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7
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"lead": "токсикоинфекции вызываются чаще всего бактериями паратифозной группы (сальмонеллами), заболевание связано с явлениями кратковременной инфекции и последующей интоксикации.",
"description": "",
"etiology": "<p>Инкубационный период при токсикоинфекциях колеблется от нескольких часов до 1—2 сут. После этого периода появляются <a href=\"/symptom/toshnota/\" title=\"Перейти на страницу симптома Тошнота\">тошнота</a>, <a href=\"/symptom/rvota/\" title=\"Перейти на страницу симптома Рвота\">рвота</a>, боли в области живота, <a href=\"/symptom/diareya/\" title=\"Перейти на страницу симптома Диарея\">понос</a>, повышается температура.<br /> Основной источник инфекции — мясо больного животного или животного-бациллоносителя. Инфицирование продуктов может происходить и в процессе обработки и хранения, при нарушении во время разделки туши целости кишечника животных-бациллоносителей, контакте с тарой, предметами оборудования, обсемененными возбудителями токсикоинфекций.</p>\r\n<p>Для возникновения токсикоинфекции имеет значение не только факт инфицирования продукта, но и степень обсеменения его. Причиной токсикоинфекции могут быть и другие продукты и блюда — винегреты, салаты, пирожные и т. д. Однако и в этом случае первоисточниками инфекции, как правило, являются животные продукты (мясо, молоко, яйца), входящие в состав блюд или находившиеся с ними в контакте через посуду, оборудование.</p>",
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"prevention": "<p>Первое, на что нужно обратить внимание — это цвет, вкус и запах пищи. Заражённые продукты пахнут, естественно, неприятно, имеют кисловатый вкус.</p>\r\n<p>Также один из признаков испорченности продукта — это газовые пузырьки, плесень. При открывании консервы следует обратить внимание на хлопок крышки, который обязательно должен присутствовать. Если его не было, то необходимо задуматься о свежести продукта.</p>",
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5430
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"diagnostics": "<p>Диагноз сложно поставить на ранних стадиях инфекции. Необходимо использовать серологические тесты.</p>",
"treatment": "<p>Лечение патогенетическое и симптоматическое. Специфических методов терапии нет. Летальность в зависимости от характера эпидемии колеблется от 1 до 25 %. В целях профилактики заболеваний лиц, выезжающих за рубеж в местности, неблагополучные по желтой лихорадке, вакцинируют. Во время пребывания на такой территории используют средства защиты от комаров – репелленты, защитные сетки.</p>",
"prevention": "<p>Вакцинация — основной способ профилактики желтой лихорадки. В районах с высоким риском заболевания, для которых характерен слабый охват прививками, важнейшим условием предотвращения эпидемий является своевременное выявление и подавление вспышек болезни посредством массовой вакцинации населения. При этом, чтобы не допустить дальнейшего распространения заболевания в регионе, где зафиксирована вспышка, важно обеспечить большой охват иммунизацией подверженного риску населения (не менее 80%).</p>\r\n<full></full>\r\n<p>Для предотвращения вспышек применяется ряд стратегий: плановая иммунизация детей грудного возраста; проведение кампаний по массовой вакцинации для расширения охвата в странах, где существует риск вспышек болезни; вакцинация лиц, совершающих поездки в районы, эндемичные по желтой лихорадке.</p>\r\n<p>Вакцина от желтой лихорадки является безопасной и недорогостоящей. При этом одна доза вакцины достаточна для формирования пожизненного иммунитета без необходимости ревакцинации.</p>\r\n<p>В редких случаях сообщается о серьезных побочных эффектах вакцины против желтой лихорадки. Показатель частоты таких «неблагоприятных проявлений после иммунизации» (НППИ), когда после введения вакцины наблюдаются поражения печени, почек и нервной системы, что делает необходимой госпитализацию, составляет от 0,4 до 0,8 на 100 000 вакцинированных.</p>\r\n<p>Уровень риска выше у лиц старше 60 лет, пациентов с тяжелым иммунодефицитом, связанным с симптоматическим ВИЧ/СПИДом или другими факторами, а также лиц с нарушениями вилочковой железы. Вакцинацию людей старше 60 лет следует проводить после тщательной оценки потенциального риска и пользы иммунизации.</p>\r\n<p>Как правило, к числу лиц, не подлежащих вакцинации, относятся:</p>\r\n<ul class=\"disc\">\r\n<li>дети грудного возраста младше 9 месяцев (кроме случаев эпидемии, когда вакцинации подлежат дети грудного возраста от 6 до 9 месяцев в районах с высоким риском инфекции);</li>\r\n<li>беременные женщины (кроме случаев вспышки желтой лихорадки и высокого риска инфекции);</li>\r\n<li>лица с тяжелыми формами аллергии на яичный белок;</li>\r\n<li>лица с тяжелым иммунодефицитом, связанным с симптоматическим ВИЧ/СПИДом или другими факторами, а также лица с нарушениями вилочковой железы.</li>\r\n</ul>\r\n<p>В соответствии с Международными медико-санитарными правилами (ММСП) страны имеют право требовать от лиц, совершающих поездки, представить свидетельство о вакцинации против желтой лихорадки. При наличии медицинских противопоказаний к вакцинации необходимо предоставить соответствующую справку от компетентных органов. ММСП — это юридически обязательный механизм, предназначенный для предотвращения распространения инфекционных заболеваний и других источников угрозы для здоровья населения. Применение к лицам, совершающим поездки, требования по предоставлению свидетельства о вакцинации оставлено на усмотрение каждому государству-участнику и в настоящее время практикуется не всеми странами.</p>",
"clinical_picture": "<p>Инкубационный период продолжается 3–6 дней. Болезнь начинается внезапно, температура тела поднимается до 39–40°, отмечаются: резкая \"></a>, \"></a>, боли в пояснице и конечностях, с ознобом\">Озноб</a>\"> с ознобом\">озноб</a></a>, \"></a>, иногда \">Рвота</a>\">\">рвота</a></a>, . Лицо, шея, верхняя часть туловища гиперемированы, веки отечны, лицо одутловато. Затем развиваются десен, , отмечается примесь крови в кале. На 4–5-й день болезни наступает ремиссия, длящаяся от нескольких часов до одних суток. В легких случаях за этим наступает выздоровление. Чаще состояние больного вновь резко ухудшается, развиваются: интоксикация, тяжелый геморрагический синдром – кровотечения из носа, желудка, кишечника, матки, появляется геморрагическая .</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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},
"code": "D55",
"name": "Анемия вследствие ферментных нарушений",
"icd_name": "Анемия вследствие ферментных нарушений",
"gender": 0,
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"cause": [
3,
0
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"periodicity": 1,
"slug": "d55_anemiya_vsledstvie_fermentnyh_narusheniy",
"lead": "относится к группе гемолитических анемий, развитие которых связано с дефицитом различных ферментов",
"description": "",
"etiology": "<p>Относительно часто встречается анемия вследствие дефицита пируваткиназы. Заболевание наследственное, передается гомозиготно.</p>\r\n<p>Пируваткиназа (а также другие ферменты гликолизного обмена) принимает участие в синтезе АТФ, дефицит этого фермента ведет к снижению содержания АТФ в эритроцитах, а это, в свою очередь, – к нарушению концентрации ионов натрия и калия в эритроцитах (Na+↑; K+↓). В результате такого сдвига возникает функциональная и морфологическая неполноценность красных кровяных клеток.</p>",
"pathogenesis": "",
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"treatment": "<p>Проводится заместительная терапия (ферментативная), используются симптоматические средства. Нередко назначение рибофлавина дает стойкий положительный эффект.</p>",
"prevention": "",
"clinical_picture": "<p>У больных обнаруживаются общие для всех гемолитических анемий клинические симптомы: <a href=\"/symptom/slabost/\" title=\"Перейти на страницу симптома Слабость\">слабость</a>, <a href=\"/symptom/uvelichenie_pecheni/\" title=\"Перейти на страницу симптома Увеличение печени\">увеличение печени</a> и селезенки, в период гемолитического криза – <a href=\"/symptom/zheltuha/\" title=\"Перейти на страницу симптома Желтуха\">желтуха</a>.</p>",
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},
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3,
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