First of all you know that GERD is caused by certain factors, and gastritis is a inflammation of the stomach lining. Now I assume the doctor did a endoscopy to dx your present illness at this time. I would also expect he did biopsies of your stomach and esophagus, and checked you for bacteria infection such as: H-pyloric and others. Nexium caused me stomach pain, but worked to heal my erode esophagus however, I found Aciphex the best drug for me in controlling my acid reflux. I have found Licorice Root Tea to help with my acid reflux. You can buy it at drugstore.com.
If you have gastritis you should at least have pinpoint the cluperate by now, but your s/s could mean something other causing you problems such as; GERD or H-pyloric(if you haven't been tested it might not be a bad idea). I would make an appointment with a GI doctor and be correctly dx if you haven't already, if so then maybe you need to discuss a change in treatment. However, GERD is a chronic disease. Treatment usually must be maintained on a long-term basis, even after symptoms have been brought under control. Issues of daily living, and compliance with long-term use of medication need to be addressed as well. This can be accomplished through follow-up, support, and education.
Gastritis is a inflammation of the gastric mucosa. Gastritis can be classified as erosive or nonerosive based on the severity of mucosal injury. It can also be classified according to the site of involvement within the stomach (ie, cardia, corpus, antrum). Gastritis can be further classified histologically as acute or chronic based on the inflammatory cell type. No classification scheme matches perfectly with the pathophysiology; a large degree of overlap exists.
Acute gastritis is characterized by polymorphonuclear cell infiltration of the mucosa of the antrum and corpus. Chronic gastritis implies some degree of atrophy (with loss of functional capacity of the mucosa) or metaplasia. It predominantly involves the antrum, with subsequent loss of G cells and decreased gastrin secretion, or the corpus, with loss of oxyntic glands, leading to reduced acid, pepsin, and intrinsic factor.H. pylori is increasingly implicated as the primary cause of nonerosive gastritis. This spiral-shaped, gram-negative organism causes almost all cases of nonerosive gastritis and its resultant complications. Infection invariably leads to gastric mucosal inflammation, which in turn alters gastric secretory physiology, leaving the mucosa more susceptible to damage by acid. Highest concentrations of H. pylori are detected in the antrum, where confined infection substantially increases the risk of prepyloric and duodenal ulceration. In some patients, infection involves the entire stomach and appears to be associated with subsequent development of gastric ulcers and gastric adenocarcinoma.
H. pylori appears to be a very common chronic infection worldwide. In developing countries, infection is most frequently acquired in childhood; suboptimal sanitary conditions, poor hygiene, low socioeconomic status, and crowded living conditions are associated with higher prevalence and earlier infection. In the USA, evidence of infection is rare in children and increases with age. Infection is more common in blacks and Hispanics than in whites.
Although the exact mode of transmission is unclear, the organism has been cultured from stool, saliva, and dental plaque, which implicates oral-oral or fecal-oral transmission. Infections tend to cluster in families and in residents of custodial institutions. Nurses and gastroenterologists appear to be at high risk, and bacteria have been transmitted by improperly disinfected endoscopes.
Superficial gastritis: The predominant infiltrating inflammatory cells in this condition are lymphocytes and plasma cells mixed with neutrophils; inflammation is superficial and may involve the antrum, corpus, or both. It is usually not accompanied by atrophy or metaplasia. Prevalence increases with age. Given the high prevalence of H. pylori-associated superficial gastritis and the relatively low incidence of clinical sequelae (ie, peptic ulcer disease), there is no clear indication to eradicate H. pylori with antibiotics in an asymptomatic patient. Most patients harbor the organism with only minimal histologic changes and no discernible clinical symptomatology.
Deep gastritis: Deep gastritis is more likely to be symptomatic (vague dyspepsia). Mononuclear cells and neutrophils infiltrate the entire mucosa to the level of the muscularis, but seldom with exudate or crypt abscesses. Distribution may be patchy, and superficial gastritis may coexist. Partial gland atrophy and metaplasia may be present. In symptomatic patients, eradication of H. pylori with antibiotics should be attempted (see Treatment under Peptic Ulcer Disease, below).
Gastric atrophy: Atrophy of gastric glands may follow various injuries, especially gastritis, most often secondary to long-standing antral (type B) gastritis. Some patients with gastric atrophy manifest autoantibodies to parietal cells, usually in association with corpus (type A) gastritis and pernicious anemia
Atrophy may occur without specific symptoms. Endoscopically, the mucosa may appear normal until atrophy is advanced, when the submucosal vascular tree may be visible. As atrophy becomes complete, acid and pepsin secretion diminish and intrinsic factor may be lost, resulting in vitamin B12 malabsorption.
Metaplasia: Two types of metaplasia are common in chronic nonerosive gastritis: mucous gland and intestinal. Mucous gland metaplasia (pseudopyloric metaplasia) occurs in the setting of severe atrophy of the gastric glands, which are progressively replaced by mucous glands (antral mucosa), especially along the lesser curve. Gastric ulcers occur most commonly at the junction of antral and corpus mucosa, but whether they occur as a cause or consequence of antrification is not clear. Intestinal metaplasia occurs in response to chronic mucosal injury. Gastric mucosa may resemble small intestinal mucosa, with goblet cells, endocrine (enterochromaffin or enterochromaffin-like) cells, and rudimentary villi, and may even assume functional (absorptive) characteristics. Intestinal metaplasia begins in the antrum and may extend to the corpus. It is classified histologically as complete (most common) or incomplete. In complete metaplasia, gastric mucosa is completely transformed into small intestinal mucosa, both histologically and functionally, with the ability to absorb nutrients and secrete peptides. In incomplete metaplasia, the epithelium assumes a histologic appearance closer to that of the large intestine and frequently exhibits dysplasia. Intestinal metaplasia is associated with stomach cancer.
Nonerosive gastritis is suspected by symptoms but diagnosed with certainty by endoscopy and biopsy. Most patients with H. pylori-associated gastritis are asymptomatic; testing for and treatment of infection are not always indicated. For patients in whom diagnosis will alter treatment, diagnostic tests to detect H. pylori consist of noninvasive and invasive techniques.
Noninvasive testing is less expensive and does not require endoscopy. Laboratory and office-based serologic assays most frequently use technology to detect IgA and IgG antibodies to H. pylori. Sensitivity and specificity are > 85% for detecting initial H. pylori infection. However, because most dyspeptic patients do not have peptic ulcer disease on endoscopy (10 to 15%) and because the role of H. pylori in the pathogenesis of nonulcerative dyspepsia remains unclear, testing every dyspeptic patient noninvasively for H. pylori would lead to unnecessary treatment in many patients. Whether it will be cost-effective to diagnose (noninvasively) and treat all dyspeptic patients has not been determined. In untreated patients, antibody titers remain elevated over time, suggesting persistent induction of an immune response. After successful eradication of the organism, qualitative serologic assays remain positive for up to 3 yr, whereas quantitative antibody levels slowly fall. Given this persistent elevation of antibody titers after eradication, serologic assays do not reliably document eradication. Because of its accuracy and low cost, serologic assay should be considered the noninvasive diagnostic test of choice for initial documentation of H. pylori infection.
Urea breath tests use 13C- or 14C-labeled urea po. In an infected patient, the organism metabolizes the urea and liberates labeled CO2, which is exhaled and can be quantified in breath samples taken 20 to 30 min after ingestion. The sensitivity and specificity are > 90%. Urea breath tests are well suited for confirming eradication of the organism after therapy. False-negative results are possible with recent antibiotic use or concomitant proton pump inhibitor therapy; therefore, follow-up testing should be delayed >= 4 wk after antibiotic therapy.
Invasive testing requires gastroscopy and mucosal biopsy and should be reserved for patients with an a priori indication for endoscopy. Although bacterial culture is highly specific, it is infrequently used in clinical practice because the fastidious nature of the organism makes culturing cumbersome. Histologic staining of gastric mucosal biopsies has a sensitivity and specificity > 90%. Given the high prevalence of the organism in the antrum, biopsies should be obtained from this area of the stomach, preferably within 1 to 2 cm of the pylorus.
A rapid urease test (RUT) is performed by placing a gastric biopsy specimen onto a gel or membrane containing urea and a pH-sensitive color indicator. If H. pylori is present, the bacterial urease hydrolyzes urea and changes the color of the media. RUT has a sensitivity and specificity > 90%. Because it is accurate, easy to perform, and relatively inexpensive, RUT should be considered the invasive diagnostic method of choice. False-negative results can occur in the setting of recent antibiotic use or treatment with proton pump inhibitors, which suppress bacteria; in these circumstances, diagnosis should be confirmed by histology.
Treatment of chronic nonerosive gastritis is directed toward H. pylori eradication (see Treatment under Peptic Ulcer Disease, below). In H. pylori-negative patients, treatment is directed at symptoms using acid-suppressive medications (eg, H2 blockers, proton pump inhibitors) or antacids.
Dee RN,C CLTC
Good comments DeeA, you may also want to try drinking 1-2 oz. of pure organic alo vera juice. This stuff really helps in soothing ulcerative and / or inflamatory conditions of the digestive system. You can get it at most heath fod stores...it is best stored in cold refrigerator and sipped about one half hour before meals in about a 1 or 2 oz. "shot glass" serving.
If this does not help you are most likely a hypochondriac.
...last part is a joke for DeeA ;)
this is the kind of tech info iv been after for ages allthough most of it goes over my head.....it seems gastritis can do all sorts of things discomfort wise....as my ailments take on a different feeling every day.(theres a pain here ..theres a pain there)....AND WITH THE THOUGHT OF REDUNDENCY A YEAR AGO AND STILL GOING ON IM CONVINCED THAT STRESS HAS A LOT TO DO WITH IT.so now with 4 main problems 1,spondylosis (which has the pins and neadles effect along with the side effects of gastritis doing the same i cant pin point the blame on either:>(( 2,mild diverticulitis 3,gastritis 4,a touch of gerd which so far has taken a dive due to licorice (i live in hope)....and yes all the worrys of having something worse are with me all the time.
doug and DeeA:you must be very divout(spelling)to be on here with constant help replys..its taken me 3 years to find this type of group.a doctor will give you very little time untill its "next patient please"but hundreds of people reading the questions are more likely to make a direct hit so to speak even though they are not doctors at least they can say "oh yeh my friend had that and it was"........
TIA steve hall ***@****