INFLAMMATION
Inflammation is defined as the local response of living mammalian tissues to injury due
>
toany agent. limit the spread of injurious agent, followed by,
> It is a body defense reaction in order to eliminate or
removal of the necrosed cells and tissues.
etiologic agents (infectious or non
Inflammation is a protective response by the body to variety ofmicrobes and their resultant ill-effects
infectious), while infectionis invasion intothe body by harmful
by toxins.
The agents causing inflammation are
1. InfectiHe agems like bacteria, viruses and their toxins, fungi, parasites.
2. Immunological agents like cell-ncdiated and antigenantibody reactions.
3. Physical agems like heat,cold, radiation, mechanical trauma.
4. Chemical agents like organic andinorganic poisons.
S. Inert materials such as foreign bodics.
Inflammation involves 2 basicprocesses :- early inflammatoryresponse and I followed by healing.
Inflammation is the visible response to an immune reaction, and activation of immune response is
almost essential before inflammatory response appears.
SIGNS OFINFLAMMATION, 4 cardinal signs of inflammation as:
rubor (redness);
tumor (swelling);
calor (heat); and
dolor (pain)
fifth sign functio laesa (loss of function) was later added by Virchow.
TYPESOF INFLAMMATION.
Depending upon the defense capacity of the host and duration of response, inflammation can be classified a
acute and chronic.
A. Acute inflammation
B. B. Chronic inflammation
Acute inflammation Chronic inflammation
"Short duration (lasting less than 2 weeks) " longer duration
" Represents the early body reaction, resolves" Occurs either after the causative agent of acute
quickly and is usually followed by healing inflammation persists for a long time/ stimulus
" The main features are: is such that it induces chronic inflammation
1. Accumulation of fluid and plasma at the from the beginning.
affected site; chronic active inflammation, is the type of
2. Intravascular activation of platelets; and chronic inflammation--there are acute
3.Polymorphonuclear neutrophils exacerbations of activity.
inflammatory cells. The characteristic feature of chronic
" Acute inflammatory response may be quite inflammation
severe and is termed as fulminant acute 1. presence of chronic inflammatory
inflammation. cells(lymphocytes, plasma cells and
macrophages)
2. granulation tissue formation
3. in specific situations as granulomatous
inflammation.
, The main function of inflammation is to move
defence mechanisms fromthe vascular system out to l
(inflammatory) stimulus, and to initiate repair. Inflammation Can
tissues, as a response to an injurious short term responses, necessary repair is
somewhat subjectively divided into ACUTE (iMmediate andrepair mechanisms). Both acute and chronic
rich in
minimal) and CHRONIC(long ternm responsc, usually Changes and Cellular Events, that follow a
inflammation have two major components: Vascular
predetermined sequence. andmake their way into the adjacent tissues.
Vascular changes allowcirculating blood cells to slow down
result fromthc activation of inflammatory cells andrepair tissue.
Cellular events
ACUTE INFLAMMATION
cells already present in the involved
The process of acute inflammation is initiated by resident immune mast cells. These cells
tissue, mainly resident macrophages,dendritic cells,histiocytes, Kupffer cells andrecognize (i.e., bind) two
possess surtace receptors known as pattern recognition receptors (PRRs), which and damage-associated
subclasses of molecules: pathogen-associated molecular patterns (PAMPs)
but which
molecular patterns (DAMPs). PAMPs are compounds that are associated with various pathogens,
host-related injury
are distinguishable from host molecules. DAMPs are compounds that are associated with
and cell damage.
the PRRs
At the onset of an infection, burn, or other injuries, these cells undergo activation (one of
recognize a PAMP or DAMP) and release inflammatory mediators responsible for the clinical signs of
inflammation.
Vasodilation and its resulting increased blood flow causes the redness (rubor) and increased heat (calor).
Increased permeability of the blood vessels results in an exudation (leakage) of plasma proteins and fluid
into the tissue (edema), which manifests itself as swelling (umor).
Some of the released mediators such as bradykinin increase the sensitivity to pain (hyperalgesia, dolor).
The mediator molecules also alter the blood vessels to permit the migration of leukocytes,
tissue. The
mainly neutrophils and macrophages, outside of the blood vessels (extravasation) into the
neutrophils migrate along a chemotactic gradient created by the local cells to reach the site of injury.
The loss of function (functio laesa) is probably the result of a neurological reflex in response to pain.
In addition to cell-derived mediators, several acellular biochemical cascade systems consisting of
preformed plasma proteins act in parallel to initiate and propagate the inflammatory response. These
include the complement system activated by bacteria and the coagulation and fibrinolysis systems activated
by necrosis, e.g. a burn or a trauma
The acute inflammatory response requires constant stimulation to be sustained. Inflammatory mediators are
short-lived and are quickly degraded in the tissue. Hence, acute inflammation begins to cease once the
stimulus has been removed
ACUTE INFLAMMATION
Acute inflammatory response by the host to any agent is a
continuous process. It can be divided into two events:
Vascular events Cellular events.
Hemodynamic changes Exudation of leucocytes
Changes in vascular permeability Phagocytosis
Inflammation is defined as the local response of living mammalian tissues to injury due
>
toany agent. limit the spread of injurious agent, followed by,
> It is a body defense reaction in order to eliminate or
removal of the necrosed cells and tissues.
etiologic agents (infectious or non
Inflammation is a protective response by the body to variety ofmicrobes and their resultant ill-effects
infectious), while infectionis invasion intothe body by harmful
by toxins.
The agents causing inflammation are
1. InfectiHe agems like bacteria, viruses and their toxins, fungi, parasites.
2. Immunological agents like cell-ncdiated and antigenantibody reactions.
3. Physical agems like heat,cold, radiation, mechanical trauma.
4. Chemical agents like organic andinorganic poisons.
S. Inert materials such as foreign bodics.
Inflammation involves 2 basicprocesses :- early inflammatoryresponse and I followed by healing.
Inflammation is the visible response to an immune reaction, and activation of immune response is
almost essential before inflammatory response appears.
SIGNS OFINFLAMMATION, 4 cardinal signs of inflammation as:
rubor (redness);
tumor (swelling);
calor (heat); and
dolor (pain)
fifth sign functio laesa (loss of function) was later added by Virchow.
TYPESOF INFLAMMATION.
Depending upon the defense capacity of the host and duration of response, inflammation can be classified a
acute and chronic.
A. Acute inflammation
B. B. Chronic inflammation
Acute inflammation Chronic inflammation
"Short duration (lasting less than 2 weeks) " longer duration
" Represents the early body reaction, resolves" Occurs either after the causative agent of acute
quickly and is usually followed by healing inflammation persists for a long time/ stimulus
" The main features are: is such that it induces chronic inflammation
1. Accumulation of fluid and plasma at the from the beginning.
affected site; chronic active inflammation, is the type of
2. Intravascular activation of platelets; and chronic inflammation--there are acute
3.Polymorphonuclear neutrophils exacerbations of activity.
inflammatory cells. The characteristic feature of chronic
" Acute inflammatory response may be quite inflammation
severe and is termed as fulminant acute 1. presence of chronic inflammatory
inflammation. cells(lymphocytes, plasma cells and
macrophages)
2. granulation tissue formation
3. in specific situations as granulomatous
inflammation.
, The main function of inflammation is to move
defence mechanisms fromthe vascular system out to l
(inflammatory) stimulus, and to initiate repair. Inflammation Can
tissues, as a response to an injurious short term responses, necessary repair is
somewhat subjectively divided into ACUTE (iMmediate andrepair mechanisms). Both acute and chronic
rich in
minimal) and CHRONIC(long ternm responsc, usually Changes and Cellular Events, that follow a
inflammation have two major components: Vascular
predetermined sequence. andmake their way into the adjacent tissues.
Vascular changes allowcirculating blood cells to slow down
result fromthc activation of inflammatory cells andrepair tissue.
Cellular events
ACUTE INFLAMMATION
cells already present in the involved
The process of acute inflammation is initiated by resident immune mast cells. These cells
tissue, mainly resident macrophages,dendritic cells,histiocytes, Kupffer cells andrecognize (i.e., bind) two
possess surtace receptors known as pattern recognition receptors (PRRs), which and damage-associated
subclasses of molecules: pathogen-associated molecular patterns (PAMPs)
but which
molecular patterns (DAMPs). PAMPs are compounds that are associated with various pathogens,
host-related injury
are distinguishable from host molecules. DAMPs are compounds that are associated with
and cell damage.
the PRRs
At the onset of an infection, burn, or other injuries, these cells undergo activation (one of
recognize a PAMP or DAMP) and release inflammatory mediators responsible for the clinical signs of
inflammation.
Vasodilation and its resulting increased blood flow causes the redness (rubor) and increased heat (calor).
Increased permeability of the blood vessels results in an exudation (leakage) of plasma proteins and fluid
into the tissue (edema), which manifests itself as swelling (umor).
Some of the released mediators such as bradykinin increase the sensitivity to pain (hyperalgesia, dolor).
The mediator molecules also alter the blood vessels to permit the migration of leukocytes,
tissue. The
mainly neutrophils and macrophages, outside of the blood vessels (extravasation) into the
neutrophils migrate along a chemotactic gradient created by the local cells to reach the site of injury.
The loss of function (functio laesa) is probably the result of a neurological reflex in response to pain.
In addition to cell-derived mediators, several acellular biochemical cascade systems consisting of
preformed plasma proteins act in parallel to initiate and propagate the inflammatory response. These
include the complement system activated by bacteria and the coagulation and fibrinolysis systems activated
by necrosis, e.g. a burn or a trauma
The acute inflammatory response requires constant stimulation to be sustained. Inflammatory mediators are
short-lived and are quickly degraded in the tissue. Hence, acute inflammation begins to cease once the
stimulus has been removed
ACUTE INFLAMMATION
Acute inflammatory response by the host to any agent is a
continuous process. It can be divided into two events:
Vascular events Cellular events.
Hemodynamic changes Exudation of leucocytes
Changes in vascular permeability Phagocytosis
