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"code": "A89",
"name": "Вирусная инфекция центральной нервной системы неуточненная",
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"lead": "Нарушение здоровья, относящееся к группе вирусные инфекции центральной нервной системы",
"description": "Энцефалит - острое воспалительное заболевание головного мозга, вызванное прямым внедрением в него вируса или реакцией гиперчувствительности в ответ на проникновение в организм вируса или иного чужеродного белка.\r\nЭнцефаломиелит - заболевание той же природы, поражающее не только головной, но и спинной мозг.\r\nАсептический менингит - воспаление мозговых оболочек, для которого характерны лихорадка, менингеальные симптомы и изменения в спиномозговой жидкости.\r\n",
"etiology": "<p>Вирусные инфекции, вызывающие первичное поражение ЦНС, могут быть эпидемическими (возбудители арбо-, полно-, ЕСНО-вирусы, вирусы Коксаки) или спорадическими (вирусы простого герпеса, ветряной оспы, эпидемического паротита). Арбовирусные энцефалиты, переносчиками которых в США служат москиты (энцефалит Сент-Луис, восточный и западный лошадиный, калифорнийский) поражают людей только в теплое время года.</p>\r\n<p>Вторичные поражения ЦНС - это обычно осложнения вирусных инфекций, обусловленные, как полагают, иммунологическими механизмами. Примерами могут служить энцефалиты, возникающие после кори, ветряной оспы, краснухи, после вакцинации против натуральной оспы, а также энцефалиты, связанные с неспецифическими инфекциями. Эти параинфекционные или постинфекционные энцефалиты (иногда определяемые как острый диссеминированный энцефаломиелит) в типичном случае возникают через 5-10 дней после начала инфекционного заболевания, и для них характерна (по данным аутопсии) периваскулярная демиелинизация; вирус в этом случае редко удается выделить из вещества мозга.</p>\r\n<p>При эпидемическом паротите (свинке) может развиваться как первичное, так и постинфекционное поражение ЦНС.</p>",
"pathogenesis": "<p>Пути проникновения вируса в организм различны. Путь распространения чаще всего гематогенный (с током крови). При комарином и клещевом энцефалитах вирус, попадая при укусе в сосудистое русло, поступает с током крови в различные органы, в том числе и в мозг. В головном мозге наиболее ранимыми оказываются структуры на дне III желудочка, подкорковые узлы, кора большого мозга, клеточные образования в мозговом стволе и спинном мозге. Возможны также контактный, алиментарный, воздушно-капельный пути передачи инфекции от человека или от животного человеку.</p>\r\n<p>Нейротропные вирусы имеют сродство (тропизм) к нервной ткани, что обеспечивается специфическими рецепторами структуры вируса. Проявления заболевания, тяжесть и особенности его течения зависят от способности организма отвечать на воздействие инфекционного агента, а также от биологической природы вируса. Иммунный ответ определяется рядом факторов, в том числе антигенными свойствами вируса, генетически детерминированной силой иммунного ответа организма человека, его реактивностью в данный момент. В этом ответе участвуют механизмы клеточного и гуморального иммунитета.</p>\r\n<p>Патогенез определяется, кроме непосредственного разрушения нейронов вирусом, токсическим действием, а также неспецифическими изменениями: поражением сосудистой стенки с повышением ее проницаемости, развитием отека, ликвородинамических нарушений.</p>",
"diagnostics": "<p>Диагностика обычно основывается на данных исследования СМЖ, важное значение при этом имеет нормальное содержание глюкозы и отрицательные результаты посева. Из СМЖ или тканей мозга иногда удается выделить вирус, однако даже в идеальных условиях вирусы, вызывающие асептический менингит и энцефалит, можно идентифицировать менее чем в половине случаев. Для точной диагностики обычно требуются парные сыворотки; диагноз подтверждается, если при повторном исследовании титр специфических антител возрастает.</p>\r\n<p>Могут быть полезны посевы из периферических органов (например, из носоглотки) и посевы кала, а также сведения о возбудителях, часто вызывающих эпидемии в данной местности.</p>\r\n<p>МРТ позволяет определить воспалительные изменения в височной доле до того, как выявятся какие-либо нарушения при ЭЭГ, КТ или сцинтиграфии мозга; полученные при МРТ данные дают возможность начать противовирусную терапию раньше, чем возникнут выраженные неврологические расстройства.</p>",
"treatment": "<p>Одним из направлений специфической терапии вирусных нейроинфекций следует считать воздействие непосредственно на вирус, находящийся в стадии активного размножения и лишенный защитной оболочки, ферментами, расщепляющими нуклеиновую кислоту вируса и тормозящими его дальнейшую репликацию. Нуклеазы назначают с учетом структуры вирусов. Рибонуклеазу применяют при заболеваниях, вызываемых РНК-содержащими вирусами (вирусы эпидемического паротита, энтеровирусы, вирусы гриппа и парагриппа, клещевого энцефалита). Дезоксирибонуклеаза показана при заболеваниях, вызываемых ДНК-содержащими вирусами (вирус простого герпеса, вирус ветряной оспы, аденовирусы). Продолжительность курса составляет 10-14 дней.</p>\r\n<p>Патогенетическая терапия включает в себя ряд направлений.</p>\r\n<ol>\r\n<li>Дегидратация и борьба с отеком мозга: осмотические диуретики, салуретики.</li>\r\n<li>Обеспечение дыхания (поддержание проходимости дыхательных путей, оксигеногерапия, гипербарическая оксигенация, при дыхательных нарушениях - интубация или трахеотомия, ИВЛ).</li>\r\n<li>Десенсибилизация (тавегил, супрастин, диазолин, димедрол).</li>\r\n<li>Поддержание гомеостаза и водно-электролитного баланса (парентеральное и энтеральное питание, хлорид калия, полиглюкин, 200 мл 4% раствора гидрокарбоната натрия).</li>\r\n<li>Устранение сердечно-сосудистых расстройств, нормализация микроциркуляции.</li>\r\n<li>Гормональная терапия.</li>\r\n<li>Восстановление метаболизма мозга).</li>\r\n</ol>\r\n<p>Симптоматическая терапия: антиконвульсанты, жаропонижающие препараты, витамины.</p>",
"prevention": "<p>Противоэпидемические мероприятия проводят в соответствии с особенностями этиологии и эпидемиологии заболевания. При возникновении заболевания предупреждение новых случаев заболевания с учетом путей распространения инфекции.</p>\r\n<p> </p>",
"clinical_picture": "<p>Вирусные инфекции ЦНС могут проявляться в трех формах. При одной из них - асимптомной - возможны лихорадка и общее недомогание, но без менингеальных явлений. Тем не менее в СМЖ могут выявляться изменения, прежде всего лимфоцитарный плеоцитоз, реже из СМЖ можно бывает выделить вирус.</p>\r\n<p>Вторая форма - менингит, для которого характерны лихорадка, головная боль, упорная рвота, общая слабость, ригидность шейных мышц и мышц спины.</p>\r\n<p>Третья форма - энцефалит - может проявляться генерализованной или очаговой дисфункцией мозга (нарушение сознания, психические изменения, эпилептические припадки, парезы) и поражением черепных нервов. Асептический менингит и энцефалит отличаются друг от друга по степени выраженности мозговой дисфункции, в то время как менингеальные симптомы одинаково свойственны обоим заболеваниям.</p>",
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},
"code": "A87",
"name": "Вирусный менингит",
"icd_name": "Вирусный менингит",
"gender": 0,
"age_min": 0,
"age_max": 84,
"cause": [
2,
4,
5,
7
],
"periodicity": 2,
"slug": "a87_virusnyy_meningit",
"lead": "Нарушение здоровья, относящееся к группе вирусные инфекции центральной нервной системы",
"description": "Вирусный менингит — воспаление серозных оболочек головного мозга, реже спинного, вызываемое инфекцией вирусной природы. Причиной возникновения в 80% являются энтеровируc. Вирусный менингит сопровождается серозным воспалительным процессом. Для серозного воспаления характерно образование серозного выпота, который пропитывает оболочки головного мозга, приводя к их утолщению. Отек мозговых оболочек вызывает нарушение оттока цереброспинальной жидкости и приводит к повышению внутричерепного давления.",
"etiology": "<p> В 80% случаев вирусный менингит обусловлен энтеровирусной инфекцией, реже причиной становится вирус эпидемического паротита, вирус Эпштейна-Барр (возбудитель инфекционного мононуклеоза), аренавирусы, цитомегаловирус, герпетическая инфекция, аденовирусы, ВИЧ.</p>",
"pathogenesis": "<p></p>\r\n<p>Возбудителями вирусных менингитов могут выступать различные вирусы, которые попадают в мозговые оболочки гематогенным, лимфогенным или периневральным путем. В зависимости от типа вируса вирусный менингит может возникнуть при контактном или воздушно-капельном заражении. К патогенетическим механизмам клинических проявлений менингита относятся воспаление и отек мозговых оболочек и нередко прилегающих тканей мозга, нарушение циркуляции в мозговых и оболочечных сосудах, гиперсекреция цереброспинальной жидкости и задержка ее всасывания, что приводит к развитию водянки мозга и повышению внутричерепного давления; перераздражение оболочек головного мозга, а также общее воздействие интоксикации.</p>",
"diagnostics": "<p>Заподозрить менингит позволяют характерные жалобы пациента, острое начало заболевания и наличие менингеальных симптомов. Для установления вирусного характера воспаления мозговых оболочек проводят люмбальную пункцию с исследованием цереброспинальной жидкости, ПЦР-исследования и выделение возбудителя.</p>\r\n<p>Анализ цереброспинальной жидкости при вирусном менингите показывает незначительное увеличение белка, нормальное содержание глюкозы и лейкоцитоз. В первые 1-2 сутки вирусный менингит может сопровождаться нейтрофильным лейкоцитозом ликвора, что более характерно для бактериального воспаления. Однако отсутствие возбудителя при микроскопии различно окрашенных мазков цереброспинальной жидкости свидетельствует в пользу вирусной этиологии заболевания. Для ее подтверждения необходимо повторное исследование ликвора спустя 12ч, при котором в случае вирусного менингита наблюдается уменьшение числа нейтрофилов и нарастание количества лимфоцитов.</p>\r\n<p>Анализ цереброспинальной жидкости позволяет дифференцировать вирусный менингит от других видов серозного воспаления мозговых оболочек (например, туберкулезного).</p>\r\n<p>Основным современным методом диагностики возбудителя при вирусном менингите является ПЦР- исследование цереброспинальной жидкости, позволяющее обнаружить геном вируса (ДНК или РНК).</p>\r\n<p>Серологические реакции для диагностики вирусного менингита показательны только в случае сравнения их результатов в начале заболевания и спустя 2-3 недели. Из-за большой длительности такой диагностики она может носить лишь ретроспективный характер.</p>\r\n<p>Пациентам, имеющим вирусный менингит, дополнительно проводят клинический анализ крови, биохимические пробы печени, определение электролитного состава крови, содержание в ней глюкозы, креатинина, липазы и амилазы. При атипичном течении вирусного менингита и сомнениях при его диагностике возможно проведение электромиографии, ЭЭГ, МРТ и КТ головного мозга.</p>",
"treatment": "<p>В отношении вирусного менингита в большинстве случаев проводится симптоматическая терапия. Пациенту рекомендован покой, постельный режим, нахождение в затемненном помещении. Для купирования головной боли назначают анальгетики. Но зачастую она значительно уменьшается после снижения внутричерепного давления в результате диагностической люмбальной пункции. Температура тела выше 38°C является показанием к приему жаропонижающих препаратов (парацетамол, ибупрофен и др.).</p>\r\n<p>Специфическая и неспецифическая противовирусная терапия вирусного менингита необходима у пациентов с ослабленным состоянием иммунной системы и у грудных детей. В таких случаях проводится внутривенное введение иммуноглобулина. Если вирусный менингит вызван вирусом герпеса или вирусом Эпштейн-Барр, то возможно применение ацикловира.</p>",
"prevention": "<p>Специфическая профилактика (вакцины) для вирусного менингита не разработана. В повседневности необходимо ограничивать контакт с больными респираторными инфекциями, гриппом, эпидемическим паротитом и другими вирусными инфекциями. Обеззараживание питьевой воды, мытье фруктов и овощей обеззараженной водой, запрет купания в водоемах важные пункты профилактики менингита.</p>\r\n<p>Важна ранняя диагностика и последующая изоляция больных на две недели. В очаге возникновения проводят дезинфекцию. Если заболевший ребенок посещал детский сад, заведение закрывают на двухнедельный карантин.</p>\r\n<p>Людям, контактировавшим с больными, в качестве профилактики внутривенно вводят иммуноглобулин, закапывают интерферон в течение недели.</p>",
"clinical_picture": "<p>Как правило, начало болезни острое, температура тела повышается до фебрильных цифр (40 С). Развивается головная боль, тошнота, многократная рвота. Наблюдается выраженная общая слабость, сопровождающаяся сонливостью, иногда оглушенностью. В более тяжелых случаях появляется спутанность сознания вплоть до его потери. Может возникать миалгия — боль в мышцах тела. Часто болезнь сопровождается диспепсическими расстройствами по типу гастроэнтерита: спастические боли в животе, жидкий стул. Аппетит отсутствует. Кожные покровы шеи и лица красные, горячие на ощупь. Сосуды склер инъецированы (красные глаза).</p>\r\n<p>При осмотре ротовой полости обнаруживается покраснение стенок глотки, дужек неба, слизистой оболочка мягкого неба, миндалин. При ощупывании затылочные, шейные, подчелюстные лимфатические узлы могут быть увеличены, чаще если возбудитель болезни вирус эпидемического паротита, цитомегаловирус, ВЭБ.</p>\r\n<p>Менингеальные симптомы (признаки, позволяющие поставить диагноз менингит) проявляются болью в затылке и по ходу позвоночника, ригидностью мышц затылка (неспособность согнуть голову вперед), характерной позой больного (поза «легавой» собаки) – в положении на боку, голова запрокинута, ноги поджаты к груди. Часто развиваются симптомы Кернига (неспособность разогнуть согнутую в колене ногу) и Брудзинского (верхний, средний, нижний). У детей может наблюдаться симптом Лесажа (подвешивания) – при поднимании за подмышечные ямки ребенок подтягивает ноги к животу.</p>\r\n<p>Вирусный менингит отличается относительно коротким течением. Уже на 3-5 сутки температура тела падает до нормальных цифр, хотя в некоторых случаях наблюдается вторая волна лихорадки. Весь период заболевания длится от 7 до 14 дней, в среднем около 10 дней.</p>",
"image": null,
"image_alt": null,
"standard_type": 3,
"danger": 79,
"published": 2,
"parent": null,
"block_rubric": 9,
"standards": [
5032
]
},
{
"id": 6085,
"symptoms": [
{
"id": 3234,
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{
"name": "Мышцы не расслабляются"
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{
"name": "Мышцы постоянно напряжены"
},
{
"name": "Мышцы сводит"
},
{
"name": "Постоянный тонус мышц"
},
{
"name": "Скованность шеи"
},
{
"name": "Ригидность мышц"
}
],
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"code": "A80",
"name": "Острый полиомиелит",
"icd_name": "Острый полиомиелит",
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"slug": "a80_ostryy_poliomielit",
"lead": "Нарушение здоровья, относящееся к группе вирусные инфекции центральной нервной системы",
"description": "Полиомиелит - острое вирусное заболевание, характеризующееся поражением нервной системы (преимущественно серого вещества спинного мозга), а также воспалительными изменениями слизистой оболочки кишечника и носоглотки. ",
"etiology": "<p>Возбудитель относится к семейству пикорнавирусов, к группе энтеровирусов (кишечным вирусам), куда входят также Коксаки- и ЕСНО-вирусы и существует в виде 3 независимых типов (I, II и III). Наиболее часто встречается 1 тип. </p>\r\n<p>Вирус устойчив во внешней среде (в воде сохраняется до 100 суток, в испражнениях — до 6 мес), хорошо переносит замораживание. Не разрушается пищеварительными соками. Разрушается при нагревании до 50 градусов Цельсия в течение 30 минут. Быстро погибает при кипячении, под действием ультрафиолетового облучения и при высушивании. Даже незначительные концентрации хлора инактивируют вирус. Источник инфекции — человек (больной или переносящий заражение бессимптомно); возбудитель выделяется через рот (несколько суток), а затем с испражнениями (несколько недель, а иногда и месяцев). Заражение может произойти воздушно-капельным путём, но чаще — при попадании в рот активного вируса (через загрязнённые руки, пищу). Механическим переносчиком вируса могут быть мухи. </p>\r\n<p>Заболеваемость полиомиелитом преобладает в летне-осенние месяцы. Чаще болеют дети от 6 месяцев до 5 лет. Большинство заболеваний связано с вирусом типа I. </p>",
"pathogenesis": "<p>Кишечная фаза </p>\r\n<p>Входными воротами для инфекции является слизистая оболочка носоглотки и тонкой кишки, в эпителии и лимфатических образованиях которых происходит первичная репродукция вируса. Затем вирус проникает в ток крови и обусловливает вирусемию. </p>\r\n<p>Фаза вирусемии </p>\r\n<p>Эта фаза характеризуется проникновением вируса во многие органы и ткани, такие как лимфатические узлы, селезенка, печень, легкие, сердечная мышца, жировая ткань, особенно бурый жир. </p>\r\n<p>Невральная фаза </p>\r\n<p>Следующим этапом развития патогенеза полиомиелита является проникновение вируса в различные органы, в частности в ЦНС. В ЦНС в патологический процесс чаще всего вовлекаются мотонейроны передних рогов спинного мозга, двигательные клетки черепных нервов. В тяжелых случаях могут поражаться нейроны задних рогов, клетки спинальных ганглиев и даже проксимальные отделы периферических нервов. В головном мозге повреждаются ретикулярная формация, вестибулярные ядра, глубинные структуры. </p>\r\n<p>Вирус действует на эндотелий сосудов, повышая их проницаемость. В результате чего происходит сдавление, отек здоровых участков нервной ткани, возникает клеточная инфильтрация, тигролиз - все это является морфологическим субстратом полиомиелита. Распространение вируса в организме человека может закончиться на любом этапе, что и определяет развитие той или иной формы полиомиелита. </p>",
"diagnostics": "<p>Лабораторные исследования: пробы крови для серологических исследований, общий анализ крови и мочи. </p>\r\n<p>Инструментальные исследования: </p>\r\n<ul>\r\n<li>Электромиография. При помощи ЭМГ регистрируются биоэлектрические потенциалы, возникающие на нервно-мышечной периферии. Поражение двигательных клеток в передних рогах спинного мозга выражается, прежде всего, четкими изменениями ритма. Это обусловлено тем, что пораженные мотонейроны возбуждаются одновременно (синхронно), что приводит с урежению колебаний потенциалов. Существует отчетливая связь между тяжестью поражения мышц и изменениями электромиограммы. ЭМГ тяжело пораженных мышц характеризуется «биоэлектрическим молчанием». </li>\r\n<li>Рентгенография конечностей для исключения вывихов, подвывихов, остеопороза.. </li>\r\n<li>Магниторезонансная томография спинного мозга - признаки атрофического процесса в передних рогах спинного мозга. </li>\r\n</ul>",
"treatment": "<p>Немедикаментозное лечение </p>\r\n<ul>\r\n<li>Лечебная физкультура занимает одно из ведущих мест в лечении больных с паралитическими формами полиомиелита. К ней необходимо приступить в раннем восстановительном периоде, то есть сразу после появления первых признаков движений в пораженных мышцах. Основная задача лечебных упражнений в раннем восстановительном периоде - тренировка основных параметров двигательной системы, которая заключается в постепенном и дозированном увеличении силы мышечного сокращения, амплитуды. На этом этапе лечения больному необходима помощь в овладении простыми движениями, а затем элементами утраченного сложного двигательного навыка. У больных с глубокими парезами при мышечной силе в пределах 1-0 балла, помимо лечения положением, применяют пассивные и пассивно-активные упражнения с переходом к активным упражнениям. </li>\r\n<li>Стимулирующий массаж пораженных конечностей, мышц спины. </li>\r\n<li>Физиолечение - магнитотерапия, биоптрон, УВЧ на пораженные сегменты спинного мозга, электростимуляция паретичных мышц импульсным током, озокеритовые или парафиновые аппликации на область паретичных мышц, суставы; электрофорез галантамина, прозерина по Вермелю. </li>\r\n<li>Иглорефлексотерапия. </li>\r\n<li>Ортопедическая профилактика паретичных конечностей с использованием шин, лонгет, валиков, мешков с песком, разработка контрактур. </li>\r\n</ul>\r\n<p> Медикаментозное лечение </p>\r\n<ul>\r\n<li>Стимулирующая терапия: антихолинэстеразные препараты - прозерин, галантамин. </li>\r\n<li>Витаминотерапия: аскорбиновая кислота, витамины группы В - В1, В6, В12. </li>\r\n<li>Последние годы в лечении полиомиелита используются анаболические стероиды (нерабол, ретаболил, метандростеналон). </li>\r\n<li>Лечение препаратами, действующими на сосудистую систему, улучшающими реологические свойства крови и микроциркуляцию, проводится в виде последовательных курсов, каждый из них длительностью 2-3 недели. </li>\r\n<li>Спазмолитическим, сосудорасширяющим, стимулирующим влиянием на спинной мозг обладает дибазол. Лечение продолжается в течение 3-4 недель, показаны повторные курсы лечения. </li>\r\n<li>Препараты, улучшающие метаболизм (ноотропы). </li>\r\n<li>Метаболические средства - фолиевая кислота, аевит, оротат калия. </li>\r\n</ul>",
"prevention": "<p>Неспецифическая направлена на общее укрепление организма, увеличение его устойчивости к различным инфекционным агентам (закаливание, правильное питание, своевременная санация хронических очагов инфекции, регулярные физические нагрузки, оптимизация цикла сон-бодровствание и др.), борьба с насекомыми, которые являются разносчиками патогенных микроорганизмов (различные виды дезинсекции), соблюдение правил личной гигиены (в первую очередь это мытье рук после улицы и после посещения туалета), тщательная обработка овощей, фруктов и других продуктов перед употреблением их в пищу. </p>\r\n<p>Специфическая профилактика заключается в проведении вакцинации против полиомиелита. </p>",
"clinical_picture": "<p>Инкубационный период при различных формах полиомиелита в среднем составляет 8–12 дней. </p>\r\n<p>Инаппарантная форма полиомиелита представляет собой носительство вируса, которое никак не проявляется клинически и может быть обнаружено только лабораторным путем. </p>\r\n<p>Абортивная (висцеральная) форма полиомиелита составляет более 80% всех случаев болезни. Клинические проявления неспецифичны; среди них преобладают общеинфекционные симптомы – лихорадка, интоксикация, головная боль, умеренные катаральные явления, боли в животе, диарея. Болезнь заканчивается через 3-7 дней полным выздоровлением; остаточных неврологических симптомов не отмечается. </p>\r\n<p>Менингеальная форма полиомиелита протекает по типу доброкачественного серозного менингита. При этом отмечается двухволновая лихорадка, головные боли, умеренно выраженные менингеальные симптомы (Брудзинского, Кернига, ригидность затылочных мышц). Через 3-4 недели наступает выздоровление. </p>\r\n<p>Паралитическая форма полиомиелита имеет наиболее тяжелое течение и исходы. В препаралитическом периоде преобладает общеинфекционная симптоматика: повышение температуры, диспепсия, ринит, фарингит, трахеит и др. Вторая волна лихорадки сопровождается менингеальными явлениями, болью в мышцах, болями в позвоночнике и конечностях, выраженной болевой чувствительностью, потливостью, спутанностью сознания и судорогами. </p>\r\n<p>Примерно на 3-6 день заболевание вступает в паралитическую фазу, характеризующуюся внезапным развитием парезов и параличей чаще нижних конечностей при сохранной чувствительности. Для параличей при полиомиелите характерны асимметричность, неравномерность, преимущественное поражение проксимальных отделов конечностей. Несколько реже при полиомиелите развиваются парезы и параличи верхних конечностей, лица, мышц туловища. Через 10-14 дней наблюдаются первые признаки мышечной атрофии. Поражение жизненно важных центров продолговатого мозга может вызвать паралич дыхательных мышц и диафрагмы и послужить причиной гибели ребенка от острой дыхательной недостаточности. </p>\r\n<p>В восстановительном периоде полиомиелита, который длится до 1 года, происходит постепенная активизация сухожильных рефлексов, восстанавливаются движения в отдельных мышечных группах. Мозаичность поражения и неравномерность восстановления обусловливает развитие атрофии и мышечных контрактур, отставание пораженной конечности в росте, формирование остеопороза и атрофии костной ткани. </p>\r\n<p>В резидуальном периоде отмечаются остаточные явления полиомиелита – стойкие вялые параличи, контрактуры, паралитическая косолапость, укорочение и деформации конечностей, вальгусная деформация стоп, кифосколиозы и пр. </p>",
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