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Benign Disorders Flashcards

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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
What is a solar lentigo
Localized proliferation of melanocytes resulting from acute or chronic exposure to sunlight "sun spot" 1-3 cm
26
Usual onset for solar lentigo
>40 yo
27
Who/where are solar lentigo most common
MC sun exposed sites MC in caucasians
28
Presentation of solar lentigo
Strictly macular 1-3 cm Light yellow, light brown, or dark brown Round, oval, with slightly irregular borders and ill defined
29
What areas are sun lentigo common?
Forehead Cheeks Nose Dorsa of hands Forearms Upper back Chest Shins Sun exposed areas!
30
Treatment of solar lentigo
Cryotherapy Laser
31
What is a acrochordon?
Very common skin colored, brown, round, or oval pedunculated papiloma Usually constricted at base >1 mm-10 mm
32
Who most commonly gets acrochordon?
middle aged and elderly females obese patients
33
Acrochordon is usually asymptomatic but can be ----
tender following trauma or torsion can become crusted or hemorrhagic
34
where are acrochordon most commonly seen?
axillae inframammary groin neck eyelids
35
over time, what happens to acrochordon?
Become larger and more in number over time
36
treatment of acrochordon
snipping electrodesiccation cryotherapy
37
what is an epidermal inclusion cyst
epidermal cysts "sebaceous cysts" collection of keratin and lipid rich debris in epithelial sac within the dermis
38
etiology of epidermal inclusion cyst
plugged pilosebaceous units traumatic implantation of epidermal cells into deeper tissues
39
epidermiology of epidermal inclusion cyst
2:1 m:f 4th and 5th decades (30-50 yo)
40
clinical findings of epidermal inclusion cyst
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
lab/diagnostics for epidermal inclusion cyst
clinical if textbook presentation C&S if recurrent infection imaging or fine needle aspiration if atypical location
42
treatment of epidermal inclusion cyst?
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
course and prognosis of epidermal inclusion cyst
asymptomatic cysts may wax and wane with periods of inflammation rarely becomes malignant: watch for rapid growth, friability, bleeding
44
what is a lipoma?
benign collection of fat cells inside thin fibrous capsulew
45
what is the MC soft tissue tumor?
lipoma
46
MC onset of lipoma
between 40 and 60 yo
47
clinical findings of lipoma
soft, painless, slow growing, subcutaneous nodules 1-10 cm in size MC location: trunk, UE, hands, head, feet
48
Laboratory tests for lipoma
clinical diagnosis biopsy if pain, movement restriction, rapidly growing, firm
49
treatment for lipoma
surgery if pain, cosmesis or dx is unclear excision
50
what is a venous lake
dark blue violaceous, asymptomatic, soft papule resulting from dilated venule lesions few in number and remain for years
51
epidemiology of venous lake
mc >50 yo
52
where is venous lake mc located
face lips ears
53
etiology of venous lake
solar exposure genetics etiology unknown
54
pathophysiology of venous lake
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
what can venous lake be confused with?
nodular melanoma pigmented bcc pyogenic granuloma
56
characteristics of venous lake
compressed with pressure lightened with diascopy dermoscopy - vascular
57
treatment of venous lake
cosmetic reasons only electrosurgery laser surgical excision
58
what is urticaria
pruritic, raised, well-circumscribed areas of erythema and edema
59
pathogenesis of urticaria
mast cells and basophils release vasoactive substances (histamine, leukotriene C4, prostaglandins) resulting in extravasation of fluid into the dermis
60
types of urticaria
type I allergic IgE response complement mediated physical mediated autoimmune idiopathic
61
clinical findings of urticaria
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
lab/diagnostics for urticaria
acute: clinical diagnosis chronic: look for underlying cause
63
management of acute urticaria
emergency dept evaluation: acute urticaria can progress to life-threatening angioedema/anaphylactic shock triple regimen therapy: H1 antihistamine + H2 antihistamine + steroid
64
MOA of H1/H2 antihistamines?
Antagonists of the histamine 1/2 binding cellular receptors
65
what are the second gen H1 antihistamines?
loratadine desloratadine fexofenadine cetirizine
66
what are the first gen H1 antihistamines
diphenhydramine hydroxyzine
67
what are the h2 antihistamines
cimetidine famotidine ranitidine
68
what is the moa of oral glucocorticoids
stabilize mast cell membrane, inhibits further histamine release
69
what are the oral glucocorticoids used in urticaria
prednisone (use for short term, 5 day non-tapering course)
70
management of chronic urticaria
antihistamines PRN refer to dermatology for further evaluation/management
71
course and prognosis of urticaria
depends on identification and treatment of underlying cause acute generally self-limiting within 24 hours chronic can impair quality of life
72
prevention of urticaria
identify and avoid etiologic cause
73
what is pyogenic granuloma?
rapidly developing vascular lesion usually following minor trauma
74
pyogenic granuloma is commonly ______
solitary, friable
75
clinical presentation of pyogenic granuloma lesion
smooth +/- crusts +/- erosions bright red dusky red violaceous brown-black papule
76
treatment of pyogenic granuloma
surgical excision ED &C can be mistaken for amelanotic nodular melanoma
77
what are types of hemangiomas?
cherry angioma capillary hemangioma strawberry angioma
78
what is the MC tumor in babies and how does it present
hemangioma endothelial hyperplasia (not vascular malformation) starts at 2-4 weeks of age and can grow as patient ages or regress F>M
79
clinical presentation of hemangioma
red soft compressible papule or nodule 1-10 cm typically solitary MC on head and neck
80
what are the 4 general types of hemangiomas?
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
if you see hemangiomas, what do you need to be concerned about and how are they evaluated?
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
treatment of hemangioma
propranolol 1st line, cardiology in most cases to monitor prednisone laser and surgical options also available
83
what is vitiligo
depigmenting disorder characterized by a patchy absence of melanocytes resulting from destruction or discontinued function of the melanocyte
84
onset of vitiligo
1/2 of all cases begins between 10-30 years of age
85
epidemiology of vitiligo
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
pathogenesis of vitiligo
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
clinical manifestations of vitiligo
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
presentation types of vitiligo
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
diagnosis of vitiligo
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
Course and management of vitiligo
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
how are glucocorticoids used in vitiligo
intermittent application of high potency for single or few macules, but if no response in 2 months, discontinue
92
how is topical photochemotherapy used in vitiligo
combines topical 8-methoxypsoralen and UVA only only used for single or small macules and may require over 100 treatments to finish
93
how is systemic photochemotherapy used for vitiligo
oral 8-MOP and UVA therapy treatment for 1 year with poor results for lip tip distribution genitals shielded and not treated
94
how is narrow-band UVB used for vitiligo
effective treatment of choice in children >6 yo
95
what is minigrafting for vitiligo
small skin grafts taken from normally pigmented skin used in refractory cases
96
what is depigmentation for vitiligo
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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