Pain Overview

Pain is the most common reason, seek medical attention from the patient to complete. Pain has sensory and emotional components and is often classified as acute or chronic pain. Acute pain is often associated with anxiety, and hyperactivity of the sympathetic nervous system (eg. As tachycardia, increased respiratory rate and increased blood pressure, sweating, dilated pupils). Chronic pain does not involve the sympathetic nervous system, but (fatigue, loss of libido, loss of appetite z. B.) and depressed mood may be associated with vegetative signs. People differ greatly in their pain tolerance. Pathophysiology of acute pain, which usually occurs in response to tissue damage, caused by the activation of peripheral pain receptors and their specific sensory A?- and C-nerve fibers (nociceptors). Chronic pain (chronic pain), which is connected to a sustained tissue damage, is probably due to persistent activation of these fibers. However, is not always possible on the severity of tissue injury include the severity of chronic or acute pain. Chronic pain may also be caused by persistent damage or dysfunction of the peripheral or central nervous system (neuropathic pain which verursacht- Neuropathic pain]). Nociceptive pain can be somatic or visceral. Somatic pain receptors located in the skin, subcutaneous tissue, fascia and other connective tissue, the periosteum, in Endoost and in the joint capsules. in general, the stimulation of these receptors produces a sharp or blunt localized pain; burning is not uncommon for participation of skin or subcutaneous tissue. Visceral pain receptors are present in most internal organs and the surrounding connective tissue. Visceral pain that is caused by the lesion of a hollow organ, can hardly be localized, dull and spasmodic and can be projected into remote areas of the skin. Visceral pain, which is caused by damage to an organ capsule or deep of other connective tissue, can be better locate and can be as sharply felt. Psychological factors modulate pain intensity at a very variable degree. Thoughts and feelings play an important role in the perception of pain. Many patients who have chronic pain, also have psychological distress, v. a. Depression and anxiety. Because certain medical conditions, such as psychiatric disorders (eg. As some Somatisierungsstörungen- somatization) are defined by self-reporting of pain, patients with poorly unexplained aches and pains often with a psychiatric disorder and thus incorrectly classified the appropriate care. Pain affect multiple cognitive domains such as attention, memory, concentration and thought content, possibly by demanding cognitive resources. Many pain syndromes are multifactorial. For example, chronic low back pain and most cancer-related pain syndromes have a prominent nociceptive component, but they can also include neuropathic pain (due to nerve damage). Pain transmission and modulation of pain fibers enter via the dorsal to the spinal cord and switched synapse in the dorsal horn. From there, they cross to the other side and pull over the side lines up to the thalamus and then to the cerebral cortex. Repetitive stimulation (eg., By an ongoing pain state) can sensitize neurons in the dorsal horn of the spinal cord, so that a weaker peripheral pain stimulus triggering acts (Bahnungsphänomen). Peripheral nerves and nerve at other levels of the CNS may also be sensitized, which produces long-term changes at synapses in cortical receptive fields (remodeling) and has an enhanced perception of pain. Substances that are released during tissue damage, incl. Those who are involved in the inflammatory cascade can sensitize peripheral nociceptors. These substances include vasoactive peptides (eg. As calcitonin-gene-related protein, substance P, neurokinin A), and other mediators (e.g., prostaglandin E2, serotonin, bradykinin, adrenaline). The modulation of the pain signal is carried out at multiple sites both on the segmental level as well as in descending pathways by numerous neurochemical mediators, incl. Endorphins (z. B. enkephalin) and monoamines (z. B. serotonin, norepinephrine). These mediators interact in a poorly understood way to increase the perception of and response to pain to maintain, to shorten or reduce. They convey the possible benefit CNS active drugs (eg. As opioids, antidepressants, anticonvulsants, membrane stabilizers) that interact with specific receptors and neurotransmitters in the treatment of chronic pain. Psychological factors are important modulators. They affect not only the expression of how patients respond to pain (eg. B.The a stoic, irritable or adversely kind) and how they behave in response to (z. B., if they make faces) but cause itself a neuronal activity that modulates neurotransmission along the pain pathway. The psychological reaction to persistent pain interacts with other CNS factors and can put as long-term changes in pain perception in motion. Basics of geriatrics in the elderly are the most common causes of pain in musculoskeletal conditions. However, the pain is often chronic and multifactorial, and the causes are unclear. NSAIDs, the risk of ulcers and gastrointestinal bleeding caused by NSAIDs is aged> 65 years, 3 to 4 times higher than in middle-aged patients. The risk depends on the drug dose and duration of therapy. Older patients at high risk of gastrointestinal side effects can range from a simultaneous administration of cytoprotective drug benefit (usually a proton pump inhibitor, occasionally the prostaglandin misoprostol). The risk of newly recognized for cardiovascular toxicity that probably at non-selective COX-1 and COX-2 inhibitors and selective COX-2 inhibitors (coxibs) which is particularly relevant for elderly patients who are more prone to cardiovascular risk factors (z. B. a history of MI or cerebrovascular or peripheral arterial disease). Both the non-selective and selective NSAIDs can impair kidney function and cause sodium and water retention; they should be used with caution in elderly patients, especially those with kidney or liver disease, heart failure or hypovolemia. Rarely NSAIDs provoke cognitive impairment and personality changes in the elderly. Indomethacin is more than other NSAIDs for confusion in the elderly verantworltich and should be avoided. Given the overall increased risk of severe toxicity in the elderly low doses as possible should be used by NSAIDs; Short-term or intermittent therapies to confirm the efficacy should be considered. NSAIDs most likely help alleviate produced by inflammation pain. Naproxen may be preferred because it appears to have a lower risk of cardiovascular side effects than other commonly prescribed NSAIDs. Opioids the half-life of opioids is prolonged in elderly patients, and they may have a greater analgesic effect than in younger patients. In elderly patients with chronic pain, seems to short-term use of opioids to relieve pain and improve physical function, but affects the mental functioning. Opioid-induced constipation and urinary retention seem more problematic in elderly patients. The risk of fracture during the first 2 weeks of treatment with opioids is higher than during treatment with NSAIDs in the elderly. Compared to other opioids transdermal buprenorphine has an opioid agonist / antagonist, a favorable risk: benefit profile in elderly patients with renal insufficiency.