pain1
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PAIN SENSATIONPAIN SENSATION PAIN SENSATIONPAIN SENSATION
According to The International Association for the Study of Pain (IASP):
Definition: Pain is an unpleasant sensory and emotional experience
associated with actual or potential tissue damage.
Significance
1) warning signal against tissue damage. Pain is one of the most
prominent symptoms of tissue damage.
2) Initiate protective reflexes which causes the subject to get rid of the
painful stimulus, or at least, to minimize tissue injury or damage
If persistent, physiological pain may progress to a If persistent, physiological pain may progress to a pathological condition pathological condition
itself, often referred to as itself, often referred to as maladaptivemaladaptive pain, in which case pain is pain, in which case pain is
dissociated from the original noxious stimulation or the healing process dissociated from the original noxious stimulation or the healing process
and thus does not represent anymore a symptom of disease but rather and thus does not represent anymore a symptom of disease but rather
abnormal sensory processing due to abnormal sensory processing due to damage to tissuesdamage to tissues (inflammatory (inflammatory
pain) or pain) or the nervous system the nervous system (neuropathic pain), or to (neuropathic pain), or to abnormal function abnormal function
of the nervous system itself (functional pain)of the nervous system itself (functional pain)..
pain resulting from activation of pain receptors may be referred to as pain resulting from activation of pain receptors may be referred to as
adaptiveadaptive or or physiologicalphysiological pain, because it minimizes tissue damage and pain, because it minimizes tissue damage and
promotes healing. promotes healing.
Classification:
Pain is classified into nociceptive, neuropathic and psychogenic; all
can be either acute or chronic. Pain is defined as chronic if persists more than 7 weeks.
1. Nociceptive is pain caused by tissue damage (inflammation) which stimulate
pain receptors (nociceptors).
1. Nociceptive is pain caused by tissue damage (inflammation) which stimulate
pain receptors (nociceptors).
2. Neuropathic: (pain due to injury of nerve pathway)
site of injury: CentralCentral Central pain (thalamic infarct).
MixedMixed Plexus avulsion, Post herpetic neuralgia.
PeripheralPeripheral Neuroma, nerve compression, phantom, neuralgias.
character: burning, tingling, numbness, pressing, squeezing, itching, constant +/-
intermittent shooting, lancinating, electric.
2. Neuropathic: (pain due to injury of nerve pathway)
site of injury: CentralCentral Central pain (thalamic infarct).
MixedMixed Plexus avulsion, Post herpetic neuralgia.
PeripheralPeripheral Neuroma, nerve compression, phantom, neuralgias.
character: burning, tingling, numbness, pressing, squeezing, itching, constant +/-
intermittent shooting, lancinating, electric.
3. Psychogenic: (difficult to differentiate whether secondary to or actual cause
of pain), anxiety, depression (30% of depressives complain of pain on initial
presentation).
3. Psychogenic: (difficult to differentiate whether secondary to or actual cause
of pain), anxiety, depression (30% of depressives complain of pain on initial
presentation).
Pain Receptors (Nociceptors)
Types of Pain Receptors
Free nerve endings which are morphologically similar but functionally
specific. They are classified according to their sensitivity into:
Polymodal Pain Receptors (most pain receptors)
These respond to a combination of mechanical, thermal, and chemical
noxious stimuli.
Mechanical Pain Receptors
respond to strong mechanical forces, such as cutting, crushing, pricking, or
even firm pressure on tissues.
Thermal Pain Receptors
respond to excessive changes in temperature (above 45oC and below 10oC).
Chemical Pain Receptors
respond to noxious chemical stimuli.
Distribution of Pain Receptors
Pain receptors are found in most tissues of the body but varies in their density.
They are abundant and widely spread in the skin and some internal
tissues such as: - the periosteum of the bone,
- arterial walls,
- joint surfaces,
- the dura of the falx and tentorium in the cranial cavity,
- the skeletal muscle,
- the parietal layer of serous membranes.
Many of the other deep tissues and viscera are poorly supplied with pain
receptors. So,
- for pain to occur, painful stimulus must by intense and widespread.
- The deep & visceral pain are poorly localized.
On the other hand, the brain itself and also the parenchymal tissues of the
liver, kidneys, and lungs have no pain receptors. They are called “pain
insensitive structures”
N.B.: Serious diseases in these structures don’t produce pain till they
extend to a pin sensitive structure like arterial wall or serous covering.
Pain Threshold:
Pain threshold is the lowest intensity of stimulus that can cause pain when
the stimulus is applied for sufficient period of time.
Pain threshold can be measured in many ways.
One of the accurate methods to quantify the threshold is heating the skin with
measured amounts of radiant heat from a calibrated electric lamp.
It has been shown that the majority of subjects begin to perceive pain when the
skin temperature reaches 45oC, and almost everyone perceives pain before the
temperature reaches 47oC.
So, it seems that the great majority of people do not show significant
differences in their sensitivity to painful stimuli. However, they differ widely in
their reaction to pain.
Stimulation of Pain Receptors:
noxious stimuli are strong enough
-----> tissue damage ------> release of
chemical agents from destructed cells
into the surrounding interstitial spaces
which are called “pain producing
compounds” (PPCs) ------> stimulate
pain receptors in the affected tissues.
PGE2
IL-1
Both threshold of pain receptors facilitating their
stimulation
The PPCs may be classified into:
1- Direct stimulators1- Direct stimulators
Substances which when reach
specific threshold directly stimulate
pain receptors ----> pain, as:
- K+ ions. - H+ ions
- Serotonin. - Histamine
- Bradykinin
2- Sensitizers2- Sensitizers
Substances which lower the threshold for
stimulation of pain receptors by direct
stimulators ----> facilitate pain
production. They include:
a) Substances released by the injured
tissues as: PGE2 & IL-1
b) Substances released by pain
receptors through antidromic impulses
as: substance P
N.B.: Substance P also stimulate mast
cells to release histamine which is a
direct stimulator.
The surface membrane of pain receptors contain several molecular receptors
which can be activated by various PPCs.
Molecular receptorFunction
Acid sensing receptor (H+)Stimulation
Purinergic receptor (ATP)Stimulation
Transient receptor potential rec. (thermal)
Stimulation
Bradykinin receptorStimulation
& sensitization
Histamine recptorStimulation
& sensitization
Serotonin receptorStimulation
& sensitization
Prostaglandin receptorsensitization
Interleukin-1 receptorsensitization
Substance P receptorsensitization
Cannabinoid receptorInhibition
Opioid receptorInhibition
Pain Tolerance:
It is the maximum intensity of pain can be tolerated by the subject without obvious
complaint.
Pain tolerance is affected by a number of factors:
- Anxiety, depression & fatigue ------> pain tolerance.
- rest, sever exercise & strong emotional excitement ------> pain tolerance.
Non Adaptation of Pain Receptors
Pain receptors do not adapt to continuing noxious stimuli.
Non adaptation to pain serves a protective function to keep the individual
trying to remove the damaging stimulus or to get away from it.
THE CHARACTER (QUALITY) of pain
1) Pricking or Cutting Pain
2) Burning Pain
3) Aching Pain
4) Throbbing Pain
5) Colicky Pain
A sharp and localized pain. It is of cutaneous origin and is caused by pricking or
cutting the skin by a sharp object.
A less well localized pain. It is usually of cutaneous origin and is caused by burns
or inflammations of the skin .
A dull-aching nature. It is more diffuse and felt coming from deeper tissues, e.g.
rheumatic pains.
is characterized by fluctuation of its intensity with arterial pulsations. It results
from localized inflammation in deep tissues, as in abscess formation.
Pain results from spasm of plain muscles in the walls of hollow viscera.
SomaticVisceral
sitesitecutaneous, deep tissuessympathetically innervated organs can be transferredto body surface
charactercharacterconstant, localisedaching, throbbing, gnawing
vague distribution and Quality deep, ache, dragging, squeezingacute: colic, paroxysmal, +/- N/V, sweating, BP and heart rate changes
Acute nociceptive pain:Acute nociceptive pain:
Fast (Immediate) physiological pain
Slow (delayed) pathophysiological pain
onset: during application of the stimulus
Duration: short duration.
Nature: pricking
Localization: well-localized
Afferent: A-delta fibers
Higher center: CC
Neurotransmitter: glutamate
Significance: * determine site & severity.
* Initiate withdrawal reflexes.
Abolished by deep pressure and not
abolished by morphine.
Shortly after application if tissue
damage occurs
Longer duration
Burning
Poorly-localized
C-fibers
Thalamus
Substance-P
* Associated with arousal, autonomic &
emotional reactions
Abolished by local anaethesia &
morphine