Pathology lecture class for MBBS students on lymphoreticular system

1. LYMPHORETICULAR
SYSTEM
Dr. Umme Kulsum Munmun
Assistant Professor
Department of Pathology
Chandpur Medical College

2. HAEMATOPOIESIS

5. NICE TO KNOW

6. Bone marrow- B
cells
Thymus – T cells
Circulate
through
blood
Secondary lymphoid
organs eg. Lymph node,
spleen, tonsil , Peyer’s
patches

7. LYMPHADENOPATHY
Antigenic
stimulation
Activation of
resident
immune cells
Primary lymphoid
follicles enlarge
(germinal center)
Enlargement of Lymph node

8. LYMPHADENOPATHY

9. LYMPHADENITIS
Inflammation of lymph node:
Secondary lymphoid follicles with
reactive germinal centers

10. LYMPHADENITIS

11. CAUSES OF LYMPHEDENOPATHY
• Viral (EBV, CMV, HIV etc)
• Bacterial (Streptococcus, Staphylococcus,
Mycobacterium, Cat- scratch disease etc)
• Fungal
• Parasitic
Infectious
Diseases
• Castleman disease
• Sarcoidosis etc
Immune
Diseases

12. CAUSES OF LYMPHEDENOPATHY
• Lymphoma
• Leukemia
• Metastatic cancers
Malignancies
• Rheumatoid arthritis
• SLE
• Drug reactions
Others

13. GENERALIZED LYMHADENOPATHY
More than two non – contiguous group of lymph
nodes

14. CAUSES OF GENERALIZED
LYMPHADENOPATHY
Infections
• TB
• HIV
• Infectious
mononucleosis
• Toxoplasmosis
Malignancy
Autoimmune
disease
Storage
diseases
Histiocytoses
Drug
reactions

15. NEOPLASTIC PROLIFERATIONS OF
WHITE BLOOD CELLS
• Present with widespread involvement of bone marrow
peripheral blood
• Liquid malignancy of either lymphoid or myeloid series
Leukemia
• Proliferations that arise as discrete mass
• Solid malignancy of lymphoid series
• Begins as malignant transformation of lymphocytes in
lymphatic system
Lymphoma

16. NEOPLASTIC PROLIFERATIONS OF
WHITE BLOOD CELLS
Lymphoid
neoplasm
B cell, T –cell or NK cell
origin
Phenotypes of neoplastic
cell closely resembles that
of a particular stage of
normal lymphocyte
maturation

17. NEOPLASTIC PROLIFERATIONS OF
WHITE BLOOD CELLS
Myeloid
neoplas
Arise from
haemopoietic
progenitors

18. LYMPHOMA
A malignant
tumour of
lymphoid
tissue

19. LYMPHOMA
Hodgkin Lymphoma
Non-Hodgkin

20. WHO CLASSIFICATIONS OF
LYMPHOID NEOPLASMS
Precursor
B-cell
Neoplasm
Peripheral
B – cell
Neoplasm
Precursor
T – cell
Neoplasm
Peripheral T
– cell /NK –
cell
Neoplasm
Hodgkin
Lymphoma

21. WHO CLASSIFICATIONS OF
LYMPHOID NEOPLASMS
• B – cell acute lymphoblastic leukaemia/lymphoma (
ALL)
Precursor
B-Cell
Neoplasm
• Follicular Lymphoma
• Diffuse large B cell lymphoma
• Marginal zone Lymphoma
• Burkitt lymphoma
• Extranodal Marginal zone lymphoma
Peripheral
B-Cell
Neoplasm

22. WHO CLASSIFICATIONS OF
LYMPHOID NEOPLASMS
• T –Cell acute lymphoblastic leukaemia/lymphoma (
ALL)
Precursor
T-Cell
Neoplasm
• Peripheral T-Cell Lymphoma
• Anaplastic Large cell lymphoma
• Mycosis fungoides
• Extranodal NK/Tcell lymphoma
• Angioimmunoblastic T Cell lymphoma
Peripheral
Cell
Neoplasm

23. WHO CLASSIFICATIONS OF
LYMPHOID NEOPLASMS
• Classical subtypes
• i. Nodular Sclerosis
• ii. Mixed cellularity
• iii. Lymphocyte rich
• iv. Lymphocyte depletion
• Lymphocyte predominance
Hodgkin
Lymphom

24. WORKING FORMULATION
• An obsolete classification of non-Hodgkin lymphomas,
first proposed in 1982.
 Low Grade
 Intermediate grade
 High grade

25. NICE TO KNOW

26. CINICAL PRESENTATIONS
Enlarged non-tender lymph
nodes (often > 2 cm)
Symotoms related to
involvement of extranodal
sites
(skin, stomach, brain etc)
Systemic symptoms (“B
symptoms”)
Fever, night sweats, weight
loss
Symptoms related to
hepatosplenomegaly
Symptoms related to
complications of bone
marrow infiltration
(Infections, anaemia, bleeding
and coagulopathies)

27. ETIOLOGY
• Exposure to radiation and certain chemicals (benzene etc)
• Infections (EBV in HL, H. pylori in gastric MALToma)
• Immunodeficiency
• Autoimmune disease
• Older age group

28. HODGKIN LYMPHOMA
• First described by Thomas Hodgkin in 1832
• Characteristic features:
 Arises in a single node or chain of nodes (esp.
cervical)
 Contains rare neoplastic distinctive giant cells
(“Reed Sternberg cells”), in a background of
abundant reactive inflammatory cells
 One of the most common cancers in young adults

29. HODGKIN LYMPHOMA

30. VARIANTS OF RS CELL

31. CLASSIFICATION
• Nodular lymphocyte predominant Hodgkin lymphoma
• Classical Hodgkin lymphoma
 Nodular sclerosis Hodgkin lymphoma
 Mixed cellularity Hodgkin lymphoma
 Lymphocyte-rich Hodgkin lymphoma
 Lymphocyte-depleted Hodgkin lymphoma

32. CLASSICAL HODGKIN LYMPHOMA
Nodular Sclerosis (66%)
-Fibrous bands and
nodules
-“Lacunar cell” variant of
cell
Mixed Cellularity (25%)
- Abundant RS cells
- Background of
lymphocytes, eosinophils,
plasma cells, neutrophils
Lymphocyte Rich (5%)
- Scattered RS cells in
lymphocyte rich
Lymphocyte Depleted
- Abundant RS cells and
mononuclear variants
- Only few background
lymphocytes

33. NODULAR LP HODGKIN
LYMPHOMA
• 5% of all Hodgkin lymphoma
• “Popcorn cells” / “L&H cells” rather than RS cells
• Background of small B-lymphocyte

34. • Distinction between Classical HL and Nodular LP
HL is based partly on immunophenotype
 Classical: CD15+ CD30+ CD45- CD20-
 NLPHL: CD15- CD30- CD45+ CD20+

35. ANN ARBOR STAGING SYSTEM
• I – Involvement of a single lymph node region or
lymphoid structure
• II – Involvement of two or more lymph node regions on
the same side of the diaphragm
• III – Involvement of lymph node regions or structures on
both sides of diaphragm
• IV – Involvement of extranodal sites

36. Prognosis of Hodgkin Lymphoma
• Generally better than non-Hodgkin lymphomas
• Depends greatly on stage (more so than histological
subtype)
• 90-100% of Stage IA and IIA curable

37. DIFFERENCES

38. NON - HODGKIN LYMPHOMA
• Very diverse group of disorders
• Unimodal age distribution, with increasnig
incidence with age
• Many arise in extranodal sites (although the
majority are nodal)

39. Divided clinically into
 Low grade
- Indolent, slow-growing, but resistant to therapy and rarely
curable
- Often present with painless generalized lymphadenopathy
 High grade
- Aggressive, rapidly progressive, but sensitive to treatment and
potentially curable
- Often present with solitary rapidly enlarging mass

40. CAUSES OF SPLENOMEGALY
• Liver disease (cirrhosis, hepatitis, portal hypertension)
• Haematologic malignancy (lymphoma, leukaemia,
myeloproliferative disorders)
• Portal or hepatic vein thrombosis
• Congestive cardiac failure
• ITP, haemolytic anaemia, thalassemia

41. DIAGNOSTIC APPROACH FOR
LYMPHADENOPATHY
• History and evaluation (Size, site, duration, tenderness,
localized/generalized, ‘B’ symptoms)
• CBC
• Mantoux test
• Microbiological test
• Serology: CMV, HIV, toxoplasmosis
• ANA, Rheumatoid factor

42. DIAGNOSTIC APPROACH FOR
LYMPHADENOPATHY
• LDH
• Imaging test
• FNA
• Biopsy and histopathology (to confirm malignancy)
• Immunohistochemistry to categorize
 Hodgkin/ Non- Hodgkin lymphoma
 B/T cell lymphoma etc
• Flowcytometry

43. CAUSES OF SPLENOMEGALY
• Infections ( malaria, TB, HIV, infectious mononucleosis
etc)
• Connective tissue disease (SLE, rheumatoid arthritis etc)
• Infiltrative disorders (sarcoidosis, amyloidosis, glycogen
storage diseases).
• Focal lesions (hemangiomas, abscess, cysts, metastasis).

44. THANK YOU