Benzodiazepines Research Paper

Tamazepam acts at many levels in the CNS, producing generalized depression. Effects may be mediated by GABA, an inhibitory neurotransmitter.

Treatment for aloprazalam drug toxicity consists of cardiac monitoring and oxygen. Naloxone can be administered at a lower dose with a gradual increase if needed to reverse respiratory depression which happens in most patients. Another treatment is the use of flumazenil which is the specific antidote for benzodiazepines. (Gershman, 2014). However, the use of this drug is controversial and does have some contraindications. It is contraindicated in patients with long-term benzodiazepines, patients who have ingested a substance that lowers the seizure threshold, or in patients who have tachycardia. The contraindications increase risk of seizures, cardiac arrest and possibly death. Because of the contraindications, most of the time flumazenil is not used for the treatment of benzodiazepine overdose. Although flumazenil is contraindicated and not used often, it can be very effective in reversing central nervous system depression associated with benzodiazepine toxicity but not effective in reversing respiratory depression. Flumazenil has a short half life of less than one hour and multiple doses may be needed for treatment. When flumazenil is used risk can be reduced by a slow dose titration of the drug

The most toxic substance tested was the combination of diazepam and secobarbital sodium with a 96 hour LD50 value of 6.31mg/kg/d when compared to the least toxic substance diazepam with its 96 hour LD50 value of 794.32mg/kg/d. This synergistic effect is due to both barbiturates such as secobarbital sodium and diazepam a benzodiazepine, both are an allosteric activator of γ-aminobutyric acid (GABA) and specifically the GABA A receptor. For diazepam binding is localised between the γ- and α- subunits. However, GABA A receptors also contain alternative allosteric modulatory sites for the binding of secobarbital sodium, however the precise location is yet to be determined. Although, the α-subunit is believed to play a role (Löscher & Rogawski, 2012; Makkar, Zhang, &

Pryazolopyrimdinone (C6H5N3) was used as a basic sedative hypnotic state that increased the GABAA receptors. GABAA is the neurotransmitter to the Central Nervous System (CNS), causing the patient to be less impulsive by blocking the Glutamate. The Citrate was not the only ingredient used to make Sildenafil Citrate. If the citrate were to be administered alone it would leave the user feeling tired rather than stimulated, while the addition of Sildenafil (C22H30N6O4S) act as a stimulant to the Corpora much like cGMP. Citrate slows down the breakdown of cGMP in the body by placing allowing the user to feel pleasure and calm rather than sedative, and the Sildenafil stimulated the cGMP to stay longer resulting in an erection of the male cannot do so

Benzodiazepine receptors are linked mainly to γ amino butyric acid (GABA) receptors, which sensitize benzodiazepine receptors to the neurotransmitter GABA, the most prominent inhibitory neurotransmitter in the central nervous system.

This medication is no longer considered the most common prescribed drug. Diazepam can be used “for the relief of anxiety, management of alcohol, reversal of status epileptics, preoperative sedation, and as an adjunct for the relief of skeletal muscle spasms” (Pharmacology and the Nursing Process, 2016). Diazepam is rapidly absorbed and this medications’ half-life can be anywhere from 10 on up to 100 hrs. Depending on several factors such as metabolic changes, kidney/liver problems, dosage of the medication, frequencies with which it is taken can in turn cause slower rates to eliminate from the body. Some side effects of Diazepam include dizziness, drowsiness, irritability, and nausea and muscle

As the Rolling Stones called them in their hit song, “Mother’s Little Helper”, “Mother needs something today to calm her down, and though she 's not really ill, there 's a little yellow pill, she goes running for the shelter of a mother 's little helper, and it helps her on her way, gets her through her busy day”, benzodiazepines were and extremely common medication in the 70s and 80s and many households had their bottle of Valium. The dependence on high dosages of benzodiazepines such as Xanax and Valium are a major clinical concern. According to Michael Liebrenz of the University of Bern, “This form of dependence is not confined to users who exceed a set amount of diazepam equivalents, but is typically found in patients who have a high-dose, long-term and/or otherwise problematic use, such as mixing BZDs, escalating dosage, using BZDs for recreational purposes, obtaining them by illegal means, and/or experiencing negative social consequences” (Liebrenz, 2016, p. 1). So the problem is not only found in patients who take large dosages, but in patients who also abuse the drug, combine multiple types of benzodiazepines and other drugs, and purchase them illegally in order to be under the influence of a benzodiazepine. This is why, for the last decade, less and less prescriptions of benzodiazepines have been dispensed in the United States. However, “over the last 20 years the quantity of benzodiazepines on each prescription has increased” (Brett, 2015, p. 152).

Dogma ketamine on the central nervous system causes an increase in cerebral oxygen consumption, cerebral blood flow, and increased intracranial pressure. Ketamine memvasodilatasi blood vessels of the brain that lead to an increase in cerebral blood flow as much as 62-80%. This effect was reduced when diazepam, midazolam, ketamine or thiopental is given before. This effect impeding the use of ketamine in patients with intracranial space occupying lesions in or head trauma. This publication offers convincing evidence that when combined with benzodiazepines (or other agents that work on the GABA receptor), and ventilation control, but not with nitrous oxide, ketamine does not increase intracranial pressure. Psikotomimetik side effects (such as

Benzodiazepines, otherwise known as benzos, are classified as medications that aid in certain disorders, such as anxiety, insomnia, panic attacks, and even loss of interest, among others.

An excess of GABA can cause excess sleepiness and drowsiness the following day after dosing.

Benzodiazepines are the common medications in the United States and in the world for treatments of a variety of anxiety disorders, sleeping disorders, epilepsy, seizures, muscle spasms, and alcohol withdrawal.1 However, there are severe adverse drug effects associated with long-term usage of benzodiazepines in elderly populations. In the United States, prescription use of benzodiazepines for the elderly have continued to be prescribed despite the warnings of risks toward elderly populations. A retrospective descriptive analysis of benzodiazepine prescriptions was performed with the 2008 LifeLink LRx Longitudinal Prescription database, it pointed out that the elderly received benzodiazepines two times more than younger adults in a 1 year period.

GABA is an amino acid that makes brains cells less sensitive to stimulation. It is made from glutamate and must be made in the brain because it cannot pass through the blood-brain barrier (Piotrowski, 2010). Excess GABA often lowers anxiety while increased GABA can cause depression. Symptoms of low GABA are anxiety, muscle tension, restlessness, insomnia, impatience, disorganization, polyuria, diaphoresis, hypertension, and diarrhea (?)

GABAA (Gamma Aminobutyric Acid) receptors are the main inhibitory neurotransmitter receptors in the mammalian brain. Although these receptors have been found in other parts of the body like liver9, smooth airway muscles of the lungs10, and several type of immune cells11,12, their main function comes in the nervous system, specifically neurons. The GABAA receptors located in the postsynaptic membrane are stimulated by GABA neurotransmitter released from the pre-synaptic neurons and functions to inhibit neuronal stimulation in the short-term (millisecond time range), while the extrasynaptic GABAA receptors are stimulated by ambient GABA in the extracellular space and confers long term inhibition.2 However, there are many types of GABAA receptors depending on the subunits that they are made up of

GHB was first synthesized about thirty years ago by Dr. H. Laborit. He was a French researcher interested in exploring the effects of GABA (gamma-aminobutyric acid) in the brain. Over the years many researchers have studied GHB’s effects. In Europe it is used as a general anesthetic, a treatment for insomnia and

Baclofen activates the GABAB receptor and give its effects. This similarirty is also observed in the drug phenibut, which activates the GABAB receptor and gives the some of its effects. Baclofen acts as an inhibitory neurotransmitter, postulated to block mono-and-polysynaptic reflexes and to block the release of excitatory transmitters. Nevertheless, baclofen is known to ‘no absue’ potenstial and do not have any substantial connection for the GHB receptor