ACUTE INFLAMMATION VASCULAR EVENTS OUTLINE Introduction Steps involve















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ACUTE INFLAMMATION VASCULAR EVENTS

OUTLINE Introduction Steps involve in inflammatory reaction Cardinal signs of inflammation Recognition of injurious agents Mechanism of acute inflammation Vascular events of acute inflammation Conclusion References

INTRODUCTION Acute It inflammation is the initial rapid response of vascularised tissue to injury. occur for a short duration. it is characterized by fluid and plasma protein exudation and a predominantly neutrophilic leukocyte accumulation. Inflammation is induced by chemical mediators that are produced by host cells in response to injurious stimuli such as; infection, trauma, foreign bodies, immune reactions and tissue necrosis.

STEPS INVOLVE IN INFLAMMATORY REACTION Recognition of injurious agents Recruitment Removal of leukocytes and plasma proteins of the agent Regulation (control) of the response Resolution (repair) CARD/INAL SIGNS OF INFLAMMATION Dolor (pain) Calor (heat) Rubor (redness) Tumour (swelling) Functio laesa (loss of function)

RECOGNITION OF INJURIOUS AGENTS Inflammatory cells express receptors designed to sense the presence of infectious pathogens and substance released from dead cells. The 1. most important two families of these receptor are; Toll-like receptors(TLRs) Theyrecognize They microbial products. are located in plasma membranes and endosomes. 2. The inflammasome It is a multi-protein cytoplasmic complex that recognizes products of dead cells

FIG 1: A, picture showing the action toll-like receptors (TLRs). B, picture showing the action of inflammasome.

MECHANISM OF ACUTE INFLAMMATION The mechanism of acute inflammatory response is a continuous process which includes; Dilation of small vessels leading to increase in blood flow Increased permeability of the microvasculature. Emigration of leukocyte from the microcirculation, their accumulation in the focus of injury and their activation to eliminate the offending agent. For the purpose of discussion it can be divided into two events; Vascular Cellular events

VASCULAR EVENTS OF ACUTE INFLAMMATION Changes in vascular flow and calibre vasodilation is induced by action of histamine on smooth muscles and it may be preceded by a transient vasoconstriction. Increased permeability of the microvasculature. protein-rich fluid moves into the extravascular tissues. The loss of fluid and increased vessel diameter lead to slower blood flow (stasis of blood flow). As stasis develops, leukocytes (principally neutrophils) becomes closer to the vascular endothelial a process called margination. This is followed by the adhesion of the neutrophils with the endothelium and soon after they migrate through the vascular wall into the interstitial tissue.

FIG 2: Picture showing vascular events in acute inflammation.

FIG 3: Diagram showing how vasodilation and increased permeability cause stasis, margination, adhension of neutrophil and eventual emigration of neutrophils

Increased Vascular Permeability mechanisms are responsible for increased vascular permeability includes; Retraction of endothelial cells resulting in opening of interendothelial spaces. Endothelial Increased injury resulting endothelial cell detachment. transport of fluid and protein by transcytosis. Response Of Lymphatic Vessels And Lymph Nodes Lymphatic vessels also participate in acute inflammation.

FIG 4: Mechanisms of increased vascular permeability in inflammation and their features and underlying causes

CONCLUSION Acute inflammation is a protective mechanism and its vascular events involve mainly vasodilation and increased permeability.

References Kumar, Vinay, Abul K. Abbas, Nelson Fausto, Stanley L. Robbins, And Ramzi S. Cotran. Robbins And Cotran Pathologic Basis Of Disease. Philadelphia: Elsevier Saunders, 2011(9 th ed). Kumar, Vinay, Abul K. Abbas, Nelson Fausto, Stanley L. Robbins, And Ramzi S. Cotran. Robbins And Cotran Pathologic Basis Of Disease. Philadelphia: Elsevier Saunders, 2017(10 th ed). Harsh Mohan. Textbook of Patholgy. Jaypee Brothers, 2010(6 th ed).

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