Bronchial Asthma

Bronchial asthma is a disease of the lungs in which an obstructive ventilation disturbance of the respiratory passages evokes a feeling of shortness of breath. The cause is a sharply elevated resistance to airflow in the airways. Despite its most strenuous efforts, the respiratory musculature is unable to provide sufficient gas exchange. The result is a characteristic asthma attack, with spasms of the bronchial musculature, edematous swelling of the bronchial wall and increased mucus secretion. In the initial stage of bronchial asthma, the patient can be totally symptom-free for long periods of time in the intervals between the attacks. As the disease progresses, increased mucus is secreted between attacks as well, which in part builds up in the airways and can then lead to secondary bacterial infections.

There are two forms of bronchial asthma from a genesis point of view:

• Non-allergic asthma (intrinsic asthma)
• Allergic asthma (extrinsic asthma)

Common to them both is a hypersensitivity of the bronchial system. However, in most cases of bronchial asthma, the two forms of asthma are coupled with each other.

A prerequisite for non-allergic bronchial asthma is a genetic predisposition. Nonspecific stimuli such as cigarette smoke, air pollution, medications, emotional factors such as shock, career or family problems, disturbed parent-child relationships but also viral, bacterial or fungal infections can trigger asthma attacks. The bronchial asthma attack can last from a few minutes to several hours; in the life-threatening Status asthmaticus, it can persist for days. In these cases, immediate hospitalization is essential.

The pathogenesis of non-allergic bronchial asthma proceeds via the reflex secretion of acetylcholine. This causes the release histamine from the mast cells of the bronchial wall. This results in immediate contraction of the smooth bronchial musculature along with overproduction of mucus. Here, the atopically inclined person reacts to environmental allergens with immediate production of antibodies. Bronchial asthma must be diagnosed early.

20% of all people suffer from exogenous/allergic asthma. They react, for example, to pollen or dust mites with severe overproduction of immunoglobulins (IgE reaction). Simplifying bronchial asthma somewhat, the following reaction pattern unfolds: the allergen induces a massive production of IgE antibodies. These bind to the surface of the mast cells in the bronchial mucous membrane and thereby effect the release of histamine, which then results in an immediate contraction of the bronchial musculature.

Besides this immediate histamine-induced reaction with bronchial asthma, other mediators are involved in the so-called inflammatory delayed reaction, which are ultimately responsible for the progressive hyperreactivity of the bronchial system in the bronchial asthma patient. In the disease's advanced stage, the victim reacts not only to the specific original allergen: nonspecific stimuli or infections suffice to provoke asthmatic symptoms.

If not adequately treated, pulmonary emphysema not infrequently develops from bronchial asthma, characterized by pneumoectasis with irreparable structural changes in the smallest broncheoles. Because to the perpetual hyperdistention of the lungs and the extra work involved in breathing, these victims are recognizable by their rigid barrel-shaped thorax and pronounced hunchback.

Bronchial Asthma Symptoms

Typical of bronchial asthma is acute shortness of breath, coughing, viscous and phlegmy sputum and difficulty exhaling. Harbingers of an attack can include sweating, sneezing, tickling in the throat and agitation. In the case of allergic asthma, there is also frequently itching around the eyes, headaches and a sensation of constriction.

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