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Taste and Food Choice
Published in Alan R. Hirsch, Nutrition and Sensation, 2023
The first effect of consuming a meal is gastric distension. Experimentally distending a rat’s stomach with air causes the taste response to sucrose, recorded in the NST, to decline, implying a less rewarding experience to the rat (Glenn and Erickson 1976). The next effect of a meal is to raise blood sugar levels. When these were increased experimentally through an intravenous infusion of glucose, taste responses to sugar in the NST also declined (Giza and Scott 1984). Similar but smaller effects on taste activity were seen with modest infusions of insulin (Giza and Scott 1987a) or glucagon (Giza, Deems, VanderWeele, and Scott 1993), both of which result in the greater availability of glucose to the muscles, though by different mechanisms. Thus, each procedure that delivered glucose to the body caused a transient reduction in sensitivity to sugars in the NST. This implies a partial loss of the pleasure that sustains eating, making termination of a meal more likely.
The Clinical Application of 5-HT Agonists and Antagonists in Gastrointestinal Disease
Published in T.S. Gaginella, J.J. Galligan, SEROTONIN and GASTROINTESTINAL FUNCTION, 2020
Timothy P. Roarty, Richard W. McCallum
Gastric retention with accumulation of acid and gastric contents can be a contributory factor in the production of GERD. McCallum and colleagues reported delayed gastric emptying of solids in a significant number of patients with GERD.21,22 Behar and Ramsey found that there was an abnormality in the gastric antral motility, but that liquid emptying was normal.23 Most studies have demonstrated delay in the mean emptying rates for either solids22,24,25 or liquids,21–26 in patients with GERD. Other investigators have reported normal emptying rates in patients with GERD.21,31–34 Gastric distension related to eating could be accentuated by any slowing of gastric emptying. It is known that gastric distension in turn promotes more frequent and complete transient relaxations of the lower esophageal sphincter (LES), which leads to recurrent reflux. Only when the basal LES pressure is less than 5 mmHg is symptomatic reflux always present, and there is a high degree of overlap with normals and asymptomatic reflux episodes. The basal LES pressure is decreased by fatty foods, smoking, and drugs such as calcium channel blockers, most anticholinergics, nitrates, aminophylline, and benzodiazepines.
Non-invasive ventilation
Published in Philip Woodrow, Nursing Acutely Ill Adults, 2015
With swallowing, some air enters the stomach. Both the trachea and oesophagus lead off the oropharynx, so positive pressure in upper airways causes more air to be swallowed, while impeding its escape (Carron et al., 2013). Air in the stomach can cause gastric distension which splints the diaphragm, reducing breath size and making breathing more difficultprovokes discomfort, nausea and/or vomiting
Ischemic gastropathy with “leopard skin” stomach
Published in Baylor University Medical Center Proceedings, 2023
Dhairya Gor, Kyle Wiseman, Rajvi Gor, Shefali Shah
Ischemic gastropathy is rarely reported and likely underrecognized, though it generally has a poor prognosis.1–3 Gastric ischemia is highly uncommon due to redundancy, anastomoses, and extensive collaterals of the vascular supply.1,5 The clinical presentation of gastric ischemia depends on the acuity and extent of ischemia development, with acute cases warranting immediate intervention.1,3 Symptoms vary but include nausea, vomiting, abdominal distension, weight loss, and gastrointestinal bleeding,3,6 similar to our patient. Gastric ischemia arises due to various underlying conditions such as hypotension, vasculitis, mechanical obstruction, or ischemia related to complications of endoscopic interventions.2–4 However, there have been only a few reports of gastric ischemia in patients with cirrhosis.1,7 In our cirrhotic patient, portal hypertension could have been a predisposing factor for ischemic gastropathy. The alteration in gastric mucosal hemodynamics with passive congestion in individuals with portal hypertension results in poor gastric perfusion, making patients susceptible to gastric ischemia.8 In addition, gastric distention contributes significantly to the development and worsening of ischemia, warranting immediate nasogastric tube placement.1
Association of Candida esophagitis with acute esophageal necrosis
Published in Baylor University Medical Center Proceedings, 2022
Muhammad Sheharyar Warraich, Bashar Attar, Shazaq Khalid, Muhammad Ali Khaqan
A 53-year-old man with a history of uncontrolled type 2 diabetes mellitus, chronic kidney disease, necrotizing pancreatitis complicated by chronic pancreatitis, and alcoholic Child B cirrhosis presented to the emergency department with 1 week of nausea, nonbloody and nonbilious vomiting, and diffuse abdominal pain. On admission, his blood pressure was 135/80 mm Hg; heart rate, 106 beats/min; respiratory rate, 30 breaths/min; and temperature, 34.4°C. The blood glucose was 675 mg/dL; bicarbonate, 16 mEq/L; anion gap, 26; pH, 7.30; urea, 36 mg/dL; creatinine, 1.4 mg/dL; hemoglobin, 8.3 g/dL; and white cell count, 17 k/μL. Blood cultures were obtained. Computed tomography of the abdomen with contrast revealed gastric distension with fluid-filled distal esophagus and changes of portal hypertension and chronic pancreatitis. The patient was diagnosed with diabetic ketoacidosis and admitted to the intensive care unit. Treatment was initiated with intravenous fluid and an insulin drip, and the patient’s condition improved.
Impact on Short-Term Complications of Early Oral Feeding in Patients with Esophageal Cancer After Esophagectomy
Published in Nutrition and Cancer, 2021
Yi Li, Zhenjun Liu, Guangyuan Liu, Qiang Fang, Lili Zhao, Pei Zhao, Jiuhui Wang, Mu Yang
The problem most associated with early oral feeding is that it may increase the incidence of anastomotic leakage and pneumonia, which are the most common and feared potential complications after esophagectomy. Therefore, anastomotic leakage and pneumonia are the main postoperative outcome measurements of nutritional route success. For instance, the commonly accepted idea is that without nasogastric decompression, gastroparesis, and paralytic ileus are common complications after gastrointestinal surgery and may lead to delay of gastric emptying, gastric distention, and an increase of anastomotic tension and incidence of aspiration and anastomotic leakage. Another concern is that the impact of early oral feeding may cause anastomotic stenosis. Increasingly, however, studies are reporting the opposite results. A systematic review reported that prophylactic nasogastric decompression after abdominal surgery could not speed up the recovery of patients after gastrointestinal surgery, but might increase the risk of postoperative complications (14), and retention of the nasogastric tube is a risk factor for postoperative respiratory tract infection (15). Moreover, early removal of the nasogastric tube and complete omission of nasogastric tube are feasible and do not increase the rate of postoperative pneumonia or the risk of anastomosis leak (12, 16). Some data suggest that the incidence of anastomosis leak in the nasogastric (NG) tube group is significantly higher than in the group without an NG tube and recommends omission of routine nasogastric tube application in the postoperative care of esophagectomy (17).