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"code": "G12",
"name": "Спинальная мышечная атрофия и родственные синдромы",
"icd_name": "Спинальная мышечная атрофия и родственные синдромы",
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"slug": "g12_spinalnaya_myshechnaya_atrofiya_i_rodstvennye_sindromy",
"lead": "Нарушение здоровья, относящееся к группе системные атрофии, поражающие преимущественно центральную нервную систему",
"description": "Термин “спинальная мышечная атрофия” (СМА), или “спинальная амиотрофия”, является широким понятием, объединяющим группу заболеваний, сопровождающихся дегенерацией двигательных нейронов в спинном мозге и (или) стволе головного мозга и характеризующихся преимущественно аутосомно-рецессивным типом наследования. ",
"etiology": "<p>В большинство случаев СМА обусловлена дефицитом протеина мотонейронов, именуемым SMN (протеин выживаемости мотонейронов) </p>\r\n<p>Этот протеин, как следует из его названия, необходим для нормального функционирования мотонейронов. </p>\r\n<p>SMN – связанная СМА обычно подразделяется на 3 категории. Тип 1 — наиболее тяжелый, с самым ранним началом, а тип 3 — наименее тяжелый, с наиболее поздним возрастом начала. Некоторые специалисты выделяют еще тип 4 для обозначения умеренной или мягкой СМА с дебютом во взрослом возрасте </p>\r\n<p>Все эти типы связаны с генетическими поломками (мутациями) на хромосоме 5, что влияет на количество синтезируемого SMN – протеина. Более высокие уровни протеина снижают тяжесть СМА. </p>\r\n<p>Существуют также формы СМА, не связанные с протеином SMN и не являющиеся результатом мутаций на хромосоме 5. </p>",
"pathogenesis": "<p>СМА вызвана мутацией в гене SMN1, который в норме производит белок SMN.</p>\r\n<p>Из-за мутации гена, у людей с СМА производится меньшее количество белка SMN, что приводит к потере моторных нейронов.</p>",
"diagnostics": "<p>При подозрении — консультация невролога и генетика. </p>\r\n<p>Биохимия крови: креатинкиназа — в норме при СМА тип I, в норме или незначительно повышена при других типах. </p>\r\n<p>Генетическое обследование: пренатально или постнатально. Тест ДНК путем определения выпадения гена SMN1. </p>\r\n<p>Электронейромиография — показывает снижение нервных импульсов, помогает дифференцировать СМА от других нервно-мышечных болезней. Сенсорная нервная проводимость обычно нормальная. </p>\r\n<p>Биопсия мышц — гистологические признаки атрофии мышечных волокон, помогает дифференцировать СМА от других нервно-мышечных болезней. </p>",
"treatment": "<p>Специального лечения пока не разработано. </p>\r\n<p>Необходимы мультипрофессиональный подход и паллиативная помощь для улучшения качества жизни. </p>\r\n<ol>\r\n<li>Помощь в передвижении и самообслуживании. </li>\r\n<li>Фиксация корпуса и конечностей (корсеты, туторы и др.). </li>\r\n<li>Физиотерапия, эрготерапия (восстановлением утраченных двигательных навыков), физическая терапия и специальные сиденья могут уменьшить развитие контрактур суставов и сколиоза. </li>\r\n<li>Дыхательные упражнения. </li>\r\n<li>Респираторная поддержка, в том числе ИВЛ (неинвазивная через маску или инвазивная через трахеостому), может понадобиться на дому при прогрессировании болезни. </li>\r\n<li>Кормление через гастростому необходимо при прогрессировании проблем с глотанием. </li>\r\n</ol>",
"prevention": "<p>Возможна только пассивная профилактика — консультирование родителей с риском СМА о возможных последствиях и пренатальная ДНК-диагностика во время беременности через биопсию ворсин хориона для принятия решения о рождении или прерывании беременности. </p>",
"clinical_picture": "<p>Наиболее тяжёлой формой является I тип спинальной мышечной атрофии (синдром Верднига-Гоффмана), манифестирующий в раннем детстве (в первые 6 месяцев). Характерен синдром «вялого ребёнка» (слабый крик, сниженная двигательная активность, вялое сосание, потеря массы тела, сниженные глотательный, сосательный и кашлевой рефлексы). Такие дети неспособны удерживать головку, переворачиваться и сидеть, отстают в моторном развитии (грубая задержка). Могут развиваться деформации суставов и конечностей, контрактуры, дыхательные и бульбарные нарушения (расстройство глотания (дисфагия), нарушение артикуляции (дизартрия) и звучности речи (дисфония). Средняя продолжительность жизни таких детей – 2 года. Причиной смерти, как правило, становится тяжёлая дыхательная недостаточность или развитие пневмонии. </p>\r\n<p>Для II типа спинальной амиотрофии характерны более поздняя манифестация (6-18 месяцев) и хронически прогрессирующее течение. У таких детей наблюдается отставание в моторном развитии, тремор пальцев, прогрессирование слабости кашлевого рефлекса, поверхностного диафрагмального дыхания и межрёберных мышц. В начале дети с данной формой заболевания могут ползать, сидеть без поддержки, а некоторые и стоять при поддержке, но эти способности утрачиваются по мере роста и увеличения массы тела. Формируются скелетные и мышечные деформации (в том числе сколиоз, деформации грудной клетки и псевдогипертрофия икроножной мышцы), контрактуры, а также возникают нарушения дыхания (вплоть до развития дыхательной недостаточности). </p>\r\n<p>Наиболее лёгкое течение из детских форм характерно для III типа спинальной мышечной атрофии (синдрома Кугельберга-Веландера). Первые проявления, как правило, обнаруживаются у детей после 1,5 лет и характеризуются сложностями с комплексными двигательными навыками (бег, подъём по ступенькам и т.п.). Симптоматика прогрессирует медленно, нарушения глотания и жевания развиваются значительно позже. </p>\r\n<p>Взрослая форма (тип IV) имеет мягкое течение, при котором наиболее часто первыми поражаются мышцы плечевого пояса. </p>",
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"code": "G10",
"name": "Болезнь Гентингтона",
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"lead": "тяжелое прогрессирующее нейродегенеративное наследственное заболевание головного мозга",
"description": "Болезнь Гентингтона - одно из тяжелейших и постоянно прогрессирующих наследственных заболеваний нервной системы, обусловленной системной дегенерацией экстрапирамидных двигательных структур и коры головного мозга.",
"etiology": "<p>Причиной болезни Гентингтона является мутация гена на 4-й хромосоме, кодирующего белок гентингтин. Нарушение синтеза этого белка предопределяет избирательное повреждение нейронов базальных ганглиев различных структур мозга, прежде всего коры и экстрапирамидной системы. Заболевание передается по аутосомно-доминантному типу, при этом патологический ген проявляется очень часто, и к 70 годам болезнь проявляется практически у всех его носителей. Дети наследуют заболевание от одного из родителей с вероятностью 50 %.</p>",
"pathogenesis": "<p>Патогенез болезни Гентингтона малоизучен, однако известно, что первопричиной ее возникновения является мутация гена на четвертой хромосоме, вследствие чего нарушается синтез белка гентингтина, происходит его кодирование. Строение данного белка представляет собой повторяющиеся триплеты аминокислотных цепочек (цитозин-аденин-гуанин), из-за мутации гена происходит увеличение количества триплетов, удлинение аминокислотной цепочки. Белок гентингтин меняет свою информацию, соединяясь с другими белками, изменяется взаимодействие между ними. Это приводит к гибели нейронов одного из отделов головного мозга, повреждению стриатума («полосатого тела»), а также коры головного мозга.</p>",
"diagnostics": "<p>Физикальное обследование, иногда в сочетании с психологическим обследованием, позволяет определить область распространения болезни. </p>\r\n<p>Медицинская визуализация (компьютерная томография(КТ), магнитно-резонансная томография (МРТ) показывает только видимую атрофию мозга на прогрессирующей стадии заболевания. Методы функциональной нейровизуализации (фМРТ и позитронно-эмиссионная томография (ПЭТ)) могут показать изменения в активности мозга до появления клинических симптомов.</p>\r\n<p>Для проведения генетической диагностики болезни Хантингтона необходим забор крови с последующим определением количества повторов ЦАГ в каждом НТТ-аллеле. Положительный результат не подтверждает диагноз, поскольку может быть получен за несколько лет до появления первых симптомов. Однако отрицательный результат однозначно свидетельствует об отсутствии вероятности развития болезни Хантингтона.</p>\r\n<p>Эмбрионы, полученные в результате экстракорпорального оплодотворения, могут быть подвержены генетической диагностике болезни Хантингтона с применением преимплантационной генетической диагностики. При этом методе забирается одна клетка из 4-8-клеточного эмбриона и затем проверяется на генетическую патологию. Полученная информация может впоследствии быть использована при выборе здорового эмбриона для имплантации. Кроме того, возможна пренатальная диагностика для эмбриона или плода в утробе матери.</p>",
"treatment": "<p>В настоящее время отсутствует возможность предупредить прогрессирование заболевания, и лечение носит чисто симптоматический характер.</p>\r\n<p>Для уменьшения гиперкинеза используют нейролептики и бензодиазепины. При депрессии показаны амитриптилин или другие антидепрессанты. При акинетикоригидной форме применяют антипаркинсонические средства, но их эффект обычно невелик. Определенную роль играет лечебная физкультура, направленная на предупреждение контрактур и деформаций, поддержание навыков передвижения.</p>",
"prevention": "<p>Единственным методом первичной профилактики является медико-генетическое консультирование. При данном заболевании МГК позволяет:</p>\r\n<ul>\r\n<li>установить диагноз и тип наследования заболевания в консультируемой семье;</li>\r\n<li>определить генетический риск у консультируемых родственников, в т.ч. с помощью ДНК-диагностики (прогностическое тестирование);</li>\r\n<li>определить прогноз потомства и наиболее эффективный способ профилактики новых случаев заболевания (в т.ч. с помощью пренатальной и преимплантационной ДНК-диагностики);</li>\r\n<li>объяснить консультируемым лицам смысл полученной и проанализированной информации, оказать помощь в решении возникающих юридических, психологических, морально-этических, социальных и иных проблем.</li>\r\n</ul>",
"clinical_picture": "<p>Симптомы болезни Хантингтона могут проявиться в любом возрасте, но чаще это происходит в 35-44 года. На ранних стадиях происходят небольшие изменения личности, когнитивных способностей и физических навыков. Обычно первыми обнаруживают физические симптомы, так как когнитивные и психические расстройства не столь выражены в ранних стадиях. Почти у всех пациентов болезнь Хантингтона в итоге проявляется схожими физическими симптомами, но начало заболевания, прогрессирование и степень когнитивных и психических нарушений различаются у отдельных лиц.</p>\r\n<p>Для начала заболевания наиболее характерна хорея — беспорядочные, неконтролируемые движения. Хорея в начале может проявляться в беспокойстве, небольших непроизвольных или незавершённых движениях, нарушении координации и замедлении скачкообразных движений глаз.</p>\r\n<p>В самом начале обычно возникают проблемы из-за физических симптомов, которые выражаются в резких, внезапных и не поддающихся контролю движениях. В других случаях, наоборот, больной двигается слишком замедленно. Возникают нарушения координации движений, речь становится невнятной. Постепенно все функции, требующие мышечного контроля, нарушаются: человек начинает гримасничать, испытывает проблемы с жеванием и глотанием. Из-за быстрого движения глаз происходят нарушения сна. Обычно больной проходит через все стадии физического расстройства, однако влияние болезни на когнитивные функции у всех очень индивидуально. Чаще всего происходит расстройство абстрактного мышления, человек перестаёт быть способным планировать свои действия, следовать правилам, оценивать адекватность своих действий. Постепенно появляются проблемы с памятью, может возникнуть депрессия и паника, эмоциональный дефицит, эгоцентризм, агрессия, навязчивые идеи, проблемы с узнаванием других людей, гиперсексуальность и усиление вредных привычек, таких как алкоголизм или игромания.</p>",
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"lead": "Хемоз — отек конъюнктивы, при котором поверхность глаза в области склер заметно увеличивается, может менять цвет и болеть. Такая патология возникает на фоне множества заболеваний глаза, установить точную причину может только врач, поэтому и самолечение в этом случае недопустимо. Особенно опасны ситуации, при которых хемоз возникает часто и склонен к длительному течению. \r\nПричины отека конъюнктивы могут быть острыми и локальными. Среди наиболее частых причин наблюдается: острое воспаление придаточного глазного аппарата и оболочек глаза, укусы насекомых, появление ячменя на глазу, орбитальный целлюлит (воспаление тканей глаза позади орбитальной перегородки), гонорейный конъюнктивит (опасная для зрения патология, которая развивается при гонореи), нарушение микроциркуляции или застой крови, которые могут быть вызваны воздействием или давлением на глаз опухолей орбитальных областей (зона вокруг глазного яблока). Часто при отеке конъюнктивы диагностируется анемия (малокровие), нефрит (воспаление, которое приводит к изменению парных органов), крапивница (кожное заболевание, преимущественно аллергического происхождения).\r\n\r\nПричинами заболевания может быть патологии глаз, черепно-мозговые травмы, бесконтрольное применение медицинских препаратов.",
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},
"code": "D62",
"name": "Острая постгеморрагическая анемия",
"icd_name": "Острая постгеморрагическая анемия",
"gender": 0,
"age_min": 0,
"age_max": 100,
"cause": [
3,
1
],
"periodicity": 1,
"slug": "d62_ostraya_postgemorragicheskaya_anemiya",
"lead": "Нарушение здоровья, относящееся к группе апластические и другие анемии",
"description": "Постгеморрагическая анемия – комплекс клинических и гематологических изменений, возникающий вследствие острой или хронической кровопотери. Постгеморрагическая анемия характеризуется бледностью, одышкой, потемнением в глазах, головокружением, гипотермией, артериальной гипотонией; в тяжелых случаях - заторможенностью, нитевидным пульсом, шоком, потерей сознания.",
"etiology": "<p>Непосредственной причиной постгеморрагической анемии является острая или хроническая потеря крови, возникшая вследствие наружного или внутреннего кровотечения. Острая постгеморрагическая анемия возникает при быстрых, массивных кровопотерях, вызванных обычно механическим повреждением стенок крупных кровеносных сосудов или полостей сердца при различных травмах и хирургических операциях, разрывом стенок сердечных камер в зоне инфаркта, разрывом аневризмы аорты и ветвей легочной артерии, разрывом селезенки, разрывом фаллопиевой трубы при внематочной беременности.</p>\r\n<p>Острая постгеморрагическая анемия характерна для обильных маточных кровотечений (менорагий, метрорагий), может сопровождать течение язвы желудка и 12-перстной кишки. У новорожденных постгеморрагическая анемия может быть вызвана плацентарным кровотечением, родовой травмой.</p>\r\n<p>Хроническая постгеморрагическая анемия обусловлена продолжительными, часто возникающими потерями небольших объемов крови при желудочно-кишечных, геморроидальных, почечных, носовых кровотечениях, нарушениях механизмов свертывания крови (ДВС-синдроме, гемофилии). Анемия может быть спровоцирована деструктивными опухолями, а также такими поражениями сосудов (наследственными или приобретенными), как ангиомы, артериовенозные аневризмы и другие дисплазии сосудов, бактериальные и иммунные васкулиты.</p>\r\n<p> </p>",
"pathogenesis": "<p>Основными факторами развития постгеморрагической анемии выступают явления сосудистой недостаточности, гиповолемия с уменьшением общего объема плазмы и циркулирующих форменных элементов, в частности, эритроцитов, осуществляющих транспорт кислорода. Этот процесс сопровождается снижением артериального давления, кровенаполнения внутренних органов и тканей, гипоксемией, гипоксией и ишемией, развитием шока.</p>\r\n<p>Степень выраженности защитно-приспособительных реакций организма определяется объемом, скоростью и источником кровотечения. В раннюю рефлекторно-сосудистую фазу компенсации кровопотери (первые сутки) благодаря возбуждению симпатико-адреналовой системы наблюдается спазм переферических сосудов и повышения сопротивления периферических сосудов. Развивается централизация кровообращения с первоочередным кровоснабжением головного мозга и сердца, уменьшение возврата крови к сердцу и сердечного выброса. Концентрация эритроцитов, Hb и гематокрит пока близки к норме («скрытая» анемия).</p>\r\n<p>Вторая фаза компенсации (2-3 сутки) сопровождается аутогемодилюцией - поступлением в кровеносное русло тканевой жидкости и восполнением объема плазмы. Усиление секреции катехоламинов и альдостерона надпочечниками, вазопрессина – гипоталамусом способствует стабильности уровня электролитов в плазме крови. Происходит прогрессирующее снижение показателей эритроцитов и гемоглобина, гематокрита; значение цветового показателя в норме (постгеморрагическая нормохромная анемия).</p>\r\n<p>В третью, костномозговую фазу компенсации (4-5 сутки) из-за недостатка железа анемия становится гипохромной, усиливается образование эритропоэтина почками. В костном мозге активируется выработка эритроцитов (эритропоэз), наблюдается гиперплазия эритроидного ростка, в периферической крови значительно повышается количество молодых форм эритроцитов (ретикулоцитов) и лейкоцитов. Уровни гемоглобина, эритроцитов и гематокрит понижены. Нормализация уровня эритроцитов и гемоглобина при отсутствии дальнейшей кровопотери происходит через 2-3 недели. При массивной или длительной кровопотере постгеморрагическая анемия приобретает гипорегенеративный характер, при истощении адаптационных систем организма развивается шок.</p>",
"diagnostics": "<p> </p>\r\n<p>В диагностике постгеморрагической анемии учитывают сведения о произошедшей острой кровопотере при внешнем кровотечении; в случае массивного внутреннего кровотечения диагноз основывается на клинических признаках в сочетании с лабораторными пробами.</p>\r\n<p>Изменения в общем анализе могут указывать на длительность кровотечения:</p>\r\n<ul>\r\n<li>в первый час — растет число тромбоцитов, уровень эритроцитов и гемоглобина в пределах нормы;</li>\r\n<li>через 2–3 часа — при сохранившемся тромбоцитозе появляется нейтрофилез, свертываемость крови достаточная, падает число эритроцитов и гемоглобин, анемию оценивают как нормохромную;</li>\r\n<li>через 5 дней — растет число ретикулоцитов, определяется низкое содержание железа в плазме.</li>\r\n</ul>\r\n<p>Для поиска места кровотечения обязательно проводят:</p>\r\n<ul>\r\n<li>анализ кала на скрытую кровь и гельминты;</li>\r\n<li>необходима фиброгастроскопия для исключения желудочного кровотеченияиз язвы, распадающейся опухоли;</li>\r\n<li>колоноскопия — осмотр нижних отделов кишечника;</li>\r\n<li>ректороманоскопия — для визуального подтверждения целостности внутренних геморроидальных узлов;</li>\r\n<li>женщин обязательно консультирует гинеколог.</li>\r\n<li>ЭКГ при постгеморрагической анемии может демонстрировать снижение амплитуды Т-зубца в стандартном и грудном отведении;</li>\r\n<li>УЗИ органов брюшной полости.</li>\r\n</ul>\r\n<p>Ультразвуковое и допплеровское исследования позволяют конкретизировать причину кровопотери.</p>",
"treatment": "<p>Первостепенное в лечении постгеморрагической анемии – установить и устранить источник кровотечения. Затем восполняют кровопотерю - под наблюдением трансфузиолога проводится неотложное переливание консервированной крови, кровезаменителей, плазмы и плазмозаменителей.</p>\r\n<p>При незначительном, но продолжительном кровотечении трансфузия цельной крови или плазмы показана в небольших гемостатических дозах. При значительной потере ОЦК</p>\r\n<p>трансфузии должны выполняться в дозах, превышающих кровопотерю на 20-30%. Тяжелая постгеморрагическая анемия лечится переливаниями больших доз крови («трансплантация крови»). В период коллапса гемотрансфузии дополняют гипертоническими кровозамещающими растворами.</p>\r\n<p>После восстановления ОЦК проводится коррекция качественного состава крови – восполнение ее компонентов: эритроцитов, лейкоцитов, тромбоцитов.</p>\r\n<p>По окончании острого периода необходимо лечение препаратами железа, витаминами группы В, С, Е. После ликвидации анемии препараты железа назначают в половинной дозе до 6-ти месяцев.Назначается симптоматическая терапия, направленная на нормализацию функциональных нарушений со стороны сердечно-сосудистой и дыхательной систем, печени, почек и др.</p>",
"prevention": "<p>Профилактика заключается в избегании травм, которые могут вызвать кровотечение. Необходимо правильно питаться, отказаться вредных привычек, своевременно лечить заболевания, которые могут вызвать кровотечения. В профилактические метода постгеморрагической анемии так же входит здоровый образ жизни и рациональное питание, при котором кровь и весь организм человека насыщается необходимым количеством витаминов и микроэлементов. В рацион питания обязательно должны входить железосодержащие продукты, такие как, свежие фрукты, бобовые, нежирное красное мясо, свежие овощи зеленых сортов, зелень и цельнозерновой хлеб.</p>\r\n<p> </p>\r\n<p> </p>\r\n<p> </p>\r\n<p> </p>\r\n<p> </p>",
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