Inflammation is the protective response to eliminate the cause of cell injury and damaged tissue. It is characterized by redness, heat, swelling, pain, and loss of function. The signs are caused by increased blood flow and vascular permeability. Inflammation can be acute, lasting minutes to days, or chronic, lasting weeks or months. Acute inflammation involves recruitment of leukocytes from the bloodstream to fight infection at the site of injury. Chronic inflammation is prolonged and involves tissue destruction by mononuclear cells and attempts at healing through fibrosis. Mediators like cytokines prolong the inflammatory response.

1. INFLAMMATION
Presenter
Suraj Chhetri
M.Optom 1st year

2. INTRODUCTION
Inflammation is the protective response intended to eliminate
the initial cause of cell injury as well as necrotic cell and tissue
resulting from the original insult.

3. CONT…
•Inflammation generally denoted by suffix itis
•E.g
•Conjuntivitis
•Belpheritis
•Uveitis

4. CAUSES OF INFLAMMATION
• Infections : bacteria , fungal, viral and parasitic
• Tissue necrosis : Several molecules released from necrotic
cells are known to trigger inflammation
• Foreign bodies : dirt , sutures
• Immune reactions : A/K/A Hypersensitivity

5. SIGNS OF INFLAMMATIONS
• Redness (rubor) :An acutely inflamed tissue appears red,
due to dilatation of small blood vessels within the damaged
area (hyperemia).

6. SIGNS OF INFLAMMATIONS
• Heat (calor): Increase in temperature is readily detected due
to increased blood flow (hyperemia) through the region,
resulting in vascular dilation and the delivery of warm blood
to the area.

7. SIGNS OF INFLAMMATIONS
• Swelling (tumor): Swelling results from edema, the
accumulation of fluid in the extravascular space as part of the
inflammatory fluid exudate.

8. SIGNS OF INFLAMMATIONS
• Pain (dolor): Pain results partly from the stretching and
distortion of tissues due to inflammatory edema and, in part
from some of the chemical mediators of acute inflammation,
especially bradykinin and some of the prostaglandins.

9. SIGNS OF INFLAMMATIONS
• Loss of function (functio laesa): Loss of function, a well-
known consequence of inflammation, was added by Virchow
(1821-1902) a/k/s father of modern pathology. Especially
seen in later phase of inflammation.

10. SEQUENTIAL STEPS OF INFLAMMATION
• The offending agent, which is located in extravascular
tissues, is recognized by host cells and molecules.
• Leukocytes and plasma proteins are recruited from the
circulation to the site where the offending agent is located.
• The leukocytes and proteins are activated and work together
to destroy and eliminate the offending substance.
• The reaction is controlled and terminated.
• The damaged tissue is repaired.

11. CONTD..
CONCLUSION
1. Recognition of the injurious agents
2. Recruitment of leukocytes
3. Removal of the agents
4. Regulation (control) of the response
5. Resolution (repair)
5 “R”s

12. ACUTE INFLAMMATION
Acute inflammation has three major components:
(1) Dilation of small vessels, leading to an increase in blood
flow
(2) Increased permeability of the microvasculature, enabling
plasma proteins and leukocytes to leave the circulation
(3) Emigration of the leukocytes from the microcirculation,
their accumulation in the focus of injury, and their activation to
eliminate the offending agent

14. CONTD…
CHANGE IN VASCULAR FLOW AND CALIBER
• Vasodilation is induced by the action of several mediators,
notably histamine, on vascular smooth muscle.
• The result is increased blood flow, which is the cause of heat
and redness (erythema) at the site of inflammation.
• The loss of fluid and increased vessel diameter lead to slower
blood flow, concentration of red cells in small vessels, and
increased viscosity of the blood.

15. CONTD…
INCREASED VASULAR PERMIABILITY (VASCULAR
LEAKAGE)
• Retraction of endothelial cells resulting in opening of inter-
endothelial spaces is the most common mechanism of vascular
leakage
• Endothelial injury resulting in endothelial cell necrosis and
detachment.

16. LEUKOCYTE RECRUITMENT TO SITE OF
INFLAMMATION
• Leukocytes are recruited from the blood into the
extravascular tissue where tissue injury, and are activated to
perform their functions.
• Leukocyte recruitment is a multistep process consisting of:
 Loose attachment to and rolling on endothelium (mediated
by selectins)
Firm attachment to endothelium (mediated by integrins)
 Passes through inter-endothelial gaps and the process
known as diapedesis

17. NEUTROPHI EVENTS IN ACUTE
INFLAMMATION

18. PHAGOCYTOSIS AND CLEARENCE OF
OFFENDING AGENT
1. Recognition and attachment of the particle (chemotaxis) to
be ingested by the leukocyte.
2. Engulfment, with subsequent formation of a phagocytic
vacuole.
3. Killing or degradation of the ingested material.

19. MEDIATORS OF INFLAMMATION

20. MORPHOLOGICAL PATTERN OF ACUTE
INFLAMMATION
1. SEROUS INFLAMMATION: Serous inflammation is
marked by the exudation of cell poor fluid into spaces
created by injury
2. FIBRINOUS INFLAMMATION: With a large increase
in vascular permeability, higher-molecular weight proteins
such as fibrinogen pass out of the blood, and fibrin is
formed and deposited in the extracellular space
3. PURULENT (SUPPURATIVE) INFLAMMATION:
Purulent inflammation is characterized by the production
of pus, an exudate consisting of neutrophils, the liquefied
debris of necrotic cells, and edema fluid.

21. CONTD..
ULCER
• An ulcer is a local defect, or excavation, of the surface of an
organ or tissue that is produced by the sloughing (shedding)
of inflamed necrotic tissue. Ulceration can occur only when
tissue necrosis and resultant inflammation exist on or near a
surface.
• Acute and chronic inflammation often coexist in ulcers, such
as peptic ulcers of the stomach or duodenum and diabetic
ulcers of the legs.

22. OUTCOME OF ACUTE INFLAMMATION
• THERE MAY BE THREE POSSIBLE OUTCOME ,
1. Complete resolution
2. Healing by connective tissue replacement (scarring or
fibrosis
3. Progression of the response to chronic inflammation

23. CHRONIC INFLAMMATION
Chronic inflammation is a response of prolonged duration
(weeks or months) in which inflammation, tissue injury, and
attempts at repair coexist, in varying combinations.
Causes
1. Persistent infections by microorganisms that are difficult to
eradicate, such as mycobacteria, these organisms often evoke
an immune reaction called delayed-type hypersensitivity

24. CONTD….
2. Hypersensitivity diseases, chronic inflammation plays an
important role in a group of diseases that are caused by
excessive and inappropriate activation of the immune system.
In autoimmune diseases self (auto) antigens evoke a self-
perpetuating immune reaction that results in chronic
inflammation and tissue
3.Prolonged exposure to potentially toxic agents, either
exogenous or endogenous.

25. MORPHOLOGICAL FEATURES OF
CHRONIC INFLAMMATION
• Infiltration with mononuclear cells, which include
macrophages, lymphocytes, and plasma cells
• Tissue destruction, induced by the persistent offending agent
or by the inflammatory cells
• Attempts at healing by connective tissue replacement of
damaged tissue, accomplished by angiogenesis (proliferation
of small blood vessels) and, in particular, fibrosis

26. CELLS AND MEDIATORS OF CHRONIC
INFLAMMATION
• It is mediated by cytokines produced by macrophages and
lymphocytes (notably T lymphocytes); bidirectional
interactions between these cells tend to amplify and prolong
the inflammatory reaction.

27. ACUTE VS CHRONIC INFLAMMATION

29. SYSTEMIC EFFECT OF INFLAMMATION
• Fever: Cytokines (TNF, IL-1) stimulate production of PGs in
hypothalamus
• In some severe infections, septic shock: Fall in blood
pressure, disseminated intravascular coagulation, metabolic
abnormalities; induced by high levels of TNF and other
cytokines

30. TISSUE REPAIR
Repair of damaged tissues occurs by two types of reactions:
1. Regeneration by proliferation of residual (uninjured) cells
and maturation of tissue stem cells
2. Deposition of connective tissue to form a scar

31. CONTD…

32. THANK YOU