Dermal Hypertrophies Flashcards

1
Q

Pathogenesis of hypertrophic scars and keloids

A

1) increased collagen and (TGF)-β synthesis by fibroblast
2) TGF-β very important proliferative phase of wound healing.
3) Expression of TGF-β1 or TGF-β2 leads to an increase in scarring,
4) expression of TGF-β3 is associated with a reduction in scarring
5) This has led to therapies, e.g. injections of recombinant TGF-β3, injections of mannose-6-phosphate which inhibits TGF-β1 and TGF-β2 signalling.
6) Proinflammatory cytokines interleukin-6 (IL-6) and IL-8 enhanced scarring
7) anti-inflammatory cytokine IL-10 decreased the amount of scar tissue.
8) propagation of a robust fibroblast response: PDGF, two transcription factors – homeobox B13 and early growth response protein 1, Wnt signaling pathway.
9) Fibroblasts from keloids increased expression of receptors for PDGF

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2
Q

Clinical features of conventional scars, hypertrophic scar and keloids

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3
Q
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4
Q

Define Vancouver scar scale

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5
Q

Name different scar scales

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6
Q

Pathology of scars

A

•histologic examination needed make this distinction between hypertrophic scars/kelloid in some (implications for treatment - eg radiation)
•In hypertrophic scars:
- increase in both the number of fibroblasts and the density of collagen fibers the dermis
- both of which are oriented parallel to the skin surface.
Keloids:
- whorls and nodules of strikingly thick, glassy, homogeneous collagen bundles
- densely packed fibrils and oriented haphazardly throughout the dermis (keloidal collagen).
-Early: abundant deposits of fibrillary collagen within the reticular dermis of keloids
-mature: often have the characteristic thick sclerotic collagen.
• In longstanding keloids - there may be a return to the earlier fibrillary pattern.
- keloidal collagen may be absent in up to 45% of keloids.
•In scars with no detectable keloidal collagen, histologic features that favor a keloid include:
•no flattening of the epidermis
•a lack of fibrosis within the papillary dermis

tongue-like advancing edge as the scar tissue extends through the reticular dermis
•a horizontal cellular fibrous band within the upper reticular dermis with a sharp demarcation from the normal-appearing papillary and reticular dermis
•prominent fascia-like fibrous bands in the deeper portion of the scar.
•Attempts to differentiate hypertrophic scars from keloids via immuno-histochemistry has led to conflicting results.
•In one study, nodules of α-smooth muscle actin (α-SMA)-positive cells (myofibroblasts) were only observed in hypertrophic scars, whereas another investigation found α-SMA expression in both hypertrophic scars (70%) and keloids (45%).

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7
Q

Histopathological differences between hypertrophic and keloids

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8
Q

Treatment of hypertrophic scars or keloids

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9
Q

Treatment of scars

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Treatment
•Prevention remains the best strategy in predisposed patients,
•There is limited evidence to support over-the-counter scar reduction products such as silicone sheeting and topical creams containing vitamin E.
•While potent topical corticosteroids are sometimes used to address pruritus, intra- lesional triamcinolone is the major first-line therapy for flattening hypertrophic scars and keloids.
•An alternative, especially for needle-averse individuals, is clobetasol propionate 0.05% cream under silicone dressing occlusion.
•Intralesional or topical corticosteroids may be combined with intralesional 5-fluorouracil.
•Surgical revision of both hypertrophic scars and keloids must be undertaken with caution given the high recurrence rates.
•Cryosurgery has been used successfully and is often combined with intralesional triamcinolone. Pulsed dye laser therapy has become popular as a modal- ity for postsurgical scar reduction and is associated with few side effects.
•Due to theoretical concerns regarding carcinogenesis, radiotherapy is reserved primarily for treatment-resistant keloids.

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10
Q

Pathogenesis of dupuytren disease

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11
Q

Clinical features of dupytren disease

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12
Q

Pathology of dupuytren disease

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13
Q

Treatment of dupuytren disease

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14
Q

Classify cutis verticis gyrata

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15
Q

Clinical features of cutis verticis gurata

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16
Q

Pathology of cutis verticis gyrata

17
Q

Differential diagnosis of cutis verticis gyrata

19
Q

Treatment of cutis verticis gyrata

20
Q

Disease associations with cutis verticis gyrata

21
Q

Pathogenesis of hyaline fibromatosis

22
Q

Clinical features of hyaline fibromatosis

23
Q

Differential diagnosis of hyaline fibromatosis

24
Q

Pathology of hyaline fibromatosis

25
Treatment of hyaline fibromatosis