Coupled with signals provided by IL-4, this interaction stimulates the B cell to begin production of a large amount of a particular type of antibody known as IgE. Secreted IgE circulates in the blood and binds to an IgE-specific receptor (a kind of Fc receptor called FcεRI) on the surface of other kinds of immune cells called mast cells and basophils, which are both involved in the acute inflammatory response. The IgE-coated cells, at this stage, are sensitized to the allergen.If later exposure to the same allergen occurs, the allergen can bind to the IgE molecules held on the surface of the mast cells or basophils. Cross-linking of the IgE and Fc receptors occurs when more than one IgE-receptor complex interacts with the same allergenic molecule and activates the sensitized cell. Activated mast cells and basophils undergo a process called degranulation, during which they release histamine and other inflammatory chemical mediators (cytokines, interleukins, leukotrienes, and prostaglandins) from their granules into the surrounding tissue causing several systemic effects, such as vasodilation, mucous secretion, nerve stimulation, and smooth-muscle contraction. This results in rhinorrhea, itchiness, dyspnea, and anaphylaxis. Depending on the individual, the allergen, and the mode of introduction, the symptoms can be system-wide (classical anaphylaxis), or localized to particular body systems. Late-phase response
After the chemical mediators of the acute response subside, late-phase responses can often occur due to the migration of other leukocytes such as neutrophils, lymphocytes, eosinophils, and macrophages to the initial site. The reaction is usually seen 2–24 hours after the original reaction.
The American Society of Health-System Pharmacists guideline recommends against the practice of stress ulcer prophylaxis in non-critically ill patients. Mechanisms
Location
The ulcerations may be superficial and confined to the mucosa, in which case they are more appropriately called erosions, or they may penetrate deeper into the submucosa. The former may cause diffuse mucosal oozing of blood, whereas the latter may erode into a submucosal vessel and produce frank hemorrhage. Lesions
The characteristic lesions may be multiple, superficial mucosal erosions similar to erosive gastroduodenitis. Occasionally, there may be a large acute ulcer in the duodenum (Curling’s ulcer).Generally, there are multiple lesions located mainly in the stomach and occasionally in the duodenum. They range in depth from mere shedding of the superficial epithelium (erosion) to deeper lesions that involve the entire mucosal thickness (ulceration). Formation
The pathogenic mechanisms are similar to those of erosive gastritis.The pathogenesis of stress ulcer is unclear but probably is related to a reduction in mucosal blood flow or a breakdown in other normal mucosal defense mechanisms in conjunction with the injurious effects of acid and pepsin on the gastroduodenal mucosa. Diagnosis
Stress ulcer is suspected when there is upper gastrointestinal bleeding in the appropriate clinical setting, for example, when there is upper gastrointestinal bleeding in elderly patients in a surgical intensive care unit (ICU) with heart and lung disease, or when there is upper gastrointestinal bleeding in patients in a medical ICU who require respirators.Stress ulcer can be diagnosed after the initial management of gastrointestinal bleeding, the diagnosis can be confirmed by upper GI endoscopy.