Acute inflammation 1

By Dr. S. Homathy

Clinical example of acute inflammation

Injurious agents(aetiological factors)

Parenchymal cells

Reversible / irreversible injury

to remove/destroy the

injurious agent and

limit tissue damage

Inflammatory reaction

vascularized connective tissue

Pathological process

Alteration in the structure and function of tissues

Direct effects reactive changes in

of injurious agents vascularized CT

on tissues

Cell injury macroscopic and

microscopic changes

Definition of Inflammation

It is a protective response of the vascular and

supporting elements of a tissue to injury

Result in the formation of a protein – rich

exudate

To prevent further injury to tissues and to remove

or destroy the injurious agent and initiate repair.

• Although it is help full, it has considerable potential to cause harm

Eg :Anaphylactic reaction to insect bite / drugs.Chronic diseases- rheumatoid arthritis /

atherosclerosisIntestinal obstruction following inflammation

in the peritoneum.

Causative agents

InfectiousPhysicalChemicalTissue NecrosisForeign Bodies (FBs)Immune “responses”, or “complexes” /

hypersensitivity reactionsAround the neoplasm

Components of the inflammatory reaction

Components of the inflammatory reaction

Circulating cells - N, E, B, L, Monocytes, platelets

Plasma proteins- clotting factors, Kininogens, complement components

Vascular wall cells – endothelial cells and smooth muscle cells.

Connective tissue cells – fibroblast and macrophages

Extracellular matrix – collagen, elastin, proteoglycan, fibronectin

Inflammatory response involve a highly complex set of events.

• Initial inflammatory stimulus

• Triggers the release of chemical mediaters from plasma and connective tissue cells

• Soluble mediators acting together or in sequence amplify the initial reaction

• Influence its evolution by vascular and cellular response.

• Inflammatory response is terminated when – Injurious stimulous is removed– Inflammatory mediators are dissipated, catabolized

/ inhibited

Inflammation

Acute inflammation Short durationLast for minutes to few

daysCharacterized by fluid

and plasma protein exudation

Neutropil leukocyte infiltration

Chronic inflammationLonger durationLast for days to yearsVascular proliferation

and scaringInflux of lymphocytes

and macrophages.

Acute inflammationIt is immediate and early response to injury

Designed to deliver leukocytes to the sites of injury

Leukocytes clear any invading microbes

Begin the process of breaking down necrotic tissues.

Cascade of events is integrated by local release of chemical mediators

It has two major componentsVascular changes

Changes in vascular caliber and flow- change in the caliber of

vesselsCauses increased blood flow

Increased vascular permeability

Structural changes permits

plasma proteins and

leucocytes to leave the

circulation

Cellular events

Cellular recruitment and activation

– Emigration of leukocytes

from the microcirculation

– Accumulate in the focus

of injury

Cardinal macroscopic changes

Vascular changes and cellular events produce

3 of the 5 classical local signs of acute

inflammation

Additional features are the consequences of mediators and leukocyte- mediated damage.

Local manifestations

• Heat (calor) described• Redness (rubor) by• Swelling (tumor) Cornelius Celsus• Pain (dolor) (1st century AD)

• Loss of function ( functio laesa)………………. ……………(described by Virchow-19th century)

Systemic manifestations

• Fever• Chills• Myalgia• Malaise

Process of acute inflammation

1. Transient vasoconstriction( within seconds)

2. Arteriolar vasodilation

3. Increased vascular permeability

4. Retardation of blood flow and stasis

5. Leukocyte extravasations and phagocytosis

6. Fibrin formation

7. Role of lymphatics

Vascular changes 1.Acute arteriolar vasodilation

Opens microvascular beds

Locally increased blood flow

Engorgement of the down-stream capillary beds

causes of increased heat and redness

Increased intravascular pressure causes an early

transudate (protein-poor filtrate of plasma) into

interstitium (vascular permeability still not increased yet)

2.Increasefd Vascular permeability (leakiness) commences– Transudate gives way to exudate (protein-rich)– Increases interstitial osmotic pressure contributing to

edema (water and ions)

• Accumulation of fluid in the extracellular space

Swelling pain due to increased pressure

8021`1. Vasodilatation

2. Exudation - Edema

3. Emigration of cells

4. Chemotaxis

3.Retardation of blood flow and stasis

outpouring of albumin rich fluid into the extravascular

tissues results

in the concentration of RBCs in small vessels and

increased viscosity of blood.

Rouleux formation of red cells further increase the viscosity

Neutrophi become oriented at the periphery of vessels and

start to stick

Swelling of the endothelium

Increase of surrounding tissue pressure

Haemoconcentration and stasis

• Normal flow

• stasis

Transudate:

An ultrafiltrate of blood plasma

permeability of endothelium is usually normal.

low protein content ( mostly albumin)

usually caused by alterations in hydrostatic or oncotic pressure.Implies a hydrostatic (pressure) problem

Exudate:

A filtrate of blood plasma mixed with inflammatory

cells and cellular debris.

permeability of endothelium is usually altered

high protein content.

caused by increased vascular permeability.

Implies an inflammatory process

• LEAKAGE OF PROTEINACEOUS

FLUID (EXUDATE, NOT TRANSUDATE)

Difference between exudates and transudate

Transudate hydrostatic imbalance

across the vascular endothelium

Low protein content( most of which is albumin – 0-1.5g/dL)

No cellsSpecific gravity <1.012Fibrin absent

Exudate Increased vascular

permeability

High protein content (1.5-6g/dL)

Also contain PNL, cellular debris and RBC

Specific gravity >1.020Fibrin present

• Fluid appears grossly clear.

• Fluid appears grossly cloudy