Lymph node pathology

Hodgkin lymphoma or Hodgkin DiseaseFrom cases of the Pathology Department - U.M.F. “Gr. T. Popa” Iasi

Fig. 23.1. SR cell: Large binucleate cell, (mirror image) with abundant amphofilic cytoplasm and large eosinophilic nucleoli surrounded by a clear halo (appearance of "owl-eye").

Fig.23.1

Classical Sternberg Reed (SR) cell and variants of SR cells

Fig. 23.2From: Stevens A. J Lowe J. Pathology. Mosby 1995

Hodgkin Disease From: Stevens A. J Lowe J. Pathology. Mosby 1995

Fig.23.3

Fig. 23.3. Involved lymph nodes are increased in volume, with LN structure completely replaced by gray - white tumoral tissue; LNs retain their individuality, but become adherent between them and deep plans.

Fig. 23.4

Fig. 23.4. Large spleen presents multiple tumoral nodules, of various sizes, white-gray in color separated by red-brown normal splenic parenchyma (appearance of rustic sausage or salami).

LH – Ann Arbor staging From: Stevens A. J Lowe J. Pathology. Mosby 1995- fig 5

From cases of the Pathology Department - U.M.F. “Gr. T. Popa” Iasi-fig 6

• Stage I (A sau B)/ IE

• Single node involvement

• Stage II / Stage II E – Two or more nodes on same

side of diaphragm

• Stage III – Lymph nodes on both sides of

the diaphragm– Spleen involvement

• Stage IV – Diffuse extranodal

involvement

• A = no additional symptoms• B = weight loss, night sweats, fever• E- extra LN involvement Fig. 23.5

Fig. 23.6. In Mixt cellularity Hodgkin lymphoma, lymph node architecture is destroyed and replaced with: (a) a proliferation of tumoral cells (classical SR cells, pleomorphic SR cells, and Hodgkin cells), and (b) reactive non-tumoral cells (lymphocytes, plasma cells, eosinophiles, macrophages), neoangiogenesis, and diffuse fibrosis.

Fig. 23.6

Nodular sclerosis Hodgkin DiseaseFrom cases of the Pathology Department - U.M.F. “Gr. T. Popa” Iasi

Fig. 23.7

Fig. 23.7-8. In nodular sclerosis Hodgkin lymphoma the lymph node structure is replaced by tumoral nodules surrounded by fibrotic bands. Tumoral nodules contain: (a) tumoral cells (lacunar cells and classical SR cells) and (b) reactive cellular elements (eosinophiles, T lymphocytes, plasma cells, and histiocytes).

Fig. 23.8

Non-Hodgkin Lymphoma From: Stevens A. J Lowe J. Pathology. Mosby 1995

Fig. 23.9. Non-Hodgkin Lymphoma-deep abdominal lymphoadenopathy: Deep abdominal lymph nodes mass with tendency to fussion.

Fig. 23.9

Fig. 23.10

Fig. 23.10. Non-Hodgkin Lymphoma-deep mediastinal lymphoadenopathy:

Mediastinal homogenous, gray tumoral block with irregular margins resulted by fusion of the tumoral lymph nodes which lost their individuality.

Small Lymphocytic Lymphoma From: Stevens A. J Lowe J. Pathology. Mosby 1995 - fig.11

From cases of the Pathology Department - U.M.F. “Gr. T. Popa” Iasi-fig.12

Fig. 23.11

Fig. 23.12

Fig. 23.11-12. Lymph node architecture is replaced by tumoral cells resembling with mature lymphocytes. Tumoral cells infiltrate lymph node capsule.

Hepatic chronic myeloid leukemiaFrom cases of the Pathology Department - U.M.F. “Gr. T. Popa” Iasi

Fig. 23.13

Fig. 23.14

Fig. 23.13-14. Liver is infiltrated by pleomorphic leukemic cells (few blast cells, numerous myelocyte cells and metamyelocyte cells and numerous mature neutrophils and eosinophiles), predominantly along of sinusoids.

Hepatic chronic lymphocytic leukemiaFrom cases of the Pathology Department - U.M.F. “Gr. T. Popa” Iasi

Fig. 23.15

Fig. 23.16

Fig. 23.15-16. Leukemic lymphocytic infiltrate is localized predominantly in the portobilliary space, which is expanded.