Acute inflammation by Dr Mohammad Manzoor Mashwani

7,285 views

Published on

Published in: Health & Medicine
  • Be the first to comment

Acute inflammation by Dr Mohammad Manzoor Mashwani

  1. 1. Acute Inflammation ByDr Mohammad Manzoor Mashwani
  2. 2. Definition• It is a rapid host response that serves to deliver leukocytes and plasma proteins, such as antibodies, to sites of infection or tissue injury.• Minutes- Hours- Days• Less than 48 hours.
  3. 3. Time course Acute inflammation: Less than 48 hours Chronic inflammation: Greater than 48 hours (weeks, months, years)Cell type Acute inflammation: Neutrophils Chronic inflammation: Mononuclear cells (Macrophages, Lymphocytes, Plasma cells).
  4. 4. ACUTE INFLAMMATIONLOCAL MANIFESTATIONS • Heat • Redness • Swelling • Pain • Loss of function 4
  5. 5. Pathogenesis: Three main processes occur at the site of inflammation, due to the release of chemical mediators :1.Increased blood flow (redness and warmth).2.Increased vascular permeability (swelling, pain & loss of function).3.Leukocytic Infiltration.
  6. 6. Cardinal Signs of Inflammation Redness : Hyperaemia. Warm : Hyperaemia. Pain : Nerve, Chemical mediators. Swelling : Exudation Loss of Function: Pain
  7. 7. MechanismInflammation 1. Vaso dilatation 2. Exudation - Edema 3. Emigration of cells 4. Chemotaxis
  8. 8. Major components of Ac. Inflammation• It has three major components:1. Alterations in vascular caliber that lead to an increase in blood flow2. Structural changes in the microvasculature that permit plasma proteins and leukocytes to leave the circulation.3. Emigration of the leukocytes from the microcirculation, their accumulation in the focus of injury, and their activation to eliminate the offending agent. 10
  9. 9. Increased Vascular Permeability (Vascular Leakage)• A hallmark of acute inflammation causing edema.• Contraction of endothelial cells resulting in increased interendothelial spaces is elicited by chemical mediators.• It is immediate transient response usually short-lived (15–30 minutes).• In some mild injuries e.g burns, x or ultraviolet radiation, certain bacterial toxins, occurs after a delay of 2 to 12 hours lasting for several hours or days, mild endothelial damage.• Late-appearing sunburn is an example of this type of leakage.• Increased transport of fluids and proteins, called transcytosis, through the endothelial cell. 11
  10. 10. 12
  11. 11. ACUTE INFLAMMATION SYSTEMIC MANIFESTATIONS• Fever• Chills• Myalgia• Malaise 13
  12. 12. ACUTE INFLAMMATION LABORATORY MANIFESTATIONS1. Leukocytosis2. Increased ESR3. Elevated serum acute phase proteins (C-reactive protein, fibrinogen, etc)1. Hypercoagulability 14
  13. 13. STIMULI for acute inflammation1. INFECTIOUS2. PHYSICAL3. CHEMICAL4. Tissue Necrosis5. Foreign Bodies (FBs)6. Immune “responses”, or “complexes”
  14. 14. ACUTE INFLAMMATION• VASCULAR EVENTS• CELLULAR EVENTS• “MEDIATORS”
  15. 15. :Lymphatics in inflammationLymphatics are responsible for draining edema.Edema: An excess of fluid in the interstitial tissue or serous cavities; either a transudate or an exudate
  16. 16. EXUDATION• AN EXUDATE: A filtrate of blood plasma. Extravascular fluid High protein concentration Contains cellular debris & High specific gravity.• Its presence implies an increase in the normal permeability of small blood vessels in an area of injury and, therefore, an inflammatory reaction.18
  17. 17. TRANSUDATE: A fluid with low protein content Little or no cellular material & Low specific gravity. It is an ultrafiltrate of plasma, resulting from osmotic or hydrostatic imbalance across the vessel wall without an increase in vascular permeability. 19
  18. 18. PUSNeutrophils + Dead cells + Microbes A purulent (infectious) inflammatory exudate. Rich in leukocytes. Mostly neutrophils Debris of dead cells & In many cases microbes. 21
  19. 19. Leukocyte exudation Divided into 4 steps 1. Margination, rolling, and adhesion to endothelium 2. Diapedesis (trans-migration across the endothelium) 3. Migration toward a chemotactic stimuli from the source of tissue injury. 4. Phagocytosis
  20. 20. PHAGOCYTOSIS• RECOGNITION• ENGULFMENT• KILLING (DEGRADATION/DIG ESTION)
  21. 21. Inflammation Outcome Fibrosis/Scar Resolution Acute Chronic Injury Inflammation Inflammation Abscess Fungus Virus Cancers Ulcer .T.B. etc Fistula Sinus
  22. 22. Downloaded from: Robbins & Cotran Pathologic Basis of Disease (on 12 May 2005 10:21 PM) © 2005 Elsevier
  23. 23. Factors affecting outcome of acute inflammation1. Severity of tissue damage2. Capacity of cells to divide3. Type of agent causing damage4. The responsiveness of the host5. Site involved 27
  24. 24. Morphologic PATTERNS of Acute INFLAMMATION• Serous (watery)• Fibrinous (hemorrhagic, rich in FIBRIN)• Suppurative (PUS)• Ulcerative
  25. 25. BLISTER, “Watery”, i.e., SEROUS
  26. 26. PUS =PURULENT ABSCESS = POCKET OF PUS
  27. 27. Ulcerative• Necrotic and eroded epithelial surface• Underlying acute and chronic inflammation• Trauma, toxins, vascular insufficiency
  28. 28. Summary 32

×