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Benign Disorders Flashcards

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Dermatology Board Prep flashcards
1
Q

What is seborrheic keratosis

A

Benign neoplasm of epidermis
Typically located on chest and back
Extremely common

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2
Q

clinical presentation of seborrheic keratosis

A

raised, stuck-on appearing papules and plques with well-defined borders
asymptomatic, but when irritated or traumatized become pruritic or painful with associated redness or bleeding

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3
Q

Etiology of seborrheic keratosis

A

Unknown, but familial autosomal dominant inheritance

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4
Q

As patients age what happens to SK

A

increase in incidence and number

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5
Q

How do SK start out?

A

flat wrinkled plaque with postage stamp appearance

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6
Q

what is lichenoid keratosis

A

inflamed seborrheic keratosis that presents as a pink shiny plaque or papule with appearance resembling nodular or cystic basal cell cancer

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7
Q

What is the term for papular seborrheic keratoses on the face of individuals with darker skin phototypes

A

dermatosis papulosa nigra

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8
Q

if you see rapid onset of numerous SKs what should you be concerned for?

A

Malignancy

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9
Q

Multiple eruptic SKs in association with a visceral cancer is referred to as the sign of —–. What is the most common associated malignancy?

A

Leser-Trelat
Adenocarcinoma of the gastrointestinal tract

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10
Q

Look for what in seborrheic keratosis

A

Waxy, stuck on verrucous appearing papules or plaques
Color variable and may range from skin colored, pink, light brown, yellow-brown, and brownish black to black
Pigmentation variable within a single lesion
Scratching surface shows scaling, rough appearance with variable amount of scale (may be considerable)
Well circumscribed

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11
Q

Where can seborrheich keratosis occur?

A

any body site

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12
Q

what is a clinical variant of seborrheic keratosis and how does it present?

A

skin tag
pedunculated 1-2 mm, furrowed, rough-surfaced polyps most commonly around neck or in axillae and show surface morphology similar to SK

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13
Q

Diagnostic Pearls for SK

A

stuck-on appearance with side lighting via penlight or dermascope
growths have coarse, waxy scale that can be removed to show raw, moist base
individual lesions grow rapidly and reach a static size without further growth

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14
Q

common features of SK on dermoscopy

A

ridges, fissures, white pinpoint milia-like cysts
comedo-like openings, all better visualized with non-polarized dermoscopy
ridges and fissures together form cerebriform pattern
vasculature pattern” looped or hairpin vessels
borders sharply demarcated
evolving seborrheic keratoses overlap with solar lentigos with broken, interrupted lines, few comedo-like openings, and borders that are scalloped or moth-eaten

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15
Q

best tests for seborrheic keratosis

A

clinical
dermoscopy to assist with differentiating between seborrheic keratosis, melanocytic nevi, and melanoma
if concern for malignancy, must biopsy

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16
Q

common histopathology findings of seborrheic keratosis

A

sharply demarcated proliferation of monotonous epidermal keratinocytes
flat, exophytic or endophytic
small, keratin-filled cysts present within the tumor

occasionally
well-dermarcated nests of basaloid cells in clonal variant
spongiosis with squamous eddies
reticulated, acanthotic, or papillomatous
variable inflammatory cell infiltrate, may be sparse lymphocytic or lichenoid

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17
Q

management of seborrheic keratosis

A

SKs are generally removed for cosmetic reasons, as lesions have no malignant potential
Reassurance regarding chronic benign nature

If multiple SKs look at it with dermoscopy and maybe biopsy
If multiple eruptive keratosis, work up for internal malignancy

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18
Q

How are seborrheic keratosis removed?

A

Cryosurgery (but scar)
Curettage and cautery
Chemical peels for small and superficial SK
Laser therapy
Shave excision for larger lesions

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19
Q

WHat is melasma?

A

Acquired light or dark brown pigmentation that occurs in exposed areas by the sun MC face

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20
Q

RFs for melasma

A

Pregnancy
Genetics
Idiopathic
Sun exposure
Ingested contraception
Medications
F>M
Hot climates

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21
Q

Clinical presentation of melasma

A

Macular
Hyperpigmented skin
Sharply defined
Usually uniform
MC on malar and frontal areas of face

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22
Q

Tests for melasma

A

Woods lamp not necessary but would show epidermal pigment enhancement

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23
Q

Treatment for melasma

A

Tri-luma QHS: fluocinolone, hydroquinone, tretinoin
Laser

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24
Q

Counseling for melasma

A

Avoidance of sun
Sunscreen >30 spf re-apply q 80 min: titanium dioxide and zinc oxide
remove estrogen exposure

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25
Q

What is a solar lentigo

A

Localized proliferation of melanocytes resulting from acute or chronic exposure to sunlight
“sun spot”
1-3 cm

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26
Q

Usual onset for solar lentigo

A

> 40 yo

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27
Q

Who/where are solar lentigo most common

A

MC sun exposed sites
MC in caucasians

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28
Q

Presentation of solar lentigo

A

Strictly macular 1-3 cm
Light yellow, light brown, or dark brown
Round, oval, with slightly irregular borders and ill defined

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29
Q

What areas are sun lentigo common?

A

Forehead
Cheeks
Nose
Dorsa of hands
Forearms
Upper back
Chest
Shins

Sun exposed areas!

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30
Q

Treatment of solar lentigo

A

Cryotherapy
Laser

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31
Q

What is a acrochordon?

A

Very common skin colored, brown, round, or oval pedunculated papiloma
Usually constricted at base >1 mm-10 mm

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32
Q

Who most commonly gets acrochordon?

A

middle aged and elderly
females
obese patients

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33
Q

Acrochordon is usually asymptomatic but can be —-

A

tender following trauma or torsion
can become crusted or hemorrhagic

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34
Q

where are acrochordon most commonly seen?

A

axillae
inframammary
groin
neck
eyelids

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35
Q

over time, what happens to acrochordon?

A

Become larger and more in number over time

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36
Q

treatment of acrochordon

A

snipping
electrodesiccation
cryotherapy

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37
Q

what is an epidermal inclusion cyst

A

epidermal cysts
“sebaceous cysts”
collection of keratin and lipid rich debris in epithelial sac within the dermis

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38
Q

etiology of epidermal inclusion cyst

A

plugged pilosebaceous units
traumatic implantation of epidermal cells into deeper tissues

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39
Q

epidermiology of epidermal inclusion cyst

A

2:1 m:f
4th and 5th decades (30-50 yo)

40
Q

clinical findings of epidermal inclusion cyst

A

asymptomatic unless inflamed or infected
inflammation results from cyst wall rupture
flesh colored, round, firm nodules +/- central pore/punctum
contents malodorous
MC on face, neck, trunk, scrotum

41
Q

lab/diagnostics for epidermal inclusion cyst

A

clinical if textbook presentation
C&S if recurrent infection
imaging or fine needle aspiration if atypical location

42
Q

treatment of epidermal inclusion cyst?

A

asymptomatic - no treatment unless cosmetic concern
inflamed - I&D
infected - I&D +/- abx therapy
surfical excision: punch, minimal incision, or elliptical excision technique (with goal to completely remove sac, performed when not inflamed)
surgical consult if cyst in atypical location

43
Q

course and prognosis of epidermal inclusion cyst

A

asymptomatic cysts may wax and wane with periods of inflammation
rarely becomes malignant: watch for rapid growth, friability, bleeding

44
Q

what is a lipoma?

A

benign collection of fat cells inside thin fibrous capsulew

45
Q

what is the MC soft tissue tumor?

A

lipoma

46
Q

MC onset of lipoma

A

between 40 and 60 yo

47
Q

clinical findings of lipoma

A

soft, painless, slow growing, subcutaneous nodules
1-10 cm in size
MC location: trunk, UE, hands, head, feet

48
Q

Laboratory tests for lipoma

A

clinical diagnosis
biopsy if pain, movement restriction, rapidly growing, firm

49
Q

treatment for lipoma

A

surgery if pain, cosmesis or dx is unclear
excision

50
Q

what is a venous lake

A

dark blue violaceous, asymptomatic, soft papule resulting from dilated venule
lesions few in number and remain for years

51
Q

epidemiology of venous lake

A

mc >50 yo

52
Q

where is venous lake mc located

A

face
lips
ears

53
Q

etiology of venous lake

A

solar exposure
genetics
etiology unknown

54
Q

pathophysiology of venous lake

A

dilated cavity lined with a single layer of flattened endothelial cells filled with red blood cells and surrounded by thin wall of fibrous tissue

55
Q

what can venous lake be confused with?

A

nodular melanoma
pigmented bcc
pyogenic granuloma

56
Q

characteristics of venous lake

A

compressed with pressure
lightened with diascopy
dermoscopy - vascular

57
Q

treatment of venous lake

A

cosmetic reasons only
electrosurgery
laser
surgical excision

58
Q

what is urticaria

A

pruritic, raised, well-circumscribed areas of erythema and edema

59
Q

pathogenesis of urticaria

A

mast cells and basophils release vasoactive substances (histamine, leukotriene C4, prostaglandins)
resulting in extravasation of fluid into the dermis

60
Q

types of urticaria

A

type I allergic IgE response
complement mediated
physical mediated
autoimmune
idiopathic

61
Q

clinical findings of urticaria

A

raised, erythematous pink skin colored wheals with central pallor
shape and size change rapidly: round, oval, acriform, annular, serpiginous
individual lesion resolves within 24 hours
+/- dermatographism
H&P should focus on underlying cause

62
Q

lab/diagnostics for urticaria

A

acute: clinical diagnosis
chronic: look for underlying cause

63
Q

management of acute urticaria

A

emergency dept evaluation: acute urticaria can progress to life-threatening angioedema/anaphylactic shock
triple regimen therapy: H1 antihistamine + H2 antihistamine + steroid

64
Q

MOA of H1/H2 antihistamines?

A

Antagonists of the histamine 1/2 binding cellular receptors

65
Q

what are the second gen H1 antihistamines?

A

loratadine
desloratadine
fexofenadine
cetirizine

66
Q

what are the first gen H1 antihistamines

A

diphenhydramine
hydroxyzine

67
Q

what are the h2 antihistamines

A

cimetidine
famotidine
ranitidine

68
Q

what is the moa of oral glucocorticoids

A

stabilize mast cell membrane, inhibits further histamine release

69
Q

what are the oral glucocorticoids used in urticaria

A

prednisone (use for short term, 5 day non-tapering course)

70
Q

management of chronic urticaria

A

antihistamines PRN
refer to dermatology for further evaluation/management

71
Q

course and prognosis of urticaria

A

depends on identification and treatment of underlying cause
acute generally self-limiting within 24 hours
chronic can impair quality of life

72
Q

prevention of urticaria

A

identify and avoid etiologic cause

73
Q

what is pyogenic granuloma?

A

rapidly developing vascular lesion usually following minor trauma

74
Q

pyogenic granuloma is commonly ______

A

solitary, friable

75
Q

clinical presentation of pyogenic granuloma lesion

A

smooth
+/- crusts
+/- erosions
bright red
dusky red
violaceous
brown-black papule

76
Q

treatment of pyogenic granuloma

A

surgical excision
ED &C

can be mistaken for amelanotic nodular melanoma

77
Q

what are types of hemangiomas?

A

cherry angioma
capillary hemangioma
strawberry angioma

78
Q

what is the MC tumor in babies and how does it present

A

hemangioma
endothelial hyperplasia (not vascular malformation)
starts at 2-4 weeks of age and can grow as patient ages or regress
F>M

79
Q

clinical presentation of hemangioma

A

red
soft
compressible papule or nodule 1-10 cm typically
solitary
MC on head and neck

80
Q

what are the 4 general types of hemangiomas?

A

simple: resolve by age 5-10
deep: lower dermis and subq fat/bluish with telangiectasias
multiple: small <2 mm papules over entire body
congenital: present at birth, purplish/telangiectasia/large veins

81
Q

if you see hemangiomas, what do you need to be concerned about and how are they evaluated?

A

If they are deep and multiple they can obstruct vital functions: vision, larynx, nose, mouth

MRI to eval
doppler and arteriography to see blood flow

82
Q

treatment of hemangioma

A

propranolol 1st line, cardiology in most cases to monitor
prednisone
laser and surgical options also available

83
Q

what is vitiligo

A

depigmenting disorder characterized by a patchy absence of melanocytes resulting from destruction or discontinued function of the melanocyte

84
Q

onset of vitiligo

A

1/2 of all cases begins between 10-30 years of age

85
Q

epidemiology of vitiligo

A

affects all races
reported and treated more frequently in races of darker skin complexion
genetic: >30% have first degree relative with vitiligo likely polygenic transmission affecting multiple gene loci responsible for immune function

86
Q

pathogenesis of vitiligo

A

autoimmune: selected melanocytes destroyed by activated lymphocytes
neurogenic: interaction of melanocytes and nerve cells
self-destruction: melanocytes destroyed by toxic substances formed as part of normal melanin biosynthesis

87
Q

clinical manifestations of vitiligo

A

individual chalk macules with sharp margin
may see loss of color to mucosal membranes, retina or hair overlying areas of depigmented skin
ranging from 5 mm to 5 cm or larger
painless and without pruritis
often seen first in sun-exposed areas
may report new macules in areas of trauma

88
Q

presentation types of vitiligo

A

generalized (MC): symmetric widespread
lip tip pattern involves skin around mouth, fingers, and toes as well as nipples and genitalia

segmental: only one side or part of body in one band that do not extend beyond
usually younger age taking 1- 2 years to progress then stops

localized vitiligo: focal to only 1-3 macules in a single sight

vitiligo universalis: confluence of macules resulting in only a few pigmented areas

89
Q

diagnosis of vitiligo

A

clinical

wood’s lamp to examine macules on lighter skin

skin biopsy in cases difficult to diagnose
histopathology: normal skin with lack of melanocytes

labs if autoimmune disorder is suspected: TSH, T4, ANA, CBC for pernicious anemia, ACTH stimulation for Addison’s

90
Q

Course and management of vitiligo

A

no cure
1/3 of aptients report few areas of spontaneous repigmentation
concern for social/psychological stress
sunburn precautions with >spf 30
cosmetic cover up: dyes or makeup to hide white macules, self tanner applied to white macules
repigmentation with topical glucocorticoids or topical photochemotherapy or systemic photochemotherapy or narrow-band UVB
minigrafting
depigmentation

91
Q

how are glucocorticoids used in vitiligo

A

intermittent application of high potency for single or few macules, but if no response in 2 months, discontinue

92
Q

how is topical photochemotherapy used in vitiligo

A

combines topical 8-methoxypsoralen and UVA
only
only used for single or small macules and may require over 100 treatments to finish

93
Q

how is systemic photochemotherapy used for vitiligo

A

oral 8-MOP and UVA therapy
treatment for 1 year with poor results for lip tip distribution
genitals shielded and not treated

94
Q

how is narrow-band UVB used for vitiligo

A

effective
treatment of choice in children >6 yo

95
Q

what is minigrafting for vitiligo

A

small skin grafts taken from normally pigmented skin used in refractory cases

96
Q

what is depigmentation for vitiligo

A

bleaching of normally pigmented skin using hydroquinone 20% (MEH)
cream is permanent and irreversible chalk white skin
recommended in patients with extensive vitiligo

Dermatology (12 decks)

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