| Factor | Mechanism | Clinical Impact |
|---|---|---|
| Corticosteroids | Inhibit fibroblast proliferation, reduce collagen synthesis, suppress inflammation | Delayed healing, increased infection risk |
| Diabetes mellitus | Impaired neutrophil function (chemotaxis, phagocytosis), hyperglycemia-induced glycation, microvascular dysfunction | Delayed healing, higher infection rates |
| Malnutrition (protein) | Insufficient amino acids for collagen synthesis; reduced fibroblast proliferation | Reduced tensile strength, delayed epithelialization |
| Advanced age | Slower proliferative response, delayed angiogenesis, reduced collagen remodeling | Delayed but not halted |
However, these are delays, not cessation. Healing still progresses, and primary intention wounds in elderly patients still achieve adequate tensile strength for suture removal at standard intervals (though infection risk is higher).
Option 0 (Corticosteroids): TRUE — Corticosteroids suppress the inflammatory phase and inhibit fibroblast function, significantly impairing healing.
Option 1 (Diabetes): TRUE — Hyperglycemia impairs neutrophil chemotaxis and phagocytosis, reducing the inflammatory response and increasing infection risk.
Option 2 (Malnutrition): TRUE — Protein deficiency directly limits collagen synthesis (collagen is 30% glycine, 11% proline). Tensile strength is reduced.
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