Primary Causes & Pathophysiology
Acid and pepsin (stomach digestive chemicals) irritate sensitive gastric (stomach) and duodenal (first bowel) lining. Impaired fundic accommodation (stomach relaxing after food) causes early fullness and bloating. Visceral hypersensitivity (extra-sensitive gut nerves) turns normal stretch into pain. Duodenal eosinophilia (allergy-type cell rise) with low-grade inflammation drives functional cases. NSAIDs (painkiller drugs) block prostaglandins (protective lining chemicals) while Helicobacter pylori causes gastritis (lining inflammation) and ulcer.
Impaired accommodation with hypersensitivity to stretch causes fullness and early satiety after normal meals
Acid sensitivity with duodenal low-grade inflammation heightens pain signalling without ulcer or mass
Mucosal break (lining sore) from acid, Helicobacter pylori or NSAIDs exposes deeper layers to acid with localised pain
Chronic bacterial inflammation alters acid control and sensitises upper gut nerves
Ulcerated mass with infiltration and outlet block causes persistent pain, fullness and early satiety
Gallbladder squeeze against stones refers pain to epigastrium through shared visceral nerves
Inflammation or mass irritates coeliac nerves and refers deep pain to upper belly with meal worsening