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54 Cards in this Set
- Front
- Back
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Inflammation |
Local reaction of vascularized to injury |
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Acute |
1. 0-2 days 2. Inflammatory Cells-Neutrophils |
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Subacute |
1. 2-14 days 2. Neutrophils, monocytes, lymphocytes, plasma cells, fibroblastic elements, angioblastic elements |
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Chronic |
1. >14 days 2. Monocytes, lymphocytes, plasma cells, macrophages, granuloma cells |
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Eosinophil |
Predominant inflammatory cells in allergic reactions and parasitic infestations |
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Other Inflammatory Cells |
Basophils, Fibroblasts (repair, scarring), Mast Cells, Platelets |
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Plasma-Derived Molecular Systems |
1. Immune System (Ab, C3, C5) 2. Kinin System (bradykinin) 3. Clotting System (thrombin)* 4. Fibrinolytic System (plasmin)* 5. Acute phase (C-reactive, ceruloplasmin, haptoglobin) |
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Cytokines (IL-1, TNF) L1 |
Very Important in treating cancer Super Cell |
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Inflammation is a protective response |
A) the initial cause of injury B) The consequences of such injury |
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Inflammation and repair can be potentially harmful |
A) Inflammatory reaction underlie many common chronic diseases B) Uncontrolled inflammatory response can lead to life-threatening hypersensitivity reactions C) Repair can produce constrictive scarring and limb immobilization |
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6 cardinal signs of inflammation |
Redness, Heat, Swelling, Pain, Loss of f(x), systemic changes |
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Inflammation is biological and _ , _ |
Physical (thermal, ionizing) Chemical (poisons) infection, trauma, immunologic, tissue death |
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Serous (Acute) |
Outpouring of watery, relatively protein poor fluid (effusion), derives from either serum or mesothelial cell secretions Pleural Effusion-in baby |
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Fibrinous (Acute) |
1. Severe Injury 2. Incr Vascular Permeability- allows leakage of larger molecules (fibrinogen) -Fibrinogen OUT 3. Extravascular Fibrin accumulates 4. Can later evolve into Fibrosis, but not yet! 5. Fibrin is Present-leads to scarring/org. |
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Suppurative (purulent) (Acute) |
1. Manifested by large amounts of pus (neutrophils, necrotic cells, and edema fluid) -edema (h20 & proteins) Neutro-dead 2. Pyogenic Bacteria more likely to cause |
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Abscesses (Acute) |
1. Focal collections of Pus 2. Central Necrotic Region-layer of preserved of neutrophils |
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Ulceration (Acute) |
1. Local Defect, excavation produced by sloughing of inflammatory necrotic tissue 2. On or Near surface (skin and mucosa) 3. Mouth, GI Tract, GU tract, lower extremeties 4. Loose surface tissue-fibroblastic proliferation/chronic inflammatory cells/scarring |
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Resolution (Acute) |
Complete tissue restoration |
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Scar Healing (Acute) |
1. After substantial tissue destruction 2. in tissues that can't regenerate (lung) |
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Abscess (Acute) |
Infections with pyogenic organisms |
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Key Events of Acute Inflammation |
1. Increase in blood flow 2. enable plasma proteins and leukocytes to leave the circulation 3. Emigration of leukocytes 4. accumulation/activation @ site of injury |
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Phagocytosis of Organisms |
1. Neutrophils-Acute 2. Macrophages- Chronic |
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Engulfment |
Pseudopods surround object forming phagosome that fuses with lysosome creating a phagolysosome |
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Phagocytosis |
1. Neutrophils/Macrophages 2. W/help of C3/Ab to grab bacteria, lysosome will mere to surface and kill bacteria |
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Oxygen-Dependent |
Hypochlorous acid-Our bleach for killing bacteria |
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Oxygen Indpendent |
Leukocyte granule proteins & enzymes |
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Mediator |
1. Originate from plasma (must be activated) or cells (granules or synthesized) 2. Bind to specific receptors 3. Can stimulate Others 4. Short Lived 5. Quickly Decay, inactivated by enzymes, or inhibited 6. Can be harmful! |
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Histamine & Serotonin (Vasoactive Amines) |
1. Arteriolar Dilation 2. Increased Permeability 3. But constricts large arteries -1 hour |
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Mast Cells (richest source) -of Vasoactive Amines -basophils and platelets |
1. First mediators likely to be released 2. Stimulated by trauma, temp, platelet aggregation, C3a, C4a, C5a, neuropeptides (P), cytokines (Il-1 and Il-8) 3. Histamine and IgE |
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Cytokines and Chemokines |
1. Polypeptides-cellular hormones 2. Mediators 3. Networks 4. Strong chemotactic-chemokines |
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***Additive Synergist |
If one cell can secrete another If equal ten depends on tissue |
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***Key Cytokines of Inflammation |
IL-1 and TNF (tumor necrosis factor) -act synergestically and are produced mainly y macrophages |
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**Acute Phase Reactions |
1. Produce Fever 2. Affect Sleep (incr) and Appetite (decr) 3. Produce acute phase proteins 4. Cause neutrophilia 5. Hemodynamic effects in shock 6. Leukocytosis |
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**Endothelial Effects |
1. Increase leukocyte adherence 2. Stimulate PGI synthesis 3. Increase Procoagulant Activity 4. Increase IL-1, IL-6, IL-8, PDGF 5. Decrease Anti-coagulant |
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**Fibroblast Effects |
1. Increase proliferation 2. Incr Collagen Synthesis 3. PGE synthesis 4. Increase Protease 5,. Collagenase Production |
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**Leukocyte Effects |
Increase Cytokine Secretion (IL-1, IL-6) and activation |
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Too much repair will cause |
Fibrosis |
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***Mediators in Inflammation 1. Vasodilation 2. Fever 3. Vascular Permeability 4. Pain |
1. PG, NO 2. IL-1, TNF, PG 3. Amines, C3a, C5a, leukotrienes 4. PG, bradykinin-aspirin inhibits bradykinin lower temp lowers pg |
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Chronic (acute & chronic inflammation) |
1. > 2 weeks 2. Inflammation, tissue destruction, and attempts to repair coexist 3. macrophages, lymphocytes, plasma cells (mononuclear) t/b 4. Tissue Destruction-induced by persistent stimulus or by inflammatory cells 5. Attempts at healing-connective tissue replacement of damaged tissue, new vessel proliferation (angiogenesis) & fibrosis |
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**Macrophages |
Key cell in chronic and granulomatous inflammation -Derive from circulating blood monocytes -Liver (kupffer cells) -Spleen/Lungs (pulmonary macro) -24-48 hrs |
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Activated Monocytes -Increase... -appear large, flat, pink, like squamous -Signals |
1. Size 2. Lysosome 3. Lysosomal enzymes 4. ability to kill organisms 5. Signals-cytokines, T cells & NK cells, bacterial endotoxins, other chemical mediators |
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Reciprocal Relationship (T cells & macrophages) |
1. M>T or T>M 2. lymphocytes >M 3. M>cytokines |
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***Granulomatous Inflammation |
Distinctive pattern of chronic inflammation -seen in limited # of infectious/non infectious -prototype: tuberculosis |
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***Granuloma |
1. Focal Area of granulomatous inflammation 2. Macrophages>Epitheliod cells 3. Surronded by mononuclear leukocytes (lymphocytes and some plasma cells) |
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Granuloma |
Epitheloid macrophages, langhans giant cell, rim of lymphocytes -foreign body-splinter-when can't be phagocytosed by single macrophage |
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***Granulation Tissue |
Histologic appearance characterized by prolifetation of fibroblasts and new thin walled delicate capillaries, in a loose ECM. -newly formed blood vessels, and scattered macrophages and other inflammatory cells -temporary structure that matures by the process of cicatrization (colleagen, contraction, devascularization-scar) |
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Chronic Inflammation and Cancer |
1. Strong Association 2. Longer, Higher Risk of Carcinogenesis |
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**Gastritis |
Gastric Adenocarcinoma MALT Helicobacterpylori |
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**Hepatitis |
Hepatocellular Carcinoma Hep B and C |
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Wound Healing |
Complete restoration of original tissue architecture and f(x) after an injury -epidermis, bronchial, GI |
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Wound Repair |
Not anatomic restoration but a f(x)nal compromise -bone marrow, liver, kidney -brain, cardiac, skeletal (incapable) |
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Primary Intention Secondary Intention |
1. Edges lined up-best 2. Edges not lined up -more granulation, epitheliazation, more fibrosis -non opposed wound margins -more necrotic debris, exudate, and fibrin to be removed |
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Contracture |
1. Sever deformity 2. Exaggeration of contraction 3. myfibroblasts 4. 2nd intention-within 6 weeks 5. Burn victims, mvmt of joints, hollow viscera |
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Keloids*** |
Accumulation of exuberant amounts of collagen -raised scars -hereditary predisposition- african american -excessive granulation tissue (proud flesh) -abnormal cell growth & ECM production in wound healing -surgery required -above skin level |
