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. 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

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. 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

12. 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.

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 ( functio laesa)……………… ……………(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. 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

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
Neutrophi become 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
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