Nervous system drugs barbiturates

NERVOUS SYSTEM DRUGS ANXIOLYTICS AND HYPNOTICS Barbiturates... 

All barbiturates have essentially die same mode of action. Depending on the dose given, tiiese drags are capable of producing central nervous system (CNS) depression and mood alteration ranging from mild excitation to mild sedation, hypnosis (sleep), and deep coma These drugs also are respiratory depressants the degree of depression... 

Hypnotics induce states of drowsiness and facilitate the onset and continuation of sleep resembling natural sleep [32]. Central nervous system (CNS) functions, in addition to the maintenance of wakefulness, are usually depressed by these drugs. Barbiturates, clinically... 

Substance-Induced Anxiety Disorder. Numerous medicines and drugs of abuse can produce panic attacks. Panic attacks can be triggered by central nervous system stimulants such as cocaine, methamphetamine, caffeine, over-the-counter herbal stimulants such as ephedra, or any of the medications commonly used to treat narcolepsy and ADHD, including psychostimulants and modafinil. Thyroid supplementation with thyroxine (Synthroid) or triiodothyronine (Cytomel) can rarely produce panic attacks. Abrupt withdrawal from central nervous system depressants such as alcohol, barbiturates, and benzodiazepines can cause panic attacks as well. This can be especially problematic with short-acting benzodiazepines such as alprazolam (Xanax), which is an effective treatment for panic disorder but which has been associated with between dose withdrawal symptoms. 

A matter of philosophical rather than practical significance is the close similarity in the optimal hydrophobicity for the random-walk process in plants and animals. In a series of papers dating bact to 1968, Hansch ( 3) has shown that drugs acting rather non-specifically in the animal central nervous system, such as anesthetics and barbiturates, also have an optimal log P in the 2.0 to 2.5 range (Table V). 

During the early twentieth century the barbiturates were used in children and adolescents for their sedative and hypnotic effects however, their safety profile and propensity to cause physical dependence led scientists in search of safer anxiolytics. The development of animal models of behavioral disorders facilitated the formulation of drugs with more specific central nervous system (CNS) effects. In 1959, chlordiazepoxide (Librium) was the first benzodiazepine (BZ) to receive a patent. It entered the market in 1960, followed by diazepam (Valium) in 1963. Today, over 35 BZs have been formulated and over 10 are available in the United States (Ballenger, 1995 Hobbs et ah, 1996). 

It is a reduction/decrease in the activity of specialized cells. For example barbiturates depress central nervous system, quinidine depresses myocardium. Certain drugs stimulate one type of cells but depress others e.g. morphine stimulates the vagus and chemoreceptor trigger zone but depresses the vomiting and cough centres. Similarly acetylcholine stimulates intestinal smooth muscle but depresses SA node in the heart. 

The benzodiazepines, the barbiturates, zolpidem, zaleplon, eszopiclone, and many other drugs bind to molecular components of the GABAa receptor in neuronal membranes in the central nervous system. This receptor, which functions... 

Tolerance—decreased responsiveness to a drug following repeated exposure—is a common feature of sedative-hypnotic use. It may result in the need for an increase in the dose required to maintain symptomatic improvement or to promote sleep. It is important to recognize that partial cross-tolerance occurs between the sedative-hypnotics described here and also with ethanol (see Chapter 23)—a feature of some clinical importance, as explained below. The mechanisms responsible for tolerance to sedative-hypnotics are not well understood. An increase in the rate of drug metabolism (metabolic tolerance) may be partly responsible in the case of chronic administration of barbiturates, but changes in responsiveness of the central nervous system (pharmacodynamic tolerance) are of greater importance for most sedative-hypnotics. In the case of benzodiazepines, the development of tolerance in animals has been associated with down-regulation of brain benzodiazepine receptors. Tolerance has been reported to occur with the extended use of zolpidem. Minimal tolerance was observed with the use of zaleplon over a 5-week period and eszopiclone over a 6-month period. 

An understanding of common mechanisms of death due to poisoning can help prepare the care-giver to treat patients effectively. Many toxins depress the central nervous system (CNS), resulting in obtundation or coma. Comatose patients frequently lose their airway protective reflexes and their respiratory drive. Thus, they may die as a result of airway obstruction by the flaccid tongue, aspiration of gastric contents into the tracheobronchial tree, or respiratory arrest. These are the most common causes of death due to overdoses of narcotics and sedative-hypnotic drugs (eg, barbiturates and alcohol). 

The most commonly abused prescription drugs are opioids and opiates such as oxycodone and morphine, central nervous system depressants such as barbiturates and benzodiazepines, and stimulants such as dextroamphetamine and methylphenidate. Brand-name painkillers such as Vicodin and OxyContin, depressants such as Valium and Xanax, and stimulants such as Ritalin and Dexedrine are commonly abused (as are some OTC cough remedies). Although helpful and safe when used appropriately, these drugs can cause serious harm when taken in unapproved ways. 

Barbiturates such as phenobarbital are weak acids. The toxicity of the barbiturate is mainly the result of the effects on the central nervous system. Only the nonionized form of the drug will distribute into the central nervous system. The proportion ionized will depend on the pKa and the pH of the blood. By increasing the pH of the blood using sodium bicarbonate administration to the poisoned patient, ionization of the barbiturate will be increased and distribution to tissues such as the brain will be decreased. Urinary excretion of the barbiturate will also be increased because the urinary pH will be increased. 

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