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In conclusion, it is advisable to briefly summarize data on the most common mechanisms of resistance among the main clinically significant microorganisms.

Causative agents of community-acquired infections

• Staphylococcus spp. - resistance to natural and semi-synthetic penicillins associated with the production of? -lactamase.

• S. pneumoniae - resistance to various levels of penicillin (some strains are resistant to third-generation cephalosporins), associated with the modification of PSB; high frequency of associated resistance to macrolides, tetracyclines, co-trimoxazole.

• H.influenzae, M.catarrhalis - resistance to semi-synthetic penicillins associated with the production of? -Lactamase.

• N.gonorrhoeae - penicillin resistance associated with the production of? -Lactamase, resistance to tetracyclines, fluoroquinolones.

• Shigella spp. - resistance to ampicillin, tetracyclines, co-trimoxazole, chloramphenicol.

• Salmonella spp. - resistance to ampicillin, co-trimoxazole, chloramphenicol. The emergence of resistance to cephalosporins III generation and fluoroquinolones.

• E.coli - for community-acquired infections FPA - resistance to ampicillin, co-trimoxazole, gentamicin is possible.

Causative agents of nosocomial infections

• Enterobacteriaceae - BLRS products (most often among Klebsiella spp.), Causing the clinical inefficiency of all cephalosporins; very high incidence of associated gentamicin / tobramycin resistance; in some institutions, there is a tendency for an increase in associated resistance to fluoroquinolones, amikacin.

• Pseudomonas spp., Acinetobacter spp., S. maltophilia - associated resistance to cephalosporins, aminoglycosides, fluoroquinolones, and sometimes carbapenems.

• Enterococcus spp. - association of resistance to penicillins, a high level of resistance to aminoglycosides, fluoroquinolones and glycopeptides.

• Staphylococcus spp. (methicillin-resistant) - associated resistance to macrolides, aminoglycosides, tetracyclines, co-trimoxazole, fluoroquinolones.

Mechanisms of resistance to tuberculosis drugs

Features of pathogenesis of tuberculosis and biology of the pathogen (slow proliferation, prolonged persistence in the body and subsequent reactivation of the infection) impose certain imprints on the formation of resistance in mycobacteria. Due to the extremely limited possibilities of genetic exchange between mycobacteria, the formation of resistance in them is almost always associated with the accumulation of chromosomal mutations in the genes coding for the target of drug action.

The terminology of the antibiotic resistance of mycobacteria is distinguished by several features, which is associated with purely practical problems. According to the WHO recommendations, depending on whether the patient received specific anti-tuberculosis therapy before isolating the pathogen, distinguish between primary and acquired resistance. Primary-resistant microorganisms include strains isolated from patients who have not received specific therapy. If the resistant strain is isolated from the patient on the background of anti-tuberculosis therapy, then the resistance is regarded as acquired. In cases where it is impossible to reliably establish the use of anti-TB drugs, use the term "initial" resistance. Micro-organisms that are resistant to rifampicin and isoniazid are considered to be multi-resistant mycobacteria.

The risk of developing mutations that mediate resistance is: 3.32 x 10-9 per cell division for rifampicin; 2.56 x 10-8 for isoniazid; 2.29 x 10-8 for streptomycin; 1,0 x 10-7 for ethambutol. The risk of simultaneous development of resistance to two drugs is less than 10-15. The likelihood of such an event is extremely low, especially given the fact that mycobacteria infection of the source of infection usually does not exceed 108 CFU. Given the above facts, the formation of multiple resistance in mycobacteria is associated with a violation of antibacterial therapy, although there is no direct evidence of this.

From the point of view of natural sensitivity to AMP, mycobacteria are not a completely homogeneous group. Thus, the “atypical” mycobacteria of M. avium-intracellulare are resistant to isoniazid and pyrazinamide, microorganisms of the M.chelonae group are resistant to isoniazid, pyrazinamide, rifampicin, streptomycin and ethambutol. But on the other hand, the listed microorganisms are highly sensitive to macrolides - azithromycin and clarithromycin, these AMPs form the basis of the therapy of the corresponding infections. Microorganisms of the M.chelonae group are also sensitive to tetracyclines and sulfonamides.


The target of rifamycin action is the enzyme DNA-dependent RNA polymerase (rpoB gene). Resistance to rifamycins (rifampicin, rifabutin, etc.) in the overwhelming majority of cases (more than 95% of strains) is associated with mutations in a relatively small fragment of the β-subunit of this enzyme. The size of this fragment is 81 base pairs (27 codons). Mutations in individual codons differ in their meaning. Thus, with mutations in codons 526 and 531, a high level of resistance to rifampicin (MIC <32.0 µg / ml) and other rifamycins are found. Mutations in codons 511, 516, 518 and 522 are accompanied by a low level of resistance to rifampicin and rifapentin, while maintaining sensitivity to rifabutin. In a small proportion of cases, resistance to rifamycins is associated with mutations in other parts of the rpoB gene.


Isoniazid is essentially a prodrug. For the manifestation of the antibacterial activity of the drug molecule must be activated inside the microbial cell, however, the chemical structure of the active form of isoniazid is not finally identified. Activation occurs under the action of the enzyme catalase-peroxidase (katG gene). Mutations in this gene (usually at position 315), resulting in a 50% reduction in enzyme activity, are found in approximately half of the isoniazid-resistant mycobacterial strains.

The second mechanism of resistance of mycobacteria to isoniazid is overproduction of targets for the action of active forms of the drug. These targets include proteins involved in the transport of precursors of mycolic acid and its biosynthesis: an acylated carrier protein (acpM gene), synthetase (kasA gene), and reductase (inhA gene) of a carrier protein. Mycolic acid is the main component of the mycobacterial cell wall. Mutations are usually detected in the promoter regions of the listed genes. The level of resistance associated with hyperproduction of targets is usually lower than with mutations in catalase-peroxidase genes.


Pyrazinamide, like isoniazid, is a prodrug. After passive diffusion inside the microbial cell, pyrazinamide is converted into pyrazinoic acid by the action of the enzyme pyrazinamidase (pncA gene). Pyrazinoic acid, in turn, inhibits fatty acid biosynthesis enzymes. In 70-90% of pyrazinamide-resistant mycobacteria strains, mutations are found in structural or promoter regions of pyrazinamidase. Here it should be noted that M.bovis has a natural resistance to pyrazinamide, thanks to a specific point mutation in codon 169.


Unlike most other microorganisms, the resistance of mycobacteria to aminoglycosides is not associated with the production of AMP. Streptomycin-resistant Mycobacterium strains have two types of mutations that lead to modification of the small subunit (23S) ribosome binding site: mutations in the genes encoding 16S rRNA (rrs) and genes encoding S23 ribosomal protein (rspL).


The target of ethambutol action is the embB protein (arabinosilotransferase), which is involved in the biosynthesis of a component of the mycobacterial cell wall - arabinogalactan. Resistance to ethambutol, in most cases, is associated with a point mutation in codon 306.


The mechanisms of resistance of mycobacteria to fluoroquinolones do not differ from the mechanisms detected in other microorganisms, and are associated with mutations in the genes of DNA gyrase.


The resistance of M. avium-intracellulare to macrolides is determined by the modification of the target of their action. In resistant strains, adenine substitution is found in the 2058 position of the 23S RNA molecule.

In conclusion, it should be noted that the mechanisms of resistance of mycobacteria to anti-tuberculosis drugs have not been established.

Mechanisms of resistance to antifungal drugs

The increased role of fungi in the etiology of hospital and some community-acquired infections led to the introduction into clinical practice of a significant number of new drugs and their widespread use, which, in turn, inevitably led to the formation of resistance. Since mushrooms, unlike bacteria, are eukaryotic organisms, it is necessary to use drugs with fundamentally different targets and mechanisms of action for the treatment of infections caused by them. A factor that significantly complicates the study of the resistance of fungi is the lack of standardization of methods for assessing their sensitivity to antifungal drugs and the difficulty in justifying the sensitivity criteria.


The mechanism of action of azoles (miconazole, ketoconazole, fluconazole, itraconazole, etc.) is to inhibit the biosynthesis of ergosterol, a substance involved in maintaining the structural integrity of the cell membrane of the fungus. The main target of the action of azoles are enzymes (14? -Methylase), carrying out the demethylation of ergosterol precursors. For fungi of the genus Candida, it has been shown that resistance to azoles may be associated with point mutations leading to amino acid substitutions. As a result of such mutations, the binding of enzymes to azoles decreases sharply, but binding to natural substrates does not suffer. Stability may result from overproduction of azo action targets. In fungi of the genus Candida and others, several transport systems are known that carry out the active elimination of azoles, which also leads to the formation of resistance of these fungi. Activation of excretion systems is often associated with changes in the structure of the membrane, leading to a decrease in the azoles entering the cells of the fungus.


The mechanism of action of allylamines (terbinafine), as well as azoles, is associated with inhibition of ergosterol biosynthesis. However, this inhibition occurs at substantially earlier stages of biosynthesis. Cases of treatment failure with terbinafine have now been reported and resistant strains have been described. Genetic and biochemical mechanisms of resistance to allylamines have not been studied enough, but it has been shown that drugs can be actively excreted from the cells of fungi by means of known transport systems.


The mechanism of the antifungal activity of polyenes (nystatin, amphotericin B, etc.) consists in the physicochemical interaction of these drugs with sterols of the cytoplasmic membrane of fungi. As a result of this interaction, pores are formed in the membrane, through which the loss of cytoplasmic content occurs, leading to the death of the fungus. Since the targets of polyenes are structural elements of the cell of the fungus, and not enzymes, the formation of resistance may be the result of complex genetic processes leading to changes in the biosynthesis of membrane components. The probability of such events is relatively small, and this is the reason for the low frequency of resistance to polyene. The biochemistry and genetics of resistance to polyena has not been studied enough, but the available data generally support the hypothesis of a decrease in the ergosterol content in the cytoplasmic membrane and an increase in the content of its analogues in resistant strains.

Evaluation of sensitivity to antifungal drugs

In connection with the occurrence of cases of ineffectiveness of antifungal therapy, a real practical need arose in determining the sensitivity of fungi to the corresponding drugs. Unfortunately, the possibilities for solving this problem are very limited. Serial dilutions on RPMI 1640 are considered standard, reproducible results are provided by a number of other methods and some commercial test systems. Detailed consideration of methods for assessing the sensitivity of fungi is beyond the scope of this chapter.

The principal points are:

1. fusion method for assessing the sensitivity of fungi;

2. the lack of criteria for the interpretation of research results for most of the combinations mushroom - drug;

3. Clinically based criteria are developed only to assess the sensitivity of Candida fungi to azoles and certain other antimycotics.

It should be noted that the use of non-standardized ("domestic" or commercial) methods for assessing the sensitivity of fungi can lead to obtaining false results and serious errors in the choice of drugs for treatment.

Mechanisms of resistance to antiviral drugs

Antiviral therapy in its effectiveness is significantly inferior to antibacterial. This is mainly due to difficulties in the development of specific drugs due to the extremely close integration of the viral genome and the host (human) genome. To date, only a very limited number of viral infections in varying degrees, is amenable to effective etiotropic therapy: herpes and CMV infections, HIV, some viral hepatitis. Accordingly, resistance to the most common antiviral drugs, antiherpetic and antiretroviral, is of key clinical importance. The main mechanisms of resistance are the formation and selection of mutations in the genes encoding enzymes involved in the metabolism of drugs, or which are direct targets for the action of drugs.

Typical for antiviral drugs is the formation of resistance during long-term therapy.

Antiherpetic drugs

Many antiherpetic drugs are active against CMV and other viruses. Acyclovir, the main antiherpetic drug, is an abnormal analogue of the guanosine nucleoside. Inside a virus-infected cell, acyclovir is phosphorylated by viral thymidine kinase and cellular phosphorylases. Acyclovir triphosphate is incorporated into growing DNA molecules and blocks their synthesis; in addition, it is a competitive inhibitor of viral DNA polymerase. Resistance to acyclovir is formed as a result of mutations in viral thymidine kinase. Two types of mutations are known: leading to a thymidine kinase deficiency and leading to a decrease in the affinity of the enzyme for acyclovir. Herpes virus strains deficient in thymidine kinase show significantly reduced virulence and cause infections mainly in immunocompromised people.

Mutations in viral DNA polymerase only lead to a moderate decrease in the sensitivity of herpes viruses to acyclovir, the clinical significance of this decrease in sensitivity has not been finally established.

In addition to acyclovir, valacyclovir is used in clinical practice, as well as famciclovir and ganciclovir. Their resistance mechanisms are the same as those of acyclovir.

Antiretroviral drugs

Among antiretroviral drugs, reverse transcriptase inhibitors and protease inhibitors are isolated. Reverse transcriptase catalyzes the synthesis of DNA from a viral RNA template. The viral protease cleaves the functionally inactive polyproteins and produces individual proteins necessary for virion assembly.

Historically, thymidine analogue zidovudine (azidothymidine) was the first reverse transcriptase inhibitor. To date, other nucleoside analogues have been registered and approved for medical use in the Russian Federation: didanosine, zalcitabine, stavudine, etc. Inside the cell, under the influence of phosphorylases, nucleoside analogs are converted to triphosphates, which are competitive inhibitors of reverse transcriptase, besides being included in the viral DNA chain, block its further synthesis.

HIV resistance to nucleoside analogs is formed quite quickly, and in this connection they are used in combination with drugs of other classes. To date, a large number of mutations in the reverse transcriptase genes, leading to the formation of resistance, have been described. Some of these mutations mediate selective resistance to zidovudine or other nucleoside analogues, others cause cross-resistance to all known drugs.

Reverse transcriptase activity can also be suppressed by compounds that differ in chemical structure from nucleosides (nevirapine). They bind to the enzyme at a site other than the catalytic center. Despite the fact that the binding of the inhibitor and the enzyme occurs outside the active center, this process leads to the suppression of catalytic activity. About 10 different mutations in reverse transcriptase genes leading to the formation of resistance have been described.

Resistance to protease inhibitors (amprenavir, indinavir, ritonavir, saquinavir) is also formed quite quickly as a result of mutations in the genes of the enzyme, so they are not used for monotherapy. Known mutations mediating resistance to individual inhibitors, as well as causing cross-resistance to several drugs.

В заключение необходимо еще раз подчеркнуть, что специфическая терапия ВИЧ-инфекции во всех случаях должна быть комбинированной и соответствовать разработанным строгим схемам, что позволяет предотвратить селекцию резистентности.

Механизмы резистентности к антипротозойным препаратам

Простейшие (Protozoa) представляют собой обширную и разнообразную по свойствам группу эукариотических микроорганизмов. Некоторые метаболические пути простейших сходны с таковыми у бактерий, этим объясняется наличие антипротозойной активности у таких антибактериальных препаратов, как нитроимидазолы и тетрациклины. В данной главе рассматриваются механизмы устойчивости простейших к наиболее известным ЛС.

Противомалярийные препараты

Появление резистентности к противомалярийным препаратам во многом связано с их массовым применением в рамках кампаний по глобальной ликвидации малярии, проводимых под эгидой ВОЗ. Наибольшее значение имеет распространение устойчивости среди P.falciparum и, в меньшей степени, среди P.vivax к дешевым препаратам массового применения: хлорохину и пириметамину/сульфадоксину.

Частота устойчивости к хлорохину варьирует в различных географических регионах даже в пределах одной страны. Так, в Кении резистентность колеблется от 18% до 70%.

Резистентность к хлорохину связана с двумя процессами: снижением транспорта препарата внутрь плазмодия и его активным выведением. Наиболее вероятным геном, ответственным за активное выведение хлорохина является pfmdr (P.falciparum multidrug resistance) - гомолог гена множественной лекарственной устойчивости млекопитающих. У устойчивых штаммов выявляется либо увеличение копийности указанного гена, либо точечные мутации. Увеличение числа копий гена pfmdr вероятно также опосредует устойчивость и к мефлохину. Генетические исследования свидетельствуют, что в формировании резистентности участвуют и другие неустановленные механизмы.

Резистентность к ингибиторам фолиевой кислоты формируется в результате мутаций в генах ферментов биосинтеза фолиевой кислоты: дигидроптероатсинтетазы и дигидрофолатредуктазы. С точечными мутациями в этих генах, а также в генах тимидилат синтетазы связана устойчивость к препарату группы бигуанидов - прогуанилу.

Активное выведение, опосредуемое продуктом гена pfmdr, вероятно, является причиной феномена множественной устойчивости P.falciparum к противомалярийным препаратам.


Ряд простейших, прежде всего T.vaginalis, G.lamblia и E.histolytica, характеризуются анаэробным метаболизмом, во многом сходным с метаболизмом анаэробных бактерий. Чувствительность этих простейших к нитроимидазолам (прежде всего к метронидазолу) объясняется способностью микроорганизмов к восстановлению нитрогруппы препаратов и, таким образом, трансформации их в активную форму, повреждающую ДНК. Донором электронов, участвующим в активации нитроимидазолов, является ферредоксин. Устойчивость анаэробных простейших к нитроимидазолам связана со снижением уровня экспрессии ферредоксина и, следовательно, со снижением способности микроорганизмов активировать препараты.

Состояние резистентности к антиинфекционным химиопрепаратам в России

На протяжении последних лет во всем мире отмечается значительный рост устойчивости возбудителей внебольничных и нозокомиальных инфекций к АМП. Возникновение антимикробной резистентности является естественным биологическим ответом на использование АМП, которые создают селективное давление, способствующее отбору, выживанию и размножению резистентных штаммов микроорганизмов.

Резистентность к АМП имеет огромное социально-экономическое значение и в развитых странах мира рассматривается как угроза национальной безопасности. Инфекции, вызванные резистентными штаммами, отличаются длительным течением, чаще требуют госпитализации и увеличивают продолжительность пребывания в стационаре, ухудшают прогноз для пациентов. При неэффективности препаратов выбора приходится использовать средства второго или третьего ряда, которые, зачастую, более дороги, менее безопасны и не всегда доступны. Все это увеличивает прямые и непрямые экономические затраты, а также повышает риск распространения резистентных штаммов в обществе.

Выделяют несколько уровней резистентности к АМП - глобальный, региональный и локальный. Прежде всего, необходимо учитывать глобальные тенденции в развитии резистентности. Примерами микроорганизмов, которые во всем мире стремительно вырабатывают резистентность к существующим АМП, являются стафилококки, пневмококк, гонококк, синегнойная палочка и др. При этом следует помнить, что антибиотикорезистентность не является тотальной, не распространяется на все микроорганизмы и АМП. Так, S.pyogenes и T.pallidum остаются универсально чувствительны к ?-лактамам; H.influenzae - к цефотаксиму или цефтриаксону.

Однако при всей важности учета глобальной картины при планировании политики антимикробной терапии более рационально опираться на данные, полученные в конкретной стране (региональные данные). Несомненно, что в такой огромной стране, как Российская Федерация, существуют значительные территориальные вариации распространения резистентности к АМП. В связи с этим неоспоримо значение территориального мониторирования резистентности и доведение его результатов до врачей различных специальностей.

В каждом лечебно-профилактическом учреждении необходимо иметь локальные данные по рези-стентности (паспорт резистентности). В первую очередь это относится к отделениям с высокой частотой применения АМП: ОРИТ, ожоговые, урологические и др. Сведения о резистентности следует приводить дифференцированно, по различным отделениям и микроорганизмам. Паспорт резистентности должен быть изложен в письменном виде и его следует регулярно, минимум один раз в год, обновлять. Удобным является его издание в виде приложения к формулярному справочнику.

Данные о состоянии резистентности в России носят разрозненный характер, зачастую они получены с нарушением методологии определения чувствительности, что ставит под сомнение их достоверность. Кроме того, наряду с этим абсолютно необходимо знать и преобладающие механизмы резистентности, в том числе на локальном уровне, что необходимо для выбора рациональной терапии.

Основной проблемой определения чувствительности микроорганизмов в России является отсутствие стандартизированных методик тестирования. Единственные существующие в нашей стране официальные рекомендации - "Методические указания по определению чувствительности микроорганизмов к антибиотикам методом диффузии в агар с использованием дисков" Минздрава СССР (1983 г.) - не описывают методики определения чувствительности "прихотливых" микроорганизмов, в частности S.pneumoniae, H.influenzae и N.gonorrhoeae, не содержат методик определения МПК, не включают критерии интерпретации для современных антибиотиков (цефалоспорины, фторхинолоны, карбапенемы). Более того специальные исследования показали, что рекомендуемая в этих документах среда АГВ непригодна для определения чувствительности к ряду АМП.

В связи с этим значительное число данных о чувствительности различных микроорганизмов к антибиотикам, полученных в микробиологических лабораториях страны, не может быть оценено и проанализировано. С осторожностью также следует относиться к публикациям в отчественных и зарубежных источниках, в которых отсутствует информация о методах определения чувствительности и критериях интерпретации.

В данной главе приведены результаты только тех исследований, которые выполнялись в соответствии с наиболее часто используемыми в мире стандартами NCCLS. Для удобства восприятия и с учетом сложившейся клинической практики, рассматриваемые микроорганизмы были подразделены на внебольничные и нозокомиальные.

Более подробную информацию по предоставленным в настоящей главе данным можно получить в Научно-методическом центре Минздрава РФ по мониторингу антибиотикорезистентности
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  1. Conclusion
    Based on the analysis of the content of the article, the following conclusions can be drawn: The most important hardening is important to begin at an early age, when the body is in the formative stage, and the mechanisms of immunobiological protection are developed. For full hardening, it is necessary to use a complex of tempering procedures, taking into account the individual characteristics of the organism. How for example age
  2. Conclusion
    In conclusion, we can give an example (of many), showing that Sytin's method is truly unique and effective. So, in the Institute of Normal Physiology. Acad. PK Anokhin RAMS in the presence of academician KV Sudakov as a result of applying this method for ten minutes a 28-year-old employee of the employee (28 years) was taken off with a pulse rate of 120 beats per minute. After
  3. Conclusion
    In conclusion of the dissertation, the results of the research are summarized, the results of solving the tasks are summarized, the prospects for further scientific research and the prospects for the use of the results are indicated, and the main conclusions are formulated: 1. Readiness for professional activity is the cumulative psychological neoplasm of the initial stages of professionalization
    In conclusion, the following should be noted. The inner world of the person we expect to see as our customer is complex and multifaceted. In everyday work with customers, one should not be limited to intuitive, sometimes superficial knowledge and notions about consumer behavior, since the true motives of behavior lie much deeper than it seems on the market.
    In conclusion, we will try to take stock of the work we have done and put forward some general provisions that we think follow from the theoretical and experimental research conducted by our research team. However, before embarking on this, it is necessary to raise the question of the degree of proof of the provisions that we intend to put forward. The monograph touches on a very wide
  6. Conclusion
    In conclusion, it is necessary to emphasize the importance of a balanced content of the described nutrients in the composition of any diet. On average, physiologically most acceptable ratio of proteins, fats and carbohydrates as 1: 1: 4. For people engaged in physical work, this ratio should be approximately equal to 1: 1: 5, and for knowledge workers - 1: 0.8: 3. Given the characteristics of carbohydrate
    In conclusion, I give an answer to another question that you, of course, ask yourself: Why are there so many feelings of guilt on our Earth, if we only suffer from this? Guilt appeared on the planet simultaneously with the separation of the sexes. In the past, we simply were without concepts of good or evil, because these concepts, generated by the mental sphere, did not exist at the very beginning of human history.
  8. Instead of conclusion
    If you have read this book, then "Conclusion" you do not need. You yourself have already done it. If you are one of those people who, like Alexander the Great, looks at the end of the book and decides to read it, then for you there are a few lines. In order for the reader to understand this book in his own way, it must be read. It is not necessary to read in a row, first. You can start reading from any chapter. Even with any small section. Select
  9. Instead of conclusion
    And instead of a conclusion, I would like to quote Rudolf Zagainov’s words: “Long-term meditations on his profession give reason to consider it not only difficult (according to technology, effort and other components), but also cruel, ruthlessly screening psychologists who cannot cope with the tasks by the will of fate they had to be taken, not corresponding to them. Be
  10. Registration of a clinical-pathoanatomical epicrisis and a conclusion on the cause of death
    The opinion of the pathologist about thanatogenesis, the mechanisms of death, taking into account the clinical and morphological data is set out in the clinical-pathoanatomical epicrisis containing the doctor's judgment about the cause of death. The conclusion about the cause of death is more accessible for understanding by relatives and representatives of non-medical departments who, according to the duty of duty, are familiar with the pathoanatomical documentation. Still
  11. Conclusion
    Dear reader! You have read the entire book. We hope that the information contained in it helped you to develop a clinical thinking, i.e. the ability to properly collect the necessary information and process it into a detailed clinical diagnosis. It is well known that recent advances in science and technology have significantly improved the recognition of internal diseases and deepened the understanding of many of their questions.
  12. Conclusion
    Diagnosis and treatment of gastritis in animals, in particular dogs, is a particularly urgent task, the solution of which is an important condition for raising the standard of living of the animal. In this paper, such concepts as chronic, acute and specific forms of gastritis were considered. The distinctive features of chronic gastritis from peptic ulcer, stomach cancer and functional disorders are given.
  13. Conclusion
    Summing up the data in the monograph, the following points should be emphasized. Along with the ever-increasing profile in medicine, new specialties are being created. And one of the first isolated obstetric anesthesiology. The first anesthesiologists in the field of obstetrics and gynecology appeared in the late 50s, and independent departments in obstetric institutions appeared in the mid-60s
    Effective emergency medical care for pregnant women, parturient women, puerperas and newborns in the acute period of obstetric and gynecological situations at the prehospital stage is a necessary condition for their successful treatment in the hospital. Its tasks include the correct recognition of pathological conditions and the skillful execution of therapeutic and tactical measures. The materials given in
  15. Conclusion
    When assessing the general layout of the dairy farm for 800 cows of the Ilyinsky state farm, the following drawbacks were noticed: there is no landscaping of the territory within the livestock facility with deciduous trees, there is an intersection of “clean” and “dirty” paths, and there are no sanitary inspection rooms and disbarriers. Also, when examining a livestock facility, the following were found: hard coatings in
  16. Conclusion
    Although the model of coronary heart disease in animal experiments differs in many ways from its clinical counterparts, it nevertheless provides important information and allows us to deepen our understanding of the mechanisms of potentially lethal ventricular rhythm disorders. On the one hand, experimental data make it possible to re-evaluate the observed clinical
  17. Conclusion
    Since the first identification of this violation, many reviews have appeared on this issue; Among the many published data, there are two aspects of interest for future researchers that deserve separate consideration. At the clinical level, the main diagnostic problem in patients with chronic recurrent ventricular tachycardia is to determine
  18. Conclusion
    Electrophysiological study with programmatic ventricular stimulation, originally used to study the mechanisms of ventricular tachycardia, is now an integral part of the clinical examination and treatment of patients with ventricular tachyarrhythmia. The sensitivity and specificity of the various methods of stimulation used in the EFI, now well studied. Adequate
    In the course of achieving the goal of our work, the analysis of available literature sources allows us to draw the following conclusions: 1. EHF-therapy has found deserved recognition in modern medicine. The success of its use is determined by shorter periods of cure, its high quality, efficiency (associated not only with a significant reduction in the duration of treatment, but also with a sharp decrease in
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