Acute Inflammation

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 leukocytes 3) Chemotaxis 4) Phagocytosis

Cellular component

Extravasation 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 wall 3) Adhesion: attach themselves to activated endothelial cells of the blood vessels 4) 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

Mediators of Inflammation 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.

Chemical mediators of inflammation by function: •

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

•

Chemotaxis: C5a, LTB4, chemokines, IL-8

•

Vasodilation: NO, PGI 2 (prostaglandin I 2)

•

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

•

Pain: bradykinin, prostaglandins

•

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

Outcomes of Acute Inflammation • Resolution: The return to normal architecture removal of dead cellular debris

• Fibrosis: is scar formation with loss architecture from more significant injury.

of

and

original

• 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. • Abscesses: localized collection of pus may form in some bacterial infections. • Chronic inflammation: Acute inflammation can continue and progress to chronic form

TISSUE DAMAGE Acute inflammation Damage neutralized & Cells can regrow

Regeneration

Restoration of normal structure & function

RESOLUTION

Damage neutralized & Cells cannot regrow

Damaging agent persists with tissue damage

Organization through Phagocytosis & Healing by repair of damaged tissue Scar formation or FIBROSIS & loss of specialized function

Organization with contd. inflammation CHRONIC INFLAMMATION

Damaging agent overcome Persistence Yes