DISEASES OF LYMPH NODES

Diseases of WBCs
I. Defective granulocytes
A. Defect in function
B. Defect in Number
II. Increase in Number of Leukocytes
A. Reactive
B. Neoplastic
- Leukemia
- Lymphoma: NHL, HL
- Plasma cell disorders
- Histiocyte disorders

A. REACTIVE PROLIFERATION OF Lymph Nodes

1. Lymphadenitis
a. Acute non-specific
 Bacterial, viral
b. Chronic non-specific
 Follicular hyperplasia
 Paracortical lymphoid hyperplasia
 Sinus histiocytosis

*The basic function of LNs is filtration of a variety of materials varying from “foreign” microorganisms & particles to the
degradation products of cells & metabolism.

*The basic anatomy reflects the primary function of LN.

*In addition, the presence of special cells reflects functions superimposed on filtration:
 o Very shortly, after the infection occurs or when the nodes begin to filter noxious particles, reactive
changes occur – usually causing enlargement of nodes
o The changes may be:
 General- in systemic infections: bacterial, viral (eg. Syphilis, Measles)
 Local- reflecting diseases in the drainage area
 Simple chronic gastric ulcer (enlarged reactive nodes in omentum)
 Local low grade inflammation
 +/- absorption of foreign particles

Basic Changes

- Subsidiary changes:
o Infiltration by neutrophils – acute inflammation
o Increased blood flow – prominent venules
o Increased plasma cells – chronic infection
o Increased eosinophils – chronic inflammation

*The qualitative and quantitative variations and combinations of these changes are very numerous in most reactive
states the appearances are non-specific.

*This is usually due to acute infections causing ACUTE LYMPHADENITIS

a. In many bacterial infections, neutrophil infiltration is a feature
 b. In the majority of acute virus infections, neutrophils are absent and the nonspecific reactive changes
previously described are seen.

*In GLANDULAR FEVER (Infectious Mononucleosis), a virus infection (EBV) of young adults, the cervical lymph nodes are
particularly involved.

B. Malignant Lymphoma
1. Non-Hodgkin’s Lymphoma
Etiology:
o Develop when there is failure of immunoregulation in the face of persistent stimulus for lymphocyte
proliferation, in:
 Human organ (allograft) recipients
 Autoimmune diseases
 Primary (congenital) immune deficiency syndromes
o Course of NHL:
 Insidious onset of peripheral, painless LN enlargement
 Lymphoma  mass local compression effect)
Bone marrow infiltration anemia
 Splenic infiltrationhypersplenismanemia
Immunologic disturbancesautoimmune hemolysisanemia
opportunistic infections
o Prognosis depends on:
 Extent (stage)
 Specific forms
 Treatment modalities

o Malignant Lymphoma classification

 Morphologic
 Nodular
 Nodular/Diffuse
  Diffuse – Large B cell
 Mantle cell
 Primary paracortical

o Classification of Non-hodgkin’s Lymphoma

 Low grade
 Small lymphocytic: Consistent with CLL, Plasmacytoid
 Follicular, predominantly small cleaved cell
 Follicular, mixed small cleaved and large cell
 Intermediate grade
 Follicular, large cell
 Diffuse, small cleaved cell
 Diffuse, mixed small and large cell
 Diffuse, large cell
 High Grade
 Large cell immunoblastic
 Small non-cleaved cell: Burkitt/Non-Burkitt
 Miscellaneous
 Cutaneous T cell
 Adult T-cell leukemia/lymphoma

2. Hodgkin’s Lymphoma
Etiology:
o Bimodal age incidence
 Early peak (15-34 y.o)
 Second peak (after 45 y.o)
o Predominance in males (except Nodular Sclerosis)
o (+) Reed-Sternberg cells
o Course:
 Symptoms of obscure mechanisms
 Fatigue
 Weight loss
 Pruritus
 Intermittent fever
 Night sweats
 Symptoms associated with:
 LN enlargement (lymphedema, mediastinal compression)
 Hematologic (anemia, increased ESR)
  Immunologic (susceptibility to infection)
o Rye classification
 Lymphocyte predominance – Few Reed sternberg cells
 Mixed cellularity- plenty Reed sternberg cells, EBV +
 Lymphocyte depletion- EBV + (most)
 Nodular sclerosis –most common, rare EBV
o Prognosis: Extent of disease is very important
 5 year survival:
 Stage I and IIA = close to 100% and most cases expect to be cured
 Stage III and IV = 50% long term, relapse-free
 Complication of combined chemotherapy and radiotherapy:
 Increased risk of developing acute leukemia or some form of NHL

Staging: Ann Arbor Staging System

*A= asymptomatic; B= presence of constitutional symptoms (fever, night sweats, weight loss > 10% of baseline of
baseline body weight in preceding 6 months)

Clinical Difference
Hodgkin’s Lymphoma Non-Hodgkin’s Lymphoma
More localized to single axial group of LNs More frequent involvement of multiple peripheral
(cervical, mediastinal, para-aortic) LNs
Orderly spread by contiguity Non-contiguous spread
Mesenteric LNs and Waldeyer’s ring rarely Waldeyer’s ring and mesenteric LNs commonly
involved involved
Extranodal involvement uncommon Extranodal involvement
DISEASES OF THE SPLEEN
A. Functions characteristic of the organ
o Filtration of unwanted elements from the blood by phagocytes:
 Related to RBCS
 Maturation of surface of RBC
 “Culling” function
 “Pitting” function
 Removal of other particulate matter from the blood
o Reserve pool and storage site
 Related to RBC
 Related to platelets
 Related to WBC
 Storage of iron and other metabolites
B. Related functions as organ of RES
o Major organ in the immune system
o Source of lymphoreticular cells and sometimes hematopoietic cells
a. Production of lymphocytes and macrophages
b. Reactivation of extramedullary hematopoiesis in severe anemia

Hypersplenism
- Triad of:
o Splenomegaly
o Decreased cellular elements of blood
o Correction of blood cytopenias by splenectomy

Congenital anomalies
- Asplenia
- Hypoplasia
- Accessory spleens

Non-specific splenitis
- In any blood-borne infection

Reactive hyperplasia
- In chronic inflammation
- Systemic antigenemia
- Immunologic-inflammatory states

Congestive Splenomegaly
- Persistent chronic venous congestion
o Systemic-cardiac decompensation
o Portal venous drainage derangement
o Obstruction of extrahepatic portal vein/splenic vein

Splenic Infarcts
- From the heart
Neoplasia
- Rare

Rupture
- In crushing injury or severe blow
- “Spontaneous rupture”
o in non-traumatic causes
THYMUS
I. Development Disorders
 Hypoplasia or aplasia (Digeorge Syndrome)
o Severe deficits on cell mediated Immunity
o Hypoparathyroidism
 CYSTS
 Hyperplasia
o Myasthenia Gravis
o Other autoimmune disease
II. Thymoma- disease of thymic epithelial cells
 Benign (encapsulated)- Cytologic, biologic
 Malignant
o Cytologically benign
o Biologically aggressive, invasive metastatic
 Cancer
o Cytologically
o Biologically