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Chapter 4. Inflammation

Chapter 4. Inflammation. CHAPTER CONTENTS. Introduction to inflammation Acute inflammation Chronic inflammation. INTRODUCTION TO INFLAMMATION. CONCEPTION Inflammation is a complex reaction to injurious agents that consists of vascular response, cellular reaction, and systemic reactions.

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Chapter 4. Inflammation

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  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. 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. 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.

  23. engulfment 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

  24. Process of phagocytosis

  25. 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

  26. 增加文字注释

  27. 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 andsynthesized in response to a stimulus • plasma-derived mediators: present in precursor form andactivated by proteolytic cleavage

  28. summary of inflammatory mediators Function Major mediators Vasodilation 5-HT,histamine, bradykinin ,PGE2 Permeability 5-HT,histamine, C3a, C5a, PAF Chemotaxis C5a, LTB4, cytokins Fever Cytokines( IL-1, 6, TNF), PG Pain PGE2 , bradykinin Tissue damage Lysosomal enzymes , NO

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

  30. 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.

  31. burn blisters

  32. Serous inflammation of skin

  33. 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.

  34. Fibrinous pericarditis

  35. Fibrinous pericarditis

  36. pseudo-membranous inflammation bacillary dysentery

  37. pseudo-membranous inflammation diphtheria

  38. 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.

  39. Abscess of kidney

  40. Abscess of brain

  41. Abscess of kidney Abscess of liver

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

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

  44. 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

  45. 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

  46. 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

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

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

  49. 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

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