1 / 21

Pain Haytham Eloqayli

Pain . Pain occur due to tissue damage: damage due to extreme mechanical, thermal or chemical stimulation.Pain is a protective mechanism: person try to remove the tissue damageloss of pain perception can cause and increase tissue damage (e.g bed sores in bedridden. Pain . Stimulus? activate pain receptor ? transmision by nerve fiber ? CNS (S.C,spinothalamic tract, brain stem, thalamus, cortex)Pain: 2 types Fast pain (acute pain, sharp pain..etc)Slow pain (chronic pain, aching pain..etc1145

andrew
Download Presentation

Pain Haytham Eloqayli

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript


    3. Pain Stimulus? activate pain receptor ? transmision by nerve fiber ? CNS (S.C,spinothalamic tract, brain stem, thalamus, cortex) Pain: 2 types Fast pain (acute pain, sharp pain..etc) Slow pain (chronic pain, aching pain..etc)

    4. Pain Stimulus: mechanical, thermal pain stimuli: extreme stimuli causing tissue damage chemical pain stimulus: tissue damage (e.g ischemia, spasm) causing release of chemical substances which activate pain receptors. Chemical substances: bradykinin, seretonin, potasium ions, proteolytic enzymes, lactic acid. Other chemical substances which enhance the pain receptors but doont directly exite them: prostaglandins, substance P. Fast pain elecited by mechanical or thermal stimulation. Slow pain elicited by all 3 types of stimulation

    5. Pain Pain receptors: for both types of pain is free nerve endings. -non adapting receptors -distributed widely in the skin, joints, arterial wall, dura distributed sparsely in the deeper tissue. Fast pain not felt in most deep tissue, its well localized Slow pain is felt both in the superficial and deep tissue, its poorly localized.

    6. Pain Nerv fibers: transmitt pain from receptors to the CNS. Ad: fast pain C: slow pain

    7. Pain CNS: S.C: dorsal horn, spinothalmic tract ? Brain stem, thalamus: conscious perception of pain ? Cortex: interpreting pain quality.

    8. Pain Spinal cord Fast pain: 1st order neuron (Ad) terminate in lamina I (lamina marginalis) 2nd order neuron leave Lamina I, cross to the contralateral side and continue up with the spinothalamic tract. Neurotransmitter in SC: glutamate Slow pain 1st order neuron (C) terminate in lamina II, III (substantia gelatinosa) 2nd order neuron: interneuron from lamina II, III to lamina V. 3rd order neuron: lamina V, cross to the contralateral side and continue up with the spinothalamic tract Neurotransmitter: substance P.

    9. Pain

    10. Pain Site of medical literature WWW. Pubmed. Com

    11. Pain Brain stem and thalamus: Fast pain: most fibers of the spinothalamic tract terminate mainly in the thalamus directly, only small amount of fibers terminate in the brain stem. Slow pain: fibers of the spinothalamic tract terminate mainly in the brain stem (one or more of 3 areas) then to the thalamus, small amount of fibers terminate directly in the thalamus. 3 areas in the brain stem: reticuler nuclei, tectal area, periaqueductal gray area.

    12. Pain

    13. Pain Analgesia System and pain control 1.analgesia system of periaqueductal gray and periventricular areas 2.Brain opiate system

    14. Pain analgesia system: Periaquiductal gray, periventriculer area (secrete enkephalin) Through 1st order neuron stimulate raphe magnus and reticuler paragigantocellularis neucli (secrete enkephalin) Through 2nd order neuron stimulate pain inhibitory complex dorsal horn (secrete serotonine) Sertonine stimulate Local neurons in dorsal horn to secrete enkephalin Result is block of signals from C and Ad and inactivation of pain pathway.

    15. Pain

    16. Pain Brain opiate system Different opiate like receptors in the brain and SC which is stimulated by internally secreted opiate like substances Result in: inactivation of pain pathway. The endogenous opiates: 3 main substances And there brakdown products: proopiomelanocortin, proenkephalin, prodynorphin.

    17. Pain Visceral Pain 1.highly localized types of damage to the viscera don not cause significant pain. So one need diffuse stimulation of pain nerve endings (ischemia, chemical damage spasm, excess distention of a hollow viscous) 2. dual transmission of pain through the referred visceral pathway and the direct parietal pathway

    18. Pain Referred pain: to feel pain in a part of the body that is remote from the tissue causing the pain visceral pain is referred to the surface of the body. Referral site localized to the dermatomal segment from which the visceral organ originated in the embryo

    19. Pain probable mechanism for referred pain -branches of visceral pain fibers are synapse in SC on the same second-order neurons that receive pain signals from the skin -When the visceral pain fibers are stimulated, pain signals from the viscera are conducted through some of the same neurons that conduct pain signals from the skin So pain from the viscera is felt on the skin.

    20. Pain

    21. Pain Parietal pain: -when the disease process often spreads to parietal surfaces (parietal peritoneum, pleura, or pericardium). -These, like the skin, are supplied with extensive pain innervations from the peripheral spinal nerves -Sharp localized

More Related