Euphoria, opioids producing

In addition, opioid medications can affect regions of the brain that mediate what one perceives as pleasure, resulting in the initial euphoria or sense of well-being that many opioids produce. Repeated abuse of opioids can lead to addiction—a chronic, relapsing disease characterized by compulsive drug seeking and abuse despite its known harmful consequences. 

Diphenoxylate Lomotil) is a meperidine derivative used as an antidiarrheal. It exhibits no morphinelike effects at low doses, but it produces mUd opioid effects, such as sedation, euphoria, and dependence, at higher doses. Its salts are highly insoluble in water, which reduces recreational use. Preparations often include atropine. 

Pharmacokinetics plays a very important role in the manner in which opioids are abused. Morphine and many of its derivatives are slowly and erratically absorbed after oral administration, which makes this route suitable for long-term management of pain but not for producing euphoria. In addition, opioids undergo considerable first-pass metabolism, which accounts for their low potency after oral administration. Heroin is more potent than morphine, although its effects arise primarily from metabolism to morphine. The potency difference is attributed to heroin s greater membrane permeability and resultant increased absorption into the brain. 

Acute administration of opioids, particularly in non-tolerant individuals, produces a syndrome of intoxication characterized by pupillary dilation and initial euphoria, followed by apathy, psychomotor retardation, slurred speech, and impaired attention and memory. Opioid overdose can produce fatal respiratory depression and thus is a medical emergency. 

There are three principal classes of opiate receptors, designated x, K, and 5, and there exist a number of drugs that are specific for each of these receptor types. However, most of the clinically used opiates are quite selective for the preceptor the endogenous opiates enkephalin, endorphin and dynorphin are selective for the p and 5, 5 and k receptors respectively. When activated by opioids these receptors produce biochemical signals that block neurotransmitter release from nerve terminals, a process that underlies their blockade of pain signaling pathways as well as other effects, such as constipation, diuresis, euphoria, and feeding. 

There are two major classes of pain medications, nonopioids and opioids. The nonopioids used to treat mild pain include agents such as acetaminophen, both steroid and nonsteroidal antiinflammatory drugs (NSAIDs), and acetylsalicylic acid. Anticonvulsants suppress neuronal firing and are also helpful in neuropathic pain. Antiinflammatory agents (e.g., NSAIDs or corticosteroids) may be particularly helpful when bony involvement occurs and are often used for low-intensity pain. Steroids decrease inflammatory edema and are useful in cases of nerve and spinal cord compression, lymphedema, visceral pain caused by organ enlargement, and bone pain. Finally, short-term corticosteroid therapy may also produce euphoria (thus ameliorating less severe depressions) as well as reverse anorexia. 

As with all opioids, meperidine is capable of producing euphoria. A few people may get a mild stimulant effect and a feeling of elation. However, instead of euphoria after a meperidine dose, some people report a feeling of dysphoria—a general feeling of discomfort and restlessness—or even disorientation and confusion. Still other people may just feel drowsy, with no noticeable positive or negative effect on their mood. 

Opioids are known to alter mood states. For example, opiates such as morphine produce euphoria and pain relief. Prolonged use of and withdrawal from opiates produce depressive-like symptoms as well. Based on the mood-altering effects of opiates, the role of endogenous opiates in psychiatric symptoms of various diseases has been studied. In addition, endogenous opioids are believed to play a role in neuronal circuitry responsible for reward and pleasure. Therefore, it is thought that perhaps the anhedonia observed in depressed patients is due to dysregulation of endogenous opioids in neuronal reward circuitry. 

Although the opioid analgesics can produce mood elevation (euphoria) in some patients and sedation in others, the more common side effect is CNS depression manifested as drowsiness.A strategy to reduce sedation or drowsiness is to decrease the analgesic dose and shorten the interval between doses. Clinicians should note that the sedative effect of opioid analgesics is additive with the sedative effects of hypnotics such as alcohol and barbiturates. These depressive agents must be avoided when opioids are prescribed. 

Opioids cause a release of endorphins producing a feeling of pleasure. Examples of abuse include heroin, a highly addictive opioid that metabolizes to morphine and readily passes into the brain producing an immediate euphoria. Pharmaceutical or medicinal abused opioids include oxycontin, hydrocodone, codeine, methadone, and propoxyphene. 

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