Common Skin Tumors Flashcards

1
Q

Cherry hemangioma

  • arise in?
  • underlying disease?
A
  • arise in middle age

- no association with underlying disease

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2
Q

Most common vascular tumor in adults?

A

cherry hemangioma

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3
Q

Location of cherry hemangioma?

A

primarily truncal

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4
Q

Cherry hemangioma, numbers?

A

multiple- up to many hundreds

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5
Q

What do cherry hemangiomas look like? size / color / etc

A

1-4 mm in size

bright red, smooth topped papules

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6
Q

How can we treat cherry hemagiomas?

A
Superficial electrodessication 
Liquid nitrogen + curettage
Shave biopsy
Pulse dye laser
Other lasers
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7
Q

Most common soft tissue tumor of infancy?

A

Infantile hemangioma (10-12% infants)

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8
Q

What is an infantile hemangioma? Neoplasm of which cells?

A

Benign endothelial cell neoplasm

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9
Q

What marker is used for Infantile hemangioma?

A

Glut-1 - a placental antigen

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10
Q

Infantile hemangioma and sex?

gestation?

A

Girls more common 3-5:1
more common premature
more common chorionic villus sampling

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11
Q

Infantile hemangioma development / progression?

A

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)

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12
Q

What complications would we be concerned about for infantile hemagiomas? Regarding location…

A

Peri-ocular may interrupt visual fields and cause atisgmatism or more severe ocular complications

Other troublesome areas include lip, anogenital, and nasal tip

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13
Q

Beard area infantile hemangiomas may be a sign of?

A

airway involvement

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14
Q

Infantile hemangioma… progression we worry about?

A

ulceration

large size - may distort normal tissue

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15
Q

Why might we be concered with multiple infantile hemangiomas?

A

may be associated with visceral (e.g. liver)

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16
Q

What congenital syndrome do we see infantile hemangiomas in?

A

Congenital syndromes (phaces)

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17
Q

Treatment of infantile hemangioma?

A

Observation (most involute spontaneously)

local wound care

pulse dyed laser

topical, intralesional and systemic steroids

beta-blockers

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18
Q

Port Wine Stain
what is it?
when is it present?

A

vascular malformation

present at birth

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19
Q

Port wine stain
persist?
gender?

A

persist to adult

not gender predilection

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20
Q

Port wine stain

Glut-1?

A

Often irregular vascular channels that do NOT stain with Glut-1

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21
Q

Port wine stain

Mutation?

A

somatic mutation in GNAQ

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22
Q

Glut-1?

A

immunohistochemical marker for juvenile hemangiomas

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23
Q

What is Klippel-Trenaunay Syndrome?

A

Complication associated with port wine stain

Overgrowth of an extremity covered by a large port wine stain

Vericose veins, venous stasis, edema, ulceration

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24
Q

Port wine stain V1 distribution?

A

Sturge Weber syndrome (10-15% in V1 distribution are associated with ocular and neurological abnormalities including glaucoma, seizures, and developmental delay)

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25
Port Wine Stain Treatment?
Pulse dye laser
26
Why treat Port Wine Stain?
persist into adulthood get worse with time dark purple, nodular, bleeding blebs
27
What is a Nevus Sebaceus?
congenital, hairless yellow-orange plaque (harmatoma) that typically occurs on the face or scalp
28
Nevus Sebaceus - lesions on the scalp are associated with?
alopecia
29
Nevus Sebaceus - do they get bigger?
Rapid growth occurs at puberty with enlargement of sebaceous glands and epidermal hyperplasia
30
Complications of nevus sebaceus?
Epidermal nevus syndrome (neurologic abnormalities) Epithelial neoplasms occur in 10-30% (trichoblastoma, syringocystadenoma papilliferum, BCC)
31
Nevus Sebaceus - treatment?
Observation | Surgical excision
32
What is a sebaceous Hyperplasia?
Common benign tumor of oil gland
33
Sebaceous Hyperplasia - - age? - induction?
increased frequency after middle age | - sunlight induced?
34
Distribution of sebaceous hyperplasia?
face>trunk>extremities
35
Sebaceous Hyperplasia | size/appearance?
primary lesion 1-6mm yellowish-white papule (globules) with central dell
36
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
37
Acrochordon - what is it?
skin tags - fibroepithelial polyps soft, flesh colored tan to brown exophytic papule (1-4 mm) with narrow base
38
acrochordon - common?
common 1/4 of all adults have | solitary or multiple
39
Large variants of acrochordon?
large variants often called soft fibroma
40
Complications of acrochordon?
recurrent trauma - torsion
41
Acrochordon treatment?
None Snip excision Cryotherapy Electrodessication - best for small lesions
42
What is a lipoma?
A benign tumor of adipose tissue
43
What is the most common form of soft tissue tumor
Lipoma
44
How should a lipoma feel?
Soft to the touch usually movable generally painless
45
Lipoma size?
Gnerally small (
46
Lipoma age?
40-60 most common but can also be found in children
47
Lipoma treatment?
none | surgical excision
48
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
49
Dermatofibroma - Distribution? Number?
80% legs | 80% solitary 20% multiple
50
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 :)
51
Dermatofibroma | what is Fitzpatrick sign?
positive dimple sign
52
Complications of Dermatofibromas?
pain pruritis
53
Dermatofibroma | treatment?
none | excision
54
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.
55
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.
56
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
57
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
58
Keloid | Treatment?
Topical steroids under occlusion Intralesional steroids Surgical excision: works best for ear keloids Surgery +/- Radiation
59
Seborrheic Keratosis - what is it?
benign tumor of the hair follicle
60
Seborrheic Keratosis - distribution?
primarily distributed head, neck, trunk
61
What are the "barnacles of life"?
seborrheic keratosis
62
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)
63
Dermatosis papulosa nigra?
variant of Seborrheic Keratosi - typically seen in Black and Asian
64
Stucco keratosis?
variant of Seborrheic Keratosi - typically seen in acral areas
65
Sign of Lesser-Trelat
variant of Seborrheic Keratosi - rapid increase in size or number - associated with internal malignancies, escpecially adenocarcinoma of the stomach (60%)
66
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
67
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.
68
Nevocellular nevi | age?
infancy to adult onset
69
Nevocellular nevi | distribution?
any skin surface including mucous membrane number of nevi increased on sun-exposed skin
70
Normal Number of nevocellular nevi? caucasian
20 years of age = 20 Australian - number peaks in 2nd-3rd decade men - 43 women 27
71
3 growth patterns of nevocellular nevi - melanocytic nevi?
intradermal junctional compound (both)
72
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
73
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
74
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
75
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)
76
Nevocellular nevi | appropriate and inappropriate treatment options (3 and 4)
``` Appropriate Shave biopsy Punch biopsy Excision Inappropriate Electrodessication Cryotherapy Dermabrasion (exception- congenital nevus?) Laser ```
77
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)
78
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
79
Blue Nevus | Treatment?
No treatment Common option for unchanging lesions Malignant blue nevus (very rare) Surgical removal Punch biopsy Excision
80
Congenital Nevi How many? Location?
May be solitary or multiple | May affect any cutaneous surface
81
Congenital vs Acquired nevi?
Primary lesion identical to acquired nevi only differ in size - 1mm to huge (i.e. think bathing trunk nevi)
82
Significance of hair on nevi?
none
83
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)
84
What percent of newborns have congenital nevi?
1%
85
Size of congenital nevi?
small 20cm
86
Congenital nevi | Treatment?
Controversial - elective surgical excision - most authorities do not recommend - recommended by some if clinically feasable
87
Medium to large congenital nevi (>10cm) occur in what fraction of newborns
1:20,000
88
What is the calculated risk for malignant melanoma in congenital nevi?
1% per year in large congenital nevi (>40cm)
89
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%
90
Dysplastic nevus | 3 types
Aytpical nevus Clarks nevus Nevus with Cytologic Aytpia and architectual disorder
91
What is acquired melanocyte prolferation
Epidermal and/or dermal proliferation cytologically atypical nevomelanocytes Abnormal growth pattern (Architectural disorder)
92
Sporadic or familial dysplastic nevus?
sporadic atypical nevi are those that occur in patients without a family history of atypical nevi
93
Dysplatic nevi | Sex ?
males = females
94
Dysplastic nevi | Age?
age of onset - usually apparent by 20
95
Dysplastic nevi | local?
any cutaneous site especially trunk
96
Dysplastic nevi | number?
solitary to hundreds
97
Dysplastic nevi | appearance?
round to oval or irregular | variation in color - tan/brown/black/red
98
Dysplastic nevi | Margins?
``` often indistinct (fuzzy) pigment bleeds into surrounding skin, irregular margins ```
99
Dysplastic nevi | size?
no limit
100
Dysplastic nevi Clinical importance Melanoma?
Melanomas are contiguous with dysplatic nevi - 6.6%-70.3% in ten studies
101
Dysplastic nevi | FAMMS?
Familial atypical mole and melanoma syndrome - risk of melanoma approaches 100%
102
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
103
FAMM pathogeneis
Germline mutations in 3 genes have been linked to a subset of hereditary melanomas and FAMM syndrome
104
Is FAMM polygenetic or multifactorial?
Found in some but not all atypical nevi | inconsistent findings in different studies
105
Dysplastic nevi treatment?
Sporadic or familial dysplastic nevi - mole mapping with dermoscopy - total body photography - remove the most atypical nevi, chanign or symptomatic nevi
106
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
107
``` 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
108
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
109
Neurofibromas
Soft flesh colored papules characterized by the "button hole sign" Less commonly appear to be deep, firm, subcu nodules
110
What causes neurofibromas
Focal proliferation of neural tissue within dermis
111
Solitary neurofibromas vs. multiple
solitary - inconsequental | many - maybe neurofibromatosis
112
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
113
Neurofibromatosis Type 1: Diagnosis requires 2 or more of the following criteria
1. 6 or more cafe au lait more than 1.5 cm in daimeter 2. two or more neurofibromas or 1 plexiform 3. Axillary or inguinal freckles (Crowe's) 4. Optic glioma 5. Two or more Lisch nodules 6. Distinctive osseous lesion, such as sphenoid wing dysplasia or thinning of long bone cortex 7. first degree relative