Alcoholmd Glossary Page - O

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O Definition
Often progressive and fatal

A phrase used to describe a serious outcome of alcoholism. As a disease, alcoholism can progress, even when it is in remission, so that a relapsing alcoholic will rapidly evolve to a full disease pattern in a short period of time. Alcoholism causes premature death through overdose; through organic complications involving the brain, liver, heart, and other organs; and by contributing to suicide, homicide, motor vehicle crashes, and other traumatic events. However, recovery is possible.


A drug initially used to control nausea associated with chemotherapy, and recently found to have a positive effect in controlling alcoholism in certain patients. It is believed that Ondansetron helps those patients with early onset alcoholism control their drinking because of its action on serotonin levels in the brain. People with a predisposition to alcoholism usually have a serotonin imbalance which makes them particularly vulnerable to impulse behavior and antisocial behavior.


Drugs used to treat the withdrawal syndrome created by opiates, meperidine, pentazocine, codeine, methadone. There are two approaches to the pharmacologic treatment of opiate withdrawal: a) opioid taper and b) clonidine. The preferred medication for outpatient opiate withdrawal is methadone. Some clinicians use a common sense tapering schedule using the patients opiate of choice. This is commonly an ineffective, short-term approach with little long-term positive effects when the patient truly has an addictive disorder in the context of a chronic somatic pain syndrome. It is difficult for addicted outpatients to comply with a tapering schedule, since loss of control is part of the symptomatology. If this treatment paradigm is used, dosage reduction of 10-20% per week (not per day) is more likely to result in better patient compliance and long term success. Clonidine, an alpha2 agonist, can be effective in suppressing some symptoms of opiate withdrawal. Initial doses of 0.3 mg q.i.d. are used to treat autonomic symptoms of withdrawal: craving, lethargy, insomnia, and muscle aches are not well suppressed. Total dosage can reach 2.0 mg/day. Lowered blood pressure and sedation are common side effects. Opiate agonists stimulate the mu site of the opiate receptor. Partial agonists partially stimulate it but have a limit or ceiling effect. Antagonists block the mu receptor.

Opiate antagonist

Opioid antagonists such as naltrexone, decrease alcohol reinforcement. Naltrexone diminishes the hedonic value of alcohol, and keeps lapses from becoming relapses. Possible mechanisms underlying naltrexone effectiveness include: craving reduction, modification of the intoxication experience, and inhibition of the primary effect of the initial drink. A supervised intake is suggested. It should be used in conjunction with supportive or relapse prevention therapy. Recently, in outpatient trials of naltrexone 50 mg p.o. daily, drinking relapses were significantly reduced. A double-blind intoxication study showed a statistically increased responsiveness to the effects of alcohol as compared to placebo. In this study, there was no decrease in psychomotor performance but greater aversive effects and decreased positive reinforcement effects of alcohol. More recently, naltrexone-treated subjects reported that the high associated with alcohol was markedly reduced as compared to placebo treated controls. Those on naltrexone also consumed less alcohol, which is speculated to be due to the loss of pleasure associated with alcohol ingestion.


Derivates of opium including heroin (diacetylmorphine), morphine, codeine, hydromorphone, ******having specific receptors abundant in limbic and cortical regions; synthetic narcotics with opiate-like properties include meperidine, methadone, pentazocine, propoxyphene; opiates play a important role in pain regulation; substance dependence refers to a compulsive drug seeking behavior with a significant daily impairment in occupational and social functioning and with a withdrawal syndrome when the abused substance is discontinued; dependence induction is a complex phenomena and might be a multimodal phenomena including mesolimbic dopaminergic pathway involved in reward induction. Opiate intoxication is most commonly encountered by the physician in the Emergency Department. The patient is sleepy or obtunded with rapid shallow respirations, cyanosis, decreased deep tendon reflexes, pin point pupils, decreased pain sensation. Needle marks (tracks) may be present if the patient uses intravenously, skin abscesses may be present if the patient uses subcutaneously (skin popping). Pulmonary edema may be present on chest X-ray. The withdrawal syndrome from opiates can vary greatly depending on the abused opiate, length, and mode of administration and underlying conditions. Shorter acting opiates (morphine, heroin, hydromorphone (Dilaudid) will produce more severe but shorter syndromes, while long-acting opiates (methadone, codeine) will produce milder but more protracted syndromes. Common mild withdrawal phenomena are: craving, anxiety, yawning, lacrimation, rhinorrhea, impaired sleep. More severe withdrawal signs and symptoms are: piloerection (goose flesh, aching of bones and muscles, nausea, vomiting and diarrhea, abdominal cramps and fever. The acute withdrawal phase may last two to ten days, but subtle sleep and mood disturbances may persist for weeks or even months.

Oral contraceptives

Increase susceptibility to alcohol (1, 3-6).


Non-residential treatment of addictive disease.


The inadvertent or deliberate consumption of a dose much larger than that either habitually used by the individual or ordinarily used for treatment of an illness, and likely to result in a serious toxic reaction or death. See also intoxication.

Oxidation and elimination

Alcohol is transformed in the liver by a specific enzyme called alcohol dehydrogenase (ADH) into a primary metabolite, acetaldehyde, which is toxic and quickly transformed by another enzyme, aldehyde dehydrogenase, into acetic acid. Antabuse blocks the ADH inducing an accumulation of acetaldehyde responsible for clinical adverse effects.

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