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Lecture notes, cheat sheets
Hospital therapy. Respiratory diseases. Pneumonia (lecture notes)
Directory / Lecture notes, cheat sheets Table of contents (expand) LECTURE No. 8. Diseases of the respiratory system. Pneumonia Pneumonia is an acute infectious and inflammatory disease of a focal nature, in which the respiratory sections and interstitial connective tissue of the lungs are involved in the pathological process. Classification by E. V. Gembitsky (1983). By etiology: 1) bacterial (indicating the pathogen); 2) viral (indicating the pathogen); 3) cornitic; 4) rickettsial; 5) mycoplasma; 6) fungal; 7) mixed; 8) infectious-allergic; 9) unknown etiology. By pathogenesis: 1) primary (independent acute inflammatory process); 2) secondary (complication of diseases of the cardiovascular system with circulatory disorders in the pulmonary circulation, chronic diseases of the kidneys, blood systems, metabolism, infectious diseases or develop against the background of chronic respiratory diseases). Clinical and morphological characteristics: 1) parenchymal (for pneumococcal pneumonia): croupous; focal; 2) interstitial. By localization and extent: unilateral; bilateral. By severity: extremely severe; heavy; moderate; mild and abortive. Downstream: sharp; protracted (radiological and clinical resolution of pneumonia). Etiology. Most pneumonia is of infectious origin. Allergic pneumonia and those caused by physical or chemical factors are rare. Bacterial pneumonia is diagnosed more often in middle-aged and elderly people; viral pneumonia - in young people. In the etiology of primary bacterial pneumonia, the leading role belongs to pneumococci. During an influenza epidemic, the role of viral-bacterial associations (usually staphylococci), as well as opportunistic microorganisms, increases. In secondary pneumonia, the leading etiological role is played by gram-negative bacteria (klebsiella pneumoniae and influenza bacillus); in the occurrence of aspiration pneumonia, the importance of anaerobic infection is great. Pathogenesis. The infectious pathogen enters from the outside into the respiratory sections of the lungs through the bronchi: inhalation and aspiration (from the nasopharynx or oropharynx). By hematogenous route, the pathogen enters the lungs mainly during secondary pneumonia or during the thrombotic genesis of pneumonia. Lymphogenous spread of infection with the occurrence of pneumonia is observed only with wounds to the chest. There is also an endogenous mechanism for the development of inflammation in the lung tissue, due to the activation of the microflora in the lungs. Its role is great in secondary pneumonia. The development of pneumonia is facilitated by unfavorable factors of the external and internal environment, under the influence of which there is a decrease in the general nonspecific resistance of the body (suppression of phagocytosis, the production of bacteriolysins, etc.) and suppression of local defense mechanisms (impaired mucociliary clearance, a decrease in the phagocytic activity of alveolar macrophages and neutrophils, etc.) . Significant importance in the pathogenesis of pneumonia is also attached to allergic and autoallergic reactions. Saprophytes and pathogenic microorganisms, becoming antigens, contribute to the production of antibodies that are fixed on the cells of the mucous membrane of the respiratory tract, where the antigen-antibody reaction occurs, which leads to tissue damage and the development of the inflammatory process. In the presence of common antigenic determinants of microorganisms and lung tissue, or when lung tissue is damaged by viruses, microorganisms, toxins and toxic substances, leading to the manifestation of its antigenic properties, autoallergic processes develop. These processes contribute to a longer existence of pathological changes and a protracted course of the disease. clinical picture. Main syndromes: 1) intoxication (general weakness, fatigue, headaches and muscle pain, shortness of breath, palpitations, pallor, loss of appetite); 2) a syndrome of general inflammatory changes (feeling hot, chills, fever, changes in acute phase blood counts: leukocytosis with a shift of the leukocyte formula to the left, an increase in ESR, fibrinogen level, α2-globulins, the appearance of C-reactive protein); 3) a syndrome of inflammatory changes in the lung tissue (appearance of cough and sputum, shortening of percussion sound), increased voice trembling and bronchophony, changes in the frequency and nature of breathing, the appearance of moist rales, radiological changes; 4) syndrome of involvement of other organs and systems. The severity of these manifestations characterizes the severity of the course of pneumonia (see Table 11). Table 11 Symptoms and course of pneumonia
At various stages of the course of pneumonia, the clinical picture may change from the addition of certain complications: pulmonary and extrapulmonary. Pulmonary: abscess formation; pleurisy (para- and metapneumonic), less often - pleural empyema; accession of an asthmatic component, the formation of pulmonary edema and the development of acute respiratory failure is possible. Extrapulmonary complications: infectious-toxic shock (with symptoms of acute vascular, acute left ventricular and renal failure, ulceration of the mucous membrane of the digestive tract and bleeding, the development of disseminated intravascular coagulation; infectious-allergic myocarditis; infective endocarditis; pericarditis; meningitis or meningoencephalitis; nephritis; hepatitis In severe croupous pneumonia, intoxication psychoses may develop, and in confluent total pneumonia - acute pulmonary heart. The main complaints of a patient with pneumonia: cough, sputum production, chest pain, aggravated by breathing and coughing, shortness of breath, impaired general well-being, fever. Cough may be dry or with sputum (mucous, mucopurulent, purulent-mucous, bloody). "Rusty" sputum is characteristic of lobar pneumonia, bloody - for pneumonia caused by Klebsiella (Fridlander's bacillus) and viral pneumonia; purulent bloody sputum indicates pneumonia of streptococcal origin. Persistent cough with a small amount of mucopurulent sputum is observed with mycoplasmal pneumonia, which is also characterized by a feeling of soreness in the throat. Pain in the side, aggravated by deep breathing and coughing, is characteristic of lobar pneumococcal pneumonia, as well as involvement of the pleura in the pathological process. With the localization of pneumonia in the lower parts of the lungs and the involvement of the diaphragmatic pleura in the process, the pain can radiate to the abdominal cavity, simulating a picture of an acute abdomen. If the upper or lower reed segment of the left lung is involved in the process, the pains are localized in the region of the heart. In 25% of patients, the complaint of shortness of breath is one of the main ones, especially with pneumonia that developed against the background of chronic respiratory diseases and heart failure. The severity of shortness of breath increases in parallel with the violation of general well-being. Symptoms of severe intoxication are most characteristic of cornitosis and mycoplasmal pneumonia, and are also observed in staphylococcal, influenza and pneumococcal (croupous) pneumonia. The patient may be disturbed by chills and an increase in body temperature to febrile. Against the general background of intoxication and febrile temperature, local symptoms appear. Diagnostics. To make an etiological diagnosis, a correct assessment of the symptoms of the disease at its very beginning is important. Hoarseness or inability to speak is characteristic of pneumonia caused by the parainfluenza virus. Lachrymation, pain in the eyes, sore throat when swallowing, copious discharge from the nose without changing other parts of the respiratory tract occur with pneumonia caused by adenovirus. The most significant for the diagnosis is the presence of a syndrome of inflammatory changes in the lung tissue. This syndrome consists of the following symptoms: 1) lag in breathing of the affected side of the chest; 2) shortening of percussion sound in the area of the projection of the lesion over a greater or lesser extent; 3) increased voice trembling and bronchophony in the same area; 4) change in the nature of breathing (hard, bronchial, weakened, etc.); 5) the appearance of pathological respiratory noises (wet, voiced fine bubbling rales and crepitus). The nature of breathing can change in different ways. In the initial stage of croupous pneumonia, breathing can be weakened, with an extended exhalation; in the hepatization phase, along with an increase in the dullness of the percussion sound, bronchial breathing is heard; with the resolution of the pneumonic focus with a decrease in percussion dullness, breathing becomes hard. With focal pneumonia, the most constant symptoms are hard breathing and moist, ringing fine bubbling rales. However, with central hilar pneumonia, physical data are presented very poorly, and recognition of pneumonia is possible only after an X-ray examination. Mycoplasma pneumonias are distinguished by the scarcity of physical data. Severe intoxication, combined with a very small number of wheezing, is observed in pneumonia caused by Klebsiella pneumonia. In some cases, during auscultation, a large number of bass and treble dry rales, uncharacteristic of the inflammatory infiltration syndrome, may come to the fore. This occurs with pneumonia that has developed against the background of chronic bronchitis; pneumonia caused by Pfeiffer's stick; in case of accession to pneumonia of an allergic component. Symptoms help to make an etiological diagnosis: 1) the detection of a small-spotted, as with rubella, rash in combination with lymphadenopathy is characteristic of adenovirus infection; 2) local enlargement of the lymph nodes indicates perifocal pneumonia; 3) fungal pneumonia combined with lesions of the mucous membranes, skin and nails; 4) hepatolienal syndrome and slight jaundice are found in cornitic and Curickettsial pneumonias; 5) for typical croupous pneumonia, the appearance of the patient is characteristic: a pale face with a feverish blush on the side of the lesion, herpetic eruptions, swelling of the wings of the nose when breathing. The most important method to clarify the presence of pneumonia and the degree of involvement of the lung tissue in the process is large-frame fluorography and X-ray examination of the chest organs. Staphylococcal pneumonias are distinguished by a clear segmentation of lung lesions with the involvement of several segments in the process. Their characteristic radiological sign is the formation of multiple cavities in the lungs of the pneumocele type on the 5-7th day from the onset of the disease, and later - necrotic cavities with the presence of fluid. Unlike true abscesses, the configuration and number of cavities change rapidly. Lobar lesion is a manifestation of croupous pneumonia or pneumonia caused by Klebsiella. The upper lobe, mainly the right lung, is most commonly affected. X-ray examination reveals an effusion in the pleural cavity. Often such an effusion occurs with streptococcal pneumonia, with pneumonia caused by Pfeiffer's stick, which is localized in the lower lobe and in 2/3 of patients captures more than one lobe of the lung. X-ray examination data are especially important in detecting pneumonia with mild auscultatory changes (interstitial and hilar pneumonia). In some cases, to clarify the diagnosis, tomography and bronchography are indicated, which help to clarify the diagnosis in cases of delayed regression of infiltrative changes, with a complicated course (abscess, effusion in the pleural cavity). They are used to exclude other pathological processes with similar clinical and radiological presentations. Bronchography reveals decay cavities in the lung tissue, as well as the presence of bronchiectasis, around which infiltrative changes (perifocal pneumonia) are possible during exacerbation. In the diagnosis of infarct pneumonia, a radionuclide study of pulmonary blood flow plays a certain role, revealing its violations. Bacteriological examination of sputum (or bronchial washings) before the appointment of antibiotics helps to detect the pathogen and determine its sensitivity to antibiotics. Not always identified microorganism is the causative agent of pneumonia. A more precise etiological diagnosis can be made using immunological studies: complement fixation reaction (RCC) and hemagglutination inhibition reaction (HITA) with viral and bacterial antigens. In the diagnosis of viral and viral-bacterial pneumonia, virological and serological studies are important (the results of a culture study of sputum, including a biological test on mice, a method of cultivating viruses in a developing chicken embryo, an immunofluorescence method, a serological method using paired sera against viruses, attach importance to only 4 -fold increase in antibody titer). Sputum examination helps to clarify the nature of pneumonia. A large number of eosinophils indicates allergic processes, the presence of atypical cells indicates pneumonia of cancerous origin; Mycobacterium tuberculosis is found in tuberculosis; elastic fibers - evidence of the collapse of lung tissue. With mycosis pneumonia, along with the detection of fungi, there is a lack of pyogenic flora due to the inhibitory effect of the waste products of fungi. According to the microscopy of Gram-stained sputum smears, we can talk about Gram-negative or Gram-positive microorganisms that live in the bronchi already on the first day of the patient's stay in the hospital. The severity of the inflammatory process is judged by the severity of acute-phase blood parameters and their dynamics (leukocytosis with a shift in the leukocyte formula, an increase in ESR, an increased content of α2-globulins, fibrinogen, the appearance of SRV, an increase in the level of sialic acids). With a prolonged course of pneumonia and the development of complications, the immunological reactivity of the body is studied. A decrease in humoral (IgM) and cellular (delayed migration of leukocytes, changes in tests characterizing the T-lymphocyte system) immunity requires immunomodulatory therapy. Treatment. Immediately after diagnosis, it is necessary to begin etiotropic therapy for pneumonia. Empirical ideas about a possible pathogen are of great importance, since bacteriological examination of sputum is carried out for quite a long time and in most patients, even with a modern approach to this study, gives uncertain and sometimes erroneous results. At the moment, penicillins have lost their importance as the drug of choice in the treatment of pneumonia. This is due to the fact that etiologically significant for the development of pneumonia, in addition to pneumococcus and Haemophilus influenzae, are obligate intracellular microorganisms - Mycoplasma pneumoniae and Chlamydia pneumoniae, which are resistant to the bactericidal effects of antibiotics of the β-lactam group. It is impossible to lose sight of the fact that hypersensitivity to these drugs quickly develops in patients. In connection with the above, in the treatment of pneumonia, much attention is paid to macrolides, which have proven effective not only against pneumococcus, but also against Mycoplasma pneumoniae, Chlarnydia pneumoniae. However, it is important not to lose sight of the fact that erythromycin, which is the standard of this group of drugs due to its low stability in an acidic environment (and hence low bioavailability), as well as the widespread prevalence of pneumococcal strains resistant to erythromycin, is losing its clinical value. meaning. As drugs of choice, it was replaced by other drugs of the macrolide class - azithromycin, roxithromycin, rovamycin, etc. A number of macrolides are also used for oral and parenteral use (for example, rovamycin). As a result, their use is justified in the severe course of the inflammatory process in the lung (for example, initially rovamycin is administered intravenously for 2-3 days, and subsequently, with a positive dynamics of the pathological process, the patient switches to taking this drug inside). The advantage of rovamycin is undeniable, since it does not interact with theophyllines, while preventing the possibility of an overdose of these drugs, since theophyllines and rovamycin are used together in the treatment of patients with chronic obstructive pulmonary diseases. It is also known that this subgroup of macrolides (16-membered macrolides) are drugs with a minimum level of side effects. In patients over 65 years of age, due to the heterogeneity of the etiological spectrum of pneumonia and with concomitant chronic obstructive pulmonary diseases, semi-synthetic penicillins can be used for initial antibiotic therapy, and in the absence of a positive effect after this therapy for 3-4 days, the use of cephalosporins is justified. It is important to recall that the spectrum of action of I and some II generation cephalosporins is gram-positive and gram-negative microorganisms, and III generation cephalosporins act mainly on gram-negative pathogens. I generation cephalosporins are represented by cephalothin (keflin), cefazolin (kefzol), etc. II generation drugs include cefuroxime (ketocef), cefoxitin (boncefin) and others. III generation cephalosporins: cefotaxime (claforan), cefoperazone (cefobid), ceftriaxone (longacef ). Aspiration pneumonia is associated with anaerobic or gram-negative microflora, which determines the use of aminoglycosides or III generation cephalosporins in combination with metronidazole-semisuccinate (500 mg intravenously 2-3 times a day). Immunodeficiency states also affect the nature of the selected drugs, which in this case depends on the nature of the pathogen. In such cases, the applied scheme consists of aminoglycosides and modern cephalosporins. The duration of effective antibiotic therapy for a patient with pneumonia is 7-10 days. When prescribing treatment, it should be taken into account that in 7-15% of cases there may be no effect from this therapy. This indicates the need to replace antibiotics, based on the results of a microbiological study. Another option is the use of alternative drugs, the so-called second-choice antibiotics: modern cephalosporins, imipenem, monobactams, fluoroquinolones. Fluoroquinolones (ofloxacin, pefloxacin, ciprofloxacin) are effective against gram-negative pathogens, including Pseudomonas aeruginosa, and some gram-positive cocci (Staphylococcus aureus), but are inactive when exposed to anaerobes. Fluoroquinolones can justifiably be considered as an alternative to macrolides in chlamydia, legionella and mycoplasma infections. Monobactam antibiotics in their modern form are represented by aztreonam (azactam), which is active mainly against gram-negative aerobes (Salmonella, Shigella, Proteus, Escherichia coli, Klebsiella, etc.); and is also stable under the action of β-lactamases. Imipenem - an antibacterial drug of the carbapenem group, is prescribed only in combination with cilastatin, which inhibits the metabolism of imipenem. The drug is highly effective against many anaerobes, gram-positive cocci and gram-negative rods. Dosing of antibiotics used in the treatment of pneumonia. 1) Penicillins: benzylpenicillin (500-000 IU intravenously every 1-000 hours or 000-6 IU every 8 hours intramuscularly), ampicillin (500-000-1 g intramuscularly every 000-000 hours or 4 g every 0,5 hours intravenously), amoxicillin (1,0-2,0 g every 6 hours orally or 8-0,5 g every 6-0,5 hours intramuscularly, intravenously), oxacillin ( 1,0 g every 8-0,5 hours orally, intramuscularly, intravenously). 2) Cephalosporins: I generation - cephalothin (keflin) (0,5-2,0 g every 4-6 hours intramuscularly, intravenously), cefazolin (kefzol) (0,5-2,0 g, every 8 hours intramuscularly, intravenously ), II generation - cefuroxime (zinacef, ketocef) (0,75-1,5 g every 6-8 hours intramuscularly, intravenously), III generation - cefotaxime (claforan) (1,0-2,0 g, maximum up to 12 g / day every 12 hours intramuscularly, intravenously), ceftriaxone (longacef, rocefin) (1,0-2,0-4,0 g every 24 hours intramuscularly, intravenously). 3) Aminoglycosides: genetamycin (80 mg every 12 hours intramuscularly, intravenously), amikacin (10-15 mg/kg every 12 hours intramuscularly, intravenously), tobramycin (brulamycin) (3-5 mg/kg every 8 hours intramuscularly, intravenously) . 4) Macrolides: erythromycin (0,5 g every 6-8 hours orally or 0,5-1,0 g every 6-8 hours intravenously), rovamycin (3,0 million IU every 8-12 hours orally or 1,5. 3,0-8 million IU every 12-XNUMX hours IV). 5) Fluoroquinolones: pefloxacin (leflacin) (400 mg every 12 hours orally, IV), ciprofloxacin (cyprobay) (500 mg every 12 hours orally or 200-400 mg every 12 hours intravenously), ofloxacin (zanocin, tarivid) (200 mg every 12 hours orally). 6) Tetracyclines: doxycycline (vibramycin) (200 mg on day 1, on subsequent days - 100 mg every 24 hours orally), minocycline (minocin) (200 mg on day 1, on subsequent days - 100 mg every 12 hours orally), aztreonam (azactam) (1,0-2,0 g every 8-12 hours), imipenem/cilstatin (thienam) (500 mg every 6-8 hours intramuscularly). It is also significant that, as a rule, a protracted or progressive course of the disease is due to inadequate initial antibiotic therapy. However, in addition to this, there are a number of local and systemic causes that lead to a long and persistent course of inflammation in the lungs: these are local airway obstruction (cancer, adenoma, mucoid blockage, etc.); bronchiectasis (congenital, acquired); cystic fibrosis; immune system defects (acquired); recurrent aspiration (achalasia, esophageal cancer, etc.); activation of latent tuberculosis infection; developing lung abscess; inadequate antibiotic therapy. Author: Mostovaya O.S. << Back: Respiratory diseases. Chronical bronchitis >> Forward: Diseases of the digestive tract. Diseases of the esophagus. Esophagitis and peptic ulcer of the esophagus
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