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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
Gastric acid is stimulated by 3 factors: Acetylcholine, from parasympathetic neurones of the vagus nerve that innervate parietal cells directlyGastrin, produced by pyloric G-cellsHistamine, produced by mast cells. This stimulates the parietal cells directly and also potentiates parietal cell stimulation by gastrin and neuronal stimulation. H2 blockers such as ranitidine are therefore an effective way of reducing acid secretion
Gastrointestinal Function and Toxicology in Canines
Published in Shayne C. Gad, Toxicology of the Gastrointestinal Tract, 2018
Gastric acid secretion is stimulated by a number of different routes and pathways, many of which can be independently blocked by various inhibitors. Without stimulation, and in the presence of fasting, gastric acid is secreted in low amounts to maintain a pH in the stomach within the range of 0.8 and 2.5 for a 24 hour period of time. Gastric acid output (acid and various fluids) is highest in the evening and lowest during the morning hours in the absence of the presence of food. The activities and kinetic parameters of many enzyme systems of the intestinal lining have also been shown to vary with the time of the day. Both circadian oscillations and the presence of both liquid and solid food play significant synergistic role in regulation of gastric emptying.
Magnitude of the problem
Published in Kathleen M Berg, Dermot J Hurley, James A McSherry, Nancy E Strange, ‘Rose’, Eating Disorders, 2018
Some patients who have induced vomiting frequently over long periods of time find that they vomit involuntarily, especially after eating larger than usual quantities of food, or vomit on such minimal provocation as hand pressure in the epigastric area. Heartburn can be a common and distressing complaint, especially in bulimia nervosa, when the lower esophageal sphincter, the valve preventing stomach contents from flowing back into the esophagus, becomes dysfunctional. Prokinetic agents (American Psychiatric Association, 2000a) such as domperidone can help by minimizing delayed gastric emptying and/or bowel transit times. H2 blockers, e.g. cimetidine and ranitidine, or proton pump inhibitors, e.g. omeprazole or pantoprazole, may also be helpful by suppressing production of gastric acid.
Proton pump inhibitor usage associates with higher risk of first episodes of pneumonia and peritonitis in peritoneal dialysis patients
Published in Renal Failure, 2022
Yujing Zhang, Jiao Li, Zijun Chen, Lingling Liu, Xiaojiang Zhan, Fenfen Peng, Qian Zhou, Xianfeng Wu, Yingsi Zeng, Liya Zhu, Yuxin Xie, Xiaochun Lai, Zebin Wang, Yueqiang Wen, Xiaoran Feng, Jianbo Liang
The mechanism of PPIs associated with pneumonia may be explained by the following reasons. As we all know, gastric acid acted as an important barrier to prevent pathogens from invading due to its lowering of the PH value of the gastrointestinal tract. PPIs inhibited the secretion of gastric acid mainly by irreversibly binding the H-K-ATPase on the cell membrane of the gastric parietal to inactivate it, thus increasing the pH value of the stomach, which in turn led to the excessive growth and colonization of pathogens [20–22]. And PPIs also reduced the acidity of the upper gastrointestinal tract, which changed the oral flora and further led to respiratory infections [23, 24]. In addition, a basic study in mice has found that the intestinal microbiota acts as a protective mediator during pneumococcal pneumonia, and the gut microbiota enhances the function of primary alveolar macrophages [25]. In a large cohort study of healthy people, it was found that PPI use significantly increased the growth of streptococci [26], while studies on streptococcal pneumonia confirmed that PPIs was associated with an increased risk of CAP caused by streptococcus pneumonia infection [27]. There was also evidence that acid inhibitors may damage immune cell function, including T lymphocytes, neutrophils, or natural killer cells [28–32], which may increase the body’s susceptibility to infection [33].
Protective effect of the solvent extracts of Portulacca oleracea against acidified ethanol induced gastric ulcer in rabbits
Published in Drug and Chemical Toxicology, 2022
Muhammad Shah Zeb Jan, Waqar Ahmad, Atif Kamil, Mir Azam Khan, Maqsood Ur Rehman, Irfan ullah, Muhammad Saeed Jan
The ethanol-induced ulcer model is widely used for investigating the testing agents or studying the efficacy of potential drugs (Strasser et al.2014). It is well known that ethanol increase histamine secretion in the stomach which in turn release hydrochloric acid from the parietal cells inside mucosa of gastric tissue via proton pump (Kumar and Kumar 2009). A membrane-bound enzyme (H+K+ATPase), located in the canalicular membrane of parietal cells, catalyzes an electroneutral exchange of H+ versus K+ into the gastric lumen with the expenditure of ATP (Reyes-Chilpa et al.2006). It is documented that gastric ulcer induced by ethanol causes reactive oxygen species (ROS) production because ethanol rapidly reaches the gastric mucosa and solubilize the protective mucous and finally releases free radicals and superoxide anion. These free radicals react with lipid to form malondialdehyde (MDA), a marker of lipid peroxidation (Zakaria et al.2011). The treatment of gastric ulcer has become a challenge in the world. Although there are some approaches used for treatment of gastric ulceration like acid neutralization, improving antioxidant level in the stomach but the most important approach is inhibition of gastric acid secretion inside the stomach (Halim et al.2017).
Educational intervention can improve appropriateness of acid suppression therapy in hospitalized geriatric patients
Published in Journal of Community Hospital Internal Medicine Perspectives, 2019
Sankalp Dwivedi, Jaya Edukulla, Sindhu Rajendra, Sandesh Murali, Serge A. Sorser, Marc S. Piper, Michael Piper, Bradley J. Warren, Harsha Ramchandani
Gastric acid plays an essential role in the digestion of protein by converting pepsinogen to the active form, pepsin. It also prevents against enteric infection, bacterial overgrowth and facilitates the absorption of vitamin B12, non-heme iron, and medications such as calcium and thyroxin [1]. Consequences of hypochlorhydria have been well defined in the literature: (1) Osteoporosis and Hip Fracture [2]; (2) Hospital acquired pneumonia and community acquired pneumonia [3,4]; (3) Clostridium difficile infection [5]; (4) Vitamin B 12 deficiency [6]; (5) Alteration in the lower intestinal microflora [7]; (6) Various forms of kidney injury have also been linked to the Proton Pump Inhibitors (PPIs) use such as acute allergic interstitial nephritis, acute kidney injury, increased incidence of chronic kidney disease and progression to end stage renal disease [8].