Terms in this set (161)

MOA:
Alcohol affects almost all cells of the body and has complex effects on the neurons in the CNS. Alcohol is a general CNS depressant. Additionally, alcohol binds with receptors in the brain reward system resulting in the release of dopamine and promoting the addictive process.
SE/ADE:
The symptoms of alcohol use include nausea; vomiting; tremors; restlessness and inability to sleep; depressed mood or irritability; increased heart rate, blood pressure, respiratory rate, and temperature; and tonic-clonic seizures. Illusions are also common. Acute overdose produces vomiting, coma, and respiratory depression. Alcohol-induced hypotension may lead to renal failure and cardiogenic shock, common causes of alcohol-related death.
hangovers manifested by malaise, nausea, headache, thirst, and a general feeling of fatigue. In alcoholics, sudden withdrawal may have life-threatening effects such as severe disorientation, psychotic symptoms (hallucinations), severe hypertension, and cardiac dysrhythmias that may progress to death.
Treatment:
Acute Phase--Detoxification
Initial treatment of acute alcohol intoxication or overdose requires implementation of the basic principles of airway, breathing, and circulation (ABCs). No antidote for alcohol is available, and stimulants should not be given.
thiamine should be started before treatment with IV glucose solution in all patients with alcoholism and continued until the client resumes a normal diet.
Abstinence Maintenance Phase—Following Detoxification
These include disulfiram (Antabuse), a daily oral medication that is a type of aversion (behavioral) therapy and prevents drinking by causing an unpleasant reaction if alcohol is consumed, and naltrexone, which blocks the desired effects of alcohol
Naltrexone (ReVia, Depade) is a pure opioid antagonist that decreases craving and pleasurable effects of alcohol and blocks the "high" of alcohol use.
Acamprosate (Campral) is used to decrease unpleasant feelings such as tension, dysphoria, anxiety, restlessness and cravings brought about by abstinence from alcohol
Ondansetron (Zofran), an antagonist of receptors in the brain reward system, decreases motivation for drinking in early onset alcoholism; and topiramate (Topamax), an anticonvulsant, may be helpful in decreasing craving for alcohol as well as cocaine.
MOA:
Sedative-hypnotic drugs act primarily on the CNS. Benzodiazepines enhance the effects of gamma-aminobutyric acid (GABA), an inhibitory neurotransmitter in the brain. Barbiturates not only enhance the inhibitory effect of GABA, but they can directly mimic the actions of GABA. Barbiturates are powerful respiratory depressants and can readily cause death by overdose.
SE/ADE:
initial euphoria and intoxication similar to that of alcohol.
Withdrawal from sedative-hypnotics can be very serious. In the first 12 to 16 hours following the last dose, the client may develop anxiety, tremors, weakness, nausea, vomiting, muscle cramps, and increased reflexes. After 24 hours, the client craves the drug and may experience delirium, grand mal seizures, and respiratory and cardiac arrest. Symptoms of withdrawal peak on the second or third day for short-acting (shorter half-life) drugs (e.g., alprazolam, secobarbital, pentobarbital) and on the seventh or eighth day for long-acting (longer half-life) drugs (e.g., diazepam, chlordiazepoxide, phenobarbital).
Treatment:
Overdoses of benzodiazepines are treated with flumazenil (Romazicon), a specific benzodiazepine antagonist
Gastric lavage may be used if the drug was taken orally within 4 to 6 hours. Dialysis may be required to decrease the drug level. Gradual withdrawal of the drug is required during withdrawal syndrome. Phenobarbital, a long-acting barbiturate, may be used to control withdrawal symptoms in a client dependent on barbiturates. Phenobarbital is then gradually withdrawn when the client is stable. To manage their symptoms safely, hospitalization is recommended during drug withdrawal for individuals who have been abusing large amounts of barbiturates.
MOA:
Important to the abuse potential of opioids is their ability to activate the brain reward system, reinforcing their addictive effect
SE/ADE:
The primary effects of opioids include analgesia, drowsiness, slurred speech, and detachment from the environment. IV use usually causes a "rush" of feelings in the lower abdomen, along with warm skin flushing and a strong sense of euphoria. Cross-tolerance among the opioids is common, but cross-tolerance to other CNS depressants does not occur. However, additive effects of other CNS depressants may lead to increased CNS depression.
Although opioid withdrawal is acutely uncomfortable, it is not usually life threatening, as is withdrawal from other CNS depressants. However, suicidal ideation may occur.
Treatment:
A narcotic antagonist such as naloxone (Narcan) should be used to reverse respiratory depression and coma induce by opioids overdose. Treatment of withdrawal syndrome is symptom-based and does not always require the use of medication. Methadone (Dolophine) in decreasing doses over 10 to 14 days is the drug most often used to decrease symptoms during opioid detoxification. Methadone is an oral opioid agonist that replaces the opioid to which the patient is addicted. Some patients obtain relief from withdrawal symptoms with the use of clonidine (Catapres), a centrally acting alpha2-adrenergic agonist that may also be used for nicotine addiction. It is most effective against autonomic GI hyperactivity (diarrhea, nausea, vomiting), but it does not decrease craving. The action of clonidine in nicotine and opioid addiction is not fully understood. Buprenorphine (Subutex) is an agonist-antagonist opioid that may be used for detoxification and maintenance therapy. Because of its action on specific opiate receptors, it can decrease the symptoms of withdrawal and suppress drug craving, yet it has a low potential for abuse.
Naltrexone (oral ReVia, injectable Vivitrol) is an opioid antagonist that blocks euphoria and all other opioid effects. It is used for abstinence maintenance therapy. Like naloxone, it will precipitate withdrawal symptoms when administered to opioid-dependent individuals.
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