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EDUCATION IS HANGING AROUND UNTIL YOU’VE CAUGHT ON
- 3. BY DR. IKRAM UL HAQUE ASSOCIAT PROFESSOR AND CONSULTANT HISTOPATHOLOGY A N M C, LAHORE
- 5. EDUCATION IS HANGING AROUND UNTIL YOU’VE CAUGHT ON Charles Darwin
- 7. INFLAMMATION Reaction of a tissue and its microcirculation to a pathogenic insult or it is a reaction which is characterized by the generation of inflammatory mediators and amount of fluid and leucocytes from the blood into extra vascular tissue
- 8. FOUR CARDINAL SIGNS OF INFLAMMATION • Rubor (redness) • Color (heat) • Tumor (swelling) • Dolar (pain) Aulus Celsus Roman Encyclopedist
- 16. ACUTE INFLAMMATIONNeutrophil Polymorphonuclear Leukocyte, PMN, PML “Leukocyte” Granulocyte, Neutrophilic granulocyte “Poly-” Polymorph
- 19. STIMULI for acute inflammation •INFECTIOUS •PHYSICAL •CHEMICAL • Tissue Necrosis • Foreign Bodies (FBs) • Immune “responses”, or “complexes”
- 20. ACUTE INFLAMMATION •VASCULAR EVENTS •CELLULAR EVENTS (PolyMorphonuclear Neutrophil, Leukocyte?, “POLY”, Neutrophil, Granulocyte, Neutrophilic Granulocyte •“MEDIATORS”
- 23. Vascular Changes • Changes in Vascular Flow and Caliber • Increased Vascular Permeability
- 24. INCREASED PERMEABILITY •DILATATION •Endothelial “gaps” •Direct Injury •Leukocyte Injury •Transocytosis (endo/exo) •New Vessels
- 35. LEAKAGE OF PROTEINACEOUS FLUID (EXUDATE, NOT TRANSUDATE)
- 36. EXTRAVASATION of PMNs • MARGINATION (PMN’s go toward wall) • ROLLING (tumbling and HEAPING) • ADHESION • TRANSMIGRATION (DIAPEDESIS)
- 37. ADHESION MOLECULES (glycoproteins) affecting ADHESION and TRANSMIGRATION • SECRETINS (from endothelial cells) • INTEGRINS (from many cells)
- 38. CHEMOTAXIS PMNs going to the site of “injury” AFTER transmigration
- 39. LEUKOCYTE “ACTIVATION” • “triggered” by the offending stimuli for PMNs to: –1) Produce eicosanoids (arachidonic acid derivatives) • Prostaglandin (and thromboxanes) • Leukotrienes • Lipoxins –2) Undergo DEGRANULATION –3) Secrete CYTOKINES
- 40. PHAGOCYTOSIS • RECOGNITION • ENGULFMENT • KILLING (DEGRADATION/ DIGESTION)
- 41. CHEMICAL MEDIATORS • From plasma or cells • Have “triggering” stimuli • Usually have specific targets • Can cause a “cascade” • Are short lived
- 43. CLASSIC MEDIATORS • HISTAMINE • SEROTONIN • COMPLEMENT • KININS • CLOTTING FACTORS • EICOSANOIDS • NITRIC OXIDE • PAF • CYTOKINES • /CHEMOKINES • LYSOSOME CONSTITUENTS • FREE RADICALS • NEUROPEPTIDES
- 44. HISTAMINE • Mast Cells, basophils • POWERFUL Vasodilator • Vasoactive “amine” • IgE on mast cell
- 45. SEROTONIN • (5HT, 5-Hydroxy- Tryptamine) • Platelets and EnteroChromaffin Cells • Also vasodilatation, but more indirect • Evokes N.O. synthetase (a ligase)
- 46. COMPLEMENT SYSTEM • >20 components, in circulating plasma • Multiple sites of action, but LYSIS is the underlying theme
- 47. KININ SYSTEM • BRADYKININ is KEY component, 9 aa’s • ALSO from circulating plasma • ACTIONS – Increased permeability – Smooth muscle contraction, NON vascular –PAIN
- 48. CLOTTING FACTORS • Also from circulating plasma • Coagulation, i.e., production of fibrin • Fibrinolysis
- 50. EICOSANOIDS (ARACHIDONIC ACID DERIVATIVES) •Part of cell membranes •1) Prostaglandins (incl. Thromboxanes) •2) Leukotrienes •3) Lipoxins (new) MULTIPLE ACTIONS AT MANY LEVELS
- 54. Lipoxins •INHIBIT chemotaxis •Vasodilatation •Counteract actions of leukotrienes
- 55. Platelet-Activating Factor (PAF) • Phospholipid • From MANY cells, like eicosanoids • ACTIVATE PLATELETS, powerfully
- 56. CYTOKINES/CHEMOKINES • CYTOKINES are PROTEINS produced by MANY cells, but usually LYMPHOCYTES and MACROPHAGES, numerous roles in acute and chronic inflammation –TNFα, IL-1, by macrophages • CHEMOKINES are small proteins which are attractants for PMNs (>40)
- 57. NITRIC OXIDE • Potent vasodilator • Produced from the action of nitric oxide synthetase from arginine
- 58. LYSOSOMAL CONSTITUENTS • PRIMARY • Also called AZUROPHILIC, or NON-specific • Myeloperoxidase • Lysozyme (Bact.) • Acid Hydrolases • SECONDARY • Also called SPECIFIC • Lactoferrin • Lysozyme • Alkaline Phosphatase • Collagenase
- 59. FREE RADICALS • O2– (SUPEROXIDE) •H2O2 (PEROXIDE) •OH- (HYDROXYL RADICAL) •VERY VERY DESTRUCTIVE
- 60. NEUROPEPTIDES • Produced in CNS (neurons) • SUBSTANCE P • NEUROKININ A
- 61. OUTCOMES OF ACUTE INFLAMMATION • 1) 100% complete RESOLUTION • 2) SCAR • 3)CHRONIC inflammation
- 62. Morphologic PATTERNS of Acute INFLAMMATION (EXUDATE) •Serous (watery) •Fibrinous (hemorrhagic, rich in FIBRIN) •Suppurative (PUS) •Ulcerative
- 63. BLISTER, “Watery”, i.e., SEROUS
- 64. FIBRINOUS
- 67. ULCERATIVE
- 69. SEQUENCE OF EVENTS • NORMAL HISTOLOGY • VASODILATATION • INCREASED VASCULAR PERMEABILITY • LEAKAGE OF EXUDATE • MARGINATION, ROLLING, ADHESION • TRANSMIGRATION (DIAPEDESIS) • CHEMOTAXIS • PMN ACTIVATION • PHAGOCYTOSIS: Recognition, Attachment, Engulfment, Killing (degradation or digestion) • TERMINATION • 100% RESOLUTION, SCAR, or CHRONIC inflammation
- 72. CAUSES of CHRONIC INFLAMMATION •1) PERSISTENCE of Infection •2) PROLONGED EXPOSURE to insult •3) AUTO-IMMUNITY
- 73. Cellular Players •LYMPHOCYTES •MACROPHAGES (aka, HISTIOCYTES) • PLASMA CELLS • EOSINOPHILS • MAST CELLS
- 77. LYMPHATIC DRAINAGE • SITE REGIONAL LYMPH NODES
- 78. SYSTEMIC MANIFESTATIONS (NON-SPECIFIC) • FEVER, CHILLS • C-Reactive Protein (CRP) • “Acute Phase” Reactants • Erythrocyte Sedimentation Rate (ESR) increases • Leukocytosis • Pulse, Blood Pressure • Cytokine Effects, e.g., TNF(α), IL-1
- 79. NORMAL SPE Serum Protein Electrophoresis In ACUTE Inflammation Alpha-1 & alpha-2 are increased, i.e., “acute phase” reactants.