INFLAMMATION: It is a protective response by a vascularized tissue against
any pathogen (bacteria, viruses, parasites) and cell injury to provide healing/
repair to that injured or infected tissue by destroying them.
TYPES OF INFLAMMATION:
1) ACUTE
INFLAMMATION
2) CHRONIC
INFLAMMATION
ACUTE INFLAMMATION:
· An immediate and early response to
injury
· Relatively short duration (from few
minutes upto few days)
· Form inflammatory exudate
· Mainly delivers neutrophil leukocytes (WBC) to the site of injury.
VASCULAR EVENTS OF ACUTE INFLAMMATION:
1) Changes
in Blood Vessel Diameter: Initial vasoconstriction followed
by vasodilation
2)
Changes in Blood Flow: Initial increase in blood velocity due vasodilation but soon blood flow
becomes slow due to increase in blood vessel permeability (loss of fluid from
blood increases blood viscosity).
3) Increase
in Vessel Permeability: Walls of blood vessels contain intercellular junctions (pores) which
normally allows the passage of small molecules (water & ions). But in acute
inflammation, endothelilal cells lining the blood vessels contracts causes the
widening of these pores, therefore allows large molecules protein & plasma
fluid to pass through the vessel walls. This process is known as exudation. Swelling caused by exudation
is called inflammatory edema.
MECHANISM OF INC. PERMEABILITY OF
VESSELS:
· Immediate transient response:
Ø It occurs in response to mild injury
Ø Permeability begins 1-2 minutes after
the onset of injury and remains about 15-30 minutes
Ø Mediated by histamine, bradykinin
& leukotrines which causes contration of endothelial cells resulting in
widening of pores
· Delayed-prolonged response:
Ø It occurs in response to moderate
injury
Ø Permeability begins 30minutes to 10
hours after the the onset of injury & reaches its peak in about 4-12 hours
Ø Permeability increases due to direct
injury of endothelial cells
· Immediate-prolomged response
Ø It occurs in response to severe
injury
Ø Permeability begins immediately after
the injury and last for one to several days
Ø Permeability increases due to
necrosis of endothelial cells.
FACTORS WHICH REGULATES TRANSPORT OF EXUDATE:
· Capillary Hydrostatic Pressure: It tends to escape the fluid out of
the vessel.
· Osmotic Pressure Of Protein In
Intersitial Space:
It tends to pull the fluid from vessels to interstitial space.
DURING INFLAMMATION EXUDATE FORMATION
OCCURS DUE TO:
Increased
capillary hydrostatic pressure due to enhance blood flow
Increased
vascular permeability allowing plama protein to enter in intersitial space
where they exert osmotic pressure & draws more fluid from the vessels
CELLULAR ( LEUKOCYTES) EVENTS:
SEQUENCE OF CELLULAR
EVENTS:
1)
MARGINATION: Normally RBC & WBC flows in the central
axis of blood vessel. During acute infalmmation, Due to increase in
permeability, the flow of blood is slow inside vessel & therefore RBC stick
together forming clumps or roulaex which is larger than WBC. These clumps
forces WBCs to the periphery towards vessel walls (endothelial cells).
2)
ADHESION: WBC
becomes attach (adhere) to the endothelial cells of vessel wall. This adhesion
is because of adhesion molecules present on the surfaces of both WBC &
endothelial cells.
3) EMIGIRATION: Adherent leukocytes leaves the blood
vessels and enters into interstitial space through intercellular junctions
(pores).
It takes
place in 2-10 minuts.
4) CHEMOTAXIS: Process by which leukocytes are attracted
towards and move towards an attractants usually a chemical substance at the
site of injury.
5) PHAGOCYTOSIS: Process by which micro-organism and
other forein body are engulfed and destroyed by neutrophils & macrophages.
This process
is divided in three steps:
I.
Recognition & Attachment: White
Blood Cells indentify the object which they have to phagocytize. Recognition
and attachment of most of the microorganism is facillitated by coating them
with serum protein called “Opsonin”
which inturn binds to specific receptors on the leukocytes.
Opsonins are (i) C3b (ii) IgG
Engulfment: Process occurs by pseudopodial extensions of leukocytes
cytoplasm which completely encloses the foreign particles forming phagosome.
Membranes of lysosomal granules fuse with it and form phagolysosomes. Lysosomes
discharge their content into phagolysosomes causing killing & degradation
of microorganis
