A Short Note On The Major Depressive Disorder ( Mdd )

Benzodiazepines are absorbed well through both per oral and parenteral administrations. However, absorption per orally is more rapid than any other route. Xanax in particular, is highly lipid soluble. Because it is highly lipid soluble, it means that it passes through the blood brain barrier more quickly. Xanax, otherwise known as alprazolam, reaches its peak in concentration in about one to two hours after administration (Griffin et al., 2013). The half-life, or the time it takes the drug to decrease by half, is about six to twenty-seven hours for adults (Griffin et al., 2013). There is a redistribution of benzodiazepines in body fat. This is a two phase process. During the first phase, there is a fast drop in the blood level as the drug is being redistributed throughout the body. During the second phase the blood level is more slow to drop than the first phase because the drug that is left in the blood is being metabolized and as that is happening it is being replaced by the drug that is being released from the body

All antidepressants work in a similar way, though there are various types of antidepressants—often called “families”—that each work a bit differently. They all, however, increase the brain’s concentration of various neurotransmitters. Antidepressants are psychiatric medications given to patients with depressive disorders to alleviate symptoms. They correct chemical imbalances of neurotransmitters in the brain which probably cause changes in mood and behavior. Antidepressants may be used for a wide range of psychiatric conditions, including social anxiety disorder, anxiety disorders. Antidepressants were initially developed in the 1950s. Their use has become progressively more common over the last twenty years. Generally speaking, anti­psychotic

Chronic intake, the delayed onset of action, drug resistance and numerous side effects force the researchers to look for the new, safe antidepressant strategies (1, 2) with rapid onset and longer time of action.

The goal of antidepressant medication is to provide some relief of the symptoms within two to six weeks. Nevertheless, not every antidepressant works for every individual. Sometimes several must be tried before finding one that produces the most beneficial results with the fewest side effects.

Some of the most common antidepressants include Prozac, Celexa, Zoloft, Paxil, Remeron and Effexor, these come capsules or tablets, studies show that the effects of these drugs can include: Nervousness and anxiety, Insomnia, Irritability, Violent thoughts and actions, Agitation, Hostility, Suicidal thoughts or suicide, Tremors, Irregular heartbeat, Aggression, Confusion and incoherent thoughts, Paranoia, Hallucinations, Psychosis,

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

This report of central nervous system depression after the administration of recommended doses of codeine in a patient with a CYP2D6 ultra-metabolizer phenotype supports genetic testing to assist in elucidating serious adverse drug reactions and in prevention of subsequent inappropriate dosing or drug selection. Genetics testing can give insight as to how our patients process the medications we prescribe them. Pharmacogenetics is a growing field with many benefits to the patient. Our duty as providers is to stay abreast of a developing technology that will provide better outcomes for our

In order to be able to treat a person with depression effectively, doctors have to sort out what kind of role the narcotics may play in the depression. If the feelings of depression is simply a part of a withdrawal due to a narcotic and are only something temporary, it is very unlikely that a antidepressant will be of any benefit. Antidepressants take a bare minimum of two to three weeks to begin working. The most effective treatment in such a case would be to try and help the person at hand to get their drug use under control or stop entirely. Both taking drugs and the withdrawal process may produce depressive symptoms themselves, makingit very difficult to know what it is that’s exactly going on, if it even seems that the depression led to taking drugs in the first place. As a result, It’s extremely vital to the treatment of the individual that the problem with narcotics is sorted out so that is will be possible to further judge whether antidepressants or other treatments used for depression will be needed. This, of course, does not mean it’s

The success of this process is predetermined in part by the livers’ ability to properly convert the drug into a less lipophilic form that cannot be reabsorbed. For alprazolam, the course of elimination relies heavily on the kidneys. Age related renal function must thereby be considered when administering alprazolam. The kidneys are responsible for removing the unbound drug in the plasma by glomerular filtration, proximal tubular secretion, and distal tubular reabsorption. The glomerular filtration rate (GFR) is roughly 20% of the renal plasma flow (Harvey, 2014). Drugs that exclusively rely on the kidneys for elimination can accumulate and have toxic effects with renal impairment. In older adults there is a progressive decline in GFR of 10% per decade following age 50 (Breenan, 2015). This change is age related, however like those with renal disease or injury, close monitoring and dosing adjustments must be carefully

Other clinical studies have implicated fluoxetine’s effects on serotonin neurotransmitters, based on the fact that serotonin is synthesized from the essential amino acid tryptophan. Patients taking fluoxetine who were in remission from major depression were given a special diet which was tryptophan-free. This rapidly decreased plasma serotonin levels, and after a short period of time (as little as 30 minutes) many of the patients began to have signs of specific depressive symptoms. Later, the reappearance of more general depressive symptoms were observed in a majority of the patients. Thus it was shown that fluoxetine has a profound effect on the neurotransmitter serotonin, and decreased

Antidepressants are psychiatric medications given to patients with depressive disorders to ease their symptoms. They are designed to correct chemical imbalances of neurotransmitters in the brain that contribute to changes in mood and behavior.“Researchers discovered the first antidepressants unintentionally in the 1950s while seeking a treatment for schizophrenia. The first antidepressant, Imipramine, marketed as Tofranil, was discovered in 1958. For schizophrenics, antidepressants only made their condition worse, but researchers soon realized that these medications are a perfect fit for patients with depression.” (NIMH). Basically NIMH is saying that you never know what you will discover about something unless you pay close attention to it. Depression is a mood disorder in which people experience feelings of intense sadness for extended periods of time. As many as one in 10 American adults report symptoms of depression, according to the Centers for Disease Control and Prevention. Antidepressants provided relief to 60% to 80% of patients, but they also caused serious side effects, including sluggishness, weight gain and occasionally death from overdose (HealthGuide). The next antidepressants, discovered in 1987-1992, were Prozac, Zoloft, and Paxil (Mayo Clinic). The new types of antidepressants were called selective serotonin reuptake inhibitors

Selective Serotonin Reuptake Inhibitors (SSRIs) are currently one of the most controversial groups of medicines, with fluoxetine, more commonly known by its brand name Prozac, at the head of the controversy. Opponents of the use of SSRI medications as a successful and safe method for treating depression and related disorders assert that the actions of the drug are an unnatural and a dangerous form of tampering with our neurochemistry. Not only are these medications incredibly safe in almost all cases, they are actually an unnatural method of modifying an already disordered, natural sequence of chemicals in the brain, and therefore are not a form of tampering, but are a method for fixing

The linkage of serotonin to depression has been known for the past five years. From numerous studies, the most concrete evidence of this connection is the decreased concentration of serotonin metabolites like 5-HIAA (5-hydroxyindole acetic acid) in the cerebrospinal fluid and brain tissues of depressed people. If depression, as suggested, is a result of decreased levels of serotonin in the brain, pharmaceutical agents that can reverse this effect should be helpful in treating depressed patients. Therefore, the primary targets of various antidepressant medications are serotonin transports of the brain. Since serotonin is activated when released by neurons into the synapse, antidepressants function at the synapse to enhance serotonin activity. Normally, serotonin's actions in the synapse are terminated by its being taken back into the neuron then releases it at which point "it is either recycled for reuse as a transmitter or broken down into its metabolic by products and transported out of the brain." As a result, antidepressants work to increase serotonin levels at the synapse by blocking serotonin reuptake (2).

As the literature remains inconclusive as to the relation between current major treatment modalities and depressive disorder, and given the extremities of the potential dangers of antidepressant medications, it is apparent that there is a need to develop new interventions, which show greater efficacy, safety, and acceptability.

Drugs rule the world, or so it appears. Many are approved for specific biological problems, as in the prevention of myocardial infarctions (heart attacks), blood clots due to trauma, surgery, stroke, etc. Conversely, others are recreational, generating instant highs or mellow lows. This essay will discuss one particular drug, chemical structure, cellular mechanism, type of inhibitor, and effects on metabolism.