Acute inflammation 1

1. Acute inflammation 1 By Dr. S. Homathy

2. Clinical example of acute inflammation

3. Injurious agents(aetiological factors) Parenchymal cells Reversible / irreversible injury to remove/destroy the injurious agent and limit tissue damage Inflammatory reaction vascularized connective tissue

4. 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

5. 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.

6. 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.

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

8. Components of the inflammatory reaction

9. Componentsof 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

10. Inflammatory response involve a highly complex set of events. • Initial inflammatory stimulus • Triggers the release of chemical mediaters from plasma and connective tissue cells

11. 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

12. Inflammation Acute inflammation Chronic inflammation Longer duration Last for days to years Vascular proliferation and scaring Influx of lymphocytes and macrophages. • Short duration • Last for minutes to few days • Characterized by fluid and plasma protein exudation • Neutropil leukocyte infiltration

13. 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

14. 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

15. 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.

16. Local manifestations • Heat (calor) described • Redness (rubor) by • Swelling (tumor) Cornelius Celsus • Pain (dolor) (1st century AD) • Loss of function (functiolaesa)………………. ……………(described by Virchow-19th century)

18. Systemic manifestations • Fever • Chills • Myalgia • Malaise

19. 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

20. 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)

21. 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 • Swellingpain due to increased pressure

22. 8021` • Vasodilatation • Exudation - Edema • Emigration of cells • Chemotaxis

23. 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 • Neutrophibecome oriented at the periphery of vessels and start to stick • Swelling of the endothelium • Increase of surrounding tissue pressure

24. Haemoconcentration and stasis • Normal flow • stasis

25. 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

26. 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

27. LEAKAGE OF PROTEINACEOUS FLUID (EXUDATE, NOT TRANSUDATE)

28. 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 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

29. Fluid appears grossly clear. • Fluid appears grossly cloudy