This is due to the fact that liquid emptying may remain normal despite advanced disease. Measurement of emptying of solids is more sensitive by scintigraphy. This test provides a physiological, non-invasive and quantitative measure of gastric emptying. Gastric scintigraphy: Gastric emptying scintigraphy of a radiolabeled solid meal is the gold standard for the diagnosis of gastroparesis. Complications of gastroparesis include esophagitis, Mallory-Weiss tear from chronic nausea/vomiting, malnutrition, volume depletion with acute renal failure (secondarily), electrolyte disturbances and bezoar formation. Treatment of constipation with an osmotic laxative has shown to improve dyspeptic symptoms as well as gastric emptying delay. Constipation may also be associated with gastroparesis. Abdominal pain in gastroparesis responds poorly to treatment. Abdominal pain or discomfort was present in 46%-89% of patients but was not the predominant symptom. In 146 patients with gastroparesis, nausea was present in 92%, vomiting in 84%, abdominal bloating in 75%, and early satiety in 60%. The GCSI scale is used to rate symptom change by either physicians or by the patient’s own self-evaluations. The GCSI total scores are based on three subscales of nausea/vomiting, post-prandial fullness/early satiety, and bloating. Also, a patient-based symptom instrument, the gastroparesis cardinal symptom index (GCSI) has been developed to assess severity of gastroparesis. A simple severity grading scale has been proposed for stratification of symptoms (Table (Table2). These symptoms are non-specific and may mimic other disorders. Symptoms of gastroparesis include nausea, vomiting, early satiety, bloating, post-prandial fullness, abdominal pain, weight loss and/or weight gain. Gastroparesis is diagnosed by the presence of delayed gastric emptying in a symptomatic patient after other potential etiologies such as ulcer disease, mechanical obstruction, gastric cancer or other malignancies are excluded. hypomotility and pyloric spasm, sensory dysfunction (such as impaired fundic relaxation, accommodation and abnormal sensation), electrical dysfunction (such as gastric arrhythmias and abnormal propagation), CNS effects resulting in nausea and vomiting, and others such as bacterial overgrowth, visceral hyperalgesia and gastrointestinal hormones. In general, several factors affect gastric motility. Although neurohumoral control of gastric emptying is incompletely understood, both motilin and ghrelin are peptides secreted by the gastrointestinal endocrine cells that have been shown to increase gastric motor function. However, these slow waves do not directly result in contraction of the gastric smooth muscle, but instead cause a simultaneous release of neurotransmitters from the enteric nerve endings, leading to smooth muscle contraction. Originating in the region of ICCs, electrical activity in the form of gastric slow waves sweeps across the stomach toward the pylorus. Neoplastic(para)-breast, small cell lung, pancreas Medications: opiates, anticholinergics, β-adrenergics, Ca-channel blockers, glucagon, THC, alcohol, tobacco, etc
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