1. ACUTE INFLAMMATION

2. ACUTE INFLAMMATION COMPONENT
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 Vasoconstriction Vasodilation
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. INCREASED VASCULAR PERMEABILITY
ACUTE INFLAMMATION
INCREASED VASCULAR PERMEABILITY
Increase in Permeability
Histamine (Mast Cells)
Seratonin (Platelets)
Time

12. INCREASED VASCULAR PERMEABILITY
ACUTE INFLAMMATION
INCREASED VASCULAR PERMEABILITY

13. HEMOCONCENTRATION AND STASIS
ACUTE INFLAMMATION
HEMOCONCENTRATION AND STASIS
Normal flow
Stasis

14. ACUTE INFLAMMATION
LEUKOCYTE ADHESION

15. ACUTE INFLAMMATION
LEUKOCYTE ADHESION

16. EMIGRATION (TRANSMIGRATION)
ACUTE INFLAMMATION
EMIGRATION (TRANSMIGRATION)

17. EMIGRATION (TRANSMIGRATION)
ACUTE INFLAMMATION
EMIGRATION (TRANSMIGRATION)

18. ACUTE INFLAMMATION
CHEMOTAXIS

19. ACUTE INFLAMMATION
AGGREGATION

20. PHAGOCYTOSIS - ATTACHMENT
ACUTE INFLAMMATION
PHAGOCYTOSIS - ATTACHMENT

21. PHAGOCYTOSIS - ENGULFMENT
ACUTE INFLAMMATION
PHAGOCYTOSIS - ENGULFMENT

22. PHAGOCYTOSIS – KILLING AND DEGRADATION
ACUTE INFLAMMATION
PHAGOCYTOSIS – KILLING AND DEGRADATION

23. ACUTE INFLAMMATION

24. ACUTE INFLAMMATION Serous Catarrhal Fibrinous Hemorrhagic Suppurative
PATTERNS
Serous
Catarrhal
Fibrinous
Hemorrhagic
Suppurative
Gangrenous
Pseudomembranous

25. ACUTE INFLAMMATION
SEROUS

26. ACUTE INFLAMMATION
SEROUS

27. ACUTE INFLAMMATION
CATARRHAL

28. ACUTE INFLAMMATION
FIBRINOUS

29. SUPPURATIVE / PURULENT
ACUTE INFLAMMATION
SUPPURATIVE / PURULENT

30. SUPPURATIVE / PURULENT - ABSCESS
ACUTE INFLAMMATION
SUPPURATIVE / PURULENT - ABSCESS

31. SUPPURATIVE / PURULENT - ABSCESS
ACUTE INFLAMMATION
SUPPURATIVE / PURULENT - ABSCESS

32. SUPPURATIVE / PURULENT - EMPYEMA
ACUTE INFLAMMATION
SUPPURATIVE / PURULENT - EMPYEMA

33. ACUTE INFLAMMATION
ULCERATIVE
Ulcers of tularemia

34. ACUTE INFLAMMATION
GANGRENOUS

35. ACUTE INFLAMMATION
GANGRENOUS
Appendix
Gallbladder

36. ACUTE INFLAMMATION
PSEUDOMEMBRANOUS

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

38. SYSTEMIC MANIFESTATIONS
ACUTE INFLAMMATION
SYSTEMIC MANIFESTATIONS
Fever
Chills
Myalgia
Discomfort

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

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