I think you need to stop acting like a gaffot and go see a gastroenterologist. An endoscopy would most likely reveal the source of your problems. There are many different ways that you could have damaged your GI tract in the past and witout an endoscopy it would be hard to tell.
Here's some info that I picked up but keep in mind, it's just one of several likely problems you could be having:
Bile reflux chemical gastropathy — Bile reflux gastropathy typically results from the regurgitation of bile into the stomach because of an operative stoma, an incompetent pyloric sphincter, or abnormal duodenal motility [28]. The degree of injury reflects the amount of exposure to bile salts. Patients who have a gastroenterostomy, for example, demonstrate the greatest degree of foveolar hyperplasia near the stoma, with decreasing inflammation proximally [13,16,29]. Bile salt concentration in gastric juice correlates with the severity of hyperplasia in these patients.
The effect of bile salts on gastric mucosa is comparable to that seen after chronic NSAID use [28]. Bile salts also appear to be a risk factor for the development of antral metaplastic gastritis [30].. Animal studies have demonstrated that bile salts and lysolecithin (derived from the metabolism of lecithin) cause acute gastric mucosal injury [31,32]. Their degree of toxicity is influenced by a number of variables including the type of bile salt, the presence or absence of deconjugation by bacteria in the intestine or stomach, the gastric pH, and the presence of pancreatic enzymes. Pancreatic enzymes in particular enhance injury from bile salts, in part because they catalyze the formation of lysolecithin from lecithin.
Lysolecithin and bile salts break down the gastric mucosal barrier [33], leading to back-diffusion of hydrogen ions and mucosal injury [31,32]. Concomitant infection by H. pylori can cause increased inflammation [34,35]. Cytoprotection from bile-induced injury by prostaglandins has been demonstrated in animal studies [36].
Diagnosis — Symptoms in patients with bile acid reflux are variable, ranging from histologic changes only without symptoms to abdominal pain, bilious vomiting and weight loss [37]. The diagnosis of bile reflux gastropathy is easiest in patients who have surgically altered anatomy predisposing to bile reflux. The demonstration of chronic gastropathy in the absence of other causes is usually sufficient. In contrast, gastropathy in patients with nonoperated stomachs should not be attributed to exposure to bile without evidence of duodenogastric reflux. Duodenogastric reflux can be demonstrated by visualization during endoscopy, bile salt analysis in gastric juice, or radionuclide scanning [28,35,38,39].
Treatment — Definitive treatment of symptomatic bile acid reflux is surgery (usually a Roux-en-Y revision), which has been associated with improvement in symptoms in 50 to 90 percent of patients in several reports [37,40-42]. Improvement is less likely in patients with delayed gastric emptying [40].
A number of medical treatments have been evaluated in small clinical trials with variable success:
Ursodeoxycholic acid significantly decreased pain and almost abolished nausea and vomiting, but did not improve histology in a placebo controlled crossover trial involving 12 patients [43]. The rationale for its use was based upon the hypothesis that changing the composition of bile acids could have a favorable effect on gastric mucosa and symptoms.
Sucralfate improved histologic features but not symptoms in a controlled trial involving 23 patients [44].
Prostaglandin E2 was ineffective in improving endoscopic features or symptoms in a double-blind crossover trial [45].
Cholestyramine combined with alginates (to improve contact time in the gastric remnant) was ineffective on symptoms or histology in a placebo controlled trial that included 32 patients
