1 / 63

Inflammation

Inflammation. Dr. Roopa. Thought for today. “ The investment u make in yourself must receive “ top priority “. When u Grow your entire world expands…. When u do not grow your whole world starts to become ‘very small’….. That smallness reflects in all areas of life including your income.”.

vala
Download Presentation

Inflammation

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Inflammation Dr. Roopa

  2. Thought for today • “ The investment u make in yourself must receive “ top priority “. When u Grow your entire world expands…. When u do not grow your whole world starts to become ‘very small’….. That smallness reflects in all areas of life including your income.”

  3. What is inflammation? Vascular response to injury

  4. Causes of inflammation • Infection • Trauma • Thermal sources • Ionizing radiation • Chemical sources • Immunologic causes • Tissue death

  5. Types of Inflammation • Acute • Chronic

  6. PRINCIPAL CELL EFFECTORS 1st 24 hours: NEUTROPHILS Bacterial infections, infarction Come from the bone marrow reserve pool Band neutrophils: less mature cells

  7. 2nd-3rd day: neutrophils are replaced by monocytes-macrophages • Tuberculosis, salmonellosis

  8. Eosinophils • Allergic reactions • Parasitic infections • Hodgkin lymphoma

  9. Mast cells and basophils • Chronic myelogenous leukemia • Myeloproliferative diseases • histamine

  10. Cellular response of leukocytes • Emigration Margination Pavementing Rolling/Tumbling Adhesion Transmigration • Chemotaxis • Phagocytosis Opsonization • Intracellular microbial killing Oxygen-dependent Oxygen-independent

  11. MARGINATION AND ROLLING .with increased vascular permeability, fluid leaves the vessel causing leukocytes to settle out of the central column and ‘marginate’ along the endothelial surface. .endo. Cells &leukocytes have complementary surface adhesion molecules which briefly stick &release causing the leukocyte to roll along the endothelium.

  12. DIAPEDESIS INSINUATION OF THE NEUTROPHILS THRU THE ENDOTHELIAL CELLS BASEMENT MEMBRANE EXTRAVASCULAR TISSUES

  13. CHEMOTAXIS NEUTROPHIL DIRECT ITS MIGRATION TOWARDS THE CHEMOATTRACTANT

  14. MARGINATION, CHEMOTAXIS AND DIAPEDESIS CAN DELIVER HUGE NUMBERS OF NEUTROPHILS IN A FEW HOURS PUS:CELLULAR ACUTE INFLAMMATORY EXUDATE WITH PMN CELLS AND CELLULAR DEBRIS

  15. PHAGOCYTOSIS FORMATION OF PHAGOSOME LYSOSOME PHAGOLYSOSOME

  16. Intracellular microbial killing: • Oxygen-dependent killing is the MOST important microbial process Phagocytosis activates HMP shunt oxidative burst suppplies electrons to NADPH oxidase superoxide anion Hydrogen peroxide

  17. Hydrogen peroxide • Oxides microbial proteins and disrupts cell walls • Myeloperoxidase-halide system of bacterial killing

  18. DEGRANULATION THE TOXIC SUBSTANCES MAY CAUSE LOSS OF FUNCTION (FUNCTIO LAESA)

  19. INCREASED BLOOD FLOW DUE TO RELAXATION OF THE TERMINAL ARTERIOLES RUBOR AND CALOR

  20. CONTRACTION OF CAPILLARY ENDOTHELIAL CELLS INCREASED VASCULAR PERMEABILITY SWELLING

  21. TUMOR MILDEST: EXTRAVASATION OF WATER, LOW MOLECULAR WEIGHT PROTEINS MODERATE: + HMW PROTEINS SEVERE: + BLOOD CELLS

  22. Calor Rubor Tumor Dolor Functio laesa

  23. MEDIATORS OF ACUTE INFLAMMATION • Exogenous: microbial products • Endogenous: 1. vasoactive amines histamine serotonin 2. Arachidonic acid metabolites cyclooxygenase pathway lipooxygenase pathway 3. Cytokines 4. Kinin system 5. Complement system

  24. Histamine • increase capillary permeability contracts postcapillary venules • Source: basophils, mast cells,platelets • Stimuli: binding of IgE binding of C3a and C5a:”anaphylotoxins” heat, cold Interleukin-1

  25. Serotonin • 5-hydroxytryptamine • Action: similar to histamine • Source: platelets

  26. Cyclooxygenase pathway Enzymes:COX-1,COX-2 Products: Platelet TxA2 -vasoconstrictor,platelet aggregator 2. Endothelial prostacyclin -vasodilator,inhibits platelet aggregation Lipooxygenase pathway Products: hydroperoxyeicosatetraenoic acid (HPETE) 5-HPETE -leukotrienes Arachidonic acid metabolites

  27. Important leukotrienes • LTB4: chemotactic for neutrophils • LTC4,LTD4,LTE4 “slow reacting substance of anaphylaxis” vasodilatation bronchoconstriction increase capillary permeability

  28. Cytokines • Soluble proteins • Secreted by numerous cells(monocytes-macrophages) • Act as “effector molecules” • IL-1 and TNF are major cytokines, that mediate inflam.. • Induce the systemic“acute phase response” • Fever, increase WBC, loss of appetite. • Synthesis of C-reactive proteins, complement components, fibrinogen, prothrombin • Synthesis of adhesion molecules • Neutrophildegranulation

  29. Kinin system • Formed during active secretion in sweat glands, salivary glands, pancreas, kidneys • End product: bradykinin • Actions: vascular permeability arteriolar dilation pain

  30. Complement system • 20 Plasma proteins • HEPATOCYTES,MACROPHAGES, GIT CELLS • Action: cell lysis

  31. COMPLEMENT CASCADE classical pathway alternative pathway

  32. OPSONIZE BACTERIA ACTIVATE PMN, MACROPHAGES REGULATES AB RESPONSE CLEARS AWAY IMMUNE COMPLEXES INFLAMMATION, TISSUE DAMAGE ANAPHYLAXIS

  33. MAC

  34. Classical pathway vs alternative pathway Bacterial surface activates the pathway Works in the absence of antibodies Less efficient • Starts with C1 + antigen-antibody • Ends with the membrane attack complex

  35. C3b: opsonin • C3a and C5a: anaphylotoxins • C5b-C9: “MAC” membrane attack complex

  36. OUTCOMES OF ACUTE INFLAMMATION • Resolution of tissue structure and function • Tissue destruction and persistent acute inflammation abscess ulcer fistula scar • Convert to chronic inflammation

  37. ABSCESS • Cavity filled with pus • Pus: neutrophils, monocytes and cellular debris • Fibrous wall • Inaccessible to circulation • Bacterial infections, especially staphylococci

  38. Ulcer • Involves epithelial surfaces • Loss of surface epithelium

  39. Fistula Abnormal communication between 2 organs or between an organ and a surface

  40. Scar • Final result of tissue destruction • Distortion of structure • Altered function

  41. CHRONIC INFLAMMATION • Occurs when the injury is persistent or recurring; or when the inflammatory reaction is insufficient to completely degrade the agent which triggered the inflammatory reaction • May also occur de novo

  42. Patterns of chronic inflammation • Chronic nonspecific inflammation • Granulomatous inflammation

  43. Chronic nonspecific inflammation • Proliferation of fibroblasts and new vessels • Increased macrophages, lymphocytes, plasma cells • Macrophage+antigen B lymphocyte activation antibody-producing plasma cells • Scarring and distortion of tissue architecture

  44. Granulomatous inflammation • Granuloma: nodular collection of macrophages called “epitheloid cells” • Surrounded by rim of lymphocytes • Macrophage+antigen presented to CD4+lymphocytes release of cytokines monocytes/macrophages transform epitheloid cells and giant cells

  45. Most characteristic: CASEOUS NECROSIS • Multinucleated giant cells Langhans giant cells foreign body giant cell • TB, fungal infections, Syphyllis, cat-scratch fever, foreign bodies

  46. HEALING REPAIR + REGENERATION NEW EPITHELIUM GROWTH

More Related