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imflamation and healing

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inflammation
Causes of cellular injury   hypoxia loss of o2 supply so cell dies/ becomes fibrotic scar tissue ( MI cells can't regenerate so heart stops to pump) ( Brain cells modify function and control impulse- no regeneration so brain stops)( skin- cells can regenerate)   trauma- will cause cellular injury   toxicity- things we inhale or ingest        
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Inflammatory response   vasomotor response ( vasoconstriction limits further bleeding and extent of injury)(vasodilation increases blood flow to help heal<hyperremia- area will get red> in diabetes there is decreased blood flow hard to heal wounds   adhesion/ chemotaxis- neutrophils break from vessels and go to area and adhere to injured area ( selectins, Icams, integrins aid in migration and adhesion)   exudation- fluid coming out of blood vessels that contain fibrinogin ( originally thin it becomes thick and clots<cellular debris>)   Fibrin barrier formation- fibrinogin is activated to fibrin which clots      
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Purpose of vasodilation   to bring WBC to injured area( leukocytosis)   netrophils and monocytes are increased   in acute inflammation that is short and first there is an increase in neutrophils   in chronic inflammation - an infection that you had for a long time there will be more lymphocytes than any other WBC   vasodilation increases o2 and nutirents   vasodilation neutralizes toxinsin the area  
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Functions of fibrin   wards off infection by forming a wall barrier around the injured area and prevents infection spreading   forms meshwork for healing   provides for homeostasis- bleeding stops- and cooagulation        
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Cardinal signs and symptoms of inflammation   hyperemia- redness or ruboor (vasodilation)   tumor- swelling (fluid)   calor- heat ( vasodilation)   Dalor -pain( from sensory nerve signals)   functo laesa- loss of function due to pain    
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Systemic signs and symptoms   malaise( weak) and fatigue (tired) fever, and myalga ( muscle pain)   leukocytosis (8,000 wbc),increase wbc synthesis in bone marrow   increase ESR (erythrocyte sedimentation rate) indicate RBC tissue breakdown   acute phase reactant- serum proteins are altered ( albumin, fibrinogen, globulin)   anorexia   hormone increase (cortisol- stress hormone from cortext of adrenal gland)  
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Types of healing   resolution- damage cells suffer but don't die   regeneration- dead cells replaced by functional cells- (GIT,GUT, skin, and bone marrow are highly regenerative)( kidney, liver, bone, lungs, and muscle are moderately regen)(brain and heart do not regenrate)   repair- healing when tissues are replaced by non functional scar tissue        
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3 levels of repair   healing by first intention- clean surgical ends of wound are together- starts from top- edges come together- no scar formation   healing by secondary intentions- deeper and larger wound ( draiing ulcer)- healing starts from below- inside comes out- works its way up - scarring is more intensive   3. - healing of infected wounds or those of high risk infection- gaping wounds need to be sutured inorder to heal        
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Delayed healing results from   infection   malnutrition   immunosupression - ( AIDS, chemo, autoimmune, transplant)   vascular problems ( diabetes, cardiac problems)   obesity    
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What helps heal   antibiotics ( can result in 2nd infection)   local application of heat or ice- ice - vasoconstrict heat- vasodilate   debrivment- remove puss and scabs and drain secretions   drug therapy ( steroids, NSAID- tylenol,immunosupressives, antihistamine      
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Biologic response modifiers will increase wbc   interleukins stimulate wbc ( lymphocyte/monocyte)   GMSF   growth factor        
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Created by: natkat
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