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 / atherosclerosis Intestinal obstruction following inflammation in the peritoneum.

Causative agents Infectious Physical Chemical Tissue Necrosis Foreign Bodies (FBs) Immune “responses”, or “complexes” / hypersensitivity reactions Around 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

Influence its evolution by vascular and cellular response. 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 Chronic inflammation Short duration Last for minutes to few days Characterized by fluid and plasma protein exudation Neutropil leukocyte infiltration Longer duration Last for days to years Vascular proliferation and scaring Influx of lymphocytes and macrophages.

Acute inflammation It 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 components Vascular changes Changes in vascular caliber and flow- change in the caliber of vessels Causes 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 Transient vasoconstriction( within seconds) Arteriolar vasodilation Increased vascular permeability Retardation of blood flow and stasis Leukocyte extravasations and phagocytosis Fibrin formation 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)

Swelling pain due to increased pressure 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` Vasodilatation Exudation - Edema Emigration of cells 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 hydrostatic imbalance across the vascular endothelium Low protein content( most of which is albumin – 0-1.5g/dL) No cells Specific gravity <1.012 Fibrin absent Exudate Increased vascular permeability High protein content (1.5-6g/dL) Also contain PNL, cellular debris and RBC Specific gravity >1.020 Fibrin present

Fluid appears grossly clear. Fluid appears grossly cloudy