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NON-NEOPLASTIC
MORPHOLOGY
• Expanded lymphatic sinus at the medulla of lymph node
• Medulla exhibits expansion of the lymphatic sinuses
• Expanded pale areas show hyperplasia of the macrophages called Histiocytes in
the medullary portion near the blood vessel
• The capillaries that supply these areas exhibit hypertrophy of the endothelial
lining epithelium
Follicular Hyperplasia • Caused by stimuli that activates humoral immune responses (reactive process)
• Presence of large oblong germinal centers (secondary follicles) which are
surrounded by a collar of small resting naïve B cells (Mantle zone)
FEATURES
1. Preservation of lymph node architecture – including the interfollicular T cell
zones & sinusoids
2. Marked variation in the shape & size of the follicles
3. Presence of frequent mitotic figures, phagocytic macrophages, recognizable light
& dark zones – all of which tend to be absent from neoplastic follicles
MORPHOLOGY
• Red pulp – expanded & is heavily congested
• Constriction of the space occupied by the white pulp
• Spleen appears heavier than normal
• Condition associated with this in the peripheral blood
• Hyperfunctioning
• Sequestration of blood cells producing
o Anemia
o Depletion of thrombocytes or platelets which are also present
in the spaces
o Increased vulnerability of the spleen to blunt trauma producing
bleeding
NEOPLASTIC
PATHOGENESIS
o Rearrangements involving the IgH locus & various proto-oncogenes
• Plasma cells
o Nuclei has a unique pattern called Spokes of Wheel or Clockface
Chromatin Pattern
o Perinuclear Halo – a pale space considered to be the Golgi Zone
where the secretory vesicles are made, and these cells are capable
of producing huge amounts of antibodies
PATHOGENESIS
• Dysregulation of BCL6, a DNA-binding zinc-finger transcriptional repressor
that is required for the formation of normal germinal centers. The majority
are of B cell lineage.
• Translocations that have in common a breakpoint in BCL6 at Chromosome
3q27