2. INTRODUCTION
• INFLAMMATION : (derived from LATIN word
inflammare To set on fire)is a localized protective
response elicited by injury or destruction of tissues
which serves to destroy ,dilute or wall of both the
injurious agent and injured tissues.
• The function of inflammation is to eliminate the initial
cause of cell injury, clear out necrotic cells and tissues
damaged and the inflammatory process, and initiate
tissue repair.
3. Intro…
• Inflammation is Response of Vascular connective
tissue towards injury
• Whenever the tissue is damage by any region
Inflammation is there if tissue is Vascularized.
• Its mean those tissue which is not Vascular there is no
Inflammation.
4. DEFINITION
• Inflammation is defined as the local response of living
tissues to injury due to any agent. It is a body defense
reaction in order to eliminate or limit the spread of
injurious agent as well as to remove the consequent
necrosed cell and tissues.
5. DEFINITION
A response of vascularized tissues to infections and damaged tissues
that brings cells and molecules of host defense from the circulation to
the sites where they are needed, in order to eliminate the offending
agents.
6. Agents causing inflammation
1.INFECTIVE AGENTS like bacteria ,viruses,fungi & parasites.
2.IMMUNOLOGICAL AGENTS like antigen antibody reactions.
3.PHYSICAL AGENTS like heat,cold,radiation,trauma
4.CHEMICAL AGENTS like organic and inorganic poisons
5.INERT MATERIALS such as foreign bodies
7. Purpose of Inflammation
Inflammation involves two processes:
a) Inflammatory response: Remove or Neutralized the cause of Injury.
b) Healing : Repair Process
8. SIGNS OF INFLAMMATION
The famous 5 cardinal signs of inflammation as:
1. Rubor: Redness
2. Tumor: Swelling
3. Color: Heat
4. Dolor: Pain
5. Functio Laesa: Loss of function
9.
10. Inflammation and Infection
INFLAMMATION
• Inflammation is a protective
response by the body to variety
of etiologic agents
INFECTION
• Invasion of harmful microbes
into the body and their resultant
ill effects by toxins
11. BRIEF INTRODUCTION
Acute Inflammation
• The initial, rapid response to infections and tissue damage is called
acute inflammation.
• Its develops within minutes or hours and is of short duration, lasting
for few hours or a few days.
• Its main characteristics are the exudation of fluid and plasma
proteins (edema) and the emigration of leukocytes, predominantly
neutrophils (also called polymorphonuclear leukocytes).
• Acute inflammation is one of the reactions of the type of host
defense known as Innate immunity
12. BRIEF INTRODUCTION
Chronic Inflammation
• If acute inflammation fails to clear the stimulus, the reaction can
progress to a protracted phase that is called chronic inflammation.
• Chronic inflammation is of longer duration and is associated with
more tissue destruction, the presence of lymphocytes and
macrophages, the proliferation of blood vessels, and the deposition of
connective tissue.
• Chronic inflammation is more prominent in the reactions of Adaptive
immunity
13. Inflammation: Acute VS. Chronic
• ACUTE INFLAMMATION
• Rapid onset
• Slow duration
• Accumulation of fluids and
plasma at the affected site
• Neutrophils are acute
inflammatory cells
• Represents early body reactions
followed by repair
• CHRONIC INFLAMMATION
• Slower onset
• Longer duration
• Occurs after the inflammation
persist for a longer time
• Lymphocytes ,plasma cells,
macrophages are chronic
inflammatory cells
• Simultaneous inflammation and
repair
14.
15. ACUTE INFLAMMATION
• The changes is acute inflammation can be described under the
following 2 headings:
1. Vascular events
2. Cellular events
16. VASCULAR EVENTS
Alteration in the microvasculature is the earliest response to tissue
injury. These alterations include :
• Haemodynamic changes
• Altered vascular permeability
17. Haemodynamic changes
Earliest features of inflammatory response result from changes in vascular
flow and calibre of small blood vessels in the injured tissue.
• TRANSIENT VASOCONSTRICTION
• PERSISTENT PROGRESSIVE VASODILATATION
• ELEVATED LOCAL HYDROSTATIC PRESSURE
• TRANSUDATION OF FLUID IN EXTRACELLULAR SPACE( swelling at local site)
• SLOWING OR STATIS
• INCREASED CONCENTRATION OF RED CELLS ( raised bloodviscosity)
• LEUCOCYTIC MARGINATION AND EMIGRATION
18. FEATURES
• Red line : appears within a few seconds due to local vasodilatation.
• Flare : bright reddish appearance surrounding the red line and result
from vasodilatation.
• Wheal : swelling or edema due to transudation of fluid into
extravascular space.
19. ALTERED VASCULAR
PERMEABILITY
• In initial stage the escape of the fluid is due to vasodilatation and
consequent elevation in hydrostatic pressure. This fluid is transudate.
• Later exudate appears by increased vascular permeability of
Microvasculation
20. MECHANISM OF INCREASED VASCULAR
PERMEABILITY
1. Contraction of endothelial cells:
• Affects venules
• Capillaries and arterioles remain unaffected
• Endothelial cells develop temporary gaps resulting vascular leakiness.
• Mediated by histamines, bradykinins etc.
• This response is immediately after the injury, reversible and for short
duration( 15-30 mins).
21.
22. 2.Retraction of endothelial cells:
• Stuctural re-organisation of endothelial cells resulting in reversible
retraction.
• Affects venules
• Onset of response 4-6 hours after injury
• Last for 2-4 hours.
23. 3. Direct injury to endothelial cells:
• Appearance of physical gap at the site of detached endothelial cells.
• Affects all levels of microvasculature
• Appears immediately after injury and lasts for several hours or days.
24. 4. Endothelial injury mediated by leukocytes:
• Adherence of leucocytes to the endothelium at the site of
inflammation.
• Activated leucocytes release proteolytic enzymes causing endothelial
injury and increased vascular leakiness
• Affects mostly venules
25. 5. Leakiness in neovascularisation:
• Newly formed capillaries under the influence of vascular endothelial
growth factor during repair.
26. CELLULAR EVENTS
• The cellular phase of inflammation consists of 2 processes:
1. Exudation of Leucocytes
2. Phagocytosis
27. EXUDATION OF LEUCOCYTES
CHANGES IN THE FORMED ELEMENTS OF BLOOD EARLY STAGE OF
INFLAMMATION
• VASODILATION
• INCREASED BLOOD FLOW
• SLOWING AND STATIS OF BLOODSTREAM
• CENTRAL STREAM WIDENS AND PERIPHERAL BECOMES NARROW
• NEUTROPHILLS COMES CLOSE TO THE VESSEL WALL
28. • Rolling and adhesion- Peripherally margination and neutrophils
slowly roll over the endothelial cells lining the vessel walls. This is
followed by transient bond between the leucocytes and endothelial
cells. It includes 3 phases:
1)Selectins
2)Integrins
3)Immunoglobulins
29. Emigration
• Neutrophill move along the endothelial surface throw out
pseudopods cross the basement membrane emigration simultaneous
of RBC due to raised hydrostatic pressure giving haemorrhagic
appearance to the inflammatory exudate.
30. Chemotaxis-
• The chemotactic factor ( cytokines, platelet factor etc) mediated
transmigration of leucocytes after crossing several barriers
(endothelium, basement membrane etc) to reach the interstitial
tissues is called chemotaxis.
31.
32. PHAGOCYTOSIS
• Phagocytosis is defined as the process of engulfment of solid
particulate material by the cells(cell-eating). The cells performing this
function are called phagocytes.
• There are mainly two types of phagocytic cells:
a) Polymorphonuclear neutrophils (PMNs) which appear early in acute
inflammatory response also called as microphages.
b) Circulating monocytes and fixed tissue mononuclear phagocytes
called Macrophages .
33. • The process of phagocytosis is similar for both polymorphs and
macrophages and involves the following 4 steps:
1.Recognition and attachment stage
2. Engulfment stage
3. Secretion stage
4. Digestion or degradation stage
