Inflammation

Dr. Mehzabin Ahmed

Inflammation ?

• It is a complex reaction in the vascularised tissues in response to cell injury, leading to accumulation of – fluid, – proteins and – leucocytes in extravascular tissues.

• It is described by adding the suffix –itis to the name of the organ or tissue involved.

Types of inflammation

• Acute inflammation is typically of short duration, few minutes to few days, in which neutrophils predominate, usually occurs with protein exudate.

• Chronic inflammation occurs over a duration of days to years, characterized by mainly lymphocytic and macrophage infiltrate with proliferation of blood vessels, tissue necrosis and fibrosis.

Acute inflammation

• It is the most common early tissue response to tissue damage and destruction.

• An inflammatory exudate fills up the site of damage.

Differences between Exudate & Transudate

The inflammatory fluid is called an exudate when it is

• Rich in proteins • Cells and tissue

debris• Has a specific

gravity greater than 1.020.

It is called a transudate when there is

• Less protein • Less number of

cells• Has a specific

gravity less that 1.012.

Clinical effects of acute inflammation

The cardinal signs of inflammation are• tumor (swelling) due to accumulation of exudate

• rubor (redness) due to vessel dilatation & blood

• calor (heat) flow to the inflamed area

• dolor (pain) due to pressure on the nerve endings from the swelling & due to chemical mediators

• loss of function due to swelling & pain

Components of acute Inflammation

• 1)       Vascular component- in the local vascular flow and alteration of the vascular permeability in acute inflammation.

• 2)       Cellular component- Neutrophils are the main effector cells of acute inflammation. They attach themselves to

Vascular component

* local vascular flow* Altered vascular

permeability

Cellular component

It involve neutrophils as the main effector cells of acute inflammation. The cellular events are:

1) Extravasation 2) Transmigration of leukocytes3) Chemotaxis 4) Phagocytosis

Cellular componentExtravasation of the PMN occurs by the following

process:1) Margination: Movement of the PMN cells close to

the vessel wall in the blood stream 2) Rolling: the PMN cells roll along the vessel wall3) Adhesion: attach themselves to activated

endothelial cells of the blood vessels4) Aggregation: collection of adjacent PMN cells

and these undergo shape changes

Transmigration: movement of the PMN cells out of the vessel lumen to the tissue space around the vessels.

Chemotaxis: Movement of the PMN cells along a concentration gradient of chemotactic factors to reach the site of inflammation.

Phagocytosis: process by which the PMN cells engulf and digest the injurious agent by releasing enzymes and superoxides

Some mediators come from plasma in precursor

forms that are activated.

Cell bound mediators are found in granules and

released immediately. Others are newly

synthesized, usually from mast cells, platelets,

neutrophils, or monocytes.

Their action is usually short- lived and decay, often

within seconds.

Mediators of Inflammation

Chemical mediators of inflammation by function:

1. Increase vascular permeability: histamine, C3a, C5a, PAF, bradykinin, LTC, LTD, LTE (leukotrienes C,D,E)

2. Chemotaxis: C5a, LTB4, chemokines, IL-8

3. Vasodilation: NO, PGI 2 (prostaglandin I 2)

4. Systemic signs: TNF (tumor necrosis factor), IL-1, IL-6

5. Pain: bradykinin, prostaglandins

6. Tissue Destruction: leukocyte lysosomal enzymes, NO (nitric oxide), reactive O2 (reactive oxygen species)

Outcomes of Acute Inflammation

1.Resolution: The return to normal architecture and removal of dead cellular debris

2.Fibrosis: is scar formation with loss of original architecture from more significant injury.

3.Organization: denotes connective tissue replacement of functional tissue and occurs with marked protein exudates, lots of fibrin exudation from plasma, areas where exudate cannot be adequately absorbed.

4.Abscesses: localized collection of pus may form in some bacterial infections.

5.Chronic inflammation: Acute inflammation can continue and progress to chronic form

TISSUE DAMAGE

Acute inflammation

Damage neutralized & Damage neutralized & Damaging agent persists

Cells can regrow Cells cannot regrow with tissue damage

Regeneration Organization through Organization with Phagocytosis & Healing contd. inflammation

by repair of damaged tissueRestoration of CHRONIC normal structure Scar formation INFLAMMATION& function or FIBROSIS

& loss of Damaging agent specialized function overcome

RESOLUTION Persistence

Yes No