Bind to receptor but only produce a partial effect • Buprenorphine – partial mu agonist, kappa antagonist
    34. 34. Opioid Classification • Antagonists – Primary activity is mu receptor antagonism • Naloxone • Naltrexone • Nalmefene • Diprenorphine
    35. 35. • Classification: – Traditional: • μ, κ, δ, ε, σ – New (?) Classification: • OP1 (δ), OP2 (κ), OP3 (μ) Opioid Receptor Pharmacology
    36. 36. Opioid Receptor Pharmacology • Mu – Supraspinal, spinal, peripheral analgesia – Respiratory depression – Euphoria/Sedation – Physical dependence – Bradycardia
    37. 37. Opioid Receptor Pharmacology • Kappa – Spinal analgesia – Sedation – Respiratory depression • Sigma (opioid receptor?) – Dysphoria/hallucinations – Hypertonia – Respiratory stimulation – tachycardia
    38. 38. Opioid Effects • Cardiovascular – Bradycardia – vagally mediated – Negligible effect on myocardial contractility – Hypotension due to histamine release • Seen with morphine, meperidine (particularly when administered IV) • Not a problem with synthetic opioids
    39. 39. Opioid Effects • Respiratory – Decrease in frequency and tidal volume – Blunts response to carbon dioxide – Cough suppressant
    40. 40. Opioid Effects • CNS – Narcosis – sedation, euphoria, hypnosis, analgesia, excitement, dysphoria – Medullary depression • Respiratory center • Cough center • Vomiting center (delayed) – Vomiting center (early) – Vagus nerve – Oculomotor nerve (miosis – dog; mydriasis – horse, cat)
    41. 41. Opioid Effects • Gastrointestinal – Salivation – Nausea – Vomiting – Nonpropulsive hypermotility – Defecation
    42. 42. Opioid Effects • Species Specific Effects – Excitement in horses (u agonists; agonists/antagonists) – Excitement in cats (dose related) – Panting in dogs – resets thermostat – Sweating in horses
    43. 43. Opioid Pharmacology: Distribution
    44. 44. Routes of Administration • SC, IM, IV • CRI • Oral • Epidural • Transdermal • Intra-articular
    45. 45. Epidural Catheter
    46. 46. Epidural Catheter
    47. 47.   Commonly Used Opioids Mu agonists  DRUG DOSE (MG/KG) ROUTE DUR ATIO N COST  (20  KG) Morphine 0.5 – 1 IM/SC 4-6 0.27 Meperidine 2 –6 IM/SC 1-2 1.47 Fentanyl .004-0.008 IV/IM/SC 1-2 4.80 Oxymorphone 0.05-0.2 IV/IM/SC 4-6 14.00 Hydromorphone 0.1-0.2 IV/IM/SC 4-6 0.76
    48. 48.   Commonly Used Opioids Mixed agonists/antagonists  DRUG DOSE (MG/KG) ROUTE DURA TION Butorphanol 0.2-0.4 IV/IM/SC 3-4 Buprenorphine 0.01-0.02 IV/IM/SC/PO 8-12
    49. 49. Reversal of Opioid Effects • Naloxone (1 ug/kg diluted in 5-10 ml normal) • Butorphanol (0.1-0.2 mg/kg)
    50. 50. Which Opioid? Which Route of Administration? • Nature of procedure – severity and expected duration of pain. • Nature of patient • Resources
    51. 51. Neuroleptanalgesia • A state of quiescence, altered awareness and analgesia produced by the administration of an opioid analgesic and a tranquilizer or sedative • Indications: – Minor surgical procedures – Diagnostic procedures – Premedication for General Anesthesia – Induction of General Anesthesia
    52. 52. Neuroleptanalgesia • Clinical Effects – Narcosis without unconsciousness – Hyper-responsive to auditory stimuli – Defecation – Respiratory depression – Bradycardia – Analgesia
    53. 53. Neuroleptanalgesia • Combinations: Acepromazine Midazolam Diazepam Oxymorphone Hydromorphone Butorphanol Morphine Buprenorphine Fentanyl
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