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patho exam 3

tissue and wound healing

QuestionAnswer
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
Created by: leh195
 

 



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