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INFLAMMATION

SYEDA RIMA ISHAQ


VISITING FACULTY

Inflammation
Inflammation is the reaction of
blood vessels, leading to the
accumulation of fluid (Serum) and
leukocytes in extra vascular tissue.

LEUKOCYTES
White

blood cells (WBCs), also called leukocytes or


leucocytes, are the cells of the immune system that are
involved in protecting the body against both
infectious disease and foreign invaders.

All

leukocytes are produced and derived from a


multipotent cell in the bone marrow known as a
hematopoietic stem cell.

INFLAMMATION
Local defense and protective response against cell injury or
irritation or Local vascular and cellular reaction, against an
irritant.

Irritating or injurious agents (Irritant)


Living:
Bacteria,
Fungi,
Virus,
Parasite
or their toxins

Non-Living:
Chemical
Physical
Mechanical

Inflammation is designated by adding the suffix (itis) to the end


of the name of the inflamed organ or tissue.

Inflammation

Inflammation can be induced by immune recognition of


infection or tissue damage (usually good)

Inflammation can be induced by immune recognition that is


hypersensitive to environmental components or
autoinflammatory or autoimmune (=disease)

The tissue & fluid are:

The fluid and proteins of plasma.


Blood vessels.
Cellular and extra cellular constituents of connective
tissue (mast cells & fibroblast).

CONNECTIVE TISSUE
Connective

tissue (CT) is one of the four


types of biological tissue that supports,
connects, or separates different types of
tissues and organs in the body. The other three
types are epithelial, muscle, and nervous
tissue. Connective tissue is found in between
other tissues everywhere in the body,
including the central nervous system. The
outer membranes covering the brain and
spinal cord are the meninges composed of
connective tissue.

Role of tissue and cells in


inflammation
The circulating cells are:

Neutrophils.

Monocytes.

Eosinophils.

Lymphocytes.

Basophils.

Platelets.

Blood stem cell

Response Of Inflammation
The main processes are:
I - Increased blood flow.
II - Increased permeability.
III - Migration of neutrophils.
IV - Chemotaxis.
V - Leucocytes recruitment & activation.

Response Of Inflammation
The main processes are:
I - Increased blood flow due to dilation of blood vessels
(arterioles) supplying the region.
II - Increased permeability of the capillaries, allowing fluid and
blood proteins to move into the interstitial spaces

Response Of Inflammation

III - Migration of neutrophils (and


perhaps a few macrophages) out of the venules and into
interstitial spaces.

Response Of Inflammation
IV - Chemotaxis
Once outside the blood vessel, a neutrophil is guided
towards an infection by various diffusing chemotactic
factors. Examples include the chemokines and the
complement peptide C5a, which is released when the
complement system is activated either via specific
immunity or innate immunity.

Response Of Inflammation
V - Leucocytes recruitment &
activation.

First step is the binding of the neutrophils to the


endothelium of the blood vessels.

The binding is due to molecules, called cell adhesion


molecules (CAMs), found on the surfaces of neutrophils
and on endothelial cells in injured tissue.

ENDOTHELIAL CELL

The endothelium is the thin layer of simple


squamous cells that lines the interior surface of
blood vessels and lymphatic vessels,[1] forming an
interface between circulating blood or lymph in the
lumen and the rest of the vessel wall. The cells that
form the endothelium are called endothelial cells.
Endothelial cells in direct contact with blood are called
vascular endothelial cells, whereas those in direct
contact with lymph are known as lymphatic
endothelial cells.

Response of Inflammation
Eosinophils.
However, in some circumstances eosinophils rather than
neutrophils predominate in acute inflammation. This tends to
occur with parasites (worms), against which neutrophils have
little success.

Response of Acute
Inflammation
Increased

Blood Flow, increased


permeability and Edema in
Inflammation:

The

increased blood flow & increased


permeability are readily visible within a
few minutes following a scratch that
does not break the skin.

Response of Acute
Inflammation
At

first, there is pale red line of


scratch.

Later

on there is accumulation of
inflammatory cells lead swelling,
(inflammation).

Finally,

there is accumulation of
interstitial fluid cause edema.

Types of inflammation

1) Acute
inflammation
2) Sub acute
inflammation:
rarely occur.

3) Chronic
inflammation

Types Of Inflammation
Inflammation is divided into:
1.

Acute Inflammation

2.

Chronic Inflammation

Acute inflammation, which occurs over seconds,


minutes, hours, and days. influx of white blood cells
and fluid from blood to fight infection and aid tissue
repair. Acute inflammation, begins within seconds to
minutes following the injury of tissues. The damage may
I-

be purely physical, or it may involve the activation of an


immune response.

1. Acute inflammation
Macroscopic signs:
Symptoms
1) Redness:
2) Hotness: Fever
3) Swelling:
4) Pain and tenderness:
5) Loss of function:Loss of
movements or restricted
movement, if near joints.

Microscopic signs:
Inflammatory response

1. Local
vascular
change

2. Formation of
inflammatory
exudate

Acute Inflammation

Vascular

stage

Prostaglandins
Arterioles

and leukotrienes affect blood vessels.

and venules dilate.

Increasing
Redness
Capillaries

blood flow to injured area

and warmth result


become more permeable.

Allowing

exudate to escape into the tissues

Swelling

and pain result

Second: Formation of inflammatory


exudates:
Immigration or infiltration of the various leukocytes, fluid
and plasma proteins outside the blood vessels into the
surrounding tissue without injury of the blood vessels.
Leukocytes seem to leave the smallest blood vessels by
inserting pseudopodia into the interendothelial junctions and
sliding through the wall by amoeboid movement.
This is also due to the increased capillary permeability
caused by the high osmotic pressure of the surroundings.

Acute Inflammation

Acute Inflammation
(Acute Bronchitis)

Types of acute inflammation


(based on type of exudates)
1-Catarrhal inflammation:
2-Serous inflammation:
3-Fibrinous inflammation:
4-Membranous inflammation:
5-Hemorrhagic inflammation:
6-Gangrenous inflammation:
7-Allergic inflammation:
8-Suppurative or purulent
inflammation:

Name

Occur in

Characterized by
Exudates rich in mucous

Catarrhal

Mild inflammation in mucous membrane of


respiratory or alimentary tracts e.g. common cold
and catarrhal appendicitis

Serous

Mild inflammation in serous surface such as pleural Extensive watery low


cavity, joint cavity where no damage in endothelium protein exudates
ex. Tuberculosis pleurisy and Common blisters

Fibrinous

Exudates rich in fibrinogen


Outpouring of exudates with high protein and less
volume ex. in lobar pneumonia due to Streptococcus
pneumonia & pericardium inflammation

Fibrinous inflammation in which network of fibrin


entangling inflammatory cells and bacteria forms
Membranous
pseudo-membrane. Example: Diphtheria , Bacillary
dysentery.
Hemorrhagic
Gangrenous

Yellowish grey pseudo


membrane rich in fibrin ,
polymorphs & necrotic
tissues

In blood vessels e.g. in plague

Exudates rich RBCs

Acute appendicitis

Necrotic tissues resulting


from thrombi or emboli
Presence of edema &

Allergic

Result to Ag Ab reaction Hypersensitivity


increase in vascularity.

Suppurative

Caused by pyogenic bacteria and is characterized


by pus formation Example: Abscess.

Large amount of Pus &


Purulent exudates produced

Chronic Inflammation
II - Chronic inflammation, which occurs over longer
times, days & months. inducer of inflammation is
not removed. Leads to tissue damage and loss of
tissue function (joint destruction, lung fibrosis, etc.)
It is associated histologically with the presence of:
Lymphocytes

and macrophages.
The proliferation of blood vessels.
Fibrosis and tissue necrosis.

Causes of Chronic inflammation

- Persistent infection.

II - Prolonged exposure to potentially toxic


agents.
III - Autoimmunity.

Chronic Inflammation
(Chronic Bronchitis)

Chronic Bronchitis

Chronic Inflammation
(Rheumatoid arthritis)

Morphological Features of
Chronic Inflammation
These are characterized by:
I - Infiltration by mononuclear cells.
II - Tissue destruction.
III - Removal of damaged tissue, (healing).

Morphological Features of
Chronic Inflammation
I - Infiltration by mononuclear cells:
The mononuclear cells are become predominant after 48 hours.
These include:

Macrophages.

Lymphocytes.

Plasma cells.

Eosinophils.

Mast cells.

Morphological Features of
Chronic Inflammation
Macrophages
Scattered

all over (microglia, Kupffer cells,


sinus histiocytes, alveolar macrophages, etc.
Circulate as monocytes and reach site of
injury within 24 48 hrs and transform
Become activated by T cell-derived
cytokines, endotoxins, and other products of
inflammation

Morphological Features of
Chronic Inflammation

T and B lymphocytes

Antigen-activated (via macrophages and dendritic cells)

Release macrophage-activating cytokines (in turn, macrophages


release lymphocyte-activating cytokines until inflammatory stimulus
is removed)

Plasma cells

Terminally differentiated B cells (of lymphocytes).

Produce antibodies.

Morphological Features of
Chronic Inflammation
Eosinophils
Found

especially at sites of parasitic


infection, or at allergic (IgE-mediated)
sites.

Eosinophils

have highly cationic


proteins, which are toxic to parasites.

Morphological Features of
Chronic Inflammation
- Tissue destruction
Occur due to:
Inflammatory cells.
Persistent infecting material.
II

Morphological Features of
Chronic Inflammation
Removal of damaged tissue,
(healing):

III -

Occur

by proliferation of small blood


vessels, (angiogenesis).
Proliferation of fibroblast, (fibrosisrepair).

Granulomatous Inflammation

Clusters of T cell-activated macrophages, which engulf and


surround indigestible foreign bodies (mycobacteria, H.
capsulatum, silica, suture material)

Resemble squamous cells, therefore called epithelioid


granulomas with peripheral lymphocytes, fibrosis &
multinucleated giant cells.

Chronic Granulomatous
Inflammation

Chronic Granulomatous
Inflammation

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