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Wound Care 1

Wound Care

Function of the skin Protection from infection/injury, Prevention of loss of body fluids, Regulation of body temp Sensory contact with environment
PRISH Pain, Redness, Impairment, Swelling, Heat
Primary Intention Wound edges are adjacent via sutures, staples, or tape Minimize scarring
Secondary Intention Wound allowed to granulate, Results in Broader scar, Wound care daily
Tertiary Intention Wound is clean, debrided and observed for 3-5 days, Left open due to delay in initial presentation, bites or obviously infected wounds
Phases of wound healing Inflammatory (up to 20 days), Proliferative (11 mo), Remodeling (2 yrs)
Initial reactions to a wound Vascular and cellular responses
Initial injury causes: vasodilation, fluid leakage into extravascular space and lymph, drainage blockage - leads to PRISH
Phases of Vascular response Vasoconstriction, plug formation and coagulation
Exposed fibrillar collage and thrombin from the injury cause: platelets to undergo activation, adhesion and aggregation
Amino acids that determine activation of platelets proline and hydroxyproline
When platelets adhere to the damaged vessel, they undergo degranulation and release cytoplasmic granules, releasing what? serotonin, ADP, thromboxane A2, fibrinogen, fibronectin and thrombospondin
What does ADP (adenosine diphosphate) do? attracts more platelets
What does thromboxane A2 do? promote platelet aggregation, degranulation and vasoconstriction
ADP and Thromboxane A2 form what? A positive feedback loop to promote formation of an unstable platelet plug
What inhibits platelet aggregation? Endothelial cells releasing prostacyclin
What is converted into fibrin Platelet derived fibrinogen
What does the fibrin plug do? Acts as a matrix for monocytes and fibroblasts
What is PDGF chemotactic for? migration of fibroblasts, smooth muscle cells, macrophages, monocytes, and neutrophils
Active platelets produce what factor for coagulation and activate what mechanism? Hagemen Factor 12 activating the intrinsic mechanism
Factor 12 activates what cascade of events? Conversion of Prothrombin to thrombin. Then thrombin converts fibrinogen to fibrin
How is a blood clot formed? Fibrin forms a loose mesh, then Factor 13 creates covalent cross links to make fibrin denser, The dense mesh catches platelets and RBCs to form the clot
What occurs after coagulation Neutrophil migration covering the affect area's walls with neutrophils
What releases histamine and what does it do Released by mast cells, basophils and platelets, Causes vasodilation and increase vessel wall permeability to allow fluid to escape from the vessel
2 categories of leukocytes PML/granulocytes and Mononuclear
Types of PML neutrophils, eosinophils, basophils
Preference for Dyes Neutrophils- no preference for dye (Most plentiful), Eosinophils- preference for red dye , Basophils- preference for basic dye
Types of mononuclear cells Monocytes - large cell, few granules and 1 nucleus; Lymphocytes - important for cell mediated immunity
Monocytes become what when they migrate from the vascular space to the tissue space Macrophages -- essential for wound healing; uses phagocytosis to kill pathogenic organisms; and are essential for angiogenesis and formation of granulation tissue
What are the chemical mediators of inflammation? Histamine, serotonin, kinins, and prostaglandins
What does serotonin do Potent vasoconstrictor - Later stages of healing: fibroblast proliferation and cross linking of collagen molecules
What do kinins do and give an example Example - bradykinin; Act as active peptides in areas of tissue destruction; Similar to histamine and rapidly destroyed
What do prostaglandins do Produced by all cells of the body Production of slow-reacting substance of anaphylaxis (SRS-A) that alter capillary permeability during the inflammatory reaction
What creates arachidonic acid and what does it do Converted from Phospholipids/phospholipase A2 Cyclo-oxygenases (COX) turn arachidonic acid into prostaglandins
What drugs inhibit the COX cascade NSAIDS, ASA, corticosteroids
What is the compliment system? Has 11 principle proteins that leak from capillaries into the tissues. An antibody binds with these and helps trigger a cascade that ultimately prevents damage by invading organisms or toxin
Modes of growth factors -Autocrine mode: exert their effect on originating cell – Paracrine mode: exert their effect on neighboring cells – Exocrine mode: exert their effect on distant cells
Characteristics of Chronic Inflammation May represent full thickness wounds covered by eschar/necrosis May represent an infected wound May contain foreign material (granuloma) Prolonged persistence of mononuclear cells May or may not have PRISH
Goals of proliferative phase - Re-epithelization creation of a permeability barrier – Neovascularization: establishment of an appropriate blood supply – Fibroplasia: reinforcement of the injured tissue
Re-epitheliazation involves: Migration of keratinocytes from wound margins in 24 hours Cells flatten and migrate in a pseudopodia fasion
Local Factors affecting epithelialization PVD, excessive surgical tension, ischemia, infection/colonization, pressure, neuropathy, radiation, foreign body reactions, hemostatic agents, extravasation of caustic drugs, adverse wound environments
Systemic Factors affecting epithelialization advancing age, malnutrition, protein deprivation, vitamin A/C deficiency, corticosteroids, anticoagulants, nicotine, NSAIDS, antineoplastic agents, chronic illness, endocrine disorders (DM), CT disorders, systemic vascular disease
3 ways that neovascularization occurs Generation of de novo vascular network Anastamosis to preexisting vessels (naturally occurring grafts) Coupling or recoupling of vessels throughout the wound space
What promotes angiogenesis? Epithelial cells are the most important cells of angiogenesis Fibronectin, heparin, and platelet factors (FGF) stimulate cell migration into wounds and stimulate epithelial cell migration and proliferation
What does fibroplasia do? Reinforces the injured tissue - fibroblasts migrate into wound within 48-72 hours to create granulation tissue and regenerate the dermal matrix Actin filaments allow movement and contractile strength
What modulates fibroblast proliferation PDGF, EGF (Epidermal), FGF (fibroblast)
What is the role of myofibroblasts? provide structure and synthesizes fibronectin, collagen, GAGs, thrombospondin, and others to alter shape
What stimulates fibronectin synthesis and what is the result? Thrombin and EGF stimulate fibronectin synthesis and secretion Fibronectin allows fibroblasts to bind to the extracellular network
2 roles of fibroblasts Migration and production of large amounts of matrix material (collagen, proteoglycans and elastin)
Most populous Types of collagen in dermis Type I: normal adult dermis Type III: most predominant synthesized collagen in wound healing; appears 48-72 hours after wound creation
2 phases that occur during granulation tissue phase Fibroplasia and Angiogensis
Importance of granulation tissue Process begins 3-4 days after wound creation - replaces provisional matrix. Is highly cellular, highly vascularized mixture of fibroblasts, endothelial cells, and macrophages Provides good integrity to wound site and very resistant to infection
3 elements of connective tissue Cells , Fibers and Amorphous Ground Substance (the last 2 form the extracellular matrix)
What is amorphous ground substance amorphous viscous gel secreted by fibroblasts that occupies the space between cells and fiber of CT
Function of ground substance Determines compliance, flexibility, and integrity of the dermis Provides strength, support, and density to tissue and reduces friction between CT fibers Protects from tissue invasion Transports cellular waste products, electrolytes and water
Characteristics of Wound Contraction Full thickness wounds begin contracting as soon as 2 weeks and reduces wound by up to 40% Myofibroblasts (mediated by actin) are the predominant mediator of this process and main cell in granulation tissue - fibronectin assists
Remodeling phase involves: Process begins after functional barrier restored Dermal macromolecules (fibronectin, hyaluronic acid, proteoglycans, and collagen) deposited during repair makes scaffold for cellular migration/tissue support Tensile strength 40% at 1 mo, 80% after 1 yr
What happens to collagen during remodeling? Lysis of Type 3 and synthesis of Type 1
Characteristics of Collagen Greek for the word “glue” Primary structure, strength and form of dermis 70% of the dry weight of skin High tensile strength and resist stretching Not homogenous => scarring Made of polypeptide chains
Type 1 Collagen Most prevalent (90%) In dermis and tendons 3 alpha-helix peptides (2 alpha-1, 1 alpha-2) diameter = 100-500 nm
Type 3 collagen Found in embryonic CT, reticular fibers 3 alpha-1 helixes 40-60nm
Biosynthesis of Collagen part 1 begins with nucleus of fibroblasts - requires magnesium and zinc for translation of DNA to RNA for protein Proline and lysine added to polypeptide chain for hydroxylation, which occurs on ribosomes and requires O2, Iron, and Vit C Creates triple helix
Biosynthesis of Collagen part 2 galactose joins triple helix and becomes procollagen Propeptides are removed via peptidase to create tropocollagen to overlap in a staged fashion Collagenous fibrils combine to form fibers and align according to lines of stress
3 types of collagenase Bacterial collagenase - works on fragmented collagen Lysosomal proteases- works on fragmented collagen Tissue collagenase - work to restore the postinjury dermis toward its normal state
What do all tissue collagenases require to function? calcium
What does hyaluronidase and other proteases do? Expose collagen fibrils for collagenases
Cells that secrete tissue collagenase are: epithelial cells, fibroblasts and macrophages, and leukocytes
Elastin characteristics Long, thin and highly contractile/hydrophobic (2% of dermal protein) Elastin, lipids, and glycoproteins form microfibrils for a scaffold for fiber orientation - microfibrils are surrounded by elastin to form solid elastic
Orientation of Elastic fibers The wavy elastic fibers are entwined among collagenous fibers Orientation of elastin varies form a horizontal arrangement in the deep dermis to more vertical arrangement closer to the epidermis Good for providing recoil
Reticular fibers characteristics Very fine, thin fibrils Form a supporting framework on which collagenous fibers are laid down Least prevalent fiber found in CT
Factors affecting CT repair Blood supply, lack of proteins, minerals, enzymes, and amino acids, Circulating hormones, Mechanical stress, Infection, Hypoxia, Lack of cellular oxygen (poor perfusion), Antineoplastic agents, antibiotics (PCN), Radiation, Steroids, cold, Malnutrition
Nutritional factors affecting CT repair Vitamin C (collagen formation) Vit A required to potentiate epithelial repair and collagen synthesis; affects macrophage availability Zinc - epithelialization/cellular proliferation - wound is weaker
Leukopenia/neutropenia do what? Decreased macrophages, reducing turgor in skin after healing
What ameliorates steroid suppression of mitotic activity in fibroblasts? Systemic Vitamin A TGF-Beta (transforming growth factor)
Surgical techniques that accelerate wound healing Steri-strips prevention of hematoma using appropriate suturing skins to prevent dead space no strangulation of tissues
Occlusive dressings can: speed healing by 40% enhance keratinocyte migration through maintaining a moist environment rich with the growth factors present as well as preventing infection
Topical antimicrobials effects inhibit cell proliferation/migration (do no harm)
Hypertrophic scarring characteristics Excessive growth of scar tissue withinthe scar margins - mounded and raised - hypervascularized, painful, and an overgrowth of collagen can form contractures Contain fibroblasts with abnormal GF due to TGF-beta Interferon/TGF-Beta antagonists to treat
Keloid Scarring characteristics Excessive growth of scar tissue beyond the scar margins Located more often on upper trunk, face, neck, and ears More common in dark skin populations
Created by: rjchokito