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ACUTE INFLAMMATION

ACUTE INFLAMMATION. ACUTE INFLAMMATION C OMPONENT. Definition: Acute inflammation is a rapid response to an injurious agent that serves to deliver mediators of host defense- leukocytes and plasma proteins-to the site of injury.

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ACUTE INFLAMMATION

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  1. ACUTE INFLAMMATION

  2. ACUTE INFLAMMATIONCOMPONENT • Definition: Acute inflammation is a rapid response to an injurious agent that serves to deliver mediators of host defense-leukocytes and plasma proteins-to the site of injury. • Acute inflammation has three major components:  (1) alterations in vascular caliber that lead to an increase in blood flow;  (2) 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. (Robbins, 7th ed.) •  When a host encounters an injurious agent, such as an infectious microbe or dead cells, phagocytes that reside in all tissues try to get rid of these agents. •  At the same time, phagocytes and other host cells react to the presence of the foreign or abnormal substance by liberating cytokines, lipid messengers, and the various other mediators of inflammation.

  3. PLASMA PROTIEN & ACUTE INFLAMMATION • Plasma proteins leave the vessels, most commonly through widened interendothelial cell junctions of the venules. The redness (rubor), warmth (calor), and swelling (tumor) of acute inflammation are caused by the increased blood flow and edema. •  Circulating leukocytes, initially predominantly neutrophils, adhere to the endothelium via adhesion molecules, transmigrate across the endothelium, and migrate to the site of injury under the influence of chemotactic agents. •  Leukocytes that are activated by the offending agent and by endogenous mediators may release toxic metabolites and proteases extracellularly, causing tissue damage. •  During the damage, and in part as a result of the liberation of prostaglandins, neuropeptides, and cytokines, one of the local symptoms is pain (dolor).

  4. Plasma proteins leave the vessels, most commonly through widened interendothelial cell junctions of the venules. The redness (rubor), warmth (calor), and swelling (tumor) of acute inflammation are caused by the increased blood flow and edema. •  Circulating leukocytes, initially predominantly neutrophils, adhere to the endothelium via adhesion molecules, transmigrate across the endothelium, and migrate to the site of injury under the influence of chemotactic agents. •  Leukocytes that are activated by the offending agent and by endogenous mediators may release toxic metabolites and proteases extracellularly, causing tissue damage. •  During the damage, and in part as a result of the liberation of prostaglandins, neuropeptides, and cytokines, one of the local symptoms is pain (dolor).

  5. ACUTE INFLAMMATION Mediators Acute inflammation INJURY

  6. ACUTE INFLAMMATION

  7. ACUTE INFLAMMATION

  8. ACUTE INFLAMMATION SEQUENCE OF EVENTS • Vasoconstriction • Vasodilation • Increased vascular permeability • Hemoconcentration and stasis • Leukocyte Adhesion • Transmigration • Chemotaxis • Aggregation • Phagocytosis

  9. ACUTE INFLAMMATION VASODILATION

  10. ACUTE INFLAMMATION VASODILATION

  11. ACUTE INFLAMMATION INCREASED VASCULAR PERMEABILITY Increase in Permeability Histamine (Mast Cells) Seratonin (Platelets) Time

  12. ACUTE INFLAMMATION HEMOCONCENTRATION AND STASIS Normal flow Stasis

  13. ACUTE INFLAMMATION LEUKOCYTE ADHESION

  14. ACUTE INFLAMMATION LEUKOCYTE ADHESION

  15. ACUTE INFLAMMATION EMIGRATION (TRANSMIGRATION)

  16. ACUTE INFLAMMATION EMIGRATION (TRANSMIGRATION)

  17. ACUTE INFLAMMATION CHEMOTAXIS

  18. ACUTE INFLAMMATION AGGREGATION

  19. ACUTE INFLAMMATION PHAGOCYTOSIS - ATTACHMENT

  20. ACUTE INFLAMMATION PHAGOCYTOSIS - ENGULFMENT

  21. ACUTE INFLAMMATION PHAGOCYTOSIS – KILLING AND DEGRADATION

  22. ACUTE INFLAMMATION

  23. ACUTE INFLAMMATION PATTERNS • Serous • Catarrhal • Fibrinous • Hemorrhagic • Suppurative • Gangrenous • Pseudomembranous

  24. ACUTE INFLAMMATION SEROUS

  25. ACUTE INFLAMMATION SEROUS

  26. ACUTE INFLAMMATION CATARRHAL

  27. ACUTE INFLAMMATION FIBRINOUS

  28. ACUTE INFLAMMATION SUPPURATIVE / PURULENT

  29. ACUTE INFLAMMATION SUPPURATIVE / PURULENT - ABSCESS

  30. ACUTE INFLAMMATION SUPPURATIVE / PURULENT - ABSCESS

  31. ACUTE INFLAMMATION SUPPURATIVE / PURULENT - EMPYEMA

  32. ACUTE INFLAMMATION ULCERATIVE

  33. ACUTE INFLAMMATION GANGRENOUS

  34. ACUTE INFLAMMATION GANGRENOUS Appendix Gallbladder

  35. ACUTE INFLAMMATION PSEUDOMEMBRANOUS

  36. ACUTE INFLAMMATION LOCAL MANIFESTATIONS • Heat • Redness • Swelling • Pain • Loss of function

  37. ACUTE INFLAMMATION SYSTEMIC MANIFESTATIONS • Fever • Chills • Myalgia • Discomfort

  38. ACUTE INFLAMMATION LABORATORY MANIFESTATIONS • Leukocytosis (granulocytosis vs. lymphocytosis) • Elevated serum acute phase proteins (C-reactive protein, fibrinogen, etc) • Increased ESR (erythrocyte sedimentation rate) • Hypercoagulability

  39. ACUTE INFLAMMATION SEQUELAE RESOLUTION Mediators Acute inflammation INJURY Chronic irritation Mediators Mediators Viral infection Autoimmune disease Chronic inflammation

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