click below
click below
Normal Size Small Size show me how
patho exam 3
tissue and wound healing
| Question | Answer |
|---|---|
| the skin is the largest | organ in the body |
| functions of the skin | serves as the first line of defense; waterproof barrier minimizes excessive water loss maintains thermoregulation contains receptors for somatic sensations participates in metabolism and activation vitamin D |
| two layers of the skin | epidermis and dermis |
| epidermis is the | upper layer of the skin |
| upper layer of the skin | stratified squamous epithelial cells; keratinocytes melanocytes, dendritic cells, tactile cells |
| tactile cells | sensory receptors for touch, cells of defense |
| keratinization | keratin is water-insoluble protein - helps keep water in the body keratinocytes filled with keratin; dead at surface |
| as you age, | ability to replace keratinocytes decreases |
| dermis contains | blood vessels skin appendages sensory receptors for pain and pressure, touch and temperature (sweat glands) smooth and skeletal muscle cells |
| two layers of the dermis | papillary layer which is superficial reticular layer which is thicker and deeper |
| papillary layer is | loosely and irregularly organized CT |
| papillary layer contains | fibroblasts, macrophages, plasma cells, mast cells, endothelial cells, adipose cells |
| reticular layer is | dense CT |
| dermal-epidermal junction (DEJ) is a barrier against | passage of substances into and out of the body |
| dermal-epidermal junction (DEJ) is framework to | restore architecture of the tissue |
| extracellular matrix (ECM) is | everything outside the cells, ground substance |
| extracellular matrix (ECM) promotes | tissue growth and wound healing |
| extracellular matrix (ECM) has | fibrous structural proteins: collagen and elastin (main fibrous proteins) |
| collagen | keeps structure |
| elastin | skin can move when needed |
| extracellular matrix (ECM) has | adhesive glycoproteins glycosaminoglycans (GAGs) |
| cell-matric and cell-cell interaction | integrins cytokines and growth factors (allow healing of skin) |
| integrins | transmit information bidirectionally bind extracellular substances adhesion molecules |
| acute wound | occurs suddenly or over brief period restoration of structural and functional integrity in 4-6 weeks (restored very quickly) |
| 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 is intact |
| partial thickness wound has | reepithelialization |
| reepithelialization | epithelial cells migrate to area and replicate by mitosis |
| full thickness wound damage | extends through epidermis and dermis |
| full thickness wound possibly extends into | subcutaneous tissue, muscle, bone |
| full thickness wound has | scar formation |
| wound healing phases | hemostasis inflammation proliferation/granulation remodeling/maturation |
| chemical mediators | neutrophils, macrophages, lymphocytes, platelets, keratinocytes, fibroblasts, endothelial cells growth factors cytokines |
| types of wound healing depends on | type of injury extend of tissue loss infection, necrotic tissue, or secondary tissue breakdown type of cells involved |
| primary intention | primary closure |
| primary intention includes | surgical closure of wound repair: formation of new ECM regeneration: reepithelialization little granulation tissue |
| secondary intention | secondary or spontaneous closure |
| secondary intention includes | 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 |
| tertiary intention includes | combination or primary and secondary intention contaminated wound cleaned, left open drainage 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: important element for bacterial killing indirect effect: modulate cytokine and growth factor activity |
| goals of hemostasis (1) | prevent additional tissue injury prepare wound for healing and regeneration |
| first phase of hemostasis | platelet adhesion, platelet activation, platelet plug |
| second phase of hemostasis | fibrin clot formation, recruitment of phagocytic cells and wound debridement |
| goals of inflammatory response (2) | to clean the wound prevent additional tissue injury prepare wound for healing and regeneration recruitment of phagocytic cells and wound debridement |
| goal of proliferative phase (3) | wound healing guided toward tissue repair |
| steps of proliferative phase | granulation tissue fibroblasts myofibroblasts endothelial cells reepithelialization |
| granulation tissue | foundation for collagen-based matrix that replaces fibrin-based provisional matric |
| fibroblasts | produce collage, adhesive proteins for ECM, develop and contract proteins to become myofibroblasts |
| endothelial cells | angiogenesis (neovascularization) |
| reepithelialization | regeneration of keratin, supply of blood/nutrients is restored |
| remodeling phase (4) | restores structural and functional integrity of skin - final process of regeneration dermal matrix not regeneration; mended |
| steps of remodeling phase (4) | 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 | 4-6 days |
| proliferative | 4-24 days |
| remodeling | 21 days-2 years |
| local factors that impede wound healing | blood flow of hypoxia infection or area infection and contamination radiation and contamination radiation exposure: damage DNA movement/tension desiccation: how dry is wound excessive edema denervation: cuts near nerve |
| systemic factors that impede wound healing | advanced age: higher age makes it harder to heal malnutrition nutritional status immune deficiency: decrease immunological cells smoking medications: glucocorticoids metabolic status: autoimmune disorders, diabetes |
| hypoxia delays or stops | wound healing process |
| hypoxia is the | leading cause of wound infection |
| hypoxia inhibits | fibroblast activity, collagen deposition in matrix |
| infection and contamination | badly contaminated wounds may overwhelm host defenses, surgical wound handling |
| contamination | necrotic tissue, foreign or exogenous material, endogenous substances |
| nutritional status plays a major role in | wound healing |
| essential macronutrients | carbohydrates and fats |
| negative nitrogen balance is | important to angiogenesis process |
| effect of negative nitrogen balance | impaired immune and inflammatory responses delayed wound healing; increased wound infection diminished angiogenesis |
| vitamin and mineral deficiencies is associated with | chronic, nonhealing wounds in nutritionally debilitated individuals |
| medications: corticosteroids promotes | breakdown of carbohydrates, fats, proteins |
| medications: corticosteroids | anti-inflammatory action impedes inflammatory phase of wound healing, various negative effects |
| medications: antineoplastic drugs | potent immunosuppressants impair reepithelialization, granulation tissue formation, angiogenesis |
| diabetes mellitus is | insufficient insulin, insulin resistance, or both |
| diabetes mellitus induces | hyperglycemia with untreated diabetes |
| hyperglycemia with untreated diabetes | chronic macrovascular disease atherosclerosis; tissue ischemia and hypoxia (delays blood perfusion to injured area) thickening of basement membranes: 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: excessive | abnormally high CT deposition resulting in altered tissue structure and function |
| fibrosis | replacement of normal tissue is excessive, nonfunctional collagen or scar tissue excess synthesis and/or delayed degradation |
| keloids | lesions of dermal scar or fibrotic tissue |
| hypertrophic scars are formed by | excessive fibrotic tissue |
| hypertrophic scars are | raised above level of surroundings |
| hypertrophic scars grow | within boundaries of original injury; regress spontaneously |
| contractures are caused by | abnormal exaggeration of wound contraction - too much activity of fibroblasts |
| contractures affects | shrinking scars severely deform wound; reduce mobility compromise mobility of involved joints |
| abnormal wound healing: deficient | insufficient deposition of dermal CT matrix weakens tissue to wound failure |
| wound dehiscence | extrafascial fascial |
| extrafascial | partial or complete separation of outer layers of sutured wound; underlying fascial layer remains intact |
| fascial | evisceration; separation of fascial layers |
| CMs of impending wound disruption | signs of infection absence of healing ridge by fifth to ninth post-op day seroma or hematoma formation increase in serous discharge |
| chronic nonhealing wounds | do not proceed through healing process progress through healing process but can't maintain structural and functional integrity arrest in inflammatory phase |
| chronic nonhealing wounds cont. | harbor bacteria; imbalance between neutrophilic proteolytic enzymes and their inhibitors increased levels of inflammatory mediators; chronic inflammation, necrosis, fibrosis |