Inflammation

INFLAMMATION: It is a protective response by a vascularized tissue against any pathogen (bacteria, viruses, parasites) and cell injury to provide healing/ repair to that injured or infected tissue by destroying them.

TYPES OF INFLAMMATION:

1) ACUTE INFLAMMATION

2) CHRONIC INFLAMMATION

ACUTE INFLAMMATION:

·     An immediate and early response to injury

·     Relatively short duration (from few minutes upto few days)

·     Form inflammatory exudate

·     Mainly delivers neutrophil leukocytes (WBC) to the site of injury.

VASCULAR EVENTS  OF ACUTE INFLAMMATION:

1) Changes in Blood Vessel Diameter:  Initial vasoconstriction followed by vasodilation

2) Changes in Blood Flow: Initial increase in blood velocity due vasodilation but soon blood flow becomes slow due to increase in blood vessel permeability (loss of fluid from blood increases blood viscosity).

3) Increase in Vessel Permeability: Walls of blood vessels contain intercellular junctions (pores) which normally allows the passage of small molecules (water & ions). But in acute inflammation, endothelilal cells lining the blood vessels contracts causes the widening of these pores, therefore allows large molecules protein & plasma fluid to pass through the vessel walls. This process is known as exudation. Swelling caused by exudation is called inflammatory edema.

MECHANISM OF INC. PERMEABILITY OF VESSELS:

·     Immediate transient response:  

Ø      It occurs in response to mild injury

Ø      Permeability begins 1-2 minutes after the onset of injury and remains about 15-30 minutes

Ø      Mediated by histamine, bradykinin & leukotrines which causes contration of endothelial cells resulting in widening of pores

·     Delayed-prolonged response:

Ø      It occurs in response to moderate injury

Ø      Permeability begins 30minutes to 10 hours after the the onset of injury & reaches its peak in about 4-12 hours

Ø      Permeability increases due to direct injury of endothelial cells

·     Immediate-prolomged response

Ø   It occurs in response to severe injury

Ø   Permeability begins immediately after the injury and last for one to several days

Ø   Permeability increases due to necrosis of endothelial cells.

FACTORS WHICH REGULATES TRANSPORT OF EXUDATE:

·     Capillary Hydrostatic Pressure: It tends to escape the fluid out of the vessel.

·     Osmotic Pressure Of Protein In Intersitial Space: It tends to pull the fluid from vessels to interstitial space.

DURING INFLAMMATION EXUDATE FORMATION OCCURS DUE TO:

Increased capillary hydrostatic pressure due to enhance blood flow

Increased vascular permeability allowing plama protein to enter in intersitial space where they exert osmotic pressure & draws more fluid from the vessels

CELLULAR ( LEUKOCYTES) EVENTS:

SEQUENCE OF CELLULAR EVENTS:

1) MARGINATION:  Normally RBC & WBC flows in the central axis of blood vessel. During acute infalmmation, Due to increase in permeability, the flow of blood is slow inside vessel & therefore RBC stick together forming clumps or roulaex which is larger than WBC. These clumps forces WBCs to the periphery towards vessel walls (endothelial cells).

2) ADHESION: WBC becomes attach (adhere) to the endothelial cells of vessel wall. This adhesion is because of adhesion molecules present on the surfaces of both WBC & endothelial cells.

3) EMIGIRATION: Adherent leukocytes leaves the blood vessels and enters into interstitial space through intercellular junctions (pores).

It takes place in 2-10 minuts.

4) CHEMOTAXIS:  Process by which leukocytes are attracted towards and move towards an attractants usually a chemical substance at the site of injury.

5) PHAGOCYTOSIS: Process by which micro-organism and other forein body are engulfed and destroyed by neutrophils & macrophages.

This process is divided in three steps:

    I.            Recognition & Attachment: White Blood Cells indentify the object which they have to phagocytize. Recognition and attachment of most of the microorganism is facillitated by coating them with serum protein called  “Opsonin” which inturn binds to specific receptors on the leukocytes.

Opsonins are (i) C3b (ii) IgG

Engulfment:  Process occurs by pseudopodial extensions of leukocytes cytoplasm which completely encloses the foreign particles forming phagosome. Membranes of lysosomal granules fuse with it and form phagolysosomes. Lysosomes discharge their content into phagolysosomes causing killing & degradation of microorganis