ERMINA WIDIYASTUTI • Reactive Disorders of Lymph Nodes • Specific Granulomatous Inflammation • Malignant Disorders of The Lymphoid System Reactive Lymphadenitis
• Infections and nonmicrobial inflammatory
stimuli often activate immune cells residing in lymph nodes, which act as defensive barriers. Any immune response against foreign antigens can lead to lymph node enlargement (lymphadenopathy) • Acute Nonspecific Lymphadenitis This form of lymphadenitis may be isolated to a group of nodes draining a local infection, or be generalized, as in systemic infectious and inflammatory conditions • Chronic Nonspecific Lymphadenitis Depending on the causative agent, chronic nonspecific lymphadenitis can assume one of three patterns: follicular hyperplasia, paracortical hyperplasia, or sinus histiocytosis. Reactive Disorders of Lymph Nodes
• Follicular Hyperplasia humoral response; B
lymphocytes large B cell germinal center • Parafollicular/Paracortical Hyperplasia Cell- mediated response; T lymphocytes paracortical hyperplasia • Sinus Hyperplasia/ Sinus Histiocytosis intense phagocytic activity by macrophages & phagocytic sinus-lining cells dilation of subcapsular & medullary sinuses SINUS HISTIOCYTOSIS • Sinus histiocytosis (also called reticular hyperplasia) refers to an increase in the number and size of the cells that line lymphatic sinusoids. • Although nonspecific, this form of hyperplasia may be particularly prominent in lymph nodes draining cancers such as carcinoma of the breast. • The lining lymphatic endothelial cells are markedly hypertrophied and macrophages are greatly increased in numbers, resulting in the expansion and distension of the sinuses. Sinus Histiocytosis This reactive pattern is characterized by distention and prominence of the lymphatic sinusoids, owing to a marked hypertrophy of lining endothelial cells and an infiltrate of macrophages (histiocytes) It often is encountered in lymph nodes draining cancers and may represent an immune response to the tumor or its products TUBERCULOUS LYMPHADENITIS
• In the case of highly virulent M. tuberculosis
or individuals with weakened resistance against tuberculosis during primary infection, lymphadenitis occurs at pulmonary hilar and cervical lymph nodes • Tuberculous meningitis and military tuberculosis occur by lymphogenous spread of M. tuberculosis Histopathology of Lymph Nodes
• M. tuberculosis grows within alveolar
macrophages and consequently forms a well- established primary lesion in the lungs. • It mostly occurs subjacent to the pleura of the upper lobe. • Some bacteria arrive at the bronchopulmonary lymph node via lymphatic vessels and form lymphadenopathy, classical Ghon complex • The primary infection begins with inhalation of M. tuberculosis and ends with T cell-mediated immune response that induces hypersensitivity against the organism • The inhaled organism is phagocytized by alveolar macrophages and transported by these cells to hilar lymph nodes • After a few weeks, T cell-mediated immunity develops in two ways. • One is formation of epithelioid cell granuloma by CD4+ cells and the other is formation of caseating granuloma by CD8+ cells • Thereafter, epithelioid granulomas are encapsulated and progress to central caseous necrosis, eventually resulting in healing • This lymphadenitis is induced by M. tuberculosis and can be seen as a part of the primary complex or secondary (organ) tuberculosis • About 90% of tuberculous lymphadenitis mainly appears in the cervical lymph node and others are in the mediastinal node • Sometimes it is difficult to distinguish among tuberculous lymphadenitis, malignant lymphoma and metastatic tumors • In the early phase of tuberculous lymphadenitis, the lymph node shows elastic hard tumor like nonspecific lymphadenitis. Inflammatory cells gradually infiltrate and periadenitis appears over time. • After the formation of abscesses in the lymph node, they enlarge and gradually change to caseous necrosis and soften. The histology of tuberculous lymphadenitis is characterized by central caseous necrosis surrounded by epithelioid cell layer and sporadic Langhans giant cells • In addition, in the outermost layer can be seen lymphocytes and fibroblasts, but no plasma cells are observed. This node is called tuberculous nodule, type IV allergic reactions against M. tuberculosis. Lymphoid Neoplasms
• Because of their overlapping clinical behavior,
the various lymphoid neoplasms can be distinguished with certainty only by the morphologic and molecular characteristics of the tumor cells. • lymphomas, tumors that produce masses in lymph nodes or other tissues LYMPHOMAS • Two groups of lymphomas are recognized: Hodgkin lymphomas and non-Hodgkin lymphomas HODGKIN’S LYMPHOMAS • Five histological subgroups : Nodular lymphocyte-predominant Lymphocytic-rich Mixed Cellularity ( intermediate progression) most common, most favorable prognosis Lymphocyte-depletion (aggressive) worse prognosis Nodular sclerosing pattern Prognosis & treatment not related to sub types, but to extent of involvement of the lymphoreticular system as a whole Reed Sternberg cells • Classic Hodgkin’s Lymphomas • Derived from activated lymphocytes; in some sub-types related to activation of B cells • Large binucleated cells with two mirror image nuclei containing large pink-staining nucleoli ( resembles owl’s eyes) popcorn cells • Usually only form a small portion of cell population, and hidden amongst sea of reactive lymphocytes, histiocytes and commonly eosinophiles NON HODGKIN’S LYMPHOMAS • Follicular (resembles lymphoid follicles without germinal center) / diffuse • Small ( as large as lymphocytes)/ Large Cell (5- 6x lymphocytes) the bigger, more aggressive Group of neoplastic proliferation of lymphoid ( T & B) or, very rarely histiocytic cells NON HODGKIN’S LYMPHOMAS • Small lymphocytic lymphomas • Follicular center cell, follicular pattern lymphomas • Diffuse large B cell lymphomas • Lymphoblastic lymphomas • Myeloma (plasmacytoma) • Cutaneus T cell lymphoma = Mycosis fungoides Diffuse Limphoma