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SBA Answers and Explanations
Published in Vivian A. Elwell, Jonathan M. Fishman, Rajat Chowdhury, SBAs for the MRCS Part A, 2018
Vivian A. Elwell, Jonathan M. Fishman, Rajat Chowdhury
The Brunner glands are located in the submucosa of the duodenum. These glands are connected to the interstitial lumen by ducts that open into certain crypts. They secrete an alkaline product that protects the duodenal mucosa from the acidic chyme and helps achieve an optimal pH for the enzymes.
Gastrointestinal Function and Toxicology in Canines
Published in Shayne C. Gad, Toxicology of the Gastrointestinal Tract, 2018
Within the proximal few centimeters of the duodenum is a large population of compound mucous glands, called Brunner’s glands. These glands are located essentially between the pylorus and the entry points of the ducts from the gall bladder and pancreas. Brunner’s glands produce large amounts of alkaline mucus, in response to the presence of secretin and various other gastrointestinal hormones, vagal stimulation, and direct stimulation. This alkaline mucus protects the sensitive intestinal mucosa from injury that could be caused by very acidic gastric secretions. The presence of copious amounts of bicarbonate ions in the mucus also helps neutralize the acid in the chyme entering the proximal small intestine. Sympathetic stimulation inhibits the secretion of mucus by the Brunner’s glands.
Gastrointestinal physiology
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2015
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
In the small intestine, which is a major site for both digestion and absorption, chyme is mixed with bile, pancreatic juice and intestinal secretions. The folded mucosal surface and the villi of the small intestine provide a large surface area for nutrient absorption. The brush-border membranes of the mucosal epithelial cells house enzymes. Simple tubular glands called the crypts of Lieberkuhn lie between the villi. The epithelia of both the villi and the crypts of Lieberkuhn contain mucus-secreting goblet cells, phagocytes and endocrine cells. Losses of small intestinal epithelial cells (which are replaced and renewed every 6 days) at the tips of the villi release enzymes such as enterokinase from the brush border of enterocytes into the lumen. Enterokinase activates pancreatic trypsin, which then activates other proteolytic enzymes. The crypts of Lieberkuhn secrete 2 to 3 L of isotonic fluid per day. Chloride is transported out of the cell, and sodium and water follow passively via paracellular spaces. Brunner’s glands in the duodenum secret alkaline fluid, which neutralizes the acidic chyme arriving form the stomach. Secretion of the small intestine is stimulated by vagal activity, and by CCK, secretin, gastrin and prostaglandins.
Utility of gastric and duodenal biopsy sampling in adult eosinophilic esophagitis patients to rule out other gastrointestinal disorders
Published in Scandinavian Journal of Gastroenterology, 2021
Willemijn E. de Rooij, Maria-Louise Haasnoot, Aaltje Lei, Marijn J. Warners, Aart Mookhoek, Albert J. Bredenoord
Typical endoscopic EoE features were present in 77 (85%) patients. Inflammatory signs, including; furrows, edema and exudates were reported in 57, 53, and 42%, respectively of these patients. Endoscopic characteristics related to fibrosis e.g., rings and strictures were observed in 51% and 14%, respectively of patients (Figure 2). Abnormal endoscopic findings of the stomach were reported in 30 (33%) patients, of which the presence of erythema (70%) was most frequently documented. Other abnormal findings were; gastritis (23%), edema (17%), mucosal defects (17%) and other remarkable anomalities (10%) e.g., hematin spots (Figure 3). Moreover, abnormal endoscopic findings of the duodenum were observed in 19 (21%) patients. Documented findings were; duodenitis (32%), erythema (26%), edema (16%) and mucosal defects (5%). Other endoscopic abnormalities of the duodenum were noted in 6 (32%) patients e.g., endoscopic signs of villous atrophy or Brunner’s glands (Figure 4).
Appropriate endoscopic treatment selection and surveillance for superficial non-ampullary duodenal epithelial tumors
Published in Scandinavian Journal of Gastroenterology, 2021
Kingo Hirasawa, Yuichiro Ozeki, Atsushi Sawada, Chiko Sato, Ryosuke Ikeda, Masafumi Nishio, Takehide Fukuchi, Ryosuke Kobayashi, Makomo Makazu, Masataka Taguri, Shin Maeda
To date, various methods of ER have been reported to treat SNADETs [5,6]. Conventional endoscopic mucosal resection (CEMR) using an electrosurgical snare after submucosal injection is a simple and swift procedure. However, it occasionally results in a piecemeal or incomplete resection, which is a known risk factor for local recurrence [7]. Moreover, in the duodenum, abundant submucosal vessels and Brunner’s glands cause difficulty in creating a sufficient mucosal lift by submucosal injection. Underwater endoscopic mucosal resection (UEMR) is an alternative for treating SNADETs [8,9]. Instead of submucosal injection, UEMR utilizes a mucosal lift created by the buoyancy of water immersion. Filling the lumen with water makes the duodenum obtuse and distended and facilitates the snaring of the lesion [10]. Meanwhile, endoscopic submucosal dissection (ESD) has been developed, which enables en bloc resection regardless of the size of the lesion. However, duodenal ESD is a technically demanding procedure that should be limited to endoscopists with extensive experience [11].
Caudal type homeoboxes as a driving force in Helicobacter pylori infection-induced gastric intestinal metaplasia
Published in Gut Microbes, 2020
Hong-Yan Chen, Yi Hu, Nong-Hua Lu, Yin Zhu
Spasmolytic polypeptide-expressing metaplasia (SPEM) is another metaplastic phenotype of gastric mucosal metaplasia caused by chronic H. pylori infection that was proposed based on findings in GC animal models.17 SPEM and goblet cell IM are recognized precancerous lesions, that are closely related to the occurrence of GC.18 When the gastric mucosa responds to acute injury, parietal cells are lost, and then the mature chief cells transdifferentiate to undergo SPEM, which occurs in the gastric fundus and corpus.17,19,20 The phenotype of SPEM is similar to that of the deep antral glands and Brunner’s glands in the duodenum with respect to the secretion of trefoil factor 2 (TFF2, also known as antispasmodic peptide) and mucin6 (MUC6),21,22 as a repair response initiated by the body to promote gastric mucosal healing and recovery. SPEM was the main pathological change to the gastric mucosa observed in Mongolian gerbils infected with H. pylori,23 and mixed glands expressing SPEM and IM could be observed with the extension of the infection period by at least one year.17 In 2004, a cohort study found that SPEM was associated with early GC in Iceland.18 To further clarify the relationship between SPEM and intestinal metaplasia, Goldenring et al.24 examined the morphological characteristics of SPEM and IM in gastric resections specimens containing SPEM and IM mixed glands, and they found that SPEM cells are located deep in the gland, and that the lineage of IM is located in the lumen of the gland. Through immunostaining for Ki67 and Muc2, they speculated that the SPEM phenotype could gradually transition to the IM phenotype, which means IM is not the only precursor/intermediate of GC.