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CLINICAL AND MORPHOLOGICAL SUBSTANTIATION OF ACUTE RESPIRATORY DISTRESS SYNDROME AND OTHER PULMONARY COMPLICATIONS IN COVID-19 Sodikova D.T.
Sodikova Dilrabo Tadidinovna - Candidate of Medical Sciences, Associate Professor,
DEPARTMENT OF GENERAL PRACTITIONERS № 2, ANDIJAN STATE MEDICAL INSTITUTE, ANDIJAN, REPUBLIC OF UZBEKISTAN
Abstract: this article concludes that severe acute respiratory distress syndrome caused by the novel coronavirus-2
(COVID-19) is considered an emergency pandemic of respiratory diseases, the clinical picture of this infection often
meets the criteria of acute respiratory distress syndrome (ARDS) with progressive stress leading to death.
The functional consequences of this specific URDS are a sharp increase in the ventilation-perfusion balance and
loss of the hypoxic vasoconstriction reflex with a pronounced component of the microvascular pulmonary artery
thrombus, which is confirmed by an increase in the level of lactate dehydrogenase and D-dimer.
The development of endothelial damage in microvascular thromboembolism in the late stages of ARDS can be
explained not only by the spread in the lungs, but also by the systemic inflammatory effect associated with the
microvascular bed of the kidneys, brain and other important organs.
Keywords: COVID-19, acute respiratory distress syndrome,pulmonary complications.
КЛИНИКО-МОРФОЛОГИЧЕСКОЕ ОБОСНОВАНИЕ ОСТРОГО РЕСПИРАТОРНОГО ДИСТРЕСС-СИНДРОМА И ДРУГИХ ЛЕГОЧНЫХ
ОСЛОЖНЕНИЙ ПРИ COVID-19 Содикова Д.Т.
Содикова Дильрабо Тадидиновна - кандидат медицинских наук, доцент, кафедра врачей общей практики № 2, Андижанский государственный медицинский институт, г. Андижан, Республика Узбекистан
Аннотация: в этой статье делается вывод о том, что тяжелый острый респираторный дистресс-синдром, вызванный новым коронавирусом-2 (COVID-19), считается чрезвычайной пандемией респираторных заболеваний, клиническая картина этой инфекции часто соответствует критериям острого респираторного дистресс-синдрома (ОРДС) с прогрессирующей нагрузкой, приводящей к смерти. Функциональными последствиями этого специфического ОРДС являются резкое увеличение вентиляционно-перфузионного баланса и потеря рефлекса гипоксической вазоконстрикции с выраженным компонентом микрососудистого тромба легочной артерии, что подтверждается повышением уровня лактатдегидрогеназы и D-димера.
Развитие повреждения эндотелия при микрососудистой тромбоэмболии на поздних стадиях ОРДС можно объяснить не только распространением в легких, но и системным воспалительным эффектом, связанным с микрососудистым руслом почек, головного мозга и других важных органов. Ключевые слова: COVID-19, острый респиратор дистресс-синдром, легочные осложнения.
UDC 616.24-002-07
Relevance. The new coronavirus infection (COVID-19) is a potentially dangerous acute respiratory disease caused by the new coronavirus (SARS-COV-2), mainly with an aspiration mechanism of transmission. COVID-19 can occur not only in the form of a light acute respiratory viral infection, but also in heavy forms that are characterized by the development of clinical cards of the respiratory distress syndrome (ORDS) and polyorgan deficiency with high mortality [1]. Throughout the passing period of the pandemic, scientific information on etiology, epidemiology, pathogenesis and morphological changes, clinical features, treatment and prevention of new coronavirus infection were replenished [3].
The distribution of COVID-19 is a particular danger regarding the decompensation of chronic diseases. The most often severe forms of COVID-19 are observed in patients with chronic obstructive pulmonary disease, obesity, diabetes, arterial hypertension, coronary heart disease, chronic kidney diseases, malignant neoplasms [6]. Pathogenesis COVID-19 is in the process of active study. In the domestic and foreign literature it is stated that the main cell receptor with which the SARS-COV-2 shell (SpikeProtein) is associated with an angiotensin-converting enzyme 2 (angiotensin-Convertingenzyme 2, ACE2). Infection occurs with the participation of transmembrane serine protease 2 (transmembraneproteaserine 2, tmprss2) required to activate the S-protein [4].
The main target of the SARS-COV-2 virus is a respiratory tract. The elveration of the 1st and 2nd types of alveolocytes occurs, the cells of the vascular endothelium, which leads to a violation of the functioning of the aerohematic barrier and the surfactant alveolar complex [15, 16]. One of the most relevant pathogenetic concepts of COVID-19 is immune dysfunction (disrevulation), which is based on the macrophage activation syndrome (macrophageactivationsyndrome, mas) [7].
The morphological signs of COVID-19 at the present stage are mainly reduced to the description of changes in early (exudative) and late (proliferative) stadies. Also verified damage to the endotheliocytes of the microcirculatory channel with disorders in the blood coagulation system, the development of DV-syndrome with multifocal microtrombosis and subsequent polyorgan dysfunction with the predominance of acute renal failure [5]. Some experts believe that in relation to the definition of lung damage at COVID-19, the term "pneumonia" absolutely does not reflect the morphology, clinical radiographic signs of the pathological process observed during the damage to the SARS-COV-2 virus.
It is proposed to use the term "viral lung damage" (viral pneumonite, virus interstacoism) [3]. A number of authors as a new title of heavy COVID-19 offers the term "microvascular obstructive pulmonary lung syndrome" [2].
Purpose of the study. Examine Patomorphogenesis of COVID-19 based on autopsy studies with the formation of the working hypothesis of the conceptual scheme of clinical and morphological phases of the development of the disease.
Materials and research methods. Retrospective, single center, controlled, nerangee. Inclusion criteria corresponded to 25 patients, 10 was carried out artificial ventilation of the lungs, three of them died. We compared the HRD clinic with non-specific severe community-hospital pneumonia and a new coronavirus infection of COVID-19.
Research results. The features of diffuse alveolar damage with a new coronavirus infection (COVID-19) pose was posed to imagine the working hypothesis of Patomorphogenesis of COVID-19 interstitial pneumonia. We offer three phases - fulminant, persistent and fibrotic, each of which is conventionally limited by certain temporary parameters and is characterized by certain morphological features. Optional activation of monocytic phagocytes, the development of generalized thrombosis of the microcirculatory channel, pathological reparation, progressive intrastallyolar and interstitial fibrosis - the main links of Pato morphogenesis of COVID-19-interstitial pneumonia.
In response to the introduction of the SARS-COV-2 virus in exudative and proliferative stages, the reactions of T-cell immunity predominate. In the fibrotic stage, the total number of T-lymphocytes is sharply reduced, the cells of humoral immunity have not been detected. The prevalence of CD8 + T-lymphocyte-suppressors over CD4 + T-lymph-cyti-helpers may be associated with the mechanisms of autoimmune lesion.
The defeat of the lungs with the development of COVID-19-interstitial pneumonia is the main reason for the drag of the disease and deaths. The identified features of Patomorphogenesis of clinical morphological phases of COVID-19-interstitial pneumonia will improve the qualification and treatment of a new coronavirus infection (COVID-19).
Output. The basis of the lesion of the lungs with a new coronavirus infection (COVID-19) is the development of the Ords (diffuse alveolar damage) with an atypical flow due to the development of COVID-19-interstitial pneumonia with a synchronous lesion of the respiratory tract and the microcirculatory bed.
The morphological signs of the fulminant phase of the progressive heavy flow of COVID-19 of the interstitial pneumonia, leading to a rapid fatal outcome (up to 10 days), correspond to the exisudative stage of the ORDS in combination with the monocytic-macrophagum hyperimmune reaction and the development of obstructive pulmonary processes in the microcirculatory stream of the lungs, or are generalized.
The morphological signs of the persistent phase of the progressive severe course of COVID-19-interstitial pneumonia leading to death (up to 20 days) correspond to the proliferative stage of the ORDS. In this phase, there is a persistence of changes in the exudative stage in combination with a monocytic-macrophageal hyperimmune reaction, the development of generalized obstructive thrombis differ processes not only in a microcirculatory line, but also in larger vessels, as well as common thrombosis and thromboembolic complications.
The morphological signs of the fibrotic phase of the progressive sediment of COVID-19-interstitial pneumonia leading to a fatal outcome (from 21 to 45 days) correspond to the fibrotic stage of ORDs with disrengenerate producersometrics and dysplastic changes, a multiplicative sharply forced fibrosis effect and fibroid models of pulmonary parenchyma.
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