Hypertrophic Prostate and Gastro-Oesophageal Reflux Disease

Question: Describe about the Hypertrophic Prostate and Gastro-Oesophageal Reflux Disease. Answer: Introduction The case of choice is that involving Mr Reginald Bowen, a 76-year-old former train driver living alone. He has a previous history of Benign Hypertrophic Prostate and Gastro-Oesophageal Reflux Disease (GORD) which are being managed by oral Omeprazole and Prostate Health Saw Palmetto 3200mg. Furthermore, his wife, Marjorie is at the Golden Oaks Nursing home for high care accommodation due to her age, and it worries Mr Bowen so much since he has been visiting her on a daily basis. The major complaints in the past 24 hours include severe abdominal pain, headache, lethargy, diarrhoea, vomiting and urinary retention. Based on the laboratory results, two faecal specimens were confirmed to contain nucleic acids of Noroviruses leading to a diagnosis of gastroenteritis. Gastroenteritis is an inflammation of the intestines and the stomach that is caused by various agents like bacteria and viruses, in this case, Norovirus (Bruggink, Dunbar Marshall 2016, pp.1521-1528). He is on an age pension a nd does not have any private health cover. Part A of this paper seeks to explore Mr Bowens anatomy and physiology in relation to gastroenteritis, its microbial mechanism and pathophysiology. Moreover, part B examines the nursing considerations and precautions in handling the case, two essential and priority problems of Mr Bowen and the evidence-based nursing interventions in the management of the two problems. Anatomy and physiology related to Mr Bowen The Norovirus gastroenteritis affects Mr Bowens part of the digestive system. First off, the digestive system consists of accessory organs like the liver, tongue, teeth, gallbladder and pancreas, and the alimentary canal (Durisch and Mueller, 2014, pp.360-365). The canal is approximately 9 meters and extends from the mouth to the anus, and it is continuous with the skin. There are organs linked along the canal, and mainly the stomach and the intestines are involved in gastroenteritis. The stomach is a J-shaped large portion that is immediately below the diaphragm in the left hypochondriac, epigastric, and umbilical regions (Betts, n.d., pp.1521-1528). It has more abundant folded mucosa into rugae. Its function is for digestion where proteases are released as well as hydrochloric acid. Again, it helps in absorption of water in dehydration, drugs like aspirin, and amino acids among others. It also controls motility and secretion of gastric juices (Betts, n.d., pp.1521-1528). The small intestine is continuous with the pylorus. It is lined with mucosa and secretes digestive juices and hormones like cholecystokinin, secretin, gastric inhibitory peptide, motilin, somatostatin, lactase and sucrase among other disaccharides (Betts, n.d., pp.1521-1528). Microbiology The Noroviruses are categorised under the Caliciviruses. Among the four types of caliciviruses, Noroviruses are the most significant in humans. They have a single strand and are RNA viruses that are positive-sense (Durisch and Mueller, 2014, pp.360-365). They have proved to be difficult to understand because of the inability to grow in a well-structured cell culture system. The best-known type of Noroviruses is the Norwalk virus that was an outbreak at an elementary school in Ohios Norwalk in 1968 (Shepherd 2011, p.4). It consists a single strand of RNA as the primary genetic material with kilobases of between 7.3 and 7.7. Around it, there are multiple copies of a protein that is unique, and it is gathered to an outer protective layer known as a capsid (Shepherd 2011, p.4). Additionally, the virus encodes Open Reading frames (ORFs) and specifically three. The largest is ORF 1 that has around 1700 amino acids. Its expression is a polyprotein precursor that is non-structural cleaved by a protease that is 3C-like. The second ORF encodes the capsid of the virus and it has approximately 500 amino acids. It also has the domains that are protruding and has a shell too. The third ORF encodes a protein that is small and basic whose function is not clearly known (Shepherd 2011, p.4). In addition, these factors make the virus very resistant to cold temperatures as well as high temperatures (White, 2014, pp.741-745). Also, disinfection does not eliminate it. Most of the viruses that are non-enveloped exhibit these characteristics making it difficult for elimination and prevention of reinfections (Nims and Plavsic, 2013, pp.358-392). The pathophysiology involved. Noroviruses are transmitted from an individual to the other through faecal-oral route, aerosols or direct contact (Whyte and Jenkins, 2012, pp.443-447). Fifty virions are enough to cause a fever, and they are very stable resisting both low and a high temperature of up to 60 degrees Celsius (Whyte and Jenkins, 2012, pp.443-447). The various forms of disinfection are also tolerated, from the use of chlorine, alcohol, vinegar, and even high concentrations of sugar. The period of incubation is approximately a day or two, and one two three-day lasting symptoms are exhibited (Whyte and Jenkins, 2012, pp.443-447). Viral shedding happens in 3 weeks after infection. The viruses attach the polymorphic histoblood group antigens (HBGAs) which supposedly serve as cofactors and receptors for infection. Their strains vary thus binding different HBGAs like A and O confirming the reinfection rates that may occur. Additionally, the lack of long-term immunity or cross-strain also contributes to the reinfection (White, 2014, pp.741-745). The norovirus affects the GIT in one way but the physiological responses of the body are varied. In the small intestines, the noroviruses damage the microvilli by releasing toxins that interrupt the transport of ions at the brush border cells causing problems of permeability (Bruggink, Dunbar and Marshall, 2016, pp.1521-1528). However, they leave an intact epithelium and mucosa, an investigation can reveal this phenomenon. Furthermore, the microvilli damage causes fat mal-absorption and D-xylose, with a dysfunction of enzymes at the brush border cells. Moreover, the damage causes the secretion of anions and a leak flux (White, 2014, pp.741-745). These changes trigger diarrhoea. The delayed emptying of the stomach and the virus-mediated variations in the gastric motility cause diarrhoea as well (White, 2014, pp.741-745). There is no invasion of the large intestines by the noroviruses hence there are no faecal leukocytes. Haematochezia rarely occurs (Whyte and Jenkins, 2012, pp.443-447). Reference list Anon, (2016). [online] Available at: https://www.sahealth.sa.gov.au/wps/wcm/connect/7dbceb80436716e69dd1dfc9302c1003/Gastro-guidelines-residential-environments_V2.0-cdcb-ics-20160401.pdf?MOD=AJPERESCACHEID=7dbceb80436716e69dd1dfc9302c1003 [Accessed 19 Sep. 2016]. Anon, (2016). [online] Available at: https://www.sahealth.sa.gov.au/wps/wcm/connect/public+content/sa+health+internet/clinical+resources/clinical+topics/clinical+handover/isbar+-+identify+situation+background+assessment+and+recommendation [Accessed 19 Sep. 2016]. Betts, J. 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