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Non neoplastic
Lymphadenopathy
By Noor Eldeeb
2nd year ENT Resident
Lymphadenopathy
Reactive
Acute
Chronic
oSpecific
•Non specific
Neoplastic
Primary
Secondary
*metastatic*
Lymphadenitis
• Inflammation of lymph nodes caused by the activation of resident
immune cells ( B cells , T cells )leading to morphologic changes in
lymph nodes
Acute Nonspecific Lymphadenitis
Mostly caused by bacterial infections
• Gross
The nodes are swollen, gray-red, and engorged.
• Microscopic
there is prominence of large reactive germinal centers containing numerous mitotic
figures.
Macrophages often contain particulate debris derived from dead bacteria or
necrotic cells and the centers of the follicles may undergo necrosis
• Clinically
Nodes are swollen and painful with abscess formation. The overlying skin is red.
Chronic Nonspecific Lymphadenitis
A wide variety of chronic immunologic stimuli may produce nonspecific
lymphadenitis.
Several different patterns of morphologic change are seen
• Follicular hyperplasia
• Paracortical hyperplasia
• Sinus histiocytosis
Clinically
lymph nodes are nontender.
Follicular hyperplasia
It is defined by the presence of secondary follicles which are surrounded
by a collar of small resting naive B cells (the mantle zone)
Germinal centers are polarized, consisting of two distinct regions:
(1) a dark zone with proliferating blast-like B cells (centroblasts) and
(2) a light zone composed of B cells with irregular or cleaved nuclear
contours (centrocytes).
Causes of follicular hyperplasia include
rheumatoid arthritis, toxoplasmosis, and early HIV infection.
Features favoring a reactive (nonneoplastic)
hyperplasia include
(1) preservation of the lymph node architecture, including the
interfollicular T-cell zones and the sinusoids
(2) marked variation in the shape and size of the follicles
(3) the presence of frequent mitotic figures, phagocytic macrophages,
and recognizable light and dark zones
Paracortical hyperplasia
• caused by stimuli that trigger T-cell–mediated immune responses,
such as acute viral infections
• The T-cell regions typically contain immunoblasts, activated T cells
three to four times the size of resting lymphocytes that have round
nuclei, open chromatin, several prominent nucleoli, and moderate
amounts of pale cytoplasm.
Sinus histiocytosis
This form of hyperplasia may be particularly prominent in lymph nodes
draining cancers
Microscopically
There is an increase in the number and size of the endothelial cells that
line lymphatic sinusoids and intrasinusoidal macrophages, which
expand and distort the sinusoids.
Chronic specific lymphadenitis
• Bacterial
TB, Syphilis, Brucellosis
• Viral
EBV , HIV
• Fungal
Histoplasmosis, coccidiomycosis
• Parasitic
Filiriasis, Toxoplasmosis
Tubercular lymphadenitis
• The characteristic element is the tuberculous granuloma * caseating
tubercle*
Stages of TB lymphadenitis
LNs.pptx
LNs.pptx
LNs.pptx

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LNs.pptx

  • 1. Non neoplastic Lymphadenopathy By Noor Eldeeb 2nd year ENT Resident
  • 3.
  • 4.
  • 5. Lymphadenitis • Inflammation of lymph nodes caused by the activation of resident immune cells ( B cells , T cells )leading to morphologic changes in lymph nodes
  • 6. Acute Nonspecific Lymphadenitis Mostly caused by bacterial infections • Gross The nodes are swollen, gray-red, and engorged. • Microscopic there is prominence of large reactive germinal centers containing numerous mitotic figures. Macrophages often contain particulate debris derived from dead bacteria or necrotic cells and the centers of the follicles may undergo necrosis • Clinically Nodes are swollen and painful with abscess formation. The overlying skin is red.
  • 7. Chronic Nonspecific Lymphadenitis A wide variety of chronic immunologic stimuli may produce nonspecific lymphadenitis. Several different patterns of morphologic change are seen • Follicular hyperplasia • Paracortical hyperplasia • Sinus histiocytosis Clinically lymph nodes are nontender.
  • 8. Follicular hyperplasia It is defined by the presence of secondary follicles which are surrounded by a collar of small resting naive B cells (the mantle zone) Germinal centers are polarized, consisting of two distinct regions: (1) a dark zone with proliferating blast-like B cells (centroblasts) and (2) a light zone composed of B cells with irregular or cleaved nuclear contours (centrocytes). Causes of follicular hyperplasia include rheumatoid arthritis, toxoplasmosis, and early HIV infection.
  • 9.
  • 10.
  • 11.
  • 12. Features favoring a reactive (nonneoplastic) hyperplasia include (1) preservation of the lymph node architecture, including the interfollicular T-cell zones and the sinusoids (2) marked variation in the shape and size of the follicles (3) the presence of frequent mitotic figures, phagocytic macrophages, and recognizable light and dark zones
  • 13. Paracortical hyperplasia • caused by stimuli that trigger T-cell–mediated immune responses, such as acute viral infections • The T-cell regions typically contain immunoblasts, activated T cells three to four times the size of resting lymphocytes that have round nuclei, open chromatin, several prominent nucleoli, and moderate amounts of pale cytoplasm.
  • 14.
  • 15. Sinus histiocytosis This form of hyperplasia may be particularly prominent in lymph nodes draining cancers Microscopically There is an increase in the number and size of the endothelial cells that line lymphatic sinusoids and intrasinusoidal macrophages, which expand and distort the sinusoids.
  • 16.
  • 17. Chronic specific lymphadenitis • Bacterial TB, Syphilis, Brucellosis • Viral EBV , HIV • Fungal Histoplasmosis, coccidiomycosis • Parasitic Filiriasis, Toxoplasmosis
  • 18. Tubercular lymphadenitis • The characteristic element is the tuberculous granuloma * caseating tubercle*
  • 19. Stages of TB lymphadenitis