Gastrointestinal Tract
Pritam S. Sahota, James A. Popp, Jerry F. Hardisty, Chirukandath Gopinath, Page R. Bouchard in Toxicologic Pathology, 2018
Parietal cells are specialized cells for acid secretion and are located in oxyntic (fundic and body) mucosa. They derive from the progenitor cells as preparietal cells before migrating down the gland to form mature parietal cells (Karam 2010). They have receptors for histamine, ACTH, acetylcholine, and gastrin (CCK2 receptor), which raise cAMP to activate the proton pump H+/K+ ATPase. Vesicles form into a canalicular system when stimulated to secrete H+ ions into the oxyntic gland and into the stomach lumen. With acid secretion by parietal cells, there is a balancing rise in pH of the venous outflow from the oxyntic mucosa called the “alkaline tide.” Deep antral gland cells all immunostain for TFF2 and mucin MUC6 are strongly stained with Alcian blue.
Stomach and duodenum
Professor Sir Norman Williams, Professor P. Ronan O’Connell, Professor Andrew W. McCaskie in Bailey & Love's Short Practice of Surgery, 2018
This is an autoimmune condition in which there are circulating antibodies to the parietal cell. This results in the atrophy of the parietal cell mass, hence hypochlorhydria and ultimately achlorhydria. As intrinsic factor is also produced by the parietal cell there is malabsorption of vitamin B12, which, if untreated, may result in pernicious anaemia. The antrum is not affected and the hypochlorhydria leads to the production of high levels of gastrin from the antral G cells. This results in chronic hypergastrinaemia. This, in turn, results in hypertrophy of the ECL cells in the body of the stomach, which are not affected by the autoimmune damage. Over time it is apparent that microadenomas develop in the ECL cells of the stomach, sometimes becoming identifiable tumour nodules. Very rarely, these tumours can become malignant. Patients with autoimmune gastritis are predisposed to the development of gastric cancer, and screening such patients endoscopically may be appropriate.
Practice Paper 9: Answers
Anthony B. Starr, Hiruni Jayasena, David Capewell, Saran Shantikumar in Get ahead! Medicine, 2016
Zollinger–Ellison syndrome describes peptic ulceration secondary to a gastrin-secreting adenoma (gastrinoma). The adenoma is usually located in the pancreas, but can be found in the stomach or small bowel. Approximately 60% of gastrinomas are malignant and have the potential to metastasize to local lymph nodes and the liver. The unregulated secretion of gastrin simulates the parietal cells in the gastric antrum to produce excessive amounts of hydrochloric acid. This disrupts the gastric and duodenal mucosa, causing peptic ulceration. The acid can also denature pancreatic enzymes, such as lipase, resulting in malabsorption and chronic diarrhoea. Diagnosis is often based upon endoscopic identification of multiple peptic ulcers in association with a raised fasting serum gastrin level. Treatment involves high-dose protein pump inhibitors and surgical resection of the adenoma. Patients with Zollinger–Ellison syndrome associated with multiple endocrine neoplasia (MEN) type 1 often have multiple adenomas that are not suitable for resection. In this situation, the patient can usually be managed using a somatostatin analogue (e.g. octreotide), which decreases gastrin secretion. Metastatic disease necessitates systemic chemotherapy.
Ultra-structural study of the indomethacin-induced apoptosis and autophagy in rat gastric parietal cells
Published in Ultrastructural Pathology, 2020
Sahar M Gebril, Yuko Ito, Eman E. Abu-Dief, Mahmoud Rezk Abdelwahed Hussein, Hoda M Elsayed, Asmaa Naser Mohammad, Usama M Abdelaal, Kazuhide Higuchi
Parietal cells (PCs) are the most predominant cell type in the gastric mucosa. They are responsible for acid secretion, and they are frequent in the isthmus and the neck of the gastric glands.9,10 Ultra-structurally, PCs have unique characteristics such as microvilli lacking the glycocalyx coat, intracellular canaliculi (ICC), numerous large mitochondria and limited protein synthetic apparatus, the rough endoplasmic reticulum (RER), and the Golgi bodies.11 The secretory activity of PCs alternates according to the physiological phases of feeding or fasting.12During fasting the PCs undergo membrane recruitment of ICC membrane into the cytoplasm with the formation of tubulovesicles (tbv) that will be ready to be added to the membrane on activation.13,14 During feeding, PCs have wide ICC with highly folded membrane studded with H +. K+ -ATPase subunits (proton pumps) for active acid formation.15,16
Localization of Helicobacter pylori gastritis and the relation of existing histopathological features with reflux esophagitis
Published in Scandinavian Journal of Gastroenterology, 2020
Serkan Yalaki, Hüseyin Pulat, Aysu Ilhan
The region secreting the gastric acid is the corpus where the parietal cells of the stomach are full. There is a relationship between the decrease in gastric acid production and the severity of corpus gastritis and atrophic gastritis caused by long-term inflammation of the corpus. In this process, it is thought that Hp infection is the main mechanism the onset of which GERD inhibits [1,2,10]. In our study, we found that, in line with this information in the literature, Hp colonization and gastritis score in the corpus were significantly lower in the RE group. Destruction of Hp may lead to increased acid secretion and may exacerbate the symptoms of RE or GERD [24,28].2427 In contrast, there are studies showing that Hp infection is common in GERD patients and that eliminating Hp leads to suffitient control of GERD symptoms and improves esophagitis [29,30].2829 Moreover, a large-scale epidemiological study (approximately 21,000 cases) showed that the decrease in the rate of Hp infection was parallel to the decrease in the prevalence of peptic ulcers and that the reemergence of GERD and/or GERD following Hp treatment was rare [31].30
An update on the latest chemical therapies for reflux esophagitis in children
Published in Expert Opinion on Pharmacotherapy, 2019
Marc Bardou, Kyle J. Fortinsky, Nicolas Chapelle, Maxime Luu, Alan Barkun
Current guidelines suggest a trial of H2RAs for patients with mild or intermittent symptoms of GERD. H2RAs inhibit histamine H2 receptors of the parietal cell thereby reducing acid secretion. While H2RAs are less effective than PPIs in producing resolution of symptoms and mucosal healing, they do have a rapid onset of action and can, therefore, provide immediate symptomatic relief [2]. While several large, well-designed trials have proven the efficacy of H2RAs in the treatment of GERD in adult patients, the evidence for their use in the pediatric population comes mainly from smaller trials [34,35]. More recently, a systematic review of 8 studies consisting of 276 children examined the efficacy of H2RAs in reducing symptoms of GERD, increasing gastric pH, and producing histologic healing [36]. While H2RAs were found to be more effective than placebo, there was only one study that suggested superior efficacy when compared to antacids. One theory for the lack of H2RA efficacy in some of these studies is a lack of proper dosing, as pediatric patients may require much higher doses per kilogram than adults [37].
Related Knowledge Centers
- Epithelium
- Gastric Mucosa
- Histamine
- Intrinsic Factor
- Stomach
- Active Transport
- Hydrochloric Acid
- Cell
- Gastric Glands
- Hydrogen Potassium Atpase