Bronchial asthma (BA) is widespread in the modern world. Every eighth inhabitant of Europe suffers from it. For successful treatment and prevention of a disease, it is necessary to know its causes and developmental characteristics.
That is why much attention is paid to the study of the pathogenesis of bronchial asthma. More on this later in the article.
What is bronchial asthma
Bronchial asthma is a chronic disease characterized by damage to the respiratory tract. Its main manifestation is recurrent attacks of obstruction, that is, blockages of the bronchi. During an attack, it is difficult for the patient to exhale due to the fact that the bronchi spasm at the height of inspiration.
Asthmatics with a long and severe course of bronchial asthma develop irreversible changes in the respiratory system. The connective tissue in the lungs grows, pneumosclerosis develops, the alveoli become thinner (this pathology is called “emphysema”). This further aggravates the course of the disease and worsens respiratory failure.
The pathophysiology of bronchial asthma is based on the increased sensitivity of the bronchi to various provoking factors, and these factors are individual for each.
Etiology and forms of bronchial asthma
The most important role in the etiology of bronchial asthma is attributed to the allergic factor. The provocateurs of the disease are divided into two large groups: endoallergens (produced inside the body) and exoallergens (come from outside). More often the second group of provoking factors becomes the cause of the disease. These include:
- Infectious pathogens – viruses, bacteria, fungi, protozoa.
- Irritants of plant origin – pollen, poplar fluff.
- Allergens of animal origin – wool, feathers, saliva, down.
- Household allergens – dust, household chemicals.
- Food – most often nuts, honey, chocolate, tomatoes cause an allergic reaction.
- Medicines – acetylsalicylic acid, antibiotics.
In some patients, asthma symptoms occur under certain weather conditions. Especially asthmatics do not tolerate rain, high humidity, cold. In this case, asthma is characterized by the absence of seizures if there is no external stimulus.
In the course of numerous studies, American scientists have found that stress can also be a trigger in the development of seizures. He is able to become the root cause of the disease, as well as aggravate the existing bronchial asthma.
Depending on the nature and characteristics of the course of the disease, the following forms of AD are distinguished:
- Atopic – develops as a result of exposure to non-infectious allergens.
- Infection-dependent – an asthma attack occurs after previous infections.
- Glucocorticoid – it is based on an imbalance in corticosteroid hormones.
- Neuropsychic – bronchial obstruction occurs due to prolonged stress.
- Aspirin – taking medications containing acetylsalicylic acid leads to the development of an attack of suffocation.
- Physical exertion asthma – the disease manifests itself after physical exertion.
General scheme of the pathogenesis of bronchial asthma
The pathogenesis of bronchial asthma is based on inflammation in the bronchial wall. Any inflammation is accompanied by increased permeability of the vessel walls.
As a result, plasma (the liquid part of the blood) seeps through them. Fluid accumulates in the bronchial mucosa, edema develops. The lumen of the organ narrows, the passage of air becomes difficult.
But why do some people develop an inflammatory process in the respiratory system when exposed to an allergen, while others do not react to it? Scientists thought about this issue for a long time and came to the conclusion that the whole point is in hereditary predisposition.
Some people from birth have increased activity of special blood cells – type 2 T-helper lymphocytes. Because of this, they release a large amount of immunoglobulin E ( IgE ), a protein that provokes an allergic reaction.
Active synthesis of IgE leads to degranulation (damage) of mast cells, which are located on the wall of the bronchi. They begin to release inflammatory mediators. It is because of these substances that the permeability of the vascular walls increases, and the inflammatory process develops.
But inflammation is only one of the mechanisms of development of bronchial asthma. In addition to him, bronchospasm takes part in the development of the attack. The smooth muscles of this tubular organ are sharply reduced, which leads to the overlap of its lumen.
An equally important role in the development of an asthma attack is played by the increased secretion of mucus by the cells of the bronchial epithelium lining the inner surface of its wall. Thus, three main factors can be distinguished in the pathogenesis of bronchial asthma and the development of asthma:
- inflammation in the bronchial wall;
- increased reactivity of the bronchial tree, due to which the muscles of this organ spasm ;
- increased production of mucus by epithelial cells.
In general, the pathogenesis of bronchial asthma can be divided into three stages:
- Immunological – occurs at the first contact of the body with an allergic agent. It is characterized by the activation of blood cells and the production of IgE .
- Immunochemical – develops upon subsequent contact with an irritant. Already produced immunoglobulins trigger the development of a reaction in the bronchial tree, which is accompanied by the synthesis of inflammatory mediators.
- Pathophysiological – manifested by active changes in the bronchial wall, described earlier. The patient has difficulty breathing, wheezing appears.
In asthmatics, as in allergy sufferers, the number of eosinophils in the blood increases. These cells belong to the group of leukocytes.
They damage the cilia on the epithelium of the bronchi, thereby impairing the evacuation of mucus, and provoke changes in the tissues. Their number in the general blood test is more than 6% speaks in favor of the diagnosis of bronchial asthma.
Features of the pathogenesis of different forms of asthma
The etiology and pathogenesis of bronchial asthma are closely interrelated. The factor that led to the attack determines the mechanism of its development. Further, we will analyze in detail the mechanisms of development of different forms of AD.
This is the most common type of disease. It develops with increased sensitivity of the bronchi to allergens of a non-infectious nature: household, animal, vegetable.
The peculiarity of the mechanism of development of bronchial asthma according to the atopic type lies in its multi-stage nature. Immunological and immunochemical phases are similar to those described in the previous section. And the pathophysiological stage is further subdivided into two stages: early and late.
An early reaction begins within minutes to 2 hours after exposure to allergens. In this case, the mucous membrane of the bronchial walls swells, the secretion of secretions increases, the muscles spasm . There is a blockage of the lumen of the organ, the passage of air is impeded.
The late stage develops approximately 6 hours after the stimulus. It is characterized by the presence of persistent inflammation in the bronchi even after the edema subsides and the spasm stops. If timely treatment is not started, the muscle tissue of the organ is replaced by connective tissue. This process is irreversible.
The infectious-dependent form of AD is typical for people of mature age. It is a complication of previously transferred acute respiratory viral infections, pneumonia, bronchitis and other pathologies of the respiratory system.
This form of asthma is characterized by slow development. Edema of the bronchi increases gradually, the patient’s condition worsens over a long time. The peak of the disease occurs two to three weeks after the infection.
The course of the infectious-dependent form is more severe. The edema, although it increases slowly, does not subside for a long time. This form of asthma is difficult to treat with traditional medications (beta- adrenergic agonists , glucocorticoids).
There are several mechanisms for the development of bronchial asthma after exposure to infectious agents:
- Allergic reaction of the slow type.
- Immediate allergic reaction (similar to the pathogenesis of the atopic form).
- Non- immunological mechanisms .
The delayed-type reaction, according to the name, is characterized by a prolonged increase in edema. At the same time, repeated exposure to the allergic agent is required to start it. The cells of the body secrete special proteins – slow-acting inflammatory mediators.
Eosinophils are also involved in the process. They synthesize a protein that damages the ciliated epithelium of the bronchi. As a result, its cells are unable to evacuate phlegm from the lumen of the organ.
A non-immunological reaction develops when the bronchial cells are directly damaged by infectious agents.
Glucocorticoids are hormones produced by the adrenal cortex. They have a powerful anti-inflammatory effect and inhibit allergic reactions. Therefore, the lack of these hormones in the body can both provoke the first attack and cause constant relapses.
The pathogenesis of the effect of glucocorticoid deficiency in bronchial asthma is as follows:
- The concentration of beta- adrenergic receptors on the bronchial epithelium decreases, which leads to a decrease in susceptibility to adrenaline, which relaxes the muscles of the bronchi.
- The activity of inflammatory mediators is not reduced and is not regulated by hormones.
- The secretion of pro-inflammatory proteins is increased , while the activity of anti- inflammatory proteins decreases.
This form of bronchial asthma most often develops with long-term treatment with glucocorticoids. The uncontrolled intake of hormones affects the adrenal glands, inhibiting their function.
In girls, hormonal BA can occur when the balance of sex hormones is disturbed. An attack is triggered by a decrease in the amount of progesterone in the blood and an increase in estrogen, which is typical for the second half of the menstrual cycle.
The neuropsychic form of bronchial asthma belongs to the group of psychosomatic diseases. These are pathologies in which prolonged stress, depression, anxiety manifest themselves in the form of a violation of the function of an organ and system.
The neuropsychic type of asthma is characterized by the absence of organic changes in the bronchial wall at the initial stages. The attack develops due to a spasm of smooth muscles. Only with a long course of the disease do persistent changes occur in the tissues of the organ.
The development of this form of AD is based on the hypersensitivity of the bronchial epithelium to histamine and acetylcholine. These substances are neurotransmitters that transmit impulses from the periphery to the central nervous system.
In addition, an asthma attack can be triggered by any exercise accompanied by a deep breath.
The pathogenesis of aspirin- type bronchial asthma is based on hypersensitivity to drugs containing acetylsalicylic acid. The substance leads to a disruption in the exchange of arachidonic acid.
This, in turn, stimulates the synthesis of leukotrienes , which cause spasm of the bronchial tree. Not only Aspirin has a similar effect, but also other non-steroidal anti-inflammatory drugs.
Another negative property of salicylates is a decrease in platelet activity. These cells play an important role in blood clotting during vascular injury and in nourishing the vessel walls. Therefore, inhibition of platelet function increases its permeability, which provokes the development of edema.
This form of asthma is most often seen in women between the ages of 30 and 40. Often, patients with aspirin asthma take anti-inflammatory drugs for pain in the back, joints, etc.
Physical stress asthma
An attack of asthma of physical exertion develops with increased physical exertion, 5 – 20 minutes after its onset. Some patients notice suffocation after 5 – 10 minutes after the end of the load.
In most cases, an exercise-induced asthma attack is not very intense. However, sometimes you have to resort to using an inhaler.
Most of the time, a person breathes through the nose. Humidified, purified and warm air has a beneficial effect on the respiratory tract and does not irritate them. With active physical exertion, breathing becomes confused, air enters through the mouth. It dries and irritates the bronchial mucosa.
Epithelial cells begin to actively release inflammatory mediators, mucosal edema develops. Spasm of the smooth muscles of the bronchial wall also takes part in the development of an attack.
Pathogenesis of asthma in children
The pathogenesis of bronchial asthma in children is based on an allergic reaction. The infectious-dependent form is much less common. It usually affects older school children.
In children, the lumen of the bronchi is narrower than in an adult, and the muscles are less developed. Therefore, the main role in the development of an attack in them is played by edema and hypersecretion of mucus. At the same time, in adults, bronchospasm is in the first place. The narrower airway lumen can explain the more severe course of asthma in childhood.
Genetic predisposition plays a significant role in the etiopathogenesis of bronchial asthma in children. A history of allergic diathesis, pollinosis, asthma in parents increases the risk of developing the disease in a child.
For many children, food is an allergen. The first attack of suffocation often develops at 5 – 6 months, when the baby begins to give complementary foods. Sometimes artificial nutrition becomes a provoking factor.
In bronchial asthma, etiology and pathogenesis are inextricably linked. But regardless of the triggering factor, the mechanism for the development of an asthma attack will include three processes: mucosal edema, smooth muscle spasm, and increased mucus secretion.
The disease is often determined by genetic predisposition. But you need to understand that a person will not inherit bronchial asthma from their parents.
Only the increased sensitivity of the immune system to certain allergens will be transmitted to it. That is, the presence of asthma in parents does not yet guarantee its development in a child.
Thus, the pathogenesis of AD is complex and multifaceted. We hope this article has clarified the features of the mechanism of development of this disease.