Inflammation is the body's mechanism for coping with agents that could damage it. In other words, inflammation is a protective response to rid the body of the cause of cell injury and the resultant necrotic cells that cell injury produces. Although the processes of acute and chronic inflammation are an important protective mechanism used by the body to deal with potentially damaging agents, they are potentially damaging to the body and must be closely regulated.

1. Inflammations
and infections

2. Introduction
• Inflammation is the body's mechanism for coping with agents that could damage
it.
• In other words, inflammation is a protective response to rid the body of the cause
of cell injury and the resultant necrotic cells that cell injury produces.
• Although the processes of acute and chronic inflammation are an important
protective mechanism used by the body to deal with potentially damaging agents,
they are potentially damaging to the body and must be closely regulated.

3. • The basic steps in acute inflammation allow white blood cells to move from the
blood to the tissue location where they are required.
• Acute inflammation can resolve completely if the inciting agent is removed, or it
can have one of several other sequelae, including chronic inflammation

4. Definition
• Definition: It is the immediate local vascular and exudative reaction of living
tissue against an injurious agent (irritants). It is the reaction of vascularized living
tissues to local injury.
• The suffix “itis” is usually added to the inflamed organs as tonsil = tonsillitis.

5. Causes of inflammation
Causes of inflammation: They include
A-Endogenous causes:
• I-immunological reactions (Ag-Ab reaction).
• Ii-some neurological and genetical disorders.
B-Exogenous Causes:
Non-living irritants: include
• 1-Physical irritants: as mechanical trauma, cold, heat or radiation. 2-
Chemical irritants: as strong or concentrated acids or alkalis.
• 3-Neutrional irritants: as in vitamin or oxygen deficiencies.
Living irritants: include
• 1-Bacteria 2-Viruses 3-Fungi 4-Parasites They produce their
effect either through direct irritation or toxin production.

6. Signs of Inflammation
Signs of Inflammation :-
• 4 cardinal signs (Celsus) – rubor (redness); – tumor (swelling); – calor (heat);–
calor (heat); – dolor (pain)
• 5th sign functio laesa (loss of function)

8. Types of Inflammation
Types of Inflammation:- Mainly of 2 types i.e. acute and chronic
• Acute Inflammation – short duration – represents the early body reaction-
followed by healing
• Chronic inflammation – longer duration – causative agent of acute inflammation
persists for a long time
• Another variant, Chronic active inflammation : stimulus is such that it induces
chronic

9. Pathological changes in acute inflammation
Two major components of inflammation:
• Vascular stages :- leads to an increased in blood flow • changes in the small blood
vessels of the microcirculation
• Cellular stages :-leads to the migration of leukocytes from the circulation • their
activation to eliminate the injurious agent.

10. Vascular stages:
Characterized – response triplet:
• 1. momentary vasoconstriction (seconds)
• 2. vasodilatation – arterioles, venules (minutes)
• 3. increased capillary permeability consequences:
Swelling
mediator release
increased viscosity
Increased blood clotting (hours)
Mediators: •histamine • NO

11. Cellular stages:
• The cellular stage of acute inflammation is marked by changes in the
endothelial cells lining the vasculature and movement of phagocytic
leukocytes into the area of injury or infection.
Cellular stages :-
• Rolling
• Margination
• Adhesion
• Transmigration across the endothelium – diapedesis
• Chemotaxis – migration
• Formation of inflammatory barrier
• Opsonization
• Phagocytosis
• Killing
• Digestion of bacteria

12. Exudation of neutrophil leukocytes I.:-
Main stages:
• Margination :- vasodilatation – stasis:-RBC forms coils in the middle of blood
vessels •granulocytes are at the wall of vessels
• Adhesion • Granulocyte adhere to the epithelium • Function of adhesive proteins •
Pavementing

13. Exudation of neutrophil leukocytes II:-
• Emigration (diapedesis) • extravasation through pores
• Chemotaxis – migration • migration to the target • Origin and function of
chemotactic substances.
• Formation of inflammatory barrier.
• Opsonization:-the coating of an antigen with antibody or complement to enhance
binding.

14. Exudation of neutrophil leukocytes III:-
• Phagocytosis
• Recognition and adherence
• Engulfment
• Intracellular killing
• Toxic oxygen
• Nitrogen products
• Lysozymes
• Killing
• Digestion of the bacteria