Inflammation, signs of and reasons for - acute

Definition and cardinal signs

Acute inflammation - the immediate, short-lived, stereotyped vascular and cellular response to tissue injury or infection, designed to contain and eliminate the insult and initiate repair
The cardinal signs (rubor, calor, tumor, dolor, functio laesa) are clinically apparent within minutes to hours of the triggering insult

Vascular phase: transient vasoconstriction, then vasodilation (rubor, calor - histamine, prostaglandins) and increased vascular permeability (tumor - oedema, from endothelial gap formation)
Cellular phase: neutrophils are recruited first (margination, rolling via selectins, firm adhesion via integrins, transmigration, chemotaxis along a gradient - e.g. IL-8, C5a, LTB4) and dominate the first 24-48 hours; phagocytose pathogens/debris and release enzymes/reactive oxygen species
Dolor (pain) - from prostaglandins/bradykinin sensitising nociceptors; functio laesa (loss of function) - the composite result of swelling, pain, and tissue disruption

Clinically recognised by the cardinal signs; laboratory correlates (raised neutrophil count, CRP) reflect the same process systemically

Outcomes of acute inflammation: complete resolution (the ideal outcome, most common with minor injury), abscess formation (walled-off collection if the insult persists), progression to chronic inflammation (if the insult is not cleared), or fibrosis/scarring (if there is substantial tissue destruction)

Wound healing, abscess formation, systemic inflammatory response syndrome (SIRS) - the exaggerated systemic form of this same process

Acute inflammation that fails to resolve within the expected timeframe (days) transitions into chronic inflammation, with a corresponding shift in the dominant cell type from neutrophils to lymphocytes/macrophages

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