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
 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.
 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.
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, alkalis, reducing
agents and bacterial toxins, etc.
 Due to tissue necrosis caused due to ischemia or
infarction.
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.
The components of acute inflammation, are
described under two broad headings-
 VASCULAR EVENTS.
 CELLULAR EVENTS.
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.
 Cellular Events-
The main function of inflammation is the
delivery of leukocytes to the site of injury.
Leukocytes ingest the offending agent, kill
microbes and degrade foreign antigens and
necrotic tissue The most important
leukocytes involved are neutrophils and
macrophages.
a) EXTRAVASATION. b) PHAGOCYTOSIS.
a) Extravasation of Neutrophils-
The migation of neutrophils from the
vascular lumen to the interstitial tissue is
called extravasation and involves the
following sequence of events: margination,
rolling and adhesion, diapedesis, chemotaxis.
b)Phagocytosis-
Physis is a process of engulfment of solid
particulate material by the cells. There are
two types of phagocytic cells-
 Polymorphonuclear neutrophils, also known
as macrophages.
 Monocytes, also known as macrophages.
Acute inflammation has local and systemic
effects, which may be-
 Beneficial Effects of Inflammation.
 Harmful Effects of Inflammation.
 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
 Fibrin formation from exuded fibrinogen,
which serves as a matrix for granulation t
formation.
 Delivery of nutrients and oxygen, which are
essential for repair and healing, by increased
blood flow through the area.
 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.
 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.
 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.
 Abscess formation: It occurs by suppuration,
when there is tissue necrosis due to
intenseneutrophilic 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.
 Chronic inflammation: If the injurious
stimulus is persistent and cannot be resolved
by the acute inflammatory response, it
progresses to chronic inflammation.
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.
 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.
 Macrophages-
Macrophages are
phagocytic cells (which
eliminates microbes
and damaged tissues)
derived from blood
monocytes during
embryonic
development and are
the key cellular
component of a
chronic inflammatory
response.
 Lymphocytes-
Lymphocytes (T
and B) get activated in
chronic inflammatory
conditions by contact
with an antigen or by
exposure to bacterial
toxins .
 Plasma Cells-
Plasma cells
produce
antibodies
directed either
against foreign
antigens or
against self-
antigens.
 Mast Cells-
Mast cells are
scattered in
connective tissues
and play a role in
acute as well as
persistent
inflammatory
reactions.
 Eosinophils-
They are
characteristically
seen in immune
reaction
mediated by IgE
and Parasitic
infection
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).
INFLAMMATION.pptx
INFLAMMATION.pptx

INFLAMMATION.pptx

  • 3.
    Inflammation is thelocal 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- Chronicinflammation 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, alkalis, reducing agents and bacterial toxins, etc.  Due to tissue necrosis caused due to ischemia or infarction.
  • 8.
    Cardinal Signs ofAcute 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 ofacute inflammation, are described under two broad headings-  VASCULAR EVENTS.  CELLULAR EVENTS.
  • 10.
    Vascular Events- The sequenceof 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- Themain function of inflammation is the delivery of leukocytes to the site of injury. Leukocytes ingest the offending agent, kill microbes and degrade foreign antigens and necrotic tissue The most important leukocytes involved are neutrophils and macrophages.
  • 12.
    a) EXTRAVASATION. b)PHAGOCYTOSIS.
  • 13.
    a) Extravasation ofNeutrophils- The migation of neutrophils from the vascular lumen to the interstitial tissue is called extravasation and involves the following sequence of events: margination, rolling and adhesion, diapedesis, chemotaxis.
  • 14.
    b)Phagocytosis- Physis is aprocess of engulfment of solid particulate material by the cells. There are two types of phagocytic cells-  Polymorphonuclear neutrophils, also known as macrophages.  Monocytes, also known as macrophages.
  • 15.
    Acute inflammation haslocal and systemic effects, which may be-  Beneficial Effects of Inflammation.  Harmful Effects of Inflammation.
  • 16.
     Dilution oftoxins, 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
  • 17.
     Fibrin formationfrom exuded fibrinogen, which serves as a matrix for granulation t formation.  Delivery of nutrients and oxygen, which are essential for repair and healing, by increased blood flow through the area.
  • 18.
     Digestion ofnormal 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.
  • 19.
     Inappropriate inflammatoryresponse: 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.
  • 20.
     Resolution: Itrefers 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.
  • 21.
     Abscess formation:It occurs by suppuration, when there is tissue necrosis due to intenseneutrophilic 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.
  • 23.
     Chronic inflammation:If the injurious stimulus is persistent and cannot be resolved by the acute inflammatory response, it progresses to chronic inflammation.
  • 25.
    Chronic inflammation isan 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.
  • 26.
     Failure toeradicate 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.
  • 28.
     Macrophages- Macrophages are phagocyticcells (which eliminates microbes and damaged tissues) derived from blood monocytes during embryonic development and are the key cellular component of a chronic inflammatory response.
  • 29.
     Lymphocytes- Lymphocytes (T andB) get activated in chronic inflammatory conditions by contact with an antigen or by exposure to bacterial toxins .
  • 30.
     Plasma Cells- Plasmacells produce antibodies directed either against foreign antigens or against self- antigens.
  • 31.
     Mast Cells- Mastcells are scattered in connective tissues and play a role in acute as well as persistent inflammatory reactions.
  • 32.
     Eosinophils- They are characteristically seenin immune reaction mediated by IgE and Parasitic infection
  • 33.
    Systemic Effectsof ChronicInflammation – 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).