Airway chronic bronchial asthma

Sympathomimetics (drugs that mimic the sympathetic nervous system) are used primarily to treat reversible airway obstruction caused by bronchospasm associated with acute and chronic bronchial asthma, exercise-induced bronchospasm, bronchitis, emphysema, bronchiectasis (abnormal condition of the bronchial tree), or other obstructive pulmonary diseases. 

W ithin the past few years a number of new drugs have been introduced to treat respiratory disorders, such as bronchial asthma and disorders that produce chronic airway obstruction. This chapter discusses the bronchodilators, dragp that have been around for a long time but are still effective in specific instances, and the newer antiasthma drugs that have proven to be highly effective in the prophylaxis (prevention) of breathing difficulty. 

Bronchial asthma is defined as a chronic inflammatory disease of the lungs it affects an estimated 9 to 12 million individuals in the U.S. Furthermore, its prevalence has been increasing in recent years. Asthma is characterized by reversible airway obstruction (in particular, bronchospasm), airway inflammation, and increased airway responsiveness to a variety of bronchoactive stimuli. Many factors may induce an asthmatic attack, including allergens respiratory infections hyperventilation cold air exercise various drugs and chemicals emotional upset and airborne pollutants (smog, cigarette smoke). 

Bronchodilation can be achieved by the use of ipratropium in conditions of increased airway resistance (chronic obstructive bronchitis, bronchial asthma). When administered by inhalation, this quaternary compound has Uttle effect on other organs because of its low rate of systemic absorption. 

Chronic exposure to fumes of heated glacial acetic acid in a canning factory has been associated with a late airway response resulting in chronic inflammation and severe bronchial asthma. Inhalation challenge induced a late asthmatic response, confirming sensitization. ... 

MicroNefrin Chronic obstructive lung disease, chronic bronchitis, bronchiolitis, bronchial asthma, and other peripheral airway diseases croup (postintubation and infectious). 

Aerosol For management of bronchial asthma in adults and children 5 or more years of age, the usual starting dose is two metered sprays inhaled 4 times/day at regular intervals. Do not exceed this dose. Not all patients will respond to the recommended dose, and a lower dose may provide efficacy in younger patients. Advise patients with chronic asthma that the effect of therapy is dependent upon its administration at regular intervals, as directed. Introduce therapy into the patient s therapeutic regimen when the acute episode has been controlled, the airway has been cleared and the patient is able to inhale adequately. 

Injection - Heart failure secondary to chronic lung disease cardiac arrhythmias brain tumor acute alcoholism delirium tremens idiosyncrasy to the drug increased intracranial or CSF pressure head injuries acute bronchial asthma upper airway obstruction. Because of its stimulating effect on the spinal cord, morphine should not be used in convulsive states (eg, status epilepticus, tetanus, strychnine poisoning) concomitantly with MAOIs or in those who have received such agents within 14 days. 

Epidural/Intrathecal administration Limit epidural or intrathecal administration of preservative-free morphine and sufentanil to the lumbar area. Intrathecal use has been associated with a higher incidence of respiratory depression than epidural use. Asthma and other respiratory conditions The use of bisulfites is contraindicated in asthmatic patients. Bisulfites and morphine may potentiate each other, preventing use by causing severe adverse reactions. Use with extreme caution in patients having an acute asthmatic attack, bronchial asthma, chronic obstructive pulmonary disease or cor pulmonale, a substantially decreased respiratory reserve, and preexisting respiratory depression, hypoxia, or hypercapnia. Even usual therapeutic doses of narcotics may decrease respiratory drive while simultaneously increasing airway resistance to the point of apnea. Reserve use for those whose conditions require endotracheal intubation and respiratory support or control of ventilation. In these patients, consider alternative nonopioid analgesics, and employ only under careful medical supervision at the lowest effective dose. 

Pulmonary disease Pilocarpine has been reported to increase airway resistance, bronchial smooth muscle tone, and bronchial secretions. Administer with caution and under close medical supervision in patients with controlled asthma, chronic bronchitis, or chronic obstructive pulmonary disease. 

It decreases reversible bronchospasm associated with chronic bronchitis, pulmonary emphysema, bronchial asthma, silicosis, tuberculosis and sarcoidosis. The resultant decrease in airway obstruction may relieve the dyspnea associated with bronchospasm. 

Asthma is a chronic inflammatory condition characterized by bronchial hyper-responsiveness and reversible airway obstruction. Cytokine release from a variety of cell types such as eosinophils, lymphocytes and other inflammatory cells produces epithelial sloughing, plasma protein extravasation from the tracheobronchial microcirculation and airway remodeling. Bronchial mucosal inflammation is present in all patients. The primary goal of asthma management is to maintain control of the disease process by reducing symptoms and improving lung function. 

Asthma is a chronic inflammation disorder of the airways that make the bronchial tubes swell and narrow, producing wheezing, chest tightness, breathlessness, and coughing symptoms. Airway narrowing in asthma is caused by inflammation, bronchospasm, and bronchial hyperactivity. Asthma does not affect the alveoli and is reversible spontaneously and by drug treatment. Asthma is fully reversible and thus is different from COPD and emphysema, which are accompanied by destruction of alveolar walls and are irreversible. 

Today, EM treatment has been established as a basic treatment for DPB. Furthermore, erythromycin has been widely applied in treating chronic airway inflammatory disorders, not only in lower airway diseases (DPB, chronic bronchitis, bronchiectasis, or bronchial asthma [31-33]) but also upper airway diseases (chronic sinusitis or exudative otitis media). Other forms of 14-membered ring macrolides, i.e., clarithromycin (CAM) [34-36] and roxithromycin (RXM) [37] have also been used for a similar purpose. 

Erythromycin is a macrolide antibiotic widely used for the treatment of upper and lower respiratory tract infections. Recent reports further showed that EM and its analogues are effective for the treatment of chronic airway diseases such as DPB, bronchial asthma, and chronic sinusitis [5, 15, 32]. This effectiveness is considered to be apart from their antimicrobial actions, because they are effective at half of the recommended dosage and even in cases without concomitant infection. Its precise mechanisms, however, remain unclear. Several cytokines including IL-1, TNF-a, and IL-8 have been reported to be elevated in HALF from patients with such airway inflammatory diseases (Table II), and to be decreased... 

To assess the effect of macrolide antibiotics on IL-8 production by inflamed airway epithelium, bronchial epithelial cells were obtained from 10 patients (3 with DPB, 5 with sinobronchial syndrome, 1 with nonatopic asthma associated with chronic sinusitis, and 1 with diffuse bronchiectasis, mean age of 54.8, all were non-or ex-smokers) under fiber optic bronchoscopy as previously reported [64, 65]. Spontaneous IL-8 release by airway epithelial cells from inflamed airways was significantly suppressed with the addition of EM and CAM, but not with ABPC in vitro [60]. Khair et al. [19] reported that EM inhibited release of IL-8 as well as of IL-6 from H. influenzae endotoxin-stimulated normal bronchial epithelial cells. 

Asthma is a common disease affecting approx 10% of the population in developed countries, and the prevalence and mortality are rising. The disease has characteristic symptoms, namely intermittent airway obstruction, airway hyperresponsiveness, and increased numbers of activated inflammatory cells and airway structural changes as a result of chronic airway inflammation. The primary underlying abnormality in bronchial asthma is thought to be the unique form of airway inflammation, including particularly eosinophils and mast cells, that gives rise to reversible airway obstruction and hyperresponsiveness. 

Asthma has been traditionally viewed as a chronic inflammatory condition characterized by airway infiltration by activated mast cells and eosinophils, orchestrated by specific Th2-type T lymphocytes (24). However, neutrophils have recently been implicated in more severe forms of asthma, and it is also increasingly evident that the bronchial epithelium, endothelium, fibroblasts, and the extracellular matrix play a dynamic role in the airway inflammation of asthma (Fig. 2). 

Bronchial hyperresponsiveness (BHR) to nonspecific stimuli is a cardinal feature of asthma and has been shown to relate to the severity of disease (30). BHR is generally regarded as a consequence of the chronic airways inflammation of asthma. Airway sensitization, mediated by IgE, appears to be closely related to nonspecific BHR, perhaps through an indirect effect of pro-inflammatory cytokines and mediators (31,32). 

Bronchial asthma is characterized by an increased responsiveness of the trachea and bronchi to various stimuli and is manifested by a widespread narrowing of the airways that changes in severity either spontaneously or as a result of therapy (91). Chronic bronchitis is defined as a condition with chronic or recurrent bronchial hypersecretion, cough and expectoration during at least 3 months for at least 2 successive years (92). Chronic bronchitis is often associated with chronic airways obstruction with minimal reversibility it is then called chronic obstructive pulmonary disease (COPD). Chronic airways obstruction in COPD is believed to be caused by either emphysema or irreversible obstructive changes in the peripheral airways, or both. There is an overlap between asthma and COPD, and many patients may have features of both diseases (93). Asthma is considered an important risk factor for the development of COPD. Bronchial hyperresponsiveness is a hallmark of asthma, whereas its importance in COPD is more obscure. Airway inflammation is a key factor for the development of bronchial hyperresponsiveness (94). Table 4 shows the main pathophysiological features of airways obstruction in asthma, chronic bronchitis, and emphysema. 

Therapeutic aerosols play a prominent role in the treatment of diseases of the lower airways, such as bronchial asthma and chronic bronchitis. It has been proposed that an increased deposition in the peripheral airways would be of value, in particular for treatment with inhaled corticosteroids. In patients with asthma, tracheobronchial deposition could be increased, practically independent of airway dimensions, by inhaling large aerosol particles extremely slowly (17,114). This could be a potentially useful approach of therapeutic importance, particularly in the treatment of patients with airways obstruction. Still, another possibility to enhance deposition of therapeutic aerosols in asthmatics could be the use of carrier gases such as helium-oxygen mixture (113). 

Asthma is an extremely complex condition characterized by variable and reversible airways obstmction combiaed with nonspecific bronchial hypersensitivity (1 3). The cause of asthma, which is not always readily diagnosed (4), remains unknown. Days, if not weeks, ate needed to document the spontaneous reversal of the airways obstmction ia some patients. Asthmatics experience both an immediate hypersensitivity response and a delayed late-phase reaction, each mediated by a different pathway. Chronic asthma has come to be viewed as an inflammatory disease (5). The late-phase reaction plays a key role ia iaduciag and maintaining the inflammatory state which ia turn is thought to iaduce the bronchial hyperresponsiveness (6). The airways obstmction results from both contraction of airways smooth muscle and excessive bronchial edema. Edema, a characteristic of inflammatory states, is accompanied, ia this case, by the formation of a viscous mucus which can completely block the small airways. 

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