Chapter 4 Inflammation and Repair
Chapter 4 Inflammation and Repair
The Inflammatory Reaction
CHARACTERISTICS OF THE INFLAMMATORY REACTION
Dilatation of blood vessels.
Migration of leukocytes through vessel walls to the site of inflammation.
Increased capillary permeability.
Extravasation of fluids.
CLINICAL MANIFESTATIONS OF INFLAMMATION
Heat and redness: dilated blood vessels.
Swelling: accumulation of fluid and exudate.
Tenderness and pain: irritation of nerve endings.
TYPES OF INFLAMMATION REACTIONS
Serous inflammation: chiefly fluid exudate.
Purulent inflammation: chiefly inflammatory cells.
Fibrinous inflammation: exudate rich in protein, which coagulates.
Hemorrhagic inflammation: many capillaries ruptured, allowing escape of red cells.
SYSTEMIC EFFECTS OF INFLAMMATION
Patient feels ill.
Elevated temperature.
Leukocytosis.
OUTCOME OF INFLAMMATION
Resolution: inflammation subsides and tissues return to normal.
Repair: replacement of damaged cells and tissues.
Large areas of destruction replaced by scar tissue.
Mediators intensify inflammatory process and generate more mediators.
CHEMICAL MEDIATORS OF INFLAMMATION
Mast cells: discharge granules containing mediators.
Kinins form from blood proteins leaking into inflamed area.
Activation of complement generates mediators.
THE ROLE OF LYSOSOMAL ENZYMES IN THE INFLAMMATORY PROCESS
Lysosomal enzymes released from leukocytes cause tissue injury.
Injury generates more mediators, which promotes further inflammation and tissue injury.
INFLAMMATION CAUSED BY ANTIGEN–ANTIBODY INTERACTION
Interaction activates complement, leading to formation of mediators. This attracts leukocytes.
Lysosomal enzymes from leukocytes cause tissue injury
HARMFUL EFFECTS OF INFLAMMATION
Inflammation usually subsides.
Persisting inflammation may cause severe tissue injury.
It may be necessary to suppress inflammatory reaction by corticosteroids to reduce tissue damage.
Infection
AN INFLAMMATION CAUSED BY A PATHOGENIC ORGANISM
Terms used to name infections:
Named by adding -itis to name of affected organ.
Cellulitis: acute spreading infection.
Abscess: tissue breakdown forming pus pockets.
Lymphadenitis: inflammation of draining lymph nodes.
Septicemia: bloodstream infection.
Factors influencing outcome:
Virulence of organism.
Dosage.
Resistance of host’s body.
CHRONIC INFECTION
Organisms and host evenly balanced.
Lymphocytes and plasma cells predominate.
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