LECTURE NOTES ON FACULTY THERAPY
Kuznetsova Yu. V.
The lecture notes presented to your attention are intended to prepare students of medical universities for passing exams. The book includes a full course of lectures on faculty therapy, is written in accessible language and will be an indispensable assistant for those who want to quickly prepare for the exam and pass it successfully.
LECTURE No. 1. Diseases
bronchopulmonary system
1. Respiratory allergies
Respiratory allergies are common allergic diseases with predominant damage to the respiratory system.
Etiology
Allergoses develop as a result of sensitization by endogenous and exogenous allergens.
Exogenous allergens of non-infectious nature include: household - washing powders, objects household chemicals; epidermal - wool, skin scales of domestic animals; pollen - pollen of various plants; food - food products; herbal, medicinal. Allergens of an infectious nature include bacterial, fungal, viral, etc.
Classification
The classification is as follows.
1. Allergic rhinitis or rhinosinusitis.
2. Allergic laryngitis, pharyngitis.
3. Allergic tracheitis.
4. Allergic bronchitis.
5. Eosinophilic pulmonary infiltrate.
6. Bronchial asthma.
Symptoms and diagnosis
Allergic rhinitis and rhinosinusitis. History - the presence of allergic diseases in the parents and close relatives of the child, the connection of diseases with allergens.
Symptomatically manifested by an acute onset: the sudden onset of severe itching, burning in the nose, bouts of sneezing, copious liquid, often foamy discharge from the nose.
Upon examination, swelling of the mucous membrane of the nasal septum, inferior and middle turbinates is revealed. The mucous membrane is pale
gray with a bluish tint, shiny surface with a marble pattern.
X-ray examination shows thickening of the mucous membrane of the maxillary and frontal sinuses and the ethmoidal labyrinth on photographs of the skull.
Positive skin tests with infectious and non-infectious allergens are characteristic.
Laboratory diagnostics revealed an increase in the level of immunoglobulin E in nasal secretions.
Allergic laryngitis and pharyngitis can occur in the form of laryngotracheitis.
Characterized by an acute onset, dryness of the mucous membrane, a feeling of soreness, soreness in the throat, attacks of dry cough, which later becomes “barking”, rough, a hoarseness of voice appears, up to aphonia.
With the development of stenosis, inspiratory shortness of breath appears, the participation of auxiliary muscles in the act of breathing, retraction of the pliable parts of the chest, flaring of the wings of the nose, and abdominal breathing acquires greater intensity and amplitude.
Obstruction of the bronchi develops due to edema, spasm and exudate and, as a consequence, obstructive ventilation failure.
The use of antibacterial agents does not have a positive effect, and the condition may even worsen.
Laboratory data - positive skin tests, an increase in the level of immunoglobulin E in the blood serum.
Allergic bronchitis occurs in the form of asthmatic bronchitis.
IN Anamnesis contains evidence of allergization of the body.
IN Unlike true bronchial asthma, asthmatic bronchitis develops spasm of large and medium-caliber bronchi, so asthma attacks do not occur.
Eosinophilic pulmonary infiltrate develops with sensibilization of the body.
The most common cause is ascariasis. In a general blood test, high eosinophilia (more than 10%) appears against the background of leukocytosis. Foci of infiltration appear in the lungs, homogeneous, without clear boundaries, which disappear without a trace after 1-3 weeks. Sometimes an infiltrate, having disappeared in one place, may appear in another.
2. Bronchial asthma
Bronchial asthma- an infectious allergic or allergic disease of a chronic course with periodically recurring attacks of suffocation caused by impaired bronchial obstruction as a result of bronchospasm, swelling of the bronchial mucosa and accumulation of viscous sputum.
Bronchial asthma is a serious health problem worldwide. It affects 5 to 7% of the Russian population. There is an increase in morbidity and mortality.
Classification (A.D. Ado and P.K. Bulatova, 1969)
1) atopic;
2) infectious allergic;
3) mixed.
1) asthmatic bronchitis;
2) bronchial asthma. Gravity:
1) mild degree:
a) intermittent: attacks of bronchial asthma less than twice a week, exacerbations are short, from several hours to several days. At night, attacks occur rarely - twice or less per month; b) persistent: attacks do not occur every day, no more than two per week.
At night, symptoms of bronchial asthma are observed more than twice a month;
2) moderate degree - manifests itself every day, requires daily use of bronchodilators. Night attacks occur more than once a week;
3) severe degree - bronchial obstruction, expressed to varying degrees constantly, physical activity is limited.
The main link in the pathogenesis of bronchial asthma is the development of sensitization of the body to a particular allergen with the occurrence of allergic inflammation in the mucous membrane of the bronchial tree.
When collecting anamnesis from a patient, it is necessary to establish the character
ter of the first attack, place and time of year, duration
and the frequency of attacks, the effectiveness of the therapy, the patient’s condition during the non-attack period.
Pathogenesis
The main link in the pathogenesis of bronchial asthma is the development of sensitization of the body to a particular allergen and the occurrence of allergic inflammation.
The main symptom is the presence of attacks of expiratory type suffocation with distant wheezing and paroxysmal cough. Forced position of the patient during an attack: the legs are lowered down, the patient sits on the bed, the body is tilted forward, with his hands resting on the bed on either side of the body.
Symptoms of respiratory failure appear (participation of auxiliary muscles in the act of breathing, retraction of intercostal spaces, cyanosis of the nasolabial triangle, shortness of breath). The chest is emphysematously distended, barrel-shaped.
Percussion box sound, the borders of the lungs shift downward. Auscultation - weakened breathing (short inhalation, long exhalation), an abundance of dry wheezing, moist rales of various sizes. From the cardiovascular system - narrowing of the boundaries of absolute cardiac dullness, tachycardia, increased blood pressure.
From the outside nervous system increased nervous excitability or lethargy, changes in autonomic reactions (sweating, paresthesia) appear.
Laboratory diagnostics
The general blood history includes lymphocytosis and eosinophilia. In the general analysis of sputum - eosinophilia, epithelial cells, macrophages, or Charcot-Leyden crystals, and Kurschmann spirals.
Instrumental research methods. X-ray shows pulmonary emphysema (increased transparency, the borders of the lungs are shifted downward). Spirography: decreased expiratory flow (pneumotachometry), decreased vital capacity, hyperventilation at rest.
Allergy examination. Skin testing with bacterial and non-bacterial allergens gives a positive result. Provocative tests with allergens are also positive.
Immunological indicators. In atopic bronchial asthma, the level of immunoglobulins A decreases and increases
In the atopic form, the number of T lymphocytes decreases, while in the infectious allergic form, it increases.
In the atopic form, the number of suppressors is reduced
And increased content of T helpers. When sensitized by fungal agents, the level of CEC increases.
Patient examination
Interview (collection of medical history, complaints). Examination (palpation, percussion, auscultation). General blood analysis. Microscopy and sputum culture.
X-ray of the chest organs. Study of external respiration parameters. Allergological, immunological examination.
Differential diagnosis
Differential diagnosis of bronchial asthma is carried out with diseases manifested by bronchospastic syndrome of non-allergic nature, which are called “syndromic asthma”; chronic obstructive bronchitis, diseases of the cardiovascular system with left ventricular failure (cardiac asthma), hysteroid breathing disorders (hysteroid asthma), mechanical blockage of the upper respiratory tract (obstructive asthma).
Differentiate with diseases of an allergic nature: polyposis, allergic bronchopulmonary aspergillosis with obstructive respiratory disorders.
It is necessary to take into account whether the patient has a combination of two
And more diseases.
IN Unlike bronchial asthma, in chronic obstructive bronchitis, the obstructive syndrome persists and does not develop reversely even with treatment with hormonal drugs, and there is no eosinophilia in the sputum analysis.
With left ventricular failure, the development of cardiac asthma is possible, which is manifested by an attack of shortness of breath at night; the feeling of lack of air and tightness in the chest will develop into suffocation.
Combined with arrhythmia and tachycardia (with bronchial asthma, bradycardia is more common). Unlike bronchial asthma, both phases of breathing are difficult. An attack of cardiac asthma may be
long-term (before using diuretics or neuroglycerin).
Hysteroid asthma has three forms. The first form is similar to a respiratory spasm. Breathing of a “hunted dog” - inhale and exhale intensified. There are no pathological signs on physical examination.
The second form of suffocation is observed in hysterical people
And caused by impaired contraction of the diaphragm. During an attack, breathing is difficult or impossible, and there is a feeling of pain in the solar plexus area.
To stop the attack, the patient is offered to inhale hot water vapor or given anesthesia.
Obstructive asthma is a symptom complex of suffocation, which is based on a violation of the patency of the upper respiratory tract.
The cause of obstruction may be tumors, foreign bodies, stenosis, or aortic aneurysm. The greatest importance in making a diagnosis belongs to tomographic examination of the chest and bronchoscopy.
The combination of symptoms of shortness of breath and suffocation also occurs in other conditions (anemic, uremic, cerebral asthma, periarthritis nodosa, carcinoid syndrome).
Hay fever, or hay fever, is an independent allergic disease in which the body becomes sensitized to plant pollen.
These diseases are characterized by: bronchospasm, rhinorrhea
And conjunctivitis. Seasonality of diseases is characteristic. It begins with the flowering period of plants and decreases when it ends.
The exacerbation stage is characterized by a persistent runny nose, pain in the eyes and lacrimation, coughing until an attack of suffocation develops.
Possible fever and arthralgia. In general blood analysis - eosinophilia (up to 20%). During the period of remission there is no clinical manifestation.
Allergic bronchopulmonary aspergillosis - a disease caused by sensitization of the body to fungi
perginelam. With this disease, damage to the alveoli, pulmonary vessels, bronchi, and other organs is possible.
The clinical sign is the symptom complex of bronchial asthma (obstructive syndrome, eosinophilia, increased immunoglobulin E).
Confirmation of the diagnosis is carried out by identifying skin sensitization to aspergillus allergens.
An example of a diagnosis. Bronchial asthma, atopic form, with frequent relapses, period of remission, uncomplicated.
The goal of treatment is to prevent the occurrence of attacks of suffocation, shortness of breath during physical activity, cough, nocturnal breathing difficulties. Elimination of bronchial obstruction. Maintaining normal lung function.
Objectives of the therapy:
1) stop exposure of the body to the allergen - the cause of the disease. In case of pollen allergy, the patient is offered to move to another area during the flowering period of the plants. In case of occupational allergies, change the place and working conditions. When eating - strict adherence to an elementary diet;
2) carry out specific desensitization followed by the production of blocking antibodies (immunoglobulin G);
3) stabilize the walls of mast cells and prevent the secretion of biologically active substances;
4) limit the impact of irritants on the respiratory tract - cold air, strong odors, tobacco smoke;
5) rehabilitation of chronic foci of infection (teeth with inflammation, sinusitis, rhinitis);
6) limit developing allergic inflammation by prescribing glucocorticoids in inhaled form;
7) prevent the use of non-steroidal anti-inflammatory drugs.
Principles of treatment.
1. Elimination of the allergen (exclusion, elimination).
2. Bronchospasm therapy:
1) selective α-adrenergic agonists (Berotec, salbutalone, Ventosin, terbutamol, phenotyrol, guoetarin);
2) non-selective adrenergic agonists (adrenaline, ephedrine, asthmapent, fulprenaline, isadrine, euspiran, novodrine);
3) phosphodiesterase antagonists, xanthines (theobramines, theophylline, euphylkin);
4) anticholinergics (atropine, ipratropine).
3. Histamine H2 receptor blockers (tavegil, fenkarol, suprastin, atosinil, pipolfen, displeron).
4. Drugs that reduce bronchial reactivity (glucocorticoids, intal, betotifen).
5. Expectorants:
1) increasing the liquid phase of sputum (thermopsis, licorice root, marshmallow, potassium iodide, alkyonium chloride);
2) mucolytics (acetylcysteine (ACC)), riboclease, deoxyribonuclease);
3) drugs that combine a mucoliptic effect with an increase in surfactant levels (bromgesin, ambro cagn, lazolvan).
6. Antibiotics.
7. Vibration massage with postural drainage.
8. Physiotherapeutic procedures, reflexology (needling
piercing, oxygen therapy).
9. Bronchoscopy, intranasal tracheobronchial examination
10. Rehabilitation in the gnotobiological department.
11. Sauna therapy.
3. Acute bronchitis
Bronchitis is a disease of the bronchi, accompanied by gradually developing inflammation of the mucous membrane with subsequent involvement of the deep layers of the walls of the bronchi.
Etiology
More often it develops with the activation and reproduction of the conditionally pathogenic flora of the body itself with a violation of mucocilar clearance due to ARVI.
Predisposing factors are cooling or sudden heating, polluted air, smoking.
Pathogens: viruses, bacteria, mixed substances, allergens. Classification:
1) acute bronchitis (simple);
In 1966-1976. The department was headed by a brilliant teacher and clinician, Professor Anna Maksimova Tokareva. Research work was carried out on the problems of hypertension, coronary heart disease, and atherosclerosis.
In 1978-1999 The department was headed by Professor Gennady Petrovich Kuznetsov. He was one of the first in our country to study the problem of cardiomyopathies. Creator and leader regional center"Diagnostics and treatment of cardiomyopathies." G. P. Kuznetsov is a laureate of the 1st All-Russian competition “Labor Glory of Russia” (2000), awarded the Provincial Prize (2007), the National Prize for the best doctors of Russia “For fidelity to the profession (2011), etc. by the American Bibliographical Institute (Los Angeles) is included among the outstanding personalities and awarded the “Medal of the 2000th Anniversary of Glory”.
In 1999-2009 The department was headed by Professor Vasily Vasilyevich Simerzin. He worked his way up from a nurse at the faculty therapy clinic to the head of the department. In 2002, under his leadership, the “Center for the Prevention and Treatment of Atherosclerosis and Dyslipidemia” was created. Professor V.V. Simerzin is a member of the board of the National Society for the Study of Atherosclerosis.
Department staff
From 2009 to 2014 The department was headed by Doctor of Medical Sciences, Associate Professor Mikhail Arkadyevich Kachkovsky - a member of the European Society of Cardiology, the European Society of Atherosclerosis, the All-Russian Scientific Society of Cardiologists, and the Russian Gastroenterological Association. Under his leadership, centers for the diagnosis and treatment of cardiomyopathies, the prevention and treatment of atherosclerosis and dyslipidemia continued to operate. Along with this, the gastroenterological focus of the department and clinic’s activities was actively developing.
Since 2014, the department has been headed by Oleg Veniaminovich Fatenkov, Doctor of Medical Sciences, Associate Professor, Chief Freelance Specialist in Therapy of the Ministry of Health of the Samara Region, a member of the board of the Russian National Society for the Study of Atherosclerosis. During this time, the educational process at the department was given a practically oriented orientation. Thanks to the creation of a research laboratory, innovative Scientific research.
The main clinical bases of the department are the Clinics of the Samara State medical university, Samara Regional Clinical Cardiology Dispensary, Samara Regional Clinical Hospital named after M.I. Kalinin, city clinical hospitals No. 3, No. 6, city clinic No. 15, Medical unit No. 2.
The department trains students, clinical interns and clinical residents in the specialty “therapy”, and conducts cycles professional retraining and improvements according to the IPO plan.
The department takes an active part in research work. Employees of the department annually make presentations at regional and all-Russian conferences. Scientific research is being conducted in the following areas: dyslipidemia and atherosclerosis, coronary heart disease, metabolic syndrome, arterial hypertension, cardiomyopathy, pathology of the esophagus, stomach, liver, etc.
1. Fluid in the pleural cavity syndrome
2. Pleural murmur syndrome
3. Pleural air syndrome
4. Inflammatory lung tissue consolidation syndrome
Diagnosis of respiratory diseases is based on clinical, instrumental, and laboratory criteria. The totality of deviations obtained during application various methods research for any pathological condition is usually called a syndrome.
1. Syndrome of fluid in the pleural cavity. A typical complaint is shortness of breath. It reflects the degree of respiratory failure due to pleural compression of the lung, which leads to a decrease in the respiratory surface in the lungs as a whole. When examining, pay attention to the protrusion and lag in the act of breathing of the corresponding half of the chest. Voice tremors and bronchotonia are weakened or absent. Percussion reveals a shortening or dullness of sound or a dull sound. On auscultation, breathing is weakened or absent.
2. Pleural murmur syndrome. Inflammation of the pleural layers can leave behind a pronounced intrapleural adhesive substrate in the form of adhesive cords, adhesions, and fibrinous pleural overlays. Such patients may have no complaints, but with severe adhesions, shortness of breath and chest pain appear during physical activity. When examining the chest, retraction and lag in the act of breathing of the affected half are noted: here you can also detect retraction of the intercostal spaces during inspiration. Voice tremors and bronchophony are weakened or absent. Percussion sound is dull. On auscultation, breathing is weakened or absent. A pleural friction rub is often heard.
3. Syndrome of air in the pleural cavity. Air may enter the pleural cavity when a subpleural cavity or abscess breaks into it. The communication of the bronchus with the pleural cavity leads to the accumulation of air in the latter, which compresses the lung. In this situation, increased pressure in the pleural cavity can lead to the closing of the hole in the pleura with pieces of damaged tissue, stopping the flow of air into the pleural cavity and the formation of a closed pneumothorax. If the connection between the bronchus and the pleural cavity is not eliminated, the pneumothorax is called an open pneumothorax.
In both cases, the main complaints are rapidly developing suffocation and chest pain. Upon examination, protrusion of the affected half of the chest and weakening of its participation in the act of breathing are determined. Voice tremors and bronchophony with closed pneumothorax are weakened or absent, with open pneumothorax they are enhanced. On percussion, tympanitis is determined in both cases. On auscultation, with a closed pneumothorax, breathing is sharply weakened or absent; with an open pneumothorax, breathing is bronchial.
In the latter case, metallic breathing may be heard as a type of bronchial breathing.
4. Inflammatory compaction syndrome of lung tissue. Compaction of lung tissue can occur not only as a result of the inflammatory process (pneumonia), when the alveoli are filled with exudate and fibrin. Compaction can occur as a result of a pulmonary infarction, when the alveoli are filled with blood, or during pulmonary edema, when edematous fluid—transudate—accumulates in the alveoli. However, compaction of the lung tissue of an inflammatory nature is most common. When an entire lobe of the lung is affected, lobar or lobar pneumonia develops; one or more segments – polysegmental pneumonia; less than one segment – focal pneumonia.
Patients complain of cough, shortness of breath, and if the pleura is involved in the inflammatory process, chest pain. On examination, the affected half of the chest lags behind in the act of breathing, which is typical for lobar pneumonia. Voice tremors and bronchophony in the compaction area are increased. The percussion sound in focal pneumonia is dull (not dull), since the area of compacted lung tissue is surrounded by normal lung tissue. With lobar pneumonia, in the initial stage the sound is dull-tympanic, in the peak stage it is dull, which in the resolution stage is gradually replaced by a clear pulmonary sound.
With focal pneumonia, auscultation reveals mixed (bronchovesicular) breathing. Dry and wet rales are heard, while wet rales are characterized as sonorous, since the inflammatory compaction of the lung tissue around the bronchi promotes better conduction of the wet rales that originate in them to the surface of the chest. If the source of inflammation is deeply located, it is not possible to detect any abnormalities during physical examination. At the same time, a large focus of inflammation, located in close proximity to the visceral pleura, gives the same abnormalities during physical examination as lobar pneumonia.
In case of lobar pneumonia, auscultation on the affected side in the initial stage reveals a weakening of vesicular breathing, crepitus and pleural friction noise; in the peak stage, bronchial breathing is heard, and there may be a pleural friction noise. In the resolution stage, bronchial breathing gradually gives way to vesicular breathing, crepitus appears, moist sonorous rales due to the penetration of liquefied exudate from the alveoli, and pleural friction noise is possible.
LECTURE 2. Clinical syndromes in respiratory diseases. Part 2
1. Lung cavity syndrome
2. Bronchospasm syndrome
3. Bronchitis syndrome
1. Lung cavity syndrome. The cavity is formed by an abscess, tuberculosis cavity, and decay of a lung tumor. A cavity formed in the lung can be detected with a diameter of at least 4 cm, communication with a bronchus, close contact with the chest wall, and a significant air content.
Patients with a destruction cavity complain of a cough with a large amount of foul-smelling yellow-green sputum. When examining the chest, a lag in the act of breathing of the affected half is detected, increased vocal tremors and bronchophony are detected, with percussion - tympanitis, with auscultation - bronchial or amphoric breathing, sonorous medium- and coarse-bubbly moist rales are heard.
2. Bronchospasm syndrome. Bronchospasm is a complex of clinical signs that occurs in the form of attacks in patients with bronchial asthma. A tendency to paroxysmal bronchospasm occurs in patients with morphologically intact bronchi and in patients with chronic bronchitis. At the moment of bronchial spasm, the patient experiences an attack of suffocation, during which exhalation is especially difficult; at the height of the attack, a cough appears with difficult to separate viscous sputum. Upon examination, the patient’s position is forced (sitting), breathing is noisy, wheezing is distant, exhalation is sharply prolonged, the veins of the neck are swollen. Accessory muscles are actively involved in the act of breathing, and diffuse cyanosis occurs. The chest is in a state of expiratory tension and has a barrel-shaped appearance. Auscultation reveals a sharply prolonged exhalation and weakening of vesicular breathing; Abundant dry whistling rales are heard in large numbers.
3. Bronchitis syndrome. With inflammation of the bronchi (bronchitis), patients complain of a cough, which at the beginning of the disease is dry, then with sputum. On examination, no deviations from the norm are detected, vocal tremor and bronchophony are not changed, and upon percussion there is a clear pulmonary sound. Auscultation - hard breathing, at the beginning of the disease dry whistling and buzzing wheezing is heard, later on moist, different-sized silent wheezing is heard, scattered throughout the lung fields.
LECTURE 3. Methods of functional diagnostics. Part 1
1. Pleural puncture
2. Sputum examination
1. Pleural puncture used to determine the nature of the pleural fluid in order to clarify the diagnosis, to remove fluid from the pleural cavity and subsequently introduce medicinal substances into it.
The puncture is usually performed along the posterior axillary line in the seventh or eighth intercostal space along the upper edge of the rib. For diagnostic purposes, 50-150 ml of liquid is removed, which is sent for cytological and bacteriological examination. For therapeutic purposes, when a large amount of fluid accumulates in the pleural cavity, 800-1200 ml are initially evacuated. Removal of a larger amount of fluid leads to a rapid displacement of the mediastinal organs to the affected side and may be accompanied by collapse. Pleural fluid can be of inflammatory (exudate) or non-inflammatory (transudate) origin. When analyzed in a clinical laboratory, the specific gravity, the amount of protein, red blood cells, leukocytes, mesothelial and atypical cells contained are determined. The specific gravity of the inflammatory fluid is 1.015 or higher, the protein content is more than 2–3%, the Rivald test is positive. The specific gravity of the transudate is less than 1.015, the amount of protein is less than 2%, the Rivald test is negative.
2. Sputum examination. Sputum is a pathological discharge of the broncho-alveolar tract, expelled during coughing and expectoration. Sputum may contain mucus, serous fluid, blood and respiratory tract cells, tissue decay elements, crystals, microorganisms, protozoa, helminths and their eggs. Examination of sputum helps to establish the nature of the pathological process in the respiratory organs, and in some cases determine its etiology.
It is better to take sputum for examination in the morning, if possible before meals and after rinsing the mouth. However, to detect tuberculosis microbacteria, sputum, if the patient produces little of it, must be collected within 1–2 days.
The daily amount of sputum ranges from 1 to 1000 ml or more. Mucous sputum is usually colorless or slightly whitish, viscous; separated, for example, in acute bronchitis. Serous sputum is also colorless, liquid, foamy. Mucopurulent sputum – yellow or greenish in color, viscous; formed in chronic bronchitis and tuberculosis. Purulent sputum is homogeneous, semi-liquid, greenish-yellow, characteristic of an abscess when it ruptures. Bloody sputum can be either pure blood in pulmonary hemorrhages or mixed.
Sputum often has no odor. Kurshman spirals can be found in sputum in the form of small, dense, tortuous whitish threads; fibrin clots (whitish and reddish tree-like branched formations found in fibrinous bronchitis, occasionally in pneumonia); small dense, greenish-yellow lumps consisting of calcified elastic fibers, crystals, cholesterol, containing Mycobacterium tuberculosis; lime grains found during the disintegration of old tuberculosis lesions; drusen of actinomycetes in the form of small yellowish grains; necrotic pieces of lung tissue; leftover food.
Microscopic examination of sputum is carried out in both native and stained preparations. For the first, pathological lumps are selected from the material poured into a Petri dish and transferred to a glass slide in such an amount that when covered with a cover glass, a thin translucent preparation is formed. The latter is viewed first at low magnification for initial orientation and search for Kurshman spirals, and then at high magnification to differentiate the shaped elements. Courshmann spirals are strands of mucus, consisting of a central dense axial thread and a spiral-shaped “matia” enveloping it, in which leukocytes (often eosinophilic) Charcot-Leyden crystals are interspersed. Kurshman spirals appear in sputum during bronchospasm, most often with bronchial asthma, less often with pneumonia.
With high magnification, leukocytes can be detected in the native preparation, a small number of which is present in any sputum, and a large number in inflammatory and, in particular, suppurative processes; Eosinophilic leukocytes can be distinguished in a native preparation by their uniform, large, shiny granularity, but they are easier to recognize when stained. Red blood cells appear during the destruction of lung tissue, pneumonia, stagnation in the pulmonary circulation, or pulmonary infarction. Flat epithelium enters the sputum mainly from the oral cavity and has no diagnostic value. Columnar ciliated epithelium is present in small quantities in every sputum, and in large quantities in cases of damage to the respiratory tract (bronchitis, bronchial asthma). Alveolar macrophages are large cells (2–3 times more leukocytes) of reticuloendothelial origin. Their cytoplasm contains abundant inclusions. The latter can be colorless (myelin grains), black from coal particles (dust cells) or yellow-brown from hemosiderin (“heart defect cells”, siderophages). Alveolar macrophages are present in small quantities in each sputum; they are more numerous in inflammatory diseases; cells of heart defects occur when red blood cells enter the cavity of the alveoli; with stagnation in the pulmonary circulation, especially with mitral stenosis; for pulmonary infarction, hemorrhage, and pneumonia.
LECTURE 4. Methods of functional diagnostics. Part 2
1. X-ray examination
2. Endoscopic examination
1. To examine the respiratory organs, fluoroscopy, radiography, bronchography and tomography of the lungs are used.
Fluoroscopy allows you to visually determine changes in the transparency of the lung tissue, detect foci of compaction or cavities in it, identify the presence of fluid or air in the pleural cavity, as well as other pathological changes.
Radiography is used to record and document changes in the respiratory organs detected during fluoroscopy on x-ray film. In pathological processes in the lungs, leading to loss of airiness and compaction of the lung tissue (pneumonia, pulmonary infarction, tuberculosis, etc.), the corresponding areas of the lungs on the film have a paler image compared to normal lung tissue. The cavity in the lung, containing air and surrounded by an inflammatory shaft, has the appearance of a dark oval-shaped spot, surrounded by a paler shadow than the shadow of the lung tissue. Fluid in the pleural cavity, which transmits fewer x-rays than lung tissue, produces a shadow on negative x-ray film that is paler than that of lung tissue.
The X-ray method allows you to determine not only the amount of fluid in the pleural cavity, but also its nature. If there is exudate in the pleural cavity, the level of its contact with the lung has an oblique line, gradually directed upward and laterally from the midclavicular line; when transudate accumulates in the pleural cavity, the level is located more horizontally.
Tomography allows for layer-by-layer X-ray examination of the lungs. It is used to diagnose tumors of the bronchi and lungs, small infiltrates, cavities and cavities located at various depths.
Bronchography is used to study the bronchi. After preliminary anesthesia, the patient is injected into the lumen of the bronchi with a contrast agent that blocks x-rays, then an x-ray of the lungs is taken and a clear image of the bronchial tree is obtained on the x-ray. This method allows you to diagnose bronchial dilatation (bronchiectasis), abscesses and lung caverns, narrowing of the lumen of large bronchi by a tumor or foreign body.
Fluorography is also a type of x-ray examination of the lungs. It is used for mass preventive examination of the population.
2. Endoscopic research methods include broncho- and thoracoscopy.
Bronchoscopy allows you to examine the mucous membrane of the trachea and bronchi of the first, second and third order. It is produced special device– a bronchoscope, to which special forceps are attached for biopsy, removal of foreign bodies, removal of polyps, photo attachment, etc. Before inserting the bronchoscope, anesthesia is performed with a 1-3% solution of dicaine of the mucous membrane of the upper respiratory tract, then the bronchoscope is inserted through the mouth and glottis into the trachea. The doctor examines the mucous membrane of the trachea and bronchi.
For histological and cytological studies, a piece of tissue from a suspicious area can be removed (biopsy) using special forceps. Bronchoscopy is used to diagnose erosions, ulcers of the bronchial mucosa and tumors of the bronchial wall, remove foreign bodies, remove bronchial polyps, treat bronchiectasis and centrally located lung abscesses. In these cases, purulent sputum is first sucked out through a bronchoscope, and then antibiotics are injected into the bronchial lumen or cavity.
LECTURE 5. Pneumonia. Etiology, pathogenesis, classification
1. Definition and etiology
2. Pathogenesis
3. Classification of pneumonia
1. Pneumonia – acute infectious exudative inflammation of the respiratory parts of the lungs, which is caused by microorganisms of various natures and covers the distal parts of the respiratory tract.
Etiology. The most common causative agents of community-acquired pneumonia are pneumococci (30–40%), mycoplasma (up to 20%) and viruses (10%). In the case of hospital-acquired pneumonia, the causative agents are usually Pseudomonas aeruginosa, Proteus, Legionella, Aspirgillus, Mycoplasma and Pneumocystis. In aspiration pneumonia, the causative agents most often are associations of gram-positive and gram-negative bacteria with anaerobic microorganisms. Such pneumonia occurs in diseases of the gastrointestinal tract, nervous system, and in patients with multiple injuries. In teenagers common cause pneumonia is Mykoplasma pneumoniae.
2. Pathogenesis. The disease occurs under conditions of superinfection or high virulence of the microorganism, on the one hand, and decreased immunity, on the other. Microorganisms penetrate into the lung tissue in one of four ways: by inhalation with air; aspiration from the oro- or nasopharynx; hematogenous spread of their distant source of infection; lymphogenous (from neighboring organs) when the chest is injured. The most typical route of infection is inhalation. A certain role in the pathogenesis of pneumonia is played by violations of the cellular mechanism of anti-infective defense, neurotrophic disorder of the bronchi and lungs associated with the effect of bacterial flora on the interoreceptor apparatus of the respiratory tract.
Predisposing factors for community-acquired pneumonia are smoking, stress, hypothermia, physical fatigue and emotional stress, prolonged exposure to a working air conditioner, impaired consciousness of any etiology, epilepsy with frequent seizures, artificial ventilation lungs, alcohol intoxication, immunodeficiency states (primary or secondary). These factors, suppressing local protective mechanisms and disrupting pulmonary circulation, lead to damage to the bronchioles and alveoli.
3. Classification of pneumonia. According to the international classification (European Respiratory Society, 1995), pneumonia is distinguished:
1) community-acquired (primary);
2) nosocomial (nosocomial), occurring 48–72 hours after hospitalization for other diseases;
3) in persons with severe immune defects;
4) atypical.
The previously widespread classification of pneumonia according to pathomorphological characteristics into lobar and focal provides relatively little information for choosing optimal etiotropic therapy. From a practical point of view, it should be considered more rational to distinguish between two main classes of pneumonia – “community-acquired” and “nosocomial-acquired”. Each class is characterized not only by its place of origin, but also has its own significant features (epidemiological, clinical, radiological, etc.), and most importantly, a certain spectrum of pathogens.
From these positions, pneumonia is distinguished that occurs in closely interacting teams, the features of which are as follows:
- usually occur earlier healthy people in the absence of background pathology;
- the disease is most common in winter time year, which is explained by the high frequency of infections with the influenza A virus, respiratory infection virus, certain epidemiological situations (viral epidemics, outbreaks of mycoplasma infection, Q-fever, etc.);
– risk factors are contact with animals, birds (ornithosis, psittacosis), contact with air conditioners (legionella pneumonia);
– main pathogens: pneumococcus, mycoplasma, legionella, chlamydia, various viruses, hemophilus influenzae.
Nosocomial (hospital-acquired) pneumonia is characterized by the following features:
– occur after two or more days of hospital stay in the absence of clinical and radiological signs of pulmonary damage during hospitalization;
– are one of the forms of nosocomial (hospital) infections and occupy third place after urinary tract infections and wound infections;
– mortality from hospital pneumonia is about 20% – risk factors are the very fact that patients are in intensive care wards, intensive care units, the presence of artificial ventilation, tracheostomy, bronchoscopic examinations, the postoperative period (especially after thoracoabdominal operations), massive antibiotic therapy, septic conditions ;
– the main pathogens are gram-negative microorganisms, staphylococcus.
Pneumonia is classified according to severity: mild, moderate, severe, and extremely severe.
1. Respiratory allergies
Respiratory allergies are common allergic diseases with predominant damage to the respiratory system.
Allergoses develop as a result of sensitization by endogenous and exogenous allergens.
Exogenous allergens of non-infectious nature include: household - washing powders, household chemicals; epidermal - wool, skin scales of domestic animals; pollen - pollen of various plants; food – food products; herbal, medicinal. Allergens of an infectious nature include bacterial, fungal, viral, etc.
The classification is as follows.
1. Allergic rhinitis or rhinosinusitis.
2. Allergic laryngitis, pharyngitis.
3. Allergic tracheitis.
4. Allergic bronchitis.
5. Eosinophilic pulmonary infiltrate.
6. Bronchial asthma.
Symptoms and diagnosis
Allergic rhinitis and rhinosinusitis. History – the presence of allergic diseases in the parents and close relatives of the child, the connection of diseases with allergens.
Symptomatically manifested by an acute onset: the sudden onset of severe itching, burning in the nose, bouts of sneezing, copious liquid, often foamy discharge from the nose.
Upon examination, swelling of the mucous membrane of the nasal septum, inferior and middle turbinates is revealed. The mucous membrane has a pale gray color with a bluish tint, the surface is shiny with a marble pattern.
X-ray examination shows thickening of the mucous membrane of the maxillary and frontal sinuses and the ethmoidal labyrinth on photographs of the skull.
Positive skin tests with infectious and non-infectious allergens are characteristic.
Laboratory diagnosis revealed an increase in the level of immunoglobulin E in nasal secretions.
Allergic laryngitis and pharyngitis can occur in the form of laryngotracheitis.
Characterized by an acute onset, dryness of the mucous membrane, a feeling of soreness, soreness in the throat, attacks of dry cough, which later becomes “barking”, rough, hoarseness appears, up to aphonia.
With the development of stenosis, inspiratory shortness of breath appears, the participation of auxiliary muscles in the act of breathing, retraction of the pliable parts of the chest, flaring of the wings of the nose, and abdominal breathing acquires greater intensity and amplitude.
Obstruction of the bronchi develops due to edema, spasm and exudate and, as a consequence, obstructive ventilation failure.
The use of antibacterial agents does not have a positive effect, and the condition may even worsen.
Laboratory data - positive skin tests, increased levels of immunoglobulin E in the blood serum.
Allergic bronchitis occurs in the form of asthmatic bronchitis.
2. Bronchial asthma
Bronchial asthma is an infectious-allergic or allergic disease of a chronic course with periodically recurring attacks of suffocation caused by impaired bronchial obstruction as a result of bronchospasm, swelling of the bronchial mucosa and accumulation of viscous sputum.
Bronchial asthma is a serious health problem worldwide. It affects 5 to 7% of the Russian population. There is an increase in morbidity and mortality.
Classification (A.D. Ado and P.K. Bulatova, 1969)
1. According to the form:
1) atopic;
2) infectious-allergic;
3) mixed.
2. By type:
1) asthmatic bronchitis;
2) bronchial asthma.
3. By severity:
1) mild degree:
a) intermittent: attacks of bronchial asthma less than twice a week, exacerbations are short, from several hours to several days. Attacks occur rarely at night - twice or less per month;
b) persistent: attacks do not occur every day, no more than twice a week. At night, symptoms of bronchial asthma are observed more than twice a month;
2) moderate degree - manifests itself every day, requires daily use of bronchodilators. Night attacks occur more than once a week;
3) severe degree - bronchial obstruction, expressed to varying degrees constantly, physical activity is limited. The main symptom is the presence of attacks of expiratory type suffocation with distant wheezing and paroxysmal cough. The forced position of the patient during an attack: the legs are lowered down, the patient is sitting on the bed, the body is tilted forward, and his hands are resting on the bed on either side of the body.
Symptoms of respiratory failure appear (participation of auxiliary muscles in the act of breathing, retraction of the intercostal spaces, cyanosis of the nasolabial triangle, shortness of breath). The chest is emphysematously distended, barrel-shaped.
Percussion-box sound, the boundaries of the lungs shift downwards. Auscultation - weakened breathing (short inhalation, long exhalation), an abundance of dry wheezing, moist rales of various sizes. From the cardiovascular system - narrowing of the boundaries of absolute cardiac dullness, tachycardia, increased blood pressure.
On the part of the nervous system, increased nervous excitability or lethargy, changes in autonomic reactions (sweating, paresthesia) appear.
The general blood history includes lymphocytosis and eosinophilia. In the general analysis of sputum - eosinophilia, epithelial cells, macrophages, or Charcot-Leyden crystals, and Kurshman spirals.
3. Allergic bronchopulmonary aspergillosis
Allergic bronchopulmonary aspergillosis is a disease caused by sensitization of the body to Asperginel fungi. With this disease, damage to the alveoli, blood vessels of the lungs, bronchi, and other organs is possible.
The clinical sign is the symptom complex of bronchial asthma (obstructive syndrome, eosinophilia, increased immunoglobulin E).
Confirmation of the diagnosis is carried out by identifying skin sensitization to aspergillus allergens.
An example of a diagnosis. Bronchial asthma, atopic form, with frequent relapses, period of remission, uncomplicated.
The goal of treatment is to prevent the occurrence of attacks of suffocation, shortness of breath during physical activity, cough, and nocturnal breathing difficulties. Elimination of bronchial obstruction. Maintaining normal lung function.
Principles of treatment.
1. Elimination of the allergen (exclusion, elimination).
2. Bronchospasm therapy:
1) selective β-adrenergic agonists (Berotec, salbutalone, Ventosin, terbutamol, phenotyrol, guoetarin);
2) non-selective adrenergic agonists (adrenaline, ephedrine, asthmapent, fulprenaline, isadrin, euspiran, novodrin);
3) phosphodiesterase antagonists, xanthines (theobramines, theophylline, euphylkin);
4) anticholinergics (atropine, ipratropine).
3. H blockers 2 - histamine receptors (tavegil, fenkarol, suprastin, atosinil, pipolfen, displeron).
4. Drugs that reduce bronchial reactivity (glucocorticoids, intal, betotifen).
5. Expectorants:
1) increasing the liquid phase of sputum (thermopsis, licorice root, marshmallow, potassium iodide, alkyonium chloride);
2) mucolytic drugs (acetylcysteine (ACC)), ribonuclease, deoxyribonuclease);
3) drugs that combine a mucoliptic effect with an increase in the level of surfactant (bromgesin, ambrocagn, lazolvan).
6. Antibiotics.
7. Vibration massage with postural drainage.
8. Physiotherapeutic procedures, reflexology (acupuncture, oxygen therapy).
9. Bronchoscopy, intranasal tracheobronchial sanitation.
10. Rehabilitation in the gnotobiological department.