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PA19.1-6 | Tuberculous Lymphadenitis — Pathology & Specimen — Part 3

Specimen Identification Practice: Step-by-Step Framework

Four-panel medical diagram showing gross and microscopic identification features of tuberculous lymphadenitis, from matted lymph nodes with caseation to H&E granulomas with Langhans giant cells. — **Panel A:** Gross lymph node specimen; multiple matted lymph nodes; thickened irregular capsule; periadenitis; cut surface; yellow-white crumbly caseous necrosis; loss of normal architecture; absence of pus; provisional diagnosis tuberculous lymphadenitis. **Panel B:** Low-power H&E; replaced lymph node architecture; pale amorphous acellular caseous necrosis; surrounding cellular infiltrate. **Panel C:** Intermediate-power H&E; confluent caseating epithelioid granulomas; central necrotic zones; granulomatous inflammation. **Panel D:** High-power H&E; epithelioid histiocytes; kidney-shaped nuclei; Langhans giant cell; peripheral horseshoe nuclei; lymphocytic cuff; eosinophilic amorphous caseous necrosis.

For PA19.5, you must be able to narrate what you see, not just label a diagram. Use this structured approach in your practical and OSCE.

For a gross specimen (pot or fresh):
1. Type: 'This is a lymph node specimen (or group of nodes).'
2. Size and number: 'Measuring approximately X × Y cm. Multiple nodes appear matted together.'
3. External surface: 'Capsule is thickened and irregular; nodes are fused — consistent with periadenitis.'
4. Cut surface: 'On bisection, the central area shows dull, yellow-white, crumbly/cheesy material (caseation) with loss of normal white pulp architecture. No liquefaction/pus.'
5. Provisional diagnosis: 'Consistent with tuberculous lymphadenitis.'

For a histological slide (H&E):
1. Low power: 'Normal lymph node architecture is replaced by large pale zones of amorphous acellular material (caseous necrosis) surrounded by cellular infiltrates.'
2. Intermediate power: 'The cellular zones consist of confluent caseating epithelioid granulomas.'
3. High power: 'Granulomas contain epithelioid histiocytes (large cells, kidney-shaped nuclei, pale syncytial cytoplasm), Langhans giant cells (peripheral horseshoe arrangement of nuclei), and a surrounding lymphocytic cuff.'
4. Central zone: 'The necrotic centre is structureless, amorphous, and eosinophilic — typical caseous necrosis.'
5. Diagnosis: 'Morphology is consistent with tuberculous lymphadenitis. ZN stain should be performed for acid-fast bacilli.'

Summary: The Complete Picture of TB Lymphadenitis

A five-panel medical diagram summarizes tuberculous lymphadenitis through clinical sites, gross pathology, immunopathogenesis, microscopic granuloma features, diagnosis, and major differentials. — **Panel A:** Clinical and gross pathology: posterior triangle cervical nodes, submandibular nodes, matted lymph nodes, cheesy yellow-white caseation, cold abscess, collar-stud abscess, sinus tract, axillary nodes, mesenteric nodes.. **Panel B:** Pathogenesis cascade: Mycobacterium tuberculosis, Th1 response, IFN-gamma, macrophage activation, epithelioid transformation, Langhans giant cell formation, granuloma, caseous necrosis, TNF-alpha, ischaemia, macrophage cytotoxicity.. **Panel C:** Microscopy: confluent caseating epithelioid granulomas, central amorphous caseous necrosis, epithelioid histiocytes, Langhans giant cells with horseshoe nuclei, lymphocytic cuff, Ziehl-Neelsen stain showing sparse acid-fast bacilli.. **Panel D:** Diagnosis: FNAC, cytology, Ziehl-Neelsen stain, biopsy, culture, GeneXpert, rifampicin resistance detection.. **Panel E:** Differentials: sarcoidosis with non-caseating granulomas and Schaumann bodies with ZN negative; fungal lymphadenitis with PAS/GMS positive organisms; cat-scratch disease with stellate necrosis and Bartonella; leprosy with perineural inflammation and modified ZN positive bacilli..

Tie the thread together before you leave this module.

Aetiology: Mycobacterium tuberculosis (occasionally M. bovis in dairy-farming regions)

Site: Cervical nodes (posterior triangle > submandibular), axillary, mesenteric

Pathogenesis: Th1-driven Type IV hypersensitivity → IFN-γ → macrophage activation → epithelioid transformation → Langhans giant cell formation → granuloma → caseous necrosis (TNF-α + ischaemia + macrophage cytotoxicity)

Gross: Matted nodes, cheesy yellow-white caseation, cold abscess, collar-stud abscess, sinus tract

Micro: Confluent caseating epithelioid granulomas; Langhans giant cells (horseshoe nuclei); central amorphous caseous necrosis; lymphocytic cuff; ZN — AFB (sparse but confirmatory)

Diagnosis: FNAC → ZN + cytology → biopsy → culture / GeneXpert (rapid, detects RIF resistance)

Key differentials: Sarcoidosis (non-caseating, Schaumann bodies, ZN−), fungal (PAS/GMS+), cat-scratch (stellate necrosis, Bartonella), leprosy (perineural, modified ZN+)

CBME link: PA19.2 covers pathogenesis; PA19.5 demands you read a gross or micro specimen and narrate systematically.

Four-panel diagram showing the sequential evolution of tuberculous granuloma from exudative phase through productive granuloma to caseous necrosis and fibrocalcification. — **Panel A:** Exudative phase (0-2 weeks) - neutrophils, macrophages, mycobacteria, acute inflammatory infiltrate. **Panel B:** Productive granuloma (2-6 weeks) - epithelioid cells, Langhans giant cells, lymphocytes, activated macrophages. **Panel C:** Caseous necrosis (6-12 weeks) - central caseous necrosis, epithelioid cell layer, lymphocyte infiltration, fibroblasts. **Panel D:** Fibrocalcification (months-years) - fibrous capsule, calcification deposits, residual caseous material, collagen fibers.