6. Pain - 1 PAIN Pain is real but also subjective...

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1 PAIN Pain is real, but also subjective. Perception of pain can vary among different people. Pain can be perceived with different intensities at different times. These factors have made it difficult to establish a firm physiological understanding of pain. It is useful to distinguish between pain and nociception . We have specific receptors that cause the perception of pain when activated. A physiological definition of a nociceptor is a receptor activated by a stimulus that causes tissue damage or would cause damage if continued. Nociceptors are the least differentiated of the sensory receptors in the skin. They generally have free nerve endings. There are several classes of cutaneous pain receptors. Thermal or mechanical nociceptors have small-diameter, thinly myelinated A δ fibers that conduct at 5-30 m/s. Activation of these nociceptors is associated with sensations of sharp prickly pain. Polymodal nociceptors are activated by a variety of high intensity mechanical, chemical, or thermal stimuli, and have small diameter, unmyelinated C fibers that conduct at 0.5-2 m/s. These make up about 40% of all C fibers. Under pressure block we first loose touch sensation, then the sharp pain carried by A δ fibers, and finally the duller, slow pain carried by C fibers. The sharp pain is more easily tolerated than the dull pain. Similarly, electrical stimulation activates the largest fibers first, and sharp pain is perceived before dull pain as the stimulus intensity is increased. Local anesthetics, on the other hand, first affect the smallest fibers. Therefore, they block dull pain first. The fact that different kinds of pain are carried over fibers with different transmission velocities is responsible for the idea of “first and second pain,” when, for example, we stub our toe. Pain or nociception usually does not adapt. In fact, the response to the pain- inducing stimulus often sensitizes. This is called hyperalgesia . The sensitization of nociceptors after injury or inflammation often results from local tissue damage and the release of a variety of chemical mediators. Tissue damage releases bradykinin and prostaglandins that sensitize the free nerve endings. The effectiveness of aspirin as a painkiller is partly because it interferes with the synthesis of prostaglandins. Also, activation of the nerve endings cause them to release substance P which acts on mast cells to release histamine which can, in turn, act on the nerve endings to increase their sensitivity. This arrangement is unusual. In most cases, receptor nerve endings are not also releasing endings. In addition, substance P and other agents can cause local vasodilation and edema, which, in turn, releases more substance P over a wider area.
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