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LYMPHOID DISORDERS

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

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