Inflammation
Content
• Inflammation
• Types of inflammation
• Changes involved in acute
inflammation
Objectives
At the end of this PDF, student will be able to
• Define “inflammation”
• Classify inflammation
• Describe the etiology of inflammation
• Identify the signs of inflammation
• Describe the changes involved in acute
inflammation
Inflammation
“Local response of living mammalian tissues to
injury due to any agent “
•
Body
defence reaction to eliminate or limit the spread of injurious agent, followed
by removal of the necrosed cells and tissues
•
Protective response
Etiology of Inflammation
•
Infective agents - bacteria, viruses and their
toxins, fungi, parasites
•
Immunological agents - cell-mediated and antigen antibody reactions
•
Physical agents - heat, cold, radiation, mechanical
trauma
•
Chemical agents - organic and inorganic poisons
Signs of inflammation
4 cardinal signs of inflammation
•
Rubor
(redness)
•
Tumor
(swelling)
•
Calor
(heat) and
•
Dolor
(pain)
Fifth sign - functio laesa (loss of
function) - Virchow
Types of inflammation
Depending upon the defense
capacity of host and duration of response
•
Acute Inflammation
•
Chronic inflammation
Acute Inflammation
•
Short duration
•
Represents early body reaction
•
Followed by repair
Main features
•
Accumulation of fluid & plasma at the
affected site
•
Intravascular activation of platelets
•
Polymorpho nuclear neutrophills (PMN) –
inflammatory cells
Chronic Inflammation
•
Longer duration
•
If causative agent of acute inflammation
persists for long periods
•
Recurrent attack of acute inflammation
Main features:
•
Presence of lymphocytes, plasma cells &
Macrophages as inflammatory cells
Changes in Acute inflammation
Two main events involved
1. Vascular events
•
Alteration of microvasculature (arteries,
capillaries & venules)
2. Cellular events
•
Exudation of leucocytes
•
Phagocytosis
Vascular events
• Alteration in the microvasculature - tissue injury
Haemodynamic Changes
Earliest features - vascular flow change, calibre of small blood vessels
1.
Irrespective of the type of injury -
transient vasoconstriction of arterioles
•
Mild
form – blood flow - 3-5 seconds
•
More
severe injury the vasoconstriction - 5
minutes
Vascular changes
2.
Persistent progressive vasodilatation
•
Mainly
arterioles
•
lesser
extent - venules and capillaries
•
Increased
blood volume - redness and warmth
3.
Progressive
vasodilatation
•
Elevate
the local hydrostatic pressure - transudation of fluid into the extracellular
space – swelling
4. Stasis of microcirculation
•
Increased
concentration of red cells - blood viscosity
5. Leucocytic margination
•
Leucocytes
stick to the vascular endothelium
•
Move
and migrate through the gaps between the endothelial cells into the
extravascular space
•
Emigration
Triple response
Flush
–
Appearance
of red line
–
Local
vasodilatation of capillaries and venules
Flare
–
Bright
reddish appearance or flush surrounding the red line
–
Vasodilatation
of the adjacent arterioles
Wheal
–
Swelling
or oedema of the surrounding
–
Transudation
of fluid into the extravascular space
Pathogenesis of altered vascular permeability
Normal circumstances - fluid balance - two
opposing sets of forces that causes:
Outward movement of fluid from microcirculation
–
intravascular
hydrostatic pressure
–
colloid
osmotic pressure of interstitial fluid
Inward movement of interstitial fluid into
circulation
–
intravascular
colloid osmotic pressure
–
hydrostatic pressure of interstitial fluid
Contraction
of endothelial cells
• Increased leakiness - venules
exclusively
• Endothelial cells - temporary gaps –
contraction - vascular leakiness - release of histamine, bradykinin and others
• Response - immediately after injury
– reversible - short duration (15-30 minutes)
• Example: immediate transient leakage
is mild thermal injury of skin of forearm
Retraction
of endothelial cells
• structural re-organisation of the
cytoskeleton of endothelial cells - reversible retraction – intercellular
junctions – venules - cytokines such as interleukin-1 (IL-1) and tumour
necrosis factor (TNF)-α - response takes 4-6 hours after injury - lasts for 2-4
hours or more
• The example invitro experimental
work only
Direct
injury to endothelial cells
• Cell necrosis, physical gaps at the
sites of detached endothelial cell - thrombosis at site initiated
• Affects – microvasculature - immediately after injury last for several hours or days or delay of 2-12 hours and last for hours or
days
Summary
• Inflammation is the local response
of living mammalian tissues to injury due to any agent
• The
four cardinal signs of inflammation are redness, swelling, heat and pain
• Inflammation
is of 2 type acute and chronic inflammation
• Acute
inflammation is of Shorter duration , represents early body reaction, followed
by repair
• Chronic
inflammation is of longer duration and occurs when the agents remains for
longer time
• Acute inflammation is characterized by cellular events and vascular events
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