• Dr. Manzoor Ahmad Mir
• Assistant Professor (Immunopathology)
• College of Applied Medical Sciences
BLISTER, “Watery”, i.e., SEROUS
Pus or Purulent
Redness
Fibrinous
What is Inflammation?

“Inflame” – to set fire.

Inflammation is “A dynamic response of vascularised tissue to injury.” OR

A reaction of a living tissue & its micro-circulation to a pathogenic insult.

It is a protective response and a defense mechanism for survival It serves to
bring defense & healing mechanisms to the site of injury.

Reaction of tissues to injury, characterized clinically by: heat, swelling,
redness, pain, and loss of function.

Pathologically
by : vasoconstriction followed by vasodilatation, stasis,
hyperemia, accumulation of leukocytes, exudation of fluid, and deposition
of fibrin.

Inflammation Involves Second-Line Defenses

If a pathogen is able to get past the body's first line
of defense, and an infection starts, the body can rely
on it's second line of defense.
Inflammatory response causes
Redness - due to capillary dilation resulting in
increased blood flow



Heat - due to capillary dilation resulting in increased
blood flow

Swelling – due to passage of plasma from the blood
stream into the damaged tissue

Pain – due mainly to tissue destruction and, to a
lesser extent, swelling.
Cardinal Signs of Inflammation

Redness : RUBOR

Heat: CALOR

Pain : DOLAR

Swelling :TUMOR

Loss of Function:
FUNCTIO LAESA
How Does Inflammation Occur?
• Microbial infections: bacterial, viral, fungal, etc.
• Physical agents: burns, trauma--like cuts, radiation
• Chemicals: drugs, toxins, battery acid etc
• Immunologic reactions: rheumatoid arthritis.
Pathogenesis: Three main processes occur at the site of inflammation, due
to the release of chemical mediators :

Increased blood flow (redness and warmth).

Increased vascular permeability (swelling, pain & loss of function).

Leukocytic Infiltration.
Inflammatory Response
Signs
Redness
Swelling
Heat
Pain
(Ruber)
(Tumor)
(Colar)
(Dolor)
Three major events
(1) Vadodilation
(2) Increased capillary permeability
(3) Influx of phagocytic cells (chemotaxis)
Cardinal Signs of Inflammation
BLISTER, “Watery”, i.e., SEROUS
Redness
 Redness : Hyperaemia.
 Warm : Hyperaemia.
 Pain : Nerve, Chemical
mediators.
 Swelling : Exudation
 Loss of Function: Pain
Pus or Purulent
Fibrinous
Types of Inflammation
 Time course
 Acute inflammation: Less than 48 hours
 Chronic inflammation: Greater than 48 hours
(weeks, months, years)
 Cell type
 Acute inflammation: Neutrophils
 Chronic
inflammation:
Mononuclear
(Macrophages, Lymphocytes, Plasma cells).
cells
Chemical Mediators:
Chemical substances synthesised or released and
mediate the changes in inflammation.
 Histamine by mast cells - vasodilatation.
 Prostaglandins – Cause pain & fever.
 Bradykinin - Causes pain.
COMPLEMENT SYSTEM
KININ AND CLOTTING SYSTEM
Vasodilation
Increased vascular
permeability
Role of
Mediators in
Different
Reactions of
Inflammation
Chemotaxis, leukocyte
recruitment and
activation
Prostaglandins
Histamine
Nitric oxide
Vasoactive amines
Bradykinin
Leukotrienes C4, D4,
E4, PAF
Substance P
C5a
Leukotriene B4
Chemokines
IL-1, TNF
Bacterial products
Fever
IL-1, TNF
Prostaglandins
Pain
Prostaglandins
Bradykinin
Tissue damage
Neutrophil and macrophage
lysosomal enzymes
Oxygen metabolites
Nitric oxide
Inflammation
Systemic Manifestations
Leukocytosis:
WBC count climbs to 15,000 or 20,000 cells/μl
most bacterial infection
Lymphocytosis:
Infectious mononucleosis, mumps,
German measles
Eosinophilia: bronchial asthma,
hay fever, parasitic infestations
Leukopenia: typhoid fever,
infection with rickettsiae/protozoa
Acute inflammation has one of four outcomes:
• Abscess formation
“A localized collection of pus (suppurative inflammation)
appearing in an acute or chronic infection, and associated with tissue destruction, and
swelling”.
• Progression to chronic inflammation
• Resolution--tissue goes back to normal
• Repair--healing by scarring or fibrosis
CAUSES OF CHRONIC INFLAMMATION
• 1) PERSISTENCE of Infection
• 2) PROLONGED EXPOSURE to insult
• 3) AUTO-IMMUNITY
Lymphatics in inflammation:
 Lymphatics are responsible for draining edema. Edema: An excess
of fluid in the interstitial tissue or serous cavities; either a
transudate or an exudate
Transudate:
• An ultrafiltrate of blood plasma
– permeability of endothelium is usually normal.
– low protein content ( mostly albumin)
Exudate:
• A filtrate of blood plasma mixed with inflammatory cells and cellular debris.
– permeability of endothelium is usually altered
– high protein content.
Pus:
• A purulent exudate: an inflammatory exudate rich in leukocytes (mostly
neutrophils) and parenchymal cell debris.
Inflammation Outcome
Fibrosis/Scar
Resolution
Injury
Acute
Inflammation
Abscess
Ulcer
Fistula
Sinus
Chronic
Inflammation
Fungus
Virus
Cancers
T.B. etc.
1.
2.
Viral infection
Persistent infections by certain microorganisms,
e.g. tubercle bacilli, Treponema pallidum, fungi, and parasites.
3.
Prolonged exposure to potentially toxic agents, either
exogenous or endogenous
e.g. of exogenous agent is particulate silica, when inhaled for
prolonged periods, results in silicosis
e.g. of endogenous agent is atherosclerosis (a chronic inflammatory
process of the arterial wall induced by endogenous toxic plasma
lipid components)
4.
Autoimmunity: immune reactions develop against the
individual's own tissues
In these diseases, autoantigens evoke immune reaction that
results in chronic tissue damage and inflammation e.g.
rheumatoid arthritis and lupus erythematosus
1.
Infiltration with mononuclear cells include




2.
Tissue destruction

3.
Macrophages
Lymphocytes
Plasma cells
Eosinophils
induced by the persistent offending agent or by
the inflammatory cells.
Healing

by connective tissue replacement of damaged
tissue, accomplished by proliferation of small
blood vessels (angiogenesis) and, in particular,
fibrosis
Examples of Diseases with Granulomatous Inflammations
Disease
Cause
Tissue Reaction
Tuberculosis
Mycobacterium
tuberculosis
Noncaseating tubercle
Caseating tubercles
Leprosy
Mycobacterium leprae
Acid-fast bacilli in
macrophages;
noncaseating granulomas
Syphilis
Treponema pallidum
Gumma: wall of
histiocytes; plasma cell
Cat-scratch disease Gram-negative bacillus Rounded or stellate
granuloma
Sarcoidosis
Unknown etiology
Noncaseating granulomas
Crohn disease
Immune reaction
against intestinal
bacterial
dense chronic inflammatory
infiltrate with noncaseating
granulomas

Thank you very much for your attention