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9 Cards in this Set
- Front
- Back
Steps of Inflammation
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1-Vasodilation
2-Vascular permeability (Edema) 3-Cellular infiltration (Pus) 4-Thrombosis (Clots) 5-Stimulation of nerve endings (Pain) |
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Cyclooxygenase-1
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Location-Present in all tissues
Fxn's-Protects gastric mucosa, supports kidney fxn, promotes platelet aggregation Inhibition by med's-Undesirable: increase risk of gastric bleeding and kidney failure Inhibition of COX-1 causes bleeding, gastric upset and decreased renal fxn. |
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Cyclooxygenase-2
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Location-Present at sites of tissue injury
Fxn's-Mediates inflam, sensitizes pain receptors, mediates fever in the brain Inhib. by med's-Desirable: results in suppression of inflam Inhibition of COX-2 results in inflam suppression |
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Histamine
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Initiates inflam response
Key mediator in inflam Stimulates pain receptor |
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H1 receptors
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In vascular smooth muscle, in bronchi.
Stimulation causes inflam response |
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H2-receptors
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In stomach
Stimulates HCl |
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NSAID's
-Prototype- |
ibuprofen (Advil, Motrin)
MOA: inhibit prostaglandin synthesis PU: for musculoskeletal d/o's (RA, OA), mild to moderate pain, reduce fever, 1y dysmennorheal pain AE: nausea, heartburn, epigastric pain, dizziness |
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Glucocorticoid
-Prototype- |
prednisone (Meticorten)
MOA: metabolized to an active glucocorticoid PU: treat inflam AE: long term -> Cushing snd |
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Antipyretics -P-
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acetaminophen (Tylenol)
MOA: reduce fever at hypothalamus and dilate peripheral blood vessels (enables sweating and dissipates heat), doesn't affect blood coagulation PU: relieve pain and fever AE: liver damage, causes less GI irritation than aspirin |