Acute and Chronic Inflammation
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Direct answer
Acute inflammation is the immediate, short-lived vascular and cellular response to injury, dominated by neutrophils and protein-rich exudation, and responsible for the cardinal signs — redness, heat, swelling, pain and loss of function. Chronic inflammation is a longer response to persistent injury in which macrophages, lymphocytes and plasma cells dominate, with simultaneous tissue destruction, attempted healing and, in some settings, granuloma formation.
What you must remember
- Acute vascular events: brief vasoconstriction, then arteriolar vasodilatation (histamine, bradykinin, nitric oxide), increased vascular permeability and stasis; increased permeability is the most important event, producing exudate.
- Acute cellular events: margination and rolling (selectins), firm adhesion (integrins binding ICAM-1), transmigration and chemotaxis toward C5a, leukotriene B4, IL-8 and bacterial peptides; defective adhesion causes leucocyte adhesion deficiency.
- Neutrophils dominate the first one to two days, then monocytes; eosinophils point to parasites and allergy; lymphocytes and macrophages suggest viruses and chronic disease.
- Mediators worth memorising: histamine from mast cells (vasodilatation, permeability), prostaglandins (pain, fever, vasodilatation — the target of aspirin), leukotrienes (bronchospasm, chemotaxis), complement fragments C3a and C5a (anaphylatoxins), and IL-1 and TNF (fever, endothelial activation, acute-phase response).
- Possible outcomes of acute inflammation: resolution, suppuration with abscess formation, organisation into fibrous scar, or progression to chronic inflammation.
- Chronic inflammation shows mononuclear infiltration, ongoing tissue destruction and repair by angiogenesis and fibrosis; typical causes are persistent microbes (tuberculosis, syphilis), prolonged toxic exposure (silicosis) and autoimmunity (rheumatoid arthritis, lupus).
- Granulomatous inflammation — epithelioid macrophages, multinucleate giant cells and lymphocytes — is caseating in tuberculosis and fungal infection, non-caseating in sarcoidosis, and a foreign-body reaction to sutures or silica; Langhans giant cells belong to tuberculosis.
- Systemic effects include fever, leucocytosis, raised ESR and acute-phase proteins such as C-reactive protein.
Common confusion
Exudate and transudate are endlessly mixed up. An exudate is protein-rich, cell-laden and produced by vascular permeability in inflammation; a transudate is protein-poor fluid formed by hydrostatic or oncotic pressure imbalance, as in congestive cardiac failure. A second favourite distinction is caseating versus non-caseating granulomas — the former essentially means tuberculosis until proven otherwise, the latter is the sarcoid signature.
Exam-focused takeaway
Theory answers should define acute inflammation, walk through vascular and cellular events with mediators, list outcomes, then contrast chronic and granulomatous patterns with causes. Viva examiners ask for the cardinal signs with their mechanisms and the difference between selectin-mediated rolling and integrin-mediated adhesion. MCQs repeatedly test anaphylatoxins, chemotactic agents, the cell type of each phase, Langhans versus foreign-body giant cells, and caseation.
Frequently asked questions
What causes the cardinal signs of inflammation?
Vasodilatation produces redness and heat, exudation produces swelling, bradykinin and prostaglandins sensitise nerve endings producing pain, and loss of function follows the rest.
Distinguish exudate from transudate.
Exudate is protein-rich with cells and high specific gravity, formed by inflamed leaky vessels; transudate is protein-poor, cell-free and formed by pressure gradients.
Name the key adhesion molecules and their roles.
Selectins mediate initial rolling of leucocytes on endothelium; integrins (LFA-1) binding ICAM-1 mediate firm adhesion before transmigration.
What is a granuloma, and when is it caseating?
A focal collection of epithelioid macrophages, often with giant cells and lymphocytes; caseation — cheese-like necrosis — is characteristic of tuberculosis.
Which cells dominate acute versus chronic inflammation?
Neutrophils dominate acute inflammation; macrophages, lymphocytes and plasma cells dominate chronic inflammation.