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.
Source of Information
