LYMPH NODES

Normal anatomy

Major zones

– Cortex

• situated beneath the capsule

• where most lymphoid follicles reside

– Paracortex

• between the cortex and the medulla

• contains mobile pool of T lymphocytes

– Medulla

• close to the hilum

• rich in lymph sinuses, arteries, and veins

• contains minor lymphocytic component

• Together with the cortex, they are called the “B zone”

LV, arteries and veins

– Afferent lymph vessels penetrate the nodal capsule to open into the marginal sinus

– Main arteries and veins pass through the hilum and radiate to the medulla, paracortex, and
inner part of the cortex

Lymph Node Evaluation

A. Biopsy

• Axillary/Cervical LN > Inguinal LN

– Inguinal LN high frequency of nonspecific chronic inflammatory

• Larger LN > Small superficial N

– Small nodes usually shows nonspecific hyperplasia

B. Needle Biopsy

• CN biopsy is adequate for the dx of metastatic CA

• FN Aspiration is used in documenting metastatic CA

C. Bacteriologic examination

• Nodes of infectious process

D. Electron microscopy

• Used in examination of Langerhans cell histiocytosis

E. Immunophenotyping

• For lymphomas: Monoclonal antibodies > Rosetting tests

• Can be performed using fresh tissue (flow cytometry) or paraffin-embedded

materials.

A. PEMs have rapid results and excellent surface Ig assessment

F. Genre rearrangement analysis

• For the ddx between benign and malignant lesions

• Markers for B or T cell derivation

• Markers for the presence of multiple lymphocytic clones in a single parent

G. Cytogenetics and molecular genetics

a. Chromosomal translocation

• Detected in malignant lymphoma

• Detected through cytogenetics, southern blot analysys, RT-PCR, and FISH

b. Chromosome copy change and chromosomal gain or deletion

• In marginal zone lymphoma: Trisomy 3, Trisomy 18, or del 6q23.3

• In CLL/small lymohocytic lymphoma: Trisomy 12

• In extranodal NK/T-cell lymphoma: del 6q21–25

• In mantle cell lymphoma: gain of 3q26

• Detected through FISH or SNP microarrays

 c. Gene mutation, amplification, and hypermethylation

• In DLBCL: point mutation in NFκB and amplification of REL

H. DNA ploidy studies

• Done through flow cytometry

Primary Immunodeficiency

TYPES OF IMMUNOLOGIC
CHARACTERISTICS
DEFICIENCY

Cortical reactive centers and medullary

Humoral type
plasma cells are scanty or absent

Thickness of the paracortical area is

Cell- mediated immunity type
greatly diminished

Lymphocyte and plasma cell content of

Defects in phagocytes and
the node is practically nil, the lymph
other cells of the accessory
node being reduced to a mass of
immune system
connective tissue and blood vessels

Patterns Of Hyperplasia

Follicular Hyperplasia

• Macroscopically: sharply-defined, onion-skin pattern surrounded by mantle of small

lymphocytes
• Microscopically: composed of an admixture of small and large lymphoid cells, irregular nuclei,
numerous mitoses, phagocytosis of nuclear debris by histiocytes - starry sky pattern

Progressively transformed germinal centers

• Large, w/ numerous small lymphocytes, indistinct borders, blurred interface

• (+) residual starry sky macrophages with scattered large lymphoid cells, epithelial cells at
periphery
• Inc. network of follicular dendritic cells

Regressively transformed germinal centers

• Small, devoid of lymphoid cells, (+) follicular dendritic cells, vascular endothelial
 • cells, & hyalinized PAS-positive intercellular material
• LPO exam: onion-skin appearance
• Prominent & numerous in CASTLEMAN DISEASE

MANTLE/MARGINAL ZONE HYPERPLASIA

• Blends with lymphoid subtype of hyaline vascular Castleman disease

• Monomorphic proliferation of small lymphoid cells with round nuclei & clear
• Benign at hematoxylin-eosin
• Diff. diagnosis: Mantle cell lymphoma

PARACORTICAL HYPERPLASIA

NODULAR FORM:
• Dermatopathic lymphadenitis and nodal reactions to malignancy
DIFFUSE FORM:
• Viral lymphadenitis, drug reactions & immunoblastic proliferation in general

SINUS HYPERPLASIA
• Also known as “sinus histiocytosis, sinus ‘catarrh’”
• Seen in nodes draining infectious or neoplastic processes

MONOCYTOID B CELLS
• IMMATURE SINUS HISTIOCYTOSIS
 originally but it is still a B-cell type, most frequent in toxoplasmosis

PLASMACYTOID DENDRITIC CELLS

• (+) pyknosis and starry sky pattern

• Common in Kikuchi necrotizing
• lymphadenitis and Castleman disease

POLYKARYOCYTES

• Used for a type of multinucleated giant cell found in lymphoid tissue

• WARTHIN-FINKELDEY GIANT
• CELL OF MEASLES

Inflammatory/ Hyperplastic diseases

Acute nonspecific lymphadenitis

• Rarely biopsied
• Microscopically, earliest change is sinus dilation resulting from increased flow of lymph,
followed by accumulation of neutrophil, vascular dilatation and edema of capsule
 • Suppurative lymphadenitis
• feature of staphyloccal infection, mesenteric lymphadenitis, lymphogranuloma venereum, and
cat-scratch disease
• Necrotizing lymphadenitis
• Seen in bubonic plague, tularemia, anthrax, melioidosis.

Chronic nonspecific lymphadentits

• Eosinophilic or xanthogranulomatous lymphadenitis depending on the type of the infiltrate.

• General features: follicular hyperplasia, prominence of postcapillary venules, increased number

of immunoblasts, plasma cells, and histiocytes; and fibrosiscapsule may appear inflamed and/or
fibrotic, and the process may extend into the Immediate perinodal tissues

Tuberculosis
• most common location is The cervical region (‘scrofula’), draining sinus that communicates with
the skin (‘scrofuloderma’) may form.
• adherent to each other and form a large multinodular mass that can be confused clinically with
metastatic carcinoma Microscopically, the appearance ranges from multiple small epithelioid
granulomas reminiscent of sarcoidosis to huge caseous masses surrounded by Langhans giant
cells, epithelioid cells, and lymphocytes.