Wound Healing Flashcards

1
Q

Wound healing occurs in non-overlapping phases: Inflammatory
Proliferative
Remodeling

A

F
Overlapping. Phase order is correct.
sometimes haemostasis added as the first stage to make 4 stages

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2
Q

The depth of the wound determines the degree of contraction and the source of keratinocytes used for re-epithelialisation.

A

T

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3
Q

Sharp wounds created by scalpels heal faster than wounds created by destructive or ablative methods.

A

T

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4
Q

Platelets are the first cell to appear in the healing process.

A

T

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5
Q

Macrophages are the most important cell in the healing process.

A

T

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6
Q

Older patients tend to heal faster.

A

F
Slower.
Patient age is a critical factor in wound healing

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7
Q

Older patients’ wounds tend to have less tensile strength which correlates with reduced amounts of collagen and a worse cosmetic outcome.

A

F

Better cosmetic outcome. Everything else is true.

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8
Q

An erosion is defined as a wound that involves structures deep to the dermis.

A

F

This is true for an ulcer. Erosion = wound with only epidermal loss.

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9
Q

A partial-thickness wound is an ulcer that involves the epidermis and varying parts of the dermis.

A

T

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10
Q

A full-thickness wound is one that involves all of the dermis and deeper structures.

A

T

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11
Q

In partial-thickness wounds, skin appendages remain and serve as reservoirs of epithelial cells to repopulate the epidermis.

A

T

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12
Q

Partial-thickness wounds heal to some extent by contraction, while there is minimal contraction in full-thickness wounds.

A

F

Other way around.

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13
Q

Second intention healing refers to the process by which an acute wound heals on its own.

A

T

Occurs primarily by contraction of myofibroblasts.

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14
Q

Primary intention healing occurs when a surgeon directs closure of the wound by approximating the wound edges.

A

T

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15
Q

The method by which a wound was created does not tend to influence its healing.

A

F Wounds created by sharp steel (eg. surgery) heal faster than others.

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16
Q

The process of wound haemostasis can be divided into two parts – development of a fibrin clot and coagulation.

A

T

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17
Q

Almost immediately after injury, polymorphonuclear leukocytes begin to adhere to the sticky endothelium of venules.

A

T

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18
Q

The term margination refers to the process by which the entire endothelial margin of the venules may be covered with neutrophils.

A

T

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19
Q

In the early inflammatory state, macrophages predominate at the site of injury.

A

F

Neutrophils and monocytes. Macrophages later.

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20
Q

As inflammation persists the number of neutrophils increases although macrophages predominate

A

F

Neutrophils decrease

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21
Q

The presence of wound contamination prolongs the neutrophilic presence within the wound.

A

T

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22
Q

Neutrophils release elastase and collagenase

A

T

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23
Q

Macrophages phagocytise, digest and kill pathogenic organisms, scavenge tissue debris and destroy remaining neutrophils

A

T

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24
Q

Macrophages tolerate severe hypoxia well.

A

T

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25
Q

The presence of macrophages may act to reduce collagen deposition

A

F

May enhance it

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26
Q

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

A

T

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27
Q

Mast calls help regular haemostasis by releasing substances such as platelet activiating factor, heparin, tryptase, chymase and t-plasminogen activator

A

T

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28
Q

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).

A

T

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29
Q

Keratinocyte migration is a late event in wound re-epithelialisation.

A

F

Early event, starts within 24hrs

30
Q

Keratinocytes use their surface integrin receptors to interact with fibronectin from the fibronectin-rich provisional matrix for their migration

A

T

31
Q

Migrating keratinocytes procude matrix metalloproteinases (MMPs) that act to degrade damaged matrix

A

T

32
Q

While epidermal cells are migrating, their proliferative potential remains intact.

A

F

Proliferative potential is inhibited.

33
Q

Within 3-5 days of the reformation of the epidermis the BMZ returns to normal

A

F

7-9days

34
Q

Collagen IV is the most abundant collagen in the BMZ.

A

T

35
Q

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

A

F

Collagen VII

36
Q

Laminins are the major collagenous extracellular matrix components

A

F

Non-collagenous

37
Q

All laminins are large heterotrimeric glycoproteins with the component chains together forming a symmetric cross-shaped structure

A

F

Asymmetrical

38
Q

Deficiency in the alpha chain of laminin-332 is associated with the blistering disease, junctional epidermolysis bullosa

A

F

Any chain can have a deficiency

39
Q

Laminin-511 has been located within the lamina densa and shows strong effects promoting human keratinocyte attachment

A

T

40
Q

At approximately day 4 fibroblasts start to migrate into the provisional matrix of the wound clot where they lay down collagen-rick matrix

A

T

fibroblasts in the wound edges begin to proliferate early after injury but donet migrate until day 4

41
Q

Granulation tissue begins to form within 5-7 days of injury.

A

F

3-4 days

42
Q

Granulation tissue consists of new vessels that migrate into the wound as well as the accumulation of fibroblasts and ground substances.

A

T

43
Q

The fibronectin matrix provides a scaffold for collagen fibrils and mediates wound contraction.

A

T

44
Q

Integrin receptors are involved only in the proliferative phase of wound repair.

A

F

Involved in all stages.

45
Q

For full-thickness wounds, contraction begins soon after wounding and peaks at 2 weeks.

A

T

46
Q

Partial-thickness wound contact less than full-thickness wounds and in direct proportion to their depth.

A

T

47
Q

Myofibroblasts within the wound align themselves along the lines of contraction.

A

T

48
Q

Angiogenesis refers to new vessel growth or neovascularisation by sprouting of pre-existing blood vessels.

A

T

49
Q

The remodelling phase of wound repair consists of the deposition of matrix materials and their subsequent change over time.

A

T

50
Q

The total amount of collagen increases early in repair, reaching a maximum between 1-2 weeks after injury.

A

F

2-3 weeks.

51
Q

Tensile strength will be 40% of strength prior to injury at 1 month

A

T

52
Q

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.

A

F

Never greater than 80% of its pre-injury strength.

53
Q

Type II collagen is the major collagen synthesised by fibroblasts in granulation tissue.

A

F

Type III collagen.

54
Q

Over the period of 1 year or more, the dermis returns to the stable pre-injury phenotype, consisting largely of type I collagen.

A

T

55
Q

Hyaluronic acid is found in the highest amounts in the first 7-10 days of wound healing.

A

F

4-5days.

56
Q

Hyaluronic acid serves as a stimulus for fibroblast proliferation and migration, and can absorb large amounts of water producing tissue oedema.

A

T

57
Q

Proteoglycans are non-sulfated glycosaminoglycans.

A

F

Sulfated. Hyalyronic acid is non-sulfated.

58
Q

Type III collagen is gradually replaced by type I collagen with ageing.

A

T

59
Q

Penicillin can impair wound strength.

A

T

60
Q

The use of occlusive dressings on acute wounds speeds healing and improves cosmesis but is NOT effective over primarily closed wounds

A

F

Is also true for primarily closed wounds

61
Q

Inflammation lasting longer than 2 weeks is chronic

A

T

Longer than the usual 2 and usually many weeks or months

62
Q

chronic inflammation occurs when a wound contains foreign bodies, necrotic tissure or is contaminated with pathogens

A

T

63
Q

chronic inflammation contains many granulocytes and mononuclear cells

A

F
characterised by absence of granulocytes but persistence of mononuclear cells, specifically lymphocytes, monocytes, and macrophages and later granulomaotus inflammation predominates

64
Q

The presence of bacterial products in the wound directly impairs healing

A

T

keratinocyte migration in chronic wounds may be directly inhibited by bacterial lipopolysaccharide

65
Q

Formation of the basement membrane zone (BMZ) is not essential for re-establishing the integrity and function of the skin

A

F

is essential

66
Q

Full thickness grafts inhibit wound contraction

A

T

much less contraction with FTSG than there is with flaps, SSG or secondary intention healing

67
Q

systemic steroids suppress wound healing

A

T
presence of systemic steroids in the first 3 days post-wounding blocks the initial inflammatory process.
causes longer healing time

68
Q

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

A

T

69
Q

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

A

T
Also Chronic debilitating illness, endocrine disorders, systemic vascular disorders, and connective tissue disease and old age

70
Q

Ascorbic acid (vitamin C) is a cofactor for the collagen cross-linking.

A

T

71
Q

wounds covered with an occlusive dressing healed up to 20% faster than those left exposed to air

A

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

72
Q

misuse of occlusive dressings can lead to the prolongation of healing

A

T

early removal or not removing gently can strip away newly fromed epithelium