A 70-year-old hypertensive man is found to have a 6 cm abdominal aortic aneurysm (AAA). The aneurysmal wall on histology shows marked loss of medial smooth muscle cells and elastic laminae with chronic inflammatory infiltrate (T cells, macrophages, B cells) and proteolytic matrix degradation. The most important protease family responsible for medial elastic tissue destruction in AAA is:

• A Serine proteases (thrombin, plasmin)
• B Matrix metalloproteinases (MMP-2, MMP-9) ✓
• C Cysteine cathepsins (cathepsin B, L)
• D Angiotensin-converting enzyme (ACE)

Explanation

Abdominal aortic aneurysm pathogenesis involves chronic adventitial and medial inflammation driven by macrophages and T cells, which elaborate matrix metalloproteinases — particularly MMP-2 (gelatinase A) and MMP-9 (gelatinase B). These MMPs degrade type IV collagen and elastin of the aortic wall, causing progressive medial atrophy, elastic tissue fragmentation, and structural weakening. Serine proteases (plasmin, elastase from neutrophils) also contribute but MMPs are the primary mediators. Risk factors include smoking (strongest), hypertension, male sex, and age; COPD (shared elastase excess) is also associated.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

Written and medically reviewed by the StethoPrep medical team.