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"code": "A98",
"name": "Геморрагическая лихорадка",
"icd_name": "Другие вирусные геморрагические лихорадки, не классифицированные в других рубриках",
"gender": 0,
"age_min": 0,
"age_max": 100,
"cause": [
2,
5,
6,
9
],
"periodicity": 1,
"slug": "a98_gemorragicheskaya_lihoradka",
"lead": "Термином \"геморрагическая лихорадка\" объединяется группа заболеваний вирусного происхождения со сходными проявлениями, при которых ведущая роль отводится поражению сосудов с развитием тромбозов или кровоточивости",
"description": "",
"etiology": "<p>Геморрагическую лихорадку могут вызывать пять основных видов вируса - тогавирусы, филовирусы, флавивирусы, аренавирусы, буньявирусы.</p>\r\n<p>Это группа инфекций, характеризующихся природной очаговостью, то есть распространением в местностях, где много диких животных, носителей вирусов и переносчиков из разряда клещей или комаров. Основные животные, которые могут быть источниками данных лихорадок это белки, летучие мыши, домашние грызуны и обезьяны.</p>\r\n<p>Для некоторых видов геморрагических лихорадок характерны и другие пути распространения. Выделяют воздушно-пылевой путь, парентеральный (через кровь и другие биологические жидкости), пищевой, водный, через контакты с зараженными животными.</p>\r\n<p>Чаще всего болеют люди, работа которых связана с животными, дикой природой и сельхозугодиями. Городские жители при заболевании в основном имеют контакты с грызунами. </p>\r\n<p> </p>",
"pathogenesis": "<p>В упрощенном виде механизмы повреждения при геморрагических лихорадках можно представить таким образом:</p>\r\n<ul>\r\n<li>повреждение сосудов вирусами или продуктами их метаболизма,</li>\r\n<li>нарушение целостности стенок сосудов, их , выделение в просвет биологически активных веществ,</li>\r\n<li>формирование из-за дефицита кровоточивости и развития так называемого ДВС-синдрома (массивного одновременного свертывания крови в одних сосудах и параллельного кровотечения из-за низкой свертываемости в других).</li>\r\n</ul>\r\n<p>В результате формируется гипоксия тканей (нехватка кислорода) и нарушения в работе сердца, легких, почек и головного мозга, происходит массивная потеря крови. При этом тяжесть болезни будет зависеть от вида лихорадки, степени активности иммунитета и особенностей организма человека. Зачастую геморрагические лихорадки протекают тяжело и заканчиваются высокой летальностью.</p>",
"diagnostics": "<p>Основа диагностики – это клиническая картина с указаниями на пребывание в неблагоприятном районе, укусы насекомых или контакт с животными. Но для подтверждения диагноза необходимо обнаружение вирусов в крови или антител к ним. Проводится:</p>\r\n<ul>\r\n<li>общий анализ крови,</li>\r\n<li>общий анализ мочи (особенно для лихорадок с почечным синдромом),</li>\r\n<li>биохимический анализ крови и мочи,</li>\r\n<li>серологические пробы,</li>\r\n<li>иммунохимические и ПЦР методы выделения вируса или антител к нему,</li>\r\n<li>при необходимости проводят выделение и исследование вирусов.</li>\r\n</ul>\r\n<p>Геморрагические лихорадки стоит различать с тяжелым капилляро-токсическим гриппом, риккетсиозами и менингококковой инфекцией – все они сопровождаются кровоточивостью и похожи по проявлениям. Кроме того, необходимо отличать эти инфекции от болезней крови с кровоточивостью (болезнь Шенляйна-Геноха или Верльгофа).</p>",
"treatment": "<p>Диагностикой и лечением занимаются врачи-инфекционисты, а иногда и реаниматологи.</p>\r\n<p>Все люди с подозрением на геморрагическую лихорадку подлежат госпитализации в боксированное отделение инфекционной больницы.</p>\r\n<p>В период острых проявлений показано парентеральное питание, в период выздоровления – легкая растительно-молочная диета с обогащением витаминами, особенно укрепляющими сосудистые стенки – витаминами РР, С или К.</p>\r\n<p>Кроме того, применяют внутривенные вливания растворов глюкозы, переливания крови, препараты железа, антигистаминные средства. При необходимости вводят тромбоцитарную массу, факторы свертывания.</p>\r\n<p>Постельный режим в изоляторе соблюдается до полного выздоровления. В дальнейшем пациент наблюдается еще достаточно длительно у инфекциониста и терапевта.</p>",
"prevention": "<p>К основным методам борьбы с геморрагическими лихорадками относят:</p>\r\n<ul>\r\n<li>уничтожение грызунов и насекомых-переносчиков,</li>\r\n<li>тщательная очистка участков жилых застроек от травы и кустарников, заболоченных мест,</li>\r\n<li>при работе в полях и лесах необходимо ношение защитной одежды, применение репеллентов,</li>\r\n<li>для профилактики некоторых видов геморрагических лихорадок разработаны вакцины – желтой лихорадки и омской геморрагической лихорадки.</li>\r\n</ul>",
"clinical_picture": "<p>Геморрагическая - это классическая инфекционная болезнь со стадийностью течения. Выделяют следующие стадии:</p>\r\n<ul>\r\n<li>инкубационную – она, в зависимости от вида вируса, может длиться от нескольких суток до трех недель,</li>\r\n<li>начальную стадию или период продрома, длящийся от суток до недели,</li>\r\n<li>период разгара болезни с проявлением всех типичных признаков геморрагической лихорадки и длящийся от одной до двух недель,</li>\r\n<li>период реконвалесценции или выздоровления (или в некоторых случаях - летальный исход).</li>\r\n</ul>\r\n<p>Выздоровление может длиться до нескольких месяцев, особенно в случае тяжелого течения и остаточных явлений.</p>\r\n<p>В начальном периоде симптомы геморрагической лихорадки обычно неспецифические. Обычно проявляются:</p>\r\n<ul>\r\n<li>симптомы общей интоксикации,</li>\r\n<li>высокая температура,</li>\r\n<li>расстройства сознания вплоть до бреда,</li>\r\n<li>точечные кровоизлияния на коже в зоне шеи и лица, склер и в области рта,</li>\r\n<li>нарушения ритма сердца с учащением или замедлением частоты,</li>\r\n<li>снижение давления,</li>\r\n<li>в анализах крови выявляется воспалительная реакция (лейкоцитоз, может быть со сдвигом) с незначительным снижением тромбоцитов.</li>\r\n</ul>\r\n<full></full>\r\n<p>В период разгара может быть:</p>\r\n<ul>\r\n<li>временное снижение температуры,</li>\r\n<li>общее улучшение состояния, после чего вновь наступает ухудшение,</li>\r\n<li>нарастает токсикоз,</li>\r\n<li>прогрессируют нарушения сознания,</li>\r\n<li>развиваются мелкие тромбозы и из мест инъекций, с поверхностей слизистых, пищеварительного и мочеполового тракта,</li>\r\n<li>нарушаются функции легких, почек, сердца.</li>\r\n</ul>\r\n<p>В периоде выздоровления постепенно все симптомы исчезают, работа органов восстанавливается.</p>",
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},
"code": "D51",
"name": "Витамин-B12-дефицитная анемия",
"icd_name": "Витамин-B12-дефицитная анемия",
"gender": 0,
"age_min": 0,
"age_max": 100,
"cause": [
3,
0
],
"periodicity": 1,
"slug": "d51_vitamin-b12-deficitnaya_anemiya",
"lead": "образование в костном мозге мега лобластов, внутрикостное мозговое разрушение эритроцитов, изменение нервной системы в виде фуникулярного миелоза",
"description": "",
"etiology": "<p>Одним из важнейших моментов биологического действия витамина В12 является активизация им фолиевой кислоты, витамин В12 способствует образованию производных фолиевой кислоты – фолатов, которые непосредственно необходимы для костномозгового кроветворения. При дефиците витамина В12 и фолатов нарушается синтез ДНК, что в свою очередь приводит к нарушению деления клеток, увеличению их размеров и качественной неполноценности. Наиболее значительно страдают клетки эритробластического ростка: вместо эритробластов в костном мозге обнаруживаются крупные клетки эмбрионального кроветворения – мегалобласты, они не способны «созреть» до полноценного эритроцита, т. е. не могут переносить гемоглобин и кислород. Средний срок жизни мегалоцитов приблизительно в 3 раза меньше, чем у «нормальных» эритроцитов. При недостатке второго кофермента витамина В12 – внутреннего фактора – имеет место другой механизм развития анемии – происходит нарушение жирового обмена с накоплением метилмалоновой кислоты, токсичной для нервной системы. Вследствие этого возникает фуникулерный миелоз – нарушение кроветворения в костном мозге и развитие анемии. В12-дефицитная анемия развивается и в результате нарушения всасывания витамина в желудочно-кишечном тракте вследствие атрофического гастрита или в результате врожденной недостаточности железистого аппарата желудка, при этом в желудочном соке отсутствует гастромукопротеин, принимающий непосредственное участие в расщеплении и всасывании В12 и его коферментов.</p>",
"pathogenesis": "",
"diagnostics": "<p>В периферической крови определяется резкое снижение количества эритроцитов (до 0,8×1012), цветовой показатель остается высоким – 1,2–1,5. Клетки красной крови неодинаковы по величине (анизоцитоз), преобладают крупные эритроциты – макроциты, у многих эритроцитов отмечается форма в виде овала, ракетки, полумесяца и иного (пойкилоцитоз).</p>\r\n<p>В пунктате костного мозга количество клеток красного ростка резко увеличено, в 3–4 раза больше клеток лейкоцитарного ростка (в норме – обратное соотношение). В плазме крови отмечается увеличение содержания свободного билирубина и железа (до 30–45 ммоль/л).</p>",
"treatment": "<p>Назначается витамин В12. Лечение начинают введением 100–300 мкг витамина подкожно или внутримышечно 1 раз в день. На 2–3-и сутки терапии эритропоэз полностью нормализуется, а на 5–6-е сутки вновь образованные полноценные эритроциты начинают поступать в кровяное русло в необходимом количестве, самочувствие больных постепенно нормализуется. После восстановления картины крови переходят на поддерживающую терапию – введение витамина В12 в дозе 50–100 мкг, которую проводят в течение всей жизни больного. При нарушениях нервной системы на первом этапе применяют нейротропные препараты.</p>\r\n<p>Прогноз</p>\r\n<p> </p>\r\n<p>При адекватной терапии благоприятный. Без лечения заболевание прогрессирует и может привести к смерти больного.</p>",
"prevention": "",
"clinical_picture": "<p>Заболевание начинается незаметно, постепенно прогрессирует <a href=\"/symptom/slabost/\" title=\"Перейти на страницу симптома Слабость\">слабость</a>, появляются <a href=\"/symptom/narushenie_serdechnogo_ritma/\" title=\"Перейти на страницу симптома Нарушение сердечного ритма\">сердцебиение</a>, <a href=\"/symptom/golovokruzhenie/\" title=\"Перейти на страницу симптома Головокружение\">головокружение</a> и <a href=\"/symptom/odyshka/\" title=\"Перейти на страницу симптома Одышка\">одышка</a>, особенно при физической нагрузке, резких движениях, снижается трудоспособность, ухудшается аппетит, возможно подташнивание. Нередко первая жалоба, с которой больные обращаются к врачу, – это жжение языка, его причиной является характерный для данного заболевания атрофический <a href=\"/symptom/glossit/\" title=\"Перейти на страницу симптома Глоссит\">глоссит</a>. Как следствие дистрофических изменений в нервной системе возникают кожные анестезии и парестезии, в тяжелых случаях нередко отмечается нарушение походки (спастический парапарез), могут наблюдаться расстройства функций мочевого пузыря и прямой кишки, нарушается сон, появляется эмоциональная неустойчивость, <a href=\"/symptom/depressiya/\" title=\"Перейти на страницу симптома Депрессия\">депрессия</a>. При осмотре больного обращают внимание на бледность кожных покровов и слизистых оболочек (обычно с желтоватым оттенком вследствие повышенного распада мегалоцитов и образования из освобождающегося гемоглобина билирубина), одутловатость лица; очень характерен ярко-красный блестящий гладкий язык (из-за резкой атрофии сосочков) – «полированный» язык. Очень характерен атрофический гастрит. Нередко при поколачивании по плоским и некоторым трубчатым костям отмечается болезненность – признак гиперплазии костного мозга. Частым симптомом В12-дефицитной анемии является <a href=\"/symptom/povyshennaya_temperatura_37-38/\" title=\"Перейти на страницу симптома Повышенная температура 37-38°\">субфебрильная температура</a>.</p>",
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5277
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},
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