Ulcerative colitis is defined as the disease that has been characterized with chronic inflammation in large bowel which is prevalent among people who are genetically susceptible and exposed to the potential environmental triggers (Genetic Home Reference, 2019). The complications result in swelling, irritation and ulcers in the large intestine. The various symptoms of ulcerative colitis are rectal pain, diarrhea, bleeding, abdominal pain, rectal pain severe weight loss, pus, fatigue and fever (Genetic Home Reference, 2019). It has been found that Eleanor has lost 9 kgs in the last two weeks. The structural and functional changes that have been occurred during the progression of ulcerative colitis results in severe weight loss among the patients. According to Elsherif, Alexakis and Mendall (2014), ulcerative colitis is an inflammatory disease which leads a catabolic generalized state. This is a disease that has been associated with the malabsorption of macronutrients and micronutrients in the body. Physiological impairment like dysfunctioning of epithelial barrier and impairment in absorptive transport mechanism results in impaired absorption and secretion of macronutrients and micronutrients in the body (Antoni, Nuding, WehkampampStange, 2014). This event results in the loss of electrolytes and water through a passive mechanism in the intestinal lumen. This leads to increased uptake of antigens in the lumen and results in enhanced mucosal membrane inflammation. The cascade of inflammation leads to stimulation of metric oxide synthase, cyclooxygenase, and Toll-like receptors and increased nitric oxide production (Mourad, BaradaampSaade, 2017). Event of expression of various immune cells leads to proinflammatory cytokine perpetuation and results in increased inflammation of mucosal membrane and dysfunctioning of epithelial barrier. Another underlying mechanism behind the malabsorption of nutrients is neutrophils crypts infiltration which results in the destruction of epithelial membrane destruction (Martini, Krug, Siegmund, Neurathamp Becker, 2017). Destruction of tight junctions of epithelial cells leads to barrier function impairment. In the case of ulcerative colitis, intercellular adhesion increases because of up-regulation of E-cadherin-catenin complex present in mucosa of inflamed bowel (Martini et al., 2017). This event results in epithelial cell death by the mechanism of apoptosis and leads to increased inflammation. The epithelial cell death results in the destruction of crypts integrity. The decrease in transepithelial resistance because of Fas ligand-mediated apoptosis on T84 cells is a mechanism contributes an increase in the flux of small molecules and restricted flux of larger molecules (LechugaampIvanov, 2017). This mechanism leads to malabsorption of macronutrients and micronutrients as well as the sever weight loss of Eleanor.
It has been found that Eleanor is encountering severe pain. Pain is defined as apperception of noxious stimulus that transmits along the central nervous system, peripheral nervous system and brain (Bullock amp Manias, 2013). The transmission of noxious stimuli information occurs in the periphery of the brain which results in the activation of nociceptors which are known as pain receptors (Bullock amp Manias, 2013). Then the impulse travels along sensory fibers (afferent) and via dorsal nerve roots. This event leads to the release of certain chemical mediators like kinins and prostaglandins (Bullock amp Manias, 2013). The peripheral afferent fiber ends in dorsal grey horns substantial gelatinosa and in the spinal cord, activation of spinothalamic tracts has occurred. The information travels and received by thalamus in order to transmit it for final processing in the cerebral cortex part where the conscious pain perception occurs. Morphine is an opioid that has been used as s single analgesic drug (Bullock amp Manias, 2013). The drug acts on the central nervous system and activates opioid receptors which are involved in the transmission of pain stimulus and its control. This activation leads to adenylate cyclase inhibition and reduction in the concentrations of cAMP, hyperpolarization of nerve membranes and potassium efflux promotion (Bullock amp Manias, 2013). This cascade results in the opening of voltage-gated calcium channels and inhibition of presynaptic transmitter release (Bullock amp Manias, 2013). Thus, morphine helps in the control of pain sensation that has been generated because of ulcerative colitis in Eleanor
The clinical manifestations that have been presented by Eleanor are diarrhea with mucus, pus and blood, weakness, fecal inconsistency, anorexia, weakness and fatigue. According to Thiagarajah, Donowitz and Verkman (2015), severe diarrhea is a clinical manifestation of ulcerative colitis which is caused due to the reduction in the process of absorption of colonic fluids. The mucus and pus in the feces of the patient suffering from ulcerative colitis is the indication of infection in large intestine (Crohns amp Colitis Foundation, 2019). In addition, the pus and mucus have been produced in the intestine because of open sore development as a consequence of inner lining inflammation of colon. According to Lillis (2018), the increase in sensitivity of colon as a result of inflammation cause pushing of stool and fecal inconsistency in the patients having the complication of ulcerative colitis. In addition, fear of abdominal cramps and pain after eating, vomiting, nausea results in complications of anorexia among the patients of ulcerative colitis (Johns Hopkins Medicines, n.d.). It has been reported that continuous diarrhea and inadequate intake of food results in weakness and fatigue in the patients.
From the case study, it has been revealed that the fluid that has been prescribed to Eleanor is Hartmanns solution 1000 ml over 6 hours. The various components of Hartmanns solution are potassium chloride, sodium chloride, calcium chloride dihydrate and sodium lactate which are dissolved in water (EMC, 2018). Hartmanns solution is isotonic in nature with pH 5.0-7.0 and osmolarity of 278Osmol/L (EMC, 2018). The excessive calcium that has been present in the solution is extracted through the body via the renal system. It has been reported that it is an active source of electrolytes and water (HPRA, 2017). Fluid that has been present in Hartmanns solution facilitates effective restoration of electrolyte balance in the body because this solution contains multiple electrolytes along with alkalinizing agent such as sodium lactate (HPRA, 2017). This solution helps in effective maintenance of pH of the physiological system. It is an active source of bicarbonates which can help in the treatment of metabolic acidosis which is a potential consequence of potassium deficiency or dehydration in the body (EMC, 2018). Also, the calcium components that are present in the solution helps in maintain cell membrane integrity, capillary permeability and integrity of the nervous system (EMC, 2018).
Antoni, L., Nuding, S., Wehkamp, J., ampStange, E. F. (2014). Intestinal barrier in inflammatory bowel disease.World Journal of Gastroenterology WJG,20(5), 1165.
Bullock, S., amp Manias, E. (2013).Fundamentals of pharmacology. Pearson Higher Education AU.
Crohns amp Colitis Foundation. (2019). What is ulcerative colitis. Retrieved from https//www.crohnscolitisfoundation.org/what-are-crohns-and-colitis/what-is-ulcerative-colitis/Elsherif, Y., Alexakis, C., ampMendall, M. (2014). Determinants of weight loss prior to diagnosis in inflammatory bowel disease a retrospective observational study.Gastroenterology Research and Practice,2014.
EMC. (2018). Compound sodium lactate solution for infusion BP. Retrieved from https//www.medicines.org.uk/emc/product/1812/smpcGenetic Home Reference. (2019). Ulcerative Colitis. Retrieved from https//ghr.nlm.nih.gov/condition/ulcerative-colitisHPRA. (2017). Hartmanns solution for infusion. Retrieved from https//www.hpra.ie/img/uploaded/swedocuments/2148236.PA0566_030_003.0dd654ff-ba16-4252-af1d-4d307db99df1.000001Hartmans20Solution20PIL.170313.pdfJohns Hopkins Medicines. (n.d.). Crohns disease Introduction. Retrieved from https//www.hopkinsmedicine.org/gastroenterology_hepatology/_pdfs/small_large_intestine/crohns_disease.pdfLechuga, S., ampIvanov, A. I. (2017). Disruption of the epithelial barrier during intestinal inflammation Quest for new molecules and mechanisms.Biochimicaet Biophysica Acta (BBA)-Molecular Cell Research,1864(7), 1183-1194.
Lillis, C. (2018). Ulcerative colitis stool A visual guide. Retrieved from https//www.medicalnewstoday.com/articles/323436.phpMartini, E., Krug, S. M., Siegmund, B., Neurath, M. F., amp Becker, C. (2017). Mend your fences the epithelial barrier and its relationship with mucosal immunity in inflammatory bowel disease.Cellular and Molecular Gastroenterology and Hepatology,4(1), 33-46.
Mourad, F. H., Barada, K. A., ampSaade, N. E. (2017). Impairment of small intestinal function in ulcerative colitis role of enteric innervation.Journal of Crohns and Colitis,11(3), 369-377.
Thiagarajah, J. R., Donowitz, M., amp Verkman, A. S. (2015). Secretory diarrhoea mechanisms and emerging therapies.Nature Reviews Gastroenterology amp Hepatology,12(8), 446.
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