#Vmt academy of practical nursing manual
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Evidence also suggests that a genetic protection against TD exists. 10 However, factors such as environmental influence, age as a risk factor, and oxidative stress suggest that TD has many features that cannot be limited to genetics alone. 9 MГјller et al have reported familial TD. 6Д®vidence suggests a genetic predisposition to TD 7, 8 however, many of these findings have not been replicated or are inconsistent. 5 However, a 2011 review of clinical studies suggests that the relationship between toxic metabolites of APDs and TD is still unclear. 4 Evidence also suggests that APDs and their metabolites may be directly toxic to neurons through oxidative stress. The basal ganglia, subcortical nuclei comprised of several brain regions including the striatum and substantia nigra, are highly innervated by dopamine neurons and are therefore especially at risk for oxidative stress and the occurrence of TD. Monoamine oxidase, the enzyme that metabolizes dopamine, and dopamine itself can cause lipid peroxidation and the alteration of antioxidant enzymes which can lead to cell death.

#Vmt academy of practical nursing free

The result of increased dopamine metabolism is an increase in the production of free radicals. With regard to the oxidative stress hypothesis, antidepressants block dopamine receptors, increasing dopamine synthesis and metabolism. With regard to the dopamine hypothesis, chronic dopamine blockade can result in upregulation of dopamine receptor responsiveness that can result in an exaggerated response of the postsynaptic dopamine receptors to dopamine. Several hypotheses have been proposed that include prolonged blockade of postsynaptic dopamine receptors leading to dopamine receptor supersensitivity, gamma-aminobutyric acid (GABA) depletion, cholinergic deficiency, oxidative stress, altered synaptic plasticity, neurotoxicity, and defective neuroadaptive signaling. The pathophysiology of TD lacks a universally accepted theory and mechanism. In this review based on our literature search, we discuss the pathophysiology and epidemiology of TD, medications that can induce TD, possible solutions for preventing TD, and treatments for managing TD and for managing TD symptoms while a patient is concurrently taking an APD. The search terms we used to gather this information included tardive dyskinesia, medication-induced tardive dyskinesia, neuroleptics, antipsychotics, typical antipsychotics, atypical antipsychotics, antiemetics, anticholinergics, antidepressants, anticonvulsants, antihistamines, antiparkinson agents, stimulants, anxiolytics, biogenic amines, mood stabilizers, oral contraceptives, incidence, prevalence, dopamine, oxidative stress, pharmacokinetic, genetic polymorphisms, gastroparesis, history, case study, epidemiology, pathophysiology, etiology, prevention, and treatment. We attempted to include as many recent (publication date of 2015 and later) articles as possible. We conducted a PubMed search using keywords and combined word searches that involved medication-induced TD as well as agents that are associated with causing or are used to treat medication-induced TD. Of course, patients need to take the medications that are causing the unwanted side effect of TD therefore, stopping the medication can be dangerous and may even induce further complications. In many patients, TD is irreversible and can persist long after the medications that may be causing the symptoms are stopped. And while many of the non-APD medications that cause TD directly or indirectly affect dopamine neurotransmission, emerging evidence suggests that isolating the definition of a TD diagnosis to dopamine agonists only is incorrect. While the DSM-V definition of TD is helpful in diagnosing dopamine antagonistвЂ“related TD, this definition falls short of the wide range of medications that can also cause TD, especially because only one of the several hypotheses for why TD occurs involves dopamine. 2 In all cases, TD must persist for at least 1 month after a medication is discontinued for a TD diagnosis.

#Vmt academy of practical nursing manual

The Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-V) classifies TD as a medication-induced movement disorder that can develop after short-term and long-term use of medications, as well as after discontinuation of, change in, or reduction in medications. 1 However, TD is also associated with a wide variety of other medications. In fact, TD occurs in 20%-50% of patients taking APDs. TD most generally occurs in individuals who are on long-term treatment with dopaminergic antagonist medications (antipsychotic drugs ). The tardive dyskinesia (TD) form of dyskinesia gets its name from the slow-or tardive-onset of involuntary movements of the face, lips, tongue, trunk, and extremities.

The term dyskinesia refers to involuntary muscle movements that can range from slight tremor to uncontrollable movement of the entire body.