Acute inflammation: vascular and cellular events and mediators
The vascular changes, neutrophil adhesion cascade and chemical mediators of acute inflammation, and how they explain exudates, leucocyte adhesion deficiency, steroid neutrophilia, NSAID-exacerbated asthma and ACE inhibitor angioedema.
Tier 2Medical sciences concept
Written with AI assistance and fact-checked against the sources below. For exam study, not clinical decisions. How notes are made
At a glance
- Acute inflammation is the rapid, stereotyped response to infection or necrosis. It brings fluid, plasma proteins and neutrophils to the site within minutes to hours.
- Vascular events: arteriolar vasodilation (redness, heat), then increased venular permeability (swelling, exudate).
- Cellular events: margination, rolling (selectins), firm adhesion (integrins), transmigration, chemotaxis, phagocytosis and killing.
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Sources
- Robbins and Cotran Pathologic Basis of Disease (10th ed.)Elsevier (Kumar, Abbas and Aster, 2020), 2020
- Cellular and Molecular Immunology (10th ed.)Elsevier (Abbas, Lichtman and Pillai, 2022), 2022
- Light RW et al. Pleural effusions: the diagnostic separation of transudates and exudates. Ann Intern Med 1972;77:507-13Annals of Internal Medicine, 1972
- Serhan CN. Pro-resolving lipid mediators are leads for resolution physiology. Nature 2014;510:92-101Nature, 2014
- ASCIA information on aspirin and NSAID allergy and hypersensitivityAU/NZAustralasian Society of Clinical Immunology and Allergy, 2024
- Last updated
- 14 November 2026
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