PA3.1-2 | Acute Inflammation — Vascular & Cellular Events, Mediators — Summary & Reflection

KEY TAKEAWAYS

Acute inflammation is a rapid, neutrophil-dominated protective response with five cardinal signs (rubor, tumor, calor, dolor, functio laesa).

Vascular events follow a set sequence: transient vasoconstriction → vasodilation → ↑permeability (endothelial contraction via histamine/leukotrienes; direct injury; transcytosis) → stasis → exudate. Exudate (protein >3 g/dL) differs fundamentally from transudate.

Leucocyte recruitment is a stepwise cascade: margination → rolling (selectins) → activation (chemokines) → firm adhesion (integrins–ICAM-1) → diapedesis (PECAM-1) → chemotaxis (C5a, LTB₄, IL-8).

Phagocytosis relies on opsonins (IgG Fc, C3b) and kills via: (i) respiratory burst (NADPH oxidase → O₂•⁻ → H₂O₂ → HOCl via MPO) and (ii) O₂-independent granule enzymes.

Mediators include: histamine (mast cells, immediate); prostaglandins/leukotrienes (COX/LOX, AA pathway — targeted by NSAIDs/montelukast); TNF + IL-1 (macrophages — fever, adhesion, acute-phase response); complement (C3a/C5a — anaphylatoxins + chemotaxis; C3b — opsonin); bradykinin (pain + permeability); NO (vasodilation + microbicidal).

Morphological patterns: serous (watery), fibrinous (fibrin, 'bread-and-butter'), suppurative/abscess (pus), ulcer (epithelial defect).

Outcomes: resolution → suppuration → organisation/fibrosis → chronic inflammation.

REFLECT

Consider a patient who develops a perianal abscess after a minor abrasion. Walk through the full sequence — from the initial breach of skin to abscess formation — naming the mediators, cells, and morphological steps involved. What would need to be different about the organism or host defences to produce resolution instead of suppuration? How does this case illustrate the dual nature of inflammation as both protective and potentially harmful?