DD 03-07-14 08-09am Common Skin Tumors - Morelli Flashcards

1
Q

(Sentile) Cherry Hemangiomas - age / how common / what it means

A
  • Typically arise in middle age
  • Most common vascular tumor in adults
  • Generally no association w/ underlying disease
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2
Q

Cherry Hemangiomas - appearance / distribution

A

Distribution: primarily truncal

Number: typically mutiple; up to many hundreds

Primary lesion:

  • 1-4 mm in size
  • bright red, smooth-topped papules
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3
Q

Cherry Hemangiomas - Treatment

A

Superficial electrodesiccation

  • best for small lesions
  • may require local anesthesia

Liquid nitrogen followed by curettage

Shave biopsy

Pulse dye laser- best for small lesions

Other vascular lasers

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4
Q

Infantile Hemangioma (Capillary / Strawberry) - defn.

A

= Benign endothelial cell neoplasm

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5
Q

Infantile Hemangioma (Capillary / Strawberry) - demographics

A

= Most common soft tissue tumor of infancy (10-12% of infants)

More common in:

  • Girls (3-5:1)
  • Premature infants (<1.5 kg)
  • Infants of mothers post-chorionic villus sampling
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6
Q

Confirmation of “Dx” of Infantile Hemangioma

A
  • Positive stain with Glut-1, a placental antigen
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7
Q

Infantile Hemangioma (Capillary / Strawberry) - development

A
  • Occasionally fully formed BUT often only a precursor lesion noted at birth
  • Rapid proliferation in first 1-3 months of life
  • Spontaneous involution over years
  • –> 50% by age 5
  • –> 70% by age 7
  • –> 90% by age 9
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8
Q

Infantile Hemangioma (Capillary / Strawberry) - troublesome areas

A

Peri-ocular
—> may interrupt visual fields & cause astigmatism or more severe ocular complications

“Beard area”
—> may be sign of airway involvement

Other troublesome areas include lip, anogenital, and nasal tip

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9
Q

Infantile Hemangioma (Capillary / Strawberry) - complications

A

Ulceration
Size
- if large, may distort normal tissue & interfere w/ function

Number
- Diffuse neonatal hemangiomatosis may be associated w/ visceral hemangiomas

Congenital syndromes (PHACES)

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10
Q

Infantile Hemangioma (Capillary / Strawberry) - treatment

A

Observation
= most involute spontaneously, without scarring

Local wound care

Pulsed dye laser

Topical, intralesional & systemic steroids

Beta-blockers

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11
Q

Port Wine Stain - overview

A

= Vascular (capillary) malformation
- Present at birth
- Persists into adulthood
= Often irregular vascular channels that do NOT stain w/ Glut-1

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12
Q

Port Wine Stain - demographics & cause

A
  • No gender or gestational predilection

- Somatic mutation in GNAQ

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13
Q

Port Wine Stain - Complications

A
  • Klippel-Trenaunay syndrome

- Sturge Weber Syndrome

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14
Q

Klippel-Trenaunay syndrome

A

= complication of port wine stain

  • Overgowth of extremity covered by large port wine stain
  • Varicose veins, venous stasis, edema, ulceration
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15
Q

Sturge Weber Syndrome

A

= complication of port wine stain

10-15% in V1 distribution are associated w/ ocular & neurologic abnormalities including:

  • glaucoma
  • seizures
  • developmental delay
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16
Q

Port Wine Stain - Treatment & Why treat

A

Pulsed dye laser

Why treat?

  • Persist into adulthood
  • Get worse with time
  • Dark purple, nodular, bleeding blebs
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17
Q

Hamartoma defn.

A

= simply put, an excess of normal tissue in a normal situation
= a benign, focal malformation that resembles a neoplasm in the tissue of its origin
- not malignant & grows at same rate as surrounding tissues
= composed of tissue elements normally found at that site, but which grow in a disorganized mass
= occur in many different parts of the body
= most often asymptomatic & undetected unless seen on an image taken for another reason.

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18
Q

Nevus Sebaceus - defn. & cause

A

= hamartoma that most commonly presents as a papillomatous yellow-orange linear plaque on face or scalp
—> Scalp lesions are associated w/ alopecia

Somatic mutations in HRAS and KRAS

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19
Q

Nevus Sebaceus - timing of growth

A

Rapid growth occurs at puberty w/ enlargement of sebaceous glands & epidermal hyperplasia

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20
Q

Nevus Sebaceus - Complications

A

Epidemal nevus syndrome
–> neurologic abnormalities

Epithelial neoplasms
- occur in 10-30%
= Basal cell carcinoma, syringocystadenoma papilliferum

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21
Q

Nevus Sebaceus - Treatment

A
  • Observation (no treatment)

- Surgical excision

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22
Q

Sebaceous Hyperplasia - defn. & appearance / distribution

A

= Common benign tumor of oil gland

Distribution:
- face > trunk > extremities

Primary lesion:
- 1-6 mm yellowish-white papule (globules) w/ central dell

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23
Q

Sebaceous Hyperplasia - age / cause

A

Increasing frequency after middle age

Possibly sunlight induced

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24
Q

Sebaceous Gland Hyperplasia - Treatment

A
  • No treatment
    = Cosmetic issue only

Electrodessication w/wo curettage

Trichloroacetic acid (50%) for 3-5 seconds

Liquid nitrogen cryotherapy (high recurrence rate)

Laser therapy (expensive)

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25
Q

Acrochordon - aka, prevalence

A
  • aka Skin tags, Fibroepithelial polyps

- Common (¼ of all adults have at least one)

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26
Q

Acrochordon (skin tags, fibroepithelial polyps) - appearnance

A
  • Solitary or multiple
  • Soft, flesh-colored tan to brown exophytic papule (1-4 mm) with narrow base

Large variants:
= oftenc alled “soft fibroma”

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27
Q

Acrochordon (skin tags, fibroepithelial polyps) - Complications

A

Recurrent trauma

Torsion

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28
Q

Acrochordon (skin tags, fibroepithelial polyps) - Treatment

A

No treatment

Snip excision

  • Narrow stalk = no anesthesia needed
  • Large stalk = usually require local anesthesia

Cryotherapy

Electrodessication- best for small lesions

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29
Q

Lipoma - defn.

A

= benign tumor of adipose tissue

- most common form of soft tissue tumor

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30
Q

Lipoma - appearance / feel

A
  • soft to touch
  • usually movable
  • generally painless
  • many are small (6cm
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31
Q

Lipoma - age

A
  • commonly found in adults from 40 to 60 yo

- can also be found in children

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32
Q

Lipoma - Treatment

A

No treatment

Surgical excision

33
Q

Dermatofibroma

A
  • aka fibrous histiocytoma

Distribution- legs (80%)

Typically solitary (80%)

Primary lesion

  • Round to oval firm nodule
  • depressed or dome-shaped
  • Several mm to 1 cm (rarely larger)
  • Skin-colored to tan to brown (rarely red, blue)
  • May scale
34
Q

Dermatofibroma (fibrous histiocytoma) - Signs, Complications

A

Positive dimple (Fitzpatrick) sign

Complications: Pain, Pruritus

35
Q

Dermatofibroma - Treatment

A

No treatment

Surgical excision

36
Q

Keloid Scar - defn., composition

A

= a type of scar
- depending on its maturity, composed of mainly type III (early) OR type I (late) collagen
= result of overgrowth of granulation tissue (collagen type 3) at site of healed skin injury, which is then slowly replaced by collagen type 1

*Keloids should not be confused w/ hypertrophic scars, which are raised scars that DO NOT grow beyond the boundaries of the original wound

37
Q

Keloids - appearance / feel

A
  • firm, rubbery lesions OR shiny, fibrous nodules

- vary in color from pink to flesh-colored or red to dark brown

38
Q

Keloids - treatment

A

Difficult
Works best w/ear keloids
Surgery +/- Radiation

39
Q

Seborrheic Keratosis - aka, defn.

A

= “Barnacles of Life”

= Benign tumor of the hair follicle

40
Q

Seborrheic Keratosis - distribution / appearance

A

Distribution- primarily head, neck, trunk

Primary lesion

  • Color- white to gray to tan to brown to black
  • Exophytic papule- “stuck-on appearance”
  • Smooth to verrucous
  • Often friable
  • Surface often studded w/ small pits (pseudohorncysts)
41
Q

Seborrheic Keratosis - Clinical Variants

A

Dermatosis papulosa nigra

Stucco keratosis

Inflamed seborrheic keratosis

Sign of Leser-Trélat

42
Q

Dermatosis papulosa nigra - demographics

A

Typically seen in Black and Asian patients

43
Q

Stucco keratosis - distribution

A

Typically acral areas
= distal portions of limbs (hands, feet)
= distal portions of head (ears, nose)

44
Q

Sign of Leser-Trélat

A
  • Rapid increase in size or number

- Associated w/ internal malignancies, esp. gastric adenocarcinoma (60%)

45
Q

Seborrheic Keratosis - Treatment

A

Cryosurgery- treatment of choice

Moisturizers

  • alpha-hydroxy acids (e.g., aqua glycolic acid)
  • Lactic acid (e.g., Am Lactin, Lac Hydrin)

Liquid Nitrogen

Surgical removal

46
Q

Nevocellular Nevi - Clinical Features - Distribution

A

Distribution:
= Any skin surface, including mucous membranes
= Number of nevi increased on sun-exposed skin

47
Q

Nevocellular Nevi - Clinical Features - Age of Onset & Number of nevi

A

Age of onset: Infancy to adulthood

20 years of age = 20 nevi

Number peaks in 2nd & 3rd decade

  • Men = 43 nevi
  • Women = 27 nevi
48
Q

Nevocellular Nevi - types

A

Moles

Melanocytic Nevi

49
Q

Nevocellular Nevi - Growth patterns

A

Intradermal nevus
Junctional nevus
Compound nevus

50
Q

Intradermal Nevus - Clinical Features

A

Location- head & neck most common

Size- variable (most <6 mm)

Primary lesion

  • Papule or nodule
  • Dome-shaped, papillated, pedunculated, cerebriform
  • Color- skin colored to tan to light brown
51
Q

Junctional Nevus - Clinical Features

A

Location: Anywhere (esp. plantar/palmar surfaces)

Size- variable, 1-5 mm

Primary lesion

  • Macule; less commonly, subtle papule
  • Surface- typically smooth
  • Color- tan to brown to black
52
Q

Compound Nevus - Clinical Features

A

Location: usually trunk & proximal extremities

Size- variable (most <6 mm)

Primary lesion

  • Papule or nodule
  • Typically dome-shaped; less commonly papillated or pedunculated
  • Color- tan to brown to black
53
Q

Nevocellular Nevi - Indications for Treatment

A

*No treatment required for most nevi
I
Indications for treatment:
- Atypical-appearing nevus
- Atypical evolution (growth, color, symptoms)
- Irritated nevus (e.g., rubbed by clothing)

54
Q

Nevocellular Nevi - Treatment Options

A

Appropriate

  • Shave biopsy
  • Punch biopsy
  • Excision biopsy

Inappropriate

  • Electrodessication
  • Cryotherapy
  • Dermabrasion (exception- congenital nevus?)
  • Laser
55
Q

Blue Nevus - defn. & reason for color

A

= dermal proliferation of melanocytes that produce abundant melanin

Blue color
= optical effect where longer wavelengths are absorbed & shorter wavelengths are reflected back (Tyndall effect)

56
Q

Blue Nevus - demographics / epidemiology

A
  • Congenital (1:3000) or acquired (up to 4% of adults)
  • Most common in Asians & whites
  • Uncommon in blacks
57
Q

Blue Nevus - appearance

A

Primary lesion-

  • blue to blue-gray to blue-white
  • papule or nodule
  • Size- 1 mm to 2 cm
58
Q

Blue Nevus - Treatment

A

No treatment

  • Common option for unchanging lesions
  • Malignant blue nevus (very rare)

Surgical removal

  • Punch biopsy
  • Excision biopsy
59
Q

Congenital Nev - Clinical Features

A
  • May be solitary or multiple
  • May affect any cutaneous surface

Primary lesion

  • identical to acquired nevi only differ in size:
  • 1 mm to huge (i.e. bathing trunk nevi)

Presence of dark hairs- no clinical significance

60
Q

Congenital Nev - Complications

A

Head, neck, posterior midline- cranial and/or leptomeningeal melanocytosis

61
Q

Congenital Nev - Prevalence

A

1% of newborns

- Medium to Large (>10cm) = 1:20,000 newborns

62
Q

Congenital nevi - sizes

A

Small (20 cm diameter)

63
Q

Congenital Nevi - Treatment

A

Highly controversial area

Elective surgical excision

  • Most authorities do not recommend
  • Recommended by some if clinically feasible
64
Q

Congenital Nevi - potentia for l/prevalence of malignancy

A

Calculated potential for malignant melanoma:
- Risk 1% per year in large congenital nevi (>40 cm diameter)

Malignant melanoma in congenital nevi:

  • 50% appear in first 3 years
  • 60% appear in first decade
65
Q

Dysplastic Nevus - aka

A

aka: Atypical Nevus, Clark’s Nevus, Nevus w/ Cytologic Atypia and Architectural Disorder

= Acquired melanocytic proliferation

  • Epidermal and/or dermal proliferation of cytologically atypical nevomelanocytes
  • Abnormal growth pattern (architectural disorder)
  • Sporadic or Familial
66
Q

Dysplastic Nevi - Demographics

A

Male = Female

Age of onset: usually apparent by 20 yo

67
Q

Dysplatic Nevi - Location / Number / Appearance

A

Location: any cutaneous site, esp. trunk

Number of lesions: solitary to hundreds

Primary lesions:

  • Round to oval to irregular
  • Variegation in color (tans, brown, black, reds)
  • Margins often irregular & indistinct (fuzzy), w/ pigment bleeding into surrounding skin
  • Size- no limit
68
Q

Dysplastic Nevi - Clinical importance

A

Melanomas are contiguous w/ dysplastic nevi
- 6.6%-70.3% in ten studies

Familial atypical mole & melanoma syndrome
- Risk of melanoma approaches 100%

69
Q

Familial Atypical Moles And Melanoma (FAMM Syndrome) - Criteria

A
  • Occurrence of malignant melanoma in 1 or more 1st- or 2nd-degree relatives
  • Presence of numerous (often >50) melanocytic nevi, some of which are clinically atypical
  • Many of associated nevi show certain histologic features
70
Q

FAMMM Syndrome - Pathogenesis

A

Germline mutations in3 genes linked to a subset of hereditary melanomas & FAMM syndrome:

  • CDK2NA mapped to 9p21
  • CDK4 mapped to 12q14
  • CMM1 mapped to 1p.

Polygenetic or multifactorial?

  • Found in some but not all atypical nevi
  • Inconsistent finding in different studies
71
Q

Treatment of Sporadic or Familial dysplastic nevi

A
  • Mole mapping w/ dermoscopy
  • Total body photography
  • Remove most atypical nevi, changing or symptomatic nevi
72
Q

Treatment of Clinically solitary dysplastic nevus

A

Reasonable to surgically remove

73
Q

Treatment of Biopsy-proven atypical nevi

A

Controversial

  • Some only excise lesions w/ moderate-severe atypia
  • NIH Consensus panel: excise w/ 2-5 mm margins
74
Q

Neurofibromatosis (Von Recklinghausen’s disease) - defect & inheritance

A

Defect in neurofibromin gene
= tumor suppressor
- on chromosome 17 for NF-1

  • AD inheritance w/ variable expression
  • 50% of cases due to spontaneous mutations
75
Q

Neurofibromatosis - Criteria for Dx

A

Must have 2 or more of the following:
1. 6+ cafe au lait macules more than 1.5 cm in diameter (or mroe than 0.5 cm diameter in children)

  1. 2+ neurofibromas or 1 plexiform neurofibroma
  2. Axillary or inguinal freckling (Crowe’s sign)
  3. Optic glioma
  4. 2+ Lisch nodules
  5. Distinctive osseous lesion (such as sphenoid wing dysplasia, thinning of long bone cortex)
  6. 1st degree relative (parent, sibling, child) w/ the disorder.
76
Q

Neurofibromas

A

= Soft flesh-colored papules characterized by “button hole sign”
- Less commonly appear to be deep, firm, subQ nodules

= Focal proliferation of neural tissue w/in dermis

  • Solitary neurofibromas are inconsequential
  • Multiple neurofibromas may be sign of neurofibromatosis
77
Q

Café-au-Lait Spots

A

= Subtle increase in # of melanocytes w/ increased melanin production
- Congenital or early childhood

Distribution- trunk and proximal extremities

Typically solitary
Multiple lesions associated with NF
- Prepubertal child- 6 or more > 5 mm
- Crowe’s sign (axillary / inguinal freckling)

78
Q

Café-au-Lait Spots - Treatment

A

No treatment- cosmetic concern only

Pigmented laser

  • Expensive
  • Variable results