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35 Cards in this Set
- Front
- Back
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Acute inflammatory response |
Erythema Heat Edema Pain Loss of Function |
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Bradykinin regulator |
ACE (angiotensin converting enzyme) inhibitors - leads to increased vasodilation, vascular permeability (lead to edema), and decreased smooth muscle contraction |
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Bradykinin Effects |
Vasodilation Vascular Permeability Decreased Smooth Muscle Contraction Pain (when combined with prostaglandin) |
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Kinin Cascade (simplified) |
Factor XII (Hagerman factor) --> prekallikrein --> kallikrein --> bradykinin |
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Main Activating Factors Between Systems |
Factor XII Plasmin |
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Classic Complement Pathway Induced |
Anitgen-Antibody complex |
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Alternative Complement Pathway Induced |
Microbial Surface (Lectin pathway similar) |
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Complement Cascade |
-Opsonization of target --> phagocytosis by macrophages -Direct lysis of pathogen cell wall -Histamine release and increased vascular permeability |
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C3a |
Chemotactic Factors Anaphylatoxins |
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C3b |
-Opsonization tag for macrophage -Leads to C5 --> C5b --> Membrane Attack Complex (MAC) |
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What activates the kinin cascade, complement system, and coagulation (clotting) system? |
Factor XII |
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Sequence of Acute Inflammation |
1. Epithelial cells release chemokines 2. Chemokines activate endothelial cells, adherence and then margination of neutrophils to endothelium 3. Mast cell degranulation, release histamines, vasodilation and permeability of endothelium 4. Neutrophils enter interstitial fluid, chemotaxis directs them toward infection to phagocytose, also send macrophage chemotactic factor to bring macrophages to infection
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Adherence |
Chemokines activate the endothelial cells to attract the neutrophils, roll along endothelial layer |
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Margination |
Accumulation of neutrophils at vessel wall prior to diapedesis |
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Diapedesis |
Endothelial wall retraction to allow neutrophil entrance into the interstitial fluid, sight of infection |
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Role of Eosinophils |
Control effect of histamine Control effect of serotonin Surface break down of parasites |
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Cytokines |
-Soluble factors that regulate the inflammatory response -Include interleukins, interferons, and tumor necrosis factor - alpha |
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Interleukins (ILs) |
-Biochemical messengers primarily produced by macrophages and lymphocytes -Help regulate the inflammatory response significantly -How white cells communicate -Induces fever [Interleukin1 goes to hypothalamus to induce fever] |
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Interferons |
-Provide protection from viral infection in uninfected cells -Secreted by cells that are dying from virus |
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Tumor Necrosis Factor-Alpha (TNF-a) |
-Primarily produced by macrophages -Promotes inflammation with both local and system effects -Increases permeability and leukocyte emigration -Part of both immediate and long term response |
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Chronic Inflammation |
-Slower onset and more protracted course -Less vascular dilation and exudation of fluids - Increased numbers of plasma cells, macrophages, and lymphocytes -Suppuration (pus formation) and granulation tissue -Body is focusing on control and eventual healing -Angiogenesis and collage deposition are key elements |
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Mast Cells |
- Produce: histamine chemotactic factors cytokines prostaglandins growth factors leukotrienes chemotactic factors -Most important activator in inflammation |
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Eosinophils |
-Secrete chemical mediators -Contain receptors for immunoglobulin/complement complexes -Lysozomes to calm down vascular effects in inflammation and dissolve surface membranes of parasites |
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Prostaglandins |
-Involved in pain response in conjunction with bradykinin -Vasodilation and edema -NSAIDS block COX pathway |
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Interleukin-1 |
-Secreted by macrophages -Moves ot hypothalamus creating an increase in temperature -Increases adhesion factors on endothelial cells to increase diapedesis |
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Systemic Manifestations of Acute Inflammation |
-Fever -Leukocytosis -Increase in level of plasma proteins |
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Histamines |
-Released by mass cells -Act as main chemotactic factor |
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Surface defenses |
-Skin -Secretions -Mucus |
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Degranulation |
Release of histamine and chemotactic factors for PMNs and eosinophils in first few minutes |
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Neutrophils |
-Removal of debris (in sterile lesions) -Killing bacteria and phagocytosis (in infections) -Short lived -Acidic environment of inflammation kills them quickly |
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Macrophages |
-Derived from monocytes -Phagocytize invading bacteria -Secrete Interleukin-1 |
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Pleiotropic Cytokines |
Particular cytokine can act on a number of different types of cells rather than a single cell type. |
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Redundant Cytokines |
The ability of a number of different cytokines to carry out the same function. |
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Multifunctional Cytokines |
The same cytokine is able to regulate a number of different functions. |
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Outcomes of Inflammation |
-Complete resolution -Healing by fibrosis and scarring -Abscess formation -Progression to chronic inflammation (granuloma) |
