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60 Cards in this Set
- Front
- Back
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Antigen
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Foreign proteins capable of eliciting an immune response
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Non-protein Antigens
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Polysaccharides and polypeptides
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Auto-Immunity
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Host molecules incite antibody response
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Inflammation Definition
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Process specific to vascularized tissues where fluids from blood vessels and WBC accumulate at site of injury to defend body
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Innate Immune protection
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Most of innate immune system are developed in utero
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Inflammation Function
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Response to pathogenic environmental insult & begins wound/ tissue healing
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Mistakes of Inflammation
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Inadequate response, misdirected response, exaggerated response.
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Acute Inflammatory Response
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Immediate
Gets Intravascular leukocytes delivered in time to extravascular locations. |
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Phlegmone
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Egyptians- 4500 years ago
Greeks- 2500 years ago 'The burning thing.’ |
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Cardinal Signs of Inflammation
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2000 years ago
Roman- Cornelius Celsus Rubor, Tumor, Calor, Dolor |
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John Hunter
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1973- Scottish surgeon
Inflammation not a problem but a curative response |
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Julius Cohnheim
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1867
Observed diapedesis under microscopic in a live frog. Student of Rudolph Virchow. |
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Elie Metchinkoff
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1880’s
Discovered process of phagocytosis. Demonstrated that both serum factors (antibodies) & cellular factors (phagocytes) are involved in immune response. |
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Sir Thomas Lewis
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Demonstrated that chemical substances made at inflammation site also mediate the response.
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Characteristics of Acute Inflammation
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1. Recent onset; short duration (few minutes to 2 days)
2. Movement of WBC neutrophils 3. Blood proteins & blood serum to extracellular space |
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Key Events in Acute Inflammation
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1. Change in diameter of small blood vessels
2. Change in vascular permeability 3. Stage of Exudation 4. Change in vascular flow |
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Exudation Definition
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Escape of fluid, proteins, & leukocytes from blood vessels into the extravascular environment resulting in edema (and pus if there are cells & cellular debris)
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Features of Changes in Vascular Flow
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1. Vasoconstriction (not important and brief)
2. Vasodilation- increases blood flow (redness and heat) 3. Increase in pressure drives out non-protein fluid and concentrates protein in vascular system. 4. Increase of viscocity, decreases blood flow and causes increased leakage. 5. Margination and Emmigration of Leukocytes |
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Features of Changes in Permeability
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Endothelium membrane becomes 'leaky. (Due to contraction of individual endothelial cells)
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Transudation
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Increased hydrostatic pressure drives protein-poor liquid out
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Exudation
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Increased permeability allows protein- rich fluid to escape
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3 responses to increased Permeability
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Immediate Transient
Immediate-sustained Delayed-prolonged leakage |
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Immediate Transient Response
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5-10 minutes after injury, lasting 15-30 minutes.
Mediated by histamine and proceeds via endothelium contraction |
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Immediate Sustained Response
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Immediately upon injury. Lasts a few hours or days.
Severe injury Related to leakage from torn vessels |
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Delayed-Prolonged Leakage
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Doesn't start for several hours. Lasts for days.
NOT involving epithelial contraction but still is leaky capillaries and venules. (i.e. sunburn response) |
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Stage of Leukocytic Exudation
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1. Stasis initiates margination, pavementing and emigrating.
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Margination of Leukocytes
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White cells travel near the periphery
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Pavementing
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A mechanism causes adhesion between Leukocytes and the walls of the capillaries and venules.
*** chemicals or genetic defects can increase or decrease pavementing and thus the inflammatory response. |
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Emigration
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Leukocytes emigrate to extravascular space to find whatever has caused the inflammation.
6-24 hours: Neutrophils 24-48 hours: Monocytes |
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Opsonins
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Serum factor antibodies
Tag foreign proteins for distruction |
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Lysosomal Enzymes
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Kill invaders in an oxygen-dependent reaction. (hydrogen peroxide)
Oxygen -independent kills with other stubstances that alter permeability of bacteria membrane. |
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Leukopenia
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Decreased circulation of leukocytes.
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Potential Defects related to Leuckocytic Exudation
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Leukopenia
Impaired Adhesion: alcohol poisening Impaired Chemotaxis & migration: Diabetes Defective Phagocytosis: Diabetes Impaired degradative ability (diminished hydrogen peroxide formation- chronic granulomatous disease) |
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Arthus Reaction
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Swarm of neutrophils digest the walls of venule.
(negative impact of inflammatory focus) |
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Lymphangitis
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Exudate and debris of tissue move through lymph. Surviving bacteria is spread as well.
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Chemical Mediators of Inflammation
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Triple response
Sir Thomas Lewis 1920's |
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Triple response
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1. Red Line: Blood vessel dilation
2. Red Flare: General Arteriolar Vasodilation (within 30 seconds) 3. White Wheal: Localized Edima caused by histamine. (within 1-3 minutes) |
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Net Result of chemical mediators
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1. Vasodilation
2. Increased Vascular Permeability 3. Chemotaxis of Leukocytes 4. Pain |
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Vasoactive Amines
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Histamines & Seratonin (5-hydroxytryptamine)
Increase permeability & Transudation |
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Agents which promote the release of Vasoactive Amines
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1. Physical Agents (heat, cold)
2. Immunological Reactions 3. Anaphylatoxins (fragments of complement proteins) 4. Allergens (cause IgE to bind to mast cells and secrete histamine) |
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Plasma Proteases
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Complements
Kinins Clotting Systems |
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Complements
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20 proteins involved in antibody-antigen immune response.
Antigen-Antibody complex binds to complement which releases histmine and neutrophilic infiltration C3a, C5a |
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C3a
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Increase vascular permeability
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C5a
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Increase vascular permeability
Enhances Chemotactic Behavior |
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Kinins
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Endogenous peptides produced by cascade caused by Factor 12 (Hageman Factor)
Bradykinin |
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Bradykinin
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Vasoactive nonapeptide
Increases permeability Pain perception |
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Clotting System Constituents
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Activated by Factor 12 (Hageman Factor)
Converts Fibronogen to fibrin Fibrinopeptides increase permeability and chemotaxis |
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Arachidonic Acid Metabolites
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20-carbon polyunsaturated fatty acid
Ingested through diet or from linoleic acid |
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NSAIDS inhibit this enzyme
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Cylooxygenase
This transforms arachidonic acid into protaglandin PGG2 |
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Cylooxygenase
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type 1: secretes mucous that protects tummy
Type 2: makes protglandin which is involved in inflammation and should be the REAL target of NSAIDS |
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5-Lipxygenase (5-LO)
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Converts Arachidonic acid into Leukotrienes
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Leukotrienes
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More potent inflammatory agent than Prostaglandins
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Mast Cells version of lysosomes
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Eosiniphil Chemotactic Factor of Anaphylaxis
(ECF-A) |
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Lymphokinines
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From lymphocyte when attacking an antigen.
Impact adhesion, histamine release, etc. |
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Exogenous Factors initiating chemical mediators
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Direct injury to blood vessels
Bacterial by-products |
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Primary Chemical Mediators related to Increased Vascular Permeability
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Vasoactive Amines (especially histamines)
Kinins (especially bradykinin) Prostaglandins |
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Primary Chemical Mediators related to Emigration of Leukocytes
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C5a
Neutrophil Lysosomal Proteins Eosinophil Chemotactic Factor of Anaphylaxis (ECF-A) |
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Opsonizing Agent
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C3b
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Tissue Damage ensues from this agent
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Neutrophil Lysosomal Products
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Endogenous Pyrogens
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Cytokinins produced by leukocytes travel to brain to raise the thermostat
Sympathetic vasoconstricion |
