wound healing Flashcards
inflammatory response results from cellular injury that ruptures cells
trauma
environmental irritants
microorganisms
free radical damage
hypoxia
surgery
inflammation
prepates injured area for healing
leukocytes (neutrophils and macrophages) remove debris and provide growth factors
nutrients (proteins, glucose, vitamins) provide the building flocks for cells
clotting factors and platelets limit damage
plasma protein system
clotting cascade to prevent further bleeding. Kinin cascade produces bradykinin which causes pain, vasodilation, and vascular permeability. Complement cascade stimulates opsonins, chemotaxic factors, and anaphylatoxins which causes release of histamine
the vascular response: histamine and bradykinin stimulate vasodilation. increased blood flow causes heat, redness, pain and edema
cellular response: chemotaxis factors attract neutrophils to move to move to the capillary walls (migrate), phagocytosis
inflammatory response
reaction to tissue damage caused by injury or infection
redness, heat, pain, swelling, loss of function
fever: caused by endogenous pyrogens, prodromal, chill, defervescence stage (sweating)
exudate (drainage)
serous: watery, plasma like
fibrinous: clotted
serosanguinous: blood tinged
sanguineous: blood
suppurative/purulent: pus
chronic inflammation
continuous exposure to irritants could result in granuloma formation, giant cell formation, cancer
stages of wound healing
inflammation: 1-2 days
proliferation and new tissue formation: 2-8 weeks for maximum strength, may involve regeneration and resolution, repair with scar tissue, but loss of function
remodeling and maturation: up to two years
factors affecting wound healing
oxygenation: reduced in COPD and atherosclerosis
circulation: reduced in elderly, CHF, DM, MI
Hydration: reduced in illness, hydration and age
Age: accelerated in young and reduced in the elderly
Immunity: reduced in HIV, stress, infection
Medications: cortisone, chemotherapy, immunomodulator
types of wound healing
first intention: must be clean, able to approximate wound edges, fasted and preferred
second intention: used in contaminated wounds, large amount of tissue lost, very slow, large scare
third intention: rarely used, to close large wounds that are cleaned enough (skin grafting)
wound healing process
macrophages dissolve clots, clear debris add TGF-B (transforming growth factor beta) to stimulate collagen precursor to procollagen
VEGE (vascular endothelial growth factor) stimulates angiogenesis
MMP (matrix metalloproteinases) remodel collagen and fibrin
collagen lattice forms, granulation tissue fills in wound, hypertrophic scar tissue overfills wound. Cicatrization (maturation) may take 1-2 years. Collagen contracts and the scar tissue becomes lighter and smoother
dysfunctional healing
wounds may fail to close or may re-open due to poor wound healing conditions
non-union: failure to adherence
dehiscence: wound edges separate, expose underlying tissues
evisceration: underlying viscera are exposed
wounds may become infected
abscess: a walls pocket of infection
sinus tract: a narrow tunnel forms
cellulitis
necrosis and gangrene may occur
fibrin or dysfunctional collagen synthesis
fistula formation
adhesions
contractures
strictures
keloids
systemic markers of vascular inflammation
homocysteine level: elevated in reduced folate levels, b vitamins, riboflavin inhibits increased endothelial damage in arteries
C-reactive protein: increases to neutralize inflammatory chemicals low risk for cardiovascular events
infectious agents found in plaques
endothelial dysfunctions: lack of nitrous oxide
COPD emphysema
pathophysiology: chronic stretching of the alveoli due to obstruction of the bronchial passageways which prevents easy expulsion of gases causing a decrease in alveolar elasticity, causes a dead space in the lung tissue
barrel chest, pink puffer
increases risk of right side heart failure , fluid retention, pneumonia
these patienrs tend to adapt to the condition by increasing quantity of RBC’s altering the pigmentation of their skin
