Back to ELM2: Pathology
Inflammation & Tissue Repair
~1 min read
Lesson 2 of 20
Notes
Inflammation & Tissue Repair
Acute Inflammation
Vascular changes: vasodilation (histamine, PGE2) → increased blood flow (rubor, calor)
Permeability changes: endothelial contraction → protein-rich exudate → oedema (tumor)
Cellular events: margination → rolling (selectins) → adhesion (integrins/ICAM) → transmigration → chemotaxis (C5a, IL-8, LTB4)
Mediators of Acute Inflammation
- Histamine: mast cells, immediate vasodilation + permeability
- Prostaglandins: COX pathway, pain and fever
- Leukotrienes: LTB4 (chemotaxis), LTC4/D4/E4 (bronchoconstriction)
- Complement: C3a/C5a (anaphylatoxins), C5a (chemotaxis), MAC (C5b-9, lysis)
- IL-1, IL-6, TNF-╬▒: systemic effects — fever, acute phase proteins, leukocytosis
Outcomes of Acute Inflammation
- Resolution (complete restoration)
- Suppuration (abscess formation)
- Organisation and fibrosis (scar)
- Progression to chronic inflammation
Granulomatous Inflammation
- Aggregates of activated macrophages (epithelioid cells) ┬▒ Langhans giant cells
- Causes: TB (caseating), Crohn's, sarcoidosis (non-caseating), foreign body, fungal infection
Wound Healing
- Primary intention: clean wound edges apposed; minimal scar
- Secondary intention: open wound, granulation tissue fills cavity; larger scar
- Key cells: platelets (haemostasis), macrophages (debridement), fibroblasts (collagen III → I), myofibroblasts (contraction)
- Growth factors: TGF-╬▓ (fibrosis), PDGF (fibroblast recruitment), VEGF (angiogenesis)