General pathology
Lecture - 5 –
Dr. Ali Zeki
Inflammation:
Definition:
It’s a protective response of living tissue to injury, its intended to localized and
to eliminate the initial cause of tissue injury.
Types of inflammation:
Inflammation can be classified according to the time course and type of cells
taking part in inflammatory response into two types:
1- Acute inflammation:
Its early response to injury and of short duration starting within few minutes
and last up to few days, and characterized by fluid and plasma proteins
exudates with predominantly neutrophils accumulation.
Causes of acute inflammation:
1- Microbial infections " pyogenic bacteria, viruses".
2- Hypersensitivity reactions " drugs , and allergies".
3- Physical agents " trauma, radiation, heat (burn), cold (frostbite)".
4- Chemical agents " acids, alkali, toxins".
5- Tissue necrosis " ischemic infraction".
Essential appearance (cardinal signs), of acute inflammation:
1- Redness:
the acutely inflamed tissue appear red for example the skin affected by
sunburn, and in conjunctivitis, this occur due to dilation of small vessels within
the damaged area.
2- Heat:
Increase in temperature at site of inflammation, its due to increased blood flow
(hyperemia).
3- Swelling:
Its due to accumulation of fluid in the extravascular apace (edema).
4- Pain:
Its partly due to the stretching and distortion of tissues due to inflammatory
edema, and also due to chemical mediators of acute inflammation like
(bradykinin and serotonin).
5- Lose of function:
the movement of inflamed part of the body inhibited by pain, while sever
swelling may physically immobilize the tissue.
Mechanisms of acute inflammation:
1- vascular (events) changes:
 Transient vasoconstriction of arterioles: seconds to few minutes, mediated
by neurogenic mechanism.
 Persistent Arteriolar vasodilatation: this lead to increase blood flow at the
site of inflammation and engorgement of downstream capillary beds, this
increment in the blood flow responsible for redness and warmth of the site of
inflammation. The engorgement of the capillary bed lead to increase in the
hydrostatic pressure and lead to ooze of low protein fluid called transudate to
the extra vascular compartment.
 Increase permeability of the vessel wall that lead to infiltrate of high
protein fluid called exudates, to the extra vascular compartment.
Note: accumulation of both exudates and transudate responsible for Oedema
at site of inflammation.
Mechanisms of increase vessels permeability:
1- Endothelial cells contraction: reversible process mediated by chemicals
(histamine and bradykinin).
2- Junction Retraction: reversible process mediated by chemicals (TNF,
AND IL-1).
3- Direct endothelial cells damage.
4- Leukocytes dependant endothelial cells injury, like in burn or infection.
5- Increase transcytosis via an intracellular vesicles pathway.
6- Leakage from newly formed blood vessels (angiogenesis).


Increase viscosity of blood due to extravasations of blood plasma.
Slow of blood flow ( Stasis).
2- cellular (events) changes:
 (Margination): Accumulation of leukocytes along the endothelial
surface and leaving the normal axial stream.
 (Pavement): Adhesion of the leukocytes to the endothelial cells.
 After tight adhesion of the leukocytes to the endothelial cells, the
leukocytes start (transmigration), by squeezing between endothelial cells at
the intercellular junctions.
 (Chemotaxis): Its migration of leukocytes toward site of inflammation
along a chemical gradient.
Types of chemotactic factors:
The chemotactic factors are either endogenous or exogenous, and these are:
1Bacterial products.
2Complement component (C5a).
3Arachidonic acid (A.A.), and leukotriene B4.
4Cytokines (IL-8).
 (Phagocytosis):
It’s the process of engulfment and internalization of particular materials
include (micro-organisms, damaged cells and tissue debris), by phagocytic
cells which are (neutrophils, monocytes and tissue macrophages).
Opsonization:
Phagocytosis is enhanced if the material to be phagocytosed is coated with
certain plasma proteins called (opsonins), this process called Opsonization, so
the opsonins promote the adhesion between the particular material and the
phagocyte cell membrane.
Types of opsonins:
1- specific antibodies of IgG class.
2- C3b component of complement.
3- Plasma fibronectin.
Microbial killing:
 Oxygen independent mechanism by lysosomal enzymes.
 Oxygen dependent mechanism, by free radicals like super-oxide anion
O2ˉ, and OH˚
Mediators of acute inflammation:
Function “role of mediators”
Vasodilatation
Increase vessel permeability
Neutrophil adhesion
Neutrophil chemotaxis
Fever
Pain
Tissue necrosis
Type of mediators
Histamine, prostaglandins, nitric oxide, and bradykinin
Histamine, leukotrienes, nitric oxide, and bradykinin
IL – 1, TNFα, C5a, and LTB4
C5a, LTB4, and bacterial components.
IL – 1, TNFα, and prostaglandins
Prostaglandins, and bradykinin
Lysosomal granules contents, and free radicals generated by neutrophils
Mediators secretes from macrophages:
Arachidonic acid metabolites, and platelets activating factor “mediators of
acute inflammation”.
Highly reactive oxygen metabolites “bacterial and cell killing” .
Proteases and hydrolytic enzymes. “ removing damaged material from areas
of injury”.
Cytokines , IL – 1 , and TNF α “ stimulate fibroblast proliferation, and
collagen synthesis”.
Growth factors “ PDGF, EGF, and FGF “stimulate growth of blood vessels,
division and migration of fibroblasts”.