A patient on long-term corticosteroid therapy develops a wound that fails to heal. Which specific mechanism explains corticosteroid-mediated impairment of wound healing?

• A Corticosteroids directly inhibit collagen fibril formation by blocking prolyl hydroxylase
• B Corticosteroids specifically deplete vitamin C causing scurvy-like impairment of cross-linking
• C Corticosteroids suppress production of growth factors (TGF-β, PDGF) and inhibit fibroblast proliferation and collagen synthesis ✓
• D Corticosteroids upregulate matrix metalloproteinases specifically in wound beds

Explanation

Corticosteroids impair wound healing through multiple mechanisms: suppression of TGF-β and PDGF production (reducing fibroblast recruitment and activation), direct inhibition of fibroblast proliferation and collagen synthesis, reduced angiogenesis, and impaired macrophage-mediated debridement (blunted inflammation). While corticosteroids do increase MMPs, the dominant anti-healing effect is reduced fibroblast activity and growth factor suppression. Prolyl hydroxylase requires vitamin C as cofactor — its inhibition is the mechanism in scurvy, not corticosteroid use.

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

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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