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tissue/wound healing
patho exam 3
| Question | Answer |
|---|---|
| largest organ in the body | skin |
| how big is the skin? | 1.2-2.2 square meters, 4-5 kilograms (9-11 pounds) |
| functions of the skin | serves as first line of defense, waterproof barrier; minimizes excessive water loss; maintains thermoregulation; contains receptors for somatic sensations; participates in metabolism and activation vitamin D |
| how does the skin maintain thermoregulation? | blood is warmer than the environment, capillaries in dermis are open for more circulation on the skin |
| two layers of the skin | epidermis and dermis |
| epidermis | upper layer of skin |
| what is the epidermis composed of? | stratified squamous epithelial cells; keratinocytes; melanocytes, dendritic cells, tactile cells |
| tactile cells | sensory receptors for touch |
| stratum basale | have stem cells that keep dividing and removing cells from top layers |
| melanocytes | produce and inject melanin that determines color of skin |
| epidermis: keratinization | keratin is water-insoluble protein; keratinocytes filled with keratin; dead at surface |
| what does keratin do? | help keep water in the body |
| what does the dermis contain? | blood vessels, skin appendages; sensory receptors for pain, touch, temperature; smooth and skeletal muscle cells |
| what do the blood vessels in the dermis do? | supply nutrients and oxygen to epidermis |
| two layers of the epidermis | papillary layer (superficial), reticular layer (thicker and deeper) |
| papillary layer of dermis | loosely and irregularly organized connective tissue |
| components of papillary layer of dermis | fibroblasts, macrophages, plasma cells, mast cells, endothelial cells, adipose cells |
| reticular layer | dense connective tissue |
| dermal-epidermal junction | barrier against passage of substances into and out of the body; framework to restore architecture of the tissue |
| extracellular matrix | ground substance, tissue growth and wound healing, fibrous structural proteins, adhesive glycoproteins, glycosaminoglycans (GAGs) |
| fibrous structural proteins in ecm | collagen and elastin |
| adhesive glycoproteins | keeps things together |
| glycosaminoglycans | make matrix like gelatin |
| cell-matrix and cell-cell interaction | integrins, cytokines and growth factors |
| cell-matrix and cell-cell interaction: integrins | transmit information bidirectionally, bind extracellular substances, adhesion molecules |
| acute wound | 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; reepithelialization |
| partial thickness wound: reepithelialization | epithelial cells migrate to area and replicate by mitosis |
| full thickness wound | damage extends 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, endothelia cells; growth factors; cytokines |
| types of wound healing depends on | type of injury; extent of tissue loss; infection, necrotic tissue, or secondary tissue breakdown; types of cells involved |
| types of wound healing | primary intention (primary closure), secondary intention (secondary or spontaneous closure), tertiary (delayed primary closure) |
| primary intention (primary closure) | surgical closure of wound, little granulation tissue |
| repair of primary intention (primary closure) | formation of new ECM |
| regeneration of primary intention (primary closure) | reepithelialization |
| 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; contaminated wound cleaned, left open for drainage |
| is scarring greater in primary or secondary intention | primary intention |
| four phases of wound healing | hemostasis, inflammatory, proliferative, remodeling |
| chemical mediators in wound healing | cytokines, growth factors, nitric oxide |
| role of cytokines | initiate healing process, produce growth factors and cytokines, stimulate expression of growth factors, develop the ECM, coordinate intercellular communication |
| role of growth factors | stimulate growth, division, differentiation of other cells; regulate intercellular communication |
| role of nitric oxide direct effect | bacterial killing |
| role of nitric oxide indirect effect | modulate cytokine and growth factor activity |
| hemostasis goals | prevent additional tissue injury, prepare wound for healing and regeneration |
| hemostasis phases | platelet adhesion, platelet activation, platelet plug; fibrin clot formation, recruitment of phagocytic cells and wound debridement |
| steps of hemostasis | vessel constriction, primary hemostasis, secondary hemostasis, stable clot formation |
| inflammatory response goals | to clean the wound, prevent additional tissue injury, prepare wound for healing and regeneration, recruitment of phagocytic cells and wound debridment |
| what does a mast cell secrete? | histamine |
| proliferative phase goal | wound healing guided toward tissue repair |
| proliferative phase steps | granulation tissue: foundation for collagen-based matrix that replaces fibrin-based provisional matrix; fibroblasts: produce collagen, adhesive for ECM; myofibroblasts, endothelial cells: angiogenesis; reepithelialization: regeneration of keratin |
| vascular endothelial growth factors mediating angiogenesis | cell mobilization, VEGF secretion, angiogenesis, wound bed |
| 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 |
| the stages of wound healing with cellular involvement | inflammatory, proliferative, remodeling |
| inflammatory phase length | 4-6 days |
| inflammatory phase steps | hemostasis (platelets), inflammation (master cells), neutrophils and monocytes, macrophages |
| proliferative phase length | 4-24 days |
| proliferative phase steps | skin resurfacing (keratinocytes), dermal restoration (endothelial cells, fibroblasts) |
| remodeling phase length | 21 days- 2 years |
| remodeling phase steps | keratinocytes, myofibroblasts; endothelial cells |
| local factors that impede wound healing | blood flow and hypoxia, infection, infection and contamination, radiation exposure, movement/tension, desiccation, excessive edema, denervation |
| systemic factors that impede wound healing | advances age, malnutrition, nutritional status, immune deficiency, smoking, medications, metabolic status |
| what does radiation exposure cause? | damage DNA of cells |
| what medications can impeded wound healing? | glucocorticoids delay healing, anticoagulants also delay |
| 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 |
| effect of negative nitrogen balance | impaired immune and inflammatory response, delayed wound healing; increased wound infection, diminished angiogenesis |
| vitamin and mineral deficiencies | associated with chronic, non-healing wounds in nutritionally debilitated individuals |
| corticosteroids promote breakdown of... | carbohydrates, fats, proteins |
| corticosteroids | anti-inflammatory action impedes inflammatory phase of wound healing, various negative effects |
| antineoplastic drugs | potent immunosuppressants; impair reepithelialization, granulation tissue formation, angiogenesis |
| diabetes mellitus | insufficient insulin, insulin resistance, or both |
| hyperglycemia with untreated diabetes | chronic macrovascular disease, atherosclerosis; tissue ischemia and hypoxia; thickening of basement membranes: diabetic lesions |
| diabetes mellitus with impaired perfusion | impaired granulocyte function and chemotaxis, reduced ability to fight infection |
| diabetes mellitus: sensory neuropathy | reduces pain sensation associated with wounds |
| abnormal wound healing: excessive | abnormally high connective tissue deposition resulting in altered tissue structure and function |
| types of abnormal wound healing: excessive | fibrosis, keloids, hypertrophic scars, contractures |
| fibrosis | replacement of normal tissue excessive, nonfunctional collagen or scar tissue, excess synthesis and/or delayed degradation |
| keloids | lesions of dermal scar or fibrotic tissue |
| hypertrophic scars | excess fibrotic tissue, raised above level of surrounding, grow within boundaries of original injury; regress spontaneously |
| 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 tissue to wound failure |
| abnormal wound healing: deficient: wound dehiscence types | extrafascial, fascial |
| wound dehiscence: extrafascial | partial or complete separation of outer layers of sutured wound; underlying fascial layer remains intact |
| wound dehiscence: fascial | evisceration; separation of fascial layers |
| clinical manifestations of impending wound disruption | signs of infection, absence of healing ridge by fifth to ninth postoperative day, seroma or hematoma formation, increase in serous discharge |
| do chronic nonhealing wounds proceed through the healing process? | no |
| chronic nonhealing wounds progress through? | healing process by cannot maintain structural and functional integrity |
| when do chronic nonhealing wounds arrest? | in inflammatory phase |
| when do chronic nonhealing wounds harbor? | bacteria; imbalance between neutrophilic proteolytic enzymes and their inhibitors |
| chronic non healing wounds have increased levels of? | inflammatory mediators; chronic inflammation, necrosis, fibrosis |
Created by:
camrynfoster