Downloaded 118 times
Uploaded byJumatil Fajar
Patologi Sistem Pernapasan (1)
Dokumen tersebut membahas tentang patologi sistem pernapasan khususnya tentang emfisema dan bronkitis kronik. Emfisema disebabkan oleh kerusakan serat elastik paru-paru yang menyebabkan hilangnya kemampuan mengembang sehingga jalan napas kecil kolaps selama ekspirasi. Bronkitis kronik ditandai dengan batuk kronis dan produksi sputum yang disebabkan oleh iritasi kronis pada bronkus akibat merokok.
More Related Content
Similar to Patologi Sistem Pernapasan (1)
![[KP 2.2.4.2] Hemoptisis Masif, Emboli Paru, Infark Paru.pptx](https://cdn.slidesharecdn.com/ss_thumbnails/kp2-230729001217-adc1ea41-thumbnail.jpg?width=640&height=640&fit=bounds)
Patologi Sistem Pernapasan (1)
- 1. Patologi Sistem Pernapasan (1) EdFriedlander, M.D., Pathologist
- 2.
- 3. • Tromboemboli parusering terjadi. • Trombi pada arteri paru yang tidak bisa dioperasi hampir selalu emboli. • Paling sering berasal dari vena dalam dari tungkai; mereka juga mungkin berasal dari vena pelvis, jarang sekali berasal dari sinus dura otak besar atau tempat-tempat lain • Trombosis pada vena tungkai sangat tidak nyaman (“tromboflebitis”), tetapi seringkali tanpa gejala. Sebagai seorang mahasiswa, anda akan membandingkan sirkumferensi betis, memeriksa tanda Homan (hati-hati jangan sampai menghancurkan trombus), dan lain-lain
- 4. • Seringkali tromboemboliparu tidak berbahaya dan kadang-kadang membentuk sesuatu atau hancur; sebagiannya mematikan. • Trias Virchow. Aturan khas untuk trombosis vena dalam dan tromboemboli paru meliputi: • Stasis karena imobilisasi dari ekstremitas; gagal jantung kongestif kanan; anemia sel sabit; obesitas • Status hiperkoagulasi karena kanker; setelah luka bakar; pembedahan, trauma berat; kehamilan; wanita yang menggunakan pil kontrasepsi oral dengan kandung estrogen tinggi; antikoagulan lupus, defisiensi antikoagulan herediter (S protein, C protein, antitrombin III, V-leiden, homosistein); perokok dan jangan lupa sindrom nefrotik, dimana pasien kehilangan kehilangan potein S dan C dalam urin mereka
- 5. • Kerusakan endotel:pemasangan infus, kadang-kadang kateter CVP bertindak sebagai nidus bagi sebuah trombus yang mengalami embolisasi. • Tidak seorang pun tahu mengapa – bayi jarang sekali meninggal karena tromboemboli paru
- 6. Tromboemboli paru menyebabkan •Kematian mendadak (“embolus sadel” menyumbat batang paru-paru dan/atau ketua arteri utama paru-paru) • “Cor pulmonale” akut (mungkin; hal ini biasanya mengharuskan penutupan 50% atau lebih dari batang arteri pulmonaris) • Peningkatan “ruang mati” paru-paru yang tidak diperfusi; bila cukup banyak paru-paru menjadi ruang mati dan sisanya menyerima seluruh darah dari jantung, maka tidak cukup oksigen disini dan hipoksemia akan terjadi • Iskemia karena kehilangan surfaktan dan kolaps alveoli (atelektasis; kadang-kadang)
- 7. Tromboemboli paru menyebabkan •Infark aktual dari bahan paru karena embolus paru dapat terjadi jika sirkulasi bronkus tidak adekuat karena gagal jantung kiri, syok, dan lain-lain • Bronkokonstriksi dan mengi (kadang-kadang, mungkin karena pengeluaran serotonin dari trombosit) • Embolisasi kronik mengakibatkan peningkatan resistensi pembuluh darah paru (“hipertensi paru”) dan kadang-kadang “cor-pulmonale”
- 8. • Setiap pasiendengan cemas, nyeri dada, sesak batuk, hemoptisis mendadak atau kematian mendadak harus membuat anda berpikir tentang emboli paru • Angiografi adalah standar emas saat pasien masih hidup • Emboli paru berubah menjadi pita-pita fibrosa yang tetap di paru seumur hidup seseorang.
- 9.
- 10.
- 11.
- 12.
- 13.
- 14.
- 15.
- 16.
- 17.
- 18.
- 19.
- 20.
- 21.
- 22.
- 23.
- 24.
- 26. •Penyakit paru obstruktifkronik (PPOK) adalah pengelompokkan tradisional dan tidak terlalu membantu dari empat penyakit berikut: • Bronkitis kronik • Emfisema • Asma • Bronkiektasis
- 27. •COPD meliputi duapenyakit yang sangat sering terjadi yang biasanya terjadi secara bersama- sama akibat merokok yaitu : •Bronkitis kronik •Emfisema
- 28. Bronkitis Kronik •Menyebabkan obstruksipada aliran udara karena udem, nekrosis, fibrosis, dan infeksi berulang dalam batang bronkus •Dinding menjadi lebih tebal dan hal ini mempersempit lubang bronkus •Meskipun penyempitan lubang bronkus mengganggu pernapasan, biasanya keparahan emfisema yang benar-benar membuat orang ini menjadi cacat
- 29. •Lingkaran setan darikolonisasi bakteri, infeksi, dan kerusakan mungkin berperan dalam perkembangan penyakit •Peningkatan sekresi mukus dan hiperplasia dari kelenjar yang mengeluarkan mukus oleh diri mereka sendiri, meskipun khas untuk bronkitis kronis, sekarang diketahui bahwa mereka tidak berkontribusi secara berarti terhadap obstruksi
- 30. Emfisema •Menyebabkan obstruksi aliranudara karena kehilangan elastisitas rekoil yang menyebabkan saluran udara kecil menjadi tertutup saat awal dari ekspirasi. •Kita semua kehilangan sebagian elastisitas ketika kita tua, tapi perokok dan orang-orang kekurangan alfa-1 antritripsin kehilangan lebih banyak, dan juga memiliki beberapa kerusakan dari septa mereka, yang bukan merupakan bagian normal dari penuaan.
- 31. •Baik emfisema danbronkitis kronis paling sering disebabkan oleh menghisap rokok. Sebagian besar perokok yang memiliki salah satu penyakit, juga memiliki penyakit lainnya.
- 32. Perokok harus bersiap-siapuntuk: •Pigmen rokok di paru-paru •Pigmen karbon di paru-paru •Kehilangan motilitas silier •Perkembangan sel goblet pada epitel kolumnar yang tersisa
- 33. Perokok harus bersiap-siapuntuk: •Hipertrofi dan hiperplasia dari kelenjar mukus dalam bronki, dengan mukus yang lebih banyak, plus peradangan dalam lamina propria kebawah melalui bronkiolus terminal. Hal ini menyebabkan terjadi penularan kapasitas ventilasi maksimum segera setelah merokok dimulai
- 34. Perokok harus bersiap-siapuntuk: •Penebalan membran basalis epitel pernapasan •Peningkatan jumlah neutrofil di dalam paru-paru •Peningkatan jumlah makrofag alveoli •Rusaknya kemampuan makrofag alveoli untuk berfungsi dengan baik •Meningkatnya produksi dan pelepasan elastase neutrofil dan makrofag
- 36. Perokok harus bersiap-siapuntuk: •Hilangnya elastisitas dari dinding alveoli •Kemungkinan kerusakan dinding alveoli •Metaplasia skuamosa dari epitel pernapasan
- 38.
- 39.
- 40. Emfisema sentriasinar / emfisemaasinar distal
- 41.
- 42.
- 43.
- 44.
- 45.
- 46. Emfisema – “goodblebs” (lepuh yang bagus)
- 47.
- 48.
- 49.
- 50.
- 51.
- 52. History of Illness •A 71 year old man, who had smoked 40 cigarettes per day throughout his adult life, had a history of "chest trouble" for 40-50 years. Three days before his death, he developed increasing cough with yellow phlegm (sputum) and shortness of breath. At autopsy, the bronchi showed advanced changes of chronic bronchitis. There was left lower lobe pneumonia, while the right lung had obvious destruction of air sac walls (emphysema), the middle lobe being transformed into an air cyst. The heart showed right ventricular wall enlargement (8 mm thick, normal is up to 5 mm).
- 53. This specimen shows a smoker's lung with cystic spaces (emphyse ma)due to destruction of airsac
- 54. •Ahli anatomi kunomendefinisikan “emfisema” sebagai dilatasi sebagian dari asinus yang permanen, dengan kerusakan yang mungkin terjadi dari beberapa dinding alveoli. •Anda akan mendiagnosis emfisema pada tes fungsi paru dengan melihat adanya pemanjangan dari waktu yang diperlukan untuk ekspirasi paksa penuh, dengan tidak adanya penyakit asma
- 55. Dua bentuk utamaemfisema •Emfisema sentrilobular (sentiasinar) menunjukkan lebih banyak dilatasi dari bronkioli respiratorius dan alveoli mereka •Biasanya dilihat sebagai emfisema perokok “karena paparan rokok paling berat pada pusat dari acini”. Dan “lebih parah pada lobus superior, karena mereka lebih banyak terpapar rokok”
- 56. •Emfisema panlobular (panasinar)melibatkan asinus secara seragam •Secara tradisional, hal ini disebabkan oleh kekurangan alfa 1-protease inhibitor (“antitripsin”) “karena darah membawa neutrofil ke semua paru secara seragam”. Dan “lebih parah di lobus lebih bawah, karena mereka memiliki lebih banyak darah”
- 57. •Saat penderita emfisemadiautopsi, kerusakan sedemikian parah sehingga anda tidak dapat membuat perbedaan, dan ini bukan sesuatu yang berarti bagi klinisi, radiologi atau pasien.
- 58. Patologinya sangat jelas •Emfisematidak disebabkan oleh udara yang terperangkap di dalam bronkiolus yang meradang (penderita asma tidak menjadi asma dari kondisi tersebut) atau memainkan instrumen musik tiup. •Masalahnya adalah kerusakan serat elastik paru-paru oleh elastase dari netrofil, monosit, kemungkinan pankreas. Tentu saja, merokok sigaret membawa banyak polimorfonukleus ke paru-paru.
- 59. •Kekurangan serum alfa-1-antitripsinadalah kesalahan metabolisme yang mana memperberat emfisema panasinar yang berkembang pada orang yang tidak merokok. •Asap rokok memperkuat elastase, menghambat anti- protease, dan mendukung infeksi dengan jalan melepaskan lebih banyak elastase. Kita tidak tahu mengapa sebagian perokok menderita emfisema yang lebih parah dibandingkan dengan perokok yang lain. •Karena kehilangan kemampuan mengembang, jalan napas yang kecil kolaps selama ekspirasi paksa.
- 60. •Pasien dengan “emfisema”klasik mengalami pink puffer, dengan PaCO2 normal, barrel chest, pursed lips, sesak, napas cepat, kurus (dia bekerja keras sepanjang waktu), kacau. Hasil pemeriksaan fisik yang konsisten hanya melambatnya ekspirasi paksa (“Dapatkah anda meniup korek api pada jarak enam inchi dengan mulut terbuka lebar”)
- 62. •Pink puffers belajaruntuk menjaga agar paru-paru mereka tetap mengembang untuk menjaga agar bronkiolus pernapasan tidak kolaps, dan hal ini membuat perubahan pada bentuk dada itu sendiri (“barrel chest”, “peningkatan diameter anterior posterior”, “peningkatan volume paru-paru total”) •Orang-orang ini tak lama kemudian menderita infeksi paru-paru akibat bakteri, dan mati akibat cor pulmonale, pneumotoraks, atau pneumonia; kurang sering akibat tromboemboli paru
- 63. Emfisema Bulosa •Menghasilkan gelembungberisi udara (jika > 2 cm, anda dapat menyebutnya “bula”) mengandung sedikit atau tidak ada jaringan paru-paru, biasanya di puncak, kadang-kadang di lokasi jaringan parut TB yang sudah lama.
- 64. •Sebagian besar kasusmungkin merupakan hasil dari emfisema yang sering terjadi, dengan paru yang tidak elastis yang “kolaps akibat berat badannya sendiri”; lobus lebih atas memiliki lebih banyak kontak dengan asap rokok karena mereka memiliki ventilasi yang lebih baik. •Gelembung dapat disingkirkan secara pembedahan, yang meringankan hirupan “pink puffers”.
- 65. •Gelembung-gelembung tersebut rentanpecah, menyebabkan pneumothorax dan kematian mendadak.
- 66.
- 67.
- 68. Bentuk-bentuk lain dariemfisema •Kompensasi (misalnya setelah pengeluaran sebuah lobus paru, lobus-lobus lain mengembang; ini salah istilah, karena tidak ada kerusakan alveoli, dan tidak ada kehilangan elastisitas) •“Ireguler” atau “traksional” (misalnya dekat dengan jaringan parut yang tertarik; salah istilah yang lain) •“Tua” (kehilangan elastisitas tanpa kehilangan bahan paru, akibat “umur yang sudah tua).
- 69. Bentuk-bentuk lain dariemfisema (lanjutan) •“Emfisema interstisial” tidak merujuk ke paru-paru. Ini berarti udara dipaksa masuk ke jaringan fibrosa tubuh, seringkali akibat dari robeknya paru itu sendiri (karena emfisema yang sebenarnya, batuk yang parah, respirator, iga patah, trauma tekanan).
- 70.
- 71. •Didefinisikan secara klinissebagai batuk menetap dengan produksi sputum selama paling sedikit tiga bulan selama paling sedikit dua tahun berturut-turut. •Penyebab yang biasa adalah rokok. •Pasien bronkitis kronik klasik adalah “blue bloater”, dengan peningkatan PaCo2, gemuk, udematosa (cor pulmonale), sianosis, menghasilkan banyak sputum, narkosis CO2.
- 72. •Gambaran yang membedakandari pasien ini adalah toleransi yang didapat terhadap hiperkarbia yang disebabkan oleh buruknya ventilasi (misalnya akibat emfisema). •Berbeda dengan “pink puffers” (yang mempertahankan kondisi hiperkarbia mereka), pasien-pasien ini tidak lagi berjuang untuk bernapas, sepanjang mereka mendapatkan oksigen yang memadai
- 73. •Karena ventilasi alveoliyang lebih buruk, hipertensi paru datang lebih dini pada pasien “bronkitis kronik” dibandingkan pasien emfisema. •Pada emfisema, hipertensi paru terjadi terutama karena kerusakan dari pembuluh darah, dengan beberapa atau tanpa lesi proliferatif yang sebenarnya. •Kekambuhan sering terjadi dan menjadi alasan seseorang dirawat dirumah sakit.
- 74. •80% diakibatkan olehinfeksi bakteri atau virus •Bakteri yang paling mematikan adalah Staphylococcus pneumonia dan Hemophilus influenza •Kematian juga disebabkan oleh cor pulmonale atau akibat tidak bernapas yang diakibatkan oleh pemberian oksiten tambahan (ingat, hiperkarbia tidak lagi merangsang pernapasan pada pasien ini). Dosis kecil dari sedatif dapat menghentikan dorongan pernapasan mereka, jadi hati-hatilah.
- 75.
- 76.
- 77.
- 78. •Meskipun sistem pemeriksaanfungsi paru cukup rumit, diagnosis utama dari “COPD” dibuat dengan jalan riwayat penyakit dan pemeriksaan fisik.
- 79.
- 80. •Sindrom yang seringditemukan (10% anak-anak, 5% dewasa) dimana bronki kecil merespon secara tidak normal terhadap berbagai rangsangan yang menyebabkan konstriksi dan/atau peradangan (biasanya keduanya). Hal ini menghasilkan episode sesak, mengi dan batuk. •Faktor sel Mast tampaknya membantu bronkokonstriksi apapun yang mencetuskan serangan
- 81. Serangan asma seringkalidirangsang oleh: •Hipersensitifitas tipe I, dari degranulasi sel mast yang dimediasi IgE yang diakibatkan oleh paparan terhadap polen, kotoran kecoak, dan alergen poten lainnya. •Infeksi virus •Polusi, asap rokok (kami tidak tahu mengapa, tetapi itu sangat potensial; orang tua yang merokok memperburuk asma pada anak), menghirup heroin / kokain
- 82. •“bau yang kuat”(cat basah merangsang sebagian penderita asma) •Aspirin; NSAIDS lain, tartrazine kuning •“Stress” •Reflux asam lambung (“sakit di ulu hati”)
- 83. •Olahraga, terutama dalamudara dingin (saluran udara yang kering dan/atau dingin sekali); perenang kompetisi pada kolam renang yang dihalogenasi adalah kelompok resiko khusus. •Chlamydia dan mycoplasma; terutama Chlamydophila pneumoniae
- 84. • Asma alergiada bila serangan pasien biasanya dicetuskan oleh hipersensitifitas yang dimediasi oleh IgE • Asma idiosinkrasi ada bila serang pasien biasanya dicetuskan oleh paparan terhadap aspirin, inhibitor cyclo-oxygenase lain, dan/atau tratrazine yellow • Apapun penyebabnya, patologi pada asma adalah peradangan dari mukosa bronkus, dengan eosinofil, dan (juga mungkin, sebagai hasil) peningkatan kerentanan dari epitel
- 85. Patologi paru-paru • Gambarankasat mata: arteri pulmonalis pada paru-paru ini telah ditembus oleh campuran putih, campuran barium-gelatin.
- 86.
- 87.
- 88.
- 89.
- 90.
- 91.
- 92.
- 93.
- 94.
- 95.
- 96.
- 97.
- 98.
- 99.
- 100.
- 101.
- 102.
- 103. Mengi juga dapatdisebabkan oleh: •Benda asing atau tumor pada saluran pernapasan bagian atas •Udem paru (terutama pada gagal jantung kongestif kiri) •Embolus paru •Bronkitis kronik •Sindrom karsinoid
- 104.
- 105. •Didefinisikan sebagai dilatasisilindris permanen dan ulkus dari bagian batang bronkus •Gambaran klinis adalah batuk kronik dengan produksi sputum, sampai beberapa cangkir sehari •Dilatasi (“-ektasis”) disebabkan oleh kontraksi dari jaringan parut disekitar bronkus, dan dari sekitar atelektasis.
- 106.
- 107.
- 108.
- 109. Bronkiektasis • Bronkiektasis terjadibila ada sumbatan atau infeksi dengan peradangan dan kerusakan bronki sehinga ada dilatasi permanen. Bila dilatasi ada, sebagaimana terlihat disini secara kasat mata di bagian telah bawah dari paru- paru, pasien memiliki infeksi berulang karena stasis pada saluran napas ini. Produksi sputum purulen dalam jumlah besar saat batuk merupakan hal yang biasa.
- 110.
- 111.
- 112.
- 113.
- 114. • Bronkiektasis memperburukinfeksi pernapasan (berat, atau mereka yang menderita penurunan daya tahan tubuh – ingat AIDS anak- anak), asma, merokok, penyakit keturunan (terutama kistik fibrosis dan diskinesis/imotiliti silier primer, termasuk Kartagener). Jika anda teraspirasi benda asing yang tinggal di sebuah bronkus, anda akan menderita bronkiektasis di daerah tersebut. Saat ini, banyak kasus bersifat idiopatik.
- 116.
- 117. •Sering (1-5% padaorang dewasa, dan sebagian anak- anak), serius, masalah kesehatan yang sudah lama diabaikan, ditandai dengan banyak episode obstruksi saluran pernapasan atas setiap malam •Korban sleep apnea semuanya terkenal suka mengorok (mengorok terkait dengan mengantuk sepanjang harus yang berlebihan dan masalah kualitas hidup lainnya).
- 118. •Sebagian besar kelebihanberat badan (lebih banyak jaringan lemak di saluran pernapasan atas atau memiliki tonsil yang sangat besar atau kelainan rahang. Sebagian besar tidur dengan posisi terlentang. Sebagian besar memiliki “leher tebal” dan/atau banyak minum.
- 119. •Ketika korban mulaimasuk tidur yang dalam, saluran pernapasan bagian atas tertutup, ia meronta, mendengkur, setengah terbangun, membuka kembali saluran napas dengan megap-megap. Siklus ini berulang setiap beberapa menit sepanjang malam, dan pasien tidak pernah tidur nyenyak.
- 120. •Sleep apnea menyebabkansakit kepala dipagi hari, mengantuk sepanjang hari, “narkolepsi”, perubahan sikap dan perilaku, gagal di sekolah dan pekerjaan, “penyakit psikiatri”, perceraian (“dia menolak untuk tidur denganku lebih lama”), “near-miss SIDS”, kematian “jantung” mendadak, snooze angina, hipertensi, dan lain-lain.
- 121. Terapi • Minta pasienuntuk TIDUR PADA SATU SISI • Obat PROTRIPTYLINE membantu otak mempertahankan jalan napas yang utuh • UVULOPALATOPHATYNGOPLASTY (operasi) dan/atau TONSILLECTOMY cukup berguna • MESIN yang menyediakan tekanan jalan napas positif berlanjut bekerja dengan baik pada sebagian besar korban • TRACHEOSTOMY adalah upaya terakhir tetapi menyembuhkan sleep apnea
- 122.
- 123.
- 124.
- 125.
- 126.
- 127.
- 128.
- 129.
- 130.
- 131.
- 132.
- 133. •Jalan napas orangyang tidak merokok secara normal steril dibawah pita suara, tetapi hampir setiap organisme mampu menyebabkan penyakit telah menyebabkan PNEUMONIA, infeksi dari bahan paru- paru. •Bronki perokok cenderung untuk mengandung beberapa Hemofilus influenza dan pneumokoki
- 134. •INFEKSI OLEH BAKTERIYANG SERING TERJADI paling sering menyebabkan eksudasi (cairan udem, lalu neutrofil dan mungkin makrofag) ke dalam rongga alveolus (“saya membatukkan lendir”) •Jika infeksi bakteri terjadi pada sebagian dalam lobus tersendiri, disebut BRONKOPNEUMONIA •Jika bakteri menyebar secara agresif, berhenti hanya pada fisura interlobaris, disebut PNEUMONIA LOBARIS.
- 135.
- 136.
- 137.
- 138.
- 139.
- 140.
- 141.
- 142.
- 143.
- 144. Pneumonia lobaris tengah • Hampirseluruh lobus tengah dari paru-paru kanan ini terlibat dengan abses kronis sebagaimana terlihat dalam potongan ini. Daerah abses berwarna kuning, dan sangat keras. Agen infeksius yang bertanggung jawab disini adalah Nocardia, yang dikenal menghasilkan peradangan yang menghasilkan abses kronik
- 145.
- 146.
- 147.
- 148.
- 149.
- 150.
- 151. • INFEKSI VIRUSDAN MIKOPLASMA paling sering menyebabkan udem ringan di interstisium, dan infiltrasi insterstisium oleh limfosit dan makrofag (“Batuk saya kering”) • TUBERKULOSIS, PNEUMOSISTIS, PNEUMONIA JAMUR memiliki patologi yang berbeda
- 152.
- 153.
- 154.
- 155.
- 156. Fungus ball (Aspergillus) •Ini adalah granuloma jamur yang dihasilkan oleh Aspergillus. Proses infeksi diduga dengan fakta bahwa lesi telah melintasi fisura. Sebuah neoplasma biasanya dibatasi oleh hambatan anatomis. Granuloma ini memiliki tepi yang tidak teratur, berwarna merah dan pusat yang keras dan berwarna orange.
- 157.
- 158.
- 159.
- 160.
- 161.
- 162.
- 163.
- 164.
- 165.
- 166. Aspergilloma paru •Potongan paruini menunjukkan aspergilloma dalam bagian atas dari lobus bawah. Perhatikan dinding fibrosa dan fibrosis parenkim yang meluas ke pleura, yang menebal.
- 167.
- 168.
- 169.
- 170.
- 171.
- 172. Aspergilloma • Bola jamurini melintasi fisura diantara lobus kanan tengah dan kanan bawah, gambaran yang lebih sering ditemukan pada jamur, dibandingkan pada bakteri, pneumonia. Bola jamur adalah massa bundar jaringan paru dikelilingi oleh rongga udara. Parenkim paru didekatnya memiliki lapisan fibrosa tipis.
- 173.
- 174. Hifa bercabang dengan bungkusproteinasea
- 175.
- 176.
- 177.
- 178.
- 179.
- 180.
- 181.
Editor's Notes
- #12 Pulmonary infarct (hemorrhagic infarct of the lung) is an area of ischemic necrosis produced by venous thrombosis on a background of passive congestion of lung. In infarct area, alveolar walls, vascular walls and bronchioles are necrotic. They appear eosinophilic (pink), homogenous, lacking the nuclei, but keep their shapes - "structured necrosis". Alveolar lumens from infarcted area are invaded by red blood cells - hemorrhagic infarct (red). (H&E, ob. x10)
- #13 Pulmonary infarct in an area of passive congestion. The hemosiderin-laden macrophages present inside the alveolar lumen are witnesses of pre-existent passive congestion. (H&E, ob. x20)
- #14 Pulmonary (hemorrhagic) infarct produced by venous thrombosis. (H&E, ob. x10)
- #15 Seen in the pulmonary artery in a left lung on cut section is a large pulmonary thromboembolus. Such thromboemboli typically originate in the leg veins or pelvic veins of persons who are immobilized. Other contributing factors include trauma to the extremities, hypercoagulable states (examples include Trousseaus syndrome in patients with carcinomas; protein C or S deficiency; use of oral contraceptives), heart failure, pregnancy, and older age.
- #16 Large thromboemboli can cause death. Medium sized thrombomboli (blocking a pulmonary artery to a lobule or set of lobules) can produce the lesion seen here--a hemorrhagic pulmonary infarction, because the patient survives. The infarct is wedge-shaped and based on the pleura. These infarcts are hemorrhagic because, though the pulmonary artery carrying most of the blood and oxygen is cut off, the bronchial arteries from the systemic circulation (supplying about 1% of the blood to the lungs) is not cut off.
- #17 Here is a "saddle embolus" that bridges across the pulmonary artery from the heart as it divides into right and left main pulmonary arteries. Such a saddle embolus is a cause for sudden death. This thromboembolus displays the typical gross appearance. The surface is somewhat irregular, and there are areas of pale tan to white admixed with dark red areas. The thrombus often has the outlines of the vein in which it formed.
- #18 Here is a larger area of infarction produced by a medium-sized thromboembolus to the lung. This infarction has begun to organize at the margins.It is also possible to have multiple small pulmonary thromboemboli that do not cause sudden death and do not occlude a large enough branch of pulmonary artery to cause infarction. However, if there are lots of small emboli, particularly if they are showered to the lungs over a period of time, then they collectively may block enough small arteries to produce pulmonary hypertension.
- #19 A closer view of a thromboembolus filling a main pulmonary artery reveals a layered appearance, typical of a thrombus that formed in a large vein of the pelvis or lower extremity.
- #20 Here a thromboembolus is packed into a pulmonary artery. Over time, if the patient survives, the thromboembolus will undergo organization and dissolution.
- #21 Here is a small peripheral pumonary artery thromboembolus. Such a small PE such as this one would probably not be noticed or cause problems unless there were many of them showered into the pulmonary circulation at once or over a period of time. This could lead to pulmonary hypertension.
- #22 The fibrous bands of connective tissue across this branch of pulmonary artery indicate organization of a remote pulmonary thromboembolus. If many pulmonary arteries are involved by this process, pulmonary hypertension could result.
- #24 This is the microscopic appearance of a pulmonary thromboembolus in a large pulmonary artery. There are interdigitating areas of pale pink and red that form the "lines of Zahn" characteristic for a thrombus. These lines represent layers of red cells, platelets, and fibrin which are layed down in the vessel as the thrombus forms.
- #36 I remember this one from the 1950's
- #40 Emphysema is an enlargement of air spaces caused by destruction of alveolar walls. Air spaces greater than one cm are bullae. This photo shows apical bullous disease with relatively little involvement of the rest of the lung.
- #42 This section of centriacinar emphysema shows the enlarged air spaces around a small airway. Respiratory epithelium remains at the arrow. The more peripheral alveoli are normal.
- #43 This photo is taken from a patient with alpha-1-antitrypsin deficiency-related emphysema. It shows an increased number of PMNs in capillaries (arrows and many more) and some alveolar and interstitial blood. These PMNs, if activated, can potentially digest the collagen and elastin of the alveolar wall. Note the megakaryocyte in a capillary (arrowhead at top). Its function is not known, but any contribution of platelets would help to preserve the integrity of the capillary bed.
- #44 Emphysema at 40x MagnificationIn the 1980s, approximately 2 million Americans were known to be afflicted with the chronic respiratory disease emphysema. By the dawn of the twenty-first century that number had ballooned to 3 million. What is perhaps even more disconcerting, however, is that the vast majority of individuals diagnosed with emphysema could have avoided the crippling disease by simply not smoking cigarettes. Similar to most other respiratory ailments, smoking is a key factor in the onset of emphysema, accounting for more than 80 percent of all cases of the disease, which tends to develop gradually as the alveoli of the lungs become increasingly damaged by tobacco smoke. Thus, emphysema most commonly afflicts individuals over the age of 45, many of which began smoking as teenagers.
- #45 Emphysema at 10x MagnificationEmphysema is characterized by a deterioration of the elasticity of the lungs, which results in collapse of the alveolar walls and degeneration of the pulmonary capillaries. Consequently, large pockets of air may fill the lungs, but cannot be readily exhaled because the damage present in the organs hinders them from effectively pushing the air out. Early signs of the disease are breathlessness during physical exertion and a mild, chronic cough. Over time, the condition gets progressively worse, especially among smokers. It may become difficult to obtain enough air even when at rest, interest in eating may decrease because the process is made arduous by breathing problems, and the production of phlegm may become a constant occupation, aggravating the cough. Other common symptoms of emphysema include wheezing, tightness of the chest, intolerance to cold environments, swelling in the extremities, and a bluish hue to the skin related to insufficient exchange of gases. Without treatment, permanent disability can result, as can heart or respiratory failure leading to death
- #46 Emphysema at 20x MagnificationThe damage to the lungs caused by emphysema is irreversible. A successful lung transplant is the closest that a patient with the disease can currently come to a cure, but many individuals that such a procedure could potentially aid are not physically fit enough to undergo it. Accordingly, other, less invasive, treatments for emphysema are much more common. Bronchodilators are often recommended to help combat constriction of the airways, corticosteroids can soothe inflammation, and oxygen therapy is typically provided to individuals in an advanced state of the disease to counteract oxygen deficiency (hypoxemia). Some emphysema patients also elect to undergo lung reduction surgery, a minimally invasive medical procedure that involves only a few small incisions, through which a small camera and stapling device can be inserted so that damaged portions of the lung can be cut away, providing healthy tissue with additional space for expansion.
- #47 The chest cavity is opened at autopsy to reveal numerous large bullaeapparent on the surface of the lungs in a patient dying with emphysema. Bullae are large dilated airspaces that bulge out from beneath the pleura. Emphysema is characterized by a loss of lung parenchyma by destruction of alveoli so that there is permanent dilation of airspaces with loss of elastic recoil.
- #48 On cut section of the lung, the dilated airspaces with emphysema are seen. Although there tends to be some scarring with time because of superimposed infections, the emphysematous process is one of loss of lung parenchyma, not fibrosis. There are two major types of emphysema: centrilobular (centriacinar) and panlobular (panacinar). The former involves primarily the upper lobes while the latter involves all lung fields, particularly the bases. Centrilobular emphysema occurs with loss of the respiratory bronchioles in the proximal portion of the acinus, with sparing of distal alveoli. This pattern is most typical for smokers. Panacinar emphysema occurs with loss of all portions of the acinus from the respiratory bronchiole to the alveoli. This pattern is typical for alpha-1-antitrypsin deficiency.
- #50 This is a more subtle appearance for centrilobular emphysema in which there are "dirty holes" that appear focally where the central portions of lung acini have lost lung parenchyma while collecting anthracotic pigment at the same time. This pattern is typical for smokers.Smokers have a greater number of neutrophils and macrophages in their alveoli. Smoking irritates alveolar macrophages, which in turn release neutrophil chemotactic factors, such as interleukin 8, thus recruiting neutrophils. In addition, nicotine is chemotactic for neutrophils, and smoke can activate the alternative complement pathway (an inflammatory cascade). Proteases, particularly elastase, are secreted by these neutrophils and macrophages. Proteases are enzymes that are capable of digesting lung tissue and these chemicals are responsible for the damage seen in emphysema. Oxidants and free radicals in smoke also inhibit the alpha-1-antitrypsin circulating in the lung that protects alveoli from proteases. Chronic irritation by smoke also can lead to chronic bronchitis with excess production of mucus. Smoke interferes with the ciliary action of the respiratory epithelium and the mucus cannot be cleared. This predisposes the smoker to secondary and repeated infections.
- #51 Microscopically at high magnification, the loss of alveolar walls with emphysema is demonstrated. Remaining airspaces are dilated.
- #52 Gross pathology of lung showing centrilobular emphysema characteristic of smoking. Closeup of fixed, cut surface shows multiple cavities lined by heavy black carbon deposits.
- #54 This lung shows emphysema (dilated air spaces) throughout the whole lung, being gross in a zone about 4 cm wide along the lateral margin, and approximately 2 cm wide along the lower margin. The inner aspect of the lower lobe exhibits considerable destruction of the pulmonary tissue, being replaced by a large cystic cavity (bulla). There is a large amount of black pigment deposited in the lung. This is carbon, derived from tar in cigarette smoke.
- #76 Microscopically, we see thickening of the bronchial basement membrane (seen also in asthma), proliferation of goblet cells, hypertrophy and hyperplasia of mucous glands, more of the various inflammatory cells, more lymphoid aggregates and follicles than usual, and often a considerable amount of scarring (histopathology update on "smoker's small airways disease": NEJM350: 2645, 2004). Even the cartilage may be thinned."Reid index" is ratio of thickness of submucosal mucous glands to entire submucosa. Normal is up to .4; increased in chronic bronchitis.Only in the most severely crippled smokers, we see widespread obliteration of the lumens of the terminal bronchioles (i.e., obstructive bronchiolitis or denser scarring). See below.
- #77 Mucous gland hyperplasia, the histologic correlate of chronic bronchitis is defined as a seromucous gland to wall thickness greater than 1/3. In this case the seromucous gland thickness (arrows) is more than 1/2 of the distance between the perichondrium and the epithelial basement membrane. Note also the goblet cell hyperplasia in the epithelium. The normal percentage of goblet cells is 20%.
- #78 In patients with chronic bronchitis/emphysema, lumens of small airways may be distorted and narrowed by mural smooth muscle hyperplasia, fibrosis, or chronic inflammation and by luminal exudate or mucus. In emphysema, airways tend to collapse because of the loss of alveolar wall supports, as seen here. Mural inflammation and luminal exudate are also shown.
- #86 Consolidation does not account for the fact that the lungs did not collapse when the chest was opened. An obstructive airways disease (chronic bronchitis/bronchiolitis, emphysema, bronchiectasis, or asthma) must be the cause. The airways show thick, mucous plugs. Find at least three of these plugs. (One is just below the center.) The alveolar parenchyma appears normal.The diagnosis is asthma.
- #87 The lung is moderately congested with blood and collapsed, due to absorption of air trapped by obstruction of airways (bronchi and bronchioles). The large and medium-sized bronchioles are thick-walled and they are filled with greyish-white, jelly-like mucus plugs. It is these plugs, rather than spasm of airway muscle, that have caused the partial collapse of the lung, unconsciousness, low arterial oxygen and high carbon dioxide. The blood vessels in the vicinity of the bronchi contain blood clot.
- #88 These lungs appear essentially normal, but are normal-appearing because they are the hyperinflated lungs of a patient who died with status asthmaticus.
- #89 This cast of the bronchial tree is formed of inspissated mucus and was coughed up by a patient during an asthmatic attack. The outpouring of mucus from hypertrophied bronchial submucosal glands, the bronchoconstriction, and dehydration all contribute to the formation of mucus plugs that can block airways in asthmatic patients.
- #90 Between the bronchial cartilage at the right and the bronchial lumen filled with mucus at the left is a submucosa widened by smooth muscle hypertrophy, edema, and inflammation (mainly eosinophils). These are changes of bronchial asthma, more specifically extrinsic asthma from type I hypersensitivity to allergens. The peripheral eosinophil count or the sputum eosinophils can be increased during an asthmatic attack.
- #91 At high magnification, the numerous eosinophils are prominent from their bright red cytoplasmic granules in this case of bronchial asthma. There are two major clinical forms of asthma that can overlap.Extrinsic asthma: there is typically an association with atopy (allergies) mediated by type 1 hypersensitivity, and asthmatic attacks are precipitated by contact with inhaled allergens. This form occurs most often in childhood.Intrinsic asthma: asthmatic attacks are precipitated by respiratory infections, exposure to cold, exercise, stress, inhaled irritants, and drugs such as aspirin. Adults are most often affected.
- #93 Mainly a bronchial disease, asthma is characterized by features in the following 3 images:-Mural inflammation (eosinophils, mast cells, lymphocytes)-Wall thickening by edema, hyperemia, fibrosis-Smooth muscle thickening (arrow)-Mucous plugs-Epithelial slough
- #94 Epithelial hyperplasia, goblet cell metaplasia (most of the epithelial cells here are goblet cells. Normally only 20% of cells should be goblet type)Subepithelial collagenosis ("basement membrane thickening")(arrow)
- #95 Mucous plugs with eosinophils and Charcot-Leyden crystals--bipyramidal hexagons fitted base to base (arrows).
- #96 Mucous plugs with Curschmann's spiral--fuzzy spiraled structures, derived from mucus (Papanicolaou stain).
- #107 Large airways are damaged by chronic inflammation related to obstructing lesions, foreign bodies, or cystic fibrosis. The airway supporting structures--cartilage and smooth muscle are destroyed. Elastic forces of the surrounding normal lung cause airway dilation. Here, the lumen contains pus and the wall is chronically inflamed and fibrotic.
- #108 With bronchiectasis, adjacent small airways are also involved. The walls lose their normal smooth muscle and become scarred, and the lumens become narrowed. This lesion accounts for the airflow obstruction of diffuse bronchiectasis.
- #111 A closer view demonstrates the focal area of dilated bronchi with bronchiectasis. Bronchiectasis tends to be localized with disease processes such as neoplasms and aspirated foreign bodies that block a portion of the airways. Widespread bronchiectasis is typical for patients with cystic fibrosis who have recurrent infections and obstruction of airways by mucus throughout the lungsThe best possible outcome following an inflammatory process is complete resolution, leaving the tissues intact and undamaged. However, chronic inflammation may occur in conjunction with some degree of scarring. Here, chronic inflammation of the bronchi has led todilation and scarring with increased tan to white collagenous tissue.
- #112 Bronchiectasis is seen here. The repeated episodes of inflammation can result in scarring, which has resulted in fibrous adhesionsbetween the lobes. Fibrous pleural adhesions are common in persons who have had past episodes of inflammation of the lung that involve the pleura. With extensive involvement, the pleural space may be obliterated.
- #113 The mid lower portion of this photomicrograph demonstrates a dilated bronchus in which the mucosa and wall is not clearly seen because of the necrotizing inflammation with destruction. This is the microscopic appearance of bronchiectasis. Bronchiectasis is not a specific disease, but a consequence of another disease process that destroys airways.
- #114 This photomicrograph shows a bronchus with increased numbers ofchronic inflammatory cells in the submucosa. Chronic bronchitis does not have characteristic pathologic findings, but is defined clinically as a persistent productive cough for at least three consecutive months in at least two consecutive years. Most patients are smokers. Often, there are features of emphysema as well. Since chronic bronchitis and emphysema often overlap, the term 'chronic obstructive pulmonary disease' (COPD) can be applied.
- #124 Gram-positive diplococci with capsule (haloe) formation, located outside neutrophils
- #125 Irregularly clustered Gram-positive cocci in and outside neutrophils.
- #126 Gram-negative diplococci phagocytized by neutrophils.
- #127 Small-sized, Gram-negative short rods mainly seen outside neutrophils.
- #128 Small-sized, Gram-negative short rods mainly seen outside neutrophils, resembling H. influenzae.
- #129 Large-sized, Gram-negative rods with capsule formation.
- #130 Gram-negative rods floating within mucoid matrices.
- #131 The mucoid matrix of P. aeruginosa is positively stained with colloidal iron.
- #132 A few large-sized rods stained red by carbolfuchsin solution are phagocytized by macrophages.
- #133 Red-stained rods are seen in the cytoplasm of macrophages. Gimenez stain is not specific for Legionella, and a variety of microbes such as H. pylori and rickettsia, are identified with this stain.
- #136 Pneumonia lobaris.
- #137 Pneumonia lobaris
- #142 PneumoniaThe alveoli are filled with inflammatory cells, carbon-layden type I pneumocytes are seen in the center of the field. The carbon is the black stuff in the middle of the field, possibly an old smoker. The white blood cells fighting this infection are polys (PMN's). The polys are the cells that look like clover and have dark-staining nuclei, they are located throughout the field.The alveoli are lined by two types of epithelial cells.TYPE I CELLS: flat cells with large cytoplasmic extensions and are the primary lining cells. These are the cells where the blood/gas exchange takes place.TYPE II CELLS: (granular pneumocytes) are thicker and contain numerous lamellar inclusion bodies. These cells secrete surfactant.The conversion of Type II cells to Type I cells occurs at a rate of about 1 percent per day.Also, note the small blood vessels containing erythrocytes.
- #143 The specimen is a slice of the left lung. The upper lobe is relatively normal, except for an old scar near the apex of the lung caused by tuberculosis. The major abnormality is that the lower lobe is uniformly consolidated (airless and solid) due to lobar pneumonia, with inflammatory cells and exuded plasma filling the airspaces. The shaggy material on the pleural surface is fibrin, a protein derived from fibrinogen in exuded plasma.
- #144 At medium power magnification, numerous neutrophils fill the alveoli in this case of acute bronchopneumonia in a patient with a high fever.Pseudomonas aeruginosa was cultured from sputum. Note the dilated capillaries in the alveolar walls from vasodilation with the acute inflammatory process.
- #146 An acid fast stain demonstrates a long filamentous organism in the center that is dark red. This is typical for Nocardia infection. This organism usually infects immunocompromised persons. Nocardiabraziliensis infections can become disseminated, often involving the brain.
- #147 This is a microscopic appearance of chronic abscessing inflammation with large areas of pink necrotic tissue present on the left that are bordered by granulation tissue with numerous prominent capillaries filled with blood.
- #148 Surgical specimen of an irregular-shaped lung nodule in a previously healthy individual Formation of grains within the abscess cavity is pathognomonic of actinomycosis (HE, low power). If grains are not included in the specimen, the histopathological diagnosis may be inflammatory pseudotumor of the lung.
- #149 Surgical specimen of an irregular-shaped lung nodule in a previously healthy individual The grains are composed of clustered thin bacteria and homogeneous matrix called Splendore-Hoeppli material (HE, high power). Neutrophilic reaction is evident.
- #150 Surgical specimen of an irregular-shaped lung nodule in a previously healthy individual Grocott stain identifies numbers of thin filamentous bacteria, Actinomycesisraelii, within the grain.
- #151 Surgical specimen of an irregular-shaped lung nodule in a previously healthy individual Grocott stain identifies numbers of thin filamentous bacteria, Actinomycesisraelii, within the grain.
- #153 Case 85. Aspergillosis of lung (49 y-o M) Surgical specimen of a lung cavity containing a fungus ball A thick-walled cavity formed in the upper lobe is associated with fibrotic lung tissue and thickened pleura (gross findings).
- #154 Case 85. Aspergillosis of lung (49 y-o M) Surgical specimen of a lung cavity containing a fungus ball Y-shaped, septum-forming basophilic hyphae are arranged in the same direction (HE). Non-viable hyphae show less basophilia.
- #155 Case 87. Candidosis of lung (55 y-o M) Fatal severe pneumonia in a septicemic patient after chemotherapy for lung cancer Sausage-shaped chains of pseudohyphae of Candida albicans show deep basophilia and vacuolation at the site of junctions. Hyphae formation predominates in such a destructive, invasive lesion.
- #156 Case 87. Candidosis of lung (55 y-o M) Fatal severe pneumonia in a septicemic patient after chemotherapy for lung cancer Grocott's silver strongly stains the pseudohyphae, except for the junctional vacuolation.
- #158 Here is the microscopic appearance of a viral pneumonia with interstitial lymphocytic infiltrates. Note that there is no alveolar exudate. Thus, the patient with this type of pneumonia will probably not have a productive cough. The most common causes for viral pneumonia are influenza A and B, parainfluenza, adenovirus, human metapneumovirus, and respiratory syncytial virus (RSV appears mostly in children). Cytomegalovirus can appear in immunocompromised hosts.Influenza A viral virulence varies considerably, as the virus undergoes genetic drift and shift with recombinations of its segmented RNA genome, particulary with shift when there are cross species shift, most often involving birds and swine. Examples include: H1N1, H1N5, H7N9.
- #159 A fungus ball composed of blue-staining hyphal elements of Aspergillus is seen here in a bronchus. Fungus balls may also form when fungi colonize cavitary lesions of tuberculosis.
- #160 Branching, septate hyphae are close-packed here and radiating outward in this aspergilloma.
- #161 The hyphae of Aspergillus are seen more clearly here. Aspergillus has a propensity to invade into blood vessels.
- #162 This well-formed granuloma has a large Langhans giant cell in the center. Two small spherules of Coccidioidesimmitis are seen in the giant cell.
- #163 Case 80. Coccidioidomycosis of lung (34 y-o F) Surgical specimen of the apical lung lesion in a Japanese student who traveled in Arizona Encapsulated caseous focus, termed coccidioidoma, closely resembles old tuberculosis (HE, low power).
- #164 Case 80. Coccidioidomycosis of lung (34 y-o F) Surgical specimen of the apical lung lesion in a Japanese student who traveled in Arizona A degenerated sporangium containing endospores is observed in the necrotic background, confirming the diagnosis of coccidioidomycosis (HE, high power).
- #165 Case 80. Coccidioidomycosis of lung (34 y-o F) Surgical specimen of the apical lung lesion in a Japanese student who traveled in Arizona Endospores in the sporandium of Coccidioides immitis are PAS-positive.
- #166 At higher magnification, the thick wall of the C. immitis spherule is seen in a giant cell in the center of this image. The spherule containsendospores. In the United States, C. immitis is endemic to the desert Southwest, but it can be found inhabiting dry plains of North and South America. In nature, C. immitis exists in a hyphal form with characteristic alternating arthrospores.
- #168 Case 81. Blastomycosis of lung (48 y-o M) Fatally progressive lung lesion in an American black Infiltration of neutrophils and macrophages is evident in the diffusely involved lung (HE). Systemic dissemination of the fungi led the patient to death.
- #169 Case 81. Blastomycosis of lung (48 y-o M) Fatally progressive lung lesion in an American black Large-sized yeasts, Blastomyces dermatitidis, reveal thick cell wall and internal eosinophilic cytoplasm, with a haloe formed between these two (HE, high power).
- #170 Case 81. Blastomycosis of lung (48 y-o M) Fatally progressive lung lesion in an American black The cell wall is stained black by Grocott's silver. Budding growth pattern of the yeast is evident.
- #171 Case 79. Histoplasmosis of lung (50 y-o M) Surgical specimen of the apical encapsulated lung lesion in a resident along the Mississippi River Small-sized round yeasts are observed in the necrotic tissue.
- #172 Case 79. Reference case 79A Systemic histoplasmosis in a child, with peripheral granulocytes infected with small yeast-form fungi (Giemsa). Capsule is not formed by Histoplasma capsulatum. The prognosis is poor.
- #174 This small, incipient lung ball (A) shows the central, necrotic lung parenchyma with invasive aspergillus (bluish organisms) pneumonia. The periphery is composed of a thick layer of PMNs that have digested the lung tissue, but a cavity has not yet formed. As a result of the digestion, vessels may be eroded and hemoptysis may occur
- #175 At high magnification (B), the PMNs are present at the top, and the necrotizing aspergillus pneumonia is at the bottom. The arrow indicates a branching hypha that has a pink, proteinaceous coat. This pink coating accounts for the dark pink layer of similar hyphae just under the PMNs in A. The nature of this coating, which has been described around fungi and helminth eggs and is called the Splendore-Hoeppli phenomenon, is unknown [5].
- #179 Case 78. Cryptococcal granuloma of lung (49 y-o M) Solitary subpleural lung nodule excised thoracoscopically An irregular-shaped yellowish nodule is seen (gross findings).
- #180 Case 78. Cryptococcal granuloma of lung (49 y-o M) Solitary subpleural lung nodule excised thoracoscopically PAS stain identifies numerous yeast-form fungi phagocytized by multinucleated giant cells.
- #181 Case 78. Cryptococcal granuloma of lung (49 y-o M) Solitary subpleural lung nodule excised thoracoscopically Electron micrograph demonstrates encapsulated round yeasts in the cytoplasm. A nucleus is recognized in the yeast.
- #182 Case 78. Reference case 78A Brushing cytology showing a multinucleated giant cell which phagocytizes numbers of PAS-positive round yeasts into the cytoplasm (PAS). When phagocytized, the size of this yeast becomes smaller, and capsule formation becomes inactive.