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| Acute Inflammation
๐ฅ Acute inflammation is a rapid, early defensive response of the body to harmful stimuli such as pathogens, damaged cells, or irritants.
It is characterised by the classical signs of โก๏ธ heat, redness, swelling, pain, and loss of function.
Its main purposes are to eliminate the cause of injury, remove necrotic debris, and initiate tissue repair.
๐ Stages of Acute Inflammation
- 1. Initiation ๐๏ธ :
- Recognition of harmful stimuli via pattern recognition receptors (PRRs) on immune cells.
- Release of inflammatory mediators such as histamine, prostaglandins, cytokines.
- 2. Vascular Changes ๐ :
- Vasodilation: Increased blood flow โ redness & heat.
- Increased vascular permeability: Plasma proteins & fluid leak into tissues โ oedema (swelling).
- 3. Cellular Events ๐งโโ๏ธ๐ฆ :
- Leukocyte recruitment: Margination โ rolling โ adhesion โ transmigration (diapedesis).
- Phagocytosis: Neutrophils & macrophages engulf debris โ fuse phagosome with lysosome โ destruction by ROS & enzymes.
๐งช Chemical Mediators of Inflammation
- Vasoactive Amines โก :
- Histamine: Mast cells, basophils, platelets โ vasodilation & permeability.
- Serotonin: Platelets & enterochromaffin cells โ similar vascular effects.
- Plasma Protein Systems ๐ฉธ :
- Complement (C3a, C5a): Anaphylatoxins โ permeability & chemotaxis. C3b acts as an opsonin.
- Coagulation: Fibrin meshwork forms a clot scaffold.
- Kinin system: Bradykinin โ vasodilation, pain, permeability.
- Arachidonic Acid Metabolites ๐ :
- Prostaglandins (COX): Pain, vasodilation, fever.
- Leukotrienes (LOX): Chemotaxis, permeability, bronchospasm.
- Cytokines & Chemokines ๐ข :
- TNF, IL-1: Fever, adhesion molecules, systemic acute phase response.
- Chemokines: Recruit leukocytes to the site.
- ROS & Nitric Oxide โ๏ธ :
- Microbicidal and signalling roles.
- Excess = tissue injury (ARDS, reperfusion injury).
๐งญ Outcomes of Acute Inflammation
- โ
Resolution: Full clearance & return to normal tissue.
- ๐ฅ Abscess: Localised pus collection when clearance fails.
- โป๏ธ Chronic inflammation: If stimulus persists โ fibrosis & immune activation.
- ๐งฑ Fibrosis/scarring: When tissue repair is incomplete.
๐ฉบ Clinical Signs & Symptoms ("Cardinal Signs")
- ๐ด Redness (Rubor): Vasodilation, hyperaemia.
- ๐ฅ Heat (Calor): Increased blood flow & metabolic activity.
- ๐ง Swelling (Tumour): Oedema from plasma leakage.
- ๐ฃ Pain (Dolor): Mediated by bradykinin, prostaglandins, pressure effects.
- โ ๏ธ Loss of Function (Functio Laesa): Pain & swelling limiting use.
๐ Clinical Relevance
- Fever in systemic inflammation is driven by IL-1 & TNF acting on the hypothalamus.
- Raised CRP & ESR are acute phase reactants produced by the liver.
- Uncontrolled acute inflammation can โ sepsis, SIRS, or chronic inflammation (e.g. Crohnโs, RA).
๐ Summary
Acute inflammation is an essential protective response, aimed at eliminating harmful agents and initiating repair.
It integrates vascular changes, leukocyte activity, and chemical mediators.
โ๏ธ While vital, if unchecked it can cause collateral tissue injury or evolve into chronic disease.