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Psychotic Depression
Question 1:
a) Describe in brief the pathophysiology of psychotic depression disorder.
b) Identify other neurotransmitters associated with psychotic depression and discuss how they function to produce the symptoms in this disorder.
Answer 1. a) Sally is suffering from number of biological changes are designated to psychotic depression disorder. Most commonly studied change is the level of cortisol in the patients with psychotic depression (Nandam, Brazel, Zhou & Jhaveri, 2020). This fact has been well established through several research studies that the level of cortisol is high in patients with psychotic depression. This high level of cortisol in an individual is termed hypercortisolemia. It has been found that the level of cortisol tend to remain high even after administering dexamethasone. Dexamethasone is a corticosteroid which works by decreasing the amount of adrenocorticotrophic hormone released by pituitary gland (Meijer & de Kloet, 2017). The low level of adrenocorticotrophic hormone thus influences the release of cortisol from adrenal gland leading to low level of it. Dexamethasone is unable to suppress the level of cortisol due to its high activity and secondary reason is that negative feedback mechanism is disturbed and it is termed dexamethasone non-suppression. Corticotropin releasing factor majorly contributes in the regulation of hypothalamus-pituitary-adrenal axis and in the regulation of stress in an individual (Söder, Clamor & Lincoln, 2019). The interrupted negative feedback mechanism leads to low level of corticotropin releasing factor, as cortisol regulates the level of corticotropin releasing factor using negative feedback. Hypothalamus-pituitary-adrenal axis is responsible for the production of glucocorticoid and in patients with psychotic depression it is unable to produce appropriate amount of glucocorticoids (chun Li et al., 2020). So, low level of glucocorticoid is not able to regulate the level of adrenocorticotrophic hormone via feedback regulation. Hypercortisolemia is responsible for enhanced activity of dopamine in patients with psychotic depression. Increased level of plasma dopamine level is as an indicative of higher dopamine activity. High level of cortisol and dopamine both serve to the pathophysiology of psychotic depression disorder as they are found to be increased in individuals with psychotic depression when compared with individuals with non-psychotic depression ( H. Andrade et al., 2016).
Hypothalamus-pituitary-thyroid axis also functions in the regulation of mood of an individual like hypothalamus-pituitary-adrenal axis. It works by hierarchical cascade producing thyrotropin releasing hormone to stimulate the release of thyroid stimulating hormone which helps in producing tri-iodothyronine (T3) and thyroxine (T4) (Fröhlich & Wahl, 2019). This cascade is important for the human system as thyroid hormone contributes directly in the development of central nervous system. Abnormal level of thyroid hormone impacts the central nervous system, contributing to the psychotic depression disorder. Psychotic depression patients show elevated levels of thyrotropin releasing hormone. It has also been reported that patients with psychotic depression show enhanced level of anti-thyroglobulin and anti-microsomal thyroid antibodies (Szpunar & Parry, 2018).
b) Neurotransmitters have been attributed for normal functioning of the brain. They are the chemical messengers that transfer signals from a neuron to the target cell. Psychotic depression interferes with the normal functioning of the brain thus, affecting the level of some neurotransmitters in it (Sheffler, Reddy & Pillarisetty, 2020). Several research studies have shown that the norepinephrine is involved in psychotic depression. Norepinephrine controls the several activities of the brain by binding to the G-protein coupled α and ß-adrenergic receptors. α-adrenergic receptors divided into α1 and α2 subtypes and ß-adrenergic receptors are divided into ß1, ß2 and ß3 (Ciccarelli, Sorriento, Coscioni, Iaccarino & Santulli, 2017). α1-adrenergic and ß-adrenergic receptors are involved in the stimulation of the signaling of the cells. α1-adrenergic receptor performs cell signaling by increasing the level of intracellular phospholipase C and ß-adrenergic receptor stimulates cell signaling by enhancing the level of cyclic adenosine monophosphate. α2-adrenergic receptor works towards halting the cell signaling by lowering the level of cyclic adenosine monophosphate (cAMP). Norepinephrine has the higher binding affinity towards α2-adrenergic receptors in comparison to α1 and ß-adrenergic receptors. So, when low levels of norepinephrine are present it binds to the α2-adrenergic receptors blocking the cell signaling and when the level of norepinephrine is increased it binds to the α1 and ß-adrenergic receptors, again initializing the cell signaling (Ehsan, Ghasemi & Nasrin, 2020). Noradrenergic receptors have nerve fibers that act as the connecting link between locus coeruleus and different part of the forebrain including the cortex, cerebellum, amygdala, hippocampus, basal ganglia, thalamus and hypothalamus. In psychotic depression different symptoms originate due to different concentration of norepinephrine at locus coeruleus. These symptoms include sad mood, tiredness, very weak concentration or thinking power, circadian rhythm, interrupted sleep or wakefulness and immune responses (Maletic, Eramo, Gwin, Offord & Duffy, 2017).
Serotonin neurotransmitter is also actively involved in the regulation of mood of an individual (Marazziti, 2017). It performs its function by regulating the release of cAMP and cAMP response element binding protein in response to external environmental stimuli. Serotonin signaling pathway, works in conjunction with signaling pathway of dopamine, glutamate, acetylcholine and γ-aminobutiric acid (GABA) (Momiyama & Nishijo, 2017). Serotonin is stored in secretory granule of nerve terminals until it is released due to environmental stimuli. After releasing into synaptic cleft it binds to G-protein coupled receptors regulating different function of brain. Serotonergic neurons connect cerebral cortex, striatum, thalamus, midbrain dopaminergic nuclei with septum, hippocampus, hypothalamus and other limbic area (Baou et al., 2016). Inhibition of proper functioning of serotonin cascade results in occurrence of symptoms like hallucinations, altered cognition, delusions and paranoia (Dackis & Gold, 2018).
Question 2. Describe the clinical nursing care and interventions for a person with psychotic depression who is first admitted to hospital (i.e. the first 24 hours).
Answer 2. Patient with psychotic depression when admitted to a hospital, the first line of treatment given is administering medication to the patient. Drugs are administered to the patient which work by modifying the pathway of specific neurotransmitters (Voineskos et al., 2020). These drugs are given in order to provide a fast relief in the symptoms of psychotic depression. Then antidepressants are administered to the patient as second line of treatment. Antidepressants are not administered as the first line of action as they can give adverse effects in some patients with psychotic depression. Some of the examples of these depressants are amitriptyline and amoxapine. This problem was associated with older antidepressants and prescribing new antideprassants can overcome this problem. But the mode of action of the newly marketed antidepressant is not known. Examples include bupropion and mirtazapine. So most of the hospitals refrain from using them on such patients due to adverse effects (Shiwaku, Fujita & Takahashi, 2020). Along with medication patient is provided with self-care and hygiene of the patient is maintained. Patient is encouraged to eat a healthy diet which will also help in improving the effect of overall treatment. Patient is provided environment to feel comfortable like back rubs at bed time to improve their sleep cycle. When the patient starts to feel energetic again certain physical activities are planned for them. Active communication with the patient is established by observing several physical activities of the patient and they are also encouraged to get involved in the conversation equally. Laugh with the patient in order to make her realize the value of happiness and being happy. Conversations at slow pace are carried out in order to provide time to the patient to respond as her nervous system becomes slow. A well designated routine is designed for the patient. Patient is educated about the methods to use for overcoming the symptoms of psychotic depression. They are taught to express their feelings and involve themselves in the activities that make them feel good as a method to ease down their symptoms. Help patient in overcoming from their delusions. The patient is examined for suicidal tendencies by asking them different set of questions. It needs to be performed as patients with psychotic depression have higher tendencies towards committing suicide. The medication of the patient is adjusted based on their symptoms in adverse conditions. The above mentioned non-pharmacological interventions to the patient suffering with psychotic depression will alleviate his happiness and will enhance the effectiveness of pharmacological treatment by improving the activity of brain. In long term treatment of the disorder consultation with the psychiatrist should be prescribed. In addition to consultation, electroconvulsive therapy and simulation techniques can be used for the treatment of the patient.
Question 3. Discuss the pharmacological and non-pharmacological interventions that can assist Viva to alleviate her symptoms as described in the case study above.
Answer 3. The patient in the case study is already administered anti-depressants and they have proven to be ineffective in her case. In most of the cases of psychotic depression it has been found that anti-depressants simply do not work or either worsens the symptoms of the patient as similar observations can be drawn from the case study (Cowen, 2019). This is the reason why doctors use anti-depressant only if it is necessary but as the second line of treatment. Several studies have been conducted in this regard to enhance the efficiency of the treatment (Gobbi et al., 2018). A combinational intervention has been proposed to provide a more efficient treatment. It involves administering anti-depressant along with anti-psychotics to the patient (Wijkstra et al., 2017). The same treatment can be used for the patient in the case study as it has proven to be more effective. Ketamine which is a receptor antagonist has been used in patient who shows resistance to the treatment of depression. It works more efficiently than the anti-depressant as it displays anti-depressant effect by using different pathways like dendritic morphogenesis, alpha-amino-3-hydroxy-5-methyl-1-4-isoxazolepropionic acid activation and opioid receptor agonism (C. Andrade, 2017). So, it can be administered to the patient in the case study as an effective treatment. It will benefit her by reducing the anxiety and overcoming the feeling of committing suicide.
Patients with psychotic depression disorder have cognitive dysfunction which interferes with their functional recovery. It has been reported that cognitive dysfunction is more severe in case of psychotic depression when compared to non-psychotic depression. So, cognitive function has been used as a non-pharmacological intervention to the patient with psychotic depression. Its efficiency has been demonstrated in a study reported by MacQueen and Memedovish (MacQueen & Memedovich, 2017). The cognitive function of a patient can be improved non-pharmacologically by involving them actively in the activities that involve mental exercises. They can be assigned tasks which require thinking. This method has been demonstrated to be successful in improving the cognitive function of patient. So, this method can also be used for patient in the case study (Morimoto, Manning, Kim & Cote, 2018). This method will subsidize the feeling of being worthless in Sally and improvement in cognitive function will enhance the effectiveness of her overall treatment of psychotic depression.
References for The Pharmacological Treatment of Resistant Depression
Andrade, C. (2017). Ketamine for depression, 2: diagnostic and contextual indications. The Journal of Clinical Psychiatry, 78(5), 555-558.
Andrade, E. H., Rizzo, L. B., Noto, C., Ota, V. K., Gadelha, A., Daruy-Filho, L., Tasso, B. d. C., Mansur, R. B., Cordeiro, Q., & Belangero, S. I. (2016). Hair cortisol in drug-naïve first-episode individuals with psychosis. Brazilian Journal of Psychiatry, 38(1), 11-16.
Baou, M., Boumba, V. A., Petrikis, P., Rallis, G., Vougiouklakis, T., & Mavreas, V. (2016). A review of genetic alterations in the serotonin pathway and their correlation with psychotic diseases and response to atypical antipsychotics. Schizophrenia research, 170(1), 18-29.
chun Li, Y., xing Zheng, X., zhe Xia, S., Li, Y., huan Deng, H., Wang, X., wei Chen, Y., song Yue, Y., He, J., & jun Cao, Y. (2020). Paeoniflorin ameliorates depressive-like behavior in prenatally stressed offspring by restoring the HPA axis-and glucocorticoid receptor-associated dysfunction. Journal of Affective Disorders.
Ciccarelli, M., Sorriento, D., Coscioni, E., Iaccarino, G., & Santulli, G. (2017). Adrenergic receptors Endocrinology of the Heart in Health and Disease (pp. 285-315): Elsevier.
Cowen, P. J. (2019). The pharmacological treatment of resistant depression–an overview.
Dackis, C. A., & Gold, M. S. (2018). The serotonin subtype of depression. Advances in Psychopharmacology: Improving Treatment Response, 107.
Ehsan, S., Ghasemi, M., & Nasrin, M. (2020). Norepinephrine, neurodevelopment and behavior. Neurochemistry International, 104706.
Fröhlich, E., & Wahl, R. (2019). The forgotten effects of thyrotropin-releasing hormone: Metabolic functions and medical applications. Frontiers in Neuroendocrinology, 52, 29-43. doi: https://doi.org/10.1016/j.yfrne.2018.06.006
Gobbi, G., Ghabrash, M. F., Nuñez, N., Tabaka, J., Di Sante, J., Saint-Laurent, M., Vida, S., Kolivakis, T., Low, N., & Cervantes, P. (2018). Antidepressant combination versus antidepressants plus second-generation antipsychotic augmentation in treatment-resistant unipolar depression. International Clinical Psychopharmacology, 33(1), 34-43.
MacQueen, G. M., & Memedovich, K. A. (2017). Cognitive dysfunction in major depression and bipolar disorder: A ssessment and treatment options. Psychiatry and Clinical Neurosciences, 71(1), 18-27.
Maletic, V., Eramo, A., Gwin, K., Offord, S. J., & Duffy, R. A. (2017). The role of norepinephrine and its α-adrenergic receptors in the pathophysiology and treatment of major depressive disorder and schizophrenia: a systematic review. Frontiers in Psychiatry, 8, 42.
Marazziti, D. (2017). Understanding the role of serotonin in psychiatric diseases. F1000Research, 6, 180-180. doi: 10.12688/f1000research.10094.1
Meijer, O. C., & de Kloet, E. R. (2017). A refill for the brain mineralocorticoid receptor: the benefit of cortisol add-on to dexamethasone therapy. Endocrinology, 158(3), 448-454.
Momiyama, T., & Nishijo, T. (2017). Dopamine and serotonin-induced modulation of GABAergic and glutamatergic transmission in the striatum and basal forebrain. Frontiers in Neuroanatomy, 11, 42.
Morimoto, S. S., Manning, K. J., Kim, J. U., & Cote, S. E. (2018). Non-Pharmacological Cognitive Remediation Strategies for Treatment of Depression and Cognitive Impairment. Current Behavioral Neuroscience Reports, 5(3), 198-209.
Nandam, L. S., Brazel, M., Zhou, M., & Jhaveri, D. J. (2020). Cortisol and Major Depressive Disorder—Translating Findings From Humans to Animal Models and Back. Frontiers in Psychiatry, 10, 974.
Sheffler, Z. M., Reddy, V., & Pillarisetty, L. S. (2020). Physiology, Neurotransmitters StatPearls [Internet]: StatPearls Publishing.
Shiwaku, H., Fujita, M., & Takahashi, H. (2020). Benzodiazepines Reduce Relapse and Recurrence Rates in Patients with Psychotic Depression. Journal of Clinical Medicine, 9(6), 1938.
Söder, E., Clamor, A., & Lincoln, T. M. (2019). Hair cortisol concentrations as an indicator of potential HPA axis hyperactivation in risk for psychosis. Schizophrenia Research, 212, 54-61.
Szpunar, M. J., & Parry, B. L. (2018). A systematic review of cortisol, thyroid-stimulating hormone, and prolactin in peripartum women with major depression. Archives of Women's Mental Health, 21(2), 149-161.
Voineskos, A. N., Mulsant, B. H., Dickie, E. W., Neufeld, N. H., Rothschild, A. J., Whyte, E. M., Meyers, B. S., Alexopoulos, G. S., Hoptman, M. J., & Lerch, J. P. (2020). Effects of Antipsychotic Medication on Brain Structure in Patients With Major Depressive Disorder and Psychotic Features: Neuroimaging Findings in the Context of a Randomized Placebo-Controlled Clinical Trial. JAMA Psychiatry.
Wijkstra, J., Lijmer, J., Burger, H., Cipriani, A., Geddes, J., & Nolen, W. A. (2017). Pharmacological treatment for psychotic depression. BJPsych Advances, 23(1), 2-2.
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