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Clin Med III: Dermatology > Benign, Neoplasms, Hyperplasias, and Pigmentary Disorders > Flashcards

Benign, Neoplasms, Hyperplasias, and Pigmentary Disorders Flashcards

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Dermatology Board Prep flashcards
1
Q
  • extremely common benign neoplasms of the epidermis
  • MC chest and the back
  • Few or hundreds of these raised, “stuck-on”-appearing papules and plaques with well-defined borders
A

Seborrheic Keratosis

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2
Q

cause of Seborrheic Keratosis?

A

unknown,
familial trait - autosomal dominant mode of inheritance

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3
Q

SKs tend to increase in incidence and number with increasing ?

A

age

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4
Q

how may SKs start of as?

A

a flat wrinkled plaque with a “postage stamp” appearance (flat seborrheic keratosis)

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5
Q

T/F: SKs are MC symptomatic

A

F: asymptomatic
but when irritated or traumatized, they may become pruritic or painful with associated redness or bleeding

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6
Q

inflamed seborrheic keratosis that presents as a pink shiny papule or plaque with an appearance that resembles that of a nodular or cystic basal cell cancer.

A

lichenoid keratosis

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7
Q

papular seborrheic keratoses (most often seen as dark brown 1-3 mm papules) on the face of individuals with darker skin phototypes.

A

Dermatosis papulosa nigra

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8
Q

Relatively rapid onset of numerous SKs
may be a cutaneous sign of ?

A

internal malignancy

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9
Q

Multiple eruptive SKs is associated with?
what is the other name for it?

A
  • visceral cancer - MC adenocarcinoma of GI tract.
  • the sign of *Leser-Trélat *
    *
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10
Q
  • Waxy, “stuck-on,” verrucous-appearing papules or plaques
  • skin-colored, pink, light brown, yellow-brown, brownish-black to black.
  • Pigmentation variable within a lesion.
  • Scratching shows scaling, rough appearance
  • Lesions are usually well-circumscribed.
  • They may occur on any body site.
A

SKs

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11
Q

pedunculated 1-2 mm, furrowed, rough-surfaced polyps appear most commonly around the neck or in the axillae
MC in middle aged and elderly

A

skin tag - acrochordon

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12
Q

The stuck-on appearance of SKs can sometimes be best appreciated with ?

A

side-lighting - Hold a penlight or dermatoscope parallel to skin surface at edge of SK

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13
Q
  • Ridges, fissures, white pinpoint milia-like cysts, and comedo-like openings - best with non-polarized dermoscopy
  • ridges + fissures = cerebriform pattern
  • looped/hairpin vessels
  • sharply demarcated borders.
  • Early evolving has many features similar to solar lentigines: broken, interrupted lines (fingerprinting), few comedo-like openings, and borders that are scalloped or moth-eaten.

these dermoscopy features are for what lesion?

A

Seborrheic Keratosis

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14
Q

how to dx SK?

A
  • clinically
  • Dermoscopy can help differentiating SK vs melanocytic nevi vs melanoma.
  • Bx if any concern for malignancy
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15
Q

histopathology findings of SKs

A
  1. Sharply demarcated proliferation of monotonous epidermal keratinocytes
  2. Flat, exophytic or endophytic
  3. Small keratin-filled cysts (ie, horn cysts) present within tumor
    - Occasional features
    - Well-demarcated intraepidermal nests of basaloid cells (Borst-Jadassohn phenomenon) 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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16
Q

mgmt pearls for SKs

A
  • removed only for cosmetic reasons
  • Patient reassurance
  • if multiple SKs, a suspicious pigmented lesion may be overlooked.
  • multiple eruptive SKs = prompt search for underlying internal malignancy, esp if patient hx or ROS is suspicious for cancer.
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17
Q

tx options for SKs

A
  1. Cryosurgery (MC) - dyspigmentation
  2. Curettage and cautery
  3. Chemical peels (eg, trichloroacetic acid) - for small and superficial SKs
  4. Laser therapy (pulsed CO2, alexandrite, and ER:YAG)
  5. Shave excision - for larger lesions
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18
Q
  • Acquired light or dark brown pigmentation that occurs in exposed areas by the sun
  • MC Face
A

Melasma

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19
Q

RF for Melasma

A
  • Pregnancy (“mask”)
  • Genetics
  • Idiopathic
  • Sun exposure
  • Ingested contraception
  • Medications (diphenylhydantoin)
    *
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20
Q
  • Macular
  • Hyperpigmented skin
  • Sharply defined
  • Usually uniform
  • MC on malar and frontal areas of face
  • F>M; Hot climates

dx?
w/u?
tx?

A
  • melasma
  • clinical; Woods lamp not needed - Shows epidermal pigment enhancement
  • Tri-Luma QHS (fluocinolone 0.01%, hydroquinone 4%, tretinoin 0.05%); laser
  • avoid sun, SPF +30 (Titanium dioxide and zinc oxide, remove estrogen exposure
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21
Q
  • Localized proliferation of melanocytes resulting from acute or chronic exposure to sunlight
  • 1-3 cm
  • Onset: >40 y/o
A

Solar Lentigo

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22
Q

Solar Lentigos are MC in who?

A
  • MC on sun exposed sites
  • MC Caucasians - Skin Type 1 and 2
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23
Q
  • Light yellow, light brown, or dark brown (variegated)
  • Round, oval, with slightly irregular borders and ill defined
  • Skin lesions strictly macular - 1-3 cm

dx? tx?

A
  • Solar Lentigo
  • Cryo, Laser
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24
Q

what are the sun exposed areas?

A
  • Forehead
  • Cheeks
  • Nose
  • Dorsa of hands
  • Forearms
  • Upper back
  • Chest
  • Shins
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25
Q

acrochordons are MC in who?

A
  • females
  • obese individuals
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26
Q

Acrochordons are MC in ___ areas

A

intertriginous

  • Axillae
  • Inframammary
  • Groin
  • Neck
  • Eyelids
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27
Q

acrochordons are seen in with what other 2 conditions

A
  1. Acanthosis Nigricans
  2. Metabolic Syndrome
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28
Q

acrochordons become larger and more in number over time especially during ?

A

pregnancy

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29
Q

tx for acrochordon

A
  1. Snipping
  2. Electrodesiccation
  3. Cryo
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30
Q

a collection of keratin and lipid rich debris in an epithelial sac within the dermis

A

Epidermal Inclusion Cyst
aka: epidermal cysts, “sebaceous cysts” - avoid using term sebaceous cyst

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31
Q

cause of Epidermal Inclusion Cyst

A
  • plugged pilosebaceous units
  • traumatic implantation of epidermal cells into deeper tissues
32
Q

Epidermal Inclusion Cyst MC in who?

A
  • 2:1 M>F
  • 4th and 5th decades (30-50 y/o)
33
Q
  • asx unless inflamed or infected - inflammation results from cyst wall rupture
  • flesh colored, round, firm nodules - +/- central pore/punctum
  • contents is malodorous - “rancid cheese”
  • MC on face, trunk, neck, scrotum
A

Epidermal Inclusion Cyst

34
Q

w/u for Epidermal Inclusion Cyst

A
  • clinical dx
  • C&S if recurrent infection
  • Imaging or FNA if atypical location (breast, bone)
35
Q

tx for epidermal inclusion cyst

A
  1. asx - none unless cosmetic concern
  2. inflamed - I&D
  3. infected - I&D, +/- abx therapy
  4. Excision: complete removal of cyst sac
    - punch, minimal incision or elliptical excision
    - best performed when cyst is not inflamed
  5. Surgical consult if cyst is located in atypical location
36
Q

course and prognosis of epidermal inclusion cyst

A
  1. asx cysts may wax and wane with periods of inflammation
  2. rarely becomes malignant - watch for rapid growth, friability, bleeding
37
Q

a benign collection of fat cells inside thin fibrous capsule
MC soft tissue tumor

A

Lipoma

38
Q
  • Onset MC between 40-60 y/o
  • soft, painless, slow growing, subcutaneous nodules
  • 1-10 cm in size
  • MC location - trunk, UE; hands, head, feet are less common

dx?
w/u?
tx?

A
  1. lipoma
  2. clinical; bx if painful, restricts movement, grows rapidly, firm
  3. surgery if painful, comesis or dx unclear
39
Q
  • Dark blue violaceous, asymptomatic, soft papule resulting from a dilated venule
  • MC on face, lips, and ears
  • MC > 50 years old
A

Venous Lake

40
Q

cause of venous lakes?

A
  • Etiology unknown
  • potentially from Solar exposure and Genetics
41
Q

Because of its dark blue or sometimes even black color, Venous lakes may be confused with ? (3)

A
  1. nodular melanoma
  2. pigmented bcc
  3. pyogenic granuloma
42
Q

ways to r/o malignancy in venous lakes?

A
  • Compressed with pressure
  • Lightened with diascopy
  • Dermoscopy = vascular
43
Q

tx for venous lakes

A

Cosmetic reasons only

  1. Electrosurgery
  2. Laser
  3. Surgical excision
44
Q

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

A

urticaria

45
Q

pathophys of urticaria

A

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

46
Q

causes of urticaria

A
  1. type I allergic IgE response
  2. complement-mediated - infectious, serum sickness, transfusion rxn
  3. physical mediated - pressure, cold, cholingergic
  4. autoimmune - SLE, RA, thyroid
  5. idiopathic
47
Q

how are urticarias categorized

A
  1. acute < 6w - infection, allergy
  2. chronic > 6w - physical, autoimmune
48
Q
  • raised, erythematous-pink-skin colored wheals with central pallor
  • shape and size change rapidly - round, oval, acriform, annular, serpiginous
  • individual lesion resolves < 24 h
  • +/- dermatographism
  • H&P should focus on underlying cause

dx?
w/u?

A
  • Urticaria
  • clinical, look for underlying cause
49
Q

general mgmt for Urticaria

A
  • ED eval - acute can progress to life-threatening angioedema/anaphylactic shock
  • Triple Therapy: H1 (1st line) + H2 + steroid is often recommended
50
Q

types of H2 antihistamines

A
  1. cimetidine(Tagamet)
  2. famotidine(Pepcid)
  3. ranitidine(Zantac)
51
Q

types of 2nd gen antihistamines

A
  • loratadine(Claritin)
  • desloratadine(Clarinex)
  • fexofenadine(Allegra)
  • cetirizine(Zyrtec)
52
Q

types of 1st gen antihistamines

A
  • diphenhydramine (Benadryl)
  • hydroxyzine (Vistaril)
53
Q

MOA of oral GC

A
  • stabilize mast cell membrane, inhibits further histamine release
  • Prednisone - short term, 5 day non-tapering course
54
Q

tx for chronic urticaria

A
  • antihistamines prn
  • refer to dermatology for further evaluation/management
55
Q

prognosis of urticaria

A
  1. depends on identification and tx of underlying cause
    - acute generally self-limiting within 24 hours
    - chronic can impair quality of life
56
Q

Rapidly developing vascular lesion usually following minor trauma
Very common solitary - Erodes, Vascular bleeds spontaneously

A

Pyogenic Granuloma

57
Q

s/s of Pyogenic Granuloma

A
  • Smooth
  • +/- crusts
  • +/- erosions
  • Bright red
  • Dusky red
  • Violaceous
  • Brown-black papule
58
Q

tx for Pyogenic Granuloma

A

Surgical excision
ED&C

59
Q

Pyogenic Granulomas can be misaken for ?

A

amelanotic nodular melanoma

60
Q

3 dx of Hemangioma

A

Cherry angioma
Capillary hemangioma
Strawberry angioma

61
Q

MC tumor in babies

A

vascular tumor - endothelil hyperplasia

NOT a vascular malformation

62
Q

s/s of hemangiomas

A
  • Red
  • Soft
  • Compressible papule nodule - 1-10cm
  • Solitary
  • MC on head and neck
63
Q

4 types of hemangiomas

A
  1. Simple: Resolve on own by year 5-10
  2. Deep (aka cavernous): Lower dermis and subq fat / bluish w/ telangiectasias
  3. Multiple: Small < 2mm papules (entire body)
  4. Congenital: Present at birth; Purplish/telangiectasia/large veins
64
Q

how can deep and multiple hemangiomas be problematic?
w/u?

A
  • obstruct vital functions - vision, larynx, nose, mouth
  • MRI to eval; doppler and arteriography to see blood flow
65
Q

tx for hemangioma

A
  • Propranolol 1st line
  • Refer to Cardiology
  • Prednisone
  • Laser and surgical possible
66
Q

a depigmenting disorder characterized by a patchy absence of melanocytes
results from a destruction or discontinued function of the melanocyte
Onset: (50%) 10-30 y/o

A

vitiligo

67
Q

?% of a patients will have a first degree relative with vitiligo

A

> 30 %

68
Q

vitiligo is likely a ___ transmission
affecting multiple gene loci responsible for immune function

A

polygenic

69
Q

3 Theories about the mechanism of destruction of melanocytes

A
  • Autoimmune: Selected melanocytes are destroyed by certain lymphocytes that have been activated for unknown reasons.
  • Neurogenic: Interaction of the melanocytes and nerve cells.
  • Self-destruction: Melanocytes are destroyed by toxic substances formed as part of normal melanin biosynthesis.
70
Q
  • individual “chalk” white macules with sharp margins - 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 pruritus
  • Often seen first in sun-exposed areas
  • May report new macules in areas of recent trauma (Koebner phenomenon)
A

vitiligo

71
Q

4 presentation types of vitiligo

A
  1. generalized
  2. segmental
  3. localized
  4. vitiligo universalis
72
Q
  • Symmetrical with widespread distribution.
  • “Lip-tip” pattern involves skin around mouth, fingers and toes, as well as nipples and genitalia

which type of vitiligo

A

generalized

73
Q
  • Only one side or part of body in one band that do not extend beyond the initial one-sided region.
  • Younger age, taking 1-2 years to progress, then stops

which type of vitiligo

A

segmental

74
Q

Focal to only 1-3 macules in a single sight

which type of vitiligo

A

localized

75
Q

Confluence of macules resulting in only a few pigmented areas.

which type of vitiligo

A

Vitiligo Universalis

76
Q

w/u for vitiligo

A
  • Clinical
  • Wood’s lamp - evaluate macules on lighter skin
  • Skin bx - required in cases difficult to dx; Histopathology - nml skin with lack of melanocytes
  • Labs if autoimmune disorder is suspected - TSH, T4, fasting glucose, ANA, CBC for pernicious anemia, ACTH stimulation for Addison’s,
77
Q

Course and Management of vitiligo

A
  • No cure
  • ⅓ of pts may report a few areas of spontaneous repigmentation
  • Concern for social / psychological stress
  • SPF >30
  • Cosmetic cover-up - Dyes or makeup to hide the white macules; Self tanner applied to the white macules

Clin Med III: Dermatology (13 decks)

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