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Bronchial asthma



Bronchial asthma is characterized by increased reactivity of the mucous membrane of the airways, leading to reversible attacks of strong and inadequate contraction of the bronchi in response to the effects of various irritants. Patients with asthma experience unpredictable attacks of severe shortness of breath, coughing and stridor (wheezing). In some patients, chronic bronchitis or pulmonary heart develops again. There is a condition with incessant seizures - status asthmaticus, which does not stop with conventional anti-asthma drugs for 1 day. This condition may end in death. It is observed in people with long-standing asthma. In some cases, the onset of an asthma attack can be associated with the exposure to an allergen to which the patient has been sensitized before, but often such an agent cannot be detected.

Traditionally, asthma is divided into two forms, exogenous, or acquired (allergic, reagin-mediated, atopic), and endogenous, or hereditary. The exogenous form is an expression of a type I hypersensitivity reaction caused by some external antigen. Varieties of bronchial asthma include atopic (allergic), occupational (including many subtypes), and allergic bronchopulmonary aspergillosis (colonization of aspergillus in the bronchi with the appearance of IgE). In contrast to the exogenous form, endogenous asthma is provided by various non-immune mechanisms: iatrogenic (action of aspirin), viral infections, cooling or inhaled irritating substances (sulfur dioxide), as well as stress and physical overload. In the table. 15.3 lists various types of asthma, factors that provoke its development, and possible mechanisms that are involved in the implementation of a particular type of disease.

Table 15.3.

Types of Asthma

.



Increased reactivity of the mucous membrane of the bronchi occurs, as a rule, against the background of chronic inflammatory processes in which many types of cells and mediators are involved. However, the relationship between such reactivity and background processes is poorly understood.

Atopic (allergic) bronchial asthma. This most common type of disease usually begins in childhood. The triggering factor is the impact of any of the environmental antigens - dust, pollen, animal dandruff, food particles, etc. Some patients have an intrafamilial relationship with the presence of atopy in any of the direct relatives. The first asthmatic attack is often preceded by allergic rhinitis, urticaria (skin allergic disease) and eczema. Patients typically have elevated serum IgE levels. A skin test with an antigen that causes the disease immediately manifests itself in a localized reddish area of ​​edema - a typical sign of an IgE-mediated type I hypersensitivity reaction. Such hypersensitivity is realized in an immediate acute response and in a late reaction.

Contact of pre-sensitized mast cells coated with IgE with the same (initial) or some cross-reacting antigen stimulates the release of mediators from these cells. If antigens are carried through the air, the first reaction will appear on sensitized mast cells located on the epithelium of the bronchial mucosa and in the thickness of its wall. Mast cells secrete mediators that reveal intracellular, dense compounds that bind epithelial cells. From this moment, the penetration of antigens to numerous mast cells located under the epithelium is facilitated. At the same time, direct stimulation of the subepithelial vagal (parasympathetic) receptors is carried out, causing bronchial contraction with the help of central and local reflex mechanisms (including those that are mediated by type C non-myelin sensitive nerve fibers). All this happens within a few minutes after antigenic stimulation.

All this is an acute, or immediate, reaction. Mediators involved in the reactions of IgG antibodies are divided into primary and secondary. Primary mediators include two groups of substances: histamine, which causes contraction of the bronchi through direct and cholinergic reflex effects, and also increases the permeability of venules and the secretion of bronchial glands; chemotaxis factors for eosinophils and neutrophils (for example, leukotriene B4), selectively attracting cells into the antigenic zone. The effect of histamine is important in the first few minutes of an asthmatic attack. Secondary mediators include 4 groups of substances: leukotrienes C4, D4 and E4 - extremely powerful mediators that provide a continuous reduction of the bronchi, increase vascular permeability and secretion of mucus; prostaglandin D2, causing narrowing of the bronchi and vasodilation; platelet activating factor, which leads to aggregation of blood plates and their release from granules of histamine and serotonin; cytokines - interleukin-1, tumor necrosis factor and interleukin-6, which were isolated in patients from mast cell granules. Thus, an acute reaction is manifested in the reduction of bronchi, edema, mucus secretion, hyperemia, and under certain conditions in hypotension, i.e. lowering blood pressure.

Then there comes a late reaction, which develops 4-8 hours after antigenic stimulation and is maintained for 12-24 hours. It is mediated by many white blood cells - neutrophils, eosinophils and lymphocytes involved in the reaction zone by chemotaxis factors and mast cell cytokines, as well as mediators secreted by the cells of a chronic inflammatory reaction. White blood cells produce mediators that stimulate a late reaction. Factors synthesized by many types of cells, first cause the release of histamine from basophils, and then the reduction of bronchi and edema. In the future, neutrophils provide alteration, and the main main protein of eosinophils causes damage to the epithelium and contraction of the bronchi. Manifestations of acute and late reactions in IgE-mediated processes help to explain the long-term nature of pathological changes in bronchial asthma and similar allergic conditions.

Non-atopic (non-reaginous) bronchial asthma. This is the second, less common, but still common type of bronchial asthma that is associated with any kind of respiratory infection. Moreover, viruses, such as rhinoviruses or parainfluenza pathogens (see Chapter 14), are much more common etiological agents than bacteria. Often the family nature of the disease is traced. Patients have a normal level of serum IgE and, as a rule, there are no other forms of allergy. Allergic skin tests are almost always negative. Respiratory viral bronchitis reduces the threshold sensitivity (in other words, increases the susceptibility) of subepithelial vagal receptors to irritants.

Iatrogenic bronchial asthma (caused by drugs). It is known that asthma provokes several pharmacological agents. Persons with recurrent rhinitis and nasal polyps have bronchial asthma caused by aspirin. Such patients are sensitive to very small doses of aspirin, and they have not only asthmatic attacks, but also urticaria. Aspirin appears to inhibit the cyclooxygenase system in arachidonic acid metabolism. In this case, the lipoxygenase system is not damaged, and the enzyme balance is shifted towards the synthesis of leukotrienes, providing a reduction in the bronchi.

Professional forms of bronchial asthma. They are caused by all kinds of fumes (fumes of hot epoxy resins, clay, plastics), organic and inorganic dust (wood, cotton, platinum and other origin), various chemicals (toluene, formaldehyde, etc.). In individuals who are already sensitive to any of these agents, an asthmatic attack occurs from minimal amounts of the agent.
The pathogenetic mechanisms of the development of occupational forms vary depending on the stimulus and include type I hypersensitivity reactions, IgG mediated, direct release of bronchial contracting substances, and unknown types of hypersensitivity reactions.

In the overwhelming majority of cases, morphological changes in bronchial asthma were studied by pathological examination in individuals who died during asthmatic



Fig. 15.13.

Bronchial asthma, status asthmaticus

.

The wall of the bronchus, containing mucus and Kurshman spirals in the lumen (right :) above); hypertrophy of the smooth muscle layer and inflammatory infiltrate are visible in the wall.

someone's fit. However, the results of a study of sputum and biopsy material indicate the same changes. Macroscopically, the lungs are characterized by increased airiness, although there may be small areas of atelectasis. Viscous and sticky mucous plugs, clogging bronchi and bronchioles, are noteworthy. Under the microscope, it is clear that these plugs contain layers of desquamated epithelium and mucus, known as H. Cursmann spirals. Numerous eosinophils and Charcot – Leiden crystals (J.M. Charcot, EVLeyden) are also determined in the cork contents. The latter are clusters of crystalloids formed by the eosinophil membrane protein. Both spirals and crystals can be observed in sputum cytological preparations. Other histological changes include thickening of the basement membrane of the bronchial epithelium, edema and inflammatory infiltration in the walls of the bronchi (Fig. 15.13), the predominance of eosinophils in inflammatory infiltrate (5-50% of all cells of the infiltrate), an increase in subepithelial mucous glands and a thickening of the smooth muscle, reflective layer prolonged reduction of the bronchi.

Bronchiectasis (bronchiectasis, bronchiectasis) is a chronic necrotizing infectious disease of the bronchi and bronchioles, leading to (or associated with) abnormal dilation (s) of these airways. Clinically, bronchiectasis is accompanied by severe and persistent cough, fever, secretion of profuse and fetid purulent sputum. At the height of the disease, coughing fits can be paroxysmal, especially when changing body position (in the morning). Chronic ventilation disorders are often accompanied by shortness of breath and cyanosis. In the later stages of the disease, a pulmonary heart develops, sometimes metastatic abscesses in the brain and amyloidosis form. With bronchiectasis, the expansion of the bronchi and the violation of their drainage function are permanent, while the reversible dilatation of the bronchi accompanies viral and bacterial pneumonia. For bronchiectasis, a polyetiological origin is characteristic. In most cases, they develop in connection with the following three conditions: obstruction of the bronchi by a tumor, foreign bodies, less often mucous plugs (in these cases, bronchiectasis is oriented to the pulmonary segment, “affected” by obstruction) or having a diffuse character, for example, with atopic asthma or chronic bronchitis; congenital or hereditary conditions, which include congenital bronchiectasis (due to a defect in the development of the bronchi), cystic fibrosis (cystic fibrosis, see chapter 22), intralobular sequestration of lung tissue, various immunodeficiency states, immobility of the cilia of the respiratory epithelium and Cartagener syndromes (see below); necrotizing pneumonia, often caused by mycobacterium tuberculosis (see chapter 14), staphylococci or mixed microbial flora.

Bronchial obstruction and infectious lesions are the main causes of bronchiectasis. After obstruction of any bronchus by a tumor or a foreign body, distal to the blockage site, air is absorbed and atelectasis occurs. The latter is often accompanied by inflammation and the presence in the lumen of secretion and exudate, leading to the expansion of the bronchi in those areas where the airways are passable. All of these changes are reversible. However, they become irreversible if the obstruction becomes permanent, especially during the period of growth of the body, since under such conditions the bronchi cannot develop normally, and if there is an infection. In the pathogenesis of bronchiectasis, the infection plays a dual role. Firstly, it causes inflammation of the wall of the bronchi with a weakening of their structure and subsequent expansion. Secondly, extensive damage to the bronchi and bronchioles causes endobronchial obliteration with atelectasis distal to it, and then the development of bronchiectasis around the atelectasis zones.

These two important factors - infection and obstruction of the bronchi - are very clearly manifested in severe bronchiectasis in children associated with cystic fibrosis (see chapter 22). With this disease, squamous metaplasia of the respiratory epithelium develops with a violation of the normal function of the mucus and cilia, the occurrence of infection, necrosis of the walls of the bronchi and bronchioles, as well as the subsequent appearance of bronchiectasis. In young children, pathological changes take the form of bronchiolitis with occlusion of the lumen by granulation tissue.

In Kartagener syndrome (M.Kartagener), consisting of a triad - bronchiectasis, sinusitis and a distorted position of internal organs (situs vescerum inversus) - there is a genetic defect in the mobility of the cilia of the respiratory epithelium. This defect is associated with a structural anomaly of the cilia, expressed in the absence or uneven distribution of dynein (contractile protein), structures on the doublets of ciliary microtubules that provide cilia mobility. The cilia immobility interferes with purification from bacteria, predisposes the sinuses and bronchi to infection, and also negatively affects cell motility during embryogenesis, which leads to situs inversus. In males suffering from this disease, infertility often develops, due to poor sperm motility. Kartagener syndrome is inherited in an autosomal recessive manner and manifests itself in different ways. About 50% of patients with defective cilia for unknown reasons do not have situs inversus. In other patients, instead of motionless cilia, there are cilia with impaired movement (ciliary dyskinesia).

Bronchiectasis usually develops in both upper lobes of the lung, in particular in those bronchi that are located more vertically. The process is more pronounced in the distal bronchi and bronchioles. When the airway is blocked by a tumor or a foreign body, the affected area is clearly limited, as a rule, to one segment. With bronchiectasis, the affected bronchi differ primarily in lumen expansion, sometimes exceeding the norm by 4 times. Extensions of the bronchi can have a cylindrical, fusiform or saccular shape. Significant expansion of even small bronchi and bronchioles allows macroscopically to trace their progress and branching almost to the visceral pleura. These extensions in some places on the cross section resemble cystic cavities.

Histological signs vary depending on the activity and duration of the process. At the height of the development of the active phase of bronchiectasis in the walls of the bronchi and bronchioles, there is exudate reflecting chronic inflammation in the acute phase. Inflammation is associated with desquamation of the respiratory epithelium and focal ulceration. In the preserved epithelium, pseudostratification (false multilayer structure) of the epithelium or true squamous metaplasia is detected. Sometimes the walls of the bronchi or bronchioles are completely destroyed, and a pulmonary abscess is formed or already formed in this zone. Over time, peribronchial fibrosis and cicatricial changes occur, contributing to an even greater deformation of the affected bronchi.

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Bronchial asthma

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