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},
"code": "K73",
"name": "Хронический гепатит",
"icd_name": "Хронический гепатит, не классифицированный в других рубриках",
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2,
7,
8,
9,
10
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"lead": "Поражение гепатоцитов, вызванное различными причинами, характеризующееся гепатоцеллюлярным некрозом и воспалением, длящееся более 6 месяцев",
"description": "",
"etiology": "<p>Вирусы гепатитов В, С, Д, Е, аутоиммунные реакции, токсины и лекарственные средства.</p>",
"pathogenesis": "<p>Под воздействием повреждающих агентов происходят цитолиз и некробиоз гепатоцитов. На фоне длительно существующего хронического гепатита часто развивается цирроз печени.</p>",
"diagnostics": "<p>Проводится на основании жалоб, данных анамнеза, объективного осмотра, лабораторно-инструментальных методов исследования. Необходимо провести биохимическое исследование крови с исследованием уровня прямого и непрямого билирубина, АЛТ, холестерина, щелочной фосфатазы. Обязательными являются проведение тимоловой пробы, оценка сулемового титра. Проводят серологическое исследование крови, электронную иммунную микроскопию. В моче определяют уровень уробилиногена.</p>\r\n<p> </p>\r\n<p>Одним из важнейших методов диагностики является биопсия печени.</p>\r\n<p>Дифференциальная диагностика</p>\r\n<p>Проводится с циррозом печени, острыми гепатитами А, В, С, Д, Е, гастроэнтеритом, а также с надпеченочной или подпеченочной желтухой.</p>",
"treatment": "<p>Необходимо соблюдение диеты. При хроническом вирусном гепатите назначают интерферон—2α.</p>",
"prevention": "",
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4948
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"code": "F83",
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3
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{
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"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": "",
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