Acute Inflammation - Definition, Pathogenesis, Causes, Mediators, Morphology, Exudate and Transudate

inflammation is a natural host protective response occurs against tissue insults such as infection tissue injury or necrosis foreign agents and hypersensitivity reactions inflammation is the first-line defense in our body against such insults and it is nonspecific inflammation usually promotes healing but if uncontrolled it may become harmful inflammation can be acute or chronic in this video I will discuss about acute inflammation and chronic inflammation I will do in a separate video acute inflammation is rapid and onset tannaz of short duration usually lasts for a few hours or few days and the characteristic microscopic feature is the

protein and fluid rich exudate which I will discuss later in this video our four major purposes of acute inflammation they are to eliminate the injurious agent to prevent the spread of the injurious agent to remove necrotic cells and tissue and to initiate the repairing process there are four major macroscopic features of acute inflammation known as hallmarks of acute inflammation they are redness or erythema pain swelling or edema and warmth at the sight of inflammation the cute inflammation consists of two events they are vascular events which occur in blood vessels and lymphatics and cellular events generated

by leukocytes predominantly neutrophils there are two phases in vascular events of blood vessels first one is increase in blood flow at the site of inflammation and the second one is increase in vascular permeability when there is a tissue injury the injured cells will secrete nitric oxide and histamine these substances cause vasodilation of blood vessels especially in capillaries and venules vasodilation results in increased blood flow at the site of inflammation this is the reason for erythema and warmth at the site of inflammation in addition histamine released by the injured cells will generate action potentials in the

pain sensory nerve fibers which induces pain when the blood flow increases blood cells get concentrated in the vessels resulting in local stasis of blood at the same time vascular permeability increases due to contraction of endothelial cells sometimes direct injury to the endothelium causes discontinuation of vessels and increases permeability and vascular endothelial growth factor increases transit osis of substances through the endothelial cells increased vascular permeability causes release of the protein and fluid rich exudate into the interstitial space which is the reason for edema lymphatics also play a role in vascular events there is an increase in

limb flow due to excess fluid accumulation in the interstitial space increased proliferation of lymph vessels to compensate the increased load and lymph nodes may become enlarged due to hyperplasia cellular events consist of three steps first one is recruitment of leukocytes to the site of inflammation from blood then recognition of the offending agent and finally removal of the offending agent neutrophils and monocytes are the predominant cell type and cellular events because they possess the ability for Fugazi ptosis these cells also promote growth and repair during the inflammatory response first let's discuss about recruitment of leukocytes there

are three steps adhesion of leukocytes to the endothelium transmigration of leukocytes into the interstitial space and chemo taxis of leukocytes towards the site of inflammation in the interstitial fluid adhesion of leukocytes to the endothelium occurs in three steps the first step is margination we know that the normal blood has a laminar flow meaning that in normal blood plasma flows peripherally closer to the endothelium and blood cells in the middle however due to the increased blood flow during the vascular events this laminar flow gets disrupted and leukocytes come in contact with the endothelium this movement of

leukocytes is called margination the second step of leukocyte adhesion is rolling this movement is initiated by selecting proteins they are expressed in leukocytes as l selectins in platelets as p selectins and in endothelial cells as e selectins the expression of ligands for these receptors is mediated by tumor necrosis factor and interleukin 1 interaction of selectins and their ligands results in attachment of leukocytes to the endothelium however these interactions are much weaker so due to the blood flow leukocytes frequently attach and get detached from the endothelium giving rise to the typical rolling movement of leukocytes this

movement of leukocytes is demonstrated later in this video third and final step is firm adhesion of leukocytes to the endothelium it is mediated by integrins expressed on leukocytes and the expression of ligands for integrins on the endothelial cells is mediated by tumor necrosis factor and interleukin 1 interaction of integrins and their ligands results in firm adhesion of leukocytes to the endothelium okay we were discussing about the cellular events of acute inflammation it had three steps recruitment of leukocytes recognition of the offending agent and removal of the offending agent in the recruitment of leukocytes there were

three steps adhesion transmigration and chemo taxis so we have discussed about adhesion now let's discuss about transmigration transmigration is the movement of leukocytes which are firmly attached to the endothelium into the interstitial space several adhesion molecules facilitate this movement of leukocytes such as platelet endothelial cell adhesion molecules in CD thirty-one after passing through the endothelial lining leukocytes secrete collagen ace's to dissolve the basement membrane and they reach the interstitial space the final step of leukocyte adhesion is chemo taxis of leukocytes towards the site of inflammation in the interstitial space this movement occurs according to a

chemical gradient these chemicals could be endogenous or exogenous endogenous substances are secreted by the host cells such as chemokines components of the complement system and arachidonic acid metabolites exogamous substances are secreted by the endurance agent itself such as bacterial products like lipids and peptides these chemotactic agents bind to g-protein coupled receptors on the leukocytes and initiate intracellular signaling Cascades which increased the cytosolic calcium and GTP levels and activate several kinases the net result is polymerization of actin and initiation of the movement of leukocytes towards the site of inflammation now we have finished the first step

of cellular events recruitment of leukocytes the next step is recognition of the offending agent leukocytes must be activated to perform their functions in order to get activated they need to recognize the offending agent first then the recognition itself initiates signaling cascades which cause activation of leukocytes leukocytes have several types of receptors to recognize the offending agent toll-like receptors recognize bacterial lipopolysaccharides bacterial proteoglycans and double strand RNA g-protein-coupled receptors usually recognize substances produced by the host cells such as prostaglandins platelet activating factors in Luca trance and they also recognize bacterial products like short bacterial peptides receptors

for opsin ins recognize proteins which cope microbes during opsonization such as antibodies complement proteins and lectins this optimization process helps to make phagocytosis more efficient receptors for cytokines recognize cytokines which are produced against microbes and into Ferrand gamma the final step of cellular events is the removal of the offending agent Fugazi ptosis and intracellular killing are the ways of removal of the offending agent at first leukocytes should bind with the offending agent then it is engulfed by the leucocyte and finally the leucocyte kills and degrades the offending agent leukocytes have several types of receptors to

engulf the offending agent such as Manas receptors scavenger receptors and receptors for obstinance this diagram shows the whole process of phagocytosis and intracellular killing within a neutrophil in the first step the neutrophil engulfs the bacterium and forms of Faygo 'some which contains the bacterium covered by a pinch of plasma membrane in the second step Fago some fuses with a lysosome and forms of Faygo lysosome this causes the release of lysosomal enzymes into the Faygo some in the third step lysosomal enzymes reactive oxygen and nitrogen species degrade the bacterium and in the fourth step the soluble

debris of bacterium are removed by exocytosis so in summary we can demonstrate the whole process of acute inflammation like this when the Endura say Junt is removed the acute inflammatory response should terminate several factors contribute to cease the inflammatory response when the offending agent is eliminated the stimulus for acute inflammation no longer persists and the mediators of acute inflammation have short half-life's neutrophils live a short duration after leaving the circulation switch of pro-inflammatory luka trans into anti-inflammatory ly pox ins liberation of anti-inflammatory cytokines from the macrophages such as transforming growth factor bead of and interleukin

10 production of anti-inflammatory lipid mediators such as protectants and neural impulses which inhibit the acute inflammatory response finally I would like to discuss the differences between an exudate and a transit 8 an exudate is a fluid which is formed in the interstitial space due to the increased vascular permeability but a transit 8 is a fluid which is formed due to an imbalance of the hydro static and osmotic forces between the vessels in the interstitial fluid exudate has a high protein content and transit 8 has a low protein content exudate has a high neutrophil content and

is rich in cellular debris but transit 8 has little or sometimes no cellular material at all exudate has a high specific gravity and transit 8 has a low specific gravity exudate clinically causes non pitting edema while transit eight causes pitting edema you