Common Skin Tumors Flashcards
Cherry hemangioma
- arise in?
- underlying disease?
- arise in middle age
- no association with underlying disease
Most common vascular tumor in adults?
cherry hemangioma
Location of cherry hemangioma?
primarily truncal
Cherry hemangioma, numbers?
multiple- up to many hundreds
What do cherry hemangiomas look like? size / color / etc
1-4 mm in size
bright red, smooth topped papules
How can we treat cherry hemagiomas?
Superficial electrodessication Liquid nitrogen + curettage Shave biopsy Pulse dye laser Other lasers
Most common soft tissue tumor of infancy?
Infantile hemangioma (10-12% infants)
What is an infantile hemangioma? Neoplasm of which cells?
Benign endothelial cell neoplasm
What marker is used for Infantile hemangioma?
Glut-1 - a placental antigen
Infantile hemangioma and sex?
gestation?
Girls more common 3-5:1
more common premature
more common chorionic villus sampling
Infantile hemangioma development / progression?
Often only a precursor lesion is noted at birth, occasionally fully formed
Rapid proliferation in the first 1-3 months of life
Spontaneous involution over years (50% by 5, 70% by 7, 90% by 9)
What complications would we be concerned about for infantile hemagiomas? Regarding location…
Peri-ocular may interrupt visual fields and cause atisgmatism or more severe ocular complications
Other troublesome areas include lip, anogenital, and nasal tip
Beard area infantile hemangiomas may be a sign of?
airway involvement
Infantile hemangioma… progression we worry about?
ulceration
large size - may distort normal tissue
Why might we be concered with multiple infantile hemangiomas?
may be associated with visceral (e.g. liver)
What congenital syndrome do we see infantile hemangiomas in?
Congenital syndromes (phaces)
Treatment of infantile hemangioma?
Observation (most involute spontaneously)
local wound care
pulse dyed laser
topical, intralesional and systemic steroids
beta-blockers
Port Wine Stain
what is it?
when is it present?
vascular malformation
present at birth
Port wine stain
persist?
gender?
persist to adult
not gender predilection
Port wine stain
Glut-1?
Often irregular vascular channels that do NOT stain with Glut-1
Port wine stain
Mutation?
somatic mutation in GNAQ
Glut-1?
immunohistochemical marker for juvenile hemangiomas
What is Klippel-Trenaunay Syndrome?
Complication associated with port wine stain
Overgrowth of an extremity covered by a large port wine stain
Vericose veins, venous stasis, edema, ulceration
Port wine stain V1 distribution?
Sturge Weber syndrome (10-15% in V1 distribution are associated with ocular and neurological abnormalities including glaucoma, seizures, and developmental delay)
Port Wine Stain Treatment?
Pulse dye laser
Why treat Port Wine Stain?
persist into adulthood
get worse with time
dark purple, nodular, bleeding blebs
What is a Nevus Sebaceus?
congenital, hairless yellow-orange plaque (harmatoma) that typically occurs on the face or scalp
Nevus Sebaceus - lesions on the scalp are associated with?
alopecia
Nevus Sebaceus - do they get bigger?
Rapid growth occurs at puberty with enlargement of sebaceous glands and epidermal hyperplasia
Complications of nevus sebaceus?
Epidermal nevus syndrome (neurologic abnormalities)
Epithelial neoplasms occur in 10-30% (trichoblastoma, syringocystadenoma papilliferum, BCC)
Nevus Sebaceus - treatment?
Observation
Surgical excision
What is a sebaceous Hyperplasia?
Common benign tumor of oil gland
Sebaceous Hyperplasia -
- age?
- induction?
increased frequency after middle age
- sunlight induced?
Distribution of sebaceous hyperplasia?
face>trunk>extremities
Sebaceous Hyperplasia
size/appearance?
primary lesion 1-6mm yellowish-white papule (globules) with central dell
Sebaceous Gland Hyperplasia
How do we treat?
No treatment
- cosmetic only
Electrodessication w/wo curettage
Trichloracetic acid (50%) for 3-6 seconds
Liquid nitrogen cryotherapy
- high recurrence rate
Laser therapy
Acrochordon - what is it?
skin tags - fibroepithelial polyps
soft, flesh colored tan to brown exophytic papule (1-4 mm) with narrow base
acrochordon - common?
common 1/4 of all adults have
solitary or multiple
Large variants of acrochordon?
large variants often called soft fibroma
Complications of acrochordon?
recurrent trauma - torsion
Acrochordon treatment?
None
Snip excision
Cryotherapy
Electrodessication - best for small lesions
What is a lipoma?
A benign tumor of adipose tissue
What is the most common form of soft tissue tumor
Lipoma
How should a lipoma feel?
Soft to the touch
usually movable
generally painless
Lipoma size?
Gnerally small (
Lipoma age?
40-60 most common but can also be found in children
Lipoma treatment?
none
surgical excision
Dermatofibroma
Dermatofibroma (superficial benign fibrous histiocytoma) is a common cutaneous nodule of unknown etiology that occurs more often in women. Dermatofibroma frequently develops on the extremities (mostly the lower legs) and is usually asymptomatic, although pruritus and tenderness can be presen
Dermatofibroma -
Distribution?
Number?
80% legs
80% solitary 20% multiple
Dermatofibroma
primary lesion?
appearance
round to oval firm nodule - depressed or dome shaped
several mm to 1cm, rarely larger
color- skin colored to tan to brown - rarely red and blue
surface may demonstrate scale :)
Dermatofibroma
what is Fitzpatrick sign?
positive dimple sign
Complications of Dermatofibromas?
pain pruritis
Dermatofibroma
treatment?
none
excision
Keloid
what is it
what is it made of?
type of scar, which depending on its maturity, is composed of mainly either type III (early) or type I (late) collagen.
What do keloids result from?
result of an overgrowth of granulation tissue (collagen type 3) at the site of a healed skin injury which is then slowly replaced by collagen type 1.
Keloid
texture / appearance?
firm, rubbery lesions or shiny, fibrous nodules and can vary from pink to flesh-colored or red to dark brown in color
What distinguishes a keloid from a hypertrophic scar?
Keloids should nto be confused with hypertrophic scars, which are raised scars that do not grow beyond the boundaries of the original wound
Keloid
Treatment?
Topical steroids under occlusion
Intralesional steroids
Surgical excision: works best for ear keloids
Surgery +/- Radiation
Seborrheic Keratosis - what is it?
benign tumor of the hair follicle
Seborrheic Keratosis - distribution?
primarily distributed head, neck, trunk
What are the “barnacles of life”?
seborrheic keratosis
Seborrheic Keratosis - primary lesion?
color - white to gray to tan to brown to black
Exophytic papule - stuck on appearance
smooth to verrucous
often friable (crumble)
surface often studded with small pits (psedohorncysts)
Dermatosis papulosa nigra?
variant of Seborrheic Keratosi - typically seen in Black and Asian
Stucco keratosis?
variant of Seborrheic Keratosi - typically seen in acral areas
Sign of Lesser-Trelat
variant of Seborrheic Keratosi
- rapid increase in size or number
- associated with internal malignancies, escpecially adenocarcinoma of the stomach (60%)
Seborrheic Keratosis
Treatment
Moisturizers
-hydroxy acids (e.g., aqua glycolic acid)
Lactic acid (e.g., Am Lactin, Lac Hydrin)
Cryosurgery- treatment of choice
Liquid Nitrogen
Surgical removal
Nevocellular Nevi
Melanocytic nevus (nevomelanocytic nevus, nevocellular nevus): benign proliferation of melanocytes, the skin cells that make the brown pigment melanin. Hence, most nevi are brown to black.
Nevocellular nevi
age?
infancy to adult onset
Nevocellular nevi
distribution?
any skin surface including mucous membrane
number of nevi increased on sun-exposed skin
Normal Number of nevocellular nevi? caucasian
20 years of age = 20
Australian - number peaks in 2nd-3rd decade
men - 43
women 27
3 growth patterns of nevocellular nevi - melanocytic nevi?
intradermal
junctional
compound (both)
Intradermal nevus - local? - size? - primary lesion?
location - head and neck most common
size - variable - most less than 6mm
primary lesion
papule or nodule
dome-shaped, papillated, pedunculated - cerebriform
color - skin colored to tan to light brown
Junctional nevus
local?
size?
primary lesion?
located anywhere - especially common on plantar and 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
local?
size?
primary lesion?
local - trunk and proximal extremities are most common sites
size - variable most less than 6mm
primary lesion
papule or nodule
typically dome shaped, less commonly papillated or pedunculated
color - tan to brown to black
Nevocellular nevi
indications to treat?
No treatment required for most nevi
Indications for treatment
Atypical-appearing nevus
Atypical evolution (growth, color, symptoms)
Irritated nevus (e.g., rubbed by clothing)
Nevocellular nevi
appropriate and inappropriate treatment options (3 and 4)
Appropriate Shave biopsy Punch biopsy Excision Inappropriate Electrodessication Cryotherapy Dermabrasion (exception- congenital nevus?) Laser
Blue nevus
dermal proliferation of melanocytes that produce abundant melanin
blue color is an otpical effect where longer wavelengths are absobred and shorter wavelengths are reflected bakc (Tyndall effect)
Blue nevus clinical features
- congenital vs acquired?
- population?
- appearance?
congenital (1:3000) acquired (up to 4% adults)
Most common in Asians and Caucasians
Primary lesion is blue to blue-gray to blue-white papule or nodule
Size 1mm to 2cm
Blue Nevus
Treatment?
No treatment
Common option for unchanging lesions
Malignant blue nevus (very rare)
Surgical removal
Punch biopsy
Excision
Congenital Nevi
How many?
Location?
May be solitary or multiple
May affect any cutaneous surface
Congenital vs Acquired nevi?
Primary lesion identical to acquired nevi only differ in size - 1mm to huge (i.e. think bathing trunk nevi)
Significance of hair on nevi?
none
Complications of congenital nevi?
head, neck, posterior midline –> cranial an or leptomeningeal melanocytosis (the two innermost layers of tissues that cover the brain and spinal cord)
What percent of newborns have congenital nevi?
1%
Size of congenital nevi?
small 20cm
Congenital nevi
Treatment?
Controversial
- elective surgical excision
- most authorities do not recommend - recommended by some if clinically feasable
Medium to large congenital nevi (>10cm) occur in what fraction of newborns
1:20,000
What is the calculated risk for malignant melanoma in congenital nevi?
1% per year in large congenital nevi (>40cm)
Malignant melanoma in congenital nevi
what fraction appear in first 3 years
what fraction appear in first decade?
first 3 years 50%
first decade 60%
Dysplastic nevus
3 types
Aytpical nevus
Clarks nevus
Nevus with Cytologic Aytpia and architectual disorder
What is acquired melanocyte prolferation
Epidermal and/or dermal proliferation cytologically atypical nevomelanocytes
Abnormal growth pattern (Architectural disorder)
Sporadic or familial dysplastic nevus?
sporadic atypical nevi are those that occur in patients without a family history of atypical nevi
Dysplatic nevi
Sex ?
males = females
Dysplastic nevi
Age?
age of onset - usually apparent by 20
Dysplastic nevi
local?
any cutaneous site especially trunk
Dysplastic nevi
number?
solitary to hundreds
Dysplastic nevi
appearance?
round to oval or irregular
variation in color - tan/brown/black/red
Dysplastic nevi
Margins?
often indistinct (fuzzy) pigment bleeds into surrounding skin, irregular margins
Dysplastic nevi
size?
no limit
Dysplastic nevi
Clinical importance
Melanoma?
Melanomas are contiguous with dysplatic nevi - 6.6%-70.3% in ten studies
Dysplastic nevi
FAMMS?
Familial atypical mole and melanoma syndrome - risk of melanoma approaches 100%
FAMM syndrome?
Criteria?
The occurence of malignant melanoma in 1 or more first or second degree relatives
The presence of numerous (often >50) melanocytic nevi, some of which are clinically atypical
Many of the associated nevi showing certain histological features
FAMM pathogeneis
Germline mutations in 3 genes have been linked to a subset of hereditary melanomas and FAMM syndrome
Is FAMM polygenetic or multifactorial?
Found in some but not all atypical nevi
inconsistent findings in different studies
Dysplastic nevi treatment?
Sporadic or familial dysplastic nevi
- mole mapping with dermoscopy
- total body photography
- remove the most atypical nevi, chanign or symptomatic nevi
Dysplastic nevi treatmetn
- clinically solitary?
- biopsy proven atypical?
reasonable to surgically remove
controversial
some only excise lesions with moderate/severe atypia
NIH consensus panel-excise with 2-5mm margins
Cafe au Lait Macules what are they when are they found how are they distributed multiple associated with?
Subtle increase in number of melanocytes with 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
Crowe’s sign
Crowe’s sign is the presence of axillary (armpit) freckling in people with neurofibromatosis type I (von Recklinghausen’s disease). These freckles occur in up to 30% of people with the disease and their presence is one of seven diagnostic criteria for neurofibromatosis
Neurofibromas
Soft flesh colored papules characterized by the “button hole sign”
Less commonly appear to be deep, firm, subcu nodules
What causes neurofibromas
Focal proliferation of neural tissue within dermis
Solitary neurofibromas vs. multiple
solitary - inconsequental
many - maybe neurofibromatosis
Neurofibromatosis - Von Recklinghausens
Inheritance?
What % de novo?
Cuase?
AD inheritance with variable expression
50% of cases due to spontaneous mutations
Defect in neurofibromin gene, a tumor suppressor, on chromosome 17 for NF-1
Neurofibromatosis Type 1: Diagnosis requires 2 or more of the following criteria
- 6 or more cafe au lait more than 1.5 cm in daimeter
- two or more neurofibromas or 1 plexiform
- Axillary or inguinal freckles (Crowe’s)
- Optic glioma
- Two or more Lisch nodules
- Distinctive osseous lesion, such as sphenoid wing dysplasia or thinning of long bone cortex
- first degree relative
