Mucosal oedema

VIII.b.1.3. Extensive disease. Rectal therapies are insufficient, and patients should receive, if outpatients, oral corticosteroids, and if in-patients oral or parenteral corticosteroids with full supportive treatment including parenteral fluids and blood transfusion. The need for intensive in-patient treatment is indicated by the presence of severe diarrhoea, anaemia, fever and tachycardia with radiographic evidence of colonic mucosal oedema on plain X-ray, or of toxic megacolon. 

The small reductions in the subglottic region of the airways secondary to mucosal oedema causes significant changes to airflow. It is this change that results in the bark-like cough and respiratory distress. 

Many corticosteroids undergo metabolism via CYP3A4 and are substrates of P-gp. They are used to suppress inflammation in the respiratory tract, reducing mucosal oedema and decreasing bronchial secretions. They are employed both to prevent acute exacerbations of chronic airways disease and to treat acute flare-ups. They may be subject to interactions when administered orally, but interactions with high-dose inhaled formulations are thought to occur due to steroid that is deposited in the oropharynx, swallowed and absorbed via the gastrointestinal tract. 

The relative importance of many of the mediators is not precisely defined but they interact to produce mucosal oedema, mucus secretion and damage to the ciliated epithelium. Breaching of the protective epithelial barrier allows hyperreactivity to be maintained by bronchoconstrictor substances or by local axon reflexes through exposed nerve fibres. Wheezing and breathlessness result. The bronchial changes also obstruct access of inhaled drug to the periphery, which is why they can fail to give full relief. 

In contrast to the acute mediator-induced bronchocon-striction and mucosal oedema characteristic of the EAR, there is now considerable evidence that the LAR is associated with inflammatory cell accumulation and activation. This situation is generally considered to be analogous to that seen in chronic airway inflammation, but some caution is needed in extrapolating the results of... 

Mucosal oedema contributes to the airway narrowing present in asthma. Contraction of endothelial cells in post-capillary venules leads to the formation of gaps which allow the outflow of plasma. This occurs in response to mediators released from inflammatory cells such as H, PGs, LTs, and platelet aaivating factor (PAF) which probably act directly on endothelial cells and bradykinin which may act via neural reflexes. In addition to obstructing the airway lumen, exuded plasma may... 

The bronchial histopathology of patients who have died of asthma shows an intense infiltration of the bronchial mucosa with inflammatory ceUs, particularly eosinophils, macrophages, lymphocytes and to a lesser extent neutrophils. Deposition of eosinophil products in the bronchial epithelium and subepithelium is a particularly prominent feature (Filley etal., 1982). Epithelial denudation, dilatation of blood vessels, mucosal oedema and hypertrophy of both submucosal glands and bronchial smooth muscle are other features. Many of these features of asthma deaths are also observed in milder and well-controlled asthmatics. Elevated numbers of eosinophils, moncytes/macrophages and activated lymphocytes are persistent features observed in bronchial biopsies... 

Histologic features in the airways of patients with OA are similar to those found in individuals with non-occupational asthma (NOA). Common pathologic sequelae include airway smooth muscle hypertrophy, mucosal oedema, increased mucus production from greater numbers of mucous secreting glands and goblet cells, and deposition of collagen beneath the basement membrane (Fabbri et al., 1993). BAL fluids from normal, NOA and OA subjects have similar inflammatory-cell count distributions (90 to 95 per cent alveolar... 

Animals given OC perorally show gastric mucosal hyperaemia, oedema, focal bleeding and focal necrosis. 

In UC, histological changes are limited to the mucosa and superficial submucosa with deeper layers being unaffected, except in fulminant colitis. The major changes are distortion of crypt architecture and basal plasma cells and basal lymphoid cell infiltrate. Mucosal vascular congestion with oedema, focal haemorrhage and inflammatory cell infiltration may also be present (Fig. 8.2). 

Fig. 11.6a,b. Transverse (a) and axial (b) views of ascending colon wall thickening, reflecting neutropenic enterocolitis characterized by marked mucosal and submucosal oedema and occasional haemorrhage... 

Acute gastritis may be subdivided on the basis of the endoscopic appearance into mild and advanced gastritis. The former exhibits a generalised oedema, moderately swollen folds, limited mucosal bleedings, and small erosions. The stomach wall is less pliable with reduced distension. The same, but more... 

Ibuprofen may cause gastric ulcers (63 ), and haematemesis has been reported (99 ). Gastric mucosal erythema and oedema with petechial haemorrhages and erosions have been reported (35 ). Tests for faecal occult blood may be positive (106 ). Ibuprofen suppositories may cause local irritation (110 ). 

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