Second-generation antihistamines, such as loratadine, cetirizine or desloratadine, selectively antagonize peripheral H1 receptors, and are less sedating, less anticholinergic, and generally preferred over the first-generation antihistamines. Fexofenadine, a new-generation antihistamine that blocks histamine H1 receptors, may be less sedating than some second-generation antihistamines.People who do not respond to the maximum dose of H1 antihistamines may benefit from increasing the dose, then to switching to another non-sedating antihistamine, then to adding a leukotriene antagonist, then to using an older antihistamine, then to using systemic steroids and finally to using ciclosporin or omalizumab.H2-receptor antagonists are sometimes used in addition to H1-antagonists to treat urticaria, but there is limited evidence for their efficacy. Systemic steroids
Oral glucocorticoids are effective in controlling symptoms of chronic hives however they have an extensive list of adverse effects such as adrenal suppression, weight gain, osteoporosis, hyperglycemia, etc. Therefore, their use should be limited to a couple of weeks. In addition, one study found that systemic glucocorticoids combined with antihistamines did not hasten the time to symptom control compared with antihistamines alone. Leukotriene-receptor antagonists
Leukotrienes are released from mast cells along with histamine. The medications, montelukast and zafirlukast block leukotriene receptors and can be used as add on treatment or in isolation for people with CU. It is important to note that these medications may be more beneficial for people with NSAID induced CU. Other
Other options for refractory symptoms of chronic hives include anti-inflammatory medications, omalizumab, and immunosuppressants. Potential anti-inflammatory agents include dapsone, sulfasalazine, and hydroxychloroquine.
Bowel sound may be increased (borborygmi) due to excessive peristaltic action of the stomach. Fullness in the left hypochondrium may also be present. Causes
The causes are divided into benign or malignant. Benign
Peptic ulcer disease
Infections, such as tuberculosis; and infiltrative diseases, such as amyloidosis. A rare cause of gastric outlet obstruction is blockage with a gallstone, also termed "Bouveret syndrome" or "Bouverets syndrome". In children congenital pyloric stenosis / congenital hypertrophic pyloric stenosis may be a cause. A pancreatic pseudocyst can cause gastric compression. Pyloric mucosal diaphragm could be a rare cause. Malignant
Tumours of the stomach, including adenocarcinoma (and its linitis plastica variant), lymphoma, and gastrointestinal stromal tumours

Pathophysiology
In a peptic ulcer it is believed to be a result of edema and scarring of the ulcer, followed by healing and fibrosis, which leads to obstruction of the gastroduodenal junction (usually an ulcer in the first part of the duodenum). Diagnosis
The most confirmatory investigation is endoscopy of upper gastrointestinal tract. Laboratory often find hypochloremic, hypokalemic, and alkalotic due to loss of hydrogen chloride and potassium. High urea and creatinine levels may also be observed if the patient is dehydrated. Abdominal X-ray may show a gastric fluid level which would support the diagnosis. Barium meal and follow through may show an enlarged stomach and pyloroduodenal stenosis.Gastroscopy may help with cause and can be used therapeutically. Differential diagnosis
The differential diagnosis of gastric outlet obstruction may include: early gastric carcinoma, hiatal hernia, gastroesophageal reflux, adrenal insufficiency, and inborn errors of metabolism.