Inflammation is the body's response to injury or infection that is characterized by redness, swelling, heat, and pain. The inflammatory process involves increased blood flow, capillary permeability, and migration of leukocytes to the site of injury. This results in local swelling, redness, heat, and pain. The outcome of inflammation depends on the severity, and can result in resolution, repair with scarring, or areas of tissue destruction. Chemical mediators intensify the inflammatory process and generate more mediators, while different types of exudates are produced depending on their protein and cellular contents.

1. INFLAMMATION
PRAKASH S,BSN RN RM

2. Learning Objectives
• List characteristics and clinical manifestations
– Acute inflammation
– Types of exudates: serous, purulent, fibrinous,
hemorrhagic
• Describe possible outcomes of an inflammatory
reaction and its harmful effects
• Explain chemical mediators of inflammation and
role in intensifying the inflammatory process
• Compare inflammation and infection

3. Inflammatory Reactions
• A nonspecific response to any agent that
causes cell injury
• Agents may be
– Physical (heat or cold)
– Chemical (concentrated acid)
– Microbiologic (bacterium or virus)

4. Local and Systemic Effects of
Inflammation
• Local effects
– Capillary dilatation
• Increased blood flow, increased warmth and
redness
– Increased capillary permeability, leading to
extravasation of fluid, leading to swelling
– Attraction of leukocytes
• Migrate to site of injury
• Adhere to endothelium of small blood vessels
• Systemic effects: fever, leukocytes

5. Local and Systemic Effects of Inflammation

6. Characteristic Signs of Inflammation
• Heat and redness
– Dilated blood vessels and slowing of blood
through vessels
• Swelling
– Accumulation of fluid and exudate due to
extravasation of plasma
• Tenderness and pain
– Irritation of nerve endings

7. Acute inflammation, ear
Extensive burn with marked fluid
extravasation
© Courtesy of Leonard Crowley, M.D./University of Minnesota Medical School

8. Inflammatory Process (1 of 2)
• Acute inflammatory process
– Polymorphonuclear leukocyte cell
• Most important cell in acute inflammatory response;
actively phagocytic cell
• Mononuclear cells (monocytes, macrophages) follow
later to clean up tissue debris

9. Inflammatory Process (2 of 2)
• Severe inflammatory process
– Systemic effects become evident (feeling ill,
fever)
– Bone marrow accelerates production of
leukocytes resulting in increased levels in
bloodstream
– Liver produces acute phase proteins such as
C-reactive protein
• Mild inflammatory process
– Self-limiting, subsides with tissue resolution

10. Outcome of Inflammation
• Depends on amount of tissue damage
– Severe inflammatory process
• Tissue damage → replacement of damage cells
→ heal with scarring
– Mild inflammatory process
• Self-limiting, subsides with tissue resolution

11. • Outcomes
– Resolution
– Repair
– Areas of destruction replaced by scar tissue
– Mediators intensify inflammatory process
– Mediators generate more mediators
Outcome of Inflammation

12. Exudate
• Fluid mixture of protein, leukocytes, and tissue
debris
• Proportion of protein and inflammatory cells vary
• Serous: primarily fluid, little protein
• Purulent: largely inflammatory cells (pus)
• Fibrinous: rich in fibrinogen; coagulates and forms
fibrin; produces a sticky film on surface of inflamed
tissue
• Adhesions: bands of fibrous tissue that bind
adjacent tissue together
• Hemorrhagic: increased red blood cells

13. Chemical Mediators of Inflammation
(1 of 2)
• Chemical agents that intensify the
inflammatory process
• Cell-derived mediators
– Mast cells: specialized connective tissue cells
with granules filled with histamine, a vasodilator
– Histamine and serotonin: also in blood platelets
– Prostaglandins
– Leukotrienes: synthesized from arachidonic acid

14. Chemical Mediators of Inflammation
(2 of 2)
• Mediators from blood plasma
– Bradykinin
– Complement
• Activated by antigen-antibody reaction
• Series of proteins that interact in a regular
sequence

15. Chemical Mediators of Inflammation

16. Lysosomal Enzymes and Antigen-
Antibody Reaction
• Lysosomal enzymes
– From cytoplasm of phagocytic cells neutrophils and
monocytes that can digest protein material
• Antigen-antibody reaction
– Activates complements generating mediators
• Harmful effects of inflammation
– Tissue injury results in part from the injurious agent
and the inflammatory reaction itself
– Adrenal corticosteroids: used to suppress a persistent
inflammatory

17. Infection
• Inflammatory process caused by disease-
producing organisms
• “itis”: suffix indicates an infection or
inflammatory process such as
appendicitis, hepatitis, colitis
• Cellulitis: acute spreading infection at any
site
• Abscess: infection associated with
breakdown of tissues, formation of pus

18. Infection
• Septicemia: overwhelming infection
where pathogenic bacteria gain access to
bloodstream
• Pathogenic: capable of producing disease
• Virulence: a measure of severity of
disease
• Host: affected individual or animal

19. Infection
© Courtesy of Leonard Crowley, M.D./University of Minnesota Medical School

20. Infection
• Involves the relationship between invading
organism and defenses of the body

21. Infection
• Factors influencing the outcome
– Virulence of organism
– Numbers of invading organisms
– Host resistance

22. Chronic Infection
• State in which the pathogenic organism
and the host are evenly matched
• Relatively quiet, smoldering inflammation,
associated with repeated attempts of the
body at healing
• Predominant cells: lymphocytes, plasma
cells, and monocytes

23. Discussion
1. How do the mediators of inflammation function?
2. What are the possible outcomes of an
inflammation?
3. An exudate high in fibrinogen can coagulate
producing fibrin that causes a sticky film on tissues
that causes normally separate tissues to adhere
together. This results from the production of:
– Serous exudate
– Purulent exudate
– Fibrinous exudate
– Hemorrhagic exudate
– None of the above