S/O MR.C.S.SHEKAR
#1003, 1ST BLOCK,
JANAPRIYA HEAVENS, GKVK POST
ALLALSANDRA,
BANGALORE- 560 065.
2. / NAME OF THE INISTITUTION / M.S RAMAIAH INSTITUTE OF
NURSING EDUCATION AND
RESEARCH
M.S.R.I.T.POST
BANGALORE-560054
3. / COURSE OF STUDY AND
SUBJECT / M.Sc NURSING (1ST YEAR)
MEDICAL SURGICAL NURSING
DISSERTATION PROTOCOL
4. / DATE OF ADMISSION TO
COURSE / 14-07-2008
5. / TITLE OF THE TOPIC:
EFFECTIVENESS OF PLANNED TEACHING PROGRAMME ON KNOWLEDGE REGARDING HOME CARE AMONG PATIENTS WITH GASTRITIS AT SELECTED HOSPITALS, BANGALORE.
RajivGandhiUniversity of Health Science, Karnataka,
Bangalore
ANNEXURE- II
PROFORMA FOR REGISTRATION OF SUBJECTS FOR
DISSERTATION
6. BRIEF RESUME OF INTENDED WORK
INTRODUCTION:
"Every human being is the author of his own health”
…. Buddha
Health is a concept that includes physical, mental, emotional, sand spiritual well-being.HistoricallyHealth was defined as the process through which a person seeks to maintain an equilibrium that promotes stability and comfort, is a dynamic process that varies according to a person’s perception of well-being1.
Wellness is the conditionin which an individual functions at optimal levels.Illness is the inability of an individual’s adaptive responses to maintain physical and emotional balance that subsequently results in an impairment of functional abilities. It is easier to measure illness than it is to measure wellness because definite parameters can be used to determine whether and individual has symptoms indicative of disease processes1.
Gastrointestinal system plays a vital role in maintaining ones health. It has the critical task of supplying essential nutrients to fuel the brain, heart, lungs and other organs ad tissues1. The GI system comprises the alimentary canal and its accessory organs, beginning at the mouth; extending through the pharynx, oesophagus, stomach, small intestine, colon, rectum, and anal canal; and ending at the anus.The GI system is responsible for the following essential bodily functions: ingestion and propulsion of food, mechanical and chemical digestion of food, absorption of nutrients into the bloodstream, and the storage and elimination of waste products from the body through feces2.
A malfunction in the GI tract or in one of the accessory GI organs can produce far-reaching metabolic effects, eventually threatening life itself. GI function also profoundly affects the quality of life by its impact on overall health1.
Gastritis is an inflammatory process of the mucosal lining of the stomach. The inflammationmay be contained within one region or be patchy in many areas. Gastric structure and functionare altered in either the epithelial or the glandular components of the gastric mucosa. The inflammationis usually limited to the mucosa, but some forms involve the deeper layers of the gastricwall. Gastritis is classified into acute and chronic forms3.
Acute gastritisis the most common form of acute gastritis is acute hemorrhagic gastritis, also called acute erosive gastritis. The gastric erosions are limited to the mucosa, which have edema and sites of bleeding. Erosions can be diffuse throughout the stomach or localized to the antrum.Acute gastritis is caused by Alcohol abuse or ingestion of aspirin or nonsteroidal anti-inflammatorydrugs (NSAIDs) are the most common causes. Other causes are steroid or digitalis medications;ingestion of corrosive agents such as lye or drain cleaners; ingestion of excessive amounts of tea,coffee, mustard, cloves, paprika, or pepper; chemotherapy or radiation to the upper abdomen;severe stress that is related to critical illness; staphylococcus food poisoning; infections (candida,cytomegalovirus, herpes virus) in immunosuppressed patients3.
Chronic gastritisdevelops gradually and is more likely to cause a dull pain and a feeling of fullness or loss of appetite after a few bites of food. The three forms of chronic inflammation of the gastric mucosa are superficial gastritis,atrophic gastritis, and gastric atrophy. Superficial gastritis, the initial stage in the developmentof chronic gastritis, leads to red, edematous surface epithelium, small erosions, anddecreased mucus content. The gastric glands remain normal. With atrophic gastritis, inflammationextends deeper into the gland area of the mucosa with loss of parietal and chief cells2, 3.Atrophic gastritis further develops into the final stage of chronic gastritis—gastric atrophy. Inthis stage, there is a total loss of glandular structure.Chronic gastritis has also been classified as type A and type B. Type A chronic gastritis, theless common form, involves the body of the stomach (fundus) rather than the antrum. Type Bgastritis is a more common nonautoimmune inflammation of the lining of the stomach. It primarilyinvolves the antrum but can affect the entire stomach as age increases. Patients withchronic gastritis have an increased risk (10%) for gastric cancer or may develop chronic irondeficiency.Untreated gastritis can also lead to hemorrhage and shock, gastric perforation, gastrointestinal(GI) obstruction, and peritonitis. The primary causes for Type A gastritis is considered primarily an autoimmune disorder.The primary cause of type B gastritis is H. pylori, which is found in nearly 100% of the cases oftype B gastritis. In both acute and chronic type B gastritis, the normal gastric mucosal barrier isdisrupted, which leads to mucosal injury3.
The immediate treatment for acute gastritis is directed toward alleviating the symptoms andwithdrawing the causative agents. The physician usually prescribes an H2 antagonist. The medicalgoal is to maintain the pH of gastric contents above 4.0. Acute hemorrhagic gastritis maydisappear within 48 hours because of rapid cell proliferation and restoration of gastric mucosa.If the bleeding is profuse and persistent, blood replacement is necessary. An infusion of vasopressin(Pitressin) or embolization of the left gastric artery is used to halt hemorrhage. Surgicalintervention is not performed unless hemorrhage is uncontrollable. In this rare situation, vagotomywith pyloroplasty is usually performed.There is no known treatment that will reverse the pathogenesis of chronic gastritis. Eradicationof H. pylori bacteria halts active gastritis in approximately 92% of the cases unless there ispermanent damage to the gastric epithelium. The medical regimen for eradicating H. pylori is acombination of bismuth salts and two antibiotics over a 2-week period. An important part ofmanagement of patients with chronic gastritis is long-term follow-up for early detection of gastriccancer. Patients who have either chronic type A or B gastritis may develop perniciousanemia; destruction of parietal cells in the fundus and body of the stomach leads to inadequatevitamin B12 absorption2, 3.
Independent cares for gastritis are to Encourage the patient to avoid aspirin and NSAIDs (indomethacin and ibuprofen) unless theyhave been prescribed. Reinforce the need to take these medications with food or to take enteric coatedaspirin. Other drugs that may contribute to gastric irritation include chemotherapeuticagents, corticosteroids, and erythromycin. Explain the importance of reading the labels of OTCdrugs to identify those that contain aspirin. Instruct the patient about the action, dosage, and frequencyof the medications (antacids, H2 antagonists, antibiotic regimen) that are administeredwhile the patient is in the hospital. Discuss the possible complications that can develop withacute or chronic gastritis (hemorrhage, pernicious anemia, iron deficiency anemia, or gastriccancer). Explain the pathophysiology and treatment of each possible complication. Discuss howingestion of caffeine and spicy foods results in irritation and inflammation of the mucosa of thestomach3.
Be sure the patient understands how smoking and alcohol aggravate gastritis and thatabstaining from both will facilitate healing and reduce recurrence. Provide information aboutvarious smoking and alcohol rehabilitation programs available in the community. Explain therationale for the need for support during this very difficult lifestyle change for permanentabstinence3.
Assist the patient in identifying her or his personal physical and emotional stressors. Reviewcoping skills that the patient has used previously to change behaviors. Talk about how to adaptthe environment to which the patient must return in order to meet the needs of lifestyle changes.Involve the family in assisting with the patient’s needed changes. Assess the family’s responseand ability to cope.
Home health care for patients with gastritis are to instruct the patient to avoid caffeine drinks, hot and spicy foods, identified aggravating foods,alcohol, smoking, salicylates, and NSAID OTC drugs. Provide a written list of symptoms ofGI bleeding and pernicious anemia (weakness, sore tongue, numbness and tingling in theextremities, anorexia, weight loss, angina, shortness of breath, palpitations). Inform thepatient of the need for lifetime vitamin B12 intramuscular injections if pernicious anemiadevelops. Reinforce the need for follow-up for early detection testing for gastric cancer.Review medication action, dosage, frequency, and side effects. Make referrals to smoking andalcohol cessation programs of the patient’s choice. Reinforce relaxation exercises and stressmanagement techniques3.
In some cases, gastritis can lead to ulcers and an increased of stomach cancer1. For most people, however, gastritis isn't serious and improves quickly with treatment but the recurrence is faster without proper homecare. Hence home care is an essential part in managing gastritis and preventing gastric cancer3.
6.1 NEED FOR THE STUDY
According to National Digestive Diseases Information Clearinghouse (USA)global prevalence of all digestive diseases were 60 to 70 million people (1996)4 with the mortality of 2,34,000(2002)5, 14 million hospitalization that is 9% of all cases(2002)6, 45 million ambulatory care visits(2000)7 and costing $107,000 billion (1992) for diagnosis and treatment7.
National Digestive Diseases Information Clearinghouse states global prevalence of gastritis and nonulcer dyspepsia was 3.7 million people and 6.4 million people respectively (1996) with the global incidence of gastritis, chronic nonulcer disease and acute nonulcer disease was 3,13,000., 4,44,000 and 8.0million new cases every year(1975) respectively, with the mortality rate from gastritis alone was 375 (2002)8 and causing disability in 30,000 people (1990–1992)7 who had gastritis and with an ambulatory care visits of 2.9 million per year (2000)6.
According to world health statistics 2008 by world health organisation Noncommunicable conditions will cause over three quarters of alldeaths in 2030 and gastric cancer rank will raise from 18 (2004) to 9th rank by 2030 with death percentage of 1.9 9.Gastric cancer is also increased in the 1–2%of people over 60 years old who develop autoimmunegastritis with loss of parietal cells due to the productionof serum autoantibodies against gastric HþKþ-ATPase,the parietal cell proton pump10.
Recent evidence from World Bank and WHO (cited in the publication Global Burden of Disease) studies show that alcohol-related Gastritis and acid peptic disease:Although alcohol isabsorbed mainly from the small intestine, the directeffect on the lining of the stomach leads to its damage called acute gastritis. Attacks of acute gastritis often lead to vomiting and usually occur with instances of heavydrinking. Repeated bouts of acute gastritis can occur inexcess alcohol consumers and is aggravated by theneglect of food. Repeated damage to the lining of thestomach leads to hyperacidity and is called acid pepticdisease9.
0.65% (83,242) of hospital consultant episodes were for gastritis and duodenitis, out of which 85% required hospital admission, 17% required emergency hospital admission ,the mean length of stay in hospitals was 6.4 days and 0.18% (94,063) of hospital bed days were for gastritis and duodenitis in England 2002-03 (Hospital Episode Statistics, Department of Health, England, 2002-03)13.Hospitalizations for gastritis and duodenitis at public hospitals occurred in 7.8 people per 10,000 population in Australia 2001-02 (Australian Hospital Data, AIHW, Australia, 2001-02)11.
Prevalence rate by Country for gastritis:
(Digestive diseases in the United States: Epidemiology and Impact – NIH Publication No. 94-1447, NIDDK, 2004)11
Country/Region / Extrapolated Prevalence / Population Estimated UsedUSA / 2,914,961 / 293,655,4051
Ireland / 39,403 / 3,969,5582
United Kingdom / 598,275 / 60,270,7082
China / 12,892,972 / 1,298,847,6242
Bangladesh / 1,403,012 / 141,340,4762
Bhutan / 21,694 / 2,185,5692
India / 10,572,391 / 1,065,070,6072
Pakistan / 1,580,257 / 159,196,3362
Sri Lanka / 197,588 / 19,905,1652
South Africa / 441,216 / 44,448,4702
Australia / 197,667 / 19,913,1442
New Zealand / 39,644 / 3,993,8172
Nurses play animportant role in patient education, particularly in relationto medication, diet, prevention, compliance withtreatment, and treatment side effects of gastritis12.Hence student researcher felt it is very important to teach regarding home care and prevent gastritis which further prevents the gastric cancer which will be the 9th ranked disease by 2030 according to world health statistics 20089.
STATEMENTOF PROBLEM
A Study to Assess the Effectiveness of Planned Teaching Programme on Knowledge Regarding Home Care among Patients with Gastritis at Selected Hospitals, Bangalore.
6.2 REVIEW OF LITERATURE
Review of literature is the key step in research process. Literature review of present study has been collected and presented under the following headings,
6.2.1General information about gastritis
6.2.2Causes of gastritis
6.2.3Diagnosis of gastritis
6.2.4Treatment of gastritis
6.2.5Home care and prevention of gastritis
A study carried out on Helicobacter pylori Eradication in Patients on Long-termTreatment With NSAIDs Reduces the Severity of GastritisA Randomized Controlledtrial using experimental research design on 305 patients were eligible for inclusion ifthey were on long-termNSAIDs and were H. pylori-positive on serologic testing and Gastritis was assessed according to the updated Sydney classification for activity, chronic inflammation, gastric glandularatrophy, intestinal metaplasia, and H. pylori density and found that 48% were on chronic gastro protectivemedication. Significant less active gastritis, inflammation, andH. pylori density was found in the eradication group comparedwith the placebo group in both corpus and antrum (P<0.001).In the corpus, less atrophy was found in the eradication groupcompared with the placebogroup and concluded that H. pylori eradication in patients on long-term NSAID therapy leads to healing of gastritis despite ongoingNSAID therapy13.
A Meta analysis was carried out on Helicobacter pylori is a risk factor for peptic ulcer disease incirrhotic patients at CochraneCentre;Barcelona, Spain using meta analysis design on 976 patients with cirrhosis and data were collected by extensive MEDLINE search ofthe literature was performed. Studies reporting theprevalence of H. pylori infection in cirrhotic patients withand without ulcers were selected. The findings of the study were seven studies with a total of976 patients with cirrhosis (275 cases with ulcer diseaseand 701 controls). The prevalence of H. pylori infection inpatients with peptic ulcer disease was higher than in thosewithout. The pooled odds ratio was 2.70 (95% CI, 1.91–3.82). H. pylori infection was associated more or lessequally with duodenal and gastric ulcers and concluded that H. pylori infection increases the risk of pepticulcer disease in patients with cirrhosis14.
A study conducted on Helicobacter pylori impairs iron absorption in infected individuals at University of Naples, Italyusing experimental research design on 55 subjects who underwent gastro endoscopy and data were collected using laboratory findings and found that H. pylori-positive subjects had lower serum level of ferritin and lower delta iron compared to H. pylori-negative subjects. That difference is significant in anaemic women and is independent of the presence of serum anti-CagA antibodies. After H. pylori eradication iron absorption test was similar to those of non-infected subjects and concluded that H. pylori infection impairs iron uptake. That mechanism, together with others, may contribute to the depletion of iron ininfected patients15.
A study was carried out on Lymphocytic Gastritis and Celiac Disease in Indian Children: Evidence of a Positive Relation at Postgraduate Institute of Medical Education and Research, Chandigarh, India using experimental research design on 164 children with CD diagnosed between June 2003 and October 2005gastric and duodenal biopsies were performed simultaneously, were enrolled prospectively. The control group was composed of 164 children without CD, matched for sex and age, who w3eere undergoing upper digestive endoscopy. H pylori was searched for in gastric biopsy specimens sectioned and stained with haematoxylin and eosin, and a modified Giemsa stain for H pylori was performed for confirmation. The Student t test was used to compare quantitative measurements between groups and findings of the study were LG was found in 69 (42.1%) patients with CD. Positive cases had a mean of 43.9 +/- 1.5 intraepithelial lymphocytes per 100 surface epithelial cells, compared with a mean of 13.4 +/- 0.4 in negative cases and 7.8 +/- 0.5 in non-CD control children (P < 0.0001). Patients not showing LG did, however, show significantly increased gastric intraepithelial lymphocytes compared with the control children. Nine of 164 CD patients, and 4 of 69 patients with LG, had positive results for H pylori and concluded that pathogenetic relation between CD and LG. CD without LG also showed increased gastric intraepithelial lymphocytes. H pylori infection may be another cause of LG in children16.
Nurses play animportant role in patient education on home care, particularly in relationto medication, diet, prevention, compliance withtreatment, and treatment side effects. Regarding prevention the widespread detection and treatment of H. pylorias a preventive measure in gastritis has been discussedbut not resolved. Until more is known about the routes bywhich H. pylori is spread, specific prevention recommendationscannot be made. Erosive gastritis fromNSAIDs can be prevented by discontinuing the use ofthese drugs. In 1998 an education campaign waslaunched to educate people, particularly an aging populationof arthritis sufferers, about the risk of ulcers fromNSAIDs and alternative drugs. As of 2001 the success ofthis campaign had not been evaluated11.
A study conducted on Immunohistochemical expression of Fhit protein inHelicobacter pylori related chronic gastritis, gastricprecancerous lesions and gastric carcinoma: correlation withconventional clinicopathologic parameters at volos general hospital, Greece using descriptive research design on 76 patients with chronic gastritis of which 33 patients had h.pylori infection by ramdom sampling technique data were collected by laboratory and histological studies. The major findings of the study were 79% of H. pylori related gastritidesshowed that the Fhit protein was either completely absentor there was a marked reduction of immunostaining.Similar results were obtained for 76.4% of cases of chronicgastritides with low and high-grade dysplasia, and 56% ofgastric adenocarcinomas. A negative result for Fhit proteinimmunostaining was strongly associated with H. pyloriinfection (P 0.0001) and with epithelial dysplasia(P 0.01) but not with intestinal metaplasia or degree ofactivity. Additionally, negative or reduced immunostainingfor Fhit was associated with the degree of dysplasia andprogress of a subset of these lesions to infiltratingadenocarcinoma (P 0.02). In gastric denocarcinomasnegative or weak immunostaining of the Fhit proteincorrelated with the histological grade (P 0.01) and clinicalstage of the disease (P 0.01) and concluded that irrespective ofhistological type, H.pylori can play an important role in the earlydevelopment and progression of some gastric cancers17.