Acute bronchitis Acute bronchitis (AB) is an inflammatory disease of the trachea and bronchi, which is characterized by an acute course and reversible diffuse lesions of the mucous membrane. AB is one of the most common respiratory diseases, which is more common in children and the elderly (more often men). This disease is more susceptible to people living in areas with a cold and humid climate, working in drafts, in damp cold rooms. OB is often combined with damage to the upper respiratory tract (rhinopharyngitis, laryngitis, tracheitis), or is observed in isolation. isolated.
Contributing factors: acute infections of the upper respiratory tract; focal infections of the paranasal sinuses and tonsils; violation of nasal breathing; cooling; smoking; decrease in the reactivity of the body (after serious illnesses, operations, with hypovitaminosis, poor nutrition, etc.).
Clinic The disease begins acutely. Sometimes symptoms of acute respiratory disease precede - runny nose, sore throat, hoarseness. The clinical picture of OB consists of symptoms of general intoxication and bronchial lesions. Symptoms of general intoxication: weakness, headache, pain in the muscles of the back and legs, aches, chills. The temperature may rise to subfebrile, sometimes high, or remain normal.
Symptoms of bronchial lesions: dry, rough, painful, unproductive cough with a small amount of mucous sputum; after 1 - 3 days, the cough becomes wet, mucopurulent sputum is coughed up. Pain in the throat and trachea decreases, the temperature decreases, the general condition improves; shortness of breath is possible - a symptom of obstruction (impaired patency) of the bronchi;
Treatment Treatment of OB is mainly symptomatic, usually outpatient, in severe cases - inpatient: bed rest at high temperature measures that eliminate bronchial irritation, facilitate breathing (airing the room, avoiding smoking, cooking, using odorous substances. plentiful warm drink (tea with raspberry , lemon, honey, lime blossom, milk with soda.
Phytotherapy with expectorant action: steam inhalation of decoctions of herbs (eucalyptus, St. John's wort, chamomile), essential oils(anise, eucalyptus, menthol); ingestion of herbal infusions of thermopsis, licorice root, marshmallow, plantain leaves, coltsfoot, thyme herb, anise fruit, eucalyptus tincture.
Drug therapy includes: - antitussive sedatives for dry painful cough (codeine, codterpine, sinekod, libexin, levopront); – bronchodilators for broncho-obstructive syndrome (salbutamol, berotek in inhalations, eufillin tablets, broncholithin in the form of syrup, etc.); – expectorants (Coldrex broncho, Doctor Mom, bronchipret, herbion primrose syrup, marshmallow syrup, etc.); – mucolytics (fluditec, fluimucil, acetylcysteine, carbocysteine, mucodin; ambroxol, bromhexine, ambrobene, lazolvan, solvin, etc.); -local antiseptics, anti-inflammatory and analgesic drugs with simultaneous damage to the nasopharynx (hexoral, strepsils, septolete, stopangin, iox, etc.); – antipyretic drugs (analgin, acetylsalicylic acid, paracetamol, etc.);
– drugs of combined action are also used: bronchodilator and antitussive (broncholitin), expectorant and anti-inflammatory (psyllium herbion syrup), expectorant and antitussive (codelac) antitussive, antiallergic and antipyretic (Coldrex Night) – general tonic (vitamins, immunomodulators); -antibacterial drugs (better taking into account the microbial spectrum) are used in the absence of the effect of symptomatic treatment, high temperature, the appearance of purulent sputum, as well as in elderly and debilitated patients. The minimum duration of treatment is 5 - 7 days. The most commonly used antibiotics are: semi-synthetic penicillins (ampicillin, amoxicillin), macrolides (erythromycin, rovamycin, azithromycin), cephalosporins (cefaclor, cephalexin), tetracyclines (doxycycline) and sulfonamides: biseptol (bactrim), sulfalene, etc.
Etiology about. bronchitis Most often, the etiological factor of acute bronchitis is various viruses, less often bacteria. Allergic acute bronchitis is possible. Bronchitis often accompanies diphtheria, typhoid fever, whooping cough. The etiology of bronchitis and their clinical features often depend on the age of children.
Bronchitis clinic Duration of fever averages 2-3 days Cough is dry and obsessive at the beginning of the disease, later - wet and productive. Auscultation reveals widespread diffuse rough dry and wet medium and large bubbling rales.
Clinical picture of acute bronchiolitis Expressed signs of respiratory failure: cyanosis of the nasolabial triangle, expiratory or mixed dyspnea, tachypnea. Often there is swelling of the chest, participation of auxiliary muscles inhalation, retraction of compliant places of the chest. Percussion reveals a boxed percussion sound. Auscultation reveals diffuse, moist, finely bubbling rales on inhalation and exhalation.
Clinic of acute obstructive bronchitis Signs of bronchial obstruction often develop already on the first day of SARS, noisy wheezing with prolonged exhalation, heard at a distance (remote wheezing). Children can be restless, often change body position. Expressed tachypnea, mixed or expiratory dyspnea; the chest is swollen, its compliant places are drawn in. Percussion sound box. Auscultation reveals a large number of scattered moist medium and large bubbles.
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Chronic bronchitis: ● chronic inflammation of the bronchial mucosa (edema); ● hypersecretion (hypercrinia); ● increased viscosity of the bronchus. secret (discrinia); ● violation of the protective cleansing function of the bronchi; ● cough (permanent or periodic) with sputum Chronic bronchitis - the main clinical manifestations (cough and sputum) persist for at least 3 months a year for at least 2 years in a row.
Slide 3: Etiology
1. Smoking (active and passive). 2. Long-term exposure to volatile substances (pollutants) = industrial and domestic (silicon, cadmium, NO 2, SO 2, etc.). 3. Viral-bacterial infection of the airways Smoker index = cf. number of cigarettes smoked per day × number of months in a year, i.e. by 12. ● HCI greater than 160 is a serious risk factor for the development of COPD. ● HCI more than 200 - "malicious" smoker
Slide 4: Forms of chronic bronchitis:
● Damage to the proximal (large and medium) bronchi ● Favorable clinical course and prognosis. ● The main clinical manifestation is a persistent or periodic cough with sputum. 1. Chron. non-obstructive bronchitis (CNB): ● Signs of unexpressed bronchial obstruction occur only during periods of exacerbation or in the most advanced stages of the disease.
Slide 5: Forms of chronic bronchitis:
● Deep degenerative-inflammatory and sclerotic changes. not only proximal, but also distal airways. ● The clinical course is usually unfavorable. ● Prolonged cough. 1. Chron. obstructive bronchitis (COB): ● Early damage to the respiratory structures and steadily increasing shortness of breath (expiratory) and the formation of COPD ● Decreased exercise tolerance.
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Slide 7: Complications of chronic bronchitis (usually COB and COPD):
● emphysema; ● respiratory failure (chronic, acute acute on the background of chronic); ● bronchiectasis; ● secondary pulmonary arterial hypertension; ● cor pulmonale (compensated and decompensated).
Slide 8: Clinical picture of CNB:
Remission phase: 1. "Smoker's cough" 2. Harsh breathing, 3. Single dry low-pitched rales. Exacerbation phase: 1. Duration. cough with mucus. or mucopurulent sputum; 2. Increase in body temperature (optional sign); 3. Unsharply expressed intoxication. 4. Dry scattered low-pitched (bass) rales in the lungs against the background of hard breathing.
Slide 9: Clinical picture of CNB:
5. Rarely during an exacerbation of CNB - moderate signs of broncho-obstructive syndrome caused by a reversible component of bronchial obstruction = mucosal edema, viscous sputum and bronchospasm): ● labored breathing (often expiratory dyspnea), ● high treble rales (with forced exhalation) against the background of hard breathing, ● bouts of unproductive cough
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Slide 10: Formation in COPD of chronic obstructive pulmonary disease (COPD)
With COB, further progression of the disease leads to the involvement in the inflammatory process not only of large and small bronchi, but also of the alveolar tissue (elastase infiltration by neutrophils and free oxygen radicals, a decrease in the elasticity of emphysema), an increasing predominance of the irreversible component of bronchial obstruction (pulmonary emphysema and peribronchial fibrosis). This is how COPD is formed: ● chronic obstructive bronchitis, ● pulmonary emphysema, ● pneumosclerosis, ● pulmonary hypertension, ● chronic cor pulmonale. e x
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Slide 11: Thus, the features of COPD:
● Involvement in the inflammatory process of not only large and medium, but also small bronchi, as well as alveolar tissue (elastase and free oxygen radicals). ● Development of broncho-obstructive syndrome, consisting of irreversible and reversible components. ● Formation of secondary diffuse emphysema. ● Progressive impairment of lung ventilation and gas exchange leading to hypoxemia and hypercapnia. ● Formation of the lung arterial hypertension and chronic cor pulmonale (CHP).
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Slide 12: Clinical picture of COPD:
1. Expiratory dyspnea, appearing or aggravated by physical exertion and coughing. 2. Attacks of hacking unproductive cough. 3. Signs of emphysema, cyanosis. 4. Prolongation of the expiratory phase, especially forced breathing. 5. Harsh or weakened breathing. 6. Scattered high-pitched dry rales with calm or forced breathing, as well as distant rales. 7. Pulmonary AH and HLS.
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Slide 13: Causes of respiratory failure in COPD:
1. Uneven bronchial obstruction (hypoventilated and non-ventilated zones with insufficient oxygenation). 2. Reducing the total area of the functioning alveolar-capillary membrane. 3. Decrease in inspiratory reserve volume (increase in chest volume and increase in its rigidity). 4. Severe fatigue of the respiratory muscles 6. Violation of gas diffusion.
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Slide 14: Radiographic signs of COB and COPD:
● increase in the total area of lung fields; ● persistent increase in lung transparency; ● depletion of the lung pattern on the periphery of the lung fields; ● flattening of the dome of the diaphragm and a significant limitation of its mobility during breathing (less than 3–5 cm); Emphysema
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Slide 15: X-ray. signs of COB and COPD:
● reduction of the transverse dimensions of the heart ("drip" or "hanging" heart); ● heaviness of the lung pattern
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slide 16: bronchiectasis
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Slide 17: Evaluation of the FVD
Tiffno index (IT) = FEV 1 / FVC (%). IT is normal more than 70-75% of FVC
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Slide 18: Evaluation of respiratory function in COB and COPD
3 stages of the course of COPD: 1st stage - FEV 1 from 50% to 69% of the proper value. 2nd stage - FEV 1 from 35% to 49% of the proper value. 3rd stage - FEV 1 less than 35% of the proper value.
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Slide 19
Bronchial asthma. COPD Emphysema of the lungs. Etiology, pathogenesis, clinic, diagnostics Moscow 2012
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Slide 20: What is asthma?
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Bronchial asthma Prevalence (Russia) Asthma prevalence rates in Russia according to the official statistics of the Ministry of Health of the Russian Federation and the results of individual epidemiological studies differ significantly: patients with bronchial asthma, of which only 1.4 million are registered
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Slide 22: DEFINITION key points
Asthma is a chronic inflammatory disease of the airways. A specific type of airway inflammation that involves many cells: mast cells, eosinophils, T-lymphocytes Causes: airway hyperreactivity, bronchial obstruction and respiratory symptoms.
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Slide 23: Hyperactivity
Increased bronchial response leading to airway obstruction under the influence of stimuli: allergens, physical activity, cold air, pollutants C hyperreactivity syndrome manifests itself in the development of acute or chronic bronchial tree obstruction, reversible on its own or under the influence of appropriate treatment with β-2 agonists, corticosteroid hormones
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Slide 24: INTERNAL FACTORS
Genetic predisposition Atopy Airway hyperreactivity Gender Race/ethnicity
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Slide 25: EXTERNAL FACTORS
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Slide 26: Bronchial obstruction
As a result of the inflammatory process, four mechanisms of bronchial obstruction occur: acute bronchospasm, edema of the bronchial wall, chronic obstruction with mucus, remodeling of the bronchial wall
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Smooth muscle dysfunction Airway inflammation Mucosal edema Inflammatory cell infiltration and activation Cell proliferation Epithelial damage Basement membrane thickening Bronchoconstriction Bronchial hyperreactivity Hyperplasia Release of inflammatory mediators Exacerbation symptoms
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Slide 28
Norma Asthma attack
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Inflammation Bronchial hyperreactivity Bronchial obstruction Symptoms of bronchial asthma Swelling of the bronchial mucosa Bronchospasm Hypersecretion of mucus Vasodilatation
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Acute inflammation Chronic inflammation Airway remodeling Increased number of inflammatory cells Epithelial damage Bronchoconstriction Mucosal edema Mucus secretion Airway constriction Bronchial hyperreactivity Decreased reversibility of bronchial obstruction Exacerbation symptoms Cell proliferation Increased extracellular matrix volume
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Slide 31: Precastma. Criteria
1. Acute or chronic lung disease with bronchial obstruction. These are obstructive bronchitis, acute pneumonia with obstruction, acute respiratory infections with obstruction. 2. Extrapulmonary manifestations of altered reactivity. 3. Eosinophilia of blood and (or) sputum. 4. Hereditary predisposition. Precastma. Criteria.
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Slide 32: CLASSIFICATION OF BRONCHIAL ASTHMA 1. Exogenous bronchial asthma - allergens come from external environment(plant pollen, mold fungi, animal hair, the smallest mites found in house dust). A special case is atopic bronchial asthma caused by a hereditary predisposition to allergic reactions 2. Endogenous bronchial asthma - an attack is caused by factors such as infection, exercise, cold air, psycho-emotional stimuli 3. Mixed genesis - attacks can occur both when an allergen is exposed to the respiratory tract, and and under the influence of the above factors
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Slide 33: PATHOGENETIC CLASSIFICATION OF BRONCHIAL ASTHMA I. Stages of asthma development 1. Biological defects in practically healthy people 2. Pre-asthma condition 3. Clinically formed asthma II. Forms of asthma /not included in the formulation of clinical diagnosis/: 1. immunological form 2. non-immunological form III. Clinical and pathogenetic variants of BA: 1. atopic / with an indication of an allergenic allergen or allergens / 2. infection-dependent / with an indication of infectious agents / 3. autoimmune 4. hormonal / with an indication of the endocrine organ, the function of which is changed, and the nature of dishormonal changes / 5 neuro-psychic 6. pronounced adrenergic imbalance 7. primary altered bronchial reactivity, suffocation during physical exertion, exposure to cold, medications, including aspirin, etc./
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Slide 34: PATHOGENETIC CLASSIFICATION OF BRONCHIAL ASTHMA (continued) IV. Severity of the course of BA: 1. Mild course 2. Moderate course 3. Severe course V. Phases of the course of BA: 1. Exacerbation 2. Fading exacerbation 3. Remission VI. Complications: 1. Pulmonary /emphysema, pulmonary insufficiency, atelectasis, pneumothorax/ 2. Extrapulmonary /myocardial dystrophy, cor pulmonale, etc./
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Slide 35: Clinical forms of bronchial asthma (1)
Allergic, atopic (exogenous) asthma - in patients with manifestation of atopy Allergic diseases in relatives Early onset, remission is often noted during puberty. Often associated with allergic rhinitis and atopic dermatitis
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Slide 36: Clinical forms of bronchial asthma (2)
Non-allergic (endogenous) asthma - in patients without manifestation of atopy Late onset Aspirin asthma Extremely hypersensitivity to aspirin and other NSAIDs
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Slide 37: Clinical forms of bronchial asthma (3)
Occupational bronchial asthma Develops as a result of contact with chemical sensitizing substances at work and is not associated with an atopic condition Sometimes occupational asthma symptoms can occur in patients with atopy (due to contact with allergens at work)
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Slide 38: The pathogenesis of clinical manifestations
The leading role in the pathogenesis of bronchial asthma is played by the increased reactivity of the bronchi, which leads to their periodic reversible obstruction. It is manifested by: increased airway resistance, lung hyperdistension, hypoxemia caused by focal hypoventilation, and a mismatch between ventilation and lung perfusion.
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Slide 39: Diagnosis
Clinical diagnostics (suffocation attacks) Laboratory diagnostics (eosinophilia in the KLA and nasal secretion, scarification tests, Ig E, special IgE, immunogram) Assessment of the function of external respiration (spirogram - FEV1, PSV). Peakflowmetry
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Slide 40: Clinical diagnosis
History and symptom assessment Physical examination Lung function assessment Allergy status to identify risk factors
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Slide 41: Questions to suspect the diagnosis of AD
Does the patient have bouts of (repeated) wheezing? An agonizing cough at night? Wheezing or cough after exercise? Wheezing, chest tightness or cough due to exposure to aeroallergens or pollutants? “Does it go down in the chest” or does the cold last more than 10 days?
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Slide 42: Asthma attack
1. Aura (most patients have it). 2. Attack. 3. Recovery (outcome).
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Slide 43: Complaints at the time of exacerbation
Whistling rales heard at a distance: paroxysmal, aggravated by expiration, stopped by inhalation of B2-agonists Cough: usually unproductive, so-called. “Suffocating” Feeling of tightness in the chest Expiratory shortness of breath, later turning into an attack of suffocation Isolation of viscous, “glassy”, difficult to separate sputum, usually in a small amount
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Slide 44: Anamnesis: Relationship between symptoms and cause, place, action (trigger factors). Atopy in blood relatives. atopic diseases. allergic reactions
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Slide 45: Trigger factors - factors that need to be identified when taking an anamnesis
Allergens (house dust mites, plant pollen, animal dander, mold, cockroaches) Irritants (tobacco smoke, air pollutants, strong odors, fumes, soot) Physical factors (exercise, cold air, hyperventilation, laughter, screaming, crying) ) Viral infection of the respiratory tract Emotional overload (stress)
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Slide 46: RISK OF DEVELOPING ASTHMA DEPENDING ON THE HEALTH OF PARENTS
Parents and relatives of the 1st degree of allergy do not have allergies. One of the parents is Allergic. diseases in both parents In both parents, the same organ is affected Risk of developing allergic diseases in children 5-10% Risk of developing allergic diseases in children 20-40% Risk of developing allergic diseases in children 40-60% Risk of developing allergic diseases in children 60 -80%
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Slide 47: Physical data
Typical position of the patient: emphasis on the shoulder girdle Facial expression: a feeling of suffering on the face, participation of mimic muscles in breathing, puffiness of the face Skin color: diffuse cyanosis On examination: signs of acute emphysema, participation in breathing of auxiliary muscles, barrel-shaped chest Percussion: box percussion sound Auscultation : weakened vesicular breathing Dry scattered rales over the entire surface of the chest: high, treble, musical, whistling rales in large numbers, along with low, bass, buzzing, buzzing, etc., especially on exhalation Signs of increasing respiratory failure Concomitant manifestations: nasal congestion, dry skin, lichenification, rashes, etc.
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Slide 49: Complete blood count.
General analysis blood in uncomplicated bronchial asthma, usually with signs of moderate inflammatory changes. Eosinophilia is characteristic (the number of eosinophils is 500-1000 µl-1). The number of eosinophils is especially increased at night and during periods of contact with the allergen.
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Slide 50: Sputum analysis
With exogenous bronchial asthma, ciliated epithelial cells (25-35%), eosinophils (5-80%), Charcot-Leiden crystals are determined in sputum. When exogenous bronchial asthma is exacerbated, the number of eosinophils in sputum increases. In endogenous bronchial asthma and chronic bronchitis, the same cellular elements are present in the sputum, but neutrophils predominate, the content of eosinophils ranges from 5 to 20%. With exacerbation of endogenous bronchial asthma total number cells in sputum increases, but the ratio between them remains the same
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Forced expiratory volume in the first second (FEV 1), Forced vital capacity (FVC) Tiffno index Peak expiratory flow (PSV) Airway hyperresponsiveness (tests with anticholinergics) Assessment of lung function
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Slide 52: Spirometry Curve flow - volume
normal Obstruction of moderate severity
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Slide 53: Spirographic examination
A – normal B – in a patient with BA 0 1 2 3 4 FEV 1 Time, sec. FEV 1 Time, sec. 0 1 2 3 4 5 5
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Slide 54: Tiffno index FEV1/FVC ratio
Normal - FEV1 / FVC > 80%, in children > 90% Any values below the data may suggest bronchial obstruction An indicator that allows you to distinguish between obstructive and restrictive processes
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Slide 55: Severity of obstruction (functional criteria)
Mild: FEV1 > 70% predicted Moderate: FEV1 = 50-69% predicted Severe: FEV1< 50% от должного
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Slide 56: Peakflowmetry
Daily spread \u003d Normally, daily fluctuations in PEF are not more than 20% PEF in - PEF y x100 ½ (PEF in + PEF y)
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Slide 57: Rules for using a peak flow meter:
The test is performed by holding the device in a horizontal position Take a maximum breath, then exhale as strongly and quickly as possible through the peak flow meter (trying not to cough) At least 3 attempts must be made. Highest score counted © AstraZeneca
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Slide 58: Controlled Asthma (CFM)
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Slide 60: Monitoring asthma with a peak flow meter allows you to:
determination of the reversibility of bronchial obstruction; assessment of the severity of the course of the disease; assessment of bronchial hyperreactivity; predicting asthma exacerbations; definition of occupational asthma; assessment of the effectiveness of treatment
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Slide 61: Investigation of bronchial hyperreactivity using provocative tests
Test with histamine or methacholine If lung function is within normal limits, and the history of the disease indicates bronchial asthma A positive result is a response to a dose of histamine<8 мг / мл Провокационная проба физической нагрузкой – используется у детей и пациентов молодого возраста с целью уточнения диагноза Провокационная проба с аллергеном или профессиональным сенсибилизатором – проводится в специализированном учереждении
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Slide 62: Timing of improvement in asthma clinical parameters
Woolcock, Clin Exp Allergy Rev 2001 100 Years Months Days Weeks No nighttime symptoms Normalization of morning PSV Normalization of FEV1 Normalization of bronchial hyperresponsiveness No need for short-acting 2 agonists Proportion of patients with improvement, %
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Slide 63: Structure of the diagnosis
Asthma - clinical form, course severity, course phase, complications Associated allergic diseases (rhinitis, conjunctivitis, atopic dermatitis) Background diseases / conditions (significant sensitization, intolerance to NSAIDs, steroid dependence, GERD, sinusitis, thyrotoxicosis, etc.) Concomitant diseases
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Slide 64: Examples of the wording of the diagnosis
BA, exogenous, atopic form, course of moderate severity, uncontrolled course, Art. exacerbations. DN 2nd degree. allergic rhinitis. Sensitization to household and pollen (cereals) allergens. Hypertonic disease. BA, endogenous, aspirin form, severe course, controlled course. DN 1st degree. Steroid addiction, Itsenko-Cushing's syndrome. Peptic ulcer of the duodenum, HP-associated. 3. BA, exogenous, atopic form, mild controlled course, stage of remission. DN-0 st. Allergic rhinitis, conjunctivitis. Sensitization to pollen allergens (weeds). GERD.
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Slide 65: COPD definition
COPD is a disease characterized by progressive bronchial obstruction that is only partially reversible. Progressive bronchial obstruction is caused by an abnormal inflammatory "response" of the lungs to inhalation exposure to damaging particles or gases.
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Slide 66: COPD includes:
chronic bronchitis chronic obstructive bronchitis chronic purulent obstructive bronchitis pulmonary emphysema pneumosclerosis pulmonary hypertension chronic cor pulmonale
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Slide 67: Differential diagnosis of asthma and COPD (I)
Signs of asthma COPD Bronchial obstruction ... bronchial obstruction, which is often reversible ... airflow limitation, which is not completely reversible ... Risk factors sensitizing damaging Smoking Not characteristic Atopy characteristic Not characteristic fluctuations in severity Presence of cor pulmonale Not typical Typical in severe course
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Slide 68: Differential diagnosis of asthma and COPD (II)
Signs of asthma COPD Type of inflammation (sputum, BAL) eosinophils Neutrophils Blood changes Possible eosinophilia In the period of exacerbation - neutrophilic leukocytosis with stab shift, increased ESR Radiography Normal, hyperair Diffuse pneumosclerosis, pulmonary emphysema<10% Ежегодное падение ОФВ1 До 30 мл >50 ml Response to treatment GCS (+++) GCS (+)
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Slide 69: Pulmonary Emphysema
The term "emphysema" (from the Greek emphysae - to inflate, inflate) denotes pathological processes in the lungs, characterized by an increased content of air in the lung tissue, due to a decrease in the elastic properties of the alveolar membranes.
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Slide 70: Etiology and pathogenesis
There are primary and secondary emphysema. The most common form is secondary diffuse emphysema, which develops as a result of chronic obstructive pulmonary diseases (acute and chronic bronchitis, bronchial asthma, etc.).
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Slide 71: RISK FACTORS FOR EMPHYSEMA
Increased intrabronchial and alveolar pressure with the development of pulmonary bloating (prolonged cough, overexertion of the external respiratory apparatus in glass blowers, wind instrument musicians, singers, etc.) Changes in lung tissue elasticity and chest mobility with age (senile emphysema). In the development of primary emphysema, hereditary factors, in particular hereditary deficiency, are important. Hereditary deficiency of alpha1-antitrypsin has an autosomal recessive pattern of inheritance.
Early 20th century The main cause of COPD is smoking. 2006 - about 1.1 billion people smoke in the world 2025 - 1.6 billion people will smoke in the world WHO, 2002 XXI century.
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Slide 75: Circulatory disorders in emphysema
Loss of elasticity, inflammatory, fibrotic changes in the lung tissue, bronchospasm lead to impaired diffusion of gases through the alveolar-capillary membranes (alveolar-capillary block) with the development of arterial hypoxemia and hypercapnia. Arterial hypoxia leads to a reflex increase in pressure in the pulmonary vessels, opening of anastomoses between them and bronchial veins and arteries, which leads to increased arterial hypoxemia, since part of the blood is switched off from the circulation of the pulmonary circulation. On the part of the pulmonary vessels, three types of changes occur: 1) the development of pulmonary hypertension due to spasm of the vessels of the pulmonary circulation, 2) the occurrence of atherosclerosis of the branches of the pulmonary artery, and 3) the desolation of the pulmonary capillaries due to the death of the interalveolar septa.
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Slide 76: Complaints of patients with emphysema (1)
Shortness of breath is the earliest and most persistent symptom of pulmonary insufficiency. 1 degree DN - shortness of breath during physical exertion, which previously did not cause it; 2nd degree DN - shortness of breath with little physical exertion; 3rd degree DN - shortness of breath at rest
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Slide 77: Complaints of patients with emphysema (2)
Decreased performance due to shortness of breath. Cough in the presence of concomitant bronchitis Often wheezing heard at a distance Palpitation
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Slide 78: Clinical signs of emphysema
Objectively, there is a barrel-shaped chest enlarged in the anteroposterior size, the costal angle is blunt, the supraclavicular fossae are dilated, the ribs run horizontally, and the intercostal spaces are dilated. Boxed percussion sound, the lower borders of the lungs are lowered, the mobility of the lower pulmonary edge is limited. On auscultation, breathing is weakened; in the presence of bronchitis, dry and moist rales are heard. The heart sounds are muffled, an accent of 11th tone on the pulmonary artery can be heard. The liver protrudes from the hypochondrium due to the omission of the lower border of the lung. Swelling of the legs, feet can be determined
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Last presentation slide: Chronic bronchitis: X-ray of a patient with emphysema
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Acute bronchitis Acute bronchitis (AB) is an inflammatory disease of the trachea and bronchi, which is characterized by an acute course and reversible diffuse lesions of the mucous membrane. AB is one of the most common respiratory diseases, which is more common in children and the elderly (more often men). This disease is more susceptible to people living in areas with a cold and humid climate, working in drafts, in damp cold rooms. OB is often combined with lesions of the upper respiratory tract (nasopharyngitis, laryngitis, tracheitis), or is observed in isolation.
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Etiology Causal factors: infectious (viruses, bacteria); physical (exposure to excessively hot or cold air); chemical (inhalation of vapors of acids, alkalis, poisonous gases); allergic (inhalation of plant pollen, organic dust).
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Contributing factors: acute infections of the upper respiratory tract; focal infections of the paranasal sinuses and tonsils; violation of nasal breathing; cooling; smoking; decrease in the reactivity of the body (after serious illnesses, operations, with hypovitaminosis, poor nutrition, etc.).
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Clinic The disease begins acutely. Sometimes symptoms of acute respiratory disease precede - runny nose, sore throat, hoarseness. The clinical picture of OB consists of symptoms of general intoxication and bronchial lesions. Symptoms of general intoxication: weakness, headache, pain in the muscles of the back and legs, aches, chills. The temperature may rise to subfebrile, sometimes high, or remain normal.
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Symptoms of bronchial lesions: dry, rough, painful, unproductive cough with a small amount of mucous sputum; after 1 - 3 days, the cough becomes wet, mucopurulent sputum is coughed up. Pain in the throat and trachea decreases, the temperature decreases, the general condition improves; shortness of breath is possible - a symptom of obstruction (impaired patency) of the bronchi;
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with percussion of the chest - no change (clear lung sound); during auscultation - hard breathing and dry rales, during the period of sputum liquefaction - moist rales of various sizes.
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Additional studies: X-ray picture of the lungs - no changes, sometimes the pulmonary pattern is enhanced and the roots of the lungs are expanded; KLA - neutrophilic leukocytosis, increased ESR.
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The prognosis is usually favorable - recovery after 2 to 3 weeks; In the absence of proper treatment, OB can acquire a protracted course (up to 1 month or longer) or become complicated.
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Complications bronchopneumonia, acute pulmonary heart failure (ALHF), chronic bronchitis.
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Treatment Treatment of OB is mainly symptomatic, usually outpatient, in severe cases - inpatient: bed rest at high temperature measures that eliminate bronchial irritation, facilitate breathing (airing the room, avoiding smoking, cooking, using odorous substances. plentiful warm drink (tea with raspberry , lemon, honey, lime blossom, milk with soda.
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When the temperature drops, the following are used: distractions for chest pains (mustard plasters, pepper plaster or warming compresses on the sternum and interscapular region, warm foot baths);
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herbal medicine with expectorant action: steam inhalations of herbal decoctions (eucalyptus, St. John's wort, chamomile), essential oils (anise, eucalyptus, menthol); ingestion of herbal infusions of thermopsis, licorice root, marshmallow, plantain leaves, coltsfoot, thyme herb, anise fruit, eucalyptus tincture.
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Drug therapy includes: antitussive sedatives for dry painful cough (codeine, codterpin, sinekod, libexin, levopront); bronchodilators for broncho-obstructive syndrome (salbutamol, berotek in inhalations, eufillin tablets, broncholithin in the form of syrup, etc.); expectorants (Coldrex broncho, Doctor Mom, bronchipret, herbion primrose syrup, marshmallow syrup, etc.); mucolytics (fluditec, fluimucil, acetylcysteine, carbocysteine, mucodin; ambroxol, bromhexine, ambrobene, lazolvan, solvin, etc.); local antiseptics, anti-inflammatory and analgesic drugs with simultaneous damage to the nasopharynx (hexoral, strepsils, septolete, stopangin, iox, etc.); antipyretic drugs (analgin, acetylsalicylic acid, paracetamol, etc.);
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drugs of combined action are also used: bronchodilator and antitussive (broncholitin), expectorant and anti-inflammatory (plantain herbion syrup), expectorant and antitussive (codelac), antitussive, antiallergic and antipyretic (Coldrex Night) general tonic (vitamins, immunomodulators); antibacterial drugs (better taking into account the microbial spectrum) are used in the absence of the effect of symptomatic treatment, high fever, the appearance of purulent sputum, as well as in elderly and debilitated patients. The minimum duration of treatment is 5 - 7 days. The most commonly used antibiotics are: semi-synthetic penicillins (ampicillin, amoxicillin), macrolides (erythromycin, rovamycin, azithromycin), cephalosporins (cefaclor, cephalexin), tetracyclines (doxycycline) and sulfonamides: biseptol (bactrim), sulfalene, etc.
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The tactics of the FAP paramedic is the appointment of treatment and the issuance of a sick leave for 5 days; Zdravpunkt - recommendations for treatment, issuance of a certificate-exemption for 3 days, during which, if necessary, the patient must contact the local doctor; SMP - rendering emergency care(antipyretic, bronchodilators) and a recommendation to call a local doctor.
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Prevention Hardening, prevention of SARS; Treatment of diseases of the upper respiratory tract, removal of polyps, treatment of deviated nasal septum; sanitary and hygienic measures - the fight against humidity, dust, smoke, smoking, etc.
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Chronic bronchitis Chronic bronchitis (CB) is a progressive diffuse lesion of the mucous membrane and deeper layers of the bronchi, caused by prolonged irritation of the bronchial tree by various harmful agents, manifested by cough, sputum, shortness of breath and impaired respiratory function. According to WHO recommendations, bronchitis can be considered chronic if it is accompanied by a persistent cough with sputum production for at least 3 months a year for 2 or more years. CB occurs mainly in people over 40 years old, in men 2-3 times more often than in women.
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Etiology In the etiology of chronic bronchitis, prolonged exposure to the bronchial mucosa of irritating factors is important, among which we can conditionally distinguish: exogenous: tobacco smoke; substances of industrial production origin; dust; climatic factors, cooling; infectious factors;
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endogenous: frequent SARS, untreated acute bronchitis, protracted bronchitis; focal URT infections; pathology of the nasopharynx, respiratory failure through the nose; hereditary violation of enzyme systems; metabolic disease. The main role in the occurrence of CB belongs to pollutants - various impurities contained in the inhaled air. The main cause of exacerbation of the disease is infection.
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Classification of CP The nature of the inflammatory process: simple (catarrhal), purulent, mucopurulent, special forms (hemorrhagic, fibrinous). Presence or absence of bronchial obstruction: non-obstructive, obstructive. The level of damage to the bronchial tree: with a primary lesion of large bronchi, with damage to small bronchi and bronchioles. Course: latent, with rare exacerbations, with frequent exacerbations, continuously relapsing.
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Phase: exacerbation, remission. Complications: pulmonary emphysema, diffuse pneumosclerosis, hemoptysis, respiratory failure (RD) (acute, chronic stage I, II, III), secondary pulmonary hypertension (transient, with or without circulatory failure).
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Diagnosis example: Chronic obstructive bronchitis, continuously relapsing course, exacerbation phase, pulmonary emphysema, diffuse pneumosclerosis. DN I - II.
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Clinic In the acute phase: patients report an increase in temperature to subfebrile, weakness, sweating, and other symptoms of general intoxication; there is an increase in cough, an increase in sputum, especially in the morning, a change in its nature (purulent) - with non-obstructive bronchitis; as the disease progresses and the small bronchi are involved in the process, a pronounced violation of bronchial patency (obstructive bronchitis) occurs with the development of shortness of breath up to suffocation. Cough unproductive "barking", sputum is excreted in a small amount; patients may complain of pain in the muscles of the chest and abdomen, which are associated with frequent coughing;
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auscultation - hard breathing, various dry and wet rales; in the blood - leukocytosis, increased ESR; in sputum - leukocytes, erythrocytes, epithelium. In remission phase: symptoms of bronchitis are absent or mild. But signs of pulmonary heart failure and emphysema (if any) persist
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Complications caused directly by infection: pneumonia; bronchiectasis; bronchospastic and asthmatic components; due to the progressive development of bronchitis: hemoptysis; emphysema; diffuse pneumosclerosis; pulmonary (respiratory) insufficiency, which leads to pulmonary hypertension, the formation of chronic cor pulmonale.
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Diagnosis A preliminary diagnosis of chronic bronchitis is made if the patient has: cough with sputum, possibly shortness of breath, hard breathing with prolonged exhalation, scattered dry and wet rales, "cough history" (long-term smoking, nasopharyngeal pathology, occupational hazards, prolonged or recurrent course of OB and etc.). The diagnosis can be confirmed: signs of inflammation of the bronchi according to bronchoscopy, examination of sputum and bronchial contents, it is necessary to exclude other diseases with similar symptoms (pneumonia, tuberculosis, bronchiectasis, pneumoconiosis, lung cancer, etc.). In obstructive CB, unlike non-obstructive CB, the following are observed: signs of pulmonary emphysema on the radiograph; violation of bronchial patency in the study of the function of external respiration (data of spirography, peak flowmetry)
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Outpatient or inpatient treatment (depending on the severity of the patient's condition, the presence of complications, the effectiveness of previous treatment): exclusion of factors that contribute to the exacerbation of the disease; a diet with a high content of vitamins and protein, (restriction of salt, liquid); in the acute phase: antibiotic therapy antibiotics are prescribed as early as possible, more often administered parenterally in large doses, in severe cases - intratracheally (through a bronchoscope); expectorants, bronchodilators; distractions; in remission phase: FTL, exercise therapy, SKL.
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The tactics of the FAP paramedic is to refer the patient to the local therapist in case of exacerbation of chronic bronchitis. Health center - refer to a shop or district doctor to clarify the diagnosis and prescribe outpatient treatment, or resolve the issue of hospitalization according to indications. SMP - providing emergency care adequately to the symptoms: at high temperature - antipyretics, with hemoptysis - hemostatic, with shortness of breath - moistened oxygen, bronchodilators, etc. Depending on the patient's condition: either hospitalization in a therapeutic department, or a recommendation to call a local doctor.
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Recipes Rp.:Tab. Libexini 0.1 №20 D.S. 1-2 tablets 3-4 times a day. Rp.: Dragee Bromhexini 0.04 №20 D.S. 2 tablets 3 times a day, regardless of food intake. Rp.: Biseptoli 480 D.t.d. No. 20 in tabl. S. 2 tablets 2 times a day after meals. Rp.:Azithromycini 0.25 D.t.d. No. 6 in caps. S. 1 capsule 1 time per day 1 hour before meals or 2 hours after meals for 5 days.
Definition. Chronic bronchitis is an inflammation of the bronchi, characterized by three main features: 1. Diffuse (uneven) nature of the lesion of the bronchial tree; 1. Diffuse (uneven) nature of the lesion of the bronchial tree; 2. Progressive chronic course with periods of exacerbations and remissions; 2. Progressive chronic course with periods of exacerbations and remissions; 3. The main clinical symptoms are: cough, sputum production and shortness of breath. 3. The main clinical symptoms are: cough, sputum production and shortness of breath. COPD COPD - chronic bronchitis, COPD; - chronic bronchitis, COPD; - bronchial asthma; - bronchial asthma; - emphysema. - emphysema.
Factors contributing to the increase in the frequency of chronic bronchitis: - growing air pollution; - an increase in smoking in some countries; - Allergization of the population; - epidemics of influenza and other viral infections. The frequency of chronic bronchitis: - 11 per 1000 visits for chronic bronchitis; - among all diseases of the bronchopulmonary apparatus, 25% are chronic bronchitis.
ETIOLOGY. - Tobacco smoking. - Alcohol abuse. - Air pollution. - Occupational hazards (organic and inorganic dust, toxic fumes and gases). - cold, humid climate. - infections. - Endogenous factors (foci of chronic infection of the nasopharynx, immunodeficiency states, hereditary predisposition). - Hypothermia, overheating. ETIOLOGY. - Tobacco smoking. - Alcohol abuse. - Air pollution. - Occupational hazards (organic and inorganic dust, toxic fumes and gases). - cold, humid climate. - infections. - Endogenous factors (foci of chronic infection of the nasopharynx, immunodeficiency states, hereditary predisposition). - Hypothermia, overheating.
Mucociliary transport system Mucous glands of the trachea and large bronchi Bronchial secret - mucus (mucin, lipids, proteins, nucleic acids, secretory immunoglobulin). Ciliated epithelium of the bronchial tree Mucociliary transport system Mucous glands of the trachea and large bronchi Bronchial secret - mucus (mucin, lipids, proteins, nucleic acids, secretory immunoglobulin). Ciliated epithelium of the bronchial tree The influence of the sympathetic n.s.
PATHOGENESIS Pathogenic factors (smoking, dust, smoke, gases, occupational hazards). Hypertrophy of the bronchial mucous glands Violation of the rheological properties of mucus (thick, liquid). Violation of mucociliary transport of inhaled particles Violation of protective mechanisms (decrease in the bactericidal activity of the bronchi, violation of specific and non-specific protection). Attachment of infection (viruses, mycoplasma, pneumococci, staphylococci, Haemophilus influenzae, etc.). Chronic inflammation of the bronchi
Morphology of chronic bronchitis: - 1.5 times increase in bronchial wall thickness; - hypertrophy of bronchial mucous glands and goblet cells; - areas of inflammation, sclerosis, degenerative and atrophic changes in all bronchial walls (panbronchitis); - purulent impregnation of the bronchial wall with areas of ulceration (possibility of bleeding). - pneumofibrosis, emphysema. - development of bronchiectasis. Morphology of chronic bronchitis: - 1.5 times increase in bronchial wall thickness; - hypertrophy of bronchial mucous glands and goblet cells; - areas of inflammation, sclerosis, degenerative and atrophic changes in all bronchial walls (panbronchitis); - purulent impregnation of the bronchial wall with areas of ulceration (possibility of bleeding). - pneumofibrosis, emphysema. - development of bronchiectasis.
Continuation. 4. According to the phase of the disease: - exacerbation; - remission; 5. Complications: - chronic obstructive bronchitis with emphysema (COPD); - pulmonary hypertension, cor pulmonale; - pulmonary (respiratory) and cardiac (according to the right ventricular type) insufficiency.
Clinical course: - cough, sputum; - hypotonic tracheobronchial dyskinesia; - shortness of breath (bronchospastic and obstructive syndrome, degree of respiratory failure). - diffuse cyanosis, acrocyanosis. - hypercapnia. Clinical course: - cough, sputum; - hypotonic tracheobronchial dyskinesia; - shortness of breath (bronchospastic and obstructive syndrome, degree of respiratory failure). - diffuse cyanosis, acrocyanosis. - hypercapnia.
Continuation. - Data of examination, percussion, auscultation (barrel chest, box tone, hard or weakened vesicular breathing, prolonged exhalation, dry wheezing). - Signs of obstruction (dyspnea on exertion, unproductive cough, prolonged expiration, wheezing on expiration, emphysema, decreased respiratory function). Continuation. - Data of examination, percussion, auscultation (barrel chest, box tone, hard or weakened vesicular breathing, prolonged exhalation, dry wheezing). - Signs of obstruction (dyspnea on exertion, unproductive cough, prolonged expiration, wheezing on expiration, emphysema, decreased respiratory function).
Pulmonary heart (cor pulmonale). Definition - a pathological condition characterized by hypertrophy and (or) dilatation of the right ventricle of the heart as a result of pulmonary hypertension caused by primary diseases of the bronchopulmonary apparatus, pulmonary vessels or thoracophrenic pathology.
Diagnosis of chronic bronchitis. - Blood (erythrocytosis, increased hematocrit and blood viscosity, with exacerbation: leukocytosis, neutrophilia, ESR. - Sputum (neutrophilic leukocytosis, bronchial epithelial cells, erythrocytes, macrophages, impaired rheological properties). - Chest X-ray (pneumofibrosis, emphysema, low standing of the diaphragm and reducing its excursion) - Bronchography (detection of bronchiectasis) - Bronchoscopy (examination of the bronchial mucosa, biopsy production).
The function of external respiration (standards): VC: male. - 4 - 5 liters. Female - 3 - 4 liters. FEV1: male - 3 - 4 liters. Female - 2 - 3 liters. Tiffno index: FEV 1 / VC x 100 (70 - 85%). MVL: husband. – 100 – 125 l min. women - 100 l min. - Lung scanning (radioisotope study).
Treatment of chronic bronchitis. 1. Etiotropic treatment: - antibacterial therapy (antibiotics intramuscularly, intravenously, aerosols), - endobronchial sanitation 2. Treatment of bronchospastic syndrome: - sympathomimetics: 1) non-selective (izadrin, alupent, isuprel); 2) selective (salbutamol, berotek): - anticholinergics (atrovent); - a combination of sympathomimetics and anticholinergics (berodual: berotek + atrovent).
Continuation 3. Correction of mucociliary insufficiency: - Sputum thinners: trypsin, chemotrypsin, mukaltin, hyaluronidase; potassium iodide; expectorant herbs. - Antitussives: libexin; bromhexine; tusuprex; codeine (drug).
Continuation. 4. Correction of immunological disorders: - decrease in the function of the cellular link of immunity: levamisole; thymus preparations (timogen, thymolin, timuran). - drugs stimulating phagocytosis: sodium nucleinate; pentoxyl; adaptogens (eleutherococcus, ginseng, pantocrine). 5. Hormone therapy (for bronchospastic and obstructive syndrome).
6. Improving the rheological properties of blood and sputum: - Anticoagulants (heparin, fraxiparin); - Disaggregants (aspirin, chimes). 7. Oxygen therapy. 8. Physiotherapy: - UHF, electrophoresis, ultrasound, coniferous baths; - Exercise therapy, chest massage. 9.Sanatorno-resort treatment: - southern coast of Crimea; - Kislovodsk (Caucasian mineral water); - Teberda, Dombay; - Local pulmonological sanatoriums.
