Giant cell (temporal) arteritis preferentially involves which layer of the vessel wall, and which cellular finding is pathognomonic?

• A Transmural granulomatous inflammation with multinucleated giant cells centred on the internal elastic lamina (IEL), often with IEL fragmentation ✓
• B Intimal fibrous thickening with foamy macrophages (atheromatous pattern)
• C Necrotising fibrinoid necrosis of the media with neutrophilic infiltration
• D Eosinophilic infiltration of adventitia with microabscesses

Explanation

Giant cell arteritis (GCA) is a granulomatous vasculitis of medium and large arteries (temporal, ophthalmic, aorta) in which T-cell-driven macrophage activation produces granulomatous inflammation focused on the internal elastic lamina. Characteristic findings are Langhans-type or foreign-body-type multinucleated giant cells engulfing elastin fragments, with fragmentation and dissolution of the IEL. This leads to intimal hyperplasia and luminal narrowing causing ischaemia (blindness, jaw claudication, stroke). Fibrinoid necrosis with neutrophils characterises polyarteritis nodosa (small-medium vessel necrotising vasculitis); eosinophilic infiltration is seen in eosinophilic granulomatosis with polyangiitis (Churg-Strauss).

Reference: Robbins & Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.