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 inflammation is the initial rapid response of vascularised tissue to injury.

It 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 of leukocytes and plasma proteins

Removal 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 most important two families of these receptor are;

1. Toll-like receptors(TLRs)

Theyrecognize microbial products.

They 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 events

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 injury resulting endothelial cell detachment.

Increased 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(9th 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(10th ed).

Harsh Mohan. Textbook of Patholgy. Jaypee Brothers, 2010(6th ed).

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