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Disease and Defense III > Common Skin Tumors > Flashcards

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
Q

Port Wine Stain Treatment?

A

Pulse dye laser

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26
Q

Why treat Port Wine Stain?

A

persist into adulthood
get worse with time
dark purple, nodular, bleeding blebs

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27
Q

What is a Nevus Sebaceus?

A

congenital, hairless yellow-orange plaque (harmatoma) that typically occurs on the face or scalp

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28
Q

Nevus Sebaceus - lesions on the scalp are associated with?

A

alopecia

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29
Q

Nevus Sebaceus - do they get bigger?

A

Rapid growth occurs at puberty with enlargement of sebaceous glands and epidermal hyperplasia

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30
Q

Complications of nevus sebaceus?

A

Epidermal nevus syndrome (neurologic abnormalities)

Epithelial neoplasms occur in 10-30% (trichoblastoma, syringocystadenoma papilliferum, BCC)

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31
Q

Nevus Sebaceus - treatment?

A

Observation

Surgical excision

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32
Q

What is a sebaceous Hyperplasia?

A

Common benign tumor of oil gland

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33
Q

Sebaceous Hyperplasia -

  • age?
  • induction?
A

increased frequency after middle age

- sunlight induced?

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34
Q

Distribution of sebaceous hyperplasia?

A

face>trunk>extremities

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35
Q

Sebaceous Hyperplasia

size/appearance?

A

primary lesion 1-6mm yellowish-white papule (globules) with central dell

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36
Q

Sebaceous Gland Hyperplasia

How do we treat?

A

No treatment
- cosmetic only

Electrodessication w/wo curettage

Trichloracetic acid (50%) for 3-6 seconds

Liquid nitrogen cryotherapy
- high recurrence rate

Laser therapy

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37
Q

Acrochordon - what is it?

A

skin tags - fibroepithelial polyps

soft, flesh colored tan to brown exophytic papule (1-4 mm) with narrow base

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38
Q

acrochordon - common?

A

common 1/4 of all adults have

solitary or multiple

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39
Q

Large variants of acrochordon?

A

large variants often called soft fibroma

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40
Q

Complications of acrochordon?

A

recurrent trauma - torsion

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41
Q

Acrochordon treatment?

A

None
Snip excision
Cryotherapy
Electrodessication - best for small lesions

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42
Q

What is a lipoma?

A

A benign tumor of adipose tissue

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43
Q

What is the most common form of soft tissue tumor

A

Lipoma

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44
Q

How should a lipoma feel?

A

Soft to the touch
usually movable
generally painless

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45
Q

Lipoma size?

A

Gnerally small (

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46
Q

Lipoma age?

A

40-60 most common but can also be found in children

47
Q

Lipoma treatment?

A

none

surgical excision

48
Q

Dermatofibroma

A

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
Q

Dermatofibroma -
Distribution?
Number?

A

80% legs

80% solitary 20% multiple

50
Q

Dermatofibroma
primary lesion?
appearance

A

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
Q

Dermatofibroma

what is Fitzpatrick sign?

A

positive dimple sign

52
Q

Complications of Dermatofibromas?

A

pain pruritis

53
Q

Dermatofibroma

treatment?

A

none

excision

54
Q

Keloid
what is it
what is it made of?

A

type of scar, which depending on its maturity, is composed of mainly either type III (early) or type I (late) collagen.

55
Q

What do keloids result from?

A

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
Q

Keloid

texture / appearance?

A

firm, rubbery lesions or shiny, fibrous nodules and can vary from pink to flesh-colored or red to dark brown in color

57
Q

What distinguishes a keloid from a hypertrophic scar?

A

Keloids should nto be confused with hypertrophic scars, which are raised scars that do not grow beyond the boundaries of the original wound

58
Q

Keloid

Treatment?

A

Topical steroids under occlusion
Intralesional steroids
Surgical excision: works best for ear keloids
Surgery +/- Radiation

59
Q

Seborrheic Keratosis - what is it?

A

benign tumor of the hair follicle

60
Q

Seborrheic Keratosis - distribution?

A

primarily distributed head, neck, trunk

61
Q

What are the “barnacles of life”?

A

seborrheic keratosis

62
Q

Seborrheic Keratosis - primary lesion?

A

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
Q

Dermatosis papulosa nigra?

A

variant of Seborrheic Keratosi - typically seen in Black and Asian

64
Q

Stucco keratosis?

A

variant of Seborrheic Keratosi - typically seen in acral areas

65
Q

Sign of Lesser-Trelat

A

variant of Seborrheic Keratosi

  • rapid increase in size or number
  • associated with internal malignancies, escpecially adenocarcinoma of the stomach (60%)
66
Q

Seborrheic Keratosis

Treatment

A

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
Q

Nevocellular Nevi

A

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
Q

Nevocellular nevi

age?

A

infancy to adult onset

69
Q

Nevocellular nevi

distribution?

A

any skin surface including mucous membrane

number of nevi increased on sun-exposed skin

70
Q

Normal Number of nevocellular nevi? caucasian

A

20 years of age = 20
Australian - number peaks in 2nd-3rd decade
men - 43
women 27

71
Q

3 growth patterns of nevocellular nevi - melanocytic nevi?

A

intradermal
junctional
compound (both)

72
Q

Intradermal nevus - local? - size? - primary lesion?

A

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
Q

Junctional nevus
local?
size?
primary lesion?

A

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
Q

Compound nevus
local?
size?
primary lesion?

A

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
Q

Nevocellular nevi

indications to treat?

A

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
Q

Nevocellular nevi

appropriate and inappropriate treatment options (3 and 4)

A 
Appropriate
Shave biopsy
Punch biopsy
Excision
Inappropriate
Electrodessication
Cryotherapy
Dermabrasion (exception- congenital nevus?)
Laser
77
Q

Blue nevus

A

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
Q

Blue nevus clinical features

  • congenital vs acquired?
  • population?
  • appearance?
A

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
Q

Blue Nevus

Treatment?

A

No treatment
Common option for unchanging lesions
Malignant blue nevus (very rare)

Surgical removal
Punch biopsy
Excision

80
Q

Congenital Nevi
How many?
Location?

A

May be solitary or multiple

May affect any cutaneous surface

81
Q

Congenital vs Acquired nevi?

A

Primary lesion identical to acquired nevi only differ in size - 1mm to huge (i.e. think bathing trunk nevi)

82
Q

Significance of hair on nevi?

A

none

83
Q

Complications of congenital nevi?

A

head, neck, posterior midline –> cranial an or leptomeningeal melanocytosis (the two innermost layers of tissues that cover the brain and spinal cord)

84
Q

What percent of newborns have congenital nevi?

A

1%

85
Q

Size of congenital nevi?

A

small 20cm

86
Q

Congenital nevi

Treatment?

A

Controversial

  • elective surgical excision
  • most authorities do not recommend - recommended by some if clinically feasable
87
Q

Medium to large congenital nevi (>10cm) occur in what fraction of newborns

A

1:20,000

88
Q

What is the calculated risk for malignant melanoma in congenital nevi?

A

1% per year in large congenital nevi (>40cm)

89
Q

Malignant melanoma in congenital nevi
what fraction appear in first 3 years
what fraction appear in first decade?

A

first 3 years 50%

first decade 60%

90
Q

Dysplastic nevus

3 types

A

Aytpical nevus
Clarks nevus
Nevus with Cytologic Aytpia and architectual disorder

91
Q

What is acquired melanocyte prolferation

A

Epidermal and/or dermal proliferation cytologically atypical nevomelanocytes

Abnormal growth pattern (Architectural disorder)

92
Q

Sporadic or familial dysplastic nevus?

A

sporadic atypical nevi are those that occur in patients without a family history of atypical nevi

93
Q

Dysplatic nevi

Sex ?

A

males = females

94
Q

Dysplastic nevi

Age?

A

age of onset - usually apparent by 20

95
Q

Dysplastic nevi

local?

A

any cutaneous site especially trunk

96
Q

Dysplastic nevi

number?

A

solitary to hundreds

97
Q

Dysplastic nevi

appearance?

A

round to oval or irregular

variation in color - tan/brown/black/red

98
Q

Dysplastic nevi

Margins?

A 
often indistinct (fuzzy)
pigment bleeds into surrounding skin, irregular margins
99
Q

Dysplastic nevi

size?

A

no limit

100
Q

Dysplastic nevi
Clinical importance
Melanoma?

A

Melanomas are contiguous with dysplatic nevi - 6.6%-70.3% in ten studies

101
Q

Dysplastic nevi

FAMMS?

A

Familial atypical mole and melanoma syndrome - risk of melanoma approaches 100%

102
Q

FAMM syndrome?

Criteria?

A

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
Q

FAMM pathogeneis

A

Germline mutations in 3 genes have been linked to a subset of hereditary melanomas and FAMM syndrome

104
Q

Is FAMM polygenetic or multifactorial?

A

Found in some but not all atypical nevi

inconsistent findings in different studies

105
Q

Dysplastic nevi treatment?

A

Sporadic or familial dysplastic nevi

  • mole mapping with dermoscopy
  • total body photography
  • remove the most atypical nevi, chanign or symptomatic nevi
106
Q

Dysplastic nevi treatmetn

  • clinically solitary?
  • biopsy proven atypical?
A

reasonable to surgically remove

controversial
some only excise lesions with moderate/severe atypia
NIH consensus panel-excise with 2-5mm margins

107
Q 
Cafe au Lait Macules
what are they 
when are they found
how are they distributed
multiple associated with?
A

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
Q

Crowe’s sign

A

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
Q

Neurofibromas

A

Soft flesh colored papules characterized by the “button hole sign”

Less commonly appear to be deep, firm, subcu nodules

110
Q

What causes neurofibromas

A

Focal proliferation of neural tissue within dermis

111
Q

Solitary neurofibromas vs. multiple

A

solitary - inconsequental

many - maybe neurofibromatosis

112
Q

Neurofibromatosis - Von Recklinghausens

Inheritance?
What % de novo?
Cuase?

A

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
Q

Neurofibromatosis Type 1: Diagnosis requires 2 or more of the following criteria

A
  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

Disease and Defense III (11 decks)

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