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Acute inflammation

The response of living tissue to injury


same as: the reaction of the microcirculation and its contents to injury

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)

controlling factors systemic features outcome

Macroscopic changes = cardinal signs


Redness swelling heat pain loss of function Rubor tumor calor dolor functio laesa

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

Killing and degradation


lysosomal contents

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

Released from damaged tissue

Clinical features
Pyrexia drowsiness lethargy leukocytosis decreased appetite acute phase proteins

Outcome of acute inflammation 1


Resolution
clearance of injury clearance of inflammatory cells and mediators replacement of any injured cells normal function resumed

spontaneous or with treatment eg pneumonia

Outcome of acute inflammtion 2


Repair
some tissue lost may not be able to regenerate therefore replacement with granulation tissue and fibrosis likely less than ideal function

Outcome of acute inflammation 3


Chronic inflammation
if injury cannot be dealt with repeated episodes

Outcome of acute inflammation 4


Suppurative inflammation
pus is more exaggerated form of acute inflammation neutrophils, dead cells, bacteria and debris if walled-off and surrounded by a fibrous rim it becomes an abscess

Outcome of acute inflammation 5


Septicaemia
organism gains access to lymphatics then blood or blood direct response heightened mortality high

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

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