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what 3 molecules mediate fever?
IL-1, TNF, PGE2
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heat, redness and swelling during inflammation are caused by what?
changes in vascularity
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what vascular changes occur during acute inflammation?
vasodilation and increased vascular permeability
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vasodilation is mediated by what molecules?
endothelial derived NO to induce vascular smooth muscle relaxation and mast cell release of histamine
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vasodilation is maintained by what class of molecules?
prostaglandins
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what results from increased vascular permeability?
movement of fluid out of vasculature, blood becomes more concentrated and flow slows (stasis)
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tissue and endothelial cell damage is marked by what 3 types of exudate?
fibrinous, purulent, sanguineous
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purulent exudate contains mostly what type of cell?
neutrophil
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define endothelial cell contraction
formation of intercellular gaps due to reversible contraction lasting for 15-30 minutes
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endothelial cell contraction is mediated by what molecules late and early?
early: histamine, bradykinin. later: leukotrienes and PAF. C3a and C5a lead to edema
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explain endothelial cell retraction
restructuring of cytoskeleton proteins that takes 4-8 hours to develop and lasts for 24 hours or more.
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endothelial cell retraction is mediated by what molecules?
IL-1, TNF, IFN-g
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activated endothelials are characterized by what?
production of PGI2 and NO, contraction, rearrangement of cytoskeletal proteins leading to retraction, increased expression of adhesions, synth and release of inflammatory mediators.
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what is the sequence of leukocyte extravasation?
margination, rolling, adhesion, emigration, chemotaxis
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rolling and adhesion are mediated by what molecules?
rolling: selectins, adhesion: integrins
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define diapedesis
transmigration of cells through the vessel wall
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diapedesis is mediated by what molecule?
PECAM-1
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Two potent chemotactic molecules are?
PAF, LTB4 (remember PAF helps in contraction)
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activation of leukocytes is characterized by what 5 factors?
leukotrienes and prostaglandins, degranulation/release of lysosomal enzymes, ROS, cytokines, cell adhesion molecules
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what cell is the hallmark of acute inflammation?
neutrophils (accumulate within 6-24 hrs)
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define cellulitis
diffuse inflammation of connective tissue with severe inflammation of dermal and subcutaneous layers of the skin. edema
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define abscess
localized area of liquefactive necrosis
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define ulcer
erosion of an epithelial surface exposing underlying connective tissue
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name 3 reasons for chronic inflammation
persistent infections, prolonged exposure to toxic agent, immune-mediated inflammatory disease
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describe granulomatous inflammation
delayed type-IV hypersensitivity, caseous necrosis, collar of mononuclear cells surrounding aggregated epithelioid histiocytes. heals by fibrosis
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list 4 diseases characterized by granulomatous inflammation
bacterial TB, parasitic toxoplasmosis, fungal histoplasmosis/mycosis, inorganic silicosis or inert foreign material
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source and function of histamine?
mast cells, vasodilation and increased vascular permeability
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Function of bradykinin?
increase vascular permeability, pain
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Source/function of NO
endothelials, vasodilation and tissue damage
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source/function of prostaglandins
membrane phospholipids, vasodilation, pain, fever
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source/function of leukotrienes
membrane phospholipids, increase vascular permeability, vascoconstriction, bronchoconstriction
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source/function of leukotriene B4
leukocyte, leukocyte activation, chemotaxis
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source/function of PAF
leukocytes and endothelials; increase vascular permeability and chemotactic
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source/function of cytokines (IL-1, TNF)
macrophage, endothelials; endothelial and leukocyte activation, fever
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function of C5a and C3a?
increase vascular permeability
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what molecules function as vasodilators?
histamine, NO, prostaglandins
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what molecules serve to increase vascular permeability
histamine, bradykinin, leukotrienes, PAF, C3a, C5a
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how do NSAIDs work to relieve inflammation?
by blocking cyclo-oxygenase activity
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how do steroids relieve inflammation
by inhibiting the release of arachidonic acid
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thromboxane A2 does what?
vasoconstriction, promotes platelet aggregation
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what works in opposition to thromboxane A2
prostacyclin which inhibits platelet aggregation
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