Giant cell arteritis (GCA) characteristically involves the extracranial branches of the carotid artery. The pathological hallmark is granulomatous transmural inflammation with medial necrosis. The vessel wall layer where the granulomatous inflammation is most concentrated and where the characteristic giant cells form in GCA is:

• A Adventitia — granulomas form around vasa vasorum with periadventitial fibrosis
• B Internal elastic lamina — granulomas form at the intima-media junction with fragmentation of the internal elastic lamina ✓
• C Intima — foam cell granulomas form in the intimal plaque overlying a lipid core
• D Outer media — granulomas form in smooth muscle layers away from the elastic lamina

Explanation

In giant cell arteritis, the granulomatous inflammation is most concentrated at the intima-media junction, specifically targeting the internal elastic lamina (IEL). CD4+ Th1 and Th17 cells recognise arterial wall antigens (particularly of the IEL), recruiting macrophages and multinucleated giant cells that phagocytose and fragment the IEL — the characteristic 'elastic lamina fragmentation' seen on elastic tissue stains. The IEL is typically discontinuous or absent in severely involved segments. This transmural inflammation also involves the media with smooth muscle destruction. Intimal proliferation occurs in later stages causing luminal narrowing and ischaemia. Adventitial granulomas are a minor component; foam cell granulomas of intimal plaques describe atherosclerosis, not GCA.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.