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Analgesics and narcotics

Analgesics are drugs that relieve pain selectively without affecting consciousness or sensory perception. This selectivity in relieving pain is the important distinction between an analgesic and an anesthetic. Analgesics are often self-prescribed and abused. Many strong analgesics can produce serious and even fatal depression of the central nervous system. Furthermore, the use of analgesics can involve such problems as addiction, fatal overdose, allergic reaction, and significant gastrointestinal irritation. Analgesics may be classified into two types: the opioids, which act on the brain; and anti-inflammatory drugs, which alleviate pain by reducing local inflammatory responses.

The opioid analgesics were once called narcotic drugs because they induce sleep and cause dependence or addiction. This term is no longer used by physicians or scientists since both dependence and addiction can be induced by many drugs other than opioids. The opioid analgesics can be used for either short-term or long-term relief of severe pain. In contrast, the anti-inflammatory compounds are non-narcotic analgesics and are used for short-term pain relief and for modest pain, such as that of headache, muscle strain, bruises, or arthritis.

The term opioid has been adopted as a general classification of all of those agents that share chemical structures, sites, and mechanisms of action with the endogenous opioid agonists. Opioid substances encompass all of the natural and synthetic chemical compounds closely related to morphine, whether they act as agonists or antagonists. Although interest in these drugs has always been high because of their value in pain relief and because of problems of abuse and addiction, interest was intensified in the 1970s and 1980s by discoveries about the naturally occurring morphine-like substances, the endogenous opioid neuropeptides.

Opioid drugs are useful in the treatment of general postoperative pain, severe pain, and other specific conditions. The use of opiates to relieve the pain associated with kidney stones or gallstones presumably depends on their ability to affect opiate receptors in these tissues and to inhibit contractility. By a similar mechanism, opiates are also able to relieve the abdominal distress and fluid loss of diarrhea. Central receptors appear to account for the ability of morhine and analogues to suppress coughing, an effect that requires lower doses than those needed for analgesia. Low doses of opiates given subcutaneously are also specifically advocated for the relief of the respiratory distress that accompanies acute cardiac insufficiency complicated by the buildup of fluid inthe lungs, even though the mechanisms of this effect are unknown and despite the fact that opiates are respiratory depressants.

The effectiveness of a given dose of an opiate drug declines with its repeated administration in the presence of intense pain. This loss in effectiveness is termed tolerance. Evidence suggests that tolerance is not due to alterations in the brain's responses to drugs. Animals exhibiting tolerance to morphine after repeated infections in a familiar environment show little or no tolerance when given the same doses and tested for pain sensitivity in new environments. Thus, a learned aspect of tolerance seems almost certain. The cellular and molecular mechanisms underlying this loss of responsiveness are not clear, however. Physical dependence and addiction in a person using intravenous administration closely follow the dynamics of drug tolerance; increasing doses are required to produce the psychological effects, while tolerance protects the brain against these respiratory depressant actions of the drug. In the tolerant individual, intense adverse reactions can be precipitated by administration of an opiate antagonist, thus revealing the dynamic internal equilibrium that previously appeared to neutralize the response of the brain to the opiates. The signs of the withdrawal response (yawning, tearing, perspiration, dilation of me pupils, nasal discharge, anxiety, tremors, elevation of blood pressure, abdominal cramps, and hyperthermia) can be viewed as signs of an activated sympathetic nervous system and to some extent an extreme, but nonspecific, arousal response. This may also suggest that tolerance in the face of increasing opiate doses is more properly viewed as a balancing mechanism by this sympathetic activation.