What is pathio-physiological treatment in bronchial asthma

The common denominator underlying the asthmatic diathesis is a nonspecific hyperirritability of the tracheobronchial tree. In asthmatics it correlates well with the clinical features of the illness.

When airway reactivity is high, lung function becomes unstable, symptoms are more severe and persistent, therapy required to control the patient’s complaints increases.

In addition, the magnitude of diurnal fluctuations in lung function becomes greater, and the patient tends to awaken at night or in early morning with breathlessness.

In both normal and asthmatic subjects, airway reactivity is known to rise following viral infections of the respiratory tract and exposure to oxidant air pollutants such as ozone and nitrogent dioxide.

Viruses have more profound consequences, and following a seemingly trivial upper respiratory tract infection, airway responsively may remain elevated for many weeks.

In contrast, with exposure to ozone, airway reactivity remains high for only a few days. Allergens can cause for weeks. If the dose of antigen is high enough, acute episodes of obstruction may occur daily for a prolonged period of time following a single exposure.

A number of causes have been postulated for the increased airway reactivity of asthma, however the basic mechanism remains unknown. The most popular hypothesis at present is at present is that or airway inflammation.

Following exposure to an initiating stimulus, mediator containing such cells as mast cells, basophils, and macrophages can be activated to release a variety of inflammatory compounds which produce direct effects on airway smooth muscle and capillary permeability, thereby more chronic one.

The latter may be brought about by the release of chemotic factors, which recruit cellular elements to the site of injury. In addition, it is thought that the acute and chronic effects of mediator release and cellular infiltration may result in epithelial damage with involvement of neural endings within the airways and the activation of an axon reflex.

In this fashion, an essentially local phenomenon can be amplified to have widespread effects throughout the tracheobronchial tree.The stimuli that interact with airway responsiveness and incite .

Episodes of asthma can be grouped into seven major categories: allergenic, pharmacologic, environmental, occupational, infectious, exercise related and emotional.

Allergic asthma is dependent on an IgE response controlled by T and B-lymphocytes and activated by the interaction of antigen with mast cell bound IgE molecules.

Most of the allergens that provoke asthma are airborne, and in order to induce a state of sensitivity, they must be reasonably abundant for considerable periods of time.

Once sensitization has occurred, however, the patient can then exhibit exquisite responsivity so that minute amounts of the offending agent can produce significant exacerbations of the disease.

Immunologic mechanisms appear to be casually related to the development of asthma in 25 to 35 percent of all cases and contributory in perhaps another third.

Higher prevalences have been suggested, but it is difficult to know how to interpret the data because of confounding factors. Allergic asthma is frequently seasonal and it is most often observed in children and young adults.

A nonseasonal form may result from allergy to feathers, animal danders, dust mites, molds, and other antigens present continuously in the environment. Exposures to antigen typically produces an immediate response in which airway obstruction develops in minutes and then resolves.

In 30 to 50 percent of patients, a second wave of Bronchoconstriction, the so-called late reaction, develops 6 to 10 hours laters. In a minority, only a late reaction occurs.

It was formerly thought that the late reaction was essential to the development of the increase in airway reactivity that follows antigen exposure. Recent data show this not to be the case.

The mechanism by which an inhaled antigen provokes an acute episode of asthma is unknown but seems to depend in part, on antigen antibody interactions on the surface of pulmonary mast cells with the subsequent generation and release of the mediators of immediate hypersensitivity.

Current postulates hold that very small antigenic particles penetrate the lung’s defenses and come in contact with mast cells that are interdigitating with the epithelium at the luminal surface of the central airways.



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