non neoplastic ln revised

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Non-neoplastic lesions of Lymph node

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Page 1: Non neoplastic ln revised

Non-neoplastic lesions of Lymph node

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Lymphadenopathy

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

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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.

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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

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ACUTE CONDITIONS:1. Cat-scratch disease2. Lymphogranuloma venereum3. Mesenteric lymphadenitis 4. Staphylococcal infection

CHRONIC CONDITIONS:With eosinophilic predominance1. Kimura’s Disease2. Langerhan’s Cell Histiocytosis3. Castleman’s diseaseGranulomatous4. Tuberculosis5. Atypical Mycobacteriosis6. Syphilis7. Lymphogranuloma venereum8. Sarcoidosis9. BrucellosisNon specific/Non granulomatous10. Leprosy11. WhipplesFungal Infection- HistoplasmosisParasitic-ToxoplasmosisViral-12. AIDS Related

Lymphadenopathy13. Infectious Mononucleosis14. Viral Lymphadenitis

Necrotizing features seen in Acute Conditions:1. Kikuchi necrotising lymphadenitis2. Tularemia3. Fungal infections (early lesions of

histoplasmosis)Miscellaneous-4. Bubonic plague 5. Anthrax6. Melioidosis

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Acute Nonspecific Lymphadenitis

• confined to a local group of nodes draining a focal infection, or

• generalized in systemic bacterial or viral infections.

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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.

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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

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• 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

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Chronic Nonspecific Lymphadenitis

• Three morphological patterns, depending on the causative agent:

follicular hyperplasia, paracortical hyperplasia, or sinus histiocytosis

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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

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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.

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Causes of follicular hyperplasia

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

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Architectural Features

Follicular Hyperplasia1)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 lymphoma1)Complete effacement of

normal architecture2)Evenly distributed

throughout cortex and medulla.

3)Size & shape of follicles- moderate variation.

4)Fading of follicles

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Follicular Hyperplasia Vs Follicular Lymphoma

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Follicular hyperplasia Follicular lymphoma

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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).

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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.)

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Sinus Histiocytosis/S.Hyperplasia

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Chronic Granulomatous Lymphadenitis

• non-necrotising: Sarcoidosis• Necrotising: TB,Cat-scratch disease, Fungal infections, lymphogranuloma venereum

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TB-matted LN,caseous necrosis

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Tuberculous Granulomatous Lymphadenitis

Caseous necrocis

Langhan’s GC

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