The Physiology Of Asthma
Medical
research in the past decades has seen an explosion
in our understanding of the allergic
processes including asthma. These processes
occur basically as a result of hyper responsiveness
that is inherent in certain individuals.
This disease process manifests
itself as a variety of symptoms, some of which
include wheezing, cough, and chest tightness,
shortness of breath and sputum production.
This can be understood by the
fact that whenever the body recognizes an antigen
that is a foreign body; it tries to remove it
or minimize its effect on body’s own cells
by a mechanism known as inflammation. It is
actually this immune response that is exaggerated
in certain individuals that leads to allergic
asthma. There are two types of responses which
human body can produce, a primary response and
a secondary response.
A primary response occurs on first
exposure to an antigen or a foreign body. It
is short lived starting after sometime and producing
less mediators or chemical substances but capable
of causing sensitization. Whenever the body
is exposed again to the same antigen, a secondary
response occurs. It occurs readily, is more
severe and produces more inflammatory mediators,
hence leading to more signs and symptoms.
These responses produce changes
in the body which constitute the signs and symptoms
of the disease. Inflammation anywhere in the
body manifests as few cardinal signs. These
include redness, heat production, pain at the
site of inflammation, swelling at the site and
inability of the tissues to perform their function.
When these changes occur in the lungs they give
rise to the symptoms of asthma. In order to
explain physiology of asthma, one should be
aware that lungs are two large, soft organs
of sponge-like consistency located within the
chest.
Heart is located in the center
of the chest. Lungs are separated from the abdomen
by a strong dome-shaped muscle, the diaphragm.
The diaphragm moves down when one inhales and
exhales air. During normal breathing, the lungs
also change shape, expanding during inspiration
and contracting during expiration.
The main function of the lungs
is to supply adequate oxygen to the blood and
to remove carbon dioxide from the blood. The
proper exchange of these gases between outside
air and the air in the depths of the lungs depends
on clear air passages. Air enters the body through
the nose and mouth and travels down into the
smaller airways which are called bronchi and
bronchioles.
The smallest airways are microscopic
in size and end in clusters of tiny air sacs
called alveoli. There are some 300 million of
these small balloon-like air sacs in the adult
lung. Each is surrounded by a network of very
fine blood vessels called capillaries. The walls
of these capillaries and those of the air sacs
are thin which permits the passage of gases
between the airway system and the blood. During
inhalation that is breathing in the lungs fill
with air containing oxygen which can then enrich
the blood.
During exhalation breathing out,
carbon dioxide which has been removed from the
blood is expelled by the lungs. When there is
excessive mucous or secretions as a result of
inflammation of the airways, it causes swelling
and tightening of the smooth muscle around the
airways, with the result that air flow is restricted
and the normal functions of the lung are affected
and finally breathing becomes more difficult.
It is not known whether all cases
of asthma require a specific stimulus or not.
The immunologic pathways, various
mediators, and inflammatory cells that participate
in allergic diseases have all been subject to
intense scrutiny. In parallel, a wide range
of drugs has become available to the practitioner
who manages allergic diseases, and for the first
time many agents are based on an understanding
of specific inflammatory pathways in allergic
disease.
But, despite this increased understanding
and the new pharmacological
agents, the worldwide epidemic of allergic
disorders continues. This epidemic was first
described with respect to asthma, but more recently
an increased incidence of other allergic diseases,
and of atrophy itself, has been identified.
Numerous theories have been put forward to explain
this epidemic, ranging from misadventures with
symptomatically effective superficial therapies
to a diminished incidence of protective infections
in early childhood.
The former is thought to have led
to an increase in allergic
diseases because of the use of drugs that
merely cover up chronic inflammatory conditions,
and the latter has been attributed to a failure
of the developing immune system to receive the
signals needed for a protective immune response. |