Presentation is loading. Please wait.

Presentation is loading. Please wait.

Chapter 4. Inflammation. CHAPTER CONTENTS Introduction to inflammation Introduction to inflammation Introduction to inflammation Introduction to inflammation.

Similar presentations


Presentation on theme: "Chapter 4. Inflammation. CHAPTER CONTENTS Introduction to inflammation Introduction to inflammation Introduction to inflammation Introduction to inflammation."— Presentation transcript:

1 Chapter 4. Inflammation

2 CHAPTER CONTENTS Introduction to inflammation Introduction to inflammation Introduction to inflammation Introduction to inflammation Acute inflammation Acute inflammation Acute inflammation Acute inflammation Chronic inflammation Chronic inflammation Chronic 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. Inflammation is a complex reaction to injurious agents that consists of vascular response, cellular reaction, and systemic reactions. a defensive response fundamentally a defensive response fundamentally be divided into acute inflammation and chronic inflammation be divided into acute inflammation and chronic inflammation

4 INTRODUCTION TO INFLAMMATION CARDINAL CLINICAL SIGNS acute inflammation has 5 cardinal signs: acute inflammation has 5 cardinal signs: redness (rubor) redness (rubor) heat (calor) heat (calor) swelling swelling pain (dolor) pain (dolor) loss of function 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: in acute inflammation: A. fever B. changes in the peripheral white blood cell count neutrophils leukocytosis neutrophil nucleus shift to the left lymphocytosisneutropenia 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 matureimmature

8 ACUTE INFLAMMATION the early response of a tissue to injury the early response of a tissue to injury the first line of defense against injury the first line of defense against injury nonspecific nonspecific changes in the microcirculation: changes in the microcirculation: exudation of fluid emigration of leukocytes exudation of fluid emigration of leukocytes the causative factors (6 points) 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 in the microcirculation a transient vasoconstriction a transient vasoconstriction (induced by action of mediators) (induced by action of mediators) dilation of arterioles, capillaries, and venules dilation of arterioles, capillaries, and venules (hyperemia) (hyperemia) stasis stasis

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

13 The microcirculatory response B. increased permeability in venules and capillaries in venules and capillaries three phases of increased permeability in acute inflammation: three phases of increased permeability in acute inflammation: (1) an immediate phase (1) an immediate phase (2) a delayed response (2) a delayed response (3) a prolonged response (3) a prolonged response these permeability changes are effected by various chemical mediators 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 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 the composition of an exudate approaches that of plasma, but rich in proteins fibrinogen is converted to fibrin rapidly fibrinogen is converted to fibrin rapidly exudation should be distinguished from transudation 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: the functions of exudation: (1) dilute the offending agent (1) dilute the offending agent (2) cause increased lymphatic flow, conveying noxious agents to the draining lymph nodes to facilitating a protective immune response (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 (3) flood the area with plasma, which contain numerous defensive proteins

17 The cellular response leukocyte infiltration plays an important role leukocyte infiltration plays an important role in limiting the spread of injury in limiting the spread of injury in defending the host tissue 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 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 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. 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. chemotactic factors: Govern the active emigration of neutrophils and the direction in which they move.

23

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 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 Function Major mediators Vasodilation 5-HT,histamine, bradykinin,PGE 2 Permeability 5-HT,histamine, C3a, C5a, PAF Chemotaxis C5a, LTB4, cytokins Fever Cytokines( IL-1, 6, TNF), PG Fever Cytokines( IL-1, 6, TNF), PG Pain PGE2, bradykinin 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

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 Abscess of kidney

41 Abscess of brain

42 Abscess of liverAbscess of kidney

43 TYPES OF ACUTE INFLAMMATION D. hemorrhagic inflammation marked hemorrhage is the predominant pathological change 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 DIAGNOSIS OF ACUTE INFLAMMATION surface structures surface structures local cardinal signs permit diagnosis local cardinal signs permit diagnosis internal organs internal organs systemic changes may first manifest systemic changes may first manifest rarely, examine a fluid exudates or tissue sample rarely, examine a fluid exudates or tissue sample

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

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

48 CHRONIC INFLAMMATION IN RESPONSE TO ANTIGENIC INJURIOUS AGENTS mechanisms 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 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 epithelioid cell langhans-type giant 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 function of chronic inflammation serves to contain and remove an injurious agent that is not easily eradicated by the body serves to contain and remove an injurious agent that is not easily eradicated by the body dependent on immunologic reactivity: dependent on immunologic reactivity: (1) direct killing by activated lymphocytes (1) direct killing by activated lymphocytes (2) interaction with antibodies (2) interaction with antibodies (3) activation of macrophages (3) activation of macrophages

63 FUNCTION AND RESULT OF CHRONIC INFLAMMATION result of chronic inflammation result of chronic inflammation associated with tissue necrosis and implies serious illness associated with tissue necrosis and implies serious illness associated fibrosis: a repair mechanism and perhaps another side effect 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 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 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 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. 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 subacute inflammation acute-on-chronic inflammation acute-on-chronic inflammation

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


Download ppt "Chapter 4. Inflammation. CHAPTER CONTENTS Introduction to inflammation Introduction to inflammation Introduction to inflammation Introduction to inflammation."

Similar presentations


Ads by Google