Endogenous bronchial asthma. Aspirin bronchial asthma.

Endogenous bronchial asthma (idiopathic) usually develops in adulthood and includes all other types of the disease (triggers are non – immune and non-obvious). With this form, there is no family history of atopic diseases (no rhinitis, conjunctivitis), the level of eosinophils in the blood and sputum is increased, seizures occur under the influence of internal stimuli (more often – portable pneumonia, chronic bronchitis or ARVI); a known allergen has not been identified; there is a hypersensitivity to bacteria or their products; no other allergic symptoms; IgE level is normal. Usually this BA occurs after 30-40 years (more often in people who already have chronic inflammatory changes in the airways and long-term contact with irritants ), beta-2-AG is poorly treated, therefore, corticosteroids are required. Hyposensitization is ineffective (since the allergen is not detected), there is no tendency to “mitigate” the course of the disease, but, on the contrary, is characterized by its steady progression due to the development of mixed airway obstruction (asthmatic form of COPD) and frequent development of AS. Aspirin bronchial asthma occurs in 7% of cases. Aspirin can sometimes cause a fatal asthma attack within minutes of taking it. This BA is based on a violation of the metabolism of arachidonic acid: aspirin blocks the production of cyclooxygenase and the metabolism proceeds along the lipoxygenase pathway (the production of bronchodilating prostaglandin E decreases and the production of bronchoconstrictors increases (prostaglandin F2a, leukotrienes , a slowly reacting substance of anaphylaxis does not occur ). intolerance to aspirin (NSAIDs, or herbal saliyylates ) – recurrent polypous rhinosinusopathy – asthma attacks Bronchial asthma from FN (8%) is more often observed in young people with asthma. It is based on excessive loss of moisture from the respiratory tract during rapid breathing. their cooling, release of mediators and bronchospasm with the following symptomatology – heaviness in the chest, vising with or without coughing, shortness of breath.A breathless attack usually occurs 15-20 minutes after FN (more often running, cycling) against the background of inhalation of cold air. Sometimes an attack appears and whether it increases after the termination of FN. Warming of the inhaled air can reduce clinical manifestations. This phenomenon is well known to asthmatics who wear a scarf around their face when walking in cold air.


Frequent complications of bronchial asthma: • respiratory: AS, EL, ODN (CDI is very rare in bronchial asthma), pneumonia, spontaneous pneumothorax (with the appearance of emphysema under the skin or in the mediastinum) at the height of the attack (often caused by medical manipulations – the use of intermittent positive pressure and lavage of the bronchi), atelectasis or collapse of the lungs (due to mucous plugs), which are often difficult to identify radiographically; • cardiac (often caused by the intake of large, toxic doses of theophylline and beta2-AG): drop in blood pressure, cardiac arrest, MI, arrhythmias, myocardial dystrophy, acute pulmonary heart (rarely chronic); • gastrointestinal (often caused by oral corticosteroids): peptic ulcer, bleeding, ulcer perforation; • metabolic: hypokalemia (due to the intake of corticosteroids and beta-2-AG) and metabolic acidosis; • hypoxic brain damage (“respiratory encephalopathy”). Bronchial asthma is not usually fatal disease, but the lethality when it bowl due nekupiruyuschimsya AU (development asphyxiation due to abrupt obstruction of small bronchi viscous sputum) or sudden death (due to a fatal Cardy-cial arrhythmias – ventricular fibrillation) caused paradoxical reacting an excessive amount of beta-2 -AH with its own adrenal system, asthmatics under stress conditions, which is accompanied by a large release of endogenous catecholamines. Phases of bronchial asthma: exacerbation, remission (stable, unstable). Criteria for exacerbation of asthma (based on the clinical picture and peak flowmetry indices ): obvious insufficiency of previous basic therapy (decreased sensitivity to I (32-AH and increased need for them by more than 4 inhalations in the previous 24 hours compared to the usual dosage), the appearance and an increase in bronchial obstruction – a decrease in FEV, or peak expiratory flow rate ( PEF ) according to the peak flow meter data , more than 25% of the individual norm, measured in the morning hours, for more than 3 days and outside of asthma attacks; violation of the drainage function of the bronchi (sputum is coughing up worse). can proceed in the form of: • an acute attack (expiratory shortness of breath, wheezing, spastic cough, or a combination of these symptoms against the background of a noticeable decrease in FEV); • a prolonged state of bronchial obstruction – prolonged (days, weeks) difficulty breathing with clinically expressed bronchial obstruction (from it the severity of FN dyspnea and shortness of breath largely depend), against which regular asthma attacks of varying severity may appear.

Arachidonic acid metabolites in the pathogenesis of pneumonia and bronchitis

The participation of arachidonic acid metabolites in the pathogenesis of inflammatory diseases of the lungs and bronchi has attracted increasing attention of researchers in recent years. Arachidonic acid (AA) is found in the phospholipids of cell membranes and makes up about 1% of free fatty acids in plasma, circulating as a complex with albumin. When a cell is activated by a stimulus that changes the types and geometric orientation of phospholipids and activates phospholipase A2, arachidonic acid is released with subsequent metabolism by the cyclooxygenase or lipoxygenase pathway. In normally functioning cells, such a stimulus can be the products of free radical lipid oxidation. The formation of prostaglandins (PG) and thromboxanes Tx ) by the cyclooxygenase pathway passes through unstable, biologically inactive PGa2 and PGN2 (Table 1). Subsequently, the synthesis of cyclooxygenase metabolites occurs in different cells in different ways, in accordance with the enzyme that predominates in these cells. Cyclooxygenase enzyme PGN- synthetase – has two isoforms called cyclooxygenase 1 (CO-1) and cyclooxygenase 2 (CO-2), which have 61% of the same amino acid sequence. CO-1 and CO-2 mediate physiological and inflammatory processes, respectively, and respond to various stimuli with the formation of prostanoids . CO-1 is present in platelets, endothelial cells, gastric mucosa, kidneys, etc. CO-2 is synthesized de novo , mainly in macrophages, but also in the lungs, heart, blood vessels, spleen and is responsible for the massive, uncontrolled production of prostanoids when cells are stimulated with bacterial endotoxins or cytokines.

The lipoxygenase pathway of AA metabolism leads to the formation of various leukotrienes (LT), monohydroxyeicosatetraenoic acids (HETE), and lipoxins (LX), the synthesis of which, as in the case of cyclooxygenase products, depends on the enzyme prevailing in the cells. Lipoxins (A and B) are trihydroxy – acids obtained from arachidonic acid as a result of the sequential action of two lipoxygenases (LO) -15-LO and 5-LO. The enzyme 5-lipoxygenase is found only in the cells of the myeloid lineage. Cells with a complete enzymatic composition (eosinophils, mast cells and basophils) are capable of generating significant amounts of sulfidopeptide leukotrienes (LTS4, LTD4, LTE4). Platelets possess the LTS4 synthetase enzyme, but do not have 5-LO. In this regard, platelets are able to generate LTS4 only from LTA4 formed by neutrophils, due to the mechanism of transcellular metabolism. A similar mechanism exists between neutrophils and vascular endothelial cells. LT biosynthesis also requires a transmembrane protein known as 5-LO-activating protein, which plays a role in binding 5-LO to cell membrane phospholipids to initiate catalysis. In normally functioning cells, hydrolysis of membrane lipids with release of AA occurs at a rather low level, which provides a low level of eicosanoid synthesis . Under physiological conditions, there are systems that inhibit the synthesis of eicosanoids . In particular, lipocortin , a highly polar protein present in various cells, including monocytes and neutrophils , has an inhibitory effect . The formation of lipoxidin is regulated by the level of circulating corticosteroids in the body, which induce its formation. The action of lipocortin is associated with inhibition of the activity of phospholipase A, in connection with which the release of AA from phospholipids is inhibited and, thus, the formation of prostaglandins, leukotrienes and platelet activating factor (PAF) is blocked . The activity of cyclooxygenase and lipoxygenase is regulated by fatty acid hydroperoxides, which activate these enzymes even in small amounts. In this case, the pathological signal grows according to the “vicious circle” mechanism. The mechanism of the return of the functioning of the system to the physiological level, apparently, is associated with autocatalysis and autoinhibition of enzymes, the reproduction of which takes a certain time.

Clinic of an attack of bronchial asthma. Objective signs of an attack of bronchial asthma.

Usually, during a severe attack, the patient is forced to sit up in bed (due to severe shortness of breath in the supine position). He takes the “coachman’s pose” – with the support of his hands to include auxiliary muscles in the breathing act (a sign of BA severity). It is difficult for him to speak (speech is intermittent, only short phrases) and breathe. The inhalation is quick, and the exhalation is long (2-4 times longer), difficult and painful. With severe obstruction, breathing is slowed down (RR 10-12 per minute) There is an unproductive, debilitating cough (sometimes it appears early in the morning and is the only symptom of AD) with a small amount of thick, sticky sputum due to impaired bronchial drainage. Sometimes, after coughing up phlegm, there is some relief. Objectively, tachypnea (more often), prolonged exhalation, suffocation, swelling of the neck veins and face, participation in the act of breathing of the auxiliary muscles of the shoulder girdle, back and abdominal wall are objectively detected ; pale cyanosis of the lips, ears; in the eyes – fear; the face and chest are covered with cold sweat, since the respiratory muscles (diaphragm, accessory muscles) perform a tremendous amount of work (often overwhelming) under significant unfavorable mechanical conditions. In a severe attack, signs of acute emphysema of the chest are determined: it “freezes” in the act of maximum inspiration, the ribs begin to take a horizontal position. It is possible to note the cushingoid face as a result of prolonged use of GCS. Percussion over the lungs reveals a box sound, omission of the diaphragm. On auscultation of the lungs against the background of often weakened breathing, a variety of dry, “musical” wheezes (or reminiscent of “squeak”) are determined (preferably at the end of exhalation), indicating the defeat of the bronchi of various sizes. They can be heard simply by the ear, at a distance (remote). Lack of vising in a patient who has other seizure symptoms is an ominous symptom indicating that the airway is severely narrowed and there is not enough air turbulence to cause vising .

In many patients, all these symptoms disappear after the end of the attack (outside of it, nothing is heard over the lungs). But in a number of patients with frequent attacks of suffocation and in the interictal period, wheezing persists. If asthma attacks are rare, then in the phase of remission, when examining the patient, the chest is usually normal, the size of the heart is small. If they are enlarged, then echocardiography , heart examination is necessary . Blood pressure during an attack may rise slightly (especially DBP). The pulse is quickened, usually more than 100 beats / min (often due to the intake of large doses of beta2-AG), sometimes weak filling. In half of patients with asthma with FEV1 less than 1.0 L, a paradoxical pulse is determined: during inspiration (decreases) and expiration (increases), the difference in SBP is more than 10 mm Hg Auscultation reveals tachycardia and muffling of heart sounds. Elderly patients may develop arrhythmias (more often AF). Bradycardia and the absence of a paradoxical pulse indicate fatigue of the respiratory muscles. The severity of the attack can also be judged by the severity of hypoxemia with hypercapnia. The patient may not have all of these symptoms. The duration of an attack of bronchial asthma is also important, since the mechanisms of bronchial obstruction change as the attack lasts. At first, its main cause is bronchospasm (it stops in a few minutes), and later – the formation of mucous plugs and edema. To stop the latter, several days of intensive treatment may be required.

Persistent bronchial asthma. Chronic bronchial asthma.

Persistent bronchial asthma – for many months, even years, there are persistent symptoms ( vising , heaviness in the chest, shortness of breath and cough) and lifestyle restrictions. It is characterized by short periods when there are no symptoms or no remissions at all, there is a chronic pathology of the airways with large variations in the data of the daytime peak fluometry . Symptoms appear in response to or without a certain factor. It is necessary to take beta-2-AG regularly, and often GCS. Episodic, intermittent bronchial asthma – episodes of attacks (obstruction of the bronchi or cough) are replaced by asymptomatic periods when treatment is not required. Symptoms may recur (usually at night, early in the morning) daily, weekly, monthly, or annually. The attack can be severe and require treatment for several days or even weeks. This form is more common in young people with atopy (eg, allergic rhinitis). There is a complete reversibility of bronchial obstruction, in the period of remission there is no airway obstruction and symptoms. Chronic bronchial asthma (usually severe, with frequent exacerbations) – clinically these persons have a combination of BA symptoms (FEV1 less than 70%; its annual decrease is 25-38 ml) and COPD (small airway damage) with the development of CDF and chronic heart disease COPD). The clinical picture of bronchial asthma consists of the following syndromes.

• Broncho – obstructive – choking and vising – noisy breathing with the presence of sound, distant wheezing associated with breathing, decreased FEV]. • Bronchopulmonary – cough, sputum production, chest pain, shortness of breath, intoxication, hypoxia. • Cardiopulmonary – tachycardia, increased blood pressure, pulmonary hypertension, decreased IOS, ECG – heart rhythm disturbances or syndromic coronary pathology. • Allergic – the appearance of an attack of suffocation upon contact with a known allergen, positive skin scarification tests, urticaria, pruritus, blood eosinophilia . • Neuropsychic – develops with prolonged hypoxemia and hypercapnia, manifests itself as respiratory encephalopathy – variable neurological symptoms: headache, drowsiness, irritability and even aggression, tremors, euphoria, inadequate behavior. With any variant of the course of bronchial asthma, the main clinical symptoms are the same (but variable, transient, usually worsening at night and provoked by triggers). More often, there is an attack of expiratory suffocation, difficulty and wheezing ( whistling ), spastic cough or a combination of these symptoms against the background of a sharp decrease in PSV; less often – heaviness in the chest, aggravated by FN. Three periods can be conventionally distinguished in the development of an asthma attack: precursors (sometimes they are absent) -> peak -> reverse development. Harbingers may appear several minutes or hours before the onset of the attack. So, with atopic bronchial asthma, it can be abundant mucous sputum, sore throat, “sand” in the eyes, vasomotor reactions from the nasal mucosa or itching of the skin around the nose; with endogenous bronchial asthma – the appearance of a dry, repeated and painful cough, often occurring in a dream, which wakes up the patient. An attack of bronchial asthma can occur at any time, anywhere. Moreover, in a number of people unexpectedly, with unexplained airway obstruction due to bronchospasm (sudden asphyxia bronchial asthma). During an attack, subjective complaints may vary (adaptation to bronchial asthma changes). So, they can quickly disappear if the patient inhales beta-2-AG in a timely manner. The peak period of an attack is characterized by the sudden appearance of expiratory suffocation (“you cannot breathe freely”), heaviness in the chest (“it is difficult for air to pass through the respiratory tract), more often in the morning, when getting out of bed (morning mobility) or at a certain time at night (an attack -“alarm clock”). Nighttime choking is often caused by daily fluctuations in cortisol, catecholamines in the blood (the maximum decrease in their levels at night) and the maximum level of histamine at this time; increased vagal tone; an increase in the level of allergens of feather pillows, bed mites; accumulation of sputum overnight; inhalation of organophosphate insecticides (which are used to treat bed, furniture); direct aspiration or gastroesophageal reflux (due to acidic stimulation of the receptors in the lower esophagus, causing bronchoconstriction ). An attack of bronchial asthma can reach a very strong force in a few minutes. It can be classified by severity as mild, moderate, and severe.

local_offerevent_note November 22, 2020

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