High-yield map
Key points before the detail
- 01
The classical signs of inflammation can be explained directly from vascular and mediator physiology.
- 02
Leukocyte recruitment follows an ordered sequence: margination, rolling, firm adhesion, transmigration and chemotaxis.
- 03
Selectins are central to rolling; integrins mediate firm adhesion to endothelial ligands such as ICAM/VCAM.
- 04
Acute inflammation can resolve, form an abscess, progress to chronic inflammation or heal by organisation and fibrosis.
What acute inflammation is trying to achieve
The purpose of acute inflammation is to deliver plasma proteins and leukocytes to a site of injury, remove the initiating stimulus and dead tissue, and create conditions for repair. The response is protective when proportionate and controlled, but can itself damage tissue when excessive, persistent or poorly localised.
The cardinal signs explained
| Sign | Main mechanism |
|---|---|
| Rubor and calor | Arteriolar vasodilation increases local blood flow. |
| Tumour | Increased vascular permeability produces protein-rich exudate and tissue oedema. |
| Dolor | Bradykinin and prostaglandin E2 sensitise nociceptors; pressure from oedema contributes. |
| Functio laesa | Pain, swelling and tissue injury impair normal function. |
How leukocytes leave the circulation
| Step | Mechanism |
|---|---|
| Margination | Slower flow and stasis move leukocytes towards the endothelial surface. |
| Rolling | Transient selectin-mediated attachments slow the cell. |
| Firm adhesion | Activated leukocyte integrins bind endothelial adhesion molecules such as ICAM and VCAM. |
| Transmigration | Leukocytes pass between endothelial cells and through the basement membrane. |
| Chemotaxis | Cells move along gradients generated by microbial products and inflammatory mediators such as C5a and leukotriene B4. |
High-yield mediators
| Mediator | Useful association |
|---|---|
| Histamine | Rapid vasodilation and increased venular permeability. |
| Bradykinin | Pain, vasodilation and increased permeability. |
| PGE2 | Pain sensitisation and fever. |
| LTB4 | Strong neutrophil chemotaxis/activation. |
| C3a and C5a | Anaphylatoxin effects; C5a is also a potent chemotactic signal. |
| TNF, IL-1 and IL-6 | Endothelial activation and systemic acute-phase effects. |
| Nitric oxide | Vasodilation and microbicidal functions depending on cellular source. |
Outcomes of acute inflammation
- Complete resolution when the cause is removed and tissue can restore normal architecture.
- Suppuration or abscess formation when pyogenic infection and tissue necrosis produce a local collection.
- Progression to chronic inflammation when the stimulus persists.
- Organisation and fibrosis when substantial tissue destruction or non-regenerating tissue prevents full restoration.
Active recall
Close the notes and answer these
Try each question from memory before revealing the answer. These public prompts are a small preview of the integrated retrieval system inside SurgAtlas.
01Which adhesion molecules are most associated with leukocyte rolling versus firm adhesion?
Selectins mediate rolling; activated leukocyte integrins mediate firm adhesion to endothelial ligands including ICAM and VCAM.
02Name three strong chemotactic signals for neutrophils.
Bacterial products, C5a and leukotriene B4 are classic examples.
03What are four broad outcomes of acute inflammation?
Resolution, suppuration/abscess, progression to chronic inflammation, or organisation/fibrosis.
Sources & editorial basis
References & editorial basis
- SurgAtlas production chapter — Acute Inflammation. Primary source for this public lesson. The public teaching is a condensed, source-derived version of the corresponding production pathology chapter.
- Robbins & Cotran Pathologic Basis of Disease. Reference for stable mechanisms of acute inflammation.
This lesson is derived from the corresponding SurgAtlas production teaching material. Where the source makes current management or guideline claims, the public lesson uses the cited contemporary guidance. It is written for education and examination preparation, not as patient-specific clinical advice.
Editorial details
Medical Doctor (MD) · MRCS Part A · Physician · Surgical Educator
SurgAtlas is an educational resource. For patient care, verify current national guidance, local antimicrobial and transfusion policies, specialty pathways and individual patient factors.
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