CELL

INFLAMMATION

PATHOLOGY
CELL INFLAMMATION
 DEFINITION- it is the local physiological action
response to tissue injury. It is protective endeavor
by the body to remove the injurious stimuli to
healing and repair
PATTERNS OF INFLAMMATION
1. Acute inflammation- short lived and may last for
few minutes to few days only it involves
infilteration of neutrophils and exudation of
fluid and plasma proteins
2. Chronic inflammation – is for longer duration and
associated with lymphocytes, macrophages,
proliferation of blood vessels and fibrosis
ACUTE INFLAMMATION
Components of acute inflammation
1. Changes in the calibre of blood vessels, resulting in increase
in blood flow
2. Structural changes in micro vasculature that allow leakage of
plasma protein and leukocytes
3. Emigration of neutrophils and their accumulation at the site
of injury
Causes of acute inflammation
 Bacterial, viral, parasites, and other infections
 Physical injuries due to trauma, and exposure to ionizing
radiation, heat and cold
 Injury caused due to exposure to chemicals such as corrosive
agents, acids, alkalis reducing agents and bacterial toxins
 Tissue necrosis caused by ischemia or infarction
ACUTE INFLAMMATION
Cardinal signs of acute inflammation
 Swelling
 Redness
 Pain
 Heat
 Loss of function

Pathological changes in acute inflammation

1. Vascular agents
2. Cellular events
3. Phagocytosis
PATHOLOGICAL REACTIONS TO
ACUTE INFLAMMATION
VASCULAR EVENTS
Vaso dilatation- dilatation of blood vessels which begins with the
arterioles followed by the capillaries and venules , this leads to local
increase in vascular flow which manifests redness and warmth
Increased permeability of the micro vasculature- escape of the
protein rich fluid into the interstitium. The accumulation of the fluid
interstitial space called edema, which give rise to local swelling.
The mechanism contributing increased vascular permeability are
contraction of endothelial cells moving intracellular junctions ,
endothelial retraction, direct endothelial injury caused by
leukocuytes and excessively leaky new formed blood vessel(neo
angiogenesis)
Loss of fluid – it results in concentration of blood cells and increase
viscosity of blood , slowing of the flow in the micro vasculature
(stasis)
Vascular stasis- sticking of leukocytes (predominantly neutrophils) to
the vascular endothelium
PATHOLOGICAL REACTIONS TO
ACUTE INFLAMMATION
CELLULAR EVENTS
Margination – vascular stasis leads to peripheral orientation
of leukocytes , which normally flow in central column of
blood stream accumulating towards the endothelial
surface of the vascular lumen . This is called margination
Rolling and adhesion – the accumulated leukocytes roll
over the endothelial cells lining the vessel wall and
adhere transiently to the endothelial cells .
Diapedesis- transmigration of leukocytes from the vascular
lumen to the interstitial tissue across the endothelium is
called diapedesis
chemotaxis- movement oriented along chemical gradient,
after extravasation into interstitial space, leukocytes
migrate towards the site of injury by chemotaxis
PATHOLOGICAL REACTIONS TO
ACUTE INFLAMMATION
PHAGOCYTOSIS- it is the engulfment of solid
particulate material cells
Types of phagocytic cells
 Microphages – polymorphonuclear neutrophils
 Macrophages- monocytes

STEPS OF PHAGOCYTOSIS
 Recognition and attachment of particle/
microbe
 Engulfment
 Killing or degradation
PATHOLOGICAL REACTIONS TO
ACUTE INFLAMMATION
 Recognition and attachment of particle/ microbe –
microbes are coated with naturally occurring factor
in the serum called opsonins, which facilitate
recognition of phagocytic cells.
 Engulfment- these cell extend pseudopods around
the particle to be engulfed and subsequently from
phagocytic phagosome. This followed by fusion of
membrane of phagosome with that lysosome,
leading to formation of phagolysosome.
 Killing or degradation- killing of bacteria by number
of bactericidal mechanisms, oxygen dependent
bactericidal mechanism and nitric oxide
mechanism.
CHEMICAL MEDIATORS OF
INFLAMMATION
Cell derived mediators Plasma derived mediators
Vaso active amines- histamine, Kinin system
serotonin
Arachidonic acid metabolites- Complement system
thromboxane, prostacyclin,
leukotrines
Platelet activating factor Clotting system
Nitric oxide and oxygen free Fibrinolytic system
redicals
Lysosomal components
EFFECTS OF INFLAMMATION
Beneficial effects of inflammation
 Dilution of toxins such as those produced by bacteria
and allows them to carried away by lymphatics by
stimulating immune response
 Entry of antibodies due to increased vascular
permeability
 Transport of drugs such as antibiotics to the site
where bacteria are multiplying
 Fibrin formation from exuded fibrinogen which serves
as matrix granulation tissue formation
 Delivery of nutrients and oxygen which are essential
for repair and healing by increased blood flow
through the area
EFFECTS OF INFLAMMATION
Harmful effects of inflammation
 Digestion of normal tissues- enzymes such as
collagenases and proteases may digest
normal tissues, resulting their destrcution
ex: type II hypersensitivity reactions
 Swelling- swelling of acute inflamed tissue
may harmful EX: swelling of epiglottis due to
haemophillus influenza in children
 Inappropriate inflammatory response- which
occur type I hypersensitivity reactions where
provoking environmental antigen .
MORPHOLOGICAL FORMS OF
ACUTE INFLAMMATION
 Ulcer- it is localized breach of surface epithelium of organ due
to inflammation of common sites of ulceration
 Abscess formation – tissue necrosis due to intense neutrophilic
infiltration in the inflamed tissue, a cavity formed which is
called abscess
 Bacterial infection of blood

Bacteremia-bacteria in the blood

Septicemia-highly pathogenic rapidly multiplying bacteria in the
blood
Pyemia- circulation of minute septic thrombi In the blood
 Cellulitis- inflammation of soft tissues
 Pesudomembranous inflammation- it is the inflammatory
response of mucosal surfaces due to denudation of the
epithelium plasma usually exudes on the surface, where it
coagulates and forms of membrane
RESULT OF ACUTE
INFLAMMATION
 Resolution – complete restoration of inflammed
tissue back to its normal state
 Fibrosis – healing by connective tissue
replacement or scarring occurs when the injury
involves substantial amounts of tissue
destruction or when damaged tissue is unable
to regenerate
 Abscess formation – necrosis due to intense
neutrophilic in the inflamed tissue
 Chronic inflammation- injurious stimuli is
persistent and cannot resolved by acute
inflammatory response
CHRONIC INFLAMMATION
Histologic features of chronic inflammation
 Mono nuclear infiltration includes
lymphocytes, plasma cells and macrophages
 Tissue destruction or necrosis- substances
released by macrophages ex: protease, lipase
 Proliferative changes there is proliferation
of blood vessels(angiogenesis) and
fibroplastic proliferation resulting in
formation of granulation tissue
CELLS INVOLVED IN CHRONIC
INFLAMMTION
 Macrophages- monocytes are recruited form circulation and
reach the site of inflammation by transmigration and
chemotaxis. In extracellular tissue monocytes are
transformed into their tissue counterpart
 Lymphocytes- these get activated in chronic inflammatory
conditions by contact with antigen or exposure to bacterial
toxins . Once activated lymphocytes produce lymphokines
which in turn stimulate monocytes and macrophages
 Plasma cells- it produce antibodies direct against foreign
antigens or against altered self antigens
 Mast cells- these are scattered in connective tissue and
play a role as well as persistent inflammatory reactions
 Eosinophils- seen in immune reactions mediated IgE and
parasite infections
MORPHOLOGICAL PATTERNS OF
CHRONIC INFLAMMATION
 Chronic non specific inflammation- it is non
specific mononuclear inflammatory cell
infiltrate of macrophages lymphocytes, and
plasma cells. These seen in peptic ulcer,
osteomyelitis, empyema crohn’s disease
 Chronic granulomatous inflammation-
granuloma is focal aggregate of activated
macrophages which are surrounded by rim of
lymphocytes and few plasma cells
SYSTEMIC EFFECTS OF CHRONIC
INFLAMMATION
 Fever
 Leukocytosis
 Anemia
 Elevated erythrocyte