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INFLAMMATION.pptx
1.
2.
3. Inflammation is the local physiological
response to tissue injury. It is a
protective endeavor by the body to
remove the injurious stimuli as well as
to initiate the process of healing and
repair
4. Acute Inflammation –
Acute inflammation is relatively short-
lived and may last for a few minutes to a few
days only, and involves infiltration by
neutrophils and exudation of fluid and
plasma proteins,
e.g., in skin repair, infiltrating leukocytes are
the major cellular components.
5. Chronic Inflammation-
Chronic inflammation is of longer duration
lasting several months to years and is
associated with lymphocytes, macrophages,
the proliferation of blood vessels, and
fibrosis.
Inflammation is terminated when the
injurious stimulus is removed or once the
mediators of inflammation have degenerated
or inhibited.
6. Etiology-
Bacterial, viral, parasites, and other infections.
Physical injuries due to trauma, and exposure to
ionizing radiation, heat, and cold.
Injury caused due to exposure to chemicals, such
as corrosive agents, acids, alkaline agents and
bacterial toxins, etc.
Due to tissue necrosis caused due to ischemia or
infarction.
7.
8. Cardinal Signs of Acute Inflammation
•Swelling (tumor) due to increased
vascular permeability.
•Redness (rubor) due to vascular
congestion/ arteriolar dilatation.
•Pain (dolor) due to release of a mediator.
•Heat (calor) due to dilation of blood
vessels.
•Loss of function (function laesa) due to
pain, swelling, injury, scar.
9. The components of acute inflammation, are
described under two broad headings-
VASCULAR EVENTS.
CELLULAR EVENTS.
10. Vascular Events-
The sequence of the hemodynamic changes in
acute inflammation is as follows:
Vasoconstriction: This is the earliest change seen
in acute inflammation.
Vasodilation: There is a dilation of the blood
vessels, which begins with the arterioles
followed by the capillaries and venules. This leads
to a local increase in vascular flow, which
manifests as redness and warmth. The primary
mediator for vasodilation is histamine.
11. Cellular Events-
The main function of inflammation is the
delivery of leukocytes to the site of injury.
Leukocytes ingest the agent, kill microbes
and degrade foreign antigens and necrotic
tissue .The most important leukocytes
involved are neutrophils and macrophages.
13. a) Extravasation of Neutrophils-
The migation of neutrophils from the
vascular lumen to the interstitial tissue is
called extravasation.
14. b)Phagocytosis-
Physis is a process of engulfment of solid
particulate material by the cells. There are
two types of phagocytic cells-
Polymorphonuclear neutrophils.
Monocytes.
15. Acute inflammation has local and systemic
effects, which may be-
Beneficial Effects of Inflammation.
Harmful Effects of Inflammation.
16. Dilution of toxins, such as those produced by
bacteria and allows them to be carried by lymphatics
thereby stimulating an immune response.
Entry of antibodies, due to increased vascular
permeability.
Transport of drugs, such as antibiotics to the site
where bacteria are multiplying.
Delivery of nutrients and oxygen, which are essential
for repair and healing, by increased blood flow
through the area.
17. Digestion of normal tissues: Enzymes, such as
collagenases and proteases may digest normal
tissues, resulting in their destruction; for example,
in type III hypersensitivity reactions, in some types
of glomerulonephritis, and in abscess cavities.
Swelling: The swelling of acutely inflamed tissues
may be harmful; for example, the swelling of
epiglottis due to Haemophilus influenzae in
children may obstruct the airway resulting in death.
18. Inappropriate inflammatory response: Such as
those which occur in type I hypersensitivity
reactions where the provoking environmental
antigen otherwise poses no threat to the
individual. Such allergic inflammatory
responses may be life-threatening, for
example,extrinsic asthma.
19. Resolution: It refers to the complete
restoration of the inflamed tissue back to its
normal state.
Fibrosis: Healing by connective tissue
replacement or scarring/fibrosis occurs when
the injury involves substantial amounts of
tissue destruction, or when the damaged
tissue is unable to regenerate.
20. Abscess formation: It occurs due to
neutrophilic infiltration in the inflamed tissue.
The abscess cavity contains pus, which is an
opaque yellowish-white liquid containing
dead leukocytes, bacteria, and debris from
destroyed cells.
21.
22. Chronic inflammation: If the injurious
stimulus is persistent and cannot be resolved
by the acute inflammatory response, it
progresses to chronic inflammation.
23.
24. Chronic inflammation is an inflammation
of prolonged duration, which can extend
over a long period of time. Chronic
inflammation usually follows recurrent
acute inflammation; however, may begin
insidiously as a low-grade, gradual
process.
25. Failure to eradicate infectious organisms, such as
Mycobacterium, fungi, protozoa, and other viruses
that can withstand host defenses.
Excessive exposure to exogenous or endogenous
irritants.
Autoimmune disease may also lead to chronic
inflammation in which the body's immune system
recognizes its own body cells as a foreign antigen.
26.
27. Macrophages-
Macrophages are
phagocytic cells (which
eliminates microbes
and damaged tissues)
and these are the key
cellular component of
a chronic inflammatory
response.
28. Lymphocytes-
Lymphocytes (T
and B) get activated in
chronic inflammatory
conditions by contact
with an antigen or by
exposure to bacterial
toxins .
29. Plasma Cells-
Plasma cells
produce
antibodies
directed either
against foreign
antigens or
against self-
antigens.
30. Mast Cells-
Mast cells are
scattered in
connective tissues
and play a role in
acute as well as
persistent
inflammatory
reactions.
32. Systemic Effectsof Chronic Inflammation –
A patient suffering from a chronic
inflammatory condition may show the
following systemic manifestations:
Fever
Leukocytosis
Anemia (of chronic disease)
Elevated erythrocyte sedimentation rate (ESR).
