1. dr.reza2006@gmail.com Dr Reza INFLAMMATION

2. dr.reza2006@gmail.com

3. Definition of Inflammation:  Inflammation is a complex reaction in living vascularized tissue to injurious agents leading to the exudation and accumulation of protein rich fluid and leucocytes in extravascular tissue, provided the injury does not destroy the tissue.  Reaction of vascularized tissue to injury

4. dr.reza2006@gmail.com Accumulation of protein rich fluid and leucocytes in extravascular tissue

5. dr.reza2006@gmail.com Purposes: A protective response to- 1. to dilute, localize and destroy the injurious agent 2. to limit tissue injury 3. to restore the tissue towards normality Harmful effect: eg, hypersensitivity reaction

6. dr.reza2006@gmail.com Acute Inflammation:  Rapid local response of living tissue to injury  Lasts for minutes to a few days  Extravascular accumulation of protein rich fluid and leucocytes, predominantly Neutrophils, ie, Exudative lesion  Stereotype,ie, wide variety of agents share the same basic features

7. dr.reza2006@gmail.com Chronic Inflammation:  Persists for weeks to months  Extravascular accumulation of Lymphocytes and Macrophages  Tissue destruction and attempts to healing by proliferation runs simultaneously, ie, Proliferative lesion  Not stereotype

8. dr.reza2006@gmail.com Cardinal signs of Acute Inflammation  Rubor or redness  Calor or heat  Tumor or swelling  Dolor or pain  Loss of function(functio laesa)

9. dr.reza2006@gmail.com

10. Aetiology of Acute Inflammation 1. Infectious agent: Bacteria, virus, fungi, protozoa 2. Immune reaction: Hypersensitivity reaction 3. Trauma: blunt/penetrating 4. Physical agent: eg, burn, ionizing radiation 5. Foreign bodies: eg, sutures, dirt 6. Chemical agent: acids, alkalies, bile 7. Tissue necrosis: eg, infarcts

11. dr.reza2006@gmail.com Events in Acute Inflammation: 1.Vascular changes: Changes in vascular flow & caliber Increased vascular permeability(Vascular leakage) 2.Exudation of blood constituents: Fluid Exudate Cellular Exudate 3.Changes in tissue tissue components

12. dr.reza2006@gmail.com Vascular changes(Flow & Caliber) Vasodilation, due to- a) Histamine b) Nitric oxide,etc Increased permeability of microvasculature Slowing of circulation/ Stasis, due to- a) Exudation b) Microcirculation packed with red cell c) Increased viscosity of blood

13. dr.reza2006@gmail.com Accounts for warmth and redness Opens microvascular beds Increased intravascular pressure causes an early transudate (protein-poor filtrate of plasma) into interstitium (vascular permeability still not increased yet)

14. dr.reza2006@gmail.com  Movie- Vasodilation

15. dr.reza2006@gmail.com Vascular changes(Vascular Leakage)

16. dr.reza2006@gmail.com Vascular changes(Vascular Leakage)

17. dr.reza2006@gmail.com Vascular changes(Vascular Leakage)

18. dr.reza2006@gmail.com Cellular events: A) Leucocyte Extravasation 1 In the limen- a) Margination b) Rolling c) Adhesion to endothelium 2 Transmigration or diapedesis across endothelum 3 Chemotaxis B) Phagocytosis

19. dr.reza2006@gmail.com leukocytes first roll, then become activated and adhere to endothelium, then transmigrate across the endothelium, pierce the basement membrane, and migrate toward chemoattractants

20. dr.reza2006@gmail.com  Movie- Leucocyte Rolling

21. dr.reza2006@gmail.com Chemotaxis: Following extravasations, leukocytes emigrate in tissues toward the site of injury by a process called chemotaxis. Exogenous chemo attractants: Exogenous chemo attractants: bacterial products, etc. Endogenous chemo attractants: Endogenous chemo attractants: components of the (LTB4), cytokines, etc.

22. dr.reza2006@gmail.com Phagocytosis Recognition and attachment Engulfment Phagosome Phagolysosome killing and degradation Oxydent dependent mechanism: I. H2O2-MPO-Halide system II. Reactive Oxygen intermediates-O2 -,H2O2, OH - Oxydent independent mechanism: killing occur by substances of lysosomal granules- Lysozyme, Lactoferrin, BPI, Defensin

23. dr.reza2006@gmail.com Systemic effects of Acute Inflammation  Fever  Sleepiness, poor appetite, chills, rigors, tachycardia (prolonged inflammation  IL-1, TNF  increased catabolism of skeletal muscle protein  wt loss)  Blood changes  Septic shock:  Immune response: Ab or cell mediated  Lymph node, Liver, Spleen: Enlarged

24. dr.reza2006@gmail.com Fever  By Pyrogrns  stimulate PG synthesis in Hypothalamus  Exogenous Pyrogrns: bacterial LPS  stimulate leucocyte to release of Endogenous pyrogen: IL-1 & TNF  PG produced which act on vasomotor centre  skin vasoconstrivtion  reduced heat loss  fever

25. dr.reza2006@gmail.com Blood changes  Leucocyte count:  Leucocytosis(by IL-1 & TNF; also left shift)  bacterial infection  Neutrophilia  most bacterial infection  Eosinophilia(by IL-5)  allergy & helminths  Lymphocytosis  viral infection, Tuberculosis  Leucopenia  Typhoid, virus, rickettsiae, protozoa  Platelet: Thrombocytopenia occur in dengue, measels  ESR: Increased Fibrinogen level is responsible for high ESR  CRP(C-reactive protein): increased (eg. RF, RA)  Acute –phase proteins: liver synthesizes acute phase protein like C reactive protein(CRP), Fibrinogen and Serum Amyloid A(SAA).

26. dr.reza2006@gmail.com Morphological Variants: 1. Suppurative or Purulent inflammation 2. Fibrinous inflammation 3. Serous inflammation 4. Serofibrinous inflammation 5. Catarrhal inflammation 6. Pseudomembranous inflammation 7. Acute inflammatory ulcer 8. Haemorrhagic inflammation 9. Necrotizing inflammation

27. dr.reza2006@gmail.com Fate of Acute Inflammation:  Resolution  Abscess formation  Turn into chronic inflammation  ulceration

28. dr.reza2006@gmail.com Acute Vs Chronic Inflammation

29. dr.reza2006@gmail.com Exudate Vs Transudate

30. dr.reza2006@gmail.com  Movie- Inflammation

31. dr.reza2006@gmail.com Thank You