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• Definition : IASP - “An unpleasant and
emotional experience associated with
actual or potential tissue damage or
describ...
• “The fifth vital sign” – American Pain Society 2003
• Identifying pain as the fifth vital sign suggests that
the assessm...
PATHOPHYSIOLOGY OF PAIN PERCEPTION
 Two major classes
 Normal or nociceptive
 Abnormal or pathophysiologic
 Nociceptio...
PAIN RECEPTORS
The receptors which mediate pain is called nociceptors
Nociceptors - Two types of nerve fibers.
a) A myeli...
Pain receptors are activated by three noxious stimuli
• Mechanical, • Thermal, • Chemical
 Mechanical :
• Excessive press...
Chemical mediators of pain acting on nociceptors
 Potassium, ATP, ADP
 Bradykinines
 Leukotrines
 Serotonin
 Histamin...
Pain threshold and pain tolerance
The pain threshold is the point at which a stimulus is perceived
as pain
It does not var...
• Pain tolerance is generally decreased:
- with repeated exposure to pain,
- by fatigue, anger, boredom, apprehension,
- s...
Age and perception of pain
• Children and the elderly may experience or express pain
differently than adults
• Infants in ...
Neuroanatomy of pain
The portions of the nervous system responsible for the
sensation and perception of pain may be divide...
 Afferent pathways terminate in the dorsal horn of the spinal cord
(1st afferent neuron)
● 2nd afferent neuron creates sp...
The brain first perceives the sensation of pain
• The thalamus, sensitive cortex :
perceiving
describing of pain
localisin...
The role of the afferent and efferent pathways in
processing of pain information
Nociceptive pain
Nociceptors: Endings of ...
Afferent pathways:
• From nociceptors  transmitted by small A-delta fibers and
C- fibers to the spinal cord  form synaps...
Efferent analgesic system
Its role: - inhibition of afferent pain signals
Mechanisms:
- pain afferents stimulates the neur...
The role of the spinal cord in pain processing
• Most afferent pain fibers terminate in the dorsal horn of the
spinal segm...
• 2nd afferent neurons transmit the impulse from the substantia
gelatinosa (SG) and laminae through the ventral and latera...
Theory of pain production and modulation
• Most rational explanation of painproduction and modulation
is based on gate con...
Stimulation of small fiber input inhibits cells in SG and
"open the gate".
• An open gate increases the stimulation of T-...
PHYSIOLOGICAL AND PSYCHOLOGICAL EFFECTS OF PAIN
Respiratory system
 Reduction in lung volume (TV, VC, FRC)
 Regional lun...
Cardiovascular system :
 Increase in HR, BP, CO, Systemic and coronary vascular resistance.
 Increase in cardiac work an...
Neuroendocrine and metabolic effects :
  Catabolic hormones e.g. ACTH, ADH, GH, Cortisol,
Catecholamines, renin, angiote...
Immunological :
 Immune dysfunction.
 Infection
 Tumour recurrence
Coagulations :
 Deep venous thrombosis and pulmonar...
CLASSIFICATION OF PAIN
A) Physiological pain
 Brief noxious stimulus
 Activates receptors
 Impulse modification
 Norma...
I) Nociceptive pain –
 Stimulation of nociceptor.
 Primary and secondary hyperalgesia and allodynia.
 Hyperalgesia – An...
II) Neuropathic pain –
“Pain associated with injury, disease or surgical section of the
peripheral and central nervous sys...
Acute pain Chronic pain
1) Pain of recent onset and
limited duration with identifiable
relation with injury of disease
1) ...
Fast Pain
 A fibers
 Sharp, well localized and pricking sensation
 Within 0.1 msec
 Accompanient of fast pain
• Refle...
Slow pain :
 C fibres
 Poorly localised, dull, throbbing, burning sensation
 After 1 sec
 Accompanient
• Unpleasantnes...
CLINICAL TYPES OF PAIN
 Somatic pain and visceral pain
 Referred pain and radiating pain
Somatic pain :
 Arises from th...
Visceral pain :
 Poorly localized
 Unpleasant
 Nausea, vomiting, decrease BP & HR profuse sweating.
 GUARDING
 Radiat...
• Acute pain is a protective mechanism that alerts the
• individual to a condition or experience that is immediately
• har...
• Chronic pain is persistent or intermittent usually defined as
lasting at least 6 months
• The cause is often unknown, of...
Psychological response to chronic pain
Intermittent pain produces a physiologic response similar to acute
pain.
Persistent...
Patho physiology of pain
Patho physiology of pain
Patho physiology of pain
Patho physiology of pain
Patho physiology of pain
Patho physiology of pain
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Patho physiology of pain

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Patho physiology of pain

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Patho physiology of pain

  1. 1. • Definition : IASP - “An unpleasant and emotional experience associated with actual or potential tissue damage or described in terms of such damage”. • Sherrington – “The psychical (pertaining to mind) adjunct (joint to) of an imperative (urgent) protective reflex”.
  2. 2. • “The fifth vital sign” – American Pain Society 2003 • Identifying pain as the fifth vital sign suggests that the assessment of pain should be as automatic as taking a patient’s BP and pulse  Pain is the most COMMON reason patients seek medical advice  Pain is a protective mechanism or a warning to prevent further injury
  3. 3. PATHOPHYSIOLOGY OF PAIN PERCEPTION  Two major classes  Normal or nociceptive  Abnormal or pathophysiologic  Nociception : “Complex series of physiologic events that occurs between the initiation of tissue damage and perception of pain” Four processes • Transduction • Transmission • Modulation • Perception
  4. 4. PAIN RECEPTORS The receptors which mediate pain is called nociceptors Nociceptors - Two types of nerve fibers. a) A myelinated nerve fibers b) C unmyelinated nerve fibers Points A Fibre nociceptor C fibre nociceptor 1) Number Less More 2) Myelination Myelinated Unmyelinated 3) Diameter 2 – 5 micron 0.4 – 1.2 micron 4) Conduction velocity 12 – 30 m/sec 0.5 – 2 m/sec 5) Neurotransmitter Glutamic acid Substance P 6) Specific stimulus More sensitive to pressure Chemical agents e.g. LA, Histamine, kinins, PG 7) Impulse conduction Noxious stimulus Fast component Thermal & mechanical stimulus, Slow component 9) Sensitivity to electrical stimulus More Less
  5. 5. Pain receptors are activated by three noxious stimuli • Mechanical, • Thermal, • Chemical  Mechanical : • Excessive pressure or tension on nerve • E.g. blow on the head, pulling of hair, pain of child birth.  Thermal : • Raising skin temperature above 450C or exposure to cold (00) is painful.  Chemical : • Endogenous – Histamine, Kinins, prostaglandin released from damaged tissue. • Exogenous – H2SO4, HCl, H2O2
  6. 6. Chemical mediators of pain acting on nociceptors  Potassium, ATP, ADP  Bradykinines  Leukotrines  Serotonin  Histamines  Prostaglandins Excitatory Inhibitory Substance P Somatostatin, acetyl choline Calcitonine gene related peptides Enkephalins, -endorphins Glutamate Norepinephrine, adrenaline Aspartate GABA ATP Glycine Chemical mediators of pain acting on CNS
  7. 7. Pain threshold and pain tolerance The pain threshold is the point at which a stimulus is perceived as pain It does not vary significantly among healthy people or in the same person over time Perceptual dominance- intense pain at one location may cause an increase in the pain threshold in another location • The pain tolerance is expressed as duration of time or the intensity of pain that an individual will endure before initiation overt pain responses. It is influenced by - persons cultural prescriptions - expectations - role behaviours - physical and mental health
  8. 8. • Pain tolerance is generally decreased: - with repeated exposure to pain, - by fatigue, anger, boredom, apprehension, - sleep deprivation • Tolerance to pain may be increased: - by alcohol consumption, - medication, hypnosis, - warmth, distracting activities, - strong beliefs or faith Pain tolerance varies greatly among people and in the same person over time A decrease in pain tolerance is also evident in the elderly, and women appear to be more tolerant to pain than men
  9. 9. Age and perception of pain • Children and the elderly may experience or express pain differently than adults • Infants in the first 1 to 2 days of life are less sensitive to pain (or they simply lack the ability to verbalise the pain experience). • A full behavioural response to pain is apparent at 3 to 12 month of life • Older children, between the ages of 15 and 18 years, tend to have a lower pain threshold than do adults • Pain threshold tends to increase with ageing • This change is probably caused by peripheral neuropathies and changes in the thickness of the skin
  10. 10. Neuroanatomy of pain The portions of the nervous system responsible for the sensation and perception of pain may be divided into three areas: 1. afferent pathways 2. CNS 3. efferent pathways The afferent portion is composed of: a) nociceptors (pain receptors) b) afferent nerve fibres c) spinal cord network
  11. 11.  Afferent pathways terminate in the dorsal horn of the spinal cord (1st afferent neuron) ● 2nd afferent neuron creates spinal part of afferent system  The portion of CNS involved in the interpretation of the pain signals are the limbic system, reticular formation, thalamus, hypothalamus and cortex. ● The efferent pathways, composed of the fibers connecting the reticular formation, midbrain, and substantia gelatinosa, are responsible for modulating pain sensation
  12. 12. The brain first perceives the sensation of pain • The thalamus, sensitive cortex : perceiving describing of pain localising • Parts of thalamus, brainstem and reticular formation: - identify dull longer-lasting, and diffuse pain • The reticular formation and limbic system: - control the emotional and affective response to pain Because the cortex, thalamus and brainstem areinterconnected with the hypothalamus and autonomic nervous system, the perception of pain is associated with an autonomic response
  13. 13. The role of the afferent and efferent pathways in processing of pain information Nociceptive pain Nociceptors: Endings of small unmyelinated and lightly myelinated afferent neurons Stimulators: Chemical, mechanical and thermal noxae Mild stimulation  positive, pleasurable sensation (e.g. tickling) Strong stimulation  pain These differences are a result of the frequency and amplitude of the afferent signal transmitted from the nerve endings to the CNS Location: In muscles, tendons, epidermis, subcutanous tissue, visceral organs - they are not evenly distributed in the body (in skin more then in internal structures)
  14. 14. Afferent pathways: • From nociceptors  transmitted by small A-delta fibers and C- fibers to the spinal cord  form synapses with neurons in the dorsal horn(DH) • From DH  transmitted to higher parts of the spinal cord and to the rest of the CNS by spinothalamic tracts *The small unmyelinated C- neurons are responsible for the transmission of diffuse burning or aching sensations *Transmission through the larger, myelinated A- delta fibers occurs much more quickly. A - fibers carry well-localized, sharp pain sensations
  15. 15. Efferent analgesic system Its role: - inhibition of afferent pain signals Mechanisms: - pain afferents stimulates the neurons in periaqueductal gray (PAG) - gray matter surrounding the cerebral aqueduct in the midbrain results in activation of efferent (descendent) anti-nociceptive pathways - from there the impulses are transmitted through the spinal cord to the dorsal horn - there thay inhibit or block transmission of nociceptive signals at the level of dorsal horn
  16. 16. The role of the spinal cord in pain processing • Most afferent pain fibers terminate in the dorsal horn of the spinal segment that they enter. Some, however, extend toward the head or the foot for several segments before terminating • The A-  fibers, some large A-delta fibers and small C- fibers terminate in the laminae of dorsal horn and in the substantia gelatinosa • The laminae than transmit specific information (about burned or crushed skin, about gentle pressure) to 2nd afferent neuron
  17. 17. • 2nd afferent neurons transmit the impulse from the substantia gelatinosa (SG) and laminae through the ventral and lateral horn, crossing in the same or adjacent spinal segment, to the other side of the cord. From there the impulse is carried through the spinothalamic tract to the brain. The two divisions of spinothalamic tract are known: 1. the neospinothalamic tract - it carries information to the mid brain, thalamus and post central gyrus (where pain is perceived) 2. the paleospinothalamic tract - it carries information to the reticular formation, pons, limbic system, and mid brain (more synapses to different structures of brain)
  18. 18. Theory of pain production and modulation • Most rational explanation of painproduction and modulation is based on gate control theory (created by Melzack and Wall) • According to this theory, nociceptive impulses are transmitted to the spinal cord through large A- delta and small C- fibers • These fibers create synapses in the SG • The cells in this structure function as a gate, regulating transmission of impulses to CNS Stimulation of larger nerve fibers (A-alfa, A-beta) causes the cells in SG to "close the gate". • A closed gate decreases stimulation of T-cells (the 2nd afferent neuron), which decreases transmission of impulses, and diminishes pain perception
  19. 19. Stimulation of small fiber input inhibits cells in SG and "open the gate". • An open gate increases the stimulation of T-cells   transmission of impulses  enhances pain perception • In addition to gate control through large and small fibers stimulation, the central nervous system, through efferent pathways, may close, partially close, or open gate. Cognitive functioning may thus modulate pain perception Action of endorphins(ED) All ED act by attaching to opiate receptors on the plasma membrane of the afferent neuron. The result than is inhibition of releasing of the neurotransmitter, thus blocking the transmission of the painful stimulus
  20. 20. PHYSIOLOGICAL AND PSYCHOLOGICAL EFFECTS OF PAIN Respiratory system  Reduction in lung volume (TV, VC, FRC)  Regional lung collapse (atelectasis)  Decrease alveolar ventilation leads to hypoxemia and hyper capnia.  Cough is decreased  Secretions are retained  Chances of chest infections are more  Increase O2 consumption  Increase metabolic substrate formation.
  21. 21. Cardiovascular system :  Increase in HR, BP, CO, Systemic and coronary vascular resistance.  Increase in cardiac work and myocardial oxygen consumption  Decrease myocardial oxygen delivery  Risk of ischaemia, infarction and deep venous thrombosis increases. Gastrointestinal and genitourinary system :  Increases intestinal secretion  Increases smooth muscle sphincter tone  Decreases gastrointestinal motility (stasis & ileus)  Increase bladder sphincter tone – retention of urine.
  22. 22. Neuroendocrine and metabolic effects :   Catabolic hormones e.g. ACTH, ADH, GH, Cortisol, Catecholamines, renin, angiotensin II, aldosteron, glucagon.   Anabolic hormones e.g. insulin and testosterone.  Ebb phase Flow phase Catabolism.  Net resulting negative nitrogen balance. Carbohydrates metabolism :  Hyperglycemia, glucose intolerance, insulin resistance. Protein metabolism :  Muscle protein catabolism Fat metabolism :  Increase lypolysis and oxidation
  23. 23. Immunological :  Immune dysfunction.  Infection  Tumour recurrence Coagulations :  Deep venous thrombosis and pulmonary embolism PSYCHOLOGICAL RESPONSE : Behaviour :  Self absorption and concern, withdrawal from inter personal contact, increase sensitivity to external stimuli, grimacing, postering, reduced activity and seeking help and attention. Affect :  Fear and anxiety  Feeling of helplessness, loss of control, depression and insomnia.
  24. 24. CLASSIFICATION OF PAIN A) Physiological pain  Brief noxious stimulus  Activates receptors  Impulse modification  Normal neural processing  Allerting mechanism  Good correlation B) Clinical pain  Prolonged noxious stimulus  Activates receptors  Peripheral and central sensitization  Two types – Nociceptive and Neuropathic
  25. 25. I) Nociceptive pain –  Stimulation of nociceptor.  Primary and secondary hyperalgesia and allodynia.  Hyperalgesia – An increased response to a stimulus which is normally painful. • Primary hyperalgesia – excessive sensitivity of pain receptors itself e.g. sunburned skin. • Secondary hyperalgesia – means facilitation of sensory transmission.  Allodynia – Pain due to a stimulus which does not normally provoke pain.  Protective function  Poor correlation
  26. 26. II) Neuropathic pain – “Pain associated with injury, disease or surgical section of the peripheral and central nervous system”  Three types :  Neural injury pain – e.g.  Nerve compression pain – e.g.  Complex regional pain syndrome  CRPS – I : Reflex symphathetic dystrophy – “Continuous pain in a portion of extremity after trauma which may include fracture but not involved major nerve, associated with symphathetic over activity”  CRPS – II : Causalgia – “Burning pain, allodynia, usually in the hand and foot after partial injury of a nerve or one of its major branches”  No correlation between injury and pain perception
  27. 27. Acute pain Chronic pain 1) Pain of recent onset and limited duration with identifiable relation with injury of disease 1) Pain which persist a month beyond the usual course of an acute disease or a reasonable time for an injury to heal 2) Signal of organic disease process 2) No such function serve 3) Usually caused by noxious stimulation 3) Cause is often unclear. Psychological and environmental factors play major role 4) Associated with potent neuroendocrinal response 4) Absent 5) Disappear with t/t of cause 5) Often unresponsive to many form of treatment 6) Opioids typically effective and indicated 6) Poorly effective 7) Most commonly – acute medical illness, MI, pancrititis, renal colic 7) Commonly in chronic backache and cancer pain. CLASSIFICATION ACCORDING TO DURATION OF PAIN
  28. 28. Fast Pain  A fibers  Sharp, well localized and pricking sensation  Within 0.1 msec  Accompanient of fast pain • Reflex withdrawal response • Sympathetic response i.e. increase BP, HR, respiration.  Not radiate.
  29. 29. Slow pain :  C fibres  Poorly localised, dull, throbbing, burning sensation  After 1 sec  Accompanient • Unpleasantness, irritation, frustration and depression. • Nausea, vomiting, sweating, bradycardia, hypotension. • Generalized reduction of skeletal muscle tone
  30. 30. CLINICAL TYPES OF PAIN  Somatic pain and visceral pain  Referred pain and radiating pain Somatic pain :  Arises from the tissue of the body other than the viscera. a) Superficial somatic pain • Skin and subcutaneous tissue. • Similar to the fast pain. b) Deep somatic pain • Muscle, joints, bones and fascia. • Similar to slow pain.  Clinical condition • Injuries • Tissue ischaemia • Inflammation of tissues • Muscle spasm
  31. 31. Visceral pain :  Poorly localized  Unpleasant  Nausea, vomiting, decrease BP & HR profuse sweating.  GUARDING  Radiates or referred to other site  C fibres. Common causes :  Inflammation of viscera  Over distension of hollow viscus.  Spasm of hollow viscus.  Chemical stimuli  Ischaemia
  32. 32. • Acute pain is a protective mechanism that alerts the • individual to a condition or experience that is immediately • harmful to the body • Sudden onset Relief - after the chemical mediators that stimulate the nociceptors, are removed • This type of pain mobilises the individual to prompt action to relieve it • Stimulation of autonomic nervous system can be observed during this type of pain (mydriasis, tachycardia, tachypnoe, sweating, vasoconstriction) • Psychological and behavioural response to acute pain - fear - general sense of unpleasantness or unease - anxiety
  33. 33. • Chronic pain is persistent or intermittent usually defined as lasting at least 6 months • The cause is often unknown, often develops insidiously, very often is associated with a sense of hopelessness and helplessness. Depression often results
  34. 34. Psychological response to chronic pain Intermittent pain produces a physiologic response similar to acute pain. Persistent pain allows for adaptation (functions of the body are normal but the pain is not reliefed) Chronic pain produces significant behavioural and psychological changes The main changes are: - depression - an attempt to keep pain - related behaviour to a minimum - sleeping disorders - preoccupation with the pain - tendency to deny pain

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