Nursing Bioscience - Assignment Example

Running Head: NURSING BIOSCIENCE ASSESSMENT First Middle, Family of Case Study Margaret is a 55 year old female who has along history of depression. Margaret has been treated for depression for a number of years with Fluoxetine Hydrochloride (a serotonin selective reuptake inhibitor – SSRI). Margaret has experienced episodes of depression where she wanted to kill herself resulting in a number of admissions to hospital. During the 6 months prior to admission, Margaret had been feeling more depressed than usual so doubled her dose of Fluoxetine without consulting her doctor. Margaret has just been admitted to hospital with symptoms of mania such as poor sleep, increased activity, rapid pressured speech, racing thoughts, inflated self – esteem, increased libido, and has spent her life savings on gym equipment. Margaret’s family members are very concerned and reported that her behavior is very out of character as she has never displayed these symptoms before. I. Describe the Possible Biological Causes of Mental Illness The origin of mental illness is said to be multi – factorial (Tyrer, 2001). The following are the possible biological factors causing mental illness: A. Genetic Linkage (Tyrer, 2001and Crawford, 2003) Twin studies Familial linkage Adoption studies B. Hypothesis on Biogenic Amines Noradrenaline, adrenaline, serotonin, and dopamine primarily the noradrenaline and serotonin are monoamine neurotransmitters that are believed to play a principal role in the mood and emotional behavior control (Russell, et al., 2009). This hypothesis states that depression is precipitated by drugs that causes decrease in monoamine, and conversely, depression is relieved by drugs that increase monoamine levels (Russell, et al., 2009). Noradrenaline The key neurotransmitter believed to be involved in the mood and emotional behavior control (Russell, et al., 2009). Believed to inhibit or stimulate different emotional reactions, namely, anxiety, aggression, stress, and sleep patterns (Russell, et al., 2009). Serotonin The principal neurotransmitter believed to be associated with mood control (Russell, et al., 2009). Involved in pain, pleasure, anxiety, panic, arousal, and sleep behavior regulation (Russell, et al., 2009). C. Receptor Sensitivity Hypothesis Additional receptor site is synthesized to compensate for little stimulation received by postsynaptic neuron (Russell, et al., 2009). Decreased receptor sensitivity of postsynaptic neuron results when increased neurotransmitter results to increased receptor site stimulation (Russell, et al., 2009). It is therefore thought that depression is a consequence of a receptor site pathological alteration. The clinical activity of an antidepressant drug is achieved by reducing the supersensitivity of the receptors (Russell, et al., 2009). D. The Permissive Hypothesis Depression or mania results from the abnormal levels of noradrenaline secondary to low levels of serotonin (Russell, et al., 2009). When serotonin is unable to control the decrease of noradrenaline to levels that are abnormally low, the patient will turn out to be depressed. On the other hand, when noradrenaline levels become unusually high due decline of levels of serotonin, the patient becomes manic (Russell, et al., 2009). E. The Neuroendocrine Hypothesis Altered function of endocrine is believed to contribute to this pathological mood state. These include thyroid or Cushing disease (Russell, et al., 2009). F. The Serotonin Only Hypothesis In 1980s, with the advent of selective serotonin reuptake inhibitors or SSRIs that downplays adrenaline role, this theory became popular (Russell, et al., 2009). The 6 – 8 week delay in clinical relief and noradrenaline role is not explained in this hypothesis (Russell, et al., 2009). II. Identify and Briefly Discuss the Function of neurotransmitters in depression To, Zepf, and Woods (2005) noted that the prevailing hypothesis in the pathogenesis of depression for many years were monoamine neurotransmitters deficit, namely, norepinephrine and serotonin. To, Zepf, and Woods added that the neurochemical basis of depression is not just a result of any one specific deficit but rather, of a more complex deficiency. Neurotransmitters serotonin, dopamine, and norepinehrine are of special interest in bipolar disorder (Russell, et al., 2009). Depression is a result of monoamines, noradrenaline and serotonin, deficiency (Russell, et al., 2009). III. Briefly outline the cause of Margaret’s mania and briefly describe other possible biological causes of mania Margaret had a long – standing history of depression and has been treated with an anti – depressant, Fluoxetine Hydrochloride ( a serotonin selective reuptake inhibitor – SSRI), for years Margaret had been feeling more depressed than usual, which made her decide to double the dosage of her own medication without consulting her physician. Rationale behind Margaret’s diagnosis include: Margaret was mistakenly diagnosed and treated for depression In mood disorder, the early manifestation is commonly a depressive illness, and the bipolar disorder could not be diagnosed until manic illness is triggered by treating the patient with antidepressant medications (Crawford, 2003) Margaret was treated alone with anti – depressant Fluoxetine Hydrochloride (a serotonin selective reuptake inhibitor – SSRI) for years. According to Crawford (2003), antidepressants can sometimes cause “switching” to mania, when used alone. To prevent this switching to mania, a mood stabilizer drug is typically added to antidepressants. Other possible biological causes of mania include: Abnormalities in the following: 1. Ventral Striatum A 30 percent reduction in the gray matter is observed in the bipolar person, which possibly contributes to the judgment loss observed in manic episode (Zubieta, 2000). 2. Hippocampus A state of anxiety can be created by the reduction of “subiculum" aids in fear recognition, which is observed in bipolar brain (Zubieta, 2000). 3. Thalamus and Ventral Part of Brain Stem More monoamine binding sites is observed in bipolar patients (Zubieta, 2000). 4. Brain Stem (Raphe) Persons with bipolar disorder exhibit a 40 percent reduction of brain stems’ raphe nucleus, which contributes to low moods and depressed episodes (Zubieta, 2000). IV. Briefly describe the DSM IV diagnosis of bipolar affective disorder and indicate whether Margaret would met the DSM IV diagnosis for this disorder DSM IV Bipolar Affective Disorder is otherwise known as manic depression. For the patient to meet the aforementioned criteria, he must have at least two or more of the following symptoms of depression (Morrison, 2003; National Institute of Mental Health, 2010): Depressed mood, markedly decreased interest in almost all of daily activities, feeling of worthlessness, guilt feeling Significant loss of weight, psychomotor agitation, insomnia, or hypersomnia, indecisiveness, and recurrent thoughts of death Margaret must also have at least three of the following symptoms which must be present to a significant degree (Morrison, 2003; National Institute of Mental Health, 2010): Feeling of grandeur or exaggerated self – esteem Decreased sleep need, talkativeness, insomnia or hypersomnia Psychomotor agitation or retardation, flight of ideas, distractability Increased in activities that are goal – oriented, excessive pleasurable activity involvement such as increased sexual desire, unrestrained buying sprees, foolish investments in business From the aforementioned criteria, it is evident that Margaret have met the symptoms of DSM IV disorder, namely: Long history of depression and treatment of SSRI Margaret was recently admitted to the hospital due to symptoms of mania Poor sleep Increased activity Rapid pressured speech Racing thoughts Inflated self – esteem Increased libido “Spent her life savings on gym equipment” “Extreme behaviour” V. List three different medications which may be used to treat Margaret as describe in the case study above. McElroy and Keck, (2000), Bozikas, Petrikis, and Kourtis (2002) and Wolfsperger, et al (2007) stated that the cornerstones of pharmacotherapy in treating the patient are the following: Lithium Valproate sodium Carbamazepine A. From the above Selected Medication, describe two side effects for each and the biological reasons for each 1. Lithium side effects Abnormal Thyroid Effects Lithium results to transient diminution of circulating thyroid hormone concentration (National Institutes of Health, 2010). Fifty percent of patients who receive two long – term treatment of lithium have thyrotropin – releasing hormone (TRH) response abnormality and 30 percent of them also have elevated thyroid stimulating (TSH) levels (Kaplan, et al., 2007). Cardiac Effects Lithium cardiac effects resembling ECG hypokalemia are caused by lithium ion intracellular potassium displacement 2. Valproate sodium Thrombocytopenia and platelet dysfunction At high dosage, Valproate affects the hematopoietic system resulting in bleeding time prolongation (Kaplan, et al., 2007) Spina bifida During the first trimester of pregnancy, valproate crosses the placenta causing neural tube defects (Kaplan, et al., 2007) 3. Carbamazepine Hepatitis Hypersensitivity hepatitis during the first few weeks resulting from liver enzyme elevation and cholestasis secondary to bilirubin and alkaline phosphatase elevation (Kaplan, et al., 2007) Blood dyscrasia Due to benign suppression of white blood cells (Kaplan, et al., 2007) 6. Briefly discuss current research relating to the biological considerations associated with suicide and affective disorder. Include at least 5 references, from journal articles (not internet) in your answer. All research used should be less than 5 years old. Relevance of suicidal behavior is credited to the decreased neurotrophin levels such as serotonin in both the prefrontal cortex and hippocampus (Dwivedi, Mondal, Rizavi, and Conley, 2005; Ernst, Mechawar, and Turecki, 2009). The major area responsible in the regulation of mood, which has also been implicated in the affective disorder and suicide pathology, is played principally by the prefrontal cortex (Dwivedi, et al, 2005). The hippocampus, an area which is involved in the cognition and stress, is also one of the major factors involved in suicidal behavior (Dwivedi, et al, 2005). The suicide risk of manic depressed patient is accounted typically to its high energy and impulsivity (Gao, et al., 2009) The increased risk of death secondary to depression has been identified and suicide risk is decreased with increased use of antidepressant (Giltay, et al., 2010; Isacsson, 2010). In evaluations of suicide risk, the serotonergic and other biological function assessment in a clinical setting is incorporated in the study (Mann, et al., 2006). Various studies suggest that elevated risk of future suicidal behaviour is demonstrated in both serotonergic system and HPA axis anomalies (Mann, et al., 2006). On the other hand, a study in the past 12 months among subjects with depressive symptoms showed an association between total cholesterol, triglycerides, BMI, and attempts in suicide (Brunner, et al., 2006). Serotonin – related genes are possible gene candidate for suicidal behaviour because of its association with the altered system function of brain serotonin and suicide attempts seen in patients who are depressed (Galfalvy, et al., 2008). REFERENCES: 1. Bozikas, V., Petrikis, P., and Kourtis, A. (2002). Treatment of Acute Mania with Topiramate in Hospitalized Patients. Progress in Neuro – Psychopharmacology and Biological Psychiatry, 26(2002), 1203 – 1206 2. Crawford, D. (2003). Bipolar and Mood Disorder. Retrieved from Mental Health Association, http://www.nevdgp.org.au/info/mentalhealth/bipolar_kit.pdf 3. Dwivedi, Y., Mondal, A., Rizavi, H., and Conley, R.(2005). Suicide Brain is related with Decreased Expression of Neurotonin. Journal of Biological Psychiatry, 2005(58), 315 – 324. 4. Ernst, C., Mechawar, N., and Turecki, G. (2009). Suicide Neurobiology. Progress in Neurobiology, 89(2009), 315 – 333. 5. Gao, K., Tolliver, B., and Kemp, D. (2009). Correlates of Historical Suicide Attempt in Rapid Cycling Bipolar Disorder. Journals in Clinical Psychiatry, 70(7), 1032 -40 6. Gill, J., Singh, H., and Nugent, K. (2003). Acute Lithium Intoxication and Neuroleptic Malignant Syndrome. Pharmacotherapy, 23(6), 1- 4. http://www.medscape.com/viewarticle/456879_2 7. Giltay, E, Zitman, F., and Menotti, E. (2010). Respiratory Function and Other Biological Risk Factors for Completed Suicide: 40 years of Follow – up of European Cohorts of the Seven Countries Study. Journal of Affective Medicine, 120(2010), 249 – 253. 8. Gonzales – Pinto, A., Lalaguna, B., and Mosquera, F. (2001). Use of Olanzapine in Dysphoric Patient. Journal of Affective Disorder, 66 (2001), 247 -253 9. Isacsson, G. (2010). The Increased Use of Antidepressants has contributed to the Worldwide Reduction in Suicide Rates. The British Journal of Psychiatry, 196(2010), 423 - 433 10. Kaplan, H., Sadock, B., and Grebb, J. (2007). Synopsis of Psychiatry. Baltimore, MA: Williams and Wilkins. 11. McElroy, S. and Keck, P. (2000). Pharmacologic Agents for the Treatment of Acute Bipolar Mania. Society of Biological Psychiatry, 48(2000), 537 – 557 12. Morrison, J. (2003). Complete List of DSM IV Codes. Retrieved from PsychNET – UK, http://www.psychnet-uk.com/dsm_iv/schizoaffective_disorder.htm 13. National Institutes of Health. (2010). Bipolar Disorder. Retrieved from http://www.nimh.nih.gov/health/publications/bipolar-disorder/complete-index.shtml#pub8 14. Russell, C., Lyndon, R., and Hendy, L. (2009). Neurotransmitters and Mood. Retrieved North East Valley Division of General Practice, http://www.nevdgp.org.au/info/topics/depression_intro.htm. 15. To, S., Zepf, R., and Woods, A. (2005). The Symptoms, Neurobiology, and Current Pharmacological Treatment of Depression. Journal of Neuroscience Nursing, 37(2), 102 – 107. 16. Tiemeier, H. (2003). Biological Risk Factors for Late Life Depression. European Journal of Epidemiology, 8(18), 745 -750. 17. Tyrer, P. (2001). Etiology of Mental Illness. International Encyclopedia of the Social and Behavioural Sciences. 18. Wolfsperger, M., Greil, W., and Rossler, W. (2007). Pharmacological Treatment of Acute Mania in Psychiatric In Patients between 1994 and 2004. Journal of Affective Disorder, 99(2007), 9 – 17. 19. Zubieta (2000). Evidence of Brain Abnormalities in Bipolar Disorder. American Journal of Psychiatry, 157(2000), 1619 Read More