FPRS wound healing and scar revision Flashcards

1
Q

What are the layers of the skin from superficial to

deep?

A

● Epidermis
● Basement membrane
● Dermis (papillary and reticular)
● Subcutis

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2
Q

What are the layers of the epidermis from superficial to deep?

A
● Stratum corneum
● Stratum lucidum
● Stratum granulosum
● Stratum spinosum
● Stratum basale
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3
Q

What are epidermal appendages?

A

Skin-associated structures including hair follicles, apocrine
glands, sebaceous glands, and eccrine (sweat) glands

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4
Q

What is the predominant type of collagen in the

basement membrane?

A

Type IV collagen

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5
Q

What are the three phases of wound healing?

A

Inflammation, proliferation, and remodeling. Some authors

also include hemostasis as the first phase.

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6
Q

What are four general categories of wound

healing?

A

● Healing by primary intention: Two wound edges are
brought together as the primary intention of the
surgeon.
● Delayed primary healing: Two wound edges are not
brought together immediately but are reapproximated
and closed at a later time
● Healing by secondary intention: A full-thickness wound
where the edges are not reapproximated and the wound
is allowed to heal by granulation and contracture
● Epithelialization Occurs in partial-thickness wounds as
epithelial cells migrate and replicate over the wound.

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7
Q

What cell types are primarily involved in the inflammatory phase?

A

After vasoconstriction and subsequent vasodilation, polymorphonuclear neutrophils arrive and predominate for the first 24 to 48 hours after injury. Following this, monocyte
migration occurs.

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8
Q

What cell type synthesizes collagen?

A

Fibroblasts

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9
Q

What cell type is responsible for wound contraction during healing?

A

Myofibroblasts containing microfilaments capable of pro-
ducing contractile forces. These cells predominate the fibroblast population during the second week of wound
healing.

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10
Q

What major events occur during the proliferative

phase of wound healing?

A

Re-epithelialization, neovascularization, collagen deposition, and wound contraction

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11
Q

During which phase of healing are keratinocytes,
fibroblasts, and endothelial cells recruited to the
wound?

A

Proliferative phase

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12
Q

During the proliferative phase, which cytokine

modulates angiogenesis and neovascularization?

A

Vascular endothelial growth factor (VEGF)

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13
Q

How does hyperbaric oxygen therapy encourage

wound healing?

A

It promotes angiogenesis, fibroblast proliferation, leukocyte
activity, and is synergistic with antibiotic therapy.

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14
Q

What is the predominant type of collagen in an

early scar?

A

Type III collagen

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15
Q

What is the approximate tensile strength of a

healing wound at 3 months?

A

50% of normal tissue

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16
Q

When is the remodeling phase of wound healing

usually complete?

A

12 months

17
Q

What are the tenets of Halsted?

A

● Gentle handling of tissues
● Aseptic technique
● Sharp anatomical dissection of tissues
● Careful hemostasis, using fine, nonirritating suture
materials in minimal amounts
● The obliteration of dead space in the wound
● Avoidance of tension

18
Q

How can local tissue factors impact wound

healing?

A

Wound healing is compromised by any tissue effect that
decreases oxygenation, increases infection risk, prolongs
inflammation, delays neovascularization, or otherwise alters
the normal process of healing. Examples include local
infection, ischemia resulting from pressure necrosis (e.g.,
diabetic neuropathy, hematoma), alteration in tissue structure resulting from radiation therapy, locally destructive processes (neoplasia, wound desiccation).

19
Q

What patients should be counseled about increased risk for postoperative infection or wound breakdown?

A

Patients with medical comorbidities, medications, or history
of recent treatments, which alter the normal healing
process or suppress the immune system. For example,
patients who have undergone chemotherapy and radiation
therapy, are taking immunosuppressants, or have diseases
that affect the vasculature (e.g., peripheral vascular disease,
diabetes, tobacco dependence.) are at increased risk for
wound complications.

20
Q

What are relaxed skin tension lines?

A

They are the lines of minimal tension on the skin. They run parallel to natural wrinkle lines and are usually perpendicular to the force of action of the underlying muscles of facial expression.

21
Q

What are some of the technique- and patient-related factors that may lead to an aesthetically unacceptable scar?

A

● Patient variables: Diabetes, chronic steroid use, systemic
vasculitis, vitamin deficiency, poor overall nutrition,
chronic renal disease, wound infection, collagen vascular
disease, sun exposure
● Technical variables: Failure to clean the wound adequately,
excessive tension on epidermal sutures, step-off between
wound edges, rough handling of tissue, prolonged suture
retention, failure to orient incision parallel to relaxed skin
tension lines, delayed wound closure

22
Q

What are some of the performance differences

between monofilament and braided suture?

A

Monofilament suture has “memory” and usually requires
more knots to secure a tie. Braided suture has more tensile
strength but creates more resistance through tissue,
induces a stronger inflammatory response, and is more
likely to serve as a reservoir for microorganisms.

23
Q

What type of surface contour is most favorable for

wound healing by secondary intention?

A

Concave surfaces

24
Q

What are some surgical options for scar revision?

A

Excision and closure with straight line, broken geometric
line, W-plasty, Z-plasty, or local flap; excision and placement
of a skin graft

25
Q

What medications may be injected into a scar to

improve its appearance?

A

Steroids (triamcinolone diacetate), antimitotic agents (5-FU

and bleomycin)

26
Q

What is the role of silicone in scar revision?

A

The mechanism by which silicone sheeting reduces the appearance of hypertrophic scars has not been clearly
elucidated. One hypothesis is that direct pressure exerted by silicone sheeting on the wound decreases scar hypertrophy. Another theory is that silicone’s ability to maintain a hydrated environment inhibits fibroblast production of
collagen and glycosaminoglycans.

27
Q

What is the primary difference between keloid

formation and hypertrophic scarring?

A

Keloids spread beyond the boundaries of the original scar,
whereas hypertrophic scars do not extend outside the
wound perimeter.

28
Q

Review some treatment options for keloids and

hypertrophic scars.

A

Occlusive dressings, intralesional steroid injections, cryo-
therapy, radiation therapy, 5-FU, BOTOX injection, tacrolimus, retinoic acid, laser therapy, re-excision combined with above treatments