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Wound Care 1
Wound Care
| Question | Answer |
|---|---|
| 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
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