The exact pathogenesis of<unk>  is not fully understood. However, gastric emptying process is the result of interaction of smooth muscles, extrinsic and enteric autonomic nervous system, and interstitial cells of Cajal (ICC). Loss of expression of neuronal nitric oxide synthase (nNOS) and loss of interstitial cells of Cajal (ICC) play pivotal role in the pathogenesis of<unk> . Recent studies suggest that the loss of antioxidant gene expression (NRF2 gene) can contribute to the development of<unk> . NRF2 regulates expression of phase II antioxidant genes such as HO-1, SOD1, SOD2, GCLC, GCLM, CAT, and GPX1. On microscopic histopathological analysis of full thickness biopsy of the gastric body. Decreased number of interstitial cells of Cajal (also called fibroblast like cells) in circular muscle layer, immune cells infiltration of gastric tissue especially myenteric plexus predominantly consisting of lymphocytes and macrophages showing CD45 and CD68 immunoreactivity, and enteric nerve fiber loss within the circular smooth muscle layer are characteristic findings of<unk> .
Gastroparesis pathophysiology
Nausea and vomiting pathophysiology
Mallory-Weiss syndrome pathophysiology
Peptic ulcer pathophysiology
Dyspepsia pathophysiology
Gastritis pathophysiology
Stomatitis pathophysiology
Ogilvie syndrome pathophysiology