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Acute inflammation
All purpose defence mechanism produced to contain and isolate injury to destroy or neutralise injury ideally resolves may become chronic to achieve healing and repair
Terminology
Add -itis to end:
hepatitis endocarditis cystitis dermatitis pleuritis (pleurisy) pneumonitis (pneumonia)
Outline
Causes macroscopic changes microscopic changes
vessels cells (including chemotaxis and phagocytosis)
Microscopic changes
Initial constriction then dilatation of vessels Increased blood flow Increased permeability Formation of exudate Migration of leucocytes through wall Oedema
Vessels
Post-capillary venules permeability = leakiness
enhances migration of cells dilution of toxins stimulate lymphatics/immune response deposition of proteins eg fibrin to form mechanical barrier
Cells
Movement of white cells from blood flow to focus of injury
margination pavementing transmigration/diapedesis
chemotaxis phagocytosis
Cells 1
Neutrophil polymorphs first cell to arrive predominant cell for first 6-24h most common polymorph mobile, phagocytic and responds to chemotaxis segmented nucleus, granular cytoplasm full of granules containing enzymes etc
Cells 2
Eosinophils especially allergy and helminth infections bilobed, red granules Basophils/mast cells especially early blue/purple cytoplasm degranulates with release of vasoactive amines
Cells 3
Monocytes/macrophages circulating/tissue second main cell of acute inflammation predominate after 24h mobile, phagocytic, responds to chemotaxis attacks and clears up bean shaped nucleus, copious cytoplasm
Chemotaxis
Bacteria fungi immune complexes toxins complement components lipoxygenase products white cell breakdown products
Phagocytosis
Recognition and attachment
mechanical contact opsonisation
Engulfment
pseudopods phagosome
Controlled by mediators
Connection between stimulus and response:
suspected substance should be present injection should cause inflammation inhibition should prevent inflammatory repsonse
Mediators
Circulating in plasma
Intracellular
preformed synthesised
Clinical features
Pyrexia drowsiness lethargy leukocytosis decreased appetite acute phase proteins
Summary
Stereotypic response to injury contain, isolate and destroy five cardinal signs vascular response cellular element controlled by mediators resolution, repair, chronic, suppuration or death