Морфологическими особенностями являются:
1. Жировая дистрофия гепатоцитов.
2. Очаги колликвационного некроза вокруг центральных отделов дольки.
3. Воспалительная клеточная инфильтрация со значительным количеством эозинофилов.
4. Наличие гранулем, не имеющих специфического строения.
5. Поражение желчных ходов с повреждением их эпителия.
6. Холестаз в перипортальных отделах.
7. Перестройка структуры печени (образование ложных долек монолобулярного типа, разделенных фиброзными септами).
Циррозы печени.
Печень обладает значительной регенераторной способностью, поэтому даже после обширного поражения печени может быть восстановлена нормальная ее архитектоника и функция. Однако если поражение клеток повторяется многократно или возникают сильные нарушения структуры, например, после мостовидных некрозов, развивается цирроз печени.
Цирроз — хроническое заболевание печени с нарастающей печеночной недостаточностью в связи с рубцовым сморщиванием и структурной перестройкой. Цирроз печени — заболевание неспецифическое; оно является конечной стадией заболеваний, приводящих к хроническому повреждению клеток печени, это состояние нереверсивное, при нем наблюдается нарушение архитектоники печени в виде фиброза и узловой регенерации. Количество соединительной ткани резко возрастает, и клетки печени не формируют дольки, а регенерируют в виде узелков, не имеющих правильной структуры дольки.
Классификация
— инфекционный (вирусы гепатита В, С);
— обменно-алиментарный (при гемохроматозе, болезни Коновалова-Вильсона);
— аутоиммунный ("люпоидный" гепатит и первичный билиарный цирроз);
— в результате обструкции желчевыводящих путей;
2. По морфологии:
а) по макроскопической картине:
— макронодулярный — узлы более 3мм в диаметре;
— микронодулярный — узлы до 3мм в диаметре;
б) по микроскопической картине:
4. По характеру течения:
Наиболее часто причиной мелкоузлового цирроза является алкоголизм. При крупноузловом циррозе, независимо от причины, наблюдается повышение риска развития рака печени.
Если выяснить причину невозможно, говорят о «криптогенном» циррозе, однако по мере развития науки все меньше случаев попадают в данную группу.
Морфологические признаки цирроза:
— нарушение долькового строения печени;
— дистрофия гепатоцитов (гидропическая, баллонная, жировая);
— наличие узлов регенератов — ложных долек (усиление регенерации, наличие митозов и амитозов гепатоцитов);
— диффузный фиброз (разрастание соединительной ткани).
Различают три морфогенетических типа цирроза:
Постнекротический цирроз чаще развивается в исходе токсической дистрофии печени и вирусного гепатита с обширными некрозами печеночной паренхимы, крайне редко — после алкогольного гепатита. Участки некроза замещены плотной рубцовой тканью. Микроскопически паренхима представлена ложными дольками, разделенными массивными полями соединительной ткани, в которых отмечается несколько триад в одном поле зрения (феномен сближения триад). Ложные дольки состоят из новообразованной печеночной ткани, могут встречаться многоядерные печеночные клетки. Для гепатоцитов характерны белковые дистрофии, липиды в них обычно не выявляются. Отмечается холестаз, пролиферация холангиол, лимфо-гистиоцитарная инфильтрация портальных трактов. Макроскопически печень уменьшена в размерах, плотная, с крупными узлами, разделенными широкими и глубокими бороздами. Это крупноузлой цирроз. Для него характерны ранняя печеночная недостаточность и поздняя портальная гипертензия.
МАКРОПРЕПАРАТ «КРУПНОУЗЛОВОЙ ЦИРРОЗ ПЕЧЕНИ». Печень уменьшена в размерах, плотная, с поверхности и на разрезе видны неравномерные узлы, в диаметре более 1 см, разделенные широкими полями соединительной ткани.
МИКРОПРЕПАРАТ «ПОСТНЕКРОТИЧЕСКИЙ ЦИРРОЗ ПЕЧЕНИ» (окраска гематоксилином и эозином). Паренхима печени представлена ложными дольками (узлами-регенератами) различной величины. В каждом узле видны фрагменты нескольких долек. Печеночные балки неразличимы, центральная вена отсутствует или смещена к периферии. Видны белковая дистрофия и некроз гепатоцитов. Встречаются гепатоциты крупных размеров, с двумя и более ядрами. Участки паренхимы разделены широкими полями соединительной ткани, в которых определяются сближенные триады и лимфогистиоцитарные инфильтраты.
Портальный цирроз развивается в финале хронического гепатита алкогольной или вирусной природы и жирового гепатоза, характеризуется однородностью микроскопической картины — тонкопетлистой соединительнотканной сетью и малой величиной ложных долек. Микроскопически паренхима представлена ложными дольками равномерной величины, разделенными узкими прослойками соединительной ткани-септами. В септах – лимфо-гистиоцитарная инфильтрация с примесью полиморфноядерных лейкоцитов, пролиферация желчных протоков. В ложных дольках — отсутствие балочного строения, характерна жировая дистрофия гепатоцитов.
Портальный цирроз развивается медленно (в течение многих лет) чаще всего при хроническом алкоголизме. Истинным портальным циррозом является первичный билиарный цирроз. Печень при первичном билиарном циррозе увеличена, плотная, на разрезе серо-зеленая, поверхность ее гладкая либо мелкозернистая. При вторичном билиарном циррозе, обусловленном обструкцией желчных путей камнем, опухолью, или инфекцией желчных путей и развитием халангита (холангитический цирроз), печень увеличена, плотная, зеленого цвета, на разрезе с расширенными, переполненными желчью протоками. Микроскопически характерны расширение и разрывы желчных капилляров, «озера желчи», явления холангита и перихолангита, развитие соединительной ткани в перипортальных полях и внутри долек.
МАКРОПРЕПАРАТ «МИКРОНОДУЛЯРНЫЙ ЦИРРОЗ ПЕЧЕНИ». Печень уменьшена в размерах, плотной консистенции, с равномерной мелкозернистой поверхностью, узлы менее 1 см в диаметре, разделены прослойками соединительной ткани.
МИКРОПРЕПАРАТ «ПОРТАЛЬНЫЙ ЦИРРОЗ ПЕЧЕНИ» (окраска гематоксилином и эозином). Паренхима представлена ложными дольками, равномерными по величине, построенными на фрагментах одной дольки. Узлы разделены узкими тяжами соединительной ткани (септами), гепатоциты в состоянии жировой дистрофии. В соединительно-тканных септах видна лимфогистиоцитарная инфильтрация, сближение триад отсутствует.
МАКРОПРЕПАРАТ «БИЛИАРНЫЙ ЦИРРОЗ ПЕЧЕНИ». Печень уменьшена в размерах, зеленовато-бурого цвета, имеет мелкозернистую поверхность. Фиксирующая жидкость окрашена в буровато-зеленый цвет.
МИКРОПРЕПАРАТ «БИЛИАРНЫЙ ЦИРРОЗ ПЕЧЕНИ» (окраска гематоксилином и эозином). В препарате определяются расширения и разрывы желчных капилляров с образованием «озер желчи», явления холангита и перихолангита, разрастание соединительной ткани в перипортальных полях и внутри долек с формированием узлов-регенератов. Гепатоциты в состоянии дистрофии.
Смешанный цирроз обладает признаками как постнекротического, так и портального цирроза.
При циррозах печени выделяют следующие типы фиброзов:
3. Портальный и перипортальный.
Клинические проявления циррозов печени характеризуются развитием следующих синдромов:
2. Печеночная энцефалопатия (снижение детоксикации в печени).
3. Геморрагический (дефицит факторов свертывания)
4. Гормональный дисбаланс (гиперэстрогения — эритема ладоней, телеангиэктазии, потеря волос, атрофия яичек, гинекомастия).
5. Отечный (снижение онкотического давления вследствие гипоальбуминемии, задержка натрия и воды, обусловленная снижением расщепления альдостерона в печени).
6. Портальная гипертензия (варикозное расширение вен пищевода, передней стенки живота («голова медузы») и геморроидальных вен, спленомегалия).
Осложнения.
— кровотечение из расширенных вен пищевода, желудка;
— переход асцита в перитонит;
— тромбоз воротной вены;
— развитие рака печени;
— печеночно-почечная недостаточность (гепато-ренальный синдром).
Наиболее важными являются печеночная недостаточность, портальная гипертензия и печеночноклеточный рак.
В результате печеночной недостаточности наблюдается снижение синтеза альбуминов, факторов свертывания крови и других белков крови, нарушается разрушение эндогенных продуктов, таких как гормоны, азотсодержащие вещества и т.д. Развивается энцефалопатия в результате нарушения детоксикации азотсодержащих веществ, синтезируемых бактериями в просвете кишечника; эти вещества действуют как медиаторы («ложные нейротрансмиттеры») в ЦНС; часто развивается печеночно-почечная недостаточность (гепато-ренальный синдром).
В результате нарушения разрушения стероидных гормонов развивается вторичный альдостеронизм, который проявляется задержкой жидкости и ионов натрия, а у мужчин исчезают вторичные половые признаки, и развивается гинекомастия в результате гиперэстрогении. Также в результате гиперэстрогении развиваются «сосудистые звездочки» на коже.
Цирроз печени является наиболее распространенной причиной портальной гипертензии. При циррозе портальная гипертензия (>7 мм рт.ст.) возникает в результате комбинации следующих факторов: повышенного кровотока в портальной вене, повышенного сопротивления в сосудах печени, внутрипеченочного артерио-венозного шунтирования. В результате портальной гипертензии развивается варикозное расширение вен пищевода и геморроидальных вен, а также развивается асцит. Варикозное расширение вен пищевода является наиболее опасным осложнением, т.к. тонкие вены пищевода легко разрываются, в результате чего развивается порой фатальное кровотечение. Также характерно расширение вен на передней брюшной стенке в виде «головы медузы Горгоны». Еще одним грозным осложнением портальной гипертензии является тромбоз портальной вены.
Цирроз печени является предопухолевым состоянием; при нем повышается риск развития печеночноклеточного рака. Опухоль часто является мультифокальной.
МАКРОПРЕПАРАТ «ПОЛИКИСТОЗ ПЕЧЕНИ». Печень увеличена в размерах на разрезе в ткани печени определяются множественные тонкостенные кисты различных размеров, заполненные желтоватым прозрачным содержимым.
Основные диагностические критерии хронических заболеваний печени
версия для печати
Кардиальный цирроз; макропрепарат.
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Инфаркт печени; макропрепарат.
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Анемический инфаркт печени; макропрепарат.
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Тромбоз воротной вены; макропрепарат.
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Синдром Бадда-Киари: облитерирующий тромбофлебит; макропрепарат.
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Синдром Бадда-Киари; микропрепарат.
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Синдром Бадда-Киари; микропрепарат.
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1.Кровоизлияние в мозг.
Данный макропрепарат — мозг. Форма органа сохранена, размеры не увеличены. Мозг бледно-желтого цвета, выражены границы между белым и серым веществом. На разрезе видны мелкие включения бурого цвета диаметром 1 мм., светло-бурые удлиненные участки (5×7 и 4×11 мм.) расположены в области коры сверху разреза. Внизу разрезы находится большое пятно диаметром 7 см. с неравномерно распределенной окраской. Участки темно-бурого цвета с размытыми границами чередуются с более светлыми. Зона хорошо отграничена от окружающей ткани.
Описание патологических изменений.
Данные патологические изменения могли развиться при:
1) разрыве;
2) разъедании стенки сосуда, что привело к массивному кровотечению и геморрагическому пропитыванию ткани мозга (участок кровоизлияния неоднородный -> сохранены частично клеточные элементы).
Мелкие включения бурого цвета представляют собой точечные кровоизлияния из вен, происшедшие при разрезе.
Светло-бурые участки — результат повышения проницаемости стенки сосуда, развившейся в результате ангионевротических нарушений, изменения микроциркуляции, тканевой гипоксии. Разрью или разъедание сосуда могли произойти в результате атеросклероза, некроза, воспаления, склероза, злокачественной опухоли.
Исход:
1) благоприятный: рассасывание крови; образование кисты на месте кровоизлияния, инкапсуляция или организация.
2) неблагоприятный: смерть в результате поражения жизненно важных центров; присоединение инфекции и нагноение.
Заключение: данные морфологические изменения свидетельствуют о разрыве или разъедании стенки сосуда, которое привело к геморрагическому пропитыванию ткани мозга.
Диагноз: Геморрагический инсульт.
6. Фибринозный перикардит.
Данный макропрепарат — сердце, заключенное в околосердечную сумку.
Форма органа сохранена, размеры .несколько увеличены. Эпикард тускло-серого цвета, Шероховатый, покрыта фибрином светло-коричневого цвета. Очагов кровоизлияния и некроза нет. Фибрин более выражен на передней стенке правого желудочка
Описания патологических изменений.
Данные патологические изменения могут развиться при ревматических болезнях с поражением сердца. В листках сердечной сорочки развивается дезорганизация соединительной ткани, поражения сосудов и иммуннопатологические процессы. Повышенная проницаемость сосудов в стадии экссудации приводит к «пропотеванию» фибриногена за их стенки и образованию «волосатого» сердца.
Исход:
1) благоприятный:
а) рассасывание фибрина;
2) неблагоприятный: облитерация полости сердечной сорочки и обызвествление образовавшейся в ней соединительной ткани (панцирное сердце).
Заключение: данные морфологические изменения свидетельствуют о том, что в листках перикарда при ревматизме развились дистрофия и экссудативное фибринозное воспаление.
Диагноз: Фибринозный перикардит (волосатое сердце).
10. Рак желудка.
Данный макропрепарат — желудок. Форма и размеры органа изменены за счет разрастания ткани белесовато-желтого цвета, которая проросла стенку желудка и значительно утолщает ее (до 10 см и более). Рельефы слизистой не выражен. В центральной части разрастания видны углубления, разрыхления и свисающие участки — изъязвления.
Описание патологических изменений.
Данные патологические изменения могли развиться в результате предраковых состояний и предраковых изменений (кишечная метаплазия и тяжелая дисплазия).
В очагах изменения эпителия происходит малигнизация клеток и развитие опухолей (или рак развивается (de novo). Руководствуясь макроскопической картиной, можно сказать, что это рак с преимущественно эндофитным инфильтрирующим ростом — инфильтративно-язвенный рак (об этом свидетельствуют изъязвления опухоли). Гистологически это может быть как аденокарценома, так и недифференцированный рак. Прогрессия, опухоль прорастает стенку желудка и значительно утолщает ее.
Исход: 1) благоприятный:
а) медленный рост рака;
б) высокодифференцйрованная аденокарценома;
в) позднее метастазирование;
2) неблагоприятный: смерть от истощения, интоксикации, матастазов; распространение рака за пределы желудка и прорастание в другие органы и ткани, вторичные некротические изменения и распад карценомы; нарушение функции желудка.
Заключение: данные морфологические изменения свидетельствуют о мутационной трансформации клеток эпителия с их малигнизацией и последующей опухолевой прогрессией, что при инфильтрирующем росте привело к прорастанию стенки желудка с изъязвлениями, которые могут представлять вторичные некротические изменения и распад опухоли.
Диагноз: Инфильтративно-язвенный рак желудка.
19. Ишемический инфаркт селезенки.
Данный макропрепарат — селезенка Форма и размеры не изменены. Цвет неоднороден — в целом он буро-красный, но от ворот к периферии органа тянутся два участка шириной 1 -2 см. более бледной окраски. Поверхность гладкая, без разрывов, геморрагии, рубцов.
Описание патологических изменений.
Данные патологические изменения свидетельствуют о том, что причиной их послужила резкое нарушение артериального кровообращения в крупных ветвях лиенапьных артерий, что привело к ишемии значительного участка паренхимы селезенки и в последствии к инфаркту. Инфаркт в селезенке чаще всего белый, реже — белый с геморрагическим венчиком, что обусловлено особенностями ангиоархитектоники органа В данном случае он скорее всего белый, так как некротические участки имеют характерный цвет и четко отграничены от интактных участков органов.
Исход:
1) благоприятный:
а) рубцевание и замещение некротических тканей;
2) неблагоприятный:
а) разрыв капсулы органа и внутрибрюшной кровотечение;
б) смерть от шока;
в) интоксикация и аугоиммунизация продуктами распада (резорбционно-некротический синдром), что усугубляет положение.
Заключение: данные морфологические изменения свидетельствуют о резких дисциркуляторных изменениях в бассейне ветвей селезеночной артерии, приводящих к развитию инфаркта
Диагноз: Острый ишемический инфаркт селезенки.
24. Мускатная печень.
Данный макропрепарат — печень. Масса и размеры уменьшены, форма сохранена. Цвет органа на разрезе пестрый, серо-желтый с красным крапом, причем пестрота увеличивается к периферии. Печень бугристая, бугристость увеличивается к периферии.
Описание патологических изменений.
Данные патологические изменения могли развиться в результате увеличения давления в венах печени, что возможно при общем (хроническая правожелудочная недостаточность) или местном венозном застое (воспаление печеночных вен, тромбоз их просветов). При этом центральные вены расширяются, что приводит к дистрофии и некрозу прилежащих гепатоцитов и расширению синусоидов. В них к центру располагаются форменные элементы, а на периферии -плазма (из-за увеличения давления в месте впадения артериального капилляра) > плазморрагия, диапедезное кровоизлияние. В следствие застоя венозной крови > гипоксия > синтез соединительной ткани клеток Купфера — формирование базальной мембраны и превращение синосоида в капилляр > гипоксия. В центральных отделах долек развивается жировая дистрофия (декомпозиция) вплоть до некроза. Из-за полной регенерации в местах гибели гепатоцитов разрастается соединительная ткань > склероз. Венозный застой > гипоксия > утолщение соединительной ткани печени (междольковой и по ходу триад). Оставшиеся периферические гепатоциты, окруженные соединительной тканью, начинают размножаться. Формируется ложная долька, кровоснабжение которой крайне плохое > гипоксия, дистрофия > некроз гепатоцитов.
Исход:
1) благоприятный: хроническое течение заболевания; устранение причины венозного полнокровия;
2) неблагоприятный: смерть от печеночной недостаточности, рак, формирование склероза и портальной гипертензии, присоединение инфекции, желтуха и т д.
Заключение: данные морфологические изменения свидетельствуют о венозном полнокровии печени и развившейся на этой почве гипоксии, которая приводит к структурной перестройки органа.
Диагноз: Мускатный цирроз печени.
27. Пристеночный тромб артерии.
Данный макропрепарат — брюшная аорта. Форма органа сохранена, размеры не увеличены. Орган светло-серого цвета. На интимен видны образования темно-серого цвета диаметром 5 мм. с неровной поверхностью, а рядом с ним, образование такой же консистенции и цвета 3×1.5 см. Это образование расположено в месте разветвления аорты.
Описание патологических изменений.
Данные морфологические изменения могли развиться в резз’льтате нарушения жирового и белкового обмена, чему способствовали такие факторы как:
— алиментарные;
— гормональные;
— нервные;
— гемодинамические;
— сосудистые;
— наследственные;
— этнические.
Нерегулируемый клеточный обмен холестерина приводит к образованию пенистых клеток и дальнейшему развитию атеросклеротических изменений, которые мы видим на интиме аорты: жировые пятна, фиброзные бляшки, образования тромботических наложений на месте изъязвления бляшки. В образовании тромботических наложений (образования темно-серого цвета плотной консистенции) принимают участки не только нарушения сосудистой стенки, но и с нарушением кровообращения, состава крови, сосудистой стенки, нарушение регуляции свертывающей, противосвертывающей и фибринолитической систем.
Особенно важным фактором в данном случае является нарушение кровообращения в виде завихрения тока крови у места бифуркации брюшной аорты. Это замедление тока крови и способствует наложению тромботических масс на изъязвленную интиму.
Исход: 1) благоприятный:
а) асептический аутолиз тромба;
б) организация; 2) неблагоприятный:
а) петрификация;
б) тромбоэмболия;
в) септическое расплавление;
г) обтурация просвета аорты.
Заключение: данные морфологические изменения свидетельствуют о дистрофических изменениях в интиме аорты, которые вместе с нарушением тока крови создали предпосылки для тромбоза.
Диагноз: Тромбоз аорты.
9Казеозная пневмония – это специфическая пневмония, характеризующаяся нарастающими казеозно-некротическими изменениями и тяжелым, быстро прогрессирующим, нередко с летальным исходом течением. Патологическая анатомия. Казеозная пневмония имеет большую протяженность – больше доли до субтотальной. Доминирует экссудативно-некротическая реакция с быстрым гнойным расплавлением, образованием множества острых полостей без наклонности к отграничению; при слиянии которых образуются гигантские полости. В стенках полостей скопления МБТ и стафилококков.
10. Зернистая дистрофия. При гистологическом исследовании в клетках,
цитоплазме видны белковые зерна. Зернистой дистрофией страдают паренхиматозные
органы, такие как почки, печень и сердце. Эту дистрофию называют мутным или
тусклым набуханием. Это связано с макроскопическими особенностями. Органы при
данной дистрофии слегка набухшие, а поверхность на разрезе тусклая, мутна, как
бы “ ошпаренная кипятком”. Зернистую дистрофию вызывает ряд причин, которые
можно распределить на 2 группы: инфекции и интоксикации.
В почках при зернистой дистрофии наблюдается увеличение в размерах, она
дрябла, может быть положительная проба Шорра (при сведении друг к другу полюсов
почки ткань почки рвется). На разрезе ткань тусклая, границы коркового и
мозгового вещества смазаны или вообще неразличимы. При этом виде дистрофии
страдает эпителий извитых канальцев почки. Если нормальные канальцы почек имеют
ровные просветы, то при зернистой дистрофии апикальный отдел цитоплазмы
разрушается и просвет приобретает звездчатую форму. Цитоплазма эпителия
почечных канальцев содержит многочисленные зерна (розового цвета). Почечная
зернистая дистрофия имеет 2 исхода: благоприятный: если убрать причину, то
эпителий канальцев вернется к норме, неблагоприятный, если патологический
фактор продолжает действовать, то процесс становится необратимым, дистрофия
переходит в некроз (часто наблюдается при отравлении почечными ядами).
11-Амилоидоз — это разновидность белковой дистрофии, являющейся осложнением многих заболеваний: инфекционной, воспалительной, опухолевой природы. В таком случае мы говорим о приобретенном (вторичном) амилоидозе. Амилоидоз может быть следствием неизвестной причины — это первичный амилоидоз. Термин амилоидоз был предложен в 1853 году Р. Вирховым. Он показал что при этом заболевании в органах появляется вещество, которое красится йодом подобно крахмалу. До Вирхова заболевание было описано К. Ракитанским под названием “сальная болезнь” за микроскопический признак амилоидоза — орган приобретает сальный блеск. Амилоид является сложным веществом — гликопротеидом, в котором глобулярные и фибриллярные белки всегда тесно связаны с мукополисахаридами. Поражение печени. В печени амилоид откладывается в синусоидах между купферовскими клетками, по ходу ретикулярной стромы долек, печеночные клетки сдавливаются и погибают от атрофии.
12- Почки. Поражение почек более важно в практическом плане, так как почки поражаются у 90% пациентов и является основной причиной смерти (от почечной недостаточности). В почке амилоид появляется под мембраной капилляров клубочков, под мембраной сосудов коркового и мозгового слоя, под мембранами прямых и извитых канальцев и в строме почки по ходу ретикулярных волокон. Это процесс постоянный: первая стадия — скрытая, латентная. Амилоид появляется в пирамидах, в клубочковых кровеносных сосудах, вторая стадия — протеинурия. Характерно большее количество белка в моче. На этой стадии примерно 50% клубочков содержат амилоид в виде небольших очаговых отложений. В строме отмечаются явления склероза, за счет растущей ишемии. В эпителии находятся признаки жировой и гиалиново-капельной дистрофии.
13-Термин «гемохроматоз печени» отражает одну из характерных черт болезни — ненормальную окраску кожи и органов вследствие отложения в них особых пигментов кровяного происхождения.Термин «пигментный цирроз» отражает сочетание пигментации кожных покровов и цирроза печени. Патологическая анатомия. На разрезе печень резко пигментирована вследствие отложения пигмента в печеночных и купферовских клетках. Соединительная ткань развивается по ходу кровеносных капилляров; она не обладает склонностью к сморщиванию, поэтому орган обычно остается увеличенным.
14- Механическая желтуха — патологический синдром, обусловленный нарушением оттока жёлчи из жёлчных протоков.
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