Non neoplastic ln revised

1. Non-neoplastic lesions of Lymph
node

2. Lymphadenopathy
• Inflammations -
Acute
Chronic nonspecific
granulomatous
• Neoplastic conditions Primary-Lymphomas
Secondary- Metastatic

3. Reactive Lymphadenitis
• Any immune response against foreign antigens-
lymph node enlargement (lymphadenopathy)
• Infections and nonmicrobial inflammatory stimuli
involve the lymph nodes, which act as defensive
barriers
• Infections that cause lymphadenitis - acute or
chronic.
• In most instances, the histologic appearance of
the nodes is entirely nonspecific.

4. PATTERN of LN HYPERPLASIA IN RESPECT TO INFECTIOUS/ INFLAMMATORY DISEASES
FOLLICULAR/
NODULAR
INTER
FOLLICULAR/
PARACORTICAL/
DIFFUSE
SINUS MIXED
HYPERPLASIA
GRANULOMATOUS
Castleman Disease Viral lymphadenitis
(EMV, CMV,
herpes)
Rosai-
Dorfman
disease
Cat-scratch
disease
Tuberculosis
Kimura Disease Post vaccination
lymphadenitis
Whipple
disease
Kikuchi
lymphadenitis
Syphilis
Florid follicular
hyperplasia (AIDS)
LCH Toxoplasmosis Toxoplasmosis
Dermatopathic
lymphadenopathy
Fungal Infections
SLE Brucellosis
Lymphogranuloma
venereum- later
stage

5. ACUTE CONDITIONS:
1. Cat-scratch disease
2. Lymphogranuloma venereum
3. Mesenteric lymphadenitis
4. Staphylococcal infection
CHRONIC CONDITIONS:
With eosinophilic predominance
1. Kimura’s Disease
2. Langerhan’s Cell Histiocytosis
3. Castleman’s disease
Granulomatous
1. Tuberculosis
2. Atypical Mycobacteriosis
3. Syphilis
4. Lymphogranuloma venereum
5. Sarcoidosis
6. Brucellosis
Non specific/Non granulomatous
1. Leprosy
2. Whipples
Fungal Infection- Histoplasmosis
Parasitic-Toxoplasmosis
Viral-
1. AIDS Related
Lymphadenopathy
2. Infectious Mononucleosis
3. Viral Lymphadenitis
Necrotizing features seen in Acute Conditions:
1. Kikuchi necrotising lymphadenitis
2. Tularemia
3. Fungal infections (early lesions of
histoplasmosis)
Miscellaneous-
1. Bubonic plague
2. Anthrax
3. Melioidosis

6. Acute Nonspecific Lymphadenitis
• confined to a local group of nodes draining a
focal infection, or
• generalized in systemic bacterial or viral
infections.

7. Morphology
• Macroscopically, inflamed nodes- swollen,
gray-red, and engorged.
• M/E- large germinal centers with numerous
mitotic figures
• Macrophages often contain particulate debris
of bacterial origin or derived from necrotic
cells.

8. Acute suppurative lymphadenitis
• Cause is a pyogenic organism, a neutrophilic
infiltrate -seen about the follicles and within
the lymphoid sinuses
• With severe infections, centers of follicles
undergo necrosis - abscess

9. • Affected nodes - tender,firm
• If abscess extensive - fluctuant and soft
• Overlying skin red, and penetration of the
infection to the skin - draining sinuses
• With control of the infection, the lymph
nodes can revert to their normal appearance
or,
• if damaged by the immune response,
undergo scarring

10. Chronic Nonspecific Lymphadenitis
• Three morphological patterns, depending on
the causative agent:
follicular hyperplasia,
paracortical hyperplasia, or
sinus histiocytosis

11. Follicular Hyperplasia
• Cause – any stimuli that activate B-cell
immune response.
• Large oblong germinal centres(Secondary
follicle light zone) surrounded by collar of
mantle zone(resting naïve B-cells- dark zone).
• Normal germinal centres:
- Polarised

12. Follicular Hyperplasia
• Tingible body macrophages:
- Macrophages pred. found in germinal centres.
- Interspersed b/w germinal centers
- Contain immunoblast nuclear debris.
- immunoblasts undergo apoptosis- if fail to
produce Ab with high affinity to Ag.

15. Causes of follicular hyperplasia
• Non-specific reactive follicular hyperplasia
• rheumatoid arthritis,
• toxoplasmosis, and
• the early stages of HIV infection
• Kimura disease

16. Architectural Features
Follicular Hyperplasia
1)Preservation of nodal
architecture.
2)Follicles-more prominent in
cortical portion.
3) Size & shape of follicles-
marked variation(elongated,
angulated, dumb-bell forms).
4)Reaction centre- sharply
demarcated
Follicular lymphoma
1)Complete effacement of
normal architecture
2)Evenly distributed
throughout cortex and
medulla.
3)Size & shape of follicles-
moderate variation.
4)Fading of follicles

17. Follicular Hyperplasia Vs Follicular
Lymphoma

18. Follicular hyperplasia Follicular lymphoma

19. Paracortical Hyperplasia
• characterized by reactive changes within the T-
cell regions of the lymph node.
• On immune activation, parafollicular T cells
transform into large proliferating immunoblasts
that can efface the B-cell follicles.
• Eg: viral infections ( EBV), following certain
vaccinations (e.g., smallpox),
• immune reactions induced by certain drugs
(eg:phenytoin).

21. Sinus Histiocytosis
• distention and prominence of the lymphatic
sinusoids, due to marked hypertrophy of
lining endothelial cells and an infiltrate of
macrophages (histiocytes).
• Seen in lymph nodes draining cancers and
may represent an immune response to the
tumor or its products.
• Rosai Dorfman Disease.(sinus histiocytosis
with massive lymphadenopathy.)

22. Sinus Histiocytosis/S.Hyperplasia

23. Chronic Granulomatous
Lymphadenitis
• non-necrotising: Sarcoidosis
• Necrotising:
TB,
Cat-scratch disease,
Fungal infections,
lymphogranuloma venereum

24. TB-matted LN,caseous necrosis

25. Tuberculous Granulomatous
Lymphadenitis
Caseous
necrocis
Langhan’s GC