Nur 231 Final Exam Review

NUR 231 FINAL EXAM REVIEW | Understand the pathophysiology, signs and symptoms, and complications of the following: Wound healing o Types of cellular healing o Resolution: minimal tissue damage, quick resolution of injury o Regeneration: tissue regeneration by new cells, only occurs if cells are able to regenerate o Replacement: original cell cannot regenerate  Result: normal cells are replaced by another type of cell (usually connective / scar tissue)  Can result in V fxn  Ex: cardiac tissue, nerve tissue o Healing precess:1st & 2nd intention o First intention: sutured (ex/ if you had stitches) o Second intention: “open healing”  Left to heal on its own  Increased fibrinous and scar tissue o Complications od healing o Loss of fxn o Contracture o Adhesions o Hypertrophic scar tissue formation (Keliod) o Ulceration o Metaplasia Inflammation process, exudate formation. 1 VASODILATION a Leads to greater blood flow to the area of inflammation; resulting in redness and heat 2 VASCULAR PERMEABILITY a Endothelial cells become “leaky” from either direct endothelial injury or via chemical mediators 3 EXUDATION a Fluid, proteins, RBCs, and WBCs escape from the intravascular space as a result of increased osmotic pressure extravascularly and increased hydrostatic pressure intravascularly Injury cells release chemical mediators vasodilation (increased blood flow) increased capillary permeability WBCs move to site of injury phagocytosis o Exudate: fluid collection at site of ^ vascular permeability o Serous: clear yellow fluid inflammatory would healing stage o Fibrinous: high amounts of fibrin (clotting factor) o Purulent: many dead WBC’s (pus)- gen sign of infection (can be green/yellow etc) o Abscess: “walled off”, protected purulent exudate. Usually needs I&D because abx can’t get to it o Hemorrhagic: if injury causes artery/vein compromise, blood collects Burns o A thermal or non-thermal injury to tissue causing acute inflammation and destruction o *thermal, chemical, electrical o Effects of burns o Inflammation: vast increased capillary permeability causes massive fluid shifts resulting in: hypovolemia, tissue swelling (airway), pain, infection (loss of skin, first line of defense), metabolic needs (^ for needs of healing) Partial-thickness (first degree) Does not penetrate past epidermis No blister. Resolves quickly Ex: sunburn Deep Partial-thickness: (second degree) Complete epidermis and part of dermis affected Blistering of epidermis Heals, but scar may remain if extensive ^ future risk of cancers in some individuals Full-thickness: (third degree) Damage through epidermis and dermis, extending into connective tissue/ nerve/ bones/ vasculature Often results in permanent disability Hemostasis “the stopping of flow of blood”  Tissue damage initiates coagulation cascade  Tissue damage vasoconstriction/vasospasm o Inhibits blood flow to allow platelet plug  Thrombocytes adhere to tissue underlying damage o Create plug; attract coagulation factors  Coagulation: inactive prothrombin & fibrinogen combine with platelets and RBCS  activate cascade to form clot COAGULATION CASCADE  Ca2+ (essential cofactor)   Prothrombin activator   Prothrombin thrombin (Vitamin K is required for synthesis)   Fibrinogen fibrin   Insoluble fibrin clot Hypersensitivity reactions o Type I: Allergic Reaction o Histamine, IgE mediated, Mast cell Reaction o Ex: Allergic, Anaphylaxis(life0threating) o Vasodilation, capillary permeability (edema), airway obstruction, hypoxia o *systemic vasodilation Low BP o *tissue edema bronchial edema o Signs & Sx  *early: pruritis, sensation, coughing, SOB  *late: dizziness, fainting, low BP, hives, edema o Type II: Cytotoxic (ABO incompatibility)