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37 Cards in this Set
- Front
- Back
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Inflammation is connected with |
repair, regeneration and healing |
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The biological meaning of theinflammation |
Protective Protects organism against initial cause of tissue injury and removes the injured tissue Harmful Scars Atherosclerosis |
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The components of inflammation Inflammation consists of: |
Vascular reactions Migration and activation of leukocytes Systemic reactions |
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The local components of inflammation |
Vascular reactions Cellular reactions |
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Acute inflammation |
Starts rapidly (in seconds or minutes) Short – termed (lasting for few days) Morphologic components: -Exudation of fluid and plasma proteins -Oedema -Reaction / emigration of neutrophils (Neu) |
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Chronic inflammation |
Develops after acute inflammation or starts slowly Long – lasting Morphological components: -Reactions of lymphocytes and macrophages -Proliferation of blood vessels -Fibrosis -Necrosis , loss of specialised tissues |
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Etiology of acute inflammation |
Infections Trauma Foreign bodies Immune reactions Tissue necrosis |
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The pathogenesis of acute inflammationincludes: |
Vascular dilatation Edema (Exudation of plasma proteins and fluid) Leukocyte emigration and accumulation |
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The mechanisms of increased vascularpermeability |
Formation of intercellular endothelial gaps: retractionof endothelial cells (immediate transient response) Endothelial injury: -Direct endothelial injury -Delayed (2-12 hrs) prolonged leakage: delayeddirect endothelial injury (apoptosis) or damage bycytokines Leu-mediated vascular injury Transcytosis Angiogenesis |
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Response of lymphatic vessels |
Increased flow to drain the tissue oedema Movement of leukocytes and cell debris along with the lymph flow Proliferation Spread of inflammation: -Lymphangitis -Lymphadenitis: reactive vs. acute purulent |
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The cellular components of acuteinflammation |
Leu Leu extravasation: Marginalization, rolling and adhaesion to the endothelium Transmigration s. diapedesis Migration in the interstitium (tissues) Neu, Mo, Ly, Eo, Ba |
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Leu adhaesion factors |
Selectins Glycoproteins Integrins Immunoglobulin superfamily ICAM-1,VCAM-1 |
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Leukocyte diapedesis |
Occurs in post-capillary venules Adhaesion factors (CD31) to cross the endothelial layer Basement membrane destruction by collagenases Binding to connective tissues by beta1integrins and CD44 |
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The cells in acute inflammation |
Neu: dominate 6 – 24 h, disappear by apoptosisin 24 – 48 h Mo: 24 – 48 h Eo: hypersensitivity Ly: viral infections Prolonged predominance of Neu predominance:Pseudomonas 2 – 4 days |
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Chemotaxis |
locomotion oriented along a chemical gradient Granulocytes, monocytes (Mo), lymphocytes(Ly) respond to chemotactic stimulus |
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Leukocyte activation by |
Microbes, Necrosis, Ag-Av, Cytokines |
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Recognition of microbes and dead tisssues |
Leukocyte receptors: Receptors for microbial products: G protein-coupled receptors Receptors for opsonins Receptors for cytokines |
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Phagocytosis |
Recognition and attachment Engulfment: phagosome Killing and degradation: phagolysosome |
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Extracellular release of leukocyteproducts |
Lysosomal enzymes Reactive [O] intermediates Metabolites of arachidonic acid |
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The mechanisms of the extracellularrelease of leukocyte products |
Unusual process! Regurgitation: phagocytic vacuole remains transiently open before closure Frustrated phagocytosis Cytotoxic release: after phagocytosis of membranolytic substances Exocytosis |
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Termination of the acute inflammatoryresponse |
The degradation of mediators Anti-inflammatory mediators: -Lipoxins -TGF-beta -Cholinergic neural impulses |
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The outcomes of acute inflammation |
Complete resolution Progression to chronic inflammation Healing by fibrosis Death |
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The main morphological patterns ofacute inflammation |
Serous inflammation Fibrinous inflammation Purulent inflammation Inflammatory ulcer |
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Serous inflammation |
Marked exudation by relatively thin fluid Examples: -Skin blister in the site of burn |
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Fibrinous inflammation |
Exudate rich in fibrinogen due to greater increase of vascular permeability Fibrin formation occurs in the exudate due to local procoagulant (e.g., microbes or cancer cells): fibrinous exudate |
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Purulent inflammation |
Exudate rich in Neu Pus Types: phlegmonous or by abscess formation Possible outcomes: -Resolution -Healing by fibrosis -Serious systemic effects, even death |
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Inflammatory ulcers |
Ulcer – a local defect of the surface of an organ or tissue that is produced by the sloughing of inflamed and / or necrotic tissue, e.g., |
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Acute inflammation: the pathogenesisof local clinical signs |
Rubor, calor, tumor – -Due to increased blood flow and oedema Dolor -Due to tissue damage -Due to production of prostaglandins, neuropeptides and cytokines Functio laesa |
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Acute inflammation: the therapeuticapproach |
Treat the cause Depending on the cause, the inflammation can be promoted or decreased In microbial infections, the inflammation is auseful reaction In trauma (and several chronic inflammatorydiseases) the inflammation has to bereduced |
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Chronic inflammation |
Chronic inflammation is inflammation of prolonged duration (weeks or months) during which -inflammation, -tissue injury and -repair coexist. |
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The etiology of chronic inflammation |
Persisting infections: tbc, lues (Treponemapallidum), certain viruses, fungi, parasites Prolonged contact with toxic substances ordamaging physical factors Immune-mediated and/ or autoimmuneinflammatory disease |
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The morphological components ofchronic inflammation |
Infiltration with mononuclear cells:macrophages, lymphocytes, plasmocytes Tissue destruction Fibrosis: |
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Macrophage is the |
dominant cellular player in chronic inflammation |
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The development of macrophage |
Bone marrow: precursor cell Circulating monocyte: half-life 24hrs Tissue macrophage: months or years |
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Macrophage activation |
Starts during phase of active inflammation Activation by -T un NK - Ly cytokines; -Bacterial endotoxins. In 48 hrs, macrophages acquire dominantstatus |
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Granulomatous inflammation |
Granuloma – focus of chronic inflammation consisting of microscopic aggregations of -Macrophages Ly Giant cells |
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Types of granuloma |
Foreign body granuloma Immune granuloma – caused by agents that induce cell-mediated immune response when the inciting agent is poorly degradable |
