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14 Cards in this Set
- Front
- Back
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Histamine
cell source: physiological response: mechanism: pharmacology: |
-biogenic amine -source: mast cells, basophils -response: vasodilation, increase vascular permeability, pain -mech: activate GPCRs--activate signaling pathway -pharm: antihistamines (H1 antagonist) |
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Bradykinin
cell source: physiological response: mechanism: pharmacology: |
-peptide -source: endothelial cells (lumen of blood vessel) -response: vasodilation, increase micro vessel permeability, pain -mech: activate GPCRs -pharm: BK receptor ANT being tested
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Complement System
cell source: physiological response: mechanism: pharmacology: |
-plasma proteins -source: synthesized by liver, circulate in blood -response: chemotaxis, promote release of mediators from neutrophils, increase vascular permeability -mech: complement protein complexes, cause osmotic lysis, activate GPCRs, mast cell degranulation |
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C-Reactive Protein
cell source: physiological response: mechanism: pharmacology: |
-plasma protein -source: produced by liver in response to cytokines and by adipocytes -response: "acute phase reactant", activate complement cascade, mediates phagocytosis, *marker for inflammation -mech: bind to phosphatidylcholine in bacteria and damaged cells, calcium dependent binding |
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Cytokines
cell source: physiological response: mechanism: pharmacology: |
-secreted proteins, ex IL-1 and TNF alpha -source: nearly all inflammatory cells -response: stimulate acute phase reactants, TNFa: fever, sepsis IL-1: fever, fibroblast & lymphocyte proliferation mech: bind to specific receptors to induce gene expression of numerous proteins thru activation of transcription factors -increase cyclooxyrgenase (fever) and lipoxygenases -increase adhesion molecule -induce collagenases (fibrosis) pharm: Etanercept, Infliximab |
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Adenosine
cell source: physiological response: mechanism: pharmacology: |
-purine nucleoside -source: all cells -response: increase extracellularly during injury and has anti-inflammatory effect to inhibit cytokine action -receptor specific (can be pro-inflammatory) mech: activate GPCRs |
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Cell Adhesion Molecules (CAMs)
cell source: physiological response: mechanism: pharmacology: |
-integrins, selectins source: endothelial cells, platelets, leukocytes response: -leukocyte adhere to endothelium is integral to repair process -endothelial adhesion molecules contribute to recruitment of activated platelets mech: mediate contact btwn 2 cells or btw cells and extracellular matrix, "contact" molecules, Ca2+ dependent |
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Prostaglandins
cell source: physiological response: mechanism: pharmacology: |
-pro-inflammatory -source: all cells -response: vasodilation/vasoconstriction, pain, fever, platelet aggregation (tromboxane) -PGE1/PGE2 directly increase blood flow and indirectly enhance edema formation mech: activate specific GPCRs pharm: NSAIDs (block prostaglandins) |
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Leukotrienes
cell source: physiological response: mechanism: pharmacology: |
-pro-inflammatory -source: macrophages, neutrophils -response: increase vascular permeability, bronchoconstriction mech: activate GPCR pharm: Zileuton, Zafirlukast |
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Gluccocorticoids
cell source: physiological response: mechanism: pharmacology: |
-anti-inflammatory -source: adrenal cortex -response: inhibit cytokines, inhibit phospholipase A, inhibit cyclooxygenase 2, inhibit cell adhesion molecules -mech: activation of nuclear receptors -pharm: steroid --most potent and effective agents for controlling chronic inflammatory diseases |
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Zafirlukast
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-cysteinyl leukotriene receptor ANT -competitive antagonist of leukotriene receptors -orally active -metabolized by CYP2C9/3A4 -inhibits cys-LTs at receptor (LTs still synthesized) -minimal side effects use- prophylactic treatment of mild asthma |
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Zileuton |
-inhibits 5-lipoxygenase, inhibiting the synthesis of leukotrienes -orally active -metabolized by CYP enzymes -inhibits production of cys-leukotrienes (decreasing bronchoconstriction and LTB4 (chemotaxis)) -few adverse effects, increase liver enzymes use: prophylactic treatment of mild asthma |
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Etanercept |
-receptor analog -prevent TNF-alpha binding |
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Infliximab |
-monoclonal antibody -binds to TNF-alpha, preventing it from binding the receptor |
