Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0184567 (acute pain)
 3,962 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

There must be a differentiation between acute and chronic pain. While acute pain should be treated causally, this is usually no longer possible when pain has become chronic. It may even become so intense that a chronic pain patient can no longer live a productive life. The pain threshold is decreased by endogenous substances like prostaglandin E, but also kallekrein and bradykinin. Hyperadrenergic stimuli can advance pain; for example, the so-called phantom-limb pain. Also important within the biorhythm is the time of day, the physical state of activity and the psychological constitution. The pain patient often uses his disease to focus the attention of the physician on him. There are central and peripheral acting analgesics available for treatment of pain. The effect of peripheral acting analgesics can be explained by inhibition of the prostaglandin synthesis, by ASS (ASA) and its descendants, the antirheumatic agents. These acidic substances are mainly concentrated in the inflammatory tissue. They act as antiphlogistics, analgetics, and antipyretics. Descendants of phenacetin act as analgetics and antipyretics. Efficacy usually lasts 3 hours. Therefore these substances should be administered regularly and in sufficient doses, according to a fixed daily schedule. This reduces unnecessary pain and avoids overdosages. To reduce side effects and tachyphylaxis, a change of analgesics in intervals of approx. 6 weeks proved satisfactory. If peripheral analgesics are no longer sufficient, for example in the final phase of a carcinoma disease, morphine and its derivatives will then be applied. To reduce the dosage, additionally a neuroleptic drug and eventually a thymoleptic drug may be administered.
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PMID:[Pain and its management with drugs]. 716 35