Visit: Inflammation ; Inflammatory cells in acute and chronic inflammation ; Acute Inflammation ; Types of Acute Inflammation ; Chronic Inflammation ; Wound Healing .

Function of chemotactic agents:

1. Recognition and engulfment of microorganisms by covering it with serum protein (opsonin).

2. Activation of leucocytes causing liberation of oxygen metabolites, enzymes etc. which kills the engulfed microorganisms.

3. These liberated toxic metabolites and proteases also cause tissue damage.

Different mediators are discussed separately but they are intimately related and their actions start in sequence.

Once started, they are quickly inactivated or destroyed by enzymes or other substances, so that inflammation may not persist.

Chemical mediators may be:

1. Exogenous - microbial products or  2. Endogenous.

         Endogenous chemical mediators:

Early phase: 

Vasoactive amines :

1. Histamine - Source: mast cells, basophils, platelets.  Action: increases vascular permeability.

2. Serotonin (5HT)- Source: platelets.  Action: similar to histamine.

Intermediate Phase:

1. Kinin system :

Kallikrein (Plasma substrate) : i) Plasma - Bradykinin ; ii) Tissue - Kallidin.  Action: i) Pain and increased vascular permeability  ; ii) Chemotaxis of neutrophils and monocytes.

2.Compliment derivatives : Action: acts by increasing vascular  permeability and chemotaxis of neutrophils monocytes (3a and 5a called anaphylatoxin).    

3. Permeability globulin : Present in plasma. Action: similar to compliment.

4. Leukotrienes : present in all leukocytes. Action: similar to compliment.

Late phase: 

1. Prostaglandins : Liberated from all leukocytes and platelets.  Action: (i) Vasodilation, pain and fever (ii) Potentiates actions of other chemical mediators.

2. Slow Reacting Substance of Anaphylaxis (SRS- A) : Liberated from mast cells, basophils and neutrophils. Action: potentiates  the actions of other chemical mediators.

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An outline of Diagnostic Techniques available in Pathology

Cellular Injury

Diagram showing Structural Changes in Reversible and Irreversible Cell Injury

Autolysis

Heterolysis

Necrosis

Coagulation (Coagulative) necrosis

Caseative (Caseous) necrosis

Liquefaction necrosis

Fat necrosis

Fibrinoid necrosis

Apoptosis

Gangrene

Pathologic Calcification

Hyaline Change

Atrophy

Hypertrophy

Hyperplasia

Metaplasia

Aplasia

Hypoplasia