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"code": "M87",
"name": "Остеонекроз",
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"lead": "Нарушение здоровья, относящееся к группе другие остеопатии",
"description": "Остеонекроз – поражение различных отделов кости множественной этиологии, возникающее в ответ на нарушение в ней кровообращения и приводящее к гибели костного мозга и трабекулярной кости.",
"etiology": "<p>Наиболее распространенные причины остеонекроза следующие:</p>\r\n<ul>\r\n<li>Серьезная травма, которая нарушила нормальное кровоснабжение кости.</li>\r\n<li>Прием кортикостероидных препаратов (преднизолон, метилпреднизолон), особенно в больших дозах и длительными курсами, которые назначаются при хронических заболеваниях.</li>\r\n<li>Злоупотребление алкоголем и табакокурение.</li>\r\n</ul>\r\n<p>Другие, редкие причины остеонекроза:</p>\r\n<ul>\r\n<li>Системная красная волчанка (СКВ).</li>\r\n<li>Декомпрессионная болезнь (дисбарический остеонекроз).</li>\r\n<li>Заболевания крови, такие как серповидноклеточная анемия.</li>\r\n<li>Синдром приобретенного иммунодефицита (СПИД).</li>\r\n<li>Лучевая терапия при онкозаболеваниях.</li>\r\n<li>Прием бифосфонатов, которые связаны с некрозом челюсти. </li>\r\n</ul>",
"pathogenesis": "<p>Остеонекроз связан с гибелью клеток костной ткани (остеоцитов) и костного мозга.</p>\r\n<p>Развитие нетравматического остеонекроза может быть обусловлено эмболией сгустками крови или каплями жира, внутрисосудистым тромбозом и внесосудистой компрессией. После сосудистого эпизода развивается репаративный процесс, направленный на удаление некротизированной кости и костного мозга и замещение их живой тканью. Если зона инфаркта невелика и не подвергается значительной нагрузке, этот процесс может быть успешным. В 80% случаев он оказывается неэффективным и зона инфаркта подвергается компрессии. Так как остеонекроз обычно поражает дистальные участки длинных костей, суставная поверхность становится уплощенной и неровной, что сопровождается усилением болей и приводит к развитию остеоартрита.</p>",
"diagnostics": "<p>На начальном этапе проводится рентгенологическое исследование. Ранние рентгенологические признаки включают локализованные очаги склероза и просветления. Позднее может появиться субхондральный симптом полулуния. Затем развивается коллапс кости и уплощение суставной поверхности с последующим развитием дегенеративных изменений.</p>\r\n<p>МРТ – является более чувствительным и специфичным методом.</p>\r\n<p>Сцинтиграфия костей менее чувствительна и менее специфична, чем МРТ, и в настоящее время выполняется редко.</p>\r\n<p>КТ требуется редко, хотя иногда она может быть полезна для выявления сдавления сустава, который не определяется на обычной рентгенограмме, а иногда не виден даже на МРТ.</p>",
"treatment": "<p>Симптоматическая терапия включает покой, ЛФК, назначение нестероидных противовоспалительных препаратов.</p>\r\n<p>Хирургическое вмешательство направлено также на то, чтобы сохранить кость и не прибегнуть к протезированию. Существует несколько направлений:</p>\r\n<p>Декомпрессия, при которой в повреждённой кости делают отверстие, оно уменьшает давление внутри кости, не позволяет возникновению сдавления. Остеотомия – удаление участка некротизированной костной ткани. Аутотрансплантация – пересадка собственной здоровой костной ткани.</p>\r\n<p>При невозможности применения вышеуказанных методов и восстановления костной ткани прибегают к эндопротезированию суставов.</p>\r\n<p> </p>",
"prevention": "<p>Основными профилактическими мероприятиями являются:</p>\r\n<ul>\r\n<li>Отказ от вредных привычек – курения и употребления алкоголя</li>\r\n<li>Подбор минимальных эффективных доз кортикостероидов</li>\r\n<li>Соблюдение правил гигиены при уходе за ротовой полостью для предупреждения разрушения челюсти</li>\r\n<li>Прекращение приема бисфосфонатов за 2 месяца до инвазивной стоматологической манипуляции. </li>\r\n</ul>\r\n<p> </p>",
"clinical_picture": "<p>Заболевание может долгое время протекать бессимптомно. Затем постепенно развивается боль, но она может возникнуть и остро. По мере прогрессирования сдавления сустава боль нарастает, усиливается при физической нагрузке.</p>\r\n<p>В развернутой стадии отмечаются боли и ограничение подвижности, при этом пассивные движения ограничиваются в меньшей степени, чем активные. Возможен клинически выраженный синовиальный выпот, особенно в коленном суставе; жидкость при этом имеет невоспалительный характер.</p>",
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"code": "M87",
"name": "Остеонекроз",
"icd_name": "Остеонекроз",
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"lead": "Нарушение здоровья, относящееся к группе другие остеопатии",
"description": "Остеонекроз – поражение различных отделов кости множественной этиологии, возникающее в ответ на нарушение в ней кровообращения и приводящее к гибели костного мозга и трабекулярной кости.",
"etiology": "<p>Наиболее распространенные причины остеонекроза следующие:</p>\r\n<ul>\r\n<li>Серьезная травма, которая нарушила нормальное кровоснабжение кости.</li>\r\n<li>Прием кортикостероидных препаратов (преднизолон, метилпреднизолон), особенно в больших дозах и длительными курсами, которые назначаются при хронических заболеваниях.</li>\r\n<li>Злоупотребление алкоголем и табакокурение.</li>\r\n</ul>\r\n<p>Другие, редкие причины остеонекроза:</p>\r\n<ul>\r\n<li>Системная красная волчанка (СКВ).</li>\r\n<li>Декомпрессионная болезнь (дисбарический остеонекроз).</li>\r\n<li>Заболевания крови, такие как серповидноклеточная анемия.</li>\r\n<li>Синдром приобретенного иммунодефицита (СПИД).</li>\r\n<li>Лучевая терапия при онкозаболеваниях.</li>\r\n<li>Прием бифосфонатов, которые связаны с некрозом челюсти. </li>\r\n</ul>",
"pathogenesis": "<p>Остеонекроз связан с гибелью клеток костной ткани (остеоцитов) и костного мозга.</p>\r\n<p>Развитие нетравматического остеонекроза может быть обусловлено эмболией сгустками крови или каплями жира, внутрисосудистым тромбозом и внесосудистой компрессией. После сосудистого эпизода развивается репаративный процесс, направленный на удаление некротизированной кости и костного мозга и замещение их живой тканью. Если зона инфаркта невелика и не подвергается значительной нагрузке, этот процесс может быть успешным. В 80% случаев он оказывается неэффективным и зона инфаркта подвергается компрессии. Так как остеонекроз обычно поражает дистальные участки длинных костей, суставная поверхность становится уплощенной и неровной, что сопровождается усилением болей и приводит к развитию остеоартрита.</p>",
"diagnostics": "<p>На начальном этапе проводится рентгенологическое исследование. Ранние рентгенологические признаки включают локализованные очаги склероза и просветления. Позднее может появиться субхондральный симптом полулуния. Затем развивается коллапс кости и уплощение суставной поверхности с последующим развитием дегенеративных изменений.</p>\r\n<p>МРТ – является более чувствительным и специфичным методом.</p>\r\n<p>Сцинтиграфия костей менее чувствительна и менее специфична, чем МРТ, и в настоящее время выполняется редко.</p>\r\n<p>КТ требуется редко, хотя иногда она может быть полезна для выявления сдавления сустава, который не определяется на обычной рентгенограмме, а иногда не виден даже на МРТ.</p>",
"treatment": "<p>Симптоматическая терапия включает покой, ЛФК, назначение нестероидных противовоспалительных препаратов.</p>\r\n<p>Хирургическое вмешательство направлено также на то, чтобы сохранить кость и не прибегнуть к протезированию. Существует несколько направлений:</p>\r\n<p>Декомпрессия, при которой в повреждённой кости делают отверстие, оно уменьшает давление внутри кости, не позволяет возникновению сдавления. Остеотомия – удаление участка некротизированной костной ткани. Аутотрансплантация – пересадка собственной здоровой костной ткани.</p>\r\n<p>При невозможности применения вышеуказанных методов и восстановления костной ткани прибегают к эндопротезированию суставов.</p>\r\n<p> </p>",
"prevention": "<p>Основными профилактическими мероприятиями являются:</p>\r\n<ul>\r\n<li>Отказ от вредных привычек – курения и употребления алкоголя</li>\r\n<li>Подбор минимальных эффективных доз кортикостероидов</li>\r\n<li>Соблюдение правил гигиены при уходе за ротовой полостью для предупреждения разрушения челюсти</li>\r\n<li>Прекращение приема бисфосфонатов за 2 месяца до инвазивной стоматологической манипуляции. </li>\r\n</ul>\r\n<p> </p>",
"clinical_picture": "<p>Заболевание может долгое время протекать бессимптомно. Затем постепенно развивается боль, но она может возникнуть и остро. По мере прогрессирования сдавления сустава боль нарастает, усиливается при физической нагрузке.</p>\r\n<p>В развернутой стадии отмечаются боли и ограничение подвижности, при этом пассивные движения ограничиваются в меньшей степени, чем активные. Возможен клинически выраженный синовиальный выпот, особенно в коленном суставе; жидкость при этом имеет невоспалительный характер.</p>",
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"code": "B56",
"name": "Африканский трипаносомоз",
"icd_name": "Африканский трипаносомоз",
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"lead": "Нарушение здоровья, относящееся к группе протозойные болезни",
"description": "Африканский трипаносомоз человека, известный также как сонная болезнь, является трансмиссивной паразитарной болезнью. Она развивается в результате инфицирования простейшими паразитами, принадлежащими к роду Trypanosoma. Они передаются людям при укусах мух цеце (род Glossina), которые приобретают инфекцию от людей или животных, являющихся хозяевами этих патогенных паразитов человека. ",
"etiology": "<p>Существуют три морфологически идентичных подвида возбудителя сонной болезни: T. brucei brucei - возбудитель заболевания у домашних и диких животных, T. brucei gambiense - возбудитель гамбийской, или западноафриканской сонной болезни людей, и T. brucei rhodesiense - возбудитель родезийской, или восточноафриканской сонной болезни людей. Эндемично в ряде регионов Африки южнее пустыни Сахара, охватывающих территории 36 стран с населением 60 млн человек. </p>\r\n<p>Заражение человека происходит при укусе насекомого-переносчика - мухи цеце (р. Glossina). Обычно заражение человека возбудителем западноафриканского трипаносомоза происходит недалеко от водоёмов и вдоль берегов рек, в то время как заражение возбудителем восточноафриканского трипаносомза - в саваннах и на местах недавно вырубленных тропических лесов. Человек является основным хозяином для T.b. gambiense, и случайным хозяином для T.b. rhodesiense, зооноза, преимущественно поражающего домашний скот и диких животных.</p>\r\n<p>Паразиты морфологически идентичны: плоские, продолговато-веретенообразны по форме, от 12 до 35 мкм в длину и 1,5 - 3,5 мкм в ширину. Подвижны, для перемещения используют тянущуюся вдоль тела волнистую полупрозрачную мембрану. Из организма инфицированного человека обычно выделяют трипомастигоит. </p>\r\n<p> </p>",
"pathogenesis": "<p>После укуса инфицированной мухи в месте входных ворот развивается местно-воспалительная реакция в виде болезненного зудящего шанкра и регионарный лимфаденит. Через 1-3 недели, после проникновения трипаносом в кровяную и лимфатическую систему развивается гемолимфатическая стадия сонной болезни. Поздняя (менингоэнцефалитическая) стадия африканского трипаносомоза обусловлена проникновением паразита в ЦНС. В ответ на инвазию иммунная система реагирует выработкой специфических антител класса IgM, позволяющих некоторое время сдерживать паразитемию. Однако высокая антигенная изменчивость трипаносом нарушает формирование специфического иммунитета, обусловливая непрерывное прогрессирование и возвратно-рецидивирующий характер сонной болезни. <br class=\"SCXW199365423\" /> </p>",
"diagnostics": "<p>Предварительная диагностика сонной болезни осуществляется на основании клинико-эпидемиологических данных, важнейшими из которых служат пребывание в эндемичных районах Африки, наличие длительной, рецидивирующей лихорадки, первичного аффекта, шейного лимфаденита, отеков, сонливости и др. </p>\r\n<p>Лабораторная диагностика основана на обнаружении паразита в мазке крови или в жидкости лимфатического узла. Для определения разницы между первой и второй стадией болезни часто требуется люмбальная пункция. </p>",
"treatment": "<p>Чем раньше назначена терапия, тем больше шансов на выздоровление. На успех лечения влияют также возраст и общее состояние пациента, стадия заболевания и чувствительность трипаносомы к препаратам. Для уничтожения возбудителя сонной болезни применяются следующие лекарства: </p>\r\n<ol>\r\n<li>Пентамидин и сурамин. Применяются на гемолимфатической стадии заболевания. Первый препарат эффективен при гамбийской форме болезни, второй – родезийской. </li>\r\n<li>Меларсопрол. Назначается на менингоэнцефалитической стадии заболевания, эффективен при обеих клинических формах. </li>\r\n<li>Эфлорнитин. Применяется при гамбийской форме, необходим для лечения пациентов, болезнь у которых достигла второй стадии. </li>\r\n<li>Нифуртимокс. Применяется совместно с эфлорнитином. Такая схема позволяет уменьшить дозировку и продолжительность применения последнего, снижая тем самым выраженность побочных реакций. </li>\r\n</ol>",
"prevention": "<p>В профилактике сонной болезни главную роль играет истребление мух цеце с помощью инсектицидных препаратов, вырубки кустарниковых зарослей близ населенных пунктов, использование средств индивидуальной защиты от укусов кровососущих насекомых в эндемичных районах Африки. В периоды эпидемических вспышек сонной болезни среди местных жителей и приезжих проводится массовая химиопрофилактика пентамидином. Иммунопрофилактика африканского трипаносомоза не разработана.</p>",
"clinical_picture": "<p>Ранняя стадия африканского трипаносомоза характеризуется как гемолимфатическая и длится около года с момента заражения. Примерно по истечении недели после укуса мухи на коже больного образуется первичное узелковое образование – шанкр. Такого рода эритематозный элемент локализуется в большинстве случаев на голове или конечностях инфицированного. Как правило, шанкр самопроизвольно заживает через несколько недель. </p>\r\n<p>Одновременно с образованием узла на теле и конечностях больного появляются розовые и фиолетовые пятна – трипаниды. Дальнейшее течение заболевания обусловливается попаданием паразитов из подкожного пространства в кровь и лимфу. На поздних стадиях африканская трипаносома проникает сквозь гематоэнцефалический барьер, что приводит к стойким нарушениям мозговой деятельности. Помимо этого, симптомы сонной болезни по мере прогрессирования патологии могут выражаться в следующих типичных состояниях: </p>\r\n<ul>\r\n<li>лихорадке; </li>\r\n<li>болезненных подкожных отеках; </li>\r\n<li>лимфадените; </li>\r\n<li>сильных головных болях; </li>\r\n<li>дневной сонливости; </li>\r\n<li>атаксической походке; </li>\r\n<li>треморе (подергивании) языка, конечностей; </li>\r\n<li>заторможенности; </li>\r\n<li>нарушении восприятия; </li>\r\n<li>судорогах; </li>\r\n<li>эпилептических припадках. </li>\r\n</ul>\r\n<p>Важно отметить, что родезийская форма болезни отличается скоротечным развитием. Интоксикация и лихорадочное состояние выражены сильнее. Намного быстрее развивается истощение. Нередко у пациентов с данной формой африканского трипаносомоза возникают сердечно-сосудистые патологии (миокардит, аритмия). Гибель инфицированного лица наступает задолго до перехода болезни в менингоэнцефалитическую стадию. В большинстве случаев летальный исход наступает по причине интеркуррентных инфекций (пневмония, малярия). </p>",
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"code": "B56",
"name": "Африканский трипаносомоз",
"icd_name": "Африканский трипаносомоз",
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"lead": "Нарушение здоровья, относящееся к группе протозойные болезни",
"description": "Африканский трипаносомоз человека, известный также как сонная болезнь, является трансмиссивной паразитарной болезнью. Она развивается в результате инфицирования простейшими паразитами, принадлежащими к роду Trypanosoma. Они передаются людям при укусах мух цеце (род Glossina), которые приобретают инфекцию от людей или животных, являющихся хозяевами этих патогенных паразитов человека. ",
"etiology": "<p>Существуют три морфологически идентичных подвида возбудителя сонной болезни: T. brucei brucei - возбудитель заболевания у домашних и диких животных, T. brucei gambiense - возбудитель гамбийской, или западноафриканской сонной болезни людей, и T. brucei rhodesiense - возбудитель родезийской, или восточноафриканской сонной болезни людей. Эндемично в ряде регионов Африки южнее пустыни Сахара, охватывающих территории 36 стран с населением 60 млн человек. </p>\r\n<p>Заражение человека происходит при укусе насекомого-переносчика - мухи цеце (р. Glossina). Обычно заражение человека возбудителем западноафриканского трипаносомоза происходит недалеко от водоёмов и вдоль берегов рек, в то время как заражение возбудителем восточноафриканского трипаносомза - в саваннах и на местах недавно вырубленных тропических лесов. Человек является основным хозяином для T.b. gambiense, и случайным хозяином для T.b. rhodesiense, зооноза, преимущественно поражающего домашний скот и диких животных.</p>\r\n<p>Паразиты морфологически идентичны: плоские, продолговато-веретенообразны по форме, от 12 до 35 мкм в длину и 1,5 - 3,5 мкм в ширину. Подвижны, для перемещения используют тянущуюся вдоль тела волнистую полупрозрачную мембрану. Из организма инфицированного человека обычно выделяют трипомастигоит. </p>\r\n<p> </p>",
"pathogenesis": "<p>После укуса инфицированной мухи в месте входных ворот развивается местно-воспалительная реакция в виде болезненного зудящего шанкра и регионарный лимфаденит. Через 1-3 недели, после проникновения трипаносом в кровяную и лимфатическую систему развивается гемолимфатическая стадия сонной болезни. Поздняя (менингоэнцефалитическая) стадия африканского трипаносомоза обусловлена проникновением паразита в ЦНС. В ответ на инвазию иммунная система реагирует выработкой специфических антител класса IgM, позволяющих некоторое время сдерживать паразитемию. Однако высокая антигенная изменчивость трипаносом нарушает формирование специфического иммунитета, обусловливая непрерывное прогрессирование и возвратно-рецидивирующий характер сонной болезни. <br class=\"SCXW199365423\" /> </p>",
"diagnostics": "<p>Предварительная диагностика сонной болезни осуществляется на основании клинико-эпидемиологических данных, важнейшими из которых служат пребывание в эндемичных районах Африки, наличие длительной, рецидивирующей лихорадки, первичного аффекта, шейного лимфаденита, отеков, сонливости и др. </p>\r\n<p>Лабораторная диагностика основана на обнаружении паразита в мазке крови или в жидкости лимфатического узла. Для определения разницы между первой и второй стадией болезни часто требуется люмбальная пункция. </p>",
"treatment": "<p>Чем раньше назначена терапия, тем больше шансов на выздоровление. На успех лечения влияют также возраст и общее состояние пациента, стадия заболевания и чувствительность трипаносомы к препаратам. Для уничтожения возбудителя сонной болезни применяются следующие лекарства: </p>\r\n<ol>\r\n<li>Пентамидин и сурамин. Применяются на гемолимфатической стадии заболевания. Первый препарат эффективен при гамбийской форме болезни, второй – родезийской. </li>\r\n<li>Меларсопрол. Назначается на менингоэнцефалитической стадии заболевания, эффективен при обеих клинических формах. </li>\r\n<li>Эфлорнитин. Применяется при гамбийской форме, необходим для лечения пациентов, болезнь у которых достигла второй стадии. </li>\r\n<li>Нифуртимокс. Применяется совместно с эфлорнитином. Такая схема позволяет уменьшить дозировку и продолжительность применения последнего, снижая тем самым выраженность побочных реакций. </li>\r\n</ol>",
"prevention": "<p>В профилактике сонной болезни главную роль играет истребление мух цеце с помощью инсектицидных препаратов, вырубки кустарниковых зарослей близ населенных пунктов, использование средств индивидуальной защиты от укусов кровососущих насекомых в эндемичных районах Африки. В периоды эпидемических вспышек сонной болезни среди местных жителей и приезжих проводится массовая химиопрофилактика пентамидином. Иммунопрофилактика африканского трипаносомоза не разработана.</p>",
"clinical_picture": "<p>Ранняя стадия африканского трипаносомоза характеризуется как гемолимфатическая и длится около года с момента заражения. Примерно по истечении недели после укуса мухи на коже больного образуется первичное узелковое образование – шанкр. Такого рода эритематозный элемент локализуется в большинстве случаев на голове или конечностях инфицированного. Как правило, шанкр самопроизвольно заживает через несколько недель. </p>\r\n<p>Одновременно с образованием узла на теле и конечностях больного появляются розовые и фиолетовые пятна – трипаниды. Дальнейшее течение заболевания обусловливается попаданием паразитов из подкожного пространства в кровь и лимфу. На поздних стадиях африканская трипаносома проникает сквозь гематоэнцефалический барьер, что приводит к стойким нарушениям мозговой деятельности. Помимо этого, симптомы сонной болезни по мере прогрессирования патологии могут выражаться в следующих типичных состояниях: </p>\r\n<ul>\r\n<li>лихорадке; </li>\r\n<li>болезненных подкожных отеках; </li>\r\n<li>лимфадените; </li>\r\n<li>сильных головных болях; </li>\r\n<li>дневной сонливости; </li>\r\n<li>атаксической походке; </li>\r\n<li>треморе (подергивании) языка, конечностей; </li>\r\n<li>заторможенности; </li>\r\n<li>нарушении восприятия; </li>\r\n<li>судорогах; </li>\r\n<li>эпилептических припадках. </li>\r\n</ul>\r\n<p>Важно отметить, что родезийская форма болезни отличается скоротечным развитием. Интоксикация и лихорадочное состояние выражены сильнее. Намного быстрее развивается истощение. Нередко у пациентов с данной формой африканского трипаносомоза возникают сердечно-сосудистые патологии (миокардит, аритмия). Гибель инфицированного лица наступает задолго до перехода болезни в менингоэнцефалитическую стадию. В большинстве случаев летальный исход наступает по причине интеркуррентных инфекций (пневмония, малярия). </p>",
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