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 Definition
 Major causes
 Cardinal signs
 Vascular components
 Cellular components
 Morphological pattern
 Systemic effect
 outcomes
 examples
Acute inflammation is the early response of a tissue
to injury.
Acute inflammation may be regarded as the first line
of defense against injury and is characterized by
changes in the microcirculation: exudation of fluid
and emigration of leukocytes from blood vessels to
the area of injury. Acute inflammation is typically of
short duration, occurring before the immune
response becomes established, and it is aimed
primarily at removing the injurious agent.
 Infections- viral, bacterial, fungal, parasitic
 Tissue necrosis- ischemia, physical and
chemical injury, trauma
 Foreign bodies- sutures, splinters, dirt
 Immune reactions
 Burns
 Toxins
 It is characterized by five cardinal signs
 Dolor (pain)
 Calor (heat)
 Rubor(redness)
 Tumor (swelling)
 Function laesa (loss of function)
 Alteration in vascular caliber
 Alteration in permeability of vasculature
 Emigration of leukocytes
 Vascular components
increased permeability and increased blood flow, which
are induced by the actions of various inflammatory
mediators. Vasodilation occurs first at the arteriole
level, progressing to the capillary level, and brings
about a net increase in the amount of blood present,
causing the redness and heat of inflammation.
Increased permeability of the vessels results in the
movement of plasma into the tissues, with resultant
stasis due to the increase in the concentration of the
cells within blood – a condition characterized by
enlarged vessels packed with cells.
 Stasis allows leukocytes to marginate along the
endothelium, a process critical to their
recruitment into the tissues. Normal flowing
blood prevents this, as the shearing force along
the periphery of the vessels moves cells in the
blood into the middle of the vessel.
 Plasma cascade systems
 The complement system, when activated, creates
a cascade of chemical reactions that promotes
opsonization, chemotaxis, and agglutination,
and produces the MAC.
 The kinin system generates proteins capable of
sustaining vasodilation and other physical
inflammatory effects.
 Bradykinin
 A vasoactive protein that is able to induce vasodilation,
increase vascular permeability, cause smooth muscle
contraction, and induce pain.
 C3
 Cleaves to produce C3a and C3b. C3a stimulates histamine
release by mast cells, thereby producing vasodilation. C3b
is able to bind to bacterial cell walls and act as an
opsonin, which marks the invader as a target for
phagocytosis.
 C5a
 Stimulates histamine release by mast cells, thereby
producing vasodilation
 Factor XII (Hageman Factor)
 Membrane attack complex
The cellular component involves leukocytes,
which normally reside in blood and must move
into the inflamed tissue via extravasation to aid
in inflammation. Some act as phagocytes,
ingesting bacteria, viruses, and cellular debris.
Others release enzymatic granules that damage
pathogenic invaders. Leukocytes also release
inflammatory mediators that develop and
maintain the inflammatory response. In general,
acute inflammation is mediated by
granulocytes, whereas chronic inflammation is
mediated by mononuclear cells such as
monocytes and lymphocytes.
 Lysosome granules
 Histamine
 INF alpha
 IL-1
 Granulomatous inflammation:
 Characterised by the formation of
granulomas, they are the result of a limited
but diverse number of diseases, which
include among others tuberculosis, leprosy,
sarcoidosis, and syphilis.
 Fibrinous inflammation:
 Inflammation resulting in a large increase in
vascular permeability allows fibrin to pass
through the blood vessels. If an appropriate
procoagulative stimulus is present, such as
cancer cells,[6] a fibrinous exudate is
 Purulent inflammation:
 Inflammation resulting in large amount of
pus, which consists of neutrophils, dead cells,
and fluid. Infection by pyogenic bacteria such
as staphylococci is characteristic of this kind
of inflammation.
 Serous inflammation:
 Characterised by the copious effusion of non-
viscous serous fluid, commonly produced by
mesothelial cells of serous membranes, but
may be derived from blood plasma. Skin
blisters exemplify this pattern of
 outcome in a particular circumstance will be
determined by the tissue in which the injury
has occurred and the injurious agent that is
causing it. Here are the possible outcomes to
inflammation
 Resolution
 The complete restoration of the inflamed
tissue back to a normal status. Inflammatory
measures such as vasodilation, chemical
production, and leukocyte infiltration cease,
and damaged parenchymal cells regenerate.
In situations where limited or short-lived
 Fibrosis
 Large amounts of tissue destruction, or
damage in tissues unable to regenerate,
cannot be regenerated completely by the
body. Fibrous scarring occurs in these areas
of damage, forming a scar composed
primarily of collagen. The scar will not
contain any specialized structures, such as
parenchymal cells, hence functional
impairment may occur.
 Abscess formation
 A cavity is formed containing pus, an opaque
 Chronic inflammation
 In acute inflammation, if the injurious agent
persists then chronic inflammation will ensue.
This process, marked by inflammation lasting
many days, months or even years, may lead
to the formation of a chronic wound. Chronic
inflammation is characterised by the
dominating presence of macrophages in the
injured tissue. These cells are powerful
defensive agents of the body, but the toxins
they release (including reactive oxygen
species) are injurious to the organism's own
tissues as well as invading agents. As a
 Inflammation is usually indicated by adding
the suffix "itis“
Acute appendicitis Acute dermatiti
Acute appendicitis Acute dermatitis

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acute inflammation

  • 1.
  • 2.  Definition  Major causes  Cardinal signs  Vascular components  Cellular components  Morphological pattern  Systemic effect  outcomes  examples
  • 3. Acute inflammation is the early response of a tissue to injury. Acute inflammation may be regarded as the first line of defense against injury and is characterized by changes in the microcirculation: exudation of fluid and emigration of leukocytes from blood vessels to the area of injury. Acute inflammation is typically of short duration, occurring before the immune response becomes established, and it is aimed primarily at removing the injurious agent.
  • 4.  Infections- viral, bacterial, fungal, parasitic  Tissue necrosis- ischemia, physical and chemical injury, trauma  Foreign bodies- sutures, splinters, dirt  Immune reactions  Burns  Toxins
  • 5.  It is characterized by five cardinal signs  Dolor (pain)  Calor (heat)  Rubor(redness)  Tumor (swelling)  Function laesa (loss of function)
  • 6.  Alteration in vascular caliber  Alteration in permeability of vasculature  Emigration of leukocytes  Vascular components increased permeability and increased blood flow, which are induced by the actions of various inflammatory mediators. Vasodilation occurs first at the arteriole level, progressing to the capillary level, and brings about a net increase in the amount of blood present, causing the redness and heat of inflammation. Increased permeability of the vessels results in the movement of plasma into the tissues, with resultant stasis due to the increase in the concentration of the cells within blood – a condition characterized by enlarged vessels packed with cells.
  • 7.  Stasis allows leukocytes to marginate along the endothelium, a process critical to their recruitment into the tissues. Normal flowing blood prevents this, as the shearing force along the periphery of the vessels moves cells in the blood into the middle of the vessel.  Plasma cascade systems  The complement system, when activated, creates a cascade of chemical reactions that promotes opsonization, chemotaxis, and agglutination, and produces the MAC.  The kinin system generates proteins capable of sustaining vasodilation and other physical inflammatory effects.
  • 8.  Bradykinin  A vasoactive protein that is able to induce vasodilation, increase vascular permeability, cause smooth muscle contraction, and induce pain.  C3  Cleaves to produce C3a and C3b. C3a stimulates histamine release by mast cells, thereby producing vasodilation. C3b is able to bind to bacterial cell walls and act as an opsonin, which marks the invader as a target for phagocytosis.  C5a  Stimulates histamine release by mast cells, thereby producing vasodilation  Factor XII (Hageman Factor)  Membrane attack complex
  • 9. The cellular component involves leukocytes, which normally reside in blood and must move into the inflamed tissue via extravasation to aid in inflammation. Some act as phagocytes, ingesting bacteria, viruses, and cellular debris. Others release enzymatic granules that damage pathogenic invaders. Leukocytes also release inflammatory mediators that develop and maintain the inflammatory response. In general, acute inflammation is mediated by granulocytes, whereas chronic inflammation is mediated by mononuclear cells such as monocytes and lymphocytes.
  • 10.  Lysosome granules  Histamine  INF alpha  IL-1
  • 11.  Granulomatous inflammation:  Characterised by the formation of granulomas, they are the result of a limited but diverse number of diseases, which include among others tuberculosis, leprosy, sarcoidosis, and syphilis.  Fibrinous inflammation:  Inflammation resulting in a large increase in vascular permeability allows fibrin to pass through the blood vessels. If an appropriate procoagulative stimulus is present, such as cancer cells,[6] a fibrinous exudate is
  • 12.  Purulent inflammation:  Inflammation resulting in large amount of pus, which consists of neutrophils, dead cells, and fluid. Infection by pyogenic bacteria such as staphylococci is characteristic of this kind of inflammation.  Serous inflammation:  Characterised by the copious effusion of non- viscous serous fluid, commonly produced by mesothelial cells of serous membranes, but may be derived from blood plasma. Skin blisters exemplify this pattern of
  • 13.  outcome in a particular circumstance will be determined by the tissue in which the injury has occurred and the injurious agent that is causing it. Here are the possible outcomes to inflammation  Resolution  The complete restoration of the inflamed tissue back to a normal status. Inflammatory measures such as vasodilation, chemical production, and leukocyte infiltration cease, and damaged parenchymal cells regenerate. In situations where limited or short-lived
  • 14.  Fibrosis  Large amounts of tissue destruction, or damage in tissues unable to regenerate, cannot be regenerated completely by the body. Fibrous scarring occurs in these areas of damage, forming a scar composed primarily of collagen. The scar will not contain any specialized structures, such as parenchymal cells, hence functional impairment may occur.  Abscess formation  A cavity is formed containing pus, an opaque
  • 15.  Chronic inflammation  In acute inflammation, if the injurious agent persists then chronic inflammation will ensue. This process, marked by inflammation lasting many days, months or even years, may lead to the formation of a chronic wound. Chronic inflammation is characterised by the dominating presence of macrophages in the injured tissue. These cells are powerful defensive agents of the body, but the toxins they release (including reactive oxygen species) are injurious to the organism's own tissues as well as invading agents. As a
  • 16.  Inflammation is usually indicated by adding the suffix "itis“ Acute appendicitis Acute dermatiti Acute appendicitis Acute dermatitis