Inflammation

Dr. Mehzabin Ahmed

 Inflammation ?
• It is a complex reaction in the vascularised
tissues in response to cell injury, leading to
accumulation of
– fluid,
– proteins and
– leucocytes in extravascular tissues.

• It is described by adding the suffix –itis to the

name of the organ or tissue involved.
 Types of inflammation
• Acute inflammation is typically of short
duration, few minutes to few days, in which
neutrophils predominate, usually occurs with
protein exudate.

• Chronic inflammation occurs over a duration

of days to years, characterized by mainly
lymphocytic and macrophage infiltrate with
proliferation of blood vessels, tissue necrosis
and fibrosis.
 Acute inflammation
• It is the most common early tissue response to
tissue damage and destruction.

• An inflammatory exudate fills up the site of

damage.
 Differences between
Exudate & Transudate
The inflammatory It is called a
fluid is called an transudate when
exudate when it is there is
• Rich in proteins
• Cells and tissue • Less protein
debris • Less number of
• Has a specific cells
gravity greater • Has a specific
than 1.020. gravity less that
1.012.
 Clinical effects of acute
inflammation
The cardinal signs of inflammation are
• tumor (swelling) due to accumulation of exudate
• rubor (redness) due to vessel dilatation & blood
• calor (heat) flow to the inflamed area
• dolor (pain) due to pressure on the nerve
endings from the swelling &
due to chemical mediators
• loss of function due to swelling & pain
 Components of acute
Inflammation
• 1)       Vascular component- in the local
vascular flow and alteration of the vascular
permeability in acute inflammation.
• 2)       Cellular component- Neutrophils are
the main effector cells of acute inflammation.
They attach themselves to
 Vascular
component
* local vascular flow
* Altered vascular permeability
 Cellular component
It involve neutrophils as the main effector cells
of acute inflammation. The cellular events
are:
1) Extravasation
2) Transmigration of leukocytes
3) Chemotaxis
4) Phagocytosis
 Cellular component
Extravasation of the PMN occurs by the following process:
1) Margination: Movement of the PMN cells close to the
vessel wall in the blood stream
2) Rolling: the PMN cells roll along the vessel wall
3) Adhesion: attach themselves to activated endothelial
cells of the blood vessels
4) Aggregation: collection of adjacent PMN cells and these
undergo shape changes
Transmigration: movement of the PMN cells
out of the vessel lumen to the tissue space
around the vessels.

Chemotaxis: Movement of the PMN cells along

a concentration gradient of chemotactic
factors to reach the site of inflammation.

Phagocytosis: process by which the PMN cells

engulf and digest the injurious agent by
releasing enzymes and superoxides
 Mediators of Inflammation
Some mediators come from plasma in precursor forms
that are activated.

Cell bound mediators are found in granules and released

immediately. Others are newly synthesized, usually
from mast cells, platelets, neutrophils, or monocytes.

Their action is usually short- lived and decay, often within

seconds.
Chemical mediators of inflammation by function:
• Increase vascular permeability: histamine, C3a, C5a, PAF,
bradykinin, LTC, LTD, LTE (leukotrienes C,D,E)

• Chemotaxis: C5a, LTB4, chemokines, IL-8

• Vasodilation: NO, PGI 2 (prostaglandin I 2)

• Systemic signs: TNF (tumor necrosis factor), IL-1, IL-6

• Pain: bradykinin, prostaglandins

• Tissue Destruction: leukocyte lysosomal enzymes, NO

(nitric oxide), reactive O2 (reactive oxygen species)
 Outcomes of Acute
Inflammation
• Resolution: The return to normal architecture and
removal of dead cellular debris

• Fibrosis: is scar formation with loss of original

architecture from more significant injury.

• Organization: denotes connective tissue replacement of

functional tissue and occurs with marked protein
exudates, lots of fibrin exudation from plasma, areas
where exudate cannot be adequately absorbed.

• Abscesses: localized collection of pus may form in some

bacterial infections.

• Chronic inflammation: Acute inflammation can continue

and progress to chronic form
 TISSUE DAMAGE

Acute inflammation

Damage neutralized & Damage neutralized & Damaging agent persists

Cells can regrow Cells cannot regrow with tissue damage

Regeneration Organization through Organization with

Phagocytosis & Healing contd. inflammation
by repair of damaged tissue
Restoration of CHRONIC
normal structure Scar formation INFLAMMATION
& function or FIBROSIS
& loss of Damaging agent
specialized function overcome
RESOLUTION Persistence

Yes