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INFLAMMATION 2

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Acute Inflammation
Def:
Acute inflammation is the type of inflammation that presents
within a short period of time (days) and is associated with
neutrophils infiltration, or lymphocyte if caused by a viral
infection, all cardinal signs of inflammation are present
Clinical Presentations of Acute Inflammation:
a. Serous formation: type of inflammation with protein-poor
fluid, for example, skin blister resulting from burning.
b. Suppurative (Purulent formation): This is a pyogenic
inflammation and pus formation in the inflamed area.

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c. Ulcerative formation: Ulcer is a loss of continuity of
epithelium in the skin or mucous membrane, it can be due
to inflammatory damage, for example, ulcerative colitis,
peptic ulcer.
d. Boils and Furuncles formation: Focal skin collection of
abscess commonly in hair follicles. Boils are smaller
e. Pseudo-membranous formation: Following clostridia,
or diphtheria infection, characterized by the formation of
pseudo-membrane composed of (necrotic tissue +
coagulated fibrin + neutrophils and macrophage + bacteria)

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Control of Acute Inflammation:
vascular, cellular, and humeral events.
1- Vascular Events:
vascular events of inflammation involve three main
processes:
- changes in vessel caliber, blood flow (hemodynamic),
and increased vascular permeability (formation of the fluid
exudates). Therefore, blood flow to the injured area may
increase up to tenfold as vessels dilated.
- Changes in the vascular flow start with rapid vasoconstriction
for a few seconds, then vasodilatation results in hyperemia and
redness, 15 minutes later, there is stasis of blood flow

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- Stasis of Blood: Decreased movement of the blood flow;
hence allows fluid, proteins, and cells to get out of the
intravascular compartment to the inflamed area. Factors
responsible for stasis Include adhesion of WBCs to
endothelium consequently slowing of the flow, and
vasodilatation of the blood vessels in the inflamed area.
Increase of Permeability of Blood Vessels: leakage of
fluids and protein from the vessels due to histamine and
other chemical mediators, (prolonged) leakage is due to
damage to the wall of blood vessels..

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The protein-rich fluid that leaves the circulation is called an
exudate. All plasma protein can be found in the exudates,
especially fibrinogen that is converted to fibrin during the
healing process, then fluids will be washed out by lymphatic
vessels

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2- Cellular Events of inflammation
- Recruitment: Cells move out of the vessels into the area of
inflammation recruited by chemotactic agents. Inflammatory cells
become activated to phagocytize offending materials, this process
occurs in steps as follows.
a. Margination and Rolling of WBCs: Moving from axial flow to the
margin of the vessels is called margination.
b.Activation and adhesion: Marginated leukocytes begin to roll on the
endothelial surface by forming transient adhesion molecules via the
selectin family of proteins: (E-selectin on endothelial cells, P-selectin
on endothelial cells and platelets, L-selectin on leukocytes).
Adhesion to endothelium occurs via selectins and integrins.

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c. Migration of Leucocytes: Passage of the cells across the wall of
blood vessels and moved to reach the site of inflammation due to the
effect of chemical mediators gradient (chemotaxis).
d. Chemotaxis: A process resulted from certain products of WBCs,
platelets, and microorganisms, which attracts WBCs towards the
inflammation area according to the high concentration of that substance.

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e. Phagocytosis:
• Define as engulfment and internalization of foreign bodies (bacteria,
viruses, etc.) in the phagosome and digestion.
• The first step in phagocytosis is
• the adhesion of the particle to be phagocytosed to the cell surface.
• Then the phagocyte ingests the attached particle by sending out
pseudopodia around it.
• Then met and fused so that the particle lies in a phagocytic vacuole
(called a phagosome) then bounded to small bodies containing
enzymatic compounds called lysosomes, to form phagolysosomes. In
which intracellular killing of microorganisms occurs. Phagocytic
cells include neutrophils, polymorph nuclear cells, eosinophils, and
monocytes.

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3-Humeral Events (Chemical Mediators):
• Chemical mediators are the cornerstone in controlling the
inflammatory Process.
• Mediators are substances produced by, from damaged tissues or
bacteria, also from endothelial cells, WBCs, and platelet (locally)
• They can be produced systemically from the liver.
• They control: vascular and cellular events and they produce the
cardinal signs in acute and chronic inflammation
• they act locally: on the neighboring cells (paracrine) or on
themselves (autocrine).
Example of action:
a-permeability b-margination
c-chemotaxis d-vasodilation and vasoconstriction
e-fever and pain f-phagocytosis…etc).

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Out come of Acute Inflammation:
The outcome means the final fate or subsequent. It includes:
a.Resolution: Complete restoration of the structures and functions
of inflamed tissue, for example, the resolution of the inflamed lung
(pneumonia) after removal of the injurious agent.
Steps of the resolution:
• Removal of inflammatory exudates, fibrin, and cells completely
• Increase lymphatic drainage to get rid of all debris (remaining
parts of cells)
• Cessation of vascular events of inflammation
• Regeneration of lost specialized cells (return of normal structure)

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b. Fibrosis: it is a feature of chronic inflammation that
occurs in three situations: if heavy deposition of fibrin or
failure to be removed completely, or if there is a large
amount of tissue necrosis or the tissue cannot regenerate
like cardiac and CNS tissues.
c. Formation of Abscess: Occurs with pyogenic bacteria
or fungal infection.
d. Developing of Chronic Inflammation: acute Process
continues as chronic inflammation.