Inflammation

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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.

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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).

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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.


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


III - Migration of neutrophils (and perhaps a few macrophages) out of the venules and into interstitial spaces.


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.


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

Acute

inflammation

3) Chronic

inflammation

2) Sub acute inflammation:

rarely occur.

Types Of Inflammation

Inflammation is divided into:

Acute Inflammation

Chronic Inflammation

I - 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 be purely physical, or it may involve the activation of an immune response.

1. Acute inflammation

Microscopic signs:

Inflammatory response

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.

1. Local vascular change

2. Formation of inflammatory exudate

Acute Inflammation

Vascular stage

Prostaglandins and leukotrienes affect blood vessels.

Arterioles and venules dilate.

Increasing blood flow to injured area

Redness and warmth result

Capillaries become more permeable.

Allowing exudate to escape into the tissues

Swelling and pain result

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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:

NameOccur inCharacterized byCatarrhal Mild inflammation in mucous membrane of respiratory or alimentary tracts e.g. common cold and catarrhal appendicitis Exudates rich in mucousSerousMild inflammation in serous surface such as pleural cavity, joint cavity where no damage in endothelium ex. Tuberculosis pleurisy and Common blistersExtensive watery low protein exudatesFibrinousOutpouring of exudates with high protein and less volume ex. in lobar pneumonia due to Streptococcus pneumonia & pericardium inflammationExudates rich in fibrinogenMembranousFibrinous inflammation in which network of fibrin entangling inflammatory cells and bacteria forms pseudo-membrane. Example: Diphtheria , Bacillary dysentery. Yellowish grey pseudo membrane rich in fibrin , polymorphs & necrotic tissues HemorrhagicIn blood vessels e.g. in plague Exudates rich RBCsGangrenousAcute appendicitisNecrotic tissues resulting from thrombi or emboliAllergicResult to Ag Ab reaction HypersensitivityPresence of edema & increase in vascularity.SuppurativeCaused by pyogenic bacteria and is characterized by pus formation Example: Abscess. Large amount of Pus & Purulent exudates produced

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Second level

Third level

Fourth level

Fifth level

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

I - 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).


I - Infiltration by mononuclear cells:

The mononuclear cells are become predominant after 48 hours.

These include:

Macrophages.

Lymphocytes.

Plasma cells.

Eosinophils.

Mast cells.


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


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.


Eosinophils

Found especially at sites of parasitic infection, or at allergic (IgE-mediated) sites.

Eosinophils have highly cationic proteins, which are toxic to parasites.


II - Tissue destruction

Occur due to:

Inflammatory cells.

Persistent infecting material.


III - Removal of damaged tissue, (healing):

Occur by proliferation of small blood vessels, (angiogenesis).

Proliferation of fibroblast, (fibrosis-repair).

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

Inflammation

Documents

nervous tissue

tissue damage

injured tissue

role of tissue

blood proteins

diseasethe tissue fluid

reaction of blood vessels

increased blood flow