Wound Healing Flashcards
Wound healing occurs in non-overlapping phases: Inflammatory
Proliferative
Remodeling
F
Overlapping. Phase order is correct.
sometimes haemostasis added as the first stage to make 4 stages
The depth of the wound determines the degree of contraction and the source of keratinocytes used for re-epithelialisation.
T
Sharp wounds created by scalpels heal faster than wounds created by destructive or ablative methods.
T
Platelets are the first cell to appear in the healing process.
T
Macrophages are the most important cell in the healing process.
T
Older patients tend to heal faster.
F
Slower.
Patient age is a critical factor in wound healing
Older patients’ wounds tend to have less tensile strength which correlates with reduced amounts of collagen and a worse cosmetic outcome.
F
Better cosmetic outcome. Everything else is true.
An erosion is defined as a wound that involves structures deep to the dermis.
F
This is true for an ulcer. Erosion = wound with only epidermal loss.
A partial-thickness wound is an ulcer that involves the epidermis and varying parts of the dermis.
T
A full-thickness wound is one that involves all of the dermis and deeper structures.
T
In partial-thickness wounds, skin appendages remain and serve as reservoirs of epithelial cells to repopulate the epidermis.
T
Partial-thickness wounds heal to some extent by contraction, while there is minimal contraction in full-thickness wounds.
F
Other way around.
Second intention healing refers to the process by which an acute wound heals on its own.
T
Occurs primarily by contraction of myofibroblasts.
Primary intention healing occurs when a surgeon directs closure of the wound by approximating the wound edges.
T
The method by which a wound was created does not tend to influence its healing.
F Wounds created by sharp steel (eg. surgery) heal faster than others.
The process of wound haemostasis can be divided into two parts – development of a fibrin clot and coagulation.
T
Almost immediately after injury, polymorphonuclear leukocytes begin to adhere to the sticky endothelium of venules.
T
The term margination refers to the process by which the entire endothelial margin of the venules may be covered with neutrophils.
T
In the early inflammatory state, macrophages predominate at the site of injury.
F
Neutrophils and monocytes. Macrophages later.
As inflammation persists the number of neutrophils increases although macrophages predominate
F
Neutrophils decrease
The presence of wound contamination prolongs the neutrophilic presence within the wound.
T
Neutrophils release elastase and collagenase
T
Macrophages phagocytise, digest and kill pathogenic organisms, scavenge tissue debris and destroy remaining neutrophils
T
Macrophages tolerate severe hypoxia well.
T
The presence of macrophages may act to reduce collagen deposition
F
May enhance it
Macrophages are essential for production of growth factors – they synthesize and secrete PDGF, fibroblast growth factor, vascular endothelial growth factor, TGF beta and TGF alpha
T
Mast calls help regular haemostasis by releasing substances such as platelet activiating factor, heparin, tryptase, chymase and t-plasminogen activator
T
The proliferation phase of wound healing involves re-epithelialisation (the creation of a permeability barrier), angiogenesis (the establishment of an appropriate blood supply) and fibroplasia (the reinforcement of injured tissue).
T
Keratinocyte migration is a late event in wound re-epithelialisation.
F
Early event, starts within 24hrs
Keratinocytes use their surface integrin receptors to interact with fibronectin from the fibronectin-rich provisional matrix for their migration
T
Migrating keratinocytes procude matrix metalloproteinases (MMPs) that act to degrade damaged matrix
T
While epidermal cells are migrating, their proliferative potential remains intact.
F
Proliferative potential is inhibited.
Within 3-5 days of the reformation of the epidermis the BMZ returns to normal
F
7-9days
Collagen IV is the most abundant collagen in the BMZ.
T
Collagen V proteins, also called anchoring fibrils span from the lamina densa to the upper papillaru dermis where that form a structure known as anchoring plaque
F
Collagen VII
Laminins are the major collagenous extracellular matrix components
F
Non-collagenous
All laminins are large heterotrimeric glycoproteins with the component chains together forming a symmetric cross-shaped structure
F
Asymmetrical
Deficiency in the alpha chain of laminin-332 is associated with the blistering disease, junctional epidermolysis bullosa
F
Any chain can have a deficiency
Laminin-511 has been located within the lamina densa and shows strong effects promoting human keratinocyte attachment
T
At approximately day 4 fibroblasts start to migrate into the provisional matrix of the wound clot where they lay down collagen-rick matrix
T
fibroblasts in the wound edges begin to proliferate early after injury but donet migrate until day 4
Granulation tissue begins to form within 5-7 days of injury.
F
3-4 days
Granulation tissue consists of new vessels that migrate into the wound as well as the accumulation of fibroblasts and ground substances.
T
The fibronectin matrix provides a scaffold for collagen fibrils and mediates wound contraction.
T
Integrin receptors are involved only in the proliferative phase of wound repair.
F
Involved in all stages.
For full-thickness wounds, contraction begins soon after wounding and peaks at 2 weeks.
T
Partial-thickness wound contact less than full-thickness wounds and in direct proportion to their depth.
T
Myofibroblasts within the wound align themselves along the lines of contraction.
T
Angiogenesis refers to new vessel growth or neovascularisation by sprouting of pre-existing blood vessels.
T
The remodelling phase of wound repair consists of the deposition of matrix materials and their subsequent change over time.
T
The total amount of collagen increases early in repair, reaching a maximum between 1-2 weeks after injury.
F
2-3 weeks.
Tensile strength will be 40% of strength prior to injury at 1 month
T
The tensile strength of a healed wound will gradually return to 100% of its pre-injury strength, although this process may take up to 1 year.
F
Never greater than 80% of its pre-injury strength.
Type II collagen is the major collagen synthesised by fibroblasts in granulation tissue.
F
Type III collagen.
Over the period of 1 year or more, the dermis returns to the stable pre-injury phenotype, consisting largely of type I collagen.
T
Hyaluronic acid is found in the highest amounts in the first 7-10 days of wound healing.
F
4-5days.
Hyaluronic acid serves as a stimulus for fibroblast proliferation and migration, and can absorb large amounts of water producing tissue oedema.
T
Proteoglycans are non-sulfated glycosaminoglycans.
F
Sulfated. Hyalyronic acid is non-sulfated.
Type III collagen is gradually replaced by type I collagen with ageing.
T
Penicillin can impair wound strength.
T
The use of occlusive dressings on acute wounds speeds healing and improves cosmesis but is NOT effective over primarily closed wounds
F
Is also true for primarily closed wounds
Inflammation lasting longer than 2 weeks is chronic
T
Longer than the usual 2 and usually many weeks or months
chronic inflammation occurs when a wound contains foreign bodies, necrotic tissure or is contaminated with pathogens
T
chronic inflammation contains many granulocytes and mononuclear cells
F
characterised by absence of granulocytes but persistence of mononuclear cells, specifically lymphocytes, monocytes, and macrophages and later granulomaotus inflammation predominates
The presence of bacterial products in the wound directly impairs healing
T
keratinocyte migration in chronic wounds may be directly inhibited by bacterial lipopolysaccharide
Formation of the basement membrane zone (BMZ) is not essential for re-establishing the integrity and function of the skin
F
is essential
Full thickness grafts inhibit wound contraction
T
much less contraction with FTSG than there is with flaps, SSG or secondary intention healing
systemic steroids suppress wound healing
T
presence of systemic steroids in the first 3 days post-wounding blocks the initial inflammatory process.
causes longer healing time
wound healing suppression caused by corticosteroids has been shown to be ameliorated with administration of local and systemic vitamin A, and a single injection of TGF-β
T
malnutrition, protein deprivation, and deficiencies of Zinc, vitamin A and vitamin C, medications such as corticosteroids, penicillamine, nicotine, NSAIDs, and antineoplastic agents can all interfere with wound healing
T
Also Chronic debilitating illness, endocrine disorders, systemic vascular disorders, and connective tissue disease and old age
Ascorbic acid (vitamin C) is a cofactor for the collagen cross-linking.
T
wounds covered with an occlusive dressing healed up to 20% faster than those left exposed to air
F
40% faster
May be by enhancement of keratinocyte migration with maintenance of a moist environment, prevention of infection, establishment of an electromagnetic current, or containment of wound fluid and the growth factors present within the wound bed
misuse of occlusive dressings can lead to the prolongation of healing
T
early removal or not removing gently can strip away newly fromed epithelium
