Rapid Review·General Pathology
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INFLAMMATION
T1Must knowGranulomatous Inflammation
P213
Focus on
A Th1 and IFN-γ dependent wall built around something the macrophage cannot digest.
Key takeaways
What a granuloma is
What a granuloma is
a pattern of chronic inflammation induced by a persistent T-cell response to certain infections, immune-mediated disease, or foreign bodies.- Granulomas wall off a resistant stimulus without eradicating it, so inflammation persists → fibrosis and organ damage.
Histology
a focus of epithelioid cells (activated macrophages with abundant pink cytoplasm) surrounded by lymphocytes, with multinucleated giant cells formed by fused activated macrophages.How a granuloma forms
What this shows
Mechanism (know this chain cold)
APC presents antigen to a CD4+ T cell and secretes IL-12 → the CD4+ cell differentiates into Th1 → Th1 secretes IFN-γ → macrophage activation → macrophages secrete TNF → epithelioid macrophages and giant cells form → granuloma.Two consequences worth knowing
Granulomas cause hypercalcemia
activated macrophages autonomously express 1α-hydroxylase → ↑ active vitamin D, independent of PTH.Caseating vs noncaseating
| Feature | Caseating Granuloma | Noncaseating Granuloma |
|---|---|---|
| Central necrosis | Present | Absent |
| Typical cause | Infectious | Noninfectious |
| Bacterial | Mycobacteria (TB, leprosy), Bartonella henselae (cat-scratch, stellate necrotizing), Listeria, T. pallidum (tertiary syphilis) | None |
| Fungal/Parasitic | Endemic mycoses (histoplasmosis), schistosomiasis | None |
| Immune-mediated | None | Sarcoidosis, Crohn disease, primary biliary cholangitis, subacute (de Quervain) thyroiditis |
| Vasculitis | None | GPA, EGPA, giant cell arteritis, Takayasu |
| Foreign body | None | Berylliosis, talcosis, hypersensitivity pneumonitis |
| Other | Catalase-positive organisms in chronic granulomatous disease | None |
A patient with sarcoidosis has a serum calcium of 12 mg/dL with a low PTH. What is the mechanism?
Activated macrophages in the granulomas express 1α-hydroxylase on their own, making active vitamin D independent of PTH. The vitamin D raises calcium absorption, and PTH is appropriately suppressed.
How it's tested
Two guaranteed angles.
(1) Hypercalcemia in sarcoidosis. The epithelioid macrophages within the noncaseating granulomas autonomously express 1α-hydroxylase, producing excess calcitriol independent of PTH, so calcium is high with a suppressed serum PTH.
(2) A patient with RA started on infliximab develops miliary TB. The mechanism is that TNF-α is required to maintain granuloma architecture, so blocking it dissolves the wall around latent bacilli and lets them disseminate. This is why a PPD or IGRA is mandatory before starting any anti-TNF agent.
Go deeper
First Aid "Granulomatous diseases" list; Pathoma Ch. 2 "Granulomatous inflammation"; SketchyImmuno Th1. Anchor the IL-12 → Th1 → IFN-γ → macrophage-activation loop (why anti-TNF biologics reactivate latent TB) and caseating (TB/fungi) vs non-caseating (sarcoid/Crohn/beryllium).
High-yield images2
Flashcards for this page
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Tuberculosis involves (...) granulomas
Sarcoidosis presents with (...) granulomas
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