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OT Physdis

imflamation and healing

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
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
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
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
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
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)
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
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
Delayed healing results from infection malnutrition immunosupression - ( AIDS, chemo, autoimmune, transplant) vascular problems ( diabetes, cardiac problems) obesity
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
Biologic response modifiers will increase wbc interleukins stimulate wbc ( lymphocyte/monocyte) GMSF growth factor
Created by: natkat on 2005-03-17



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