Does anybody here have a pathophysiology for pain?

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    Hello, i just need a pathophysiology of pain.. specifically post-op pain.. Does anybody here have it? thanks in advance..
  2. 4 Comments so far...

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    I would think the pathophysiology of pain would differ on circumstances. But for post op pain it would be related to surgical incision. So then pain is related to the degree of receptor stimulation by processes causing tissue injury.

    Normal somatosensory processing involves interaction between afferent systems activated by tissue injury and accompanying inflammation. The primary afferent system includes nociceptors (A-delta and C- fibers), signal processing in the dorsal horn of the spinal cord, ascending neural pathways, and thalamic and other specialized brain structures.
    Does that help?
    beatot likes this.
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    I have two sources on the pathophysiology of pain. I'm just going to post the text of what I've got for you and you can extrapolate what you need from them. Post-operative pain would be a tissue injury.

    From Pharmacology: An Introduction, Fifth edition, by Henry Hitner and Barbar Nagle, pages 195-6. . ."The sensation of pain is comprised of at least two elements: the local irritation (stimulation of peripheral nerves) and the recognition of pain (within the CNS). Free nerve endings called nociceptors are located in the skin, muscle, joints, bones, and viscera. Nociceptors respond to tissue injury. When there is no injury, there is no pain stimulus, so the nociceptors are quiet. When a pain generating event happens, biochemical changes occur within the localized area of the injury. Usually, prostaglandins, histamine, bradykinins, serotonin, and Substance P are among the peripheral neurotransmitters released that trigger nociceptors to wake up. Nociceptors alert the brain to the intensity of the pain by increasing the frequency of signals sent to specialized areas within the CNS.

    The signals travel through the spinal cord into the area called the dorsal horn where they are rerouted to the appropriate area of the brain that can interpret the intensity and quality of pain present. Pain signals are sent up A-delta nociceptor and C-nociceptor fibers in the ascending pathways to the brain. If the signal is passed through the A-delta fibers (myelinated), the pain is consciously experienced as sharp. If the signal is passed through C fibers (unmyelinated), dull, aching pain is felt.

    Pain management and selection of the most appropriate analgesic depends on the type and duration of pain. Nociceptive pain can only occur when all neural equipment (nerve cells, nerve endings, spinal cord, and brain) is working properly. When pain results from abnormal signals or nerves damaged by entrapment, infection, amputation, or diabetes, it is called neuropathic pain.

    Pain duration is either acute or chronic. Acute pain usually appears in association with an observable injury (e.g., sunburn, broken foot, muscle sprain, or headache) and disappears when the injury heals. Chronic pain persists for weeks, months, or years even with analgesic therapy. Nociceptive pain can be either acute or chronic while neuropathic pain is chronic, even through it may be intermittent. If an injury doesn't heal or the pain is not adequately inhibited, nociceptors get "really irritated", a condition known as peripheral sensitization, and send so many signals through the CNS that the patient overresponds to even normal stimuli, such as a feather or brush touched to the area. In neuropathic conditions sensitization can also occur within the spinal neurons observed as over responsiveness (hyperanalgesia), prolonged pain, or the spread of pain to an uninjured area (referred pain).

    No matter what type of pain is present, relief from pain (analgesia) is the therapeutic goal. The specialized medical discipline of pain management has changed the spectrum of therapy and the types of drugs used, especially to achieve satisfactory analgesia as soon as possible. Inadequate control of pain can delay healing. With chronic pain, psychological and emotional changes occur that cause the patient to become tired and irritable; patients develop insomnia, significant stress responses such as increased heart rate and blood pressure, depression, impaired resistance to infection, and even increased sensitization to pain. The psychological component associated with the inability to permanently relieve the pain intensifies the response to pain by stimulating the CNS."

    From Pathophysiology: A 2-in-1 Reference for Nurses by Springhouse, Springhouse Publishing Company Staff, pages 286-9. . ."Pain is the result of a complex series of steps from a site of injury to the brain, which interprets the stimuli as pain. Pain that originates outside the nervous system is termed nociceptive pain; pain in the nervous system is neurogenic or neuropathic pain.

    Nociception. . .Nociception begins when noxious stimuli reach pain fibers. Sensory receptors called nociceptors—which are free nerve endings in the tissues—are stimulated by various agents, such as chemicals, temperature, or mechanical pressure. If a stimulus is sufficiently strong, impulses travel via the afferent nerve fibers along sensory pathways to the spinal cord, where they initiate autonomic and motor reflexes. The information also continues to travel to the brain, which perceives it as pain. Several theories have been developed in an attempt to explain pain.

    Nociception consists of four steps: transduction, transmission, modulation, and perception.

    Transduction. . .Transduction is the conversion of noxious stimuli into electrical impulses and subsequent depolarization of the nerve membrane. These electrical impulses are created by algesic substances that sensitize the nociceptors and are released at the site of injury or inflammation. Examples include hydrogen ions and potassium ions, serotonin, histamine, prostaglandins, bradykinin, and substance P.

    Transmission. . .A-delta fibers and C fibers transmit pain sensations from the tissues to the CNS.

    A-delta fibers are small diameter, lightly myelinated fibers. Mechanical or thermal stimuli elicit a rapid or fast response. These fibers transmit localized, sharp, stinging, or pinpricking type pain sensation. A-delta fibers connect with secondary neuron groupings on the dorsal horn of the spinal cord.

    C fibers are smaller and unmyelinated. They connect with second order neurons in lamina I and II (the latter includes the substantia gelatinosa, an area in which pain is modulated). C fibers respond to chemical stimuli, rather than heat or pressure, triggering a slow pain response, usually within 1 second. This dull ache or burning sensation isn't localized and leads to two responses: an acute response transmitted immediately through fast pain pathways, which prompts the person to evade the stimulus, and lingering pain transmitted through slow pathways, which persists or worsens.

    The A-delta and C fibers carry the pain signal from the peripheral tissues to the dorsal horn of the spinal cord. Excitatory and inhibitory interneurons and projection cells (neurons that connect pathways in the cerebral cortex of the CNS and peripheral nervous system) carry the signal to the brain by way of crossed and uncrossed pathways. An example of a crossed pathway is the spinothalamic tract, which enters the brain stem and ends in the thalamus. Sensory impulses travel from the medial and lateral lemniscus (tract) to the thalamus and brain stem. From the thalamus, other neurons carry the information to the sensory cortex, where their pain is perceived and understood.

    Another example of a crossed pathway is the ascending spinoreticulothalamic tract, which is responsible for the psychological components of pain and arousal. A this site, neurons synapse with interneutons before they cross to the opposite side of the cord and made their way to the medulla and, eventually, the reticular activating system, mesencephalon, and thalamus. Impulses then are transmitted to the cerebral cortex, limbic system, and basal ganglia.

    After stimuli are delivered, responses from the brain must be relayed back to the original site. Several pathways carry the information in the dorsolateral white columns to the dorsal horn of the spinal cords. Some corticospinal tract neurons end in the dorsal horn and allow the brain to pay selective attention to certain stimuli while ignoring others. This allows transmission of the primary signal while suppressing the tendency for signals to spread to adjacent neurons.

    Modulation. . .Modulation refers to modifications in pain transmission. Some neurons from the cerebral cortex and brain stem activate inhibitory processes, thus modifying the transmission. Substances—such as serotonin from the mesencephalon, norepinephrine from the pons, and endorphins from the brain and spinal cord—inhibit pain transmission by decreasing the release of nociceptive neurotransmitters. Spinal reflexes involving motor neurons may initiate a protective action such as withdrawal from a pinprick or may enhance the pain, as when trauma causes a muscle spasm in the injured area.

    Perception. . .Perception is the end result of pain transduction, transmission, and modulation. It encompasses the emotional, sensory, and subjective aspects of the pain experience. Pain perception is thought to occur in the cortical structures of the somatosensory cortex and limbic system. Alertness, arousal, and motivation are believed to result from the action of the reticular activating system and limbic system. Cardiovascular responses and typical fight or flight responses are thought to involve the medulla and hypothalamus.

    The following three variables contribute to the wide variety of individual pain experiences:
    • pain threshold—level of intensity at which a stimulus is perceived as pain
    • perceptual dominance—existence of pain at another location that's given more attention
    • pain tolerance—duration or intensity of pain to be endured before a response is initiated.
    Neurogenic pain. . .Neurogenic pain is associated with neural injury. Pain results from spontaneous discharges from the damaged nerves, spontaneous dorsal root activity, or degeneration of modulating mechanisms. Neurogenic pain doesn't activate nociceptors, and there's no typical pathway for transmission."
    Last edit by Daytonite on Apr 17, '07
    blue_yuina and beatot like this.
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    thanks a lot sirs, esp. to mr. daytonite. i was able to make my patho bec. of your research. ^_^ God bless.
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    Quote from beatot
    thanks a lot sirs, esp. to mr. daytonite. i was able to make my patho bec. of your research. ^_^ God bless.
    I know this is way late but this question still shows up really high Google so I thought I'd share a great resource I found while doing similar research for a paper on Neuropathic Pain.

    These videos are really specific, and wouldn't necessarily help for a postoperative pain pathophysiology (maybe... I don't know), but they're awesome for both Nociceptive and Neuropathic Pain.

    Nociceptive Pain Overview
    Neuropathic Pain Overview
    Pathophysiology of Neuropathic Pain

    -Tommy


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