Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Portal hypertension is defined as an increase of the portal venous pressure over 20 cm H2O or 7 mm Hg, respectively. It may be induced by different types of portal venous stenosis or obstruction, primarily by cirrhosis and fibrosis of the liver and, less frequent by posthepatic disorders such as the Budd-Chiari-syndrome or congestive heart failure. Portal hypertension is followed by ectasia and phlebosclerosis of the portal vein, by splenomegaly, ascites and by various types of collateral circulation. Among these, oesophageal varices, are most important since they often lead to acute upper gastrointestinal haemorrhage, the major complication of portal hypertension. Bleeding from oesophaeal varices is essentially based on atrophy of the squamous epithelium, caused by ischemia from local hypoxia and venous stasis. Portal hypertension and the frequently compromised blood clotting mechanism due to reduced synthesis of clotting factors in the liver aggravate the bleeding. Atrophy of the esophageal mucosa presents an area of decreased resistance likely to ulcerate with easy erosion of the varices--usually lying very superficially--; with mechanical irritation by food or peptic erosion from gastroesophageal reflux being frequent inducers of hemorrhage.
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PMID:[Pathologic-anatomic reflections on portal hypertension (author's transl)]. 624 21

Cystic fibrosis (CF), the most common lethal autosomal recessive disease in white populations, is characterized by dysfunctional chloride ion transport across epithelial surfaces. Although recurrent pulmonary infections and pulmonary insufficiency are the principal causes of morbidity and death, gastrointestinal symptoms commonly precede the pulmonary findings and may suggest the diagnosis in infants and young children. The protean gastrointestinal manifestations of CF result primarily from abnormally viscous luminal secretions within hollow viscera and the ducts of solid organs. Bowel obstruction may be present at birth due to meconium ileus or meconium plug syndrome. Complications of meconium ileus include volvulus, small bowel atresia, perforation, and meconium peritonitis with abdominal calcifications. Older children with CF may present with bowel obstruction due to distal intestinal obstruction syndrome or colonic stricture, and tenacious intestinal residue may serve as a lead point for intussusception or cause recurrent rectal prolapse. Radiologic studies often demonstrate thickened intestinal mucosal folds in older children and uncommonly show colonic pneumatosis, peptic esophageal stricture due to gastroesophageal reflux, and duodenal ulcer. Appendicitis due to inspissated secretions is uncommon. Obstruction of ducts and ductules produces exocrine pancreatic insufficiency, pancreatitis, cholestasis, cholelithiasis, and cirrhosis with portal hypertension. On imaging studies, the pancreas is commonly small and largely replaced by fat, sometimes displays calcifications, and is rarely replaced by macrocysts. Radiologic features of hepatobiliary disease include an enlarged radiolucent liver from steatosis, gallstones, a shrunken nodular liver, splenomegaly, and portosystemic collateral vessels. With the improved survival of CF patients, an increased risk for developing gastrointestinal carcinomas has been established, many occurring as early as the 3rd decade.
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PMID:Gastrointestinal manifestations of cystic fibrosis: radiologic-pathologic correlation. 883 77

This article presents commonly encountered and clinically significant entities affecting the gastrointestinal (GI) system with emphasis on assisting the clinician in developing management strategies to reduce the associated risks. Xerostomia, osteoradionecrosis, gastroesophageal reflux disease, and ulcerative diseases occurring in the proximal portion of the GI system and antibiotic-associated diarrhea, pseudomembranous colitis, adynamic ileus, and malabsorption problems occurring in the distal portion are presented. Lastly, suggestions for managing patients who have splenomegaly and splenectomy are addressed.
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PMID:Gastrointestinal diseases and considerations in the perioperative management of oral surgical patients. 1808 27

Laparoscopic splenectomy was first reported in 1991-1992 by several groups. The impact and role of laparoscopy for splenectomy can be considered as significant as that for gallbladder disease, achalasia, esophageal reflux, and adrenal disease. In many centers, the laparoscopic approach is now routine for most cases of elective splenectomy. The laparoscopic approach is associated with reduced morbidity, especially pulmonary, wound, and infectious complications. This article reviews a standardized approach to laparoscopic and hand-assisted splenectomy and covers indications, operative strategy, and complications. Several special considerations, including massive splenomegaly, postsplenectomy thrombosis of the portosplenic venous system, and accessory spleens are also discussed.
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PMID:Laparoscopic splenectomy: standardized approach. 2142 69

We present the unique case of adult hyperinsulinism hyperammonemia syndrome (HI/HA). This condition is rarely seen in children and even more infrequently in adults. A 27-year-old female with HI/HA, generalized tonic-clonic seizures, staring spells, and gastroesophageal reflux disease presented with diffuse abdominal pain, hypoglycemia, confusion, and sweating. She reported a history of significant nausea, vomiting, and diarrhea, which had been present intermittently over the past year. On examination, she was found to have a soft, nontender, and mildly distended abdomen without splenomegaly or masses. She had a normal blood pressure and was tachycardic (130 bpm). Her initial complete blood count and basic metabolic panel, excluding glucose, were within normal limits. She was found to have an elevated peripherally drawn venous ammonia (171 mmol/L) and near hypoglycemia (blood glucose 61 mg/dL), which were drawn given her history of HI/HA. She was continued on home carglumic acid and diazoxide, glucose was supplemented intravenously, and she was started on levetiracetam for seizure prophylaxis. An upper endoscopy (esophagogastroduodenoscopy [EGD]) was performed and was unremarkable, and biopsies taken were within normal limits. Following the EGD, she underwent a gastric emptying study that showed delayed emptying (216 minutes), consistent with a new diagnosis of gastroparesis, the likely etiology of her initial abdominal pain on presentation. This was subsequently treated with azithromycin oral solution. We present this case to raise awareness of this rarely encountered syndrome and to provide the basic principles of treatment.
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PMID:Hyperinsulinism Hyperammonemia Syndrome, a Rare Clinical Constellation. 2696 38