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| Acute Inflammation
π₯ 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 β‘οΈ 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.
π Stages of Acute Inflammation
- 1. Initiation ποΈ :
- Recognition of harmful stimuli via pattern recognition receptors (PRRs) on immune cells.
- Release of inflammatory mediators such as histamine, prostaglandins, cytokines.
- 2. Vascular Changes π :
- Vasodilation: Increased blood flow β redness & heat.
- Increased vascular permeability: Plasma proteins & fluid leak into tissues β oedema (swelling).
- 3. Cellular Events π§ββοΈπ¦ :
- Leukocyte recruitment: Margination β rolling β adhesion β transmigration (diapedesis).
- Phagocytosis: Neutrophils & macrophages engulf debris β fuse phagosome with lysosome β destruction by ROS & enzymes.
π§ͺ Chemical Mediators of Inflammation
- Vasoactive Amines β‘ :
- Histamine: Mast cells, basophils, platelets β vasodilation & permeability.
- Serotonin: Platelets & enterochromaffin cells β similar vascular effects.
- Plasma Protein Systems π©Έ :
- Complement (C3a, C5a): Anaphylatoxins β permeability & chemotaxis. C3b acts as an opsonin.
- Coagulation: Fibrin meshwork forms a clot scaffold.
- Kinin system: Bradykinin β vasodilation, pain, permeability.
- Arachidonic Acid Metabolites π :
- Prostaglandins (COX): Pain, vasodilation, fever.
- Leukotrienes (LOX): Chemotaxis, permeability, bronchospasm.
- Cytokines & Chemokines π’ :
- TNF, IL-1: Fever, adhesion molecules, systemic acute phase response.
- Chemokines: Recruit leukocytes to the site.
- ROS & Nitric Oxide βοΈ :
- Microbicidal and signalling roles.
- Excess = tissue injury (ARDS, reperfusion injury).
π§ Outcomes of Acute Inflammation
- β
Resolution: Full clearance & return to normal tissue.
- π₯ Abscess: Localised pus collection when clearance fails.
- β»οΈ Chronic inflammation: If stimulus persists β fibrosis & immune activation.
- π§± Fibrosis/scarring: When tissue repair is incomplete.
π©Ί Clinical Signs & Symptoms ("Cardinal Signs")
- π΄ Redness (Rubor): Vasodilation, hyperaemia.
- π₯ Heat (Calor): Increased blood flow & metabolic activity.
- π§ Swelling (Tumour): Oedema from plasma leakage.
- π£ Pain (Dolor): Mediated by bradykinin, prostaglandins, pressure effects.
- β οΈ Loss of Function (Functio Laesa): Pain & swelling limiting use.
π 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 β sepsis, SIRS, or chronic inflammation (e.g. Crohnβs, RA).
π 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.
βοΈ While vital, if unchecked it can cause collateral tissue injury or evolve into chronic disease.