SEMESTER-III
UNIT-1 PATHOLOGY-I
“INFLAMMATION”
PRESENTED BY
MR. SACHIN SHARMA
MR. SACHIN SHARMA([Link]. N.)
YOU WILL LEARN ABOUT
W H AT I S I N FA L M M AT I O N ?
INTRODUCTION
DEFINITION
CAUSES
CLINICAL SIGN
MEDIATOR
DIFFERENTS TYPES
MR. SACHIN SHARMA([Link]. N.)
INTRODUCTION
The term inflammation is derived from the Latin
word inflamao meaning ignite or set alight.
Inflammation is the initial and instantaneous
response to any injury.
During inflammation leukocytes are transported to
the injured site; where they act by not allowing the
microbes to further invade the site (tissue) and help
begin the process of necrotic tissue break-down.
Inflammation may be either acute or chronic.
MR. SACHIN SHARMA([Link]. N.)
DEFINITION
Inflammation is the local response of living
mammalian tissues to an injury resulting from any
agent. It is a defensive reaction of the body, so that the
spread of injurious agents can either be eliminated or
limited, and the resulting necrosed cells and tissues
can be removed.
MR. SACHIN SHARMA([Link]. N.)
CAUSES
Physical Agent
Chemical Agent
Immunological
Biological Agent
MR. SACHIN SHARMA([Link]. N.)
CLINICAL SIGN
Rubor (Redness)
Tumour (Swelling)
Calor (Heat)
Dolor (Pain)
MR. SACHIN SHARMA([Link]. N.)
WHAT IS MEDIATOR OF
INFLAMMATION?
“Chemical substance which mediate the
process of acute inflammation.”
Properties:-
These mediator are released either from
cell or plasma protein arrived.
MR. SACHIN SHARMA([Link]. N.)
MEDIATOR
Cell-derived Mediator
Plasma-derived Mediator
MR. SACHIN SHARMA([Link]. N.)
Cell-derived Mediator
Release either from their storage in cell granule or
synthesized in cell.
1. Vasoactive amine
2. Arachidonic acid metabolites
3. Lysosomal components
4. Platelet activating factor
5. Cytokine
6. Nitric oxide and oxygen metabolites
MR. SACHIN SHARMA([Link]. N.)
Source mediator main action
Mast cell Histamine permeability
Cell Platelet Serotonin permeability
derived [Link] Prosta Gyinding.
Leukotriene permeability
Lysosomal ezy.
Platelet permeability
activating
factor
Cytokines fever
MR. SACHIN SHARMA([Link]. N.)
Plasma-derived Mediator
Common site is liver after release they require
activation.
Products of:-
1. Kinin system (blood protein)
2. Clotting system
3. Fibrinolytic system
4. Complement system
MR. SACHIN SHARMA([Link]. N.)
DIFFERENTS TYPES
Acute Inflammation
Chronic Inflammation
MR. SACHIN SHARMA([Link]. N.)
Acute Inflammation
Acute inflammation is the earliest response a
tissue produces after an injury.
Acute inflammation is the first line of defense
against an injury and undergoes changes in the
microcirculation, such as exudation of fluid and
migration of leukocytes from blood vessels at the
injured site.
Acute inflammation is of short duration which
occurs before the immune response becomes
established, and is aimed at removing the
injurious agent.
MR. SACHIN SHARMA([Link]. N.)
Conti…
Changes seen during the process of acute inflammation
can be explained as:
1. Vascular events (early)
2. Cellular events (late).
MR. SACHIN SHARMA([Link]. N.)
Vascular events (early)
The earliest response to tissue injury is seen in the
form of changes in the microvasculature
(arterioles, capillaries, and venules), including
changes in the vascular permeability and changes
in blood flow (haemodynamic changes).
MR. SACHIN SHARMA([Link]. N.)
MR. SACHIN SHARMA([Link]. N.)
MR. SACHIN SHARMA([Link]. N.)
MR. SACHIN SHARMA([Link]. N.)
MR. SACHIN SHARMA([Link]. N.)
MR. SACHIN SHARMA([Link]. N.)
Contraction of endothelia cell
Retraction of endothelial cell
Direct injury to endothelial cell
Endothelial injury mediated by leukocytes
Neovascularization
MR. SACHIN SHARMA([Link]. N.)
MR. SACHIN SHARMA([Link]. N.)
Systemic effect of acute
inflammation
1. Fever
2. Leukocytosis
3. Lymphangitis
4. Shock
MR. SACHIN SHARMA([Link]. N.)
Causes
Persistent infections
Prolong exposure
Progression from acute inflammation
Autoimmunity
MR. SACHIN SHARMA([Link]. N.)
Granulomatous Inflammation
MR. SACHIN SHARMA([Link]. N.)
DEFINITION
The granulomatous inflammatory
response is a special type of chronic
inflammation characterised by often focal
collections of macrophages, epithelioid
cells and multinucleated giant cells
MR. SACHIN SHARMA([Link]. N.)
Conti…
Formation of granuloma (aggregation of epithelioid cells)
is a distinctive feature of granulomatous inflammation.
Granulomatous inflammation is a form of chronic
inflammation characterised by collections of activated
macrophages, often with T-lymphocytes, and sometimes
associated with central necrosis.
An activated macrophage, appearing as a modified
epithelial cell, is an epithelioid cell. Fusion of epithelioid
cells with each other results in the formation of multi-
nucleated giant cells. Thus, basically granulomas comprise
of epithelioid cells, but also contain multi-nucleated giant
cells. Lymphocytes and plasma cells. (occasionally) are
seen surrounding these giant cells.
MR. SACHIN SHARMA([Link]. N.)
Conti…
Two or more macrophagic cells may fuse
together in an attempt to engulf a single
particle, and the fused cells are known as giant
cells, which are of the following two types:
MR. SACHIN SHARMA([Link]. N.)
1. Foreign Body-type Giant Cells:
These giant cells are formed on exposure of an
individual to foreign un-digestible substances like
medical devices, prostheses, and biomaterials. In this
type of giant cells, the nucleiare arranged in an
irregularly scattered manner.
MR. SACHIN SHARMA([Link]. N.)
2. Langhans Giant Cells
These are multi-nucleated giant cells, the
nuclei shows peripheral arrangement, forming
a horse-shoe pattern (a circle or semicircle).
Giant cells are formed by fusion of
macrophages, perhaps by a concerted attempt
of two or more cells to engulf a single particle.
Langerhans
MR. SACHIN SHARMA([Link]. N.)
Systemic effect of chronic
inflammation
1. Fever
2. Endocrine and metabolic response
3. Autonomic responses
4. Behavioral responses
5. Leukocytosis
6. Leukopenia
7. Weight loss
MR. SACHIN SHARMA([Link]. N.)
THANK
YOU
MR. SACHIN SHARMA([Link]. N.)
