By Gisela Dallenbach-Hellweg, Magnus Knebel Doeberitz, Marcus J. Trunk
The moment version of this atlas presents a close histopathological prognosis of cervical ailment emphasizing carcinogenesis, and correlating morphologic alterations with scientific facets. directions of the way to acquire and deal with tissue samples are by way of an outline of the traditional histology, of the motion of steroid hormones at the cervix, and of many of the sorts of regeneration and irritation. The part on etiology and pathogenesis of HPV-induced neoplasia has been enlarged to provide an explanation for new insights into mobile and nuclear deregulation on the molecular point. A bankruptcy on immunohistochemistry has been additional together with subtle detection equipment, e.g., with p16 for the early differential prognosis of premalignant lesions. the newest advances in molecular organic examine, with predictive subdivision of neoplasias, facilitate the alternative of the right kind treatment. All chapters – supported by means of over 20 new microphotographs – were revised to incorporate advances within the interpretation and administration of cervical sickness. The tumor nomenclature is tailored to the hot WHO type; the ICD-O code has been added. The reference checklist is up to date with correct publications.
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Additional info for Color Atlas of Histopathology of the Cervix Uteri
14–18) The normal endocervical mucosa consists of mucus-producing tubules and clefts (mucosal infoldings, usually called glands), loosely arranged in a fibrous stroma. A single layer of tall, columnar epithelial cells covers the mucosal surface and lines the intricate folds, clefts, and tubules. The small nuclei are basally placed during the early proliferative phase. The clear cytoplasm contains abundant mucus, especially in the late proliferative phase (Fig. 14). Where the endocervical mucosa merges with the isthmic mucosa, endometrial-type glands intermingle with endocervical glands (Figs.
25). With mucin stains, a faint positive reaction may be detected in the superficial cell layer, which may include the flattened atrophic remnants of columnar cells that originally covered the reserve cells (Figs. 26, 27). Fig. 19. Hyperplasia of reserve cells in descending repair. H&E Descending Repair Fig. 20. Hyperplasia of reserve cells. Immunohistochemical reaction with cytokeratin 13 Fig. 21. Hyperplasia of reserve cells differentiating into squamous metaplasia. H&E 25 26 Normal Histology, Regeneration, and Repair Fig.
H&E Descending Repair Fig. 20. Hyperplasia of reserve cells. Immunohistochemical reaction with cytokeratin 13 Fig. 21. Hyperplasia of reserve cells differentiating into squamous metaplasia. H&E 25 26 Normal Histology, Regeneration, and Repair Fig. 22. Hyperplasia of reserve cells differentiating into squamous metaplasia. Immunohistochemical reaction with cytokeratin 13 Fig. 23. Monocellular mucin formation in squamous metaplasia. H&E Descending Repair Fig. 24. Monocellular and multicystic mucin formation in squamous metaplasia.