1. Chapter 4. Inflammation

2. CHAPTER CONTENTS Introduction to inflammation Acute inflammation
Chronic inflammation

3. INTRODUCTION TO INFLAMMATION
CONCEPTION
Inflammation is a complex reaction to injurious agents that consists of vascular response, cellular reaction, and systemic reactions.
a defensive response fundamentally
be divided into acute inflammation and chronic inflammation

4. INTRODUCTION TO INFLAMMATION
CARDINAL CLINICAL SIGNS
acute inflammation has 5 cardinal signs:
redness (rubor)
heat (calor)
swelling
pain (dolor)
loss of function
increased blood flow
to the inflamed area
accumulation of fluid
release of chemicals that stimulate nerve endings
a combination of factors

5. redness
heat
swelling
pain

6. INTRODUCTION TO INFLAMMATION
SYSTEMIC CLINICAL SIGNS
in acute inflammation:
A. fever
B. changes in the peripheral white blood cell count
neutrophils leukocytosis
neutrophil nucleus shift to the left
lymphocytosis
neutropenia
C. changes in plasma protein levels
the levels of certain plasma proteins increase
entry of pyrogens and release prostaglandins
bone marrow release
or production
viral infection

7. neutrophil nucleus shift to the left
immature
mature
neutrophil nucleus shift to the left

8. ACUTE INFLAMMATION the early response of a tissue to injury
the first line of defense against injury
nonspecific
changes in the microcirculation:
exudation of fluid emigration of leukocytes
the causative factors (6 points)

9. MORPHOLOGIC AND FUNCTIONAL CHANGES
the two main components of the acute inflammatory:
the microcirculatory response
the cellular response

10. The microcirculatory response
vasodilation and stasis
increased permeability
exudation of fluid

11. The microcirculatory response
A. vasodilation and stasis
in the microcirculation
a transient vasoconstriction
(induced by action of mediators)
dilation of arterioles, capillaries, and venules
(hyperemia)
stasis

12. The microcirculatory response
B. increased permeability
in venules and capillaries
active contraction of actin
filaments in endothelial cells
direct damage to endothelial
cells
leukocyte-mediated
endothelial injury
transcytosis increased
permeability increase
(reversible)

13. The microcirculatory response
B. increased permeability
in venules and capillaries
three phases of increased permeability in acute inflammation:
(1) an immediate phase
(2) a delayed response
(3) a prolonged response
these permeability changes are effected by various chemical mediators

14. The microcirculatory response
C. exudation of fluid
exudation: increased passage of fluid out of the microcirculation because of increased vascular permeability
the composition of an exudate approaches that of plasma, but rich in proteins
fibrinogen is converted to fibrin rapidly
exudation should be distinguished from transudation

15. Grossly, fibrin is seen on an acute inflamed serosal surface that changes to a rough, yellowish bread and
butter-like surface, covered by fibrin and coagulated
proteins.

16. The microcirculatory response
C. exudation of fluid
the functions of exudation:
(1) dilute the offending agent
(2) cause increased lymphatic flow, conveying noxious agents to the draining lymph nodes to facilitating a protective immune response
(3) flood the area with plasma, which contain numerous defensive proteins

17. The cellular response leukocyte infiltration plays an important role
in limiting the spread of injury
in defending the host tissue
Acute inflammation is characterized by the active emigration of inflammatory cells from the blood into the area of injury.

18. The cellular response
extravasation: the process of the leukocytes from the vessel lumen to the interstitial tissue.
3 steps of extravasation :
(1) margination, rolling and adhesion to endothelium in the lumen
(2) transmigration across the endothelium
(3) migration toward the site of injury

19. A. types of cells involved
The cellular response
A. types of cells involved
neutrophils
(polymorphonuclear leukocytes)
phagocytic cell of the macrophage system
lymphocytes and plasma cells

20. The cellular response
B. margination, adhesion and transmigration of neutrophils

21. The cellular response C. emigration of neutrophils take 2-10minutes
intercellular junctions
basement membrane

22. The cellular response
D. chemotactic factors
chemotaxis: In the interstitial tissue, neutrophils move toward the site of injury, oriented along a chemical gradient.
chemotactic factors: Govern the active emigration of neutrophils and the direction in which they move.

24. The cellular response E. phagocytosis recognition
opsonization: the agent has been coated with immunoglobulin or complement factor 3b (opsonins).
engulfment
the agent + opsonins phagosome
microbial killing
phagosome fuses with lysosomes, therefore the enzymes can access to the engulfed microorganism and kill them
engulfment

25. Process of phagocytosis

26. The cellular response diapedesis F. erythrocyte
the orderly flow of blood is disturbed in the dilated vessels
erythrocyte form heavy aggregates and sludging
erythrocyte enter an inflamed area passively
diapedesis
hemorrhagic inflammation

27. 增加文字注释

28. MEDIATORS OF ACUTE INFLAMMATION
A variety of endogenous chemical mediators play some important roles in the modulation of inflammatory response.
originated from cells or plasma:
cell-derived mediators:
sequestered in intracellular granules and synthesized in response to a stimulus
plasma-derived mediators:
present in precursor form and activated by proteolytic cleavage

29. summary of inflammatory mediators
Function Major mediators
Vasodilation HT,histamine, bradykinin ,PGE2
Permeability HT,histamine, C3a, C5a, PAF
Chemotaxis C5a, LTB4, cytokins
Fever Cytokines( IL-1, 6, TNF), PG
Pain PGE2 , bradykinin
Tissue damage Lysosomal enzymes , NO

30. TYPES OF ACUTE INFLAMMATION
A. serous inflammation
B. fibrinous inflammation
C. suppurative (purulent inflammation)
D. hemorrhagic inflammation

31. TYPES OF ACUTE INFLAMMATION
A. serous inflammation
occur in skin, and in peritoneal, pleural and pericardial cavities
accumulation of excessive clear watery fluid with a variable protein content
Catarrhal inflammation is a mild exudative inflammation of a surface mucous membrance without apparent tissue destruction.

32. burn blisters

33. Serous inflammation of skin

34. TYPES OF ACUTE INFLAMMATION
B. fibrinous inflammation
large amounts of fibrinogen pass the vessel wall, and fibrins are formed in the extracellular spaces
Pseudomembranous inflammation is the fibrinous inflammation occurred on a mucosal surface, and a membranous film consisting mainly of fibrin mixed with necrotic cells appears on the surface of the affected mucosa.

35. Fibrinous pericarditis

36. Fibrinous pericarditis

37. pseudo-membranous inflammation
bacillary dysentery

38. pseudo-membranous inflammation
diphtheria

39. TYPES OF ACUTE INFLAMMATION
C. suppurative (purulent inflammation)
the formation of purulent exudates or pus
Pus is made up of neutrophils, necrotic cells and edema fluid.
Abscess is a localized collection of purulent inflammation accompanied by liquefactive necrosis.

40. Abscess of kidney

41. Abscess of brain

42. Abscess of kidney
Abscess of liver

43. TYPES OF ACUTE INFLAMMATION
D. hemorrhagic inflammation
marked hemorrhage is the predominant pathological change

44. COURSE OF ACUTE INFLAMMATION
A. resolution
B. repair
C. suppuration
D. chronic inflammation

45. DIAGNOSIS OF ACUTE INFLAMMATION
surface structures
local cardinal signs permit diagnosis
internal organs
systemic changes may first manifest
rarely, examine a fluid exudates or tissue sample

46. CHRONIC INFLAMMATION
the sum of the responses mounted by tissue against a persistent injurious agent
commonly show
A. immune response
B. phagocytosis
C. necrosis
D. repair

47. CHRONIC INFLAMMATION the main features include
(1) mononuclear cell infiltration
macrophages play dominant rolls
(2) tissue destruction
(3) granulation tissue formation and fibrosis
be distinguished from acute inflammation

48. CHRONIC INFLAMMATION IN RESPONSE TO ANTIGENIC INJURIOUS AGENTS
mechanisms
injurious agent
antigens
tissue damage
self antigens
some days
chemotactic factors
accumulation of chronic inflammatory cells
activated T lymphocytes, plasma cells, macrophages

49. CHRONIC INFLAMMATION IN RESPONSE TO ANTIGENIC INJURIOUS AGENTS
morphologic types
A. granulomatous chronic inflammation
B. nongranulomatous chronic inflammation

50. granulomatous chronic inflammation
a special type of chronic inflammation
character: the formation of granuloma
granuloma: an aggregate of macrophages
two types:
epithelioid cell granuloma
foreign body granuloma

51. granulomatous chronic inflammation
characteristic features:
the formation of epithelioid cell granuloma
epithelioid cell: activated macrophages that appear as large cells with abundant pale, foamy cytoplasm
langhans-type giant cell: derived from fusion of macrophages and characterized by nuclei around the periphery of the cell

52. epithelioid cell granuloma
langhans-type
giant cell
epithelioid cell

53. granulomatous chronic inflammation
Granulomas are usually surrounded by lymphocytes, plasma cells, fibroblasts, and collagen.

54. granulomatous chronic inflammation
causes
(1) When macrophages have successfully phagocytosed the injurious agent but it survives inside them
(2) When an active T lymphocyte-mediated cellular immune response occurs

55. granulomatous chronic inflammation
changes in affected tissues:
granulomas expand and fuse with adjacent granulomas to
form large
masses

56. granulomatous chronic inflammation
changes in affected tissues:
in many infectious granulomas, central caseous necrosis is a common feature

57. granulomatous chronic inflammation
caseous necrosis:
gross: yellowish-white and resembles crumbly cheese
microscopic: finely granular, pink, and amorphous

58. nongranulomatous chronic inflammation
characteristic features:
The accumulation of sensitized lymphocytes, plasma cells, and macrophages in the injured area.
These cells are scattered diffusely throughout the tissue.
Scattered tissue necrosis and fibrosis are common.

59. nongranulomatous chronic inflammation
causes and changes in affected tissues:
A. chronic viral infections
B. chronic autoimmune diseases
C. chronic chemical intoxications
D. chronic nonviral infections
E. allergic inflammation and metazoal infections

60. CHRONIC INFLAMMATION IN RESPONSE TO NONANTIGENIC INJURIOUS AGENTS
characteristic features:
the formation of foreign body granuloma
foreign body giant cells: numerous nuclei dispersed throughout the cell
foreign material is usually identifiable in the center of the granuloma
tissue necrosis is not an associated feature
(figure 4-19)

61. Foreign body granuloma

62. FUNCTION AND RESULT OF CHRONIC INFLAMMATION
function of chronic inflammation
serves to contain and remove an injurious agent that is not easily eradicated by the body
dependent on immunologic reactivity:
(1) direct killing by activated lymphocytes
(2) interaction with antibodies
(3) activation of macrophages

63. FUNCTION AND RESULT OF CHRONIC INFLAMMATION
associated with tissue necrosis and implies serious illness
associated fibrosis: a repair mechanism and perhaps another side effect

64. MIXED ACUTE AND CHRONIC INFLAMMATION
chronic inflammation may follow acute inflammation
or result from repeated bouts of acute inflammation
features of both types of inflammation may coexist in certain circumstances

65. CHRONIC SUPPURATIVE INFLAMMATION
It is difficult to remove the large amounts of pus associated with chronic suppurative inflammation.
The surrounding viable tissue responds with a longstanding inflammatory process in which areas of suppuration alternate with areas of chronic inflammation and fibrosis.

66. CHRONIC SUPPURATIVE INFLAMMATION
The difference between an acute and chronic abscess lies in the thickness of the fibrous wall; both form are filled with pus.

67. Abscess of liver

68. RECURRENT ACUTE INFLAMMATION
if there is predisposing cause, repeated attacks of acute inflammation may occur
Each attack of acute inflammation is follwed by incomplete resolution that leads to a progressively increasing number of chronic inflammatory calls and fibrosis.
subacute inflammation
acute-on-chronic inflammation

69. CLINICAL AND PATHOLOGIC DIAGNOSIS
difficult
Precise diagnosis usually requires recourse to a full range of clinical and pathologic studies.
table 4-9