Kuliah Sambil Ngaji

Posted on Sabtu, 30 April 2011

Segala puji bagi Allah, Rabb semesta alam. Shalawat dan salam kepada Nabi kita Muhammad, keluarga dan sahabatnya.
Kegiatan kuliah terasa amat menyibukkan. Sibuk dengan berbagai tugas, harus buat presentasi, menyusun laporan praktikum dan lebih sibuk lagi jika sudah menginjak semester-semester akhir. Apakah mungkin kesibukan ini bisa dibarengi dengan menuntut ilmu agama? Jawabannya, mungkin sekali. Segala kemudahan itu datang dari Allah. Maka bisa saja seorang engineer menjadi pakar fiqih. Bisa jadi pula seorang ekonom menjadi pakar hadits. Atau seorang ahli biologi menjadi hafizh Al Qur’an. Semua itu bisa terwujud karena anugerah dan kemudahan dari Allah.

Realitas, Lebih Banyak Menyia-nyiakan Waktu
Mahasiswa sebenarnya punya banyak waktu senggang. Cuma sebagian mahasiswa saja yang benar-benar menyia-nyiakan waktunya. Tidak setiap saat ia mesti mendapatkan tugas. Tidak setiap hari mesti kerjakan laporan praktikum. Mahasiswa yang tidak pintar membagi waktu saja yang selalu “sok sibuk”.
Sebagian mahasiswa masih bisa menyisihkan waktu untuk renang dengan shohib dekatnya. Ia masih sempat juga untuk fitness meskipun di kala laporan praktikum menumpuk. Ia juga masih sempat berpetualang menjelajah berbagai gunung meskipun minggu depan ada ujian mid. Ia masih bisa begadang semalam suntuk untuk menanti pertandingan Liga Champions meskipun katanya ada banyak tugas yang mesti diselesaikan. Sebagiannya pula bisa menyisihkan waktu untuk update status setiap jam di FB (Facebook), twitter dan semacamnya. Mau tidur, mau makan, mau renang, bahkan mau ke WC sekali pun bisa ada statusnya di jejaring sosial tadi. Namun soal ngaji (istilah untuk mendalami ilmu agama) bisa menjadi nomor sekian baginya. Padahal aneh kan, hal-hal tadi bisa ia lakukan. Sedangkan berkaitan dengan urusan akhiratnya di mana ia wajib mempelajari Islam karena ibadah-ibadah tertentu akan ia lewati setiap harinya. Setiap muslim tentu mesti mengetahui bagaimanakah ia harus berwudhu yang benar sehingga shalatnya pun bisa sah. Ia pun harus tahu apa saja yang termasuk pembatal-pembatal shalat, sehingga shalatnya tidak jadi sia-sia. Ia pun harus tahu bagaimana mandi wajib.
Lihatlah mereka bisa menyisihkan waktu untuk hal-hal dunia yang kadang sia-sia. Namun untuk hal yang menyangkut akhirat mereka, di mana tentu ini lebih urgent, mereka tidak bisa membagi waktu dengan baik. Benarlah firman Allah Ta’ala,

يَعْلَمُونَ ظَاهِرًا مِنَ الْحَيَاةِ الدُّنْيَا وَهُمْ عَنِ الْآَخِرَةِ هُمْ غَافِلُونَ

“Mereka hanya mengetahui yang lahir (saja) dari kehidupan dunia; sedang mereka tentang (kehidupan) akhirat adalah lalai.” (QS. Ar Ruum: 7).
Syaikh Abu Bakr Jabir Al Jazairi hafizhohullah menjelaskan, “Mereka mengetahui kehidupan dunia secara lahiriah saja seperti mengetahui bagaimana cara mengais rizki dari pertanian, perindustrian dan perdagangan. Di saat itu, mereka benar-benar lalai dari akhirat. Mereka sungguh lalai terhadap hal yang wajib mereka tunaikan dan harus mereka hindari, di mana penunaian ini akan mengantarkan mereka selamat dari siksa neraka dan akan menetapi surga Ar Rahman.” (Aysarut Tafasir, 4/124-125)

Beberapa Sampel
Beberapa orang bisa membuktikan bahwa mereka di samping kuliah di pagi hari, sore harinya masih bisa “ngaji” (menuntut ilmu agama). Bahkan ada di antara mahasiswa yang bisa menjadi hafizh Al Quran dengan sempurna di masa kuliahnya. Ada pula yang bisa menguasai ilmu aqidah dengan baik padahal ia seorang dokter. Setelah kuliah pun ia bisa menyusun beberapa buku berkaitan dengan masalah aqidah dari hasil ia belajar di saat-saat kuliah dulu (paginya kuliah, sorenya ia duduk di majelis ilmu). Ada pula yang amat pakar dalam bahasa Arab dan menjadi seorang ustadz yang mumpuni dalam hal aqidah serta ilmu lainnya, padahal ia adalah sarjana biologi. Yang lainnya lagi adalah seorang dosen (lulus S3), namun tidak diragukan ia sangat mumpuni dalam ilmu hadits hasil dari belajar dulu bersama beberapa ustadz di saat-saat ia kuliah. Bahkan di Arab Saudi sendiri ada seorang ulama yang dulunya adalah seorang yang belajar ilmu Teknik Kimia. Dan saat ini, beliau menjadi imam dan ulama yang jadi rujukan. Ia pun memiliki situs yang berisi berbagai fatwa yang sering dikunjungi dari berbagai negara. Ada lagi ulama yang dahulunya belajar ilmu teknik mesin. Saat lulus ia mendalami ilmu hadits dan menjadi hafizh al quran. Karya-karya beliau dalam tulisan pun amat banyak. Dua ulama yang kami sebutkan di sini adalah Syaikh Sholeh Al Munajjid dan Syaikh Musthofa Al Adawi hafizhohumallah.
Itu sekedar beberapa contoh riil yang kami ketahui. Kami yakin masih banyak contoh-contoh lainnya yang mungkin para pembaca sendiri mengetahuinya. Ini pertanda bahwa orang yang belajar ilmu umum (ilmu teknik, ekonomi, IT, dll) sebenarnya tidak terhalang untuk belajar agama bahkan bisa menjadi ulama atau pun ustadz karena kerajinannya di luar jam kuliah untuk mengkaji Islam. Itulah karunia Allah untuk mereka-mereka tadi.

Mulai Belajar Islam
Kalau sudah tahu demikian, Anda selaku mahasiswa seharusnya tidak usah ragu lagi untuk menaruh perhatian pada ilmu diin (ilmu agama). Cobalah mulai dengan mempelajari Islam mulai dari dasar. Terutama pelajarilah hal-hal yang wajib yang jika Anda tidak mengetahuinya maka bisa terjerumus dalam dosa atau bisa meninggalkan kewajiban. Inilah ilmu yang wajib dipelajari.
Selaku mahasiswa wajib punya ilmu aqidah dan tauhid yang benar sesuai dengan pemahaman generasi terbaik Islam (salafush sholeh). Cobalah mempelajari beberapa tulisan karya Syaikh Muhammad bin Abdul Wahhab seperti Qowa’idul Arba’ (empat kaedah memahami syirik), Tsalatsatul Ushul (tiga landasan dalam mengenal Allah, Islam dan Nabi shallallahu ‘alaihi wa sallam), dan Kitab Tauhid (pelajaran tauhid dan syirik secara lebih detail). Kitab-kitab aqidah pun ada yang mudah dipelajari seperti Al ‘Aqidah Al Wasithiyah karya Ibnu Taimiyah dan Al ‘Aqidah Ath Thohawiyah karya Abu Ja’far Ath Thohawiy.
Anda pun wajib mempelajari fiqih secara bertahap terutama pelajaran bagaimana cara wudhu yang benar, bagaimana cara mandi wajib, dan bagaimana shalat yang benar serta berbagai hal yang berkaitan dengan hal-hal tadi. Amat mudah jika Anda menguasai dari fiqh madzhab sebagaimana anjuran para ulama. Karena di negeri ini menganut madzhab Syafi’i, Anda bisa belajar dari berbagai kitab fiqh Syafi’iyah. Pelajari dari matan-matan yang ringkas seperti kitab Al Ghoyah wat Taqrib karya Abu Syuja’ dan Minhajuth Tholibin karya Imam An Nawawi. Inilah kitab dasar yang bisa Anda kuasai. Setelah itu bisa melanjutkan dengan kitab fiqih yang lebih advance dengan mendalami dalil-dalil lebih jauh. Baru setelah itu bisa menelaah berbagai pendapat ulama dan perselisihan mereka dalam hal fiqih sehingga akhirnya kita tidak fanatik pada satu madzhab atau satu imam. Anda pun bisa menguasai fiqih melalui berbagai buku hadits seperti dari kitab ‘Umdatul Ahkam karya ‘Abdul Ghoni Al Maqdisi dan kitab Bulughul Marom karya Ibnu Hajar Al Asqolani. Untuk memahami kitab-kitab fiqih ini, Anda bisa memiliki berbagai kitab syarh (penjelasan) dari masing-masing kitab.
Buku-buku yang kami sebutkan di atas sudah cukup mudah ditemukan saat ini di berbagai toko buku Islam bahkan sudah banyak yang diterjemahkan. Sehingga tidak ada alasan bagi yang belum menguasai bahasa Arab untuk terus belajar. Namun jika Anda sambil menguasai bahasa Arab terutama menguasai grammar-nya dalam ilmu Nahwu dan Sharaf itu lebih baik. Karena menguasai bahasa tersebut bisa membuat Anda meneliti lebih jauh kitab-kitab ulama secara lebih mandiri.
Selain mempelajari hal-hal di atas, tambahkan pula dengan mempelajari berbagai kitab akhlaq dan tazkiyatun nufus (manajemen hati). Juga janganlah sampai tinggalkan hafalan Al Qur’an. Karena orang yang menghafal Al Qur’an sungguh memiliki banyak keutamaan dan faedah di tengah-tengah umat. Lebih-lebih di akhirat hafalan Al Qur’an ini membuat dia lebih ditinggikan derajat di surga. Lalu para ulama pun menganjurkan untuk menghafal berbagai matan atau berbagai kitab ringkas seperti menghafalkan kitab kecil yang berisi 42 hadits yaitu Al Arba’in An Nawawiyah. Menghafal seperti ini memudahkan kita menguasai ilmu Islam dengan lebih mudah.

Sabar dalam Belajar
Kalau dilihat, terasa begitu banyak yang harus dipelajari. Sebenarnya tidak juga karena mempelajari berbagai buku di atas itu bertingkat-tingkat. Ada yang lebih dasar, baru setelah itu beranjak pada yang lebih lanjut. Jadi belajar yang baik adalah secara bertahap. Sehingga di sini butuh kesabaran dalam belajar dan belajar butuh waktu yang lama. Yang terbaik pula adalah belajar di majelis ilmu lewat guru. Lihatlah sya’ir Imam Asy Syafi’i,

أَخِي لَنْ تَنَالَ الْعِلْمَ إلَّا بِسِتَّةٍ سَأُنْبِيكَ عَنْ تَفْصِيلِهَا بِبَيَانِ

ذَكَاءٌ وَحِرْصٌ وَاجْتِهَادٌ وَبُلْغَةٌ وَصُحْبَةُ أُسْتَاذٍ وَطُولُ زَمَانٍ

Saudaraku … ilmu tidak akan diperoleh kecuali dengan enam perkara yang akan saya beritahukan perinciannya : (1) kecerdasan, (2) semangat, (3) sungguh-sungguh, (4) berkecukupan, (5) bersahabat (belajar) dengan ustadz, (6) membutuhkan waktu yang lama.

Pintar Bagi Waktu
Modal yang penting “nyambi” belajar Islam adalah pintar membagi waktu. Cobalah membagi waktu mulai dari Shubuh hari sudah bisa menghafal Al Qur’an. Butuh satu jam untuk menyisihkan waktu kala itu. Setelah itu sediakan waktu untuk persiapan kuliah di pagi hari. Pukul 7 atau 8 sudah bisa berangkat ke kampus. Di waktu-waktu shalat atau waktu senggang saat di kampus bisa digunakan untuk muroja’ah Al Qur’an atau mengerjakan tugas-tugas kampus sehingga tidak menumpuk keesokan harinya. Pulang kampus di siang atau sore hari bisa istirahat sejenak untuk menghilangkan rasa capek. Di sore hari sehabis ‘Ashar bisa digunakan untuk mengikuti berbagai majelis ilmu sampai dengan waktu ‘Isya. Di waktu malam bisa digunakan untuk mengerjakan tugas kuliah. Sebelum tidur bisa digunakan menghafal berbagai matan, mengulang hafalan Al Qur’an atau mengulang pelajaran yang ikuti di kajian.
Jadi cuma kepintaran saja membagi waktu, niscaya kita bisa kuliah sambil “ngaji”. Dan jangan lupakan minta pertolongan Allah agar dimudahkan mempelajari agama di samping kuliah. Doa ini amat menolong. Jika kita memohon kemudahan pada Allah, pasti segala urusan tadi akan begitu mudah. Berbeda halnya jika kita bergantung pada diri sendiri yang begitu lemah.
Semoga Allah mudahkan kita selaku mahasiswa untuk dapat meraih keduanya, bahkan bisa menjadi pakar pula dalam ilmu agama dan bisa turut membantu dakwah agar tersebar seantero negeri kita ini.
Wallahu waliyyut taufiq.

Panggang-Gunung Kidul, 24 Jumadal Ula 1432 H (27/04/2011)
www.rumaysho.com

Kuliah Sambil Menimba Ilmu Agama

Kegiatan kuliah terasa amat menyibukkan. Sibuk dengan berbagai tugas, harus buat presentasi, menyusun laporan praktikum dan lebih sibuk lagi jika sudah menginjak semester-semester akhir. Apakah mungkin kesibukan ini bisa dibarengi dengan menuntut ilmu agama? Jawabannya, mungkin sekali. Segala kemudahan itu datang dari Allah. Maka bisa saja seorang engineer menjadi pakar fiqih. Bisa jadi pula seorang ekonom menjadi pakar hadits. Atau seorang ahli biologi menjadi hafizh Al Qur’an. Semua itu bisa terwujud karena anugerah dan kemudahan dari Allah.

Realitas, Lebih Banyak Menyia-nyiakan Waktu
Mahasiswa sebenarnya punya banyak waktu senggang. Cuma sebagian mahasiswa saja yang benar-benar menyia-nyiakan waktunya. Tidak setiap saat ia mesti mendapatkan tugas. Tidak setiap hari mesti kerjakan laporan praktikum. Mahasiswa yang tidak pintar membagi waktu saja yang selalu “sok sibuk”.
Sebagian mahasiswa masih bisa menyisihkan waktu untuk renang dengan shohib dekatnya. Ia masih sempat juga untuk fitness meskipun di kala laporan praktikum menumpuk. Ia juga masih sempat berpetualang menjelajah berbagai gunung meskipun minggu depan ada ujian mid. Ia masih bisa begadang semalam suntuk untuk menanti pertandingan Liga Champions meskipun katanya ada banyak tugas yang mesti diselesaikan. Sebagiannya pula bisa menyisihkan waktu untuk update status setiap jam di FB (Facebook), twitter dan semacamnya. Mau tidur, mau makan, mau renang, bahkan mau ke WC sekali pun bisa ada statusnya di jejaring sosial tadi. Namun soal ngaji (istilah untuk mendalami ilmu agama) bisa menjadi nomor sekian baginya. Padahal aneh kan, hal-hal tadi bisa ia lakukan. Sedangkan berkaitan dengan urusan akhiratnya di mana ia wajib mempelajari Islam karena ibadah-ibadah tertentu akan ia lewati setiap harinya. Setiap muslim tentu mesti mengetahui bagaimanakah ia harus berwudhu yang benar sehingga shalatnya pun bisa sah. Ia pun harus tahu apa saja yang termasuk pembatal-pembatal shalat, sehingga shalatnya tidak jadi sia-sia. Ia pun harus tahu bagaimana mandi wajib.
Lihatlah mereka bisa menyisihkan waktu untuk hal-hal dunia yang kadang sia-sia. Namun untuk hal yang menyangkut akhirat mereka, di mana tentu ini lebih urgent, mereka tidak bisa membagi waktu dengan baik. Benarlah firman Allah Ta’ala,
يَعْلَمُونَ ظَاهِرًا مِنَ الْحَيَاةِ الدُّنْيَا وَهُمْ عَنِ الْآَخِرَةِ هُمْ غَافِلُونَ
“Mereka hanya mengetahui yang lahir (saja) dari kehidupan dunia; sedang mereka tentang (kehidupan) akhirat adalah lalai.” (QS. Ar Ruum: 7).
Syaikh Abu Bakr Jabir Al Jazairi hafizhohullah menjelaskan, “Mereka mengetahui kehidupan dunia secara lahiriah saja seperti mengetahui bagaimana cara mengais rizki dari pertanian, perindustrian dan perdagangan. Di saat itu, mereka benar-benar lalai dari akhirat. Mereka sungguh lalai terhadap hal yang wajib mereka tunaikan dan harus mereka hindari, di mana penunaian ini akan mengantarkan mereka selamat dari siksa neraka dan akan menetapi surga Ar Rahman.” (Aysarut Tafasir, 4/124-125)

Beberapa Sampel
Beberapa orang bisa membuktikan bahwa mereka di samping kuliah di pagi hari, sore harinya masih bisa “ngaji” (menuntut ilmu agama). Bahkan ada di antara mahasiswa yang bisa menjadi hafizh Al Quran dengan sempurna di masa kuliahnya. Ada pula yang bisa menguasai ilmu aqidah dengan baik padahal ia seorang dokter. Setelah kuliah pun ia bisa menyusun beberapa buku berkaitan dengan masalah aqidah dari hasil ia belajar di saat-saat kuliah dulu (paginya kuliah, sorenya ia duduk di majelis ilmu). Ada pula yang amat pakar dalam bahasa Arab dan menjadi seorang ustadz yang mumpuni dalam hal aqidah serta ilmu lainnya, padahal ia adalah sarjana biologi. Yang lainnya lagi adalah seorang dosen (lulus S3), namun tidak diragukan ia sangat mumpuni dalam ilmu hadits hasil dari belajar dulu bersama beberapa ustadz di saat-saat ia kuliah. Bahkan di Arab Saudi sendiri ada seorang ulama yang dulunya adalah seorang yang belajar ilmu Teknik Kimia. Dan saat ini, beliau menjadi imam dan ulama yang jadi rujukan. Ia pun memiliki situs yang berisi berbagai fatwa yang sering dikunjungi dari berbagai negara. Ada lagi ulama yang dahulunya belajar ilmu teknik mesin. Saat lulus ia mendalami ilmu hadits dan menjadi hafizh al quran. Karya-karya beliau dalam tulisan pun amat banyak. Dua ulama yang kami sebutkan di sini adalah Syaikh Sholeh Al Munajjid dan Syaikh Musthofa Al Adawi hafizhohumallah.
Itu sekedar beberapa contoh riil yang kami ketahui. Kami yakin masih banyak contoh-contoh lainnya yang mungkin para pembaca sendiri mengetahuinya. Ini pertanda bahwa orang yang belajar ilmu umum (ilmu teknik, ekonomi, IT, dll) sebenarnya tidak terhalang untuk belajar agama bahkan bisa menjadi ulama atau pun ustadz karena kerajinannya di luar jam kuliah untuk mengkaji Islam. Itulah karunia Allah untuk mereka-mereka tadi.

Mulai Belajar Islam
Kalau sudah tahu demikian, Anda selaku mahasiswa seharusnya tidak usah ragu lagi untuk menaruh perhatian pada ilmu diin (ilmu agama). Cobalah mulai dengan mempelajari Islam mulai dari dasar. Terutama pelajarilah hal-hal yang wajib yang jika Anda tidak mengetahuinya maka bisa terjerumus dalam dosa atau bisa meninggalkan kewajiban. Inilah ilmu yang wajib dipelajari.
Selaku mahasiswa wajib punya ilmu aqidah dan tauhid yang benar sesuai dengan pemahaman generasi terbaik Islam (salafush sholeh). Cobalah mempelajari beberapa tulisan karya Syaikh Muhammad bin Abdul Wahhab seperti Qowa’idul Arba’ (empat kaedah memahami syirik), Tsalatsatul Ushul (tiga landasan dalam mengenal Allah, Islam dan Nabi shallallahu ‘alaihi wa sallam), dan Kitab Tauhid (pelajaran tauhid dan syirik secara lebih detail). Kitab-kitab aqidah pun ada yang mudah dipelajari seperti Al ‘Aqidah Al Wasithiyah karya Ibnu Taimiyah dan Al ‘Aqidah Ath Thohawiyah karya Abu Ja’far Ath Thohawiy.
Anda pun wajib mempelajari fiqih secara bertahap terutama pelajaran bagaimana cara wudhu yang benar, bagaimana cara mandi wajib, dan bagaimana shalat yang benar serta berbagai hal yang berkaitan dengan hal-hal tadi. Amat mudah jika Anda menguasai dari fiqh madzhab sebagaimana anjuran para ulama. Karena di negeri ini menganut madzhab Syafi’i, Anda bisa belajar dari berbagai kitab fiqh Syafi’iyah. Pelajari dari matan-matan yang ringkas seperti kitab Al Ghoyah wat Taqrib karya Abu Syuja’ dan Minhajuth Tholibin karya Imam An Nawawi. Inilah kitab dasar yang bisa Anda kuasai. Setelah itu bisa melanjutkan dengan kitab fiqih yang lebih advance dengan mendalami dalil-dalil lebih jauh. Baru setelah itu bisa menelaah berbagai pendapat ulama dan perselisihan mereka dalam hal fiqih sehingga akhirnya kita tidak fanatik pada satu madzhab atau satu imam. Anda pun bisa menguasai fiqih melalui berbagai buku hadits seperti dari kitab ‘Umdatul Ahkam karya ‘Abdul Ghoni Al Maqdisi dan kitab Bulughul Marom karya Ibnu Hajar Al Asqolani. Untuk memahami kitab-kitab fiqih ini, Anda bisa memiliki berbagai kitab syarh (penjelasan) dari masing-masing kitab.
Buku-buku yang kami sebutkan di atas sudah cukup mudah ditemukan saat ini di berbagai toko buku Islam bahkan sudah banyak yang diterjemahkan. Sehingga tidak ada alasan bagi yang belum menguasai bahasa Arab untuk terus belajar. Namun jika Anda sambil menguasai bahasa Arab terutama menguasai grammar-nya dalam ilmu Nahwu dan Sharaf itu lebih baik. Karena menguasai bahasa tersebut bisa membuat Anda meneliti lebih jauh kitab-kitab ulama secara lebih mandiri.
Selain mempelajari hal-hal di atas, tambahkan pula dengan mempelajari berbagai kitab akhlaq dan tazkiyatun nufus (manajemen hati). Juga janganlah sampai tinggalkan hafalan Al Qur’an. Karena orang yang menghafal Al Qur’an sungguh memiliki banyak keutamaan dan faedah di tengah-tengah umat. Lebih-lebih di akhirat hafalan Al Qur’an ini membuat dia lebih ditinggikan derajat di surga. Lalu para ulama pun menganjurkan untuk menghafal berbagai matan atau berbagai kitab ringkas seperti menghafalkan kitab kecil yang berisi 42 hadits yaitu Al Arba’in An Nawawiyah. Menghafal seperti ini memudahkan kita menguasai ilmu Islam dengan lebih mudah.

Sabar dalam Belajar
Kalau dilihat, terasa begitu banyak yang harus dipelajari. Sebenarnya tidak juga karena mempelajari berbagai buku di atas itu bertingkat-tingkat. Ada yang lebih dasar, baru setelah itu beranjak pada yang lebih lanjut. Jadi belajar yang baik adalah secara bertahap. Sehingga di sini butuh kesabaran dalam belajar dan belajar butuh waktu yang lama. Yang terbaik pula adalah belajar di majelis ilmu lewat guru. Lihatlah sya’ir Imam Asy Syafi’i,
أَخِي لَنْ تَنَالَ الْعِلْمَ إلَّا بِسِتَّةٍ سَأُنْبِيكَ عَنْ تَفْصِيلِهَا بِبَيَانِ

ذَكَاءٌ وَحِرْصٌ وَاجْتِهَادٌ وَبُلْغَةٌ وَصُحْبَةُ أُسْتَاذٍ وَطُولُ زَمَانٍ
Saudaraku … ilmu tidak akan diperoleh kecuali dengan enam perkara yang akan saya beritahukan perinciannya : (1) kecerdasan, (2) semangat, (3) sungguh-sungguh, (4) berkecukupan, (5) bersahabat (belajar) dengan ustadz, (6) membutuhkan waktu yang lama.

Pintar Bagi Waktu
Modal yang penting “nyambi” belajar Islam adalah pintar membagi waktu. Cobalah membagi waktu mulai dari Shubuh hari sudah bisa menghafal Al Qur’an. Butuh satu jam untuk menyisihkan waktu kala itu. Setelah itu sediakan waktu untuk persiapan kuliah di pagi hari. Pukul 7 atau 8 sudah bisa berangkat ke kampus. Di waktu-waktu shalat atau waktu senggang saat di kampus bisa digunakan untuk muroja’ah Al Qur’an atau mengerjakan tugas-tugas kampus sehingga tidak menumpuk keesokan harinya. Pulang kampus di siang atau sore hari bisa istirahat sejenak untuk menghilangkan rasa capek. Di sore hari sehabis ‘Ashar bisa digunakan untuk mengikuti berbagai majelis ilmu sampai dengan waktu ‘Isya. Di waktu malam bisa digunakan untuk mengerjakan tugas kuliah. Sebelum tidur bisa digunakan menghafal berbagai matan, mengulang hafalan Al Qur’an atau mengulang pelajaran yang ikuti di kajian.
Jadi cuma kepintaran saja membagi waktu, niscaya kita bisa kuliah sambil “ngaji”. Dan jangan lupakan minta pertolongan Allah agar dimudahkan mempelajari agama di samping kuliah. Doa ini amat menolong. Jika kita memohon kemudahan pada Allah, pasti segala urusan tadi akan begitu mudah. Berbeda halnya jika kita bergantung pada diri sendiri yang begitu lemah.

Internet Download Manager v6.05 Build 14

Internet Download Manager v6.05 Build 14 (IDM) integrates seamlessly into Microsoft Internet Explorer, Netscape, MSN Explorer, AOL, Opera, Mozilla, Mozilla Firefox, Mozilla Firebird, Avant Browser, MyIE2, and all other popular browsers to automatically handle your downloads. It is a tool to increase download speeds by up to 5 times, resume and schedule downloads. Comprehensive error recovery and resume capability will restart broken or interrupted downloads due to lost connections, network problems, computer shutdowns, or unexpected power outages. Simple graphic user interface makes IDM user friendly and easy to use.Internet Download Manager has a smart download logic accelerator that features intelligent dynamic file segmentation and safe multipart downloading technology to accelerate your downloads. Unlike other download managers and accelerators Internet Download Manager segments downloaded files dynamically during download process and reuses available connections without additional connect and login stages to achieve best acceleration performance. You can also drag and drop files, or use Internet Download Manager from command line. Internet Download Manager supports proxy servers, ftp and http protocols, firewalls, redirects, cookies, authorization, MP3 audio and MPEG video content processing. Internet Download Manager can dial your modem at the set time, download the files you want, then hang up or even shut down your computer when it’s done. Other features include multilingual support, zip preview, download categories, scheduler pro, sounds on different events, HTTPS support, queue processor, html help and tutorial, enhanced virus protection on download completion, progressive downloading with quotas (useful for connections that use some kind of fair access policy or FAP like Direcway, Direct PC, Hughes, etc.), built-in download accelerator, and many others.

HF RS

Mendapatkan update manual antivirus ESET NOD32, EAV dan ESS

NOD32 Update Viewer memungkinkan anda untuk mendapatkan update manual antivirus ESET NOD32, EAV dan ESS.
Program ini sebenarnya ditujukan hanya untuk pengguna terdaftar dari ESET NOD32 untuk melihat dan memeriksa anti-virus database, sehingga membuatnya bebas tanpa melanggar,
Memperluas fungsionalitas dan meningkatkan keandalan untuk mendapatkan update antivirus ESET NOD32, EAV dan ESS.

Fitur:
* Menampilkan isi perbaruan pada semua server perusahaan dan Eset mirrors.
* Menampilkan nyata versi file (bukan dari update.ver).
* Cek dan update daftar server Eset.
* Perbandingan konten update NOD32 anda sekarang dan tempat lain (new-hijau; lama-merah).
* Dalam mode otomatis dapat memeriksa update setiap saat.
* Mendukung proxy server.
* Bekerja dengan mirror pada HTTP, HTTPS, dan FTP.
* Bekerja dengan mirror dengan otorisasi (... tp: / / username: password @ host ...).
* Bekerja tanpa NOD32.

Download aplikasinya silahkan langsung ke TKP klik disini

Download Eset Nod32 Offline Update 6050 (20110417)

Download update full file - 37.35 MB

via mediafire.com

List Info Virus

Update 6050 (20110417) - 2011-04-17

BAT/Shutdown.NBO (2), JS/Exploit.Pdfka.OVB.Gen, JS/Exploit.Pdfka.OVC, MSIL/Injector.FO, Win32/Adware.GabPath, Win32/Adware.Mirar, Win32/Adware.SystemSecurity.AG (4), Win32/Adware.SystemSecurity.AH (2), Win32/Adware.XPAntiSpyware.AB (3), Win32/Agent.SLG (2), Win32/AutoRun.Agent.ABK, Win32/AutoRun.Delf.JY (2), Win32/AutoRun.IRCBot.FC, Win32/AutoRun.Spy.Banker.G, Win32/Dorkbot.A, Win32/Hoax.ArchSMS.JE, Win32/Injector.FVH, Win32/Injector.FVI, Win32/Injector.FVJ, Win32/Injector.FVK, Win32/Injector.FVL, Win32/IRCBot.NEC (2), Win32/Kelihos.A, Win32/KillAV.NMA, Win32/Kryptik.MSI, Win32/Kryptik.MSJ, Win32/Kryptik.MSK, Win32/Kryptik.MSL, Win32/LockScreen.YL, Win32/PSW.FakeMSN.NAO, Win32/PSW.Tibia.NEA, Win32/PSW.VB.NFA, Win32/Spatet.I, Win32/Spatet.Q, Win32/Spy.Banker.QEP, Win32/Spy.Banker.USJ, Win32/Spy.Banker.UVM, Win32/Spy.Banker.VIN, Win32/Spy.Banker.VSP (5), Win32/Spy.SpyEye.CA, Win32/Spy.Zbot.JF, Win32/Spy.Zbot.YW (2), Win32/TrojanDownloader.Agent.QQH (2), Win32/TrojanDownloader.Delf.QLB (2), Win32/TrojanDownloader.FakeAlert.BBT, Win32/TrojanDownloader.FakeAlert.BHH, Win32/TrojanDownloader.Small.PED (2), Win32/TrojanDownloader.Stohil.S (2), Win32/TrojanDropper.Delf.NWH (2), Win32/VB.PSU (2)

Local Server Mirror/Update ESET NOD32 V4

Pada tutorial kali ini kita akan membuat mirror server update ESET NOD32 V4 sederhana lebih simpel, stabil dan mudah dalam pembuatannya.
Tapi untuk membuatnya kita membutuhkan File License.
Pada dasarnya ESET NOD32 V3 dan V4 sudah dibekali dengan mirror yang otomatis akan melakukan generate pada waktu ada update baru.
Dan file hasil generate tersebut bisa diarahkan ke sebuah folder. Perhatikan perbedaan antara kedua gambar dibawah :

Tanpa Memasukkan File License

Dengan File License

Pada gambar terlihat perbedaan antara dimasukkan License dan tidak.
Yang menjadi pertanyaan sekarang adalah, bagaimana cara mendapatkan atau mencari License tersebut, sebenarnya tidak sulit untuk mencari license menggunakan Google, hanya saja perlu sedikit trik.
Nanti akan saya berikan satu buah License untuk anda.
Setelah License didapat, sekarang saatnya untuk menginstallnya.

Download file nod32.lic (valid until 20-05-2011).
Masuk ke halaman utama ESET NOD32
Pencet F5 untuk masuk ke halaman Setup
Klik submenu Licenses, letaknya di bawah menu Miscellaneous.
Klik Add, cari letak file nod32.lic yang telah kita download. Kemudian klik Open. OK.

Setelah kita memasukkan License tadi, akan terlihat masa berlaku license tersebut, sehingga jika sudah habis masa berlakunya, kita harus mencari lagi license yang baru. Oke, sampai disini seharusnya kita sudah mendapatkan tab Mirror pada menu (F5 > Update > Setup) seperti gambar paling atas.
Sekarang saatnya melakukan konfigurasi dengan file update dengan Webserver.
Disini saya tidak akan membahas bagaimana cara konfigurasi webserver, kita bisa menggunakan Apache, Xitami, IIS atau yang lain.

Konfigurasi File Update:

Buatlah folder “nod_upd4” atau terserah anda, di dalam folder public webserver (Apache = htdocs, IIS = wwwroot)
Buka halaman utama ESET NOD32
Pencet F5 > Update >Setup > Mirror
Klik Folder, kemudian arahkan ke Folder nod_upd4 yang telah kita buat, OK, OK, OK
Sekarang coba lakukan update, setelah selesai update, seharusnya folder nod_upd4 sudah terisi file-file hasil generate update.
Untuk nge-cek apakah server mirror anda sudah berjalan dengan lancar, buka browser internet kesayangan anda, kemudian ketikkan http://IP_SERVER_MIRROR/nod_upd4
Harusnya akan muncul seperti ini :

Jika sudah muncul gambar seperti diatas, berarti server mirror yang kita buat sudah berhasil.
Sekarang saatnya setting pada masing-masing klien.

Konfigurasi Client :

Pada halaman utama ESET NOD32, tekan tombol F5 pada keyboards.
Maka akan muncul window seperti dibawah :

Lihat urutan angka yang sudah saya tandai pada gambar diatas.
Setelah muncul window tersebut, klik update (1), kemudian Edit (2), akan muncul lagi window seperti pada gambar.
Masukkan IP Address komputer mirror (3), karena komputer mirror saya tadi memliki IP 10.10.10.11 dan folder update nya nod_upd, maka penulisannya :

http://10.10.10.11/nod_upd

Kemudian klik Add (4). dan OK (5).
Setting Client sudah selesai, sekarang test dengan menjalankan update.

Semoga bermanfaat.

Cara Upade ESET NOD32 Online alternative Mirror Server

Beberapa waktu terakhir NOD32 agak sulit sekali update secara otomatis. entah mengapa penyebabnya. sehinga kita harus cari lain untuk updatenya
salah satu cara update ialah melalui mirorr server nod32
Untuk mencari miror serverbisa kita tanyakan pada mbah Google caranya :

Cari Mirror Server di Google
Syntak /eset_upd/ diikuti dengan bulan dan tahun
Contoh "/eset_upd/ Mei-2010"
Setelah Ketemu Alamat urlnya
Contoh : http://www.nikka.active.by/eset_upd/
Pada halaman utama ESET NOD32, tekan tombol F5 pada keyboards
Maka akan muncul window seperti dibawah :
Lihat urutan angka yang sudah saya tandai pada gambar diatas.
Setelah muncul window tersebut, klik update (1), kemudian tombol Edit (2), akan muncul lagi window seperti pada gambar.
Masukkan Alamat server mirror yg anda temukan di google tadi (3),
Contoh : http://www.nikka.active.by/eset_upd/
Kemudian klik Add (4). dan OK (5).
Setting sudah selesai,
Sekarang anda bisa meng-Update Eset secara online tanpa menggunakan Username dan Password.
Untuk Memudahkan Server mirror anda bisa pilih salah satu dari server yang saya berikan dibawah ini..
http://www.nikka.active.by/eset_upd/
http://nod.botans.org/update/
http://www.lanita.net/nod32/
http://www.chetupon.ac.th/eset_upd/
http://av.theon.ru/nod3/
http://update.citynov.ru/ess/
http://www.znamensk.net/eset_upd/
http://novts.novline.ru/ess/
http://update.homelan.lg.ua/Update-Nod32/
http://info.grad.ku.ac.th/track/download/nod32/
http://silvery.vfose.ru/nod_upd/
http://nod32.hallsoft.net/
http://www.phokiri.ac.th/ftp/eset_upd/
http://ironnet.info/updates/eset_upd/

Jika pada saat meng-update terdapat pesan server failed, silakan anda ganti dengan server lainnya.

Perhatian !!!
Silakan anda baca caranya dengan teliti sebelum anda bertanya.
Jika server mirror tidak bisa gunakan, anda dapat melakukan Update secara Offline, untuk caranya akan saya jelaskan pada postingan berikutnya

Update Manual Avira

Untuk para pengguna setia Avira, saya menyediakan link update manual avira.

Link ini berasal dari MF, semoga kecepatan mendownload tidak menganggu kebosanan Anda, hahaha..

01 Mei 2011 MF

Pathophysiology of Chronic Obstructive Pulmonary Disease (COPD)

Pathophysiology

Pathologic changes in chronic obstructive pulmonary disease (COPD) occur in the large (central) airways, the small (peripheral) bronchioles, and the lung parenchyma. Most cases of COPD are the result of exposure to noxious stimuli, most often cigarette smoke. The normal inflammatory response is amplified in persons prone to COPD development. The pathogenic mechanisms are not clear but are most likely diverse. Increased numbers of activated polymorphonuclear leukocytes and macrophages release elastases in a manner that cannot be counteracted effectively by antiproteases, resulting in lung destruction.
The primary offender has been found to be human leukocyte elastase, with synergistic roles suggested for proteinase-3 and macrophage-derived matrix metalloproteinases (MMPs), cysteine proteinases, and a plasminogen activator. Additionally, increased oxidative stress caused by free radicals in cigarette smoke, the oxidants released by phagocytes, and polymorphonuclear leukocytes all may lead to apoptosis or necrosis of exposed cells. Accelerated aging and autoimmune mechanisms have also been proposed as having roles in the pathogenesis of COPD.^{[3, 4]}
Cigarette smoke causes neutrophil influx, which is required for the secretion of MMPs; this suggests, therefore, that neutrophils and macrophages are required for the development of emphysema.
Studies have also shown that in addition to macrophages, T lymphocytes, particularly CD8⁺, play an important role in the pathogenesis of smoking-induced airflow limitation.
To support the inflammation hypothesis further, a stepwise increase in alveolar inflammation has been found in surgical specimens from patients without COPD versus patients with mild or severe emphysema. Indeed, mounting evidence supports the concept that dysregulation of apoptosis and defective clearance of apoptotic cells by macrophages play a prominent role in airway inflammation, particularly in emphysema.^[5]Azithromycin (Zithromax) has been shown to improve this macrophage clearance function, providing a possible future treatment modality.^[6]
In patients with stable COPD without known cardiovascular disease, there is a high prevalence of microalbuminuria, which is associated with hypoxemia independent of other risk factors.^[7]

Chronic bronchitis

Mucous gland hyperplasia (as seen in the images below) is the histologic hallmark of chronic bronchitis. Airway structural changes include atrophy, focal squamous metaplasia, ciliary abnormalities, variable amounts of airway smooth muscle hyperplasia, inflammation, and bronchial wall thickening.

Histopathology of chronic bronchitis showing hyperplasia of mucous glands and infiltration of the airway wall with inflammatory cells.

Histopathology of chronic bronchitis showing hyperplasia of mucous glands and infiltration of the airway wall with inflammatory cells (high-powered view). Damage to the endothelium impairs the mucociliary response that clears bacteria and mucus. Inflammation and secretions provide the obstructive component of chronic bronchitis. Neutrophilia develops in the airway lumen, and neutrophilic infiltrates accumulate in the submucosa. The respiratory bronchioles display a mononuclear inflammatory process, lumen occlusion by mucus plugging, goblet cell metaplasia, smooth muscle hyperplasia, and distortion due to fibrosis. These changes, combined with loss of supporting alveolar attachments, cause airflow limitation by allowing airway walls to deform and narrow the airway lumen.
In contrast to emphysema, chronic bronchitis is associated with a relatively undamaged pulmonary capillary bed. The body responds by decreasing ventilation and increasing cardiac output. This V/Q mismatch results in rapid circulation in a poorly ventilated lung, leading to hypoxemia and polycythemia. Eventually, hypercapnia and respiratory acidosis develop, leading to pulmonary artery vasoconstriction and cor pulmonale. With the ensuing hypoxemia, polycythemia, and increased CO₂ retention, these patients have signs of right heart failure and are known as "blue bloaters."

Emphysema

Emphysema is a pathologic diagnosis defined by permanent enlargement of airspaces distal to the terminal bronchioles. This leads to a dramatic decline in the alveolar surface area available for gas exchange. Furthermore, loss of alveoli leads to airflow limitation by 2 mechanisms. First, loss of the alveolar walls results in a decrease in elastic recoil, which leads to airflow limitation. Second, loss of the alveolar supporting structure leads to airway narrowing, which further limits airflow.
Emphysema has 3 morphologic patterns:

Centriacinar
Panacinar
Distal acinar, or paraseptal

Centriacinar emphysema is characterized by focal destruction limited to the respiratory bronchioles and the central portions of the acini. This form of emphysema is associated with cigarette smoking and is typically most severe in the upper lobes.
Panacinar emphysema involves the entire alveolus distal to the terminal bronchiole. The panacinar type is typically most severe in the lower lung zones and generally develops in patients with homozygous alpha1-antitrypsin (AAT) deficiency.
Distal acinar emphysema, or paraseptal emphysema, is the least common form and involves distal airway structures, alveolar ducts, and sacs. This form of emphysema is localized to fibrous septa or to the pleura and leads to formation of bullae (as seen in the images below). The apical bullae may cause pneumothorax. Paraseptal emphysema is not associated with airflow obstruction.

Gross pathology of advanced emphysema. Large bullae are present on the surface of the lung.

Gross pathology of a patient with emphysema showing bullae on the surface. The gradual destruction of alveolar septae (shown in the image below) and of the pulmonary capillary bed in emphysema leads to a decreased ability to oxygenate blood. The body compensates with lowered cardiac output and hyperventilation. This V/Q mismatch results in relatively limited blood flow through a fairly well oxygenated lung with normal blood gases and pressures in the lung, in contrast to the situation in chronic bronchitis. Because of low cardiac output, the rest of the body suffers from tissue hypoxia and pulmonary cachexia. Eventually, these patients develop muscle wasting and weight loss and are identified as "pink puffers."

At high magnification, loss of alveolar walls and dilatation of airspaces in emphysema can be seen.

Emphysematous destruction and small airway inflammation

Emphysematous destruction and small airway inflammation often are found in combination in individual patients, leading to the spectrum that is known as COPD. When emphysema is moderate or severe, loss of elastic recoil, rather than bronchiolar disease, is the dominant mechanism of airflow limitation. By contrast, when emphysema is mild, bronchiolar abnormalities are most responsible for the majority of the deficit in lung function. Although airflow obstruction in emphysema is often irreversible, bronchoconstriction due to inflammation accounts for some reversibility. Airflow limitation is not the only pathophysiologic mechanism by which symptoms occur.

Dynamic hyperinflation

Lung volumes, particularly dynamic hyperinflation, have also been shown to play a crucial role in the development of dyspnea perceived during exercise. In fact, the improvement in exercise capacity brought about by several treatment modalities, including bronchodilators, oxygen therapy, lung volume reduction surgery (LVRS), and maneuvers learned in pulmonary rehabilitation, is more likely due to delaying dynamic hyperinflation rather than improving the degree of airflow obstruction.^{[8, 9, 10, 11, 12, 13, 14, 15]}Additionally, hyperinflation (defined as the ratio of inspiratory capacity to total lung capacity [IC/TLC]) has been shown to predict survival better than forced expiratory volume in 1 second (FEV₁).

source : emedicine.medscape.com

Bronchitis

Bronchitis is one of the top conditions for which patients seek medical care. It is characterized by inflammation of the bronchial tubes (or bronchi), the air passages that extend from the trachea into the small airways and alveoli. (See Clinical Presentation.)
Chronic bronchitis is defined clinically as cough with sputum expectoration for at least 3 months a year during a period of 2 consecutive years. Chronic bronchitis is associated with hypertrophy of the mucus-producing glands found in the mucosa of large cartilaginous airways. As the disease advances, progressive airflow limitation occurs, usually in association with pathologic changes of emphysema. This condition is called chronic obstructive pulmonary disease. (See Clinical Presentation.)
When a stable patient experiences sudden clinical deterioration with increased sputum volume, sputum purulence, and/or worsening of shortness of breath, this is referred to as an acute exacerbation of chronic bronchitis, as long as conditions other than acute tracheobronchitis are ruled out. (See Diagnosis.)
Triggers of bronchitis may be infectious agents, such as viruses or bacteria, or noninfectious agents, such as smoking or inhalation of chemical pollutants or dust. Bronchitis typically occurs in the setting of an upper respiratory illness; thus, it is observed more frequently in the winter months. (See Etiology.)
Allergens and irritants can produce a similar clinical picture. Asthma can be mistakenly diagnosed as acute bronchitis if the patient has no prior history of asthma. In one study, one third of patients who had been determined to have recurrent bouts of acute bronchitis were eventually identified as having asthma. Generally, bronchitis is a diagnosis made by exclusion of other conditions such as sinusitis, pharyngitis, tonsillitis, and pneumonia. (See Diagnosis.)
Acute bronchitis is manifested by cough and, occasionally, sputum production that last for no more than 3 weeks. Although bronchitis should not be treated with antimicrobials, it is frequently difficult to refrain from prescribing them. Accurate testing and decision-making protocols regarding who might benefit from antimicrobial therapy would be useful but are not currently available. (See Treatment and Management, as well as Medication.)
To see complete information on Pediatric Bronchitis, please go to the main article by clicking here.

Pathophysiology

During an episode of acute bronchitis, the cells of the bronchial-lining tissue are irritated and the mucous membrane becomes hyperemic and edematous, diminishing bronchial mucociliary function. Consequently, the air passages become clogged by debris and irritation increases. In response, copious secretion of mucus develops, which causes the characteristic cough of bronchitis.
In the case of mycoplasmal pneumonia, bronchial irritation results from the attachment of the organism (Mycoplasma pneumoniae) to the respiratory mucosa, with eventual sloughing of affected cells. Acute bronchitis usually lasts approximately 10 days. If the inflammation extends downward to the ends of the bronchial tree, into the small bronchi (bronchioles), and then into the air sacs, bronchopneumonia results.
Chronic bronchitis is associated with excessive tracheobronchial mucus production sufficient to cause cough with expectoration for 3 or more months a year for at least 2 consecutive years. The alveolar epithelium is both the target and the initiator of inflammation in chronic bronchitis.
A predominance of neutrophils and the peribronchial distribution of fibrotic changes result from the action of interleukin 8, colony-stimulating factors, and other chemotactic and proinflammatory cytokines. Airway epithelial cells release these inflammatory mediators in response to toxic, infectious, and inflammatory stimuli, in addition to decreased release of regulatory products such as angiotensin-converting enzyme or neutral endopeptidase.
Chronic bronchitis can be categorized as simple chronic bronchitis, chronic mucopurulent bronchitis, or chronic bronchitis with obstruction. Mucoid sputum production characterizes simple chronic bronchitis. Persistent or recurrent purulent sputum production in the absence of localized suppurative disease, such as bronchiectasis, characterizes chronic mucopurulent bronchitis.
Chronic bronchitis with obstruction must be distinguished from chronic infective asthma. The differentiation is based mainly on the history of the clinical illness: patients who have chronic bronchitis with obstruction present with a long history of productive cough and a late onset of wheezing, whereas patients who have asthma with chronic obstruction have a long history of wheezing with a late onset of productive cough.
Chronic bronchitis may result from a series of attacks of acute bronchitis, or it may evolve gradually because of heavy smoking or inhalation of air contaminated with other pollutants in the environment. When so-called smoker's cough is continual rather than occasional, the mucus-producing layer of the bronchial lining has probably thickened, narrowing the airways to the point where breathing becomes increasingly difficult. With immobilization of the cilia that sweep the air clean of foreign irritants, the bronchial passages become more vulnerable to further infection and the spread of tissue damage.

Etiology

Respiratory viruses are the most common causes of acute bronchitis, and cigarette smoking is indisputably the predominant cause of chronic bronchitis.

Viral and becterial infections in acute bronchitis

The most common viruses include influenza A and B, parainfluenza, respiratory syncytial virus, and coronavirus, although an etiologic agent is identified only in a minority of cases.^[1]
Acute bronchitis is usually caused by infections, such as those caused by Mycoplasma species, Chlamydia pneumoniae, Streptococcus pneumoniae, Moraxella catarrhalis, and Haemophilus influenzae, and by viruses, such as influenza, parainfluenza, adenovirus, rhinovirus, and respiratory syncytial virus. Exposure to irritants, such as pollution, chemicals, and tobacco smoke, may also cause acute bronchial irritation.
Bordetella pertussis should be considered in children who are incompletely vaccinated, though studies increasingly report this bacterium as the causative agent in adults as well.^[2]

Smoking and other causes of chronic bronchitis

Cigarette smoking is indisputably the predominant cause of chronic bronchitis. Common risk factors for acute exacerbations of chronic bronchitis are advanced age and low forced expiratory volume in one second (FEV₁).^[3]Most (70-80%) acute exacerbations of chronic bronchitis are estimated to be due to respiratory infections.^[4]
Estimates suggest that cigarette smoking accounts for 85-90% of chronic bronchitis and chronic obstructive pulmonary disease. Studies indicate that smoking pipes, cigars, and marijuana causes similar damage. Smoking impairs ciliary movement, inhibits the function of alveolar macrophages, and leads to hypertrophy and hyperplasia of mucus-secreting glands.
Smoking can also increase airway resistance via vagally mediated smooth muscle constriction. Unless some other factor can be isolated as the irritant that produces the symptoms, the first step in dealing with chronic bronchitis is for the patient to stop smoking.
Air pollution levels have been associated with increased respiratory health problems among people living in affected areas. The Air Pollution and Respiratory Health Branch of the National Center for Environmental Health directs the fight of the US Centers for Disease Control and Prevention against respiratory illness associated with air pollution.
According to the Healthy People 2000 report, each year in the United States, health costs of human exposure to outdoor air pollutants range from $40 to $50 billion, and an estimated 50,000 to 120,000 premature deaths are associated with exposure to air pollutants. In addition, the report states that those with asthma experience more than 100 million days of restricted activity, costs related to asthma exceed $4 billion, and about 4,000 people die of the condition each year.
A growing body of literature has demonstrated that specific occupational exposures are associated with the symptoms of chronic bronchitis. The list of agents includes coal, manufactured vitreous fibers, oil mist, cement, silica, silicates, osmium, vanadium, welding fumes, organic dusts, engine exhausts, fire smoke, and secondhand cigarette smoke.

source : emedicine.medscape.com

Bronchiectasis

Bronchiectasis is an uncommon disease that results in the abnormal and permanent distortion of one or more of the conducting bronchi or airways, most often secondary to an infectious process. First described by Laennec in 1819, later detailed by Sir William Osler in the late 1800s, and further defined by Reid in the 1950s, bronchiectasis has undergone significant changes in regard to its prevalence, etiology, presentation, and treatment.^[1]
Bronchiectasis can be categorized as a chronic obstructive pulmonary lung disease manifested by airways that are inflamed and easily collapsible, resulting in air flow obstruction with shortness of breath, impaired clearance of secretions often with disabling cough, and occasionally hemoptysis. Severe cases can result in progressive impairment with respiratory failure.^{[2, 3]}
Bronchiectasis most often presents as (1) a focal process involving a lobe, segment, or subsegment of the lung or (2) a diffuse process involving both lungs. The former is by far the most common presentation of bronchiectasis, while the latter is most often associated with systemic illnesses, such as cystic fibrosis (CF), sinopulmonary disease, or both. The majority of this article will address non-CF related bronchiectasis.
Diagnosis is usually based on a compatible clinical history of chronic respiratory symptoms, such as a daily cough and viscid sputum production, and characteristic radiographic findings on CT scans, such as bronchial wall thickening and luminal dilatation.

Pathophysiology

Bronchiectasis is an abnormal dilation of the proximal and medium-sized bronchi (>2 mm in diameter) caused by weakening or destruction of the muscular and elastic components of the bronchial walls. Affected areas may show a variety of changes, including transmural inflammation, edema, scarring, and ulceration, among other findings. Distal lung parenchyma may also be damaged secondary to persistent microbial infection and frequent postobstructive pneumonia. Bronchiectasis can be congenital or acquired but is most often the latter.^[1]
Congenital bronchiectasis usually affects infants and children and results from developmental arrest of the bronchial tree. The more commonly acquired forms occur in adults and older children and require an infectious insult, impairment of drainage, airway obstruction, and/or a defect in host defense. The tissue is also damaged in part by the host response of neutrophilic proteases, inflammatory cytokines, nitric oxide, and oxygen radicals. This results in damage to the muscular and elastic components of the bronchial wall. Additionally, peribronchial alveolar tissue may be damaged, resulting in diffuse peribronchial fibrosis.^[4]
The result is abnormal bronchial dilatation with bronchial wall destruction and transmural inflammation. The most important functional finding of altered airway anatomy is severely impaired clearance of secretions from the bronchial tree.
Impaired clearance of secretions causes colonization and infection with pathogenic organisms, contributing to the common purulent expectoration observed in patients with bronchiectasis. The result is further bronchial damage and a vicious cycle of bronchial damage, bronchial dilation, impaired clearance of secretions, recurrent infection, and more bronchial damage.^[5]
In 1950, Reid characterized bronchiectasis as cylindrical, cystic, or varicose in nature.^[6]
Cylindrical bronchiectasis involves diffuse mucosal edema, with resultant bronchi that are dilated minimally but have straight, regular outlines that end squarely and abruptly (see the image below).

Cylindrical bronchiectasis with signet-ring appearance. Note that the luminal airway diameter is greater than the diameter of the adjacent vessel.
Cystic or saccular bronchiectasis has ulceration with bronchial neovascularization and a resultant ballooned appearance that may have air-fluid levels (see the image below).

Cystic and cylindrical bronchiectasis of the right lower lobe on a posterior-anterior chest radiograph.
Varicose bronchiectasis has a bulbous appearance with a dilated bronchus and interspersed sites of relative constriction and, potentially, obstructive scarring. The latter may subsequently result in postobstructive pneumonitis and additional parenchymal damage (see the image below).

Varicose bronchiectasis with alternating areas of bronchial dilatation and constriction.

source : emedicine.medscape.com

Bronchiolitis

Bronchiolitis is an acute inflammatory injury of the bronchioles that is usually caused by a viral infection. Although it may occur in persons of any age, severe symptoms are usually only evident in young infants; the larger airways of older children and adults better accommodate mucosal edema. Bronchiolitis usually affects children younger than 2 years, with a peak in infants aged 3-6 months. Acute bronchiolitis is the most common cause of lower respiratory tract infection in the first year of life. It is generally a self-limiting condition and is most commonly associated with respiratory syncytial virus.
Bronchiolar injury and the consequent interplay between inflammatory and mesenchymal cells can lead to diverse pathological and clinical syndromes. Bronchioles are small airways, less than 2 mm in diameter, and lack cartilage and submucosal glands. The terminal bronchiole, a 16th generation airway, is the final conducting airway that terminates in the respiratory bronchioles. The acinus (ie, the gas exchange unit of the lung) consists of respiratory bronchioles, the alveolar duct, and alveoli. The bronchiolar lining consists of surfactant-secreting Clara cells and neuroendocrine cells, which are the source of bioactive products such as somatostatin, endothelin, and serotonin.
Wilhelm Lange first described obliterative bronchiolitis (OB) in 1901 by reporting 2 cases of interstitial bronchiolar disorder. In 1985,^[1]bronchiolitis obliterans-organizing pneumonia (BOOP) was described as a separate condition with different clinical, radiographic, and prognostic features than OB. BOOP is a histopathologic lesion, not a specific diagnosis. Its pathologic hallmark is proliferative bronchiolitis or bronchiolitis obliterans in association with organizing pneumonia. BOOP and OB are beyond the scope of this article and are not discussed further.

Pathophysiology

Bronchiolitis is very contagious. The virus that causes it is spread from person to person by direct contact with nasal secretions, airborne droplets, and fomites.
The effects of bronchiolar injury include the following:

Increased mucus secretion
Bronchial obstruction and constriction
Alveolar cell death, mucus debris, viral invasion
Air trapping
Atelectasis
Reduced ventilation that leads to ventilation/perfusion mismatch
Labored breathing

Ninety percent of cases are caused by respiratory syncytial virus (RSV). Other causes of bronchiolitis are addressed in Causes. Complex immunologic mechanisms play a role in the pathogenesis of RSV bronchiolitis. Type 1 allergic reactions mediated by immunoglobulin E may account for some clinically significant bronchiolitis. Infants that are breastfed with colostrum rich in immunoglobulin A appear relatively protected from bronchiolitis.

source : emedicine.medscape.com

Atelectasis

The term atelectasis is derived from the Greek words ateles and ektasis, which mean incomplete expansion. Atelectasis is defined as diminished volume affecting all or part of a lung. Pulmonary atelectasis is one of the most commonly encountered abnormalities in chest radiology findings. Recognizing an abnormality due to atelectasis on chest x-ray films can be crucial to understanding the underlying pathology. Several types of atelectasis exist; each has a characteristic radiographic pattern and etiology. Atelectasis is divided physiologically into obstructive and nonobstructive causes.

Obstructive atelectasis

Obstructive atelectasis is the most common type and results from reabsorption of gas from the alveoli when communication between the alveoli and the trachea is obstructed. The obstruction can occur at the level of the larger or smaller bronchus. Causes of obstructive atelectasis include foreign body, tumor, and mucous plugging. The rate at which atelectasis develops and the extent of atelectasis depend on several factors, including the extent of collateral ventilation that is present and the composition of inspired gas. Obstruction of a lobar bronchus is likely to produce lobar atelectasis; obstruction of a segmental bronchus is likely to produce segmental atelectasis. Because of the collateral ventilation without a lobe or between segments, the pattern of atelectasis often depends on collateral ventilation, which is provided by the pores of Kohn and the canals of Lambert.

Nonobstructive atelectasis

Nonobstructive atelectasis can be caused by loss of contact between the parietal and visceral pleurae, compression, loss of surfactant, and replacement of parenchymal tissue by scarring or infiltrative disease. Examples of nonobstructive atelectasis are described below.
Relaxation or passive atelectasis results when a pleural effusion or a pneumothorax eliminates contact between the parietal and visceral pleurae. Generally, the uniform elasticity of a normal lung leads to preservation of shape even when volume is decreased. The different lobes also function differently, eg, the middle and lower lobes collapse more than the upper lobe in the presence of pleural effusion, while the upper lobe may be affected more by pneumothorax.
Compression atelectasis occurs from any space-occupying lesion of the thorax compressing the lung and forcing air out of the alveoli. The mechanism is similar to relaxation atelectasis.
Adhesive atelectasis results from surfactant deficiency. Surfactant normally reduces the surface tension of the alveoli, thereby decreasing the tendency of these structures to collapse. Decreased production or inactivation of surfactant leads to alveolar instability and collapse. This is observed particularly in acute respiratory distress syndrome (ARDS) and similar disorders.
Cicatrization atelectasis results from diminution of volume as a sequela of severe parenchymal scarring and is usually caused by granulomatous disease or necrotizing pneumonia. Replacement atelectasis occurs when the alveoli of an entire lobe are filled by tumor (eg, bronchioalveolar cell carcinoma), resulting in loss of volume.

Right middle lobe syndrome

Right middle lobe syndrome is a disorder of recurrent or fixed atelectasis involving the right middle lobe and/or lingula. It can result from either extraluminal (bronchial compression by surrounding lymph nodes) or by intraluminal bronchial obstruction. It may develop in the presence of a patent lobar bronchus without identifiable obstruction. Inflammatory processes and defects in the bronchial anatomy and collateral ventilation have been designated as the nonobstructive causes of middle lobe syndrome.^[1]Timely medical intervention in patients (especially children) with middle lung syndrome, including fiberoptic bronchoscopy with bronchoalveolar lavage, prevents bronchiectasis that may be responsible for recurrent infections and an ultimately unfavorable outcome of chronic atelectasis.^[2]
Middle lobe syndrome has been reported as a pulmonary manifestation of primary Sjögren syndrome. Transbronchial biopsies performed in such patients revealed lymphocytic bronchiolitis in the atelectatic lobes. Atelectasis responds well to glucocorticoid treatment, suggesting that the peribronchiolar lymphocytic infiltrates may play an important role in the development of middle lobe syndrome in these patients.^[3]

Rounded atelectasis

Rounded atelectasis represents folded atelectatic lung tissue with fibrous bands and adhesions to the visceral pleura. Incidence is high in asbestos workers (65-70% of cases), most likely due to a high degree of pleural disease. Affected patients typically are asymptomatic, and the mean age at presentation is 60 years.

Pathophysiology

The mechanism of obstructive and nonobstructive atelectasis is quite different and is determined by several factors.

Obstructive atelectasis

Following obstruction of a bronchus, the circulating blood absorbs the gas in the peripheral alveoli, leading to retraction of the lung and an airless state within a few hours. In the early stages, blood perfuses the airless lung; this results in ventilation-perfusion mismatch and arterial hypoxemia. A filling of the alveolar spaces with secretions and cells may occur, thereby preventing complete collapse of the atelectatic lung. The uninvolved surrounding lung tissue distends, displacing the surrounding structures. The heart and mediastinum shift toward the atelectatic area, the diaphragm is elevated, and the chest wall flattens.
If the obstruction is removed, any complicating postobstructive infection subsides and the lung returns to its normal state. If the obstruction is persistent and infection continues to be present, fibrosis develops and the lung becomes bronchiectatic.

Nonobstructive atelectasis

The loss of contact between the visceral and parietal pleurae is the primary cause of nonobstructive atelectasis. A pleural effusion or pneumothorax causes relaxation or passive atelectasis. Pleural effusions affect the lower lobes more commonly than pneumothorax, which affects the upper lobes. A large pleural-based lung mass may cause compression atelectasis by decreasing lung volumes.
Adhesive atelectasis is caused by a lack of surfactant. The surfactant has phospholipid dipalmitoyl phosphatidylcholine, which prevents lung collapse by reducing the surface tension of the alveoli. Lack of production or inactivation of surfactant, which may occur in ARDS, radiation pneumonitis, and blunt trauma to the lung, cause alveolar instability and collapse.
Middle lobe syndrome (recurrent atelectasis and/or bronchiectasis involving the right middle lobe and/or lingula) has recently been reported as the pulmonary manifestation of primary Sjögren syndrome.
Scarring of the lung parenchyma leads to cicatrization atelectasis.
Replacement atelectasis is caused by filling of the entire lobe by a tumor such as bronchoalveolar carcinoma.

Platelike atelectasis

Also called discoid or subsegmental atelectasis, this type is seen most commonly on chest radiographs. Platelike atelectasis probably occurs because of obstruction of a small bronchus and is observed in states of hypoventilation, pulmonary embolism, or lower respiratory tract infection. Small areas of atelectasis occur because of inadequate regional ventilation and abnormalities in surfactant formation from hypoxia, ischemia, hyperoxia, and exposure to various toxins. A mild-to-severe gas exchange abnormality may occur because of ventilation-perfusion mismatch and intrapulmonary shunt.

Postoperative atelectasis

Atelectasis is a common pulmonary complication in patients following thoracic and upper abdominal procedures. General anesthesia and surgical manipulation lead to atelectasis by causing diaphragmatic dysfunction and diminished surfactant activity. The atelectasis is typically basilar and segmental in distribution. After induction of anesthesia, atelectasis increases from 1 to 11% of total lung volume. End-expiratory lung volume is also found to be decreased.
In 2009 study, a recruitment maneuver plus positive end-expiratory pressure (PEEP) reduced atelectasis to 3 ±4%, increased end-expiratory lung volume, and increased the PaO₂/FiO₂ ratio from 266 ±70 mm Hg to 412 ±99 mm Hg. It was found that the PEEP alone did not reduce the amount of atelectasis or improve oxygenation, but a recruitment maneuver followed by PEEP reduced atelectasis and improved oxygenation

Aortic Coarctation

Coarctation of the aorta is a narrowing of the aorta most commonly found just distal to the origin of the left subclavian artery. Most patients with coarctation have juxtaductal coarctation. Older terms, such as preductal (infantile-type) or postductal (adult-type), are often misleading.

Pathophysiology

The vascular malformation responsible for coarctation is a defect in the vessel media, giving rise to a prominent posterior infolding (the "posterior shelf"), which may extend around the entire circumference of the aorta. The gross pathology of coarctation varies considerably. The lesion is often discrete but may be long, segmental, or tortuous in nature.

Histology

The coarctated aortic segment reveals an intimal and medial lesion consisting of thickened ridges that protrude posteriorly and laterally into the aortic lumen. The ductus (ie, patent embryonic remnant) or ligamentum arteriosus (closed and fibrosed) inserts at the same level anteromedially. Intimal proliferation and disruption of elastic tissue may occur distal to the coarctation. At this site, infective endarteritis, intimal dissections, or aneurysms may occur. Cystic medial necrosis occurs commonly in the aorta adjacent to the coarctation site and acts as a substrate for late aneurysm formation or aortic dissection in some patients.

Embryology

Coarctation is due to an abnormality in development of the embryologic left fourth and sixth aortic arches that can be explained by 2 theories, the ductus tissue theory and the hemodynamic theory.
In the ductus tissue theory, coarctation develops as the result of migration of ductus smooth muscle cells into the periductal aorta, with subsequent constriction and narrowing of the aortic lumen. Commonly, coarctation becomes clinically evident with closure of the ductus arteriosus. This theory does not explain all cases of coarctation. Clinically, coarctation may occur in the presence of a widely patent ductus arteriosus, and it may occur quite distant from the insertion of the ductus arteriosus, such as in the transverse arch or abdominal aorta.
In the hemodynamic theory, coarctation results from reduced volume of blood flow through the fetal aortic arch and isthmus. In a normal fetus, the aortic isthmus receives a relatively low volume of blood flow. Most of the flow to the descending aorta is derived from the right ventricle through the ductus arteriosus. The left ventricle supplies blood to the ascending aorta and brachiocephalic arteries, and a small portion goes to the aortic isthmus. The aortic isthmus diameter is 70-80% of the diameter of the neonatal ascending aorta.
Based on this theory, lesions that diminish the volume of left ventricular outflow in the fetus also decrease flow across the aortic isthmus and promote development of coarctation. This helps to explain the common lesions associated with coarctation, such as ventricular septal defect, bicuspid aortic valve, left ventricular outflow obstruction, and tubular hypoplasia of the transverse aortic arch. This theory does not explain isolated coarctation without associated intracardiac lesions.

source : emedicine.medscape.com

Heart Failure

Posted on Sabtu, 23 April 2011

Signs and symptoms of heart failure include tachycardia and manifestations of venous congestion (eg, edema) and low cardiac output (eg, fatigue). Breathlessness, a cardinal symptom of left ventricular (LV) failure, may manifest with progressively increasing severity. (See Clinical Presentation.)
Heart failure can be classified according to a variety of factors. The New York Heart Association (NYHA) classification for heart failure is based on the relation between symptoms and the amount of effort required to provoke them, and The American College of Cardiology/American Heart Association (ACC/AHA) heart failure guidelines complement the NYHA classification to reflect the progression of disease.

Pathophysiology

The common pathophysiologic state that perpetuates the progression of heart failure is extremely complex, regardless of the precipitating event. Compensatory mechanisms exist on every level of organization, from subcellular all the way through organ-to-organ interactions. Only when this network of adaptations becomes overwhelmed does heart failure ensue.
Most important among the adaptations are the Frank-Starling mechanism, in which an increased preload helps to sustain cardiac performance; alterations in myocyte regeneration and death; myocardial hypertrophy with or without cardiac chamber dilatation, in which the mass of contractile tissue is augmented; and activation of neurohumoral systems. The release of norepinephrine by adrenergic cardiac nerves augments myocardial contractility and includes activation of the renin-angiotensin-aldosterone system [RAAS], the sympathetic nervous system [SNS], and other neurohumoral adjustments that act to maintain arterial pressure and perfusion of vital organs.
In acute heart failure, the finite adaptive mechanisms that may be adequate to maintain the overall contractile performance of the heart at relatively normal levels become maladaptive when trying to sustain adequate cardiac performance.
The primary myocardial response to chronic increased wall stress is myocyte hypertrophy, death/apoptosis, and regeneration.^[1]This process eventually leads to remodeling, usually the eccentric type. Eccentric remodeling further worsens the loading conditions on the remaining myocytes and perpetuates the deleterious cycle. The idea of lowering wall stress to slow the process of remodeling has long been exploited in treating heart failure patients.^[2]
The reduction of cardiac output following myocardial injury sets into motion a cascade of hemodynamic and neurohormonal derangements that provoke activation of neuroendocrine systems, most notably the above-mentioned adrenergic systems and RAAS.
The release of epinephrine and norepinephrine, along with the vasoactive substances endothelin-1 (ET-1) and vasopressin, causes vasoconstriction, which increases afterload and, via an increase in cyclic adenosine monophosphate (cAMP), causes an increase in cytosolic calcium entry. The increased calcium entry into the myocytes augments myocardial contractility and impairs myocardial relaxation (lusitropy).
The calcium overload may induce arrhythmias and lead to sudden death. The increase in afterload and myocardial contractility (known as inotropy) and the impairment in myocardial lusitropy lead to an increase in myocardial energy expenditure and a further decrease in cardiac output. The increase in myocardial energy expenditure leads to myocardial cell death/apoptosis, which results in heart failure and further reduction in cardiac output, perpetuating a cycle of further increased neurohumoral stimulation and further adverse hemodynamic and myocardial responses.
In addition, the activation of the RAAS leads to salt and water retention, resulting in increased preload and further increases in myocardial energy expenditure. Increases in renin, mediated by decreased stretch of the glomerular afferent arteriole, reduce delivery of chloride to the macula densa and increase beta1-adrenergic activity as a response to decreased cardiac output. This results in an increase in angiotensin II (Ang II) levels and, in turn, aldosterone levels, causing stimulation of the release of aldosterone. Ang II, along with ET-1, is crucial in maintaining effective intravascular homeostasis mediated by vasoconstriction and aldosterone-induced salt and water retention.
The concept of the heart as a self-renewing organ is a relatively recent development.^[3]This new paradigm for myocyte biology has created an entire field of research aimed directly at augmenting myocardial regeneration.
The rate of myocyte turnover has been shown to increase during times of pathologic stress.^[1]In heart failure, this mechanism for replacement becomes overwhelmed by an even faster increase in the rate of myocyte loss. This imbalance of hypertrophy and death over regeneration is the final common pathway at the cellular level for the progression of remodeling and heart failure.

Ang II

Research indicates that local cardiac Ang II production (which decreases lusitropy, increases inotropy, and increases afterload) leads to increased myocardial energy expenditure. Ang II has also been shown in vitro and in vivo to increase the rate of myocyte apoptosis.^[4]In this fashion, Ang II has similar actions to norepinephrine in heart failure.
Ang II also mediates myocardial cellular hypertrophy and may promote progressive loss of myocardial function. The neurohumoral factors above lead to myocyte hypertrophy and interstitial fibrosis, resulting in increased myocardial volume and increased myocardial mass, as well as myocyte loss. As a result, the cardiac architecture changes, which, in turn, leads to further increase in myocardial volume and mass.

Myocytes and myocardial remodeling

In the failing heart, increased myocardial volume is characterized by larger myocytes approaching the end of their life cycle. As more myocytes drop out, an increased load is placed on the remaining myocardium, and this unfavorable environment is transmitted to the progenitor cells responsible for replacing lost myocytes. Progenitor cells become progressively less effective as the underlying pathologic process worsens and myocardial failure accelerates. These features, namely the increased myocardial volume and mass, along with a net loss of myocytes, are the hallmark of myocardial remodeling. This remodeling process leads to early adaptive mechanisms, such as augmentation of stroke volume (Starling mechanism) and decreased wall stress (Laplace mechanism), and later, to maladaptive mechanisms, such as increased myocardial oxygen demand, myocardial ischemia, impaired contractility, and arrhythmogenesis.
As heart failure advances, there is a relative decline in the counterregulatory effects of endogenous vasodilators, including nitric oxide (NO), prostaglandins (PGs), bradykinin (BK), atrial natriuretic peptide (ANP), and B-type natriuretic peptide (BNP). This occurs simultaneously with the increase in vasoconstrictor substances from the RAAS and the adrenergic system. This fosters further increases in vasoconstriction and thus preload and afterload, leading to cellular proliferation, adverse myocardial remodeling, and antinatriuresis, with total body fluid excess and worsening heart failure (HF) symptoms.

Systolic and diastolic failure

Systolic and diastolic heart failure each result in a decrease in stroke volume. This leads to activation of peripheral and central baroreflexes and chemoreflexes that are capable of eliciting marked increases in sympathetic nerve traffic. While there are commonalities in the neurohormonal responses to decreased stroke volume, the neurohormone-mediated events that follow have been most clearly elucidated for individuals with systolic heart failure. The ensuing elevation in plasma norepinephrine directly correlates with the degree of cardiac dysfunction and has significant prognostic implications. Norepinephrine, while directly toxic to cardiac myocytes, is also responsible for a variety of signal-transduction abnormalities, such as down-regulation of beta1-adrenergic receptors, uncoupling of beta2-adrenergic receptors, and increased activity of inhibitory G-protein. Changes in beta1-adrenergic receptors result in overexpression and promote myocardial hypertrophy.

ANP and BNP

ANP and BNP are endogenously generated peptides activated in response to atrial and ventricular volume/pressure expansion. ANP and BNP are released from the atria and ventricles, respectively, and both promote vasodilation and natriuresis. Their hemodynamic effects are mediated by decreases in ventricular filling pressures, owing to reductions in cardiac preload and afterload. BNP, in particular, produces selective afferent arteriolar vasodilation and inhibits sodium reabsorption in the proximal convoluted tubule. BNP inhibits renin and aldosterone release and, therefore, adrenergic activation as well. ANP and BNP are elevated in chronic heart failure. BNP, in particular, has potentially important diagnostic, therapeutic, and prognostic implications.
For more information, see Natriuretic Peptides in Congestive Heart Failure.

Other vasoactive systems

Other vasoactive systems that play a role in the pathogenesis of heart failure include the ET receptor system, the adenosine receptor system, vasopressin, and tumor necrosis factor-alpha (TNF-alpha). ET, a substance produced by the vascular endothelium, may contribute to the regulation of myocardial function, vascular tone, and peripheral resistance in heart failure. Elevated levels of ET-1 closely correlate with the severity of heart failure. ET-1 is a potent vasoconstrictor and has exaggerated vasoconstrictor effects in the renal vasculature, reducing renal plasma blood flow, glomerular filtration rate (GFR), and sodium excretion.
TNF-alpha has been implicated in response to various infectious and inflammatory conditions. Elevations in TNF-alpha levels have been consistently observed in heart failure and seem to correlate with the degree of myocardial dysfunction. Experimental studies suggest that local production of TNF-alpha may have toxic effects on the myocardium, thus worsening myocardial systolic and diastolic function.
Thus, in individuals with systolic dysfunction, the neurohormonal responses to decreased stroke volume result in temporary improvement in systolic blood pressure and tissue perfusion. However, in all circumstances, the existing data support the notion that these neurohormonal responses contribute to the progression of myocardial dysfunction in the long term.

Heart failure with normal ejection fraction

In diastolic heart failure (heart failure with normal ejection fraction [HFNEF]), the same pathophysiologic processes leading to decreased cardiac output that occur in systolic heart failure also occur, but they do so in response to a different set of hemodynamic and circulatory environmental factors that depress cardiac output.
In HFNEF, altered relaxation, and increased stiffness of the ventricle (due to delayed calcium uptake by the myocyte sarcoplasmic reticulum and delayed calcium efflux from the myocyte) occur in response to an increase in ventricular afterload (pressure overload). The impaired relaxation of the ventricle leads to impaired diastolic filling of the left ventricle (LV).

LV chamber stiffness

An increase in LV chamber stiffness occurs secondary to any one of the following 3 mechanisms or to a combination thereof:

Rise in filling pressure
Shift to a steeper ventricular pressure-volume curve
Decrease in ventricular distensibility

A rise in filling pressure is the movement of the ventricle up along its pressure-volume curve to a steeper portion, as may occur in conditions such as volume overload secondary to acute valvular regurgitation or acute LV failure due to myocarditis.
A shift to a steeper ventricular pressure-volume curve results most commonly not only from increased ventricular mass and wall thickness, as observed in aortic stenosis and long-standing hypertension, but also from infiltrative disorders (eg, amyloidosis), endomyocardial fibrosis, and myocardial ischemia.
Parallel upward displacement of the diastolic pressure-volume curve is generally referred to as a decrease in ventricular distensibility. This is usually caused by extrinsic compression of the ventricles.

Concentric LV hypertrophy

Whereas volume overload, as observed in chronic aortic and/or mitral valvular regurgitant disease, shifts the entire diastolic pressure-volume curve to the right, indicating increased chamber stiffness, pressure overload that leads to concentric LV hypertrophy (LVH, as occurs in aortic stenosis, hypertension, and hypertrophic cardiomyopathy) shifts the diastolic pressure-volume curve to the left along its volume axis so that at any diastolic volume ventricular diastolic pressure is abnormally elevated, although chamber stiffness may or may not be altered. Increases in diastolic pressure lead to increased myocardial energy expenditure, remodeling of the ventricle, increased myocardial oxygen demand, myocardial ischemia, and eventual progression of the maladaptive mechanisms of the heart that lead to decompensated heart failure.

Arrhythmias

While life-threatening rhythms are more common in ischemic versus nonischemic cardiomyopathy, arrhythmia imparts a significant burden in all forms of heart failure. In fact, some arrhythmias even perpetuate heart failure. The most significant of all rhythms associated with heart failure are the life-threatening ventricular arrhythmias. Structural substrates for ventricular arrhythmias common in heart failure, regardless of the underlying cause, include the following:

Ventricular dilatation
Myocardial hypertrophy
Myocardial fibrosis

At the cellular level, myocytes may be exposed to increased stretch, wall tension, catecholamines, ischemia, and electrolyte imbalance. The combination of these factors contributes to an increased incidence of arrhythmogenic sudden cardiac death in patients with heart failure.

source : emedicine.medscape.com

Asthma

Posted on Jumat, 22 April 2011

Asthma is a chronic condition in your lungs that has two main components. When you have asthma, two things happen inside your lungs --- constriction, the tightening of the muscles surrounding the airways, and inflammation, the swelling and irritation of the airways. Constriction and inflammation cause narrowing of the airways, which may result in symptoms such as wheezing, coughing, chest tightness, or shortness of breath. Furthermore, there is increasing evidence that, if left untreated, asthma can cause long-term loss of lung function.
When you have asthma and are exposed to a trigger, the airways leading to the lungs become more inflamed or swollen than usual, making it harder for you to breathe. The airways also get smaller due to a tightening of the muscles surrounding the airways, and they get "stuffed up" due to a build-up of mucus.

Several triggers can cause your asthma symptoms to flare up, and may include allergies, infections, and strong odors or fumes that you may come in contact with at your home or office. Once you are exposed to a trigger and have a reaction, your airways also become more sensitive to other triggers. So, it's important to manage your asthma every day. Airway inflammation may always be there ---even when you are not having a lot of symptoms.
Prevalence of asthma
Seventeen million Americans, five million of them children have asthma. The incidence has increased over 50% in the last fifteen years. There are over five hundred thousands hospitalizations each year, making asthma on of the top five most expensive diseases our healthcare system must cover.
Despite the prevalence, however, asthma can be controlled. Our goal, almost universally met, is that every patient enjoys a completely full life without any limitations. With understanding of the disease process and of the various medications available, patients should be able to meet this goal. Education and record keeping are key to achieving this goal.
Categorizing Asthma
Asthma is often put into categories or groups based on the "triggers" that cause the asthma symptoms or attacks. These categories or types of asthma are:
Allergic asthma
Allergic asthma is triggered by an allergic reaction to allergens such as pollens or pet dander. People with this type of asthma typically have a personal and/or family history of allergies (such as hay fever) and/or eczema (skin problem resulting in itching, a red rash, and sometimes small blisters).
Seasonal asthma

Tree pollen, grass pollen, molds spores or flowers releasing pollen can all be triggers of seasonal asthma. For example, some people find that their asthma is worse in the spring when there is an increase in flowering plants. Others find their asthma is worse in the late summer or early fall when ragweed and leaves from trees are more likely to cause problems. With careful attention and a calendar, it is simple to identify a root cause of one's asthma without the need for painful skin testing.
Non-allergic asthma
For some people with asthma, asthma attacks have nothing to do with allergies. Although these people get the same symptoms and have the same changes in their airways as patients with allergic asthma, their asthma is not triggered by allergies. Like any patient with asthma, however, asthma attacks may be triggered or made

worse by one or more non-allergic asthma triggers including materials (irritants) in the air you breathe, such as tobacco smoke, wood smoke, room deodorizers, pine odors, fresh paint, household cleaning products, cooking odors, workplace chemicals, perfumes, and outdoor air pollution. Respiratory infections, such as the common cold, Influenza, or a sinus infection may also give you symptoms. Finally, exercise, cold air, sudden changes in air temperature, and even gastro esophageal reflux (heartburn) may be triggers for people with non-allergic asthma.
Exercise-induced asthma

Exercise-induced asthma (EIA) simply refers to asthma symptoms that are triggered by exercise or physical activity. These symptoms are usually noticed during or shortly after exercise. Exercising in the winter seems to be particularly bad for patients with this type of asthma as cold air and sudden changes in the temperature of the air one breathes are normally found at this time of year.
Nocturnal asthma
Can occur in a patient with any type of asthma. It refers to asthma symptoms that seem worse in the middle of the night, typically between 2 and 4 AM.
Things that can cause asthma symptoms to get worse at night may include sinus infections or postnasal drip caused by allergens like dust mites or pet dander. Your body clock may also play some role: levels of substances your body makes like adrenaline and steroids, both of which protect against asthma, are lowest between 4 and 8 AM, making it easier for people with asthma to get symptoms during these times of the night.

From: www.healthcaresouth.com/pages/asthmadef.htm