[Durgical](https://durgical.com/en/) › [DurgiPedia](https://durgical.com/en/durgipedia/) › [General pathology](https://durgical.com/en/general-pathology/) › [Inflammation](https://durgical.com/en/general-pathology/#a-inflammation) › Inflammation: the cardinal signs and its five steps [General pathology](https://durgical.com/en/general-pathology/) · [Inflammation](https://durgical.com/en/general-pathology/#a-inflammation) # Inflammation: the cardinal signs and its five steps - Topic Inflammation is how living tissue answers injury or infection: it brings blood, fluid and white cells to the spot, cleans up, then repairs. Updated 2026-11-01 ## Key points - Cardinal signs: rubor (redness), calor (heat), tumor (swelling), dolor (pain) and functio laesa (loss of function). - Redness and heat come from arteriolar dilation; swelling from leaky venules; pain from bradykinin and prostaglandin E2 acting on nerve endings. - Five steps: recognise the cause, recruit leukocytes, remove the agent, regulate the response, then resolve and repair. - Acute = hours to days, oedema and neutrophils; chronic = weeks or longer, lymphocytes, macrophages, plasma cells, tissue destruction and fibrosis. - Neutrophils dominate the first 6–24 hours; monocytes and macrophages take over by 24–48 hours. ## What it is Inflammation is the response of vascularised tissue to infection or damage. It brings plasma proteins and leukocytes from the blood to the injured site to destroy the cause, clear dead tissue and start repair. It is protective, but when it is too strong, aimed at the wrong target or never switched off, it becomes the disease itself, from anaphylaxis to rheumatoid arthritis and atherosclerosis. ## Step by step - Recognition: sentinel cells (macrophages, dendritic cells, mast cells) detect microbes or dead-cell products through receptors such as Toll-like receptors. - Sensors such as the inflammasome trigger the release of IL-1, TNF, histamine, prostaglandins and chemokines. - Recruitment: arterioles dilate, venules leak, and neutrophils roll, stick and squeeze out toward the site. - Removal: leukocytes engulf and kill the microbes and clear necrotic debris. - Regulation: short-lived mediators decay and anti-inflammatory signals (IL-10, TGF-β, lipoxins) switch the response off. - Resolution and repair: fluid drains through lymphatics; tissue regenerates or is replaced by a scar. ## Acute vs chronic inflammation | Feature | Acute | Chronic | | --- | --- | --- | | Onset and duration | Fast (minutes to hours); lasts days | Slow (days to weeks); lasts months or years | | Main cells | Neutrophils | Macrophages, lymphocytes, plasma cells | | Vascular changes | Marked vasodilation and oedema | Less oedema; growth of new vessels (angiogenesis) | | Tissue damage | Usually mild and self-limited | Often progressive, with fibrosis | | Local and systemic signs | Prominent: redness, heat, pain, fever | Subtler; may be silent for years | | Typical example | Acute appendicitis | Rheumatoid arthritis, tuberculosis | ## Clinical notes - Anti-inflammatory drugs act on specific steps of this sequence: NSAIDs on prostaglandins, glucocorticoids on many genes, biologics on TNF or IL-6. - Inflammation that fails to switch off underlies many chronic diseases: rheumatoid arthritis, inflammatory bowel disease, atherosclerosis. - People who cannot mount inflammation (severe neutropenia, long-term glucocorticoids) may have serious infections with few local signs. ## Memory aid Red, hot, swollen, sore and stuck: four Latin words from antiquity plus the one that stops the part from working. ## Test yourself Think of the answer, then tap the question to see it. ## Which vascular change explains the redness and heat of inflammation? Arteriolar dilation, mainly from histamine, nitric oxide and prostaglandins, which increases blood flow to the area. ## Which leukocyte predominates on the first day of acute inflammation, and which replaces it? Neutrophils in the first 6–24 hours; monocytes, which become macrophages, by 24–48 hours. ## When does inflammation become harmful rather than protective? When it is excessive, aimed at the body's own tissues or harmless antigens, or does not stop, as in autoimmune disease, allergy and chronic infection. [Add to my cards (3)](https://durgical.app/estudiar/?add=/en/general-pathology/inflammation-the-cardinal-signs-and-its-five-steps/) ## Related - [Vascular changes in acute inflammation: vasodilation, leakage, exudate vs transudate](https://durgical.com/en/general-pathology/vascular-changes-in-acute-inflammation-vasodilation-leakage-exudate-vs-transudat/) - [Leukocyte recruitment: rolling, adhesion, transmigration, chemotaxis](https://durgical.com/en/general-pathology/leukocyte-recruitment-rolling-adhesion-transmigration-chemotaxis/) - [Mediators of inflammation: the table to know](https://durgical.com/en/general-pathology/mediators-of-inflammation-the-table-to-know/) - [Patterns of acute inflammation: serous, fibrinous, purulent, abscess, ulcer](https://durgical.com/en/general-pathology/patterns-of-acute-inflammation-serous-fibrinous-purulent-abscess-ulcer/) - [Chronic inflammation: causes, cells and features](https://durgical.com/en/general-pathology/chronic-inflammation-causes-cells-and-features/) - [Systemic effects of inflammation: fever, acute-phase proteins, leukocytosis, sepsis](https://durgical.com/en/general-pathology/systemic-effects-of-inflammation-fever-acute-phase-proteins-leukocytosis-sepsis/) - [Tissue repair: regeneration or scar; labile, stable and permanent cells](https://durgical.com/en/general-pathology/tissue-repair-regeneration-or-scar-labile-stable-and-permanent-cells/) ## Related conditions - [Acute appendicitis](https://durgical.com/en/conditions/acute-appendicitis/) - [Cellulitis of the leg](https://durgical.com/en/conditions/cellulitis-of-the-leg/) - [Community-acquired pneumonia](https://durgical.com/en/conditions/community-acquired-pneumonia/) - [Septic Arthritis of the Knee](https://durgical.com/en/conditions/septic-arthritis-of-the-knee/) - [Gout](https://durgical.com/en/conditions/gout/) - [Rheumatoid arthritis](https://durgical.com/en/conditions/rheumatoid-arthritis/) - [Sepsis and septic shock](https://durgical.com/en/conditions/sepsis-and-septic-shock/) - [Abscess, furuncle and carbuncle](https://durgical.com/en/conditions/abscess-furuncle-and-carbuncle/) ## Elsewhere in DurgiPedia - [Acute inflammation: vascular and cellular events](https://durgical.com/en/immunology/acute-inflammation-vascular-and-cellular-events/) - [The physiology of inflammation](https://durgical.com/en/physiology/the-physiology-of-inflammation/) - [Cytokines: the table to know](https://durgical.com/en/immunology/cytokines-the-table-to-know/) - [Neutrophil](https://durgical.com/en/immunology/neutrophil/) - [Monocyte and macrophage](https://durgical.com/en/immunology/monocyte-and-macrophage/) [← All of general pathology](https://durgical.com/en/general-pathology/) Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given. Sources: [17.5 Inflammation and Fever](https://openstax.org/books/microbiology/pages/17-5-inflammation-and-fever) (OpenStax (Microbiology), 2016); [4.6 Tissue Injury and Aging](https://openstax.org/books/anatomy-and-physiology-2e/pages/4-6-tissue-injury-and-aging) (OpenStax (Anatomy and Physiology 2e), 2022); [Appendicitis](https://www.ncbi.nlm.nih.gov/books/NBK493193/) (StatPearls (NCBI Bookshelf), 2024). ## **Spotted a mistake?** We are always improving for the community. Tell us what is wrong and our team will review it. Report a mistake Representative model, for educational purposes only. --- Source: https://durgical.com/en/general-pathology/inflammation-the-cardinal-signs-and-its-five-steps/ License: CC BY 4.0 (https://creativecommons.org/licenses/by/4.0/). Cite as: DurgiPedia (durgical.com), https://durgical.com/en/general-pathology/inflammation-the-cardinal-signs-and-its-five-steps/