Inflammation Lecture

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12/14/2011

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Inflammation Lecture

  1. 1. Inflammation-1 "Opportunities are usually disguised by hard work, so most people dont recognize them." - Ann Landers DR EJAZ WARIS
  2. 2. Inflammation-2 INFLAMMATI0N Dr. SHAHILA JALEEL Histopathology SZH,Lahore Shashi-Mar 2000
  3. 3. Introduction:“Inflame” – to set fire. Inflammation is “dynamic response of vascularised tissue to injury.” Is a protective response. Serves to bring defense & healing mechanisms to the site of injury.
  4. 4. INTROD………. Injurious stimuli cause a protective vascular connective tissue reaction called “inflammation” • Dilute • Destroy • Isolate • Initiate repair Acute and chronic forms
  5. 5. Lewis Triple Response:  Flush: capillary dilatation.  Flare: arteriolar dilatation.  Weal: exudation, edema.
  6. 6. Gastric Ulcer:
  7. 7. Inflammation-8 Laryngitis: DR EJAZ WARIS
  8. 8. Acute Enteritis:
  9. 9. Inflammation-10 Pneumonia DR EJAZ WARIS
  10. 10. Inflammation-11 Cardinal Signs of Inflammation  Rubor : Redness – Hyperaemia.  Calor : Warm – Hyperaemia.  Dolor : Pain – Nerve, Chemical med.  Tumor: Swelling – Exudation  Loss of Function: DR EJAZ WARIS
  11. 11. The 5 Cardinal Signs of Heat Redness Swelling Pain Loss Of Func.
  12. 12. Inflammation-13 Inflammation Two main components: vascular reaction cellular reaction Two main types: acute chronic Chemical mediators DR EJAZ WARIS
  13. 13. Inflammation-14 Cells of inflammation DR EJAZ WARIS
  14. 14. Circulating cells
  15. 15. Inflammation-16 DR EJAZ WARIS
  16. 16. Inflammation-17 DR EJAZ WARIS
  17. 17. Inflammation-18 DR EJAZ WARIS
  18. 18. Inflammation-19 DR EJAZ WARIS
  19. 19. Inflammation-20 DR EJAZ WARIS
  20. 20. Inflammation-21 DR EJAZ WARIS
  21. 21. Connective tissue matrix Made up of : A)collagen fibers B)elastic fibers C)glycoproteins D)proteoglycans
  22. 22. Connective tissue cells
  23. 23. Inflammation-24 DR EJAZ WARIS
  24. 24. Inflammation-25 DR EJAZ WARIS
  25. 25. Inflammation-26 DR EJAZ WARIS
  26. 26. Inflammation-28 Acute Inflammation - Mechanism 1.Alterations in vascular calibre leading to increased blood flow 2.Microvasculature structural changes 3.Leukocyte emigration DR EJAZ WARIS
  27. 27. Inflammation-29 Vascular changes  A Inconstant transient vasoconstriction of arterioles for few seconds followed by vasodilation 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) DR EJAZ WARIS
  28. 28.  Vascular permeability (leakiness) commences Transudate gives way to exudate (protein-rich) Increases interstitial osmotic pressure contributing to edema (water and ions) slowing of circulation (increased permeability of the vasculature) stasis Leukocyte migration
  29. 29. Inflammation-31 Vascular changes continued  B)increased vascular permeability vascular leakage leading to escape of protein rich fluid into the interstitium is the hall mark of acute inflammation exudate transudate edema pus DR EJAZ WARIS
  30. 30.  An exudate is an extravascular fluid that has a high protein concentration cellular debris high specific gravity. Its presence implies an increase in the normal permeability of small blood vessels in an area of injury . A transudate is a fluid with low protein content (most of which is albumin) little or no cellular material low specific gravity It is essentially an ultrafiltrate of blood plasma that results from osmotic or hydrostatic imbalance across the vessel wall without an increase in vascular permeability
  31. 31. Inflammation-33  Edema denotes an excess of fluid in the interstitial tissue or serous cavities; it can be either an exudate or a transudate.  Pus, a purulent exudate, is an inflammatory exudate rich in leukocytes (mostly neutrophils), the debris of dead cells and, in many cases, microbes. DR EJAZ WARIS
  32. 32.  IMMEDIATE TRANSIENT RESPONSE – RESPONSE TO MINOR INJURY IMMEDIATE SUSTAINED RESPONSE – RESPONSE TO MORE SERIOUS INJURY, CONTINUES FOR SEVERAL DAYS, DAMAGE TO VESSELS DELAYED RESPONSE – INCREASES IN CAPILLARY PERMEABILITY, DELAYED 4-24 HR, RADIATION INJURIES, SUNBURN
  33. 33. Inflammation-37 How does endothelium becomes leaky in inflammation?  1)formation of endothelial gaps in venules  2)cytoskeletal reorganization  3)increased transcytosis  4)direct endothelial injury  5)leukocyte dependent injury  6)delayed prolonged leakage  7)leakage from new blood vessels DR EJAZ WARIS
  34. 34. Inflammation-39 Mechanism of Inflammation: DR EJAZ WARIS
  35. 35. Inflammation-40 DR EJAZ WARIS
  36. 36. Inflammation-41 Leukocyte emigration/extravasation  Sequence of events in the journey of leukocytes from the lumen to the interstitial tissue  Margination  Pavementing  Rolling  Adhesion  Transmigration/diapedesis DR EJAZ WARIS
  37. 37. Adhesion molecules Play an important role in acute inflammation 4 families Family no 1: Selectins E-selectin,P-selectin,L-selectin Family no 2:Ig-family adhesion proteins ICAM-I,ICAM-II,PECAM-I,VCAM-I
  38. 38. Adhesion moleculesFamily no 3:IntegrinsLFAMAC-1VLA-4Family no 4:Mucin like glycoproteinsCD-34Glycam-1
  39. 39. Inflammation-45 DR EJAZ WARIS
  40. 40. Inflammation-46 Neutrophil Margination DR EJAZ WARIS
  41. 41. Inflammation-47 Vascular changes DR EJAZ WARIS
  42. 42. Inflammation-48 Pneumonia - Exudation DR EJAZ WARIS
  43. 43. "Each time you are honest and conductyourself with honesty, a success force willdrive you toward greater success. Eachtime you lie, even with a little white lie,there are strong forces pushing youtoward failure."

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