DD 03-07-14 08-09am Common Skin Tumors - Morelli Flashcards
(Sentile) Cherry Hemangiomas - age / how common / what it means
- Typically arise in middle age
- Most common vascular tumor in adults
- Generally no association w/ underlying disease
Cherry Hemangiomas - appearance / distribution
Distribution: primarily truncal
Number: typically mutiple; up to many hundreds
Primary lesion:
- 1-4 mm in size
- bright red, smooth-topped papules
Cherry Hemangiomas - Treatment
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
Infantile Hemangioma (Capillary / Strawberry) - defn.
= Benign endothelial cell neoplasm
Infantile Hemangioma (Capillary / Strawberry) - demographics
= 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
Confirmation of “Dx” of Infantile Hemangioma
- Positive stain with Glut-1, a placental antigen
Infantile Hemangioma (Capillary / Strawberry) - development
- 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
Infantile Hemangioma (Capillary / Strawberry) - troublesome areas
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
Infantile Hemangioma (Capillary / Strawberry) - complications
Ulceration
Size
- if large, may distort normal tissue & interfere w/ function
Number
- Diffuse neonatal hemangiomatosis may be associated w/ visceral hemangiomas
Congenital syndromes (PHACES)
Infantile Hemangioma (Capillary / Strawberry) - treatment
Observation
= most involute spontaneously, without scarring
Local wound care
Pulsed dye laser
Topical, intralesional & systemic steroids
Beta-blockers
Port Wine Stain - overview
= Vascular (capillary) malformation
- Present at birth
- Persists into adulthood
= Often irregular vascular channels that do NOT stain w/ Glut-1
Port Wine Stain - demographics & cause
- No gender or gestational predilection
- Somatic mutation in GNAQ
Port Wine Stain - Complications
- Klippel-Trenaunay syndrome
- Sturge Weber Syndrome
Klippel-Trenaunay syndrome
= complication of port wine stain
- Overgowth of extremity covered by large port wine stain
- Varicose veins, venous stasis, edema, ulceration
Sturge Weber Syndrome
= complication of port wine stain
10-15% in V1 distribution are associated w/ ocular & neurologic abnormalities including:
- glaucoma
- seizures
- developmental delay
Port Wine Stain - Treatment & Why treat
Pulsed dye laser
Why treat?
- Persist into adulthood
- Get worse with time
- Dark purple, nodular, bleeding blebs
Hamartoma defn.
= 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.
Nevus Sebaceus - defn. & cause
= 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
Nevus Sebaceus - timing of growth
Rapid growth occurs at puberty w/ enlargement of sebaceous glands & epidermal hyperplasia
Nevus Sebaceus - Complications
Epidemal nevus syndrome
–> neurologic abnormalities
Epithelial neoplasms
- occur in 10-30%
= Basal cell carcinoma, syringocystadenoma papilliferum
Nevus Sebaceus - Treatment
- Observation (no treatment)
- Surgical excision
Sebaceous Hyperplasia - defn. & appearance / distribution
= Common benign tumor of oil gland
Distribution:
- face > trunk > extremities
Primary lesion:
- 1-6 mm yellowish-white papule (globules) w/ central dell
Sebaceous Hyperplasia - age / cause
Increasing frequency after middle age
Possibly sunlight induced
Sebaceous Gland Hyperplasia - Treatment
- 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)
Acrochordon - aka, prevalence
- aka Skin tags, Fibroepithelial polyps
- Common (¼ of all adults have at least one)
Acrochordon (skin tags, fibroepithelial polyps) - appearnance
- Solitary or multiple
- Soft, flesh-colored tan to brown exophytic papule (1-4 mm) with narrow base
Large variants:
= oftenc alled “soft fibroma”
Acrochordon (skin tags, fibroepithelial polyps) - Complications
Recurrent trauma
Torsion
Acrochordon (skin tags, fibroepithelial polyps) - Treatment
No treatment
Snip excision
- Narrow stalk = no anesthesia needed
- Large stalk = usually require local anesthesia
Cryotherapy
Electrodessication- best for small lesions
Lipoma - defn.
= benign tumor of adipose tissue
- most common form of soft tissue tumor
Lipoma - appearance / feel
- soft to touch
- usually movable
- generally painless
- many are small (6cm
Lipoma - age
- commonly found in adults from 40 to 60 yo
- can also be found in children
Lipoma - Treatment
No treatment
Surgical excision
Dermatofibroma
- 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
Dermatofibroma (fibrous histiocytoma) - Signs, Complications
Positive dimple (Fitzpatrick) sign
Complications: Pain, Pruritus
Dermatofibroma - Treatment
No treatment
Surgical excision
Keloid Scar - defn., composition
= 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
Keloids - appearance / feel
- firm, rubbery lesions OR shiny, fibrous nodules
- vary in color from pink to flesh-colored or red to dark brown
Keloids - treatment
Difficult
Works best w/ear keloids
Surgery +/- Radiation
Seborrheic Keratosis - aka, defn.
= “Barnacles of Life”
= Benign tumor of the hair follicle
Seborrheic Keratosis - distribution / appearance
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)
Seborrheic Keratosis - Clinical Variants
Dermatosis papulosa nigra
Stucco keratosis
Inflamed seborrheic keratosis
Sign of Leser-Trélat
Dermatosis papulosa nigra - demographics
Typically seen in Black and Asian patients
Stucco keratosis - distribution
Typically acral areas
= distal portions of limbs (hands, feet)
= distal portions of head (ears, nose)
Sign of Leser-Trélat
- Rapid increase in size or number
- Associated w/ internal malignancies, esp. gastric adenocarcinoma (60%)
Seborrheic Keratosis - Treatment
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
Nevocellular Nevi - Clinical Features - Distribution
Distribution:
= Any skin surface, including mucous membranes
= Number of nevi increased on sun-exposed skin
Nevocellular Nevi - Clinical Features - Age of Onset & Number of nevi
Age of onset: Infancy to adulthood
20 years of age = 20 nevi
Number peaks in 2nd & 3rd decade
- Men = 43 nevi
- Women = 27 nevi
Nevocellular Nevi - types
Moles
Melanocytic Nevi
Nevocellular Nevi - Growth patterns
Intradermal nevus
Junctional nevus
Compound nevus
Intradermal Nevus - Clinical Features
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
Junctional Nevus - Clinical Features
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
Compound Nevus - Clinical Features
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
Nevocellular Nevi - Indications for Treatment
*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)
Nevocellular Nevi - Treatment Options
Appropriate
- Shave biopsy
- Punch biopsy
- Excision biopsy
Inappropriate
- Electrodessication
- Cryotherapy
- Dermabrasion (exception- congenital nevus?)
- Laser
Blue Nevus - defn. & reason for color
= dermal proliferation of melanocytes that produce abundant melanin
Blue color
= optical effect where longer wavelengths are absorbed & shorter wavelengths are reflected back (Tyndall effect)
Blue Nevus - demographics / epidemiology
- Congenital (1:3000) or acquired (up to 4% of adults)
- Most common in Asians & whites
- Uncommon in blacks
Blue Nevus - appearance
Primary lesion-
- blue to blue-gray to blue-white
- papule or nodule
- Size- 1 mm to 2 cm
Blue Nevus - Treatment
No treatment
- Common option for unchanging lesions
- Malignant blue nevus (very rare)
Surgical removal
- Punch biopsy
- Excision biopsy
Congenital Nev - Clinical Features
- 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
Congenital Nev - Complications
Head, neck, posterior midline- cranial and/or leptomeningeal melanocytosis
Congenital Nev - Prevalence
1% of newborns
- Medium to Large (>10cm) = 1:20,000 newborns
Congenital nevi - sizes
Small (20 cm diameter)
Congenital Nevi - Treatment
Highly controversial area
Elective surgical excision
- Most authorities do not recommend
- Recommended by some if clinically feasible
Congenital Nevi - potentia for l/prevalence of malignancy
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
Dysplastic Nevus - aka
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
Dysplastic Nevi - Demographics
Male = Female
Age of onset: usually apparent by 20 yo
Dysplatic Nevi - Location / Number / Appearance
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
Dysplastic Nevi - Clinical importance
Melanomas are contiguous w/ dysplastic nevi
- 6.6%-70.3% in ten studies
Familial atypical mole & melanoma syndrome
- Risk of melanoma approaches 100%
Familial Atypical Moles And Melanoma (FAMM Syndrome) - Criteria
- 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
FAMMM Syndrome - Pathogenesis
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
Treatment of Sporadic or Familial dysplastic nevi
- Mole mapping w/ dermoscopy
- Total body photography
- Remove most atypical nevi, changing or symptomatic nevi
Treatment of Clinically solitary dysplastic nevus
Reasonable to surgically remove
Treatment of Biopsy-proven atypical nevi
Controversial
- Some only excise lesions w/ moderate-severe atypia
- NIH Consensus panel: excise w/ 2-5 mm margins
Neurofibromatosis (Von Recklinghausen’s disease) - defect & inheritance
Defect in neurofibromin gene
= tumor suppressor
- on chromosome 17 for NF-1
- AD inheritance w/ variable expression
- 50% of cases due to spontaneous mutations
Neurofibromatosis - Criteria for Dx
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)
- 2+ neurofibromas or 1 plexiform neurofibroma
- Axillary or inguinal freckling (Crowe’s sign)
- Optic glioma
- 2+ Lisch nodules
- Distinctive osseous lesion (such as sphenoid wing dysplasia, thinning of long bone cortex)
- 1st degree relative (parent, sibling, child) w/ the disorder.
Neurofibromas
= 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
Café-au-Lait Spots
= 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)
Café-au-Lait Spots - Treatment
No treatment- cosmetic concern only
Pigmented laser
- Expensive
- Variable results
