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Mental Health Emergencies - Essay Example

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This paper 'Mental Health Emergencies' tells us that the case involves Jack, a 28-year-old male who has been pacing up and down the restaurant, who appears agitated, and who cannot seem to sit still regardless of attempts by his friends to calm him down.  The patient is likely suffering from schizophrenia. …
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Mental Health Emergencies
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?Mental Health Introduction The case involves Jack, a 28 year old male who has been pacing up and down the restaurant, who appears agitated, and who cannot seem to sit still regardless of attempts by his friends to calm him down. The patient is likely suffering from schizophrenia. This is a possible diagnosis because schizophrenia patients usually manifest anxiety, emotional distance, delusions, anger, and argumentativeness. In evaluating the patient’s behaviour, he seems to be manifesting these behaviours. He is pacing up and down the restaurant and is agitated and anxious; he also is emotionally distancing himself from his staff and friends, not wanting to be touched and disregarding their efforts to calm him down. He appears angry and argumentative. He is also delusional, speaking incoherently in a stream of words and thinking how “screwed up the world is.” His wanting desperately to speak to his sister is also part of his delusion, most likely thinking that his sister may be in grave danger and that he may be suspicious of everyone else but his sister. Such behaviours are associated to the diagnosis as outlined specifically by the Diagnostic and Statistical Manual of Mental Disorders which specifies the above symptoms as possible symptoms of schizophrenia. Authors First and Allan (2011) also discuss how these symptoms, particularly auditory hallucinations and delusions, are key symptoms of schizophrenia which, coupled with agitation can really further support a strong diagnosis for schizophrenia. Glick, Berlin, and Fishkind (2008) also discuss how agitation among these patients is one of the main causes of their hospital or emergency room visits. They associate this symptom with the increase in dopamine levels for patients (Glick, et.al., 2008). Based on such condition and behaviour, this paper shall now provide an evaluation of the patient’s symptoms. It will first defend the diagnosis, detailing reasons why the symptoms match the diagnosis. This paper will then evaluate the medical assessments which would be conducted on the patient in order to determine the medical cause for his behaviour. A discussion on schizophrenia would then follow, including its incidence, current theories and current management strategies. This paper will also discuss the biological causes and social factors associated with schizophrenia. A conclusion will finally summarize and establish an overall evaluation of the patient and his associated condition. Body I believe that the patient has schizophrenia. The patient manifests delusions, specifically, delusions about how “screwed up” the world is. This delusion is based on a false belief to which the person sticks even when other people prove these delusions to be untrue. Schizophrenic patients often have bizarre delusions, including delusions of persecution about what they believe other people are doing to them (Van Os and Kapur, 2009). The fact that the patient is mumbling things to himself, claiming how “screwed up” the world is implies that he has some ideas or some thoughts about the world which are bizarre and not based on reality. His delusions and thoughts are also associated with thought disorders which are seen among schizophrenia patients (Van Os and Kapur, 2009). He cannot answer coherently, choosing instead to mutter a stream of words which are very much unresponsive to the question being asked. He is also talking in a garbled fashion, which further supports his incoherence and disorientation (Buckley, et.al., 2009). The patient also manifests thought blocking, when he suddenly stopped talking and stood still in the middle of his muttering and pacing (National Institute of Mental Health, 2009). Schizophrenia patients also manifest movement disorders which can manifest as agitated body movements. These individuals may repeat movements over and over and some may become catatonic (National Institute of Mental Health, 2009). For this patient, he displayed agitated and repetitive movements by pacing up and down the restaurant. Medical assessment There would be various medical assessments which I would conduct in order to determine that there is no medical cause for the patient’s symptoms (Mayo Foundation, 2010). However, these assessment processes may be difficult to carry out because the patient refused to be touched and approaching him caused further agitation. Nevertheless, in the event that I would be permitted to assess him, I would need to take his height and weight, check his vital signs, including his heart rate, blood pressure and temperature (Mayo Foundation, 2010). I would also need to auscultate his heart and lungs to assess any abnormal rhythms (Mayo Foundation, 2010). There is a need to check his temperature for any fevers which may be causing his symptoms. The other tests including CBC, screening for drugs and alcohol, and thyroid function would have to be carried out in the laboratory upon the patient’s admission (Mayo Foundation, 2010). Other more specific assessments would also have to be carried out by a mental health provider or expert who can make a more accurate and specific assessment of the patient’s symptoms, his thoughts, feelings, as well as his behaviour (Mayo Foundation, 2010). Such mental health provider can also rule out the possibility that the patient may be suffering from other mental health illnesses. In order to make an assessment of schizophrenia, I would consider his disorientation, agitation, pacing and repetitive movements, his refusal to be touched, and his rambling speech about the world being “screwed up,” to be determinants of a schizophrenia diagnosis (Csernansky, 2002). Based on Magnetic Resonance Imaging, patients with a schizophrenia diagnosis have been known to manifest abnormalities in their neocortical and limbic regions which have been considered significant points of concern for patients manifesting psychotic symptoms (Laruelle, et.al., 1996). Loss of volume of gray and white matter and an increase of ventricular volume over time has also been seen in imaging studies of these patients (Laruelle, et.al., 1996). Affectations in these parts of the brain cause the manifestation of symptoms like agitation, repetitive movements, rambling speech and disorientation. Schizophrenia This is considered a severe mental condition which afflicts about 7 per 1000 of the adult population in the 15-35 age group (WHO, 2012). Its incidence is at 3-10,000, but its prevalence is high due to its chronic manifestation. This disease affects close to 24 million people in the world and although it is considered treatable, such treatment can be effective more during the initial stages (WHO, 2012). About 50% of individuals with this disease are not being administered appropriate care and about 90% of individuals with untreated schizophrenia are found in developing nations (WHO, 2012). There are various theories which explain the development of schizophrenia. Some studies indicate that the dopamine system within the mesolimbic processes leads to the positive symptoms of schizophrenia (Laruelle, et.al., 1996). The distribution of the D2 receptor within these areas of the brain is also said to impact on the manifestation of schizophrenia, especially during its acute phase (Jones and Pillowsky, 2002). Other psychological processes have also been apparent in the development of this disease. Cognitive biases have been considered in these patients at risk for diagnosis under stressful conditions (Jones and Pillowsky, 2002). Other cognitive processes may refer to global neurological gaps, including memory loss. Recent studies indicate that some individuals suffering this disease may be emotionally reactive, especially when stressed; such sensitivity may make them more susceptible to the manifestation of the symptoms (Horan, et.al., 2003). Studies also indicate that the elements of delusion can refer to the emotional causes of the disorder; moreover, how individuals interpret these experiences can impact on general symptomatology (Smith, et.al., 2006). Schizophrenia may also refer to slight differences in brain structures, seen in about 40% to 50% of these cases (Smith, et.al., 2010). Based on neuropsychological tests as well as brain imaging activities seeking to evaluate functional disparities in brain functions and activities, differences in frontal lobes, the hippocampus and the temporal lobes can be most apparent among schizophrenic patients (Kircher and Thienel, 2006). The function of the dopamine in the mesolimbic pathway has been mostly associated to phenothiazone drugs which impact on dopamine function, often decreasing psychotic symptoms (Laruelle, et.al., 1996). This theory is also reinforced by the fact that amphetamines which support dopamine release may aggravate the symptoms for the disorder (Laruelle, et.al., 1996). The dopamine hypothesis also suggests that over-stimulation of the D2 receptors has been known to cause schizophrenia. Supporting evidence in imaging studies were established during the mid-1990s (Jones and Pillowsky, 2002). This theory is considered unidimensional mostly because the recently used medications also seem to be as effective as the older medications; moreover, these new medications impact on serotonin functions and may have more than a dopamine blocking impact (Jones and Pillowsky, 2002). Theories have also been forwarded on the impact of the neurotransmitter glutamate on the decreased function of the NMDA glutamate reception to the manifestation of schizophrenia; this interest has been credited to the unusually low levels of glutamate receptors seen in the post-mortem brains of patients suffering from the disorder (Konradi and Heckers, 2003). This was also supported by the discovery of glutamate blocking drugs like phenycyclidine and ketamine manifesting similar symptoms and cognitive issues linked with schizophrenia (Lahti, et.al., 2009). Decreased glutamate function is associated with unfavourable performance on tests which require frontal lobe and hippocampal function; moreover, glutamate is said to impact on dopamine function which is significantly implicated in schizophrenia, suggesting that glutamate has a significant impact on the pathways for the disorder (Coyle, et.al., 2003). The main treatment administered for schizophrenia is antipsychotic medications; and more often than not, it also supported by psychological therapy (Van Os and Kapur, 2009). Hospitalizations can be recommended for the more severe manifestations of the disease. Community support is also recommended, mostly with community visits of community mental health teams and other support groups for these patients (Van Os and Kapur, 2009). Antipsychotic medications for schizophrenia can help manage the positive symptoms of the disorder for 7-14 days; these drugs however, do not address the negative symptoms of the disorder (Van Os and Kapur, 2009). Antipsychotic medications may be typical or atypical; and preferences are often based on drop-out and symptom relapse rates (Van Os and Kapur, 2009). Favourable response rates may also be considered as a determinant for drug choice. Clozapine is considered an effective medication for those who do not respond well to other drugs; however, it can have serious side effects like agranulocytosis in some patients (Van Os and Kapur, 2009). Typical antipsychotics have also been known to cause extrapyramidal side effects while the atypical drugs have been linked with diabetes and weight gain. Atypical antipsychotics have manifested with fewer extrapyramidal side effects; however, these differences have been negligible (Ananth, et.al., 2004). Psychosocial interventions for this disorder include family therapy, cognitive remediation, cognitive behavioural therapy, and skills training (Pharoah, et.al., 2010). Family therapy has been prescribed in order to help the patient and his family manage and cope with the symptoms of the disorder; this type of therapy has also been applied in order to prevent or reduce incidents of relapse and hospitalizations (Pharoah, et.al., 2010). Cognitive remediation and cognitive behavioural therapy has been known to assist the patient in blocking the manifestation of the symptoms (Dixon et.al., 2009). It helps the patient avoid negative thinking which may lead to anxiety or stress and the manifestation of agitation. In other words, these types of therapies also help the patient manage or cope with his symptoms. This disease has been associated with heritability, strongest among first degree relatives and more than 40% of monozygotic twins (Van Os and Kapur, 2009). Environmental factors for this disorder are said to include drug use and prenatal stress. Parenting does not have a significant impact, however, with strong parental support, schizophrenic patients often cope better with their symptoms (Picchioni and Murray, 2007). Social isolation, drug abuse (cannabis, cocaine, amphetamine), immigration, racial discrimination, and family issues are also elements which impact on the manifestation of this disorder (Van Os and Kapur, 2009). Conclusion Based on the symptoms manifested by the patient, he seems to be suffering from schizophrenia. He appears agitated and disorientated; is pacing up and down the restaurant; does not want to be touched; rambles about the world being “screwed up”; is delusional; is being incoherent; and stops suddenly in the middle of his rambling. These symptoms support a diagnosis of schizophrenia because schizophrenics usually manifest delusions, agitation, disorientation, repetitive movements, thought blocking (suddenly stops in the middle of a thought), and refusal to be touched. There is a need to assess his vital signs in order to rule out other possible causes of his symptoms; moreover, a drug and alcohol test is also essential for the same purposes. Various theories have been forwarded explaining schizophrenia, including the dopamine hypothesis, and other neuropsychological pathways to the disorder. Management processes include antipsychotic medications, psychotherapies, and community support. Under these considerations and interventions, the patient may effectively recover and cope with his symptoms. An effective assessment of his symptoms must however be undertaken first before any definitive diagnosis can be set forth. References Ananth, J., Parameswaran, S., Gunatilake, S., Burgoyne, K., et.al., 2004. Neuroleptic malignant syndrome and atypical antipsychotic drugs. Journal of Clinical Psychiatry, 65(4), 464–70. Buckley, P., Miller, B., Lehrer, D., and Castle, D., 2009. Psychiatric comorbidities and schizophrenia. Schizophrenia Bulletin, 35(2), 383–402. Coyle, J., Tsai, G., and Goff, D., 2003. Converging evidence of NMDA receptor hypofunction in the pathophysiology of schizophrenia. Annals of the New York Academy of Sciences, 1003, 318–27. Csernansky, J., 2002. Schizophrenia: A new guide for clinicians. London: CRC Press. Dixon, L., Dickerson, F., and Bellack, A., 2010. The 2009 schizophrenia PORT psychosocial treatment recommendations and summary statements. Schizophrenia Bulletin, 36(1), 48–70. First, M. and Tasman, A., 2011. Clinical guide to the diagnosis and treatment of mental disorders. Sydney: John Wiley & Sons. Glick, R., Berlin, J., and Fishkind, A., 2008. Emergency psychiatry: principles and practice. London: Lippincott Williams & Wilkins. Horan, W., and Blanchard, J., 2003. Emotional responses to psychosocial stress in schizophrenia: the role of individual differences in affective traits and coping. Schizophrenia Research, 60(23), 271–83. Jones, H. and Pilowsky, L., 2002. Dopamine and antipsychotic drug action revisited. British Journal of Psychiatry, 181, 271–275. Kircher, T. and Thienel, R., 2006. The boundaries of consciousness. Amsterdam: Elsevier; 2006. Konradi, C. and Heckers, S., 2003. Molecular aspects of glutamate dysregulation: implications for schizophrenia and its treatment. Pharmacology and Therapeutics, 97(2), 153–79. Lahti, A., Weiler, M., Michaelidis, B., Parwani, A., and Tamminga, C., 2001. Effects of ketamine in normal and schizophrenic volunteers. Neuropsychopharmacology, 25(4), 455–67 Laruelle, M., Abi-Dargham, A., and van Dyck, C., 1996. Single photon emission computerized tomography imaging of amphetamine-induced dopamine release in drug-free schizophrenic subjects. Proc. Natl. Acad. Sci. U.S.A., 93(17), 9235–40. Mayo Foundation, 2010. Paranoid schizophrenia [online]. Available at: http://www.mayoclinic.com/health/paranoid-schizophrenia/DS00862/DSECTION=tests-and-diagnosis [Accessed 14 October 2012]. National Institute of Mental Health, 2009. What are the symptoms of schizophrenia? [online]. Available at: http://www.nimh.nih.gov/health/publications/schizophrenia/what-are-the-symptoms-of-schizophrenia.shtml [Accessed 17 October 2012]. Pharoah, F., Mari, J., Rathbone, J., and Wong, W., 2010. Family intervention for schizophrenia. Cochrane Database Syst Rev, 12. Picchioni, M. and Murray, R., 2007. Schizophrenia. BMJ, 335(7610), 91–5. Smith, B., Fowler, D., and Freeman, D., 2006. Emotion and psychosis: links between depression, self-esteem, negative schematic beliefs and delusions and hallucinations. Schizophrenia Res, 86(1–3), 181–8. Van Os, J. and Kapur, S., 2009. Schizophrenia. Lancet, 374(9690), 635–45. World Health Organization, 2012. Schizophrenia: What is schizophrenia? [online]. Available at: http://www.who.int/mental_health/management/schizophrenia/en/ [Accessed 15 October 2012]. Read More
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