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  • Laporan PA Lengkap

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    diah
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    This document lists and describes various types of tumors and lesions that can occur in the colon, liver, and oral cavity. It includes descriptions of adenomas, adenocarcinomas, hepatocellular carcinomas, odontogenic keratocysts, ameloblastomas, pleomorphic adenomas, fatty liver, cirrhosis, and various benign polyps. For the villous adenoma, it provides microscopic details such as hypercellularity, nuclear features, loss of goblet cells, and lack of epithelial cell maturation. It also notes that approximately 15% of colon cancers have DNA mismatch repair defects causing microsatellite instability.

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    This document lists and describes various types of tumors and lesions that can occur in the colon, liver, and oral cavity. It includes descriptions of adenomas, adenocarcinomas, hepatocellular carcinomas, odontogenic keratocysts, ameloblastomas, pleomorphic adenomas, fatty liver, cirrhosis, and various benign polyps. For the villous adenoma, it provides microscopic details such as hypercellularity, nuclear features, loss of goblet cells, and lack of epithelial cell maturation. It also notes that approximately 15% of colon cancers have DNA mismatch repair defects causing microsatellite instability.

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    © All Rights Reserved
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    Download as docx, pdf, or txt
    8 views13 pages

    Laporan PA Lengkap

    Uploaded by

    diah
    This document lists and describes various types of tumors and lesions that can occur in the colon, liver, and oral cavity. It includes descriptions of adenomas, adenocarcinomas, hepatocellular carcinomas, odontogenic keratocysts, ameloblastomas, pleomorphic adenomas, fatty liver, cirrhosis, and various benign polyps. For the villous adenoma, it provides microscopic details such as hypercellularity, nuclear features, loss of goblet cells, and lack of epithelial cell maturation. It also notes that approximately 15% of colon cancers have DNA mismatch repair defects causing microsatellite instability.

    Copyright:

    © All Rights Reserved
    Download as DOCX, PDF, TXT or read online from Scribd
    Flag for inappropriate content
    Download as docx, pdf, or txt
    of 13

    1.

    Kista Odontogenik : dentigerous radicular


    2. Ameloblastoma : follicular

    3. Ameloblastoma : plexiform

    4. Tumor Warthin
    5. Pleomorphic adenoma

    6. Polip Hiperplastik
    7. Polip Hemartomatous : Juvenile Polyp
    8. Polip Hemartomatous : Peutz Jeghers Polyp

    9. Polip Adenoma : Displasia low grade


    10. Polip Adenoma : Displasia high grade

    11. Polip Adenoma : tubular

    12. Polip Adenoma : Villious


    The villous processes are lined by columnar epithelium with low-grade dysplasia. There is
    hypercellularity and nuclear overcrowding. The nuclei are slightly enlarged, elongated, and
    hyperchromatic but are still uniform and maintain their polarity. Nucleoli are not prominent. There is
    some loss of goblet cell mucin. Mitotic activity is not significantly increased. Architecturally, the
    glands show crowding and branching. There is lack of maturation as the epithelial cells move from
    crypts to the surface. The cytologic features impart a basophilic appearance to the adenomatous
    epithelium on routine H&E staining.

    13. Polip Adenoma : tubulo-villious


    14. Adenomakarsinoma kolorektal : invasi pT1

    15. Adenomakarsinoma kolorektal : invasi pT2

    16. Adenomakarsinoma Kolorektal : Well Differentiated


    a. Well-differentiated adenocarcinoma of right-sided colon: tumoral invasion into
    muscularis propria (HE staining, ×100).
    b. Moderately-differentiated adenocarcinoma (HE × 200). The glands are lined by
    neoplastic cells with hyperchromatic nuclei. The tumor was accompanied with small
    mucinous lakes lind by well-differentiated epithelial cells. The tumor invades all
    intestinal wall.
    17. Adenomakarsinoma kolorektal : Poor differential

    Sekitar 15% dari karsinoma kolorektal (CRC), termasuk Kanker Kolorektal Non-
    poliposis Herediter (HNPCC; Sindrom Lynch), CRC sporadis sisi kanan, dan
    adenokarsinoma bergerigi menunjukkan jalur perbaikan ketidaksesuaian DNA yang
    rusak (MMR) yang menyebabkan ketidakstabilan mikrosatelit (MSI).
    Tumor ini menunjukkan hipermutasi, lebih cenderung berdiferensiasi buruk dengan
    sedikit atau tanpa pembentukan kelenjar atau menunjukkan diferensiasi musinus.
    Pola pertumbuhan sering dibatasi. Limfosit yang menginfiltrasi tumor selalu ada.
    18. Fatty Liver

    Vakuola lemak

    Nutrisi parenteral total (TPN) dapat menyebabkan cedera hepatoseluler yang


    mengakibatkan steatosis makrovesikuler, di mana inti hepatosit dipindahkan oleh satu
    atau lebih vakuola lemak, atau steatosis mikrovesikuler, di mana tetesan lemak
    didistribusikan dengan halus di dalam sitoplasma hepatosit. Steatohepatitis (seperti
    yang terlihat di sini) terdiri dari steatosis dengan sel inflamasi yang bercampur. Ada
    juga empedu yang pecah akibat kolestasis
    19. Sirosis
    Nodul

    Infeksi hepatitis B kronis sering mengakibatkan sirosis dengan nodul hepatosit yang
    rusak dan beregenerasi dipisahkan oleh pita fibrosa yang mengandung infiltrat sel
    inflamasi kronis yang menonjol dan reaksi duktular. Nodul < 3 mm disebut sebagai
    mikronodular sirosis, sedangkan yang > 3 mm disebut macronodular.
    20. Karsinoma hepatoselular : pola trabekular
    21. Karsinoma hepatoselular : pola pseudoglandular

    22. Karsinoma hepatoselular : Pola Solid


    23. Karsinoma Hepatoselular : Grade 2

    24. Karsinoma Hepatoselular : Grade 3


    25. Karsinoma Hepatoselular : Grade 4

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