Include the of H. pylori. MO 5.3
Acute gastritis refers to the inflammation of the gastric mucosa. Acute gastritis is categorized into two that is erosive and non-erosive. Erosive acute gastritis is characterized by superficial erosions, hemorrhagic and deep erosion. No-erosive acute gastritis is attributed to Helicobacter pylori which is the main cause of non-erosive acute gastritis. Several etiologies cause acute gastritis. Bacteria such as H.pylori trigger the inflammation of the gastric mucosa. H.pylori is a spiral-shaped bacteria that invade the stomach, triggering gastric mucosa inflammation. Frequent consumption of non-steroidal anti-inflammatory drugs such as ibuprofen interferes with the protective mechanism of the gastric mucosa. Individuals with extreme physiological stress possess acute gastritis characterized by severe burns in the stomach. Additionally, increased alcohol, caffeine and exposure to cigarette smoking can irritate the stomach mucosa (Yang & Hu, 2022). Direct trauma to blood vessels to the gastric mucosa lining can result in ischemia which may damage the mucosal lining impairing the rich blood supply to the stomach.
Depending on the etiology, acute gastritis encompasses different pathogenesis—Invasion of H.pylori bacteria in the stomach. One can access to H.Pylori through the consumption of contaminated food. H.pylori infections invade the gastric mucosal lining by activating a number of toxins and enzymes such as interleukins which ultimately attract polymorphs and monocytes that cause acute gastritis. Prolonged consumption of NSAIDs such as aspirin interferes with the gastric mucosal lining leading to decreased production of gastric mucus and increased susceptibility to gastric acid. Increased gastric acid in the gastric mucosa causes acute gastritis,
The clinical manifestation of acute gastritis is recurrent stomach upset, nausea, abdominal bloating, indigestion, burning or gnawing ache in the stomach between meals or at night, hiccups vomiting blood, loss of appetite and black or tarry stool (Nisa, 2018).
Yang, H., & Hu, B. (2022). Immunological perspective: Helicobacter pylori infection and gastritis. Mediators of inflammation, 2022.
Nisa, S. (2018). Gastritis (Warm-e-media): A review with Unani approach. Int. J. Adv. Sci. Res, 3(3), 43–45.