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patho
tissue and wound healing chapter 39
| Question | Answer |
|---|---|
| structure of skin | largest organ in the body 1.2 - 2.2 Sq meters 4 - 5 kilograms (9-11 lbs) |
| functions of the skin | serves as first line of defense; waterproof barrier minimizes excessive water loss maintain thermoregulation contains receptors for somatic sensations participates in metabolism and activation of vitamin D |
| two layers of the skin | epidermis and dermis |
| epidermis | upper layer of skin |
| what is epidermis made of | stratified squamous epithelial cells; keratinocytes |
| types of cells in the epidermis | melanocytes, dendritic (Langerhans) cells. Tactile (merkel) cells: sensory receptors for touch |
| keratinization of epidermis | keratin is water-insoluble protein keratinocytes filled with keratin; dead at surface helps to keep water in the body |
| dermis | below the epidermis |
| dermis contains | blood vessels skin appendages sensory receptors for pain, touch, temperature, smooth and skeletal muscle |
| two layers of the dermis | papillary layer (superficial) reticular layer (thicker and deeper) - forms connective tissue |
| papillary layer | loosely and irregularly organized connective tissue fibroblasts, macrophages, plasma cells, mast cells, endothelium cells, adipose cells. it is more flexible and better able to get nutrients |
| reticular layer | dense connective tissue |
| Dermal - epidermal junction (DEJ) | barrier against passage of substances into and out of the body framework to restore architecture of the tissue |
| extracellular matrix (ECM) | ground substance tissue growth and wound healing fibrous structural proteins collagen (keeps structure) and elastin (allows for flexibility) adhesive glycoproteins glycosaminoglycans (GAGs) |
| cell-matrix and cell-cell interactions | integrins and cytokines and growth factors |
| integrins | transmit information bidirectionally bind extracellular substances adhesion molecules |
| acute wound | 4-6 weeks occurs suddenly or over brief period restoration of structural and functional integrity in four to six weeks |
| chronic wound | occurs over long period does not heal in organized and timely manner impairment of structural and functional integrity |
| partial thickness wound | damage extends through epidermis; dermis intact re-epithelialization: epithelial cells migrate to area and replicate by mitosis |
| full thickness wound | damage through epidermis and dermis possibly extends into subcutaneous tissue, muscle, bone scar formation |
| wound healing phases | hemostasis inflammation proliferation/granulation remodeling/maturation |
| chemical mediators | neutrophils, macrophages, lymphocytes, platelets, keratinocytes, fibroblasts, endothelial cells growth factors cytokines |
| type of wound healing depends on | type of injury extent of tissue loss infection, necrotic tissue, or secondary tissue breakdown type of cells involved |
| primary intention (primary closure) | surgical closure of wound repair: formation of new ECM regeneration: re-epithelialization little granulation tissue |
| secondary intention (secondary or spontaneous closure) | full thickness wound heals without closure attempt large amount of granulation tissue longer healing time; larger scar skin grafting; skin substitutes |
| tertiary intention (delayed primary closure) | combination of primary and secondary intention contamination wound cleaned, left open drainage (to avoid infection) scarring> primary intention and < secondary intention |
| role of chemical mediators-cytokines | initiate healing process produce growth factors and cytokines stimulate expression of growth factors develop the ECM coordinate intercellular communication |
| role of chemical mediators-growth factors | stimulate growth, division, differentiation of other cells regulate intercellular communication |
| role of chemical mediators-nitric oxide | direct effect: bacteria killing indirect effect: modulate cytokine and growth factor activity |
| hemostasis goal | prevent additional tissue injury prepare wound for healing and regeneration |
| phases of hemostasis | 1. platelet adhesion, platelet activation, platelet plug 2. fibrin clot formation recruitment of phagocytic cells and wound debridement |
| inflammatory response goals | to clean the wound prevent additional tissue injury prepare wound for healing and regeneration recruitment of phagocytic cells and wound debridement mast cells |
| what do mast cells do | secrete histamine signal inflammatory response |
| proliferative phase goal | wound healing guided toward tissue repair |
| steps proliferative phase - granulation tissue | foundation for collagen-based matrix that replaces fibrin-based provisional matrix |
| steps proliferative phase - fibroblasts | produce collagen, adhesive proteins for ECM (opening) |
| steps proliferative phase - myofibroblasts | help to close the wound |
| steps proliferative phase - endothelial cells | angiogenesis (neovascularization) new vessel formation |
| re-epithelialization | regeneration of keratinocytes |
| remodeling phase of wound healing | restores structural and functional integrity of skin dermal matrix not regenerated; mended |
| remodeling phase of wound healing steps | wound contraction and closure continuous turnover of collagen decreased capillary density declining cellular content mature scar tissue devoid of skin appendages maturation of scar tissue continues for minimum of one year |
| length of stages of wound healing- inflammatory | 4-6 days |
| length of stages of wound healing- proliferative | 4-24 days |
| remodeling | 21 days-2 years |
| local factors that impede wound healing | blood flow and hypoxia infection and contamination radiation exposure movement/tension desiccation (dryness) excessive edema denervation |
| systemic factors that impede wound healing | advanced age ( older = harder to heal) malnutrition nutritional status immune deficiency smoking medications (glucocorticoids) metabolic status (autoimmune disorders, diabetes) |
| hypoxia | delays or stops wound healing process, leading cause of wound infection, inhibits fibroblast activity, collagen deposition in matrix |
| infection and contamination | badly contaminated wounds may overwhelm host defenses. surgical wound healing |
| contamination | necrotic tissue, foreign or exogenous material, endogenous substances |
| nutritional status | major role in wound healing |
| essential macronutrients | carbohydrates and fats |
| effective negative nitrogen balance | impaired immune and inflammatory responses delayed wound healing; increased wound infection diminished angiogenesis |
| vitamin and mineral deficiencies | associated with chronic, non-healing wounds in nutritionally debilitated individuals |
| medications - corticosterioids | promote breakdown of carbohydrates, fats, proteins anti-inflammatory action impedes inflammatory phase of wound healing various negative effects |
| medications - anti-neoplastic drugs | potent immunosuppressants impair re-epithelialization, granulation tissue formation, angiogenesis |
| metabolic status - Diabetes mellitus | insufficient insulin, insulin resistance, or both |
| DM - hyperglycemia with untreated diabetes | chronic macrovascular disease atherosclerosis; tissue ischemia and hypoxia thickening of basement membrane: diabetic lesions |
| DM - with impaired perfusion | impaired granulocyte function and chemotaxis reduced ability to fight infection |
| DM - sensory neuropathy | reduces pain sensation associated with wounds |
| Abnormal wound healing - excess | abnormally high connective tissue deposition resulting in altered tissue structure and function |
| Abnormal wound healing (excess) - fibrosis | replacement of normal tissue is excessive, nonfunctional collagen or scar tissue excess synthesis and/or delayed degradation |
| Abnormal wound healing (excess)- keloids | lesions of dermal scar or fibrotic tissue |
| Abnormal wound healing (excess) - hypertrophic scars | excess fibrotic tissue raised above level of surrounding grow within boundaries of original injury; regress spontaneously |
| Abnormal wound healing (excess) - contractures | abnormal exaggeration of wound contraction shrinking scars severely deform wound; reduce mobility compromise mobility of involved joints |
| abnormal wound healing - deficient | insufficient deposition of dermal connective tissue matrix weakens tissues to wound failure |
| abnormal wound healing (deficient) - wound dehiscence | extrafascial: partial or complete separation of outer layers of sutured wound; underlying fascial layer remains intact fascial: evisceration; seperation of fascial layers |
| abnormal wound healing - CM of impending wound disruption | signs of infection absence of healing ridge of 5th-9th postoperative day seroma or hematoma increase in serous discharge |
| abnormal wound healing (deficient) - chronic non-healing wounds | -dont go through healing process -progress through healing process but cannot maintain structural and functional integrity -arrest in inflammatory -harbor bacteria; imbalance between neutrphilic proteolytic enzymes and their inhibitors |
| abnormal wound healing (deficient) - chronic non-healing wounds can cause | increased levels of inflammatory mediators; chronic inflammation, necrosis, fibrosis |
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ago24