CHAPTER I BEGINNING 1.1 Background There are seven organ system in our body.

They are Respiration system, Cardiovascular system, Neurobehavior, Urinary and Reproduction system, Gastroenterology, uscle and Bone, and the last is !ndocrine and etabolic system. They "ork interratedly in our body #or human survival. $iseases o# the gastrointestinal system are commonly re#erred to as digestive diseases. The digestive system is composed o# the mouth, esophagus, stomach, and small large intestines, and the accessory organs o# digestion% liver, gallbladder, and pancreas. $igestive diseases are disorders or in#lammation o# any o# these organs. The site o# body&s digestive processes, the gastrointestinal 'G() system has the critical task o# suplying esential nutrients to #uel the brain, heart, and lungs. Gastrointestinal 'G() #uction also pro#oundly a##ect the *uality o# li#e by its impact on overall health. The importance o# digestive diseases and their implications #or health care have o#ten been minimi+ed. The group o# diseases involving the gastrointestinal tract vary #rom mild to severe. The chronicity o# the diseases and the symptoms can e##ect the person&s ability to maintain a desired li#e, style. -sychosocial stressors o#ten intensi#y the symptoms. 1.. This -aper /ill $iscuss 0bout 1...1 1o"&s the anatomy and physiology o# Gastrointestinal 'G()2 1.... /hat is the pathophysiology2 1...3 1o" do the types and classi#ication o# Gastritis2 1...4 /hat is the ethiology o# Gastritis2 1...5 /hat is the clinical appearances o# Gastritis2 1...6 /hat is the diagnostic assesment #or Gastritis2 1...7 /hat are the theraphy #or Gastritis patient2

1.3 Goal 1.3.1 To describe the anatomy and physiology o# Gastrointestinal 1.3.. To describe the pathophysiology 1.3.3 To describe the types and classi#ication o# Gastritis 1.3.4 To describe the etiology o# Gastritis 1.3.5 To describe the clinical appearances o# Gastritis 1.3.6 To describe the diagnostic assessment o# Gastritis 1.3.7 To describe the theraphy #or Gastritis patients.

CHAPTER II .

GASTRITIS ..1 0natomy and -hysiology o# Gastrointestinal 8ystem The gastrointestinal system consists o# the mouth, pharyn9, esophagus, stomach, and small and large intestines. 0ccessory organs include liver, gallbladder, and pancreas. The accessory organs #ound in the mouth are the teeth and salivary glands. The gastrointestinal system produces both e9ocrine and endocrine secretions. !9ocrine secretions prepare #ood #or absorption by diluting it to the osmolality o# plasma 'isotonic), altering the p1 #or hydrolysis, and hydroly+ing comple9 #oods. The e9ocrine secretions also protect the mucosa #rom physical and chemical irritants. !ndocrine secretions play a ma:or role in the control and coordination o# secretory and motor activities involved in the digestion and absorption o# #ood. ..1.1 outh The mouth, also re#erred to as the buccal cavity or the oral cavity, is commonly considered the beginning o# the gastrointestinal tract. echanical and chemical digestion begins in the mouth. The teeth and tongue aid in mechanical breakdo"n, "hereas the secretion o# the salivary glands begins basic starch digestion and lubricate #ood to aid in s"allo"ing. ..1.. 8alivary Glands The salivary glands consist o# the parotid, subma9illary, and sublingual glands. There are some small salivary glands #ound in the lips, buccal mucosa, and palate. The parotid gland is located anteriorly to the e9ternal ear and "raps around the mandible. The parotids are the largest o# the salivary glands; each "eighs appro9imately 14 to 3< g. The parotid gland produces ptyalin 'salivary amylase), "hich begin the chemical breakdo"n and starches.

The subma9illary gland is smaller, "eighing 7 to 1< g, and is located in#eriorly to the mylohyoid muscle. The subma9illary gland produces a mi9ture o# mucous and serous secretions. The sublingual glands are located beneath the #loor o# the mouth and "eigh appro9imately 3 g. The sublingual glands consist o# predominantly mucous acini "ith a #e" serous acini. The primary purpose o# the sublingual gland secretions is lubrication. ..1.3 =ropharyn9 The oropharyn9 is the midpoint o# the upper respiratory tract and digestive tract. The superior boundary is at a hori+ontal line that "ould connect the so#t palate "ith the second cervical vertebra. The in#erior line "ould connect hori+ontally the tip o# the epiglottis and the base o# the tongue. The nasopharyn9 lies bet"een the oropharyn9 and the hypopharyn9. The contents o# the oropharyn9 include the so#t palate, the uvula, the tonsils and their pillars, and the base o# the tongue. ..1.4 !sophagus The esophagus is a hollo" muscular tube appro9imately .5 cm in length. (t begins in the neck at the lo"er border o# the #i#th cervical vertebra and connects the hypopharyn9 to the cardia o# the stomach. =n each side o# the esophagus are the thyroid lobes and parathyroids. ..1.5 8"allo"ing $eglutition 's"allo"ing) can be divided into several phases. The #irst is voluntary, in "hich the tongue moves up"ard and back"ard, #orcing a bolus o# #ood into the pharyn9. The #ollo"ing phases are involuntary and involve trans#er and transport. Trans#er results in changes in the pharyngeal and upper esophagus, "hile transport involves the middle and lo"er esophagus. ..1.6 -eritoneal Cavity The abdomen is the largest cavity in the human body. The structure in the cavity are protected and covered by peritoneum,

"hich is made up o# serous membrane composed o# mesothelium and a thin layer o# irregular connective tissue. The parietal peritoneum is the tissue that lines the abdominal "all. The mesentery is a double #old o# parietal peritoneum that is #an shaped and encircles the :e:unum and ileum attaching them to the posterior abdominal "all. ..1.7 8tomach The #unction o# stomach is to alter the consistency and the composition o# ingested #oods. The ingested #oodstu##s are li*ui#ied into cyme as the stomach mi9es the material "ith gastric secretions. The cyme is then released in a regulated manner into the duodenum #or #urther digestion and absorption.

..1.> 8mall (ntestine The small intestine is divided into #our layers, mucosa 'innermost layer), submucosa, muscularis e9terna, and serosa 'outer layer). 0s in outer segments o# the gastrointestinal tract, the mucosa is separated #rom the submucosa by the muscularismucosae. The submucosa contains the connective tissue, lymphatics, blood vessels, and nerves. eissner&s ple9us in the submucosa. The muscularis e9terna consists o# an inner circular layer and an outer longitudinal layer. 0uerbach&s 'myenteric) ple9us lies bet"een the t"o muscle layers.

..1.? @arge (ntestine The colon is appro9imately 15< cm '4A to 5 #t) in length. The terminal ileum :oins the colon at the ileocecal valve. The appendi9 arises #rom the cecum medially, about . cm '1 inch) belo" the :unction o# the ileum and cecum. The cecum is continous "ith the ascending colon, "hich goes #rom the cecum to the undersur#ace o# the right lobe o# the liver. The colon then e9tends to the le#t, becoming the transverse colon. The transverse colon has a mesentery and there#ore a "ide range o# movement. The cecum, ascending colon, and pro9imal hal# o# the transverse colon are derived #rom the midgut. The innervations and vascular supply are shared "ith the small intestine. The transvers colon continues to the le#t and slightly up"ard, #orming the splenic #le9ure. The splenic #le9ure is slightly higher than the hepatic #le9ure and is in #ront o# and above the le#t kidney. 0s the colon turns do"n"ard, it becomes the descending colon. The sigmoid colons begins at the point "here the descending colon crosses the iliac artery at the rim o# the pelvis. The mesentery o# the sigmoid colon attaches it to the posterior 'retroperitoneal) "all o# the pelvis.near the midsacrum, the sigmoid colon becomes the rectum. The rectum descends in #ront o# the sacrum and coccy9. The upper portion o# the rectum is in the peritoneal cavity, but the distal 1. to 15 cm has no peritonel covering. This area loes behind the bladder in male "ith the seminal vesicles on either side. (n the #emale the distal 1. to 15 cm is #ound posterior to the uterus. The rectal ampulla is the lo"est part o# the rectum and is #oun anterior to the posterior aspect o# the prostate in the male. (n the #emale the rectal ampulla is attached to the posterior "all o# the vagina. The distal hal# o# the transverse colon, splenic #le9ure, descending sigmoid, and rectum are derived #rom the hindgut. The in#erior mesenteric artery supplies this portion o# the large

intestineand rectum. The nervous is innervations is #rom the sacral parasympathetic #ibers. The "all o# the colon is divided into the same #our layers as the small intestine% mucosa, submucosa, muscularis e9terna, and serosa. There are no villi #ound in the large intestine. The simple columnar epithelialsur #ace is #lat and is broken into polygonal units by cle#ts. Goblet cell openings are #ound on the epithelial sur#ace. (n the center o# polygonal units are crypts o# @ieberkuhn. 0t the bottom o# the crypts are proli#erating undi##erentiated epithelial cells and occasionally argenta##in cells. Cell rene"al begins in the crypts. The cells then migrate up"ard to the sur#ace and e9trude into the lumen. The mucosa, submucosa, and circular muscle layer #orm semilunar #olds dividing the haustra 'sacculations). The semilunar #olds are crescent shaped and e9tendone third o# the "ay around the "all o# the intestine. The longitudinal muscle layer is incomplete in the large colon. (t is called teniae coli and is noticeable band in the colon "all. Batty tags 'appendices epiplociae) pro:ect #rom the serosa coat o# the colon; this mark another di##erence bet"een the large and small intestine. The liver is the largest organ in the body, "eighting 1.4 to 1.> kg '3 to 4 lb). it is a comple9 organ "ith many #unctions, including the production o# bile, protein metabolism, carbohydrate metabolism, #at metabolism, coagulation, and deto9i#ication, ad storage o# certain minerals and vitamins. Be#ore e9amining the #unctions o# the liver, it is necessary to e9amine its anatomic structur, blood supply, and ductal system. The liver is located under the diaphragm in the upper right portion o# the abdominal cavity. The superior sur#ace o# the liver is under the right and le#t halves o# the diaphragm. The in#erior sur#ace is above '#rom the right to le#t) the hepatic #le9ure o# 6he

colon, the upper pole o# the right kidney, the #irst portion o# the duodenum, the in#erior vena cava, and the stomach. The liver normally e9tends #rom the #i#th intercostals space to :ust belo" the right costal margin. The liver is divided into t"o lobes "ith the right si9 times larger than the le#t in adult, and three times larger in in#ants. The #alci#orm ligament separates the lobes. The right lobe is #urther subdivided into *uadrate and caudate lobes. Riedel&s lobe is common accessory lobe on the right that is lateral on the gallbladder. This is #unctional as "ell as anatomic division o# the liver created by the #alci#orm ligament. The division is determined largely by the liver&s vascular supply. The liver has a dual blood supply% the portal vein and the hepatic artery. The portal vein brings nutrients #rom the gastrointestinal system, and the hepatic artery provides the arterial circulation. /ithin the liver, branches o# the hepatic artery, the portal vein, and bile ducts in the portal tract, described as the portal triad, accompany each other and empty into sinusoids. The portal vein is #ormed by the superior mesenteric vein also empties into this system. The portal vein has several tributaries, o# "hich the le#t gastric vein anastomoses "ith the esophageal veins, "hich empty into the vena cava. The liver is composed o# comple9 circulatory system involving the hepatic artery, portal vein, sinusoids, central vein, and hepatic vein. The biliary system includes the bile canaliculi. $uctules, hepatic duct, and common duct. There are several cell types present in the liver. The parenchymal cell, or hepatocyte, is the most important. The cemical actions that occur in the liver take place in the paren chymal cells. Cup##er 'reticuloendothelial) cells are those cells that line the sinusoids. ..1.1< Gallbladder

>

The gallbladder is a pear,shaped sac,6 to > cm '3 to 4 inches) long , and attached to the in#erior sur#ace o# the liver. (ts :oined to the billiary tree by the cystic duct at the point "here the hepatic duct becomes the common bile duct. The mucosa o# the gallbladder is columnar epithelium overlying a lamina propria. The mucosa is in multiple, irregular #olds that increase its absorptive area. The #ibromuscular layer #orm the #rame"ork o# the sac. (t is a mi9ture o# longitudinal smooth muscle #ibers and dense #ibous tissue. The #ibromuscular is covered by a subserous asdventitia. The seerous layer is continuous "ith the serosa o# the liver. ..1.11 -ancreas The pancreas an important accessory organ o# digestion, is located transversely across the posterior "all o# the abdomen. (t is about .< cm '1< inches) long and "eigths 6< to 16< g. the head o# the pancreas is situated in the concavity o# the duodenal loop on the right side o# then vertebral coloumn at the level o# the #irst lumbar vertebra. The body o# the pancreas e9tends le#t"ard and superiorly to the hilum o# the spleen. The terminal portion o# the pancreas is the tail. The pancreas resembles the salivary glands histologically. The di##erence bet"een the t"o is the presence o# islets o# langerhans "ithin the pancreas. The pancreas has both e9ocrine and endocrine #unctions. 0cinar cells secrete the e9ocrine product , bicarbonate and pancreatic en+yme, and the endocrine secretions o# insulin, glucagon , and gastrin are #rom the alpha , beta , and delta cells o# islets o# langerhans. The blood supply o# the pancreas is #orm the superior and in#erior pancreatiduodenal arteries and #rom branches o# the splenic artery. The venous #lo" #rom the body and tail o# the pancreas is through the splenicvein , and the head emptyes directly into the portal vein. The lymphatic system drains through the pancreatiduodenal nodes to the celiac nodes.

... -athophysiology Gastritis re#ers to any di##use lesion in the gastric mucosa that can be identi#ied histologically as in#lamed. Gastritis may occur as an acute or a chronic disorder and is more common in the eldery population. The ported incidence o# chronic gastritis associated "ith gastrointestinal bleeding has #luctuated over the last #e" years #rom 4<D to 1<D. This shi#t is probably related to success#ul utili+ation o# endoscopic diagnostic procedures. The incidence o# acute gastritis is undetermined e9cept "hen associated "ith gastrointestinal bleeding. 0cute gastritis is responsible #or 1<D to 3<D upper gastrointestinal bleeding. ..3 Types and Classi#ication 1. 0cute Gastritis 0cute gastritis is a short,lived in#lammatory process a##ecting the mucosa o# the stomach. (t involves erosion o# the mucosa. The mucosa is spotted "ith submucosal hemorrhages that resemble ecchymoses and may be round or linear. There may also be shallo" erosions that appear as bro"n spots or red petechiae or small breaks in the mucosa. The hemorrhagic erosions usually involved the glandular layer, are e9tremely shallo", and are #ound any"here in the stomach. 0cute gastritis is more common in gastric ulcer than duodenal ulcer. The di##erences bet"een gastritis erosion and gastric ulcer is that in erosion the muscularis mucosa is uninvolved and healing leaves no scar. The mechanicm that results in erosion and hemorrhage is a back di##usion o# hydrogen ions and mucosal ischemia. The disruption o# the gastric mucosal barrier allo"s the back di##usion o# the hydrogen ion, "hich stimulates the release o# vasoactive substance, increased capillary permeability and in#lammation. There are a number o# drugs , stimuli and circumstance associated "ith acute gastritis, including aspirin, anty,in#lammatory agents, alcohol, corticosteroids,ma:or physiologis stress, and instense emotional reactions.

1<

The most common cause o# acute super#icial gastritis is alcohol. 8tress ulcers are #orm o# acute gastritis. The term stress ulcer is actually a misnomer since the lesions are not ulcers. 8teroids appear to potentiate the action o# other #actors in acute gastritis. Nonsteroidal anti,in#lammatory agents used #or the treatment o# rheumatoid arthritis probably a##ect gastric mucosa because they "ork by inhibiting prostaglandin synthesis. -rostaglandins have a cytoprotective #unction on the gastric mucosa. (t appears that patient taking both nonsteroidal anti,in#lammatory agents and aspirin are at a greater risk #or bleeding #rom acute erosive gastritis. The treatment protocol #or the patient "ith rheumatoid arthritis is not stopped, but the patient "ill need to be observed and treated #or erosion as indicated. .. Chronic Gastritis Chronic gastritis is o#ten re#erred to as a nonerosive, nonspeci#ic gastritis that is #urther di##erentiated by the histologic appearance o# the gastric mucosa into super#icial gastritis, athropic gastritis, or gastric athropy. 8uper#icial gastritis is characteri+ed by an in#lammatory in#iltration o# the lamina propria. @ymphocytes, plasma cells, eisonophils are #ound in the outer one third o# the mucosa. The gastric glands are not involved. (n athropic gastritis there is loss o# #undic glands, parietal cells, and chie# cells. The muscularis mucosa is split and thickened, and marked in#lammation is present. Gastric athropy re#ers to marked or total glands loss "ith minimal in#lammation. The mucosa is thinned. T"o additional #eatures may be seen in three types o# chronic gastritis% intestinal metaplasia and pseudopyloric metaplasia. (ntestinal metaplasia is the replacement o# normal gastric cells by cells identical to those o# the normal small intestine. (ntestinal metaplasia in greater in more severe degrees o# gastric athropy. The sur#ace o# the normal stomach is columnar, "here as the small intestine has a prominent brush border and may contain goblet and -oneth&s cells. /hen intestinal metaplasia occur,

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the stomach ac*uires the appearance and the absorptive capacity seen in the small intestine. Cancer is much more likely to develop in intestinali+ed gastric mucosa in comparison to the rare instances o# carcinoma o# the intestinal epithelium in the small intestine. (n pseudopyloric metaplasia the normal #undic glands are replaced by clear,staining mucous glands that can not be distinguished #rom mucous glands in the antral gland or cardial glands mucosa. The replacement may be partial or total. $iagnosis o# pseudopyloric metaplasia is made by biopsy. (t is imperative that the location o# the biopsy be care#ully stated on pathology slips so that the pathologist does not mistake normal antral gland mucosa #or pseudopyloric metaplasia or vice versa. Chronic gastritis has also been divided into type 0 and type B. Type 0 gastritis involves the #undus. There are circulating parietal cell antibodies and high serum gastrin levels. -ernicious anemia evolves almost e9clusively #rom type 0 gastritis. The relationship o# the parietal cell antibodies and intrinsic #actor lends support #or the hypothesis that type 0 gastritis has an autoimmune background. Type B gastritis involves the #undus and the antrum. There is a lack o# parietal cell antibodies, and appro9imately 1< D o# patient "ith type B gastritis "ill have gastrin cell antibodies. (n type 0 gastritis, there is a marked reduction in acid secretion, hypergastrinemia, and eventually impaired vitamin B1. absorption. Type B has less reduction o# acid secretions, normal gastrin levels, and only rare impairment o# vitamin B1. absorption. 0s the mucosa o# the stomach changes "ith atrophy, the acid secretion is reduced, resulting in achlorhydria or hypochlorhydria. 0trophic gastritis and gastric atrophy as associated "ith an increase in gastric malignancies. There is a high rate o# cell death and increased cell turnover in atrophic gastritis. !vidence is available to document in the increased mucosal nuclear activity supporting the premalignant state. The highest mitotic rates are #ound in areas o# intestinal metaplasia.

1.

Eitamin B1. re#er to cyanocobalamin 'CN,Cbl). 1umans depend on dietary sources o# vitamin B1. provided by #oods o# animal origin. The animal daily re*uirement is <.6 to 1.. FgGd. the vitamin is stored in the liver. The liver stores o# vitamin B1. are su##icient to last 3 to 5 years. Under normal condition o# gastric acidity, dietary vitamin B 1. enter the :e:unum bound to proteins. -ancreatic protoases remove the protein, and the vitamin B1. binds "ith the intrinsic #actor, secreted in the stomach by parietal cells. (ntrinsic #actor is crucial to protect vitamin B1. #rom bacterial destruction. (n the distal ileum the intrinsic #actor vitamin B 1. comple9 attaches to speci#ic brush border reseptors. 0 p1 e*ual to or greater than 5.7 and the presence o# divalent cations, particularly calcium, are re*uired #or binding 'attachment). =nce vitamin B 1. enters in the cell, in binds "ith transcobalamin '((), a transport protein, and is carried to the liver. Eitamin B1. de#iciency is di##icult to detect early because o# the liver stores that continue to supply it. Conditions associated "ith vitamin B1. di#iciency o# pancreatic en+ymes. -rophylactic intramuscular in:ections o# vitamin B1. may be used to prevent the se*uelae associated "ith a vitamin B1. de#iciency. ..3 !tiology The etiology o# chronic gastritis caused many, mainly the #ollo"ing% 1. 0cute gastritis cause o# the continued #ailure to remove or cure is not timely, shall not be treated, it "ill repeatedly attack, and gradually progress to chronic gastritis. .. $rinking alcohol can caused gastric hyperemia, edema, and even erosion, i# long,term alcohol consumption, mucosal cells could be dehydration and precipitation, chronic gastric rusulting in#lammation, and the higher the concentration o# alcohol the stronger the e##ect. 3. Caused by smoking nicotine can stimulate gastric acid secretion, resulting local in#lammation, the nicotine in tobacco is derived

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#rom central nausea, vomiting, but also to accelerate intestinal peristalsis, causing digestive disorders. 4. $rugs over a long period o# clinical observation it is concluded, the #ollo"ing used o# drugs, aspirin, -henylbuta+one, prednisone, indomethacin, ibupro#en, can cause gastric mucosal lesions, i# the long,term e##ect on the gastric mucosa may cause chronic gastritis. 5. Control diet, or overeating, or too cold hot, or #re*uently eat certain spicy #ood 'such as chili, bamboo shoots, rice, apple, plum, peach, etc.), can cause chronic gastritis; long,term partial eclipse, the lack o# protein in #ood or vitamin B, also can cause chronic in#lammation o# gastric mucosa. 6. =ther diseases such as pulmonary heart disease, liver cirrhosis, portal hypertension, could make long,term mucosal congestion, blocked circulation, nutrition, produced by the gastric mucosal barrier causing chronic in#lammation; oral cavity, nasopharyn9 or nasal cavity o# chronic in#lammation o# the bacteria or to9in into the stomach to stimulate gastric so in#lammatory, chronic gastritis can occur. 7. 0utonomic dys#unction caused by various reasons, long,term mental stimulation, depression, #atigue, etc., caused by autonomic dys#unction, may lead to digestive dys#unction, are mani#ested in the stomach stomach spasm o# contraction, so that occurrence o# gastric mucosal ischemia, edema, abnormal gastric acid secretion can also 'too much or too little), long,term e##ects can occur in the gastric mucosa o# chronic gastritis. >. Bile re#lu9 in normal human liver bile secretion by bile duct into the intestines to digest #ood, and some patients have chronic in#lammation as biliary system, or pyloric dys#unction, bile re#lu9 can occur. Bile the stomach can damage the gastric mucosal barrier, 1 H by the in#iltration o# the gastric mucosa in the stomach cavity, stimulate mast cells to histamine secretion increased, capillary congestion, reduce gastric mucosal blood #lo", bile and

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gastrin stimulate pepsin secretion, to increase gastric acid secretion and increased gastric in:ury, gastric in#lammation occurs, erosion, bleeding and other symptoms. ..4 Clinical 0ppearance ..5.1 0ssessment 1. 0cute gastritis a. 8tomach 1. 0symptomatic; or vague complaints o# postprandial distress a#ter a large meal; or vague ulcerlike distress, particularly relieved by #ood .. assive gastrointestinal hemorrhage

3. 1istory o# aspirin or alcohol intake 4. 1istory o# hematemesis or melena 5. Nasogastric aspirate or stool heme positive #or blood 'in hospitali+ed patient) .. Chronic gastritis a. 8tomach 1. =#ten asymptomatic .. $i##use, epigastric burning or pain that increase a#ter eating large amounts; relieved by a small amount o# antacid 3. Eomiting b. -ernicious anemia 1. ay be #irst clinical sign o# chronic gastritis

.. /eakness, numbness and tingling in e9tremities; #ever; pallor; anore9ia; "eight loss

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3. 8mooth or bee#y red tongue ..5.. Nursing $iagnosis and Nursing (ntervention Nursing $iagnosis Tissue cerebral, per#usion, alteration in% renal, Nursing (ntervention 1. Give patient nothing by mouth, and keep patient is *uiet i# a hemorrhage possibility .. 3. aintain intravenous #leids and blood as ordered onitor vital sign, CE- or 8"an,Gan+ catheter, blood "ork, and urinary output 4. =bserve patient #or early signs o# hypovolemic shock and initiate replacement o# #luid volume 5. (nsert a large,bore nasogastric tube 6. (nstitute ice "ater or saline lavage as orderd #or gastrointestinal bleeding 7. -repare patient #or diagnostic Nutrition, alteration in% less than body re*uirement .. procedures 1. -rovide #re*uent 'appro9imately si9) small #eeding o# bland #ood per day onitor intake and output antiemectics as 3. Record nausea and vomiting 4. 0dminister =ral mucous membrane, alteration in ordered 1. Noti#y physician o# smooth or bee#y red tongue, since this may 16 considered

cardiopulmonary,

gastrointestinal, pepheral

be an indication o# instrinsic #actor de#iciency

..5.3 -atient education 1. (denti#y agents that are irritating to the gastric mucosa, including aspirin, aspirin,containing compounds, over,the,counter agents, alcohol, prescription drugs such as indomethacin, phenylbuta+one, reserpine, nicotine, sulindac, and napro9en. .. -rovide patient "ith in#ormation related to the cause,and,e##ect relationship o# above agents and gastritis. 3. (denti#y need #or asymptomatic patient "ith chronic gastritis to continue to see physician regularly. 4. $iscuss bland diets, amounts o# #ood ingested, use o# antacids, and their relationship to pain management. ..5.4 !valuation -atient =utcome $ata (ndicating That =utcome is

Reached Gastrointestinal hemorrhage ceases 1. Blood limits .. 1ematemesis and melena are @aboratory studies are "ithin normal limits absent 1. 8erum vitamin B1. level is "ithin normal limits .. Normal 8chilling test '>D to 4<D pressure, pulse, and

respirations are "ithin normal

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o#

original

oral

dose

o#

radioactive vitamin B1. appears in a .4,hour urine specimen 3. !ndoscopy demonstrates normal mucosa 'acute episode) or absence o# polyps and carcinoma There is no pain 'chronic gastritis) 1. -atient report a history o#

#re*uent, small #eedings o# bland #oods 'chronic gastritis) .. -atient identi#ies causative agents involved in acute gastritis an omits these #rom his intake. ..5 $iagnostic 0ssessment

1. 0cuted Gastritis a. Nasogastric aspiration Branks blood or heme,positive aspirate b. !ndoscopy !rosions, super#icial ulcerations, and di##use oo+ing o# blood "hen procedure is done during acute phase; a#ter 3 days, lesions "ill begin to heal c. 0ngiographic visuali+ation To detect and treat lesions "ith in#usion o# vasopressin d. $ouble,contrast barium study 8uper#icial gastric erosion. Can not be used to detect bleeding lesions .. Chronic Gastritis a. 8erum gastrin

1>

!levated% in a #e" patients "ith type B, the level "ill be normal or lo" b. 8erum parietal cell antibodies -resence suggest gastritis c. -entagastrin stimulation Normal gastric secretion #or person&s age and se9 "ould indicate minimal likelihood o# gastritis. $iminished gastric secretions increase likelihood o# gastritis d. 8erum pepsinogen ( levels !levated in super#icial gastritis. @o" level in atrophic gastritis re#lect absence o# chie# cells e. 8chilling test 0ssessment o# vitamin B1. absorption by measuring urinary e9cretion o# an oraldose o# radiolabeled vitamin B1. #. Barium s"allo" "ith double contrast 0ppearance o# a Ibald #undusJ and thinning o# gastric ruage g. !ndoscopy "ith biopsy and cytology Biopsy necessary to obtain a de#initive diagnosis. Cytology o# multiple biopsy sites through the stomach is used to rule out gastric carcinomas h. $i##erential diagnosis Rule out Kollinger,!llision syndrome vs. chronic gastritis. 1igh serum gastrin and high serum pepsinogen levels are andicative o# Kollinger, !llision syndrome; may also indicative multiple poorly healed ulcers. ..6 The Therapy

1. 0cute gastritis a. 8urgical 1?

-artial gastrectomy, pyloroplasty, vagotomy, or total gastrectomy may be indicated #or managing patient "ith ma:or bleeding #rom erosive gastritis b. Chemotherapeutic 1. 1istamine receptor antagonist Ranitidine 'Kantac), 1<< mg po *id, parenteral cimetidine 'Tagamet), 3<< mg *6h in 1<< ml o# $ 5/ over .< min; dosage should maintain gastric p1 at 77. .. 0ntacids 0ntacids recommended to help maintain alkaline p1. 0ntacids '3< ml *.h) have been sho"n to be ><D to ?<D e##ective to keeping p1 above 4.< 3. Bluid volume replacement (ntravenous #luid replacement durng bleeding episode to maintain volume. Blood replacement may re*uired "hen gastrointestinal hemorrhage is associated "ith acute gastritis 4. -ituitary hormone Easopressin '-ritressin) per angiography or (E, .< units in 1<< units $5/ over 1< min, may be used in severe cases and may be repeated *3,4h i# rebleeding occurs; may lose e##icacy a#ter repeated doses c. !lectromechnical (ce "ater or saline lavage used in patient "ith gastrointestinal bleeding. @aser therapy "ith direct coagulation o# bleeding spots through an endoscopic approach may be utili+ed. d. 8upportive

.<

Removal o# causative agents 'alcohol, aspirin, non,steroidal anti, in#lammatory agents). /ithholding o# #ood and #luids until vomiting and in#lammation subside; then bland diet o# medium temperature in acute gastritis "ithout bleeding "ill assist healing process. .. Chronic gastritis a. Chemotherapeutic 1. 0ntacids to reduce or alleviate symptoms .. Eitamins Eitamin C 'ascorbic acid) to #acilitate iron absorption in the patient "ith achlorhydria7< Eitamin B1. in:ections 'cyanocobalamin, 1 mgGml 1<<Fg) b. !lectromechanical Routine endoscopy to asses #ormation o# gastric polyps and gastric carcinomas in patients diagnosed "ith atrophic gastritis and gastric atrophy Routine 8chilling test or serum vitamin B1. levels to evaluated intrinsic #actor de#iciency

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CHAPTER III CLOSING 3.1 Conclusion The gastrointestinal system consists o# the mouth, pharyn9, esophagus, stomach, and small and large intestines. 0ccessory organs include liver, gallbladder, and pancreas. The accessory organs #ound in the mouth are the teeth and salivary glands. Gastritis devided into t"o types "hich are acute gastritis and chronic gastritis. The therapy #or acute gastritis by surgery such as partial gastrectomy, pyloroplasty, vagotomy, or total gastrectomy may be indicated #or managing patient "ith ma:or bleeding #rom erosive gastritis. Chemotherapeutic such as histamine receptor antagonist, antacids, #luid volume replacement and pituitary hormone, electromechnical and supportive. The therapy #or chronic gastritis by Chemotherapeutic using antacids and vitamins, and the last electromechanical. 3.. 8uggestion Bor the ne9t "riter, it "ould be better i# the paper #ocus on gastritis and the theraphy to cure and to care gastritis patient.

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REFERENCES
http://www.disease-symptoms.com/the-etiology-of-chronic-gastritis-caused

pringhouse. 1??>. Mastering Medical-Surgecal Nursing. 8pringhouse sorporation United states o# 0merika

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