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Health, Medicine, Nursing
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Addiction and Clonidine (Research Paper Sample)


The paper is contrasting and comparing Addiction and Clonidine

Addiction and Clonidine
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18, 15, 2014
Table of Content
 TOC \o "1-3" \h \z \u  HYPERLINK \l "_Toc387360537" Executive summary  PAGEREF _Toc387360537 \h 1
 HYPERLINK \l "_Toc387360538" Pharmacodynamics  PAGEREF _Toc387360538 \h 3
 HYPERLINK \l "_Toc387360539" Pharmacokinetics  PAGEREF _Toc387360539 \h 4
 HYPERLINK \l "_Toc387360540" General discussion and conclusion  PAGEREF _Toc387360540 \h 4
 HYPERLINK \l "_Toc387360541" Reference List  PAGEREF _Toc387360541 \h 6

Executive summary
By description, Addiction simply refers to a case where one is physically or psychologically enslaved to a given practice, or to any kind of habit-forming substance to an extent that the cessation of such habit leads to great trauma to such an individual. Some of the best examples of addictions include: food, drug and exercise addiction. Some of the symbols of such behaviors are: denial, continued consumption regardless of the effects, and substance pre-occupation. As its short term effect, addiction usually leads to an immediate satisfaction of the substance being abused while deadly and harmful consequences always arise in the long run. Finally, the addict’s body will tend to adjust so as to incorporate the substance in its normal functioning, a condition where one becomes psychologically dependent on the drug (Rogge & Taft, 2009). On the other hand, clonidine is a sympatholytic drug that is employed in treatment of disorders such as anxiety, ADHD and high blood pressure. It is categorized as a2 adrenergic agonist. Another point worth noting is that clonidine does not have any addictive effects and it lacks any entertaining value, although its combination with other potent substances has proved to be abusive (Guha 2012).
Clonidine has currently been employed in treatment of alcohol and opiate addiction, resulting in its possible abuse. Most people are now combining clonidine with other substances to achieve desired addictive purposes. This is to say that clonidine is now being abused due to lack of other opiate maintenance drugs like methadone, which are deemed difficult to acquire (Melnikova 2012). Therefore, there is no use in selling clonidine as people have begun to develop addiction to it hence not need to actually let it out on a regular basis.
Turning to addiction interventions, the addict’s body may simply react towards abstaining from the substances that are addictive (withdrawal). However, this process might result in undesired body reactions. For instance, there is a high possibility of occurrence of hormonal and/or chemical imbalance due to failure to re-introduce former substances. Lastly, significant psychological stress could occur if the substances that the body was used to are not available (Golan et al. 2011).
There are a number of therapeutic methods of curbing addiction, one of them being methadone maintenance. With this approach, a drug is administered in a clinical locale where there is full supervision. This process leads to a slow but steady increase in levels of brain opiate whereas the high feeling is not produced at all. The drug then remains in the system for a reasonably long time so as to prevent the addicts from re-using the addictive substance.
Another alternative is one that deeply stimulates the addicts’ brain. In this approach, the DBS procedure is meant to target a number of brain parts, PFC being the major one. In a similar manner, clonidine is seen to work this way. It targets most receptors like a2 and a2A of such brain parts, binds on them and inhibit release of norepinephrine and thus a general reduction in sympathetic tone is achieved (Stockwell 2011).
Therefore, it is safe to assert that clonidine is can help counter addiction to some substances already mentioned. However, when it is combined with other potent drugs, it can be addictive.
Clonidine is seen to have high specificity for a2 receptors that are presynaptic, located in the vasomotor center in the stem of the brain. As soon as it gets to the brain, it reacts by binding on the a2 receptors, a process that leads to a reduction in the levels of presynaptic calcium. This as well hinders norepinephrine release and thus achieves a general reduction in sympathetic tone. More still, clonidine produces antihypertensive impacts as a result of agonism on the imidazoline receptors. This action tends to facilitate actions such as sympathy-inhibitory so as to lower the levels of blood pressure (Marstrand et al. 2010).
As a treatment model of ADHD, clonidine directly raises the PFC’s noradrenergic tone by binding to postsynaptic receptors (the kind of receptors known as adrenergic a2A), whereas, indirectly, the locus coeruleus’ norepinephrine input is raised.
As a blood pressure drug, clonidine, which is an imidazoline-offshoot and hypotensive agent, tends to cross the barrier on the blood-brain, moves to hypothalamus and then prompts a significant reduction in the addict’s or patient’s blood pressure. The process occurs as this drug is able to arouse alpha-adrenoceptors (otherwise known as a2 receptors) in the stem of the patient’s brain. As a result, the existing sympathetic outflow is completely minimized from the central nervous system. As an adjunct treatment of severe pain caused by cancer, clonidine is administered as some kind of infusion (epidural). This is a case where the present opiate analgesic is unable to completely suppress such pain. Thus, since clonidine helps to reduce the sympathetic tones, it is an appropriate drug that can help withdraw most addicts from several substances, although it is associated with several side effects as seen below under the section of pharmacokinetics.
Starting with addiction, most of the addicts’ bodies usually find recreational value in the abused drugs. Most, if not all of the physiological functions of their bodies adapt to such substances and thus cause them to completely dependent on such substances to do any kind of activity.
With clonidine, its overdose may lead to a patient experiencing difficulties in breathing, feeling dizzy, cold, extreme/unusual tiredness and pinpoint eye pupils. Patients may also experience potassium loss, an incident that is portrayed through: increased thirst, mental changes, dryness of the mouth, nausea, pain of the muscles and weak pulse. With excessive sodium loss, patients may react by exhibiting confusion, muscle crumps, seizures and irritability (Williams 2012).
General discussion and conclusion
As substantiated above, clonidine indeed lacks any recreational value...
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