Aerosol Airtek is intended for the treatment of bronchial asthma in patients who are indicated for combination therapy with long-acting ß2-adrenergic agonists and inhaled corticosteroids, namely:
- in case of insufficient control of the disease against the background of constant monotherapy with inhaled corticosteroids with periodic use of short-acting β2-adrenergic agonists;
- in case of adequate control of the disease during therapy with inhaled corticosteroids and long-acting β2-adrenergic agonists.
Features of application
Pregnant
Prescribing Airtek during pregnancy is advisable only in cases where the expected benefit to the mother outweighs the possible risk to the fetus. For the treatment of pregnant women, low effective doses of fluticasone propionate are prescribed to maintain adequate control of asthma symptoms.
Children
Children and adolescents under 16 years of age who are treated with high doses of fluticasone propionate (usually ≥1000 mcg/day) are at particular risk for systemic effects. Systemic effects are usually caused by treatment in high doses for a long time. Possible systemic effects include Cushing's syndrome, Cushingoid signs, adrenal suppression, acute adrenal crisis, growth retardation in children and adolescents, decreased bone mineralization, cataracts and glaucoma, less commonly possible mental disorders and behavioral changes, including psychomotor hyperactivity, sleep disturbances, agitation, depression or aggression.
It is recommended to regularly monitor the growth dynamics of children receiving inhaled GCS for a long time. The dose of inhaled corticosteroids should be reduced to the minimum effective dose to control asthma symptoms.
“Traps” that you can fall into when treating bronchial asthma
| Figure 1. People with asthma often have a reduced outlook for the future, although some tend to underestimate the severity of their symptoms. |
What is the differential diagnosis between asthma and COPD? What are the causes of possible diagnostic errors? What is the main role of b-agonists in the treatment of bronchial asthma? How are corticosteroids prescribed?
Despite the increased competence of doctors and the availability of effective treatments, mortality from bronchial asthma remains high. Many deaths and even most hospitalizations could be prevented with proper treatment.
It must be remembered that managing patients with asthma is a complex and lengthy process.
- Chronic bronchial asthma
Underestimation of the degree of respiratory failure. The severity of the patient’s condition and the degree of incompetence of his respiratory system may not be recognized if we neglect to carefully ascertain all manifestations of the disease and construct a diagram of measurements of the maximum flow rate (MSF) of exhaled air.
People with asthma often have reduced prospects for the future, although some tend to underestimate the severity of their symptoms. To identify such an underestimation, you need to ask the patient in detail whether he has a cough or wheezing at night or during physical activity.
If patients are unable to achieve the best possible lung function, then to correct this condition, it is necessary to first calculate the normal MSP of exhaled air for a given patient, using the chart included with the peak flow meter.
If the measured MRV is more than 20% less than the calculated one, it is worth conducting a study of the reversibility of this condition, which is done by comparing the MRV or vital capacity (VC) before and after treatment.
The necessary therapy may be as little as a single dose of a bronchodilator, but if this does not increase the MOP by 20%, the calculated level, more serious measures may be needed, such as a three-week course of systemic corticosteroids (30 mg prednisolone per day for adults). In this way, the best achievable level of MSP is determined, which is used to guide subsequent treatment.
Sometimes patients report a decrease in shortness of breath, but the MSP values do not change. In such cases, it is necessary to measure VC using a spirometer, which can confirm the improvement not determined by the MSP (Fig. 2). All doctor's offices are currently equipped with spirometers.
| Figure 2. Change in vital capacity under the influence of a course of corticosteroids. MSP may not change, but an increase in vital capacity indicates an improvement in the condition |
Bronchial asthma disguised as chronic obstructive pulmonary disease (COPD). Patients who suffer from shortness of breath and are diagnosed with COPD or emphysema may have an underlying bronchospastic element due to asthma.
Such patients should undergo a reversibility study as described above. Any improvement in lung function can be supported by adequate treatment of asthma. In the absence of improvement in pulmonary function, the use of corticosteroids is not justified, but only leads to unwanted side effects such as osteoporosis.
What a doctor should remember when observing patients with bronchial asthma |
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Chronic use of short-acting b-agonists . Treatment of asthma with chronic use of β-agonists has been shown to increase pulmonary hyperresponsiveness and worsen bronchial asthma [1]. If a patient is using beta-agonists routinely rather than occasionally, their use should be followed by inhaled corticosteroids or, if corticosteroids are already being used, by increasing the dose sufficient to control asthma. Thus, b-agonists are reserved for cases of shortness of breath and wheezing.
The latest guidelines for the treatment of bronchial asthma in Britain recommend starting with a high dose of inhaled or systemic corticosteroids to achieve rapid control, then gradually reducing the dose to the minimum that ensures the patient feels normal and optimal values of MSP or vital capacity against the background of minimal use of a bronchodilator (Fig. 3) . The rapid relief achieved with corticosteroids improves the patient's mood and increases his confidence in treatment.
| Figure 3. It is recommended to start with high doses of corticosteroids, and then gradually reduce the dose to the minimum (optimal MRP or VC values) |
Recent evidence suggests that corticosteroids should be started as early as possible in all asthmatics, not only to control symptoms but also to prevent progressive structural lung damage caused by chronic inflammation [2,3]. This means that corticosteroids should be preferred over b-agonists once the diagnosis is confirmed by the MCP chart. β-agonists remain reserve drugs of last resort.
Possibility of alternative treatment. Although inhaled corticosteroids should be the cornerstone of asthma treatment, some other medications may be used in cases that are difficult to treat. It has been proven that theophyllines have an anti-inflammatory effect in fairly small doses, but their possible interaction with other drugs must be taken into account in each individual case.
It is advisable to prescribe ipratropium to elderly patients. Nedocromil and cromoglycate are sometimes effective.
Long-acting bronchodilators such as salmeterol may provide relief, especially at night, by blocking bronchoconstrictor mechanisms. However, it is necessary that all of the above drugs be accompanied by the use of adequate doses of corticosteroids.
Inhalation technique. It is important to ensure that patients develop proper inhaler handling skills. The doctor should help you choose the type of inhaler that is most convenient for the patient and check its performance. To do this, the doctor's office must have a full set of inhalers.
Spacers. Used in conjunction with aerosol inhalers, spacers facilitate drug penetration into the lungs and reduce both pharyngeal accumulation and systemic absorption through swallowing.
Spacers help coordinate drug release with inhalation. This is especially important when inhaled corticosteroids are used. Since corticosteroids are only used twice daily, the bulky spacer can be kept at home.
Spacers provide better accumulation of the drug in the lungs than nebulizers. It is necessary to use them correctly: shake the inhaler so that the medicine is mixed with the carrier, and inject the mixture once, followed by a quick inhalation [4].
Trigger factors. Unrecognized trigger factors can be at home, at work, or on vacation, that is, almost anywhere. Anamnesis will help identify the source. For example, with occupational bronchial asthma, the condition improves during vacations and on weekends. The absence of the irritant reduces or eliminates the manifestations of the disease and reduces the need for medications.
An often overlooked problem may be secondhand smoke. Drugs such as b-blockers and nonsteroidal anti-inflammatory drugs (NSAIDs) can also cause asthma.
- Attack of bronchial asthma
Use of nebulizers (nebulizers) without background corticosteroid therapy. When treating an acute asthmatic attack without oral corticosteroids, nebulizers are still used, which deliver a higher dose of beta-agonists. This does relieve bronchospasm, but since a high dose of b-agonists does not affect the accompanying inflammatory process, it is necessary to immediately give the patient oral corticosteroids to prevent the attack from worsening; the effect of bronchodilators decreases as swelling of the mucous membrane increases.
If the severity of the attack is such that a nebulizer is required, systemic corticosteroids should be prescribed. Even with a moderate attack, bronchodilators alone provide only temporary relief and there is a risk of a recurrence of the attack - possibly in the dead of night!
Delayed administration of oral corticosteroids. If anti-inflammatory therapy is not carried out, swelling of the mucous membrane increases in patients, which leads to recurrence of attacks. These patients often require hospitalization and high doses of corticosteroids for several days before their condition stabilizes.
Patients susceptible to rapid-onset attacks require corticosteroids and bronchodilators as early as possible. They must be able to recognize worsening conditions, have corticosteroids on hand at all times, and know how to use them. These patients should not be forced to wait for a physician to see them (Figure 4).
| Figure 4. Dependence of the development of acute attacks on the time of administration of corticosteroids and as a result of the use of long courses of systemic corticosteroid therapy. (1) Corticosteroids are prescribed immediately after the attack occurs: recovery occurs quickly. (2) Corticosteroids given after 6 hours: recovery delayed. (3) Corticosteroids are prescribed after 12 hours: the attack is severe and prolonged, recovery is slow |
Patients with gradual onset of attacks may want to wait and see if an increased dose of inhaled corticosteroids combined with a bronchodilator helps.
Inadequate course of systemic corticosteroids. Sometimes prescribed corticosteroids are canceled until the attack is completely relieved, which leads to continued bronchial hyperreactivity and another attack.
Such a chain of events can lead the patient to the false conclusion that he has bronchial asthma, which is difficult to treat.
The situation can be corrected by a long course of corticosteroids, continuing for several days after the condition has stabilized, and gradually reducing their dose until the minimum maintenance level is reached.
Stop monitoring the patient after an acute attack or hospitalization. Difficulties arise when discontinuing a systemic corticosteroid and prescribing an inhaled one. During this transition period, careful monitoring is necessary; Once the condition has stabilized, the dose of inhaled corticosteroid is gradually reduced to the minimum required so that the disease does not manifest itself and pulmonary function is optimal.
The goal of subsequent treatment is to maintain the highest SMR achieved in the hospital after a course of systemic corticosteroids.
A consultation some time after discharge provides a good opportunity to review the patient's management plan, find out what is wrong, and make appropriate adjustments.
- Differential diagnosis
Coughing and wheezing with purulent sputum is sometimes mistaken for a lung infection. However, the sputum of asthmatic patients contains much more eosinophils than polymorphic cells and bacteria. In old age, left ventricular failure and cardiac asthma should suggest preexisting bronchial asthma. Be careful with b-blockers!
Sudden shortness of breath may be due to pneumothorax or pulmonary embolism. Wheezing occurs with pulmonary tuberculosis, bronchial carcinoma, or a foreign body and can be clearly localized. Therefore, a chest x-ray should be performed in any patient with adult-onset asthma.
- Priority measures
After making a diagnosis, the doctor’s main goal is to free the patient from the manifestations of the disease and optimize lung function, as well as establish control over the disease. To do this, specially trained medical personnel must educate patients and check that they are following all instructions correctly.
Of course, in some cases this may be difficult, but the vast majority of patients can master the prescribed action plan.
All patients must:
- be able to recognize the onset of an attack
- know how to use high doses of b-agonists;
- start taking prednisolone orally on your own;
- know when to call the doctor or go to the hospital;
- Anyone suffering from attacks should be provided with corticosteroids.
References
1. Sears MR, Taylor DR et al. Regular inhaled b-agonist treatment in bronchial asthma. Lancet 1990;336:1491–1396. 2. Tari Haahtela et al. Comparinson of terbutaline with budesonide in newly detected asthma. N Engl J Med 1991;325:388–392. 3. Redingon AK, Howarth PH Airway remodeling in asthma. Thorax 1997;52:310–312. 4. O'Callaghan C., Barry P. Spacer devices in the treatment of asthma. BMJ 1997;314:1061–1062.
Spirometry for chronic bronchial asthma
A barrel chest in chronic bronchial asthma occurs due to air retention in the peripheral parts of the lungs, which leads to constant maintenance of the chest in a state of inspiration. The trapped air is not exhaled and uselessly occupies most of the lungs (residual volume). This reduces the volume of air (vital capacity) entering the lung.
Air is retained due to chronic inflammation, causing swelling of the lining of the peripheral bronchioles. When treated with corticosteroids, the swelling subsides and air is released. This is proven by an increase in vital capacity determined spirometrically. MSP may not change (see Fig. 2.)
Note!
Asthma attack
- Promptly initiate corticosteroid therapy if asthma is so severe that it requires the use of bronchodilator nebulizers
- Patients prone to frequent attacks should have their own supply of corticosteroids and know how to use them
- Every asthmatic patient should have a written plan for managing their condition.
Chronic asthma/COPD
- Every patient must undergo an allergy test
- Use an adequate dose of corticosteroids to prevent bronchodilator dependence
- Use bronchodilators only to stop an attack
Overdose
Signs and symptoms that can be expected in an overdose of salmeterol, typical of excessive stimulation with β2-agonists, include dizziness, tremor, headache, tachycardia, increased systolic blood pressure. If treatment with the drug must be discontinued as a result of an overdose of the β2-agonist included in the drug, appropriate steroid replacement therapy should be prescribed. Additionally, hypokalemia may occur, so serum potassium levels should be monitored and the need for potassium replacement therapy should be considered.
Salmeterol + Fluticasone (Salmeterolum + Fluticasonum)
Salmeterol stimulates β2-adrenergic receptors, which are located in the membranes of smooth muscle cells of the bronchi, uterus, gastrointestinal tract, bladder detrusor, blood vessels (vessels of skeletal muscles, lungs, coronary vessels). In this case, the smooth muscles of the bronchi relax, the tone and contractile activity of the myometrium, bladder, gallbladder and bile ducts decrease, motility and tone of the stomach and intestines decrease, and blood vessels dilate.
Salmeterol is lipophilic, due to which it not only penetrates well into the membranes of bronchial smooth muscle cells, but is also retained in the lipid layer of the membranes, creating a kind of depot of the substance in the immediate vicinity of the receptor. This delays the activation of β2-adrenergic receptors (apparently, the low rate of diffusion through the lipid layers of the membrane determines the delayed onset of the substance’s action on the receptor and is the reason for the slow development of the drug’s effect).
Relaxation of smooth muscles upon stimulation of β2-adrenergic receptors coupled to Gs proteins that stimulate adenylate cyclase is associated with an increase in cAMP levels and activation of cAMP-dependent protein kinase in smooth muscle cells. cAMP-dependent protein kinase A inhibits myosin light chain kinase, as a result, the phosphorylation of myosin light chains is disrupted and its interaction with actin does not occur. cAMP-dependent protein kinase A inhibits phospholamban (Ca2+-ATPase inhibitor), as a result, in smooth muscle cells the activity of Ca2+-ATPase, which transports Ca2+ from the cytoplasm to the sarcoplasmic reticulum, increases and the concentration of cytoplasmic Ca2+ decreases. All this leads to a decrease in the tone and contractile activity of smooth muscles. An increase in blood glucose levels is possible, since β2-adrenergic receptors control the process of glycogenolysis in the liver and skeletal muscles and insulin secretion in the pancreas, and when they are stimulated, phosphorylase is activated and glycogen breakdown increases, resulting in an increase in blood glucose levels.
Insulin secretion increases when β2-adrenergic receptors are stimulated.
The anti-inflammatory effect of fluticasone is due to interaction with intracellular glucocorticoid receptors - the formation of dimers of the glucocorticoid-glucocorticoid receptor complex (release of the receptor from bonds with heat shock proteins 70 and 90 and immunophilin). After which the activated receptor penetrates into the nucleus, binds to glucocorticoid-sensitive regulatory elements of DNA - a specific effect on gene expression (activation and suppression). And interaction with other protein transcription factors, including NFκB and AP-1, which regulate the expression of many proteins of the immune system, leads to suppression of the expression of genes encoding some cytokines, collagenase and stromelysins.
Note!
Description of the drug Airtek air. d/ing. dosage 25/250mcg/dose cont. 120 doses on this page are a simplified author’s version of the apteka911 website, created on the basis of the instructions for use.
Before purchasing or using the drug, you should consult your doctor and read the manufacturer's original instructions (attached to each package of the drug). Information about the drug is provided for informational purposes only and should not be used as a guide to self-medication. Only a doctor can decide to prescribe the drug, as well as determine the dose and methods of its use.
