Inflammation, fever lecture.pdf - Inflammation Definition\u200b patterns of cellular and tissue injury that manifests as inflammation very broad and

Inflammation, fever lecture.pdf - Inflammation...

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Inflammation: Definition : patterns of cellular and tissue injury that manifests as inflammation, very broad and generic term Dr. Cabrera lecture Response to 3 things: 1. Eliminates initial cause of cellular injury (ex. Splinter, swelling in the area) 2. Remove damaged tissue 3. Generate new tissue Adam’s book Inflammation occurs in response to injury/antigen Central purpose: to contain injury or destroy microorganism Causes : 1. exogenous (mechanical → BP cuff being on for too long, physical → MVA, cuts, chemical, biological → bacteria/germ) 2. indogenous (circulatory d/o → cardiac → hypoxia , not perfusing effectively ; immunocomplex formation → cancer pt, immunocompromised, complex, multi-d/o formation) Processes of inflammation : 1. Vasodilation - natural body’s response, increase in blood flow to area , will turn red 2. Vascular permeability - epithelial cells become leaky from either direct cell injury or via chemical mediators (histamine or prostaglandins) → swelling 3. Exudation - substance/matter → fluid, proteins, RBC and WBC’s escape from intravascular space as a result as increased osmotic pressure extravascularly and increased hydrostatic pressure intravascularly 4. Vascular Stasis - slowing of blood in blood stream with vasodilation and fluid exudate to allow chemical mediators and inflammatory cells to collect and respond to stimuli Adams: 1. Vasodilation 2. Vascular Permeability 3. Cellular infiltration 4. Thrombosis 5. Stimulation of nerve endings Steps of Inflammation from Gould's book: 1. Bradykinin is released from the injured cells 2. Bradykinin activates pain receptors 3. Sensation of pain stimulates mast cells and basophils to release histamine 4. Bradykinin and histamine cause capillary dilation → causes increase of blood flow and capillary permeability 5. Break in skin allows bacteria to enter the tissue → migration of neutrophils and monocytes go to the injury site 6. Neutrophils phagocytize the bacteria 7. Macrophages leave the bloodstream and phagocytose microbes
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*Histamine is the key chemical mediator. It is stored in mast cells and directly stimulates pain receptors Classic s/s: Redness (erythema) swelling (increased fluid and protein) heat/warmth (vasodilation) pain and discomfort loss of function Nursing intervention : RICE -Rest, Ice, Compression, Elevation Inflammation medications: Goal: to prevent/decrease inflammatory response intensity and reduce fever NSAIDS MOA: -stop prostaglandin synthesis (prostaglandin promotes inflammation) -target 2 enzymes (COX 1 and COX 2); Cyclooxygenase - key enzyme for prostaglandin biosynthesis . COX-1 present in all tissues, reduces gastric secretions and promotes blood flow in renal system & platelet aggregation COX-2 present ONLY at injury site 1. Non-steroidal anti-inflammatory drugs a. Nonselective NSAIDS → ibuprofen (Advil , Motrin) - tx of mild to moderate inflammation - will target both COX 1&2 b. COX-2 Selective NSAIDS → celecoxib (Celebrex) - tx of moderate - severe inflammation - has analgesia (relief of pain), anti-inflammatory, antipyretic (reduces fever) effects
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