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MSK II Exam I > Skin Path (Gomez) > Flashcards

Skin Path (Gomez) Flashcards

1
Q

Fibroepithelial Polyps (FEP)

A 
Also known as 
skin tags
acrochordon
fibroma molle
squamous papilloma

Occur in individuals usually age 30 or greater and particularly in obese individuals
Associated with areas of rubbing by clothing; collar of neck or groin
Has vascular supply and variable stroma from fatty to fibrous

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2
Q

Epithelial Inclusion & Pilar Cysts

A

Also known as
epidermal cyst
follicular infundibular cyst
wen

Occur in areas with lots of hair follicles (face, scalp, trunk)
Caused by obstruction of hair follicle at infundibulum

  • Filled with keratinous debris
    Lining of cysts
    • Epithelial inclusion: squamous epithelium with a granular cell layer
    • Trichilemmal/pilar: squamous epithelium with no granular cell layer

Rupture (trauma) → pain and
* foreign body granulomatous giant cell inflammatory reaction to the keratinaceous debris

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3
Q

Seborrheic Keratosis (SK)

A

Proliferation of * epidermal basal cells
Usually middle-aged or older
Roundish, flat & elevated
“Postage stamp” appearance
On non-exposed skin (trunk, proximal extremities, lateral neck)
Many have mutations in fibroblast growth factor receptor 3
Removed for cosmetic reasons or untrained clinician thinks it resembles a malignant melanoma
* Sign of Leser-Trélat – acute onset of SKs with malignancies (GI mostly)

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4
Q

Adnexal Neoplasms

A 
Overwhelming majority (99%) are benign
Arise from the ductal and glandular epithelial cells of adnexa

Benign adnexal tumors are
Symmetrical, small (<1 cm), superficial, vertically orientated

Malignant adnexal tumors are 
Asymmetrical, large, deep, wide
Sebaceous carcinoma 
Most common type of malignant adnexal neoplasm, but quite uncommon
Eccrine carcinoma 
Apocrine carcinoma

Hundreds of different neoplasms arise from or have adnexal features!!!
(eccrine or apocrine glands or ducts, hair-bulb germinal epithelium or sebaceous glands)

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5
Q

Cowden syndrome

A

multiple tricholemmomas with dominant inheritance (hair follicles)

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6
Q

Muir-Torre syndrome

A

sebaceous adenomas with association colorectal malignancy (variant of Lynch)

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7
Q

Turban tumor

A

massive confluent cylindromas (forehead and scalp - eccrine gland)

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8
Q

cylindroma occurs where?

A

forehead

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9
Q

trichoepithelioma occurs where?

A

eyes, nose, cheek

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10
Q

Dermal Lumps and Bumps- colors

A

Hemangioma - Red

Xanthomas – Yellow

Fibrohistiocytic lesions – normal tan-brown skin tone or darker

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11
Q

Benign Fibrous Histiocytoma

A 
More common name is * dermatofibroma
Benign 
In adults, frequently on the legs of young – middle aged women
Tan-brown, usually <1.0 cm
May occasionally be tender
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12
Q

Some Benign Skin Pigment Disorders

A

↑ melanin in keratinocytes: Normal number melanocytes

  • Suntan
  • Freckles
  • Café au lait spots
  • Melasma

↑ melanin in keratinocytes: small ↑ melanocytes
- Solar lentigo

Acquired pigmentation

  • Skin tattoo
  • Amalgam tattoo

↓ melanin in keratinocytes

  • Acute transient vitiligo
  • Albinism

Loss of melanocytes
- Chronic vitiligo

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13
Q

Suntan

A

Due to ultraviolet light exposure

UVB exposure →
↑ melanosomes in melanocytes →
↑ melanin per keratinocyte→
↑ protection against solar radiation 
	(mid-UV [UVB] spectrum)
  • Chronic skin damage and neoplasia also induced by exposure to ultraviolet radiation
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14
Q

hypermelanosis

A

small spots = freckles (ephelides)

large area = cafe au lait spot

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15
Q

Neurofibromatosis Type 1

A 
Autosomal dominant disorder
* NF1 gene mutation that blocks encoding of neurofibromin (RAS inhibitor)
* Neurofibromas (including plexiform)
Can develop * malignant nerve sheath tumors
* Café au lait spots (macules)
Freckles in axilla
Optic nerve gliomas
* Lisch nodules on iris
      (melanotic hamartomas)
Macrocephaly
Scoliosis
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16
Q

Melasma (Chloasma)

A

= mask of pregnancy

Blotchy hypermelanosis
Symmetrical
Cheeks and forehead
Less frequently on upper lip and neck

Women&raquo_space;> men

Occurs with
Pregnancy
Oral contraceptives
Menopause

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17
Q

Acanthosis Nigricans

A
  • Epidermal hyperplasia of stratum spinosum and hyperpigmentation

Prefers flexural regions
axillae, skin folds of neck, groin and anogenital regions

  • 80% occur with benign conditions
  • Autosomal dominant forms with variable penetrance
    • Onset during childhood or puberty
  • Also occur with * obesity or endocrine abnormalities
  • 20% are paraneoplastic
  • *Malignancy (adenocarcinoma) signals the epidermis to undergo epidermal hyperplasia.
  • Usually middle-aged or older individuals
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18
Q

Tattoo = Acquired Pigmentation

A

Intentional or incidental (pencil “lead” breaking in skin or oral amalgam injury)
May mimic pigmented lesions if incidental
May “bleed” if pigment travels into dermis & macrophages move
Will fade over time as pigments move deeper and out of dermis

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19
Q

Solar Lentigo

A

(Lentigo Senilis, Lentigo Simplex)

Benign, discrete hyperpigmented macule on chronically sun exposed skin
Back of hands and the forehead

Variable increase in number of junctional melanocytes
Increased melanin pigment in keratinocytes

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20
Q

what lentigo or lentiginous means

A

Note: “lentigo or lentiginous” means a proliferation of melanocytes

Lentigo maligna is the name given to an in situ melanoma arising in sun exposed skin and not related to a benign solar lentigo

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21
Q

Macular (or Patch) Skin Depigmentation

A

Loss of melanin in keratinocytes

  • Acute transient vitiligo
  • — e.g. keratinolytic agents that remove layers of pigmented keratinocytes
  • Albinism
  • — Defect in tyrosinase, an enzyme necessary for melanin production

Permanent lack or loss of melanocytes:
Chronic vitiligo

22
Q

Melanocytic (Nevocellular) Nevi

A

Benign Neoplasms of Melanocytes

  1. Neoplastic nested melanocyte proliferation (clusters)
    - Junctional: Basal epidermal nests (Maculopapular)
    - Compound: Basal epidermal & dermal nests (Papular)
    - Intradermal: Dermal nests: Papular to nodular
  2. Acquired mutations in NRAS and BRAF are commonly found
    - Mutations induce melanocyte neoplasia short of malignancy
23
Q

Postulated Natural History of Nevi

A

Stage:
I- Junctional (nests of melanocytes along base of the epidermis)

II- Compound (nests of melanocytes at base of the epidermis and in the dermis)

III- Intradermal = Dermal (nests of melanocytes present only in the dermis)

IV- Neurotized (melanocytes change appearance from epithelioid to spindled shape)

24
Q

Congenital Nevus

A

Present at birth (birthmark)

Benign, but melanoma can arise in the larger congenital nevi

Extensive deep dermal to subcutaneous growth with proliferative nodules

25
Q

Blue Nevus

A

Intradermal, roughly wedge-shaped and slightly raised skin surface

Thin, delicate * melanocytes in a dense reactive fibrotic stroma

Melanin pigment in melanocytes, melanophages, or other adjacent structures cause the bluish color

Benign with no significant risk for development of melanoma

26
Q

Spitz Nevus= Spindle & Epithelioid Cell Nevus

A

Usually in children and young adults
red or brown
can mimic a melanoma (clinically and histologically)
Characteristic raining down melanocyte pattern and Kamino bodies (eosinophilic amorphous globules)

27
Q

Halo Nevus

A
  • Involuting (regressing) nevus with extensive * lymphocyte infiltration and depigmentation of surrounding skin
28
Q

Dysplastic (Clark) Nevus

A

Gross appearance is worrisome for melanoma
Asymmetric
Border irregular
Color uneven
Diameter > 6 mm
Occur on non-sun or sun exposed skin
Melanocyte nests at the tips of rete ridges
* Rete ridges are often “bridged” (connected at their bases)
* Reactive fibrosis of papillary dermis

Two forms
Sporadic: not prone to malignancy
Familial dysplastic nevus syndrome 
- Autosomal dominant 
- * 50% chance of melanoma by age 60
29
Q

Malignant Melanoma

A

Subtypes

  • Lentigo maligna (in situ sun exposed area)
  • Lentigo maligna melanoma (invasive lesion similar to lentigo maligna)
  • Superficial spreading (invasive, mostly horizontal growth phase)
  • Nodular (invasive, mostly vertical growth phase)
  • Acral lentiginous (palms, soles and subungual; non-caucasian; in situ or invasive)

May occur in any skin location and occasionally in the eye, mucous membranes of the genitalia, anus, oral cavity, or other sites
Most melanomas occur in sun damaged skin (also occur in non-sun exposed skin)
- Occurs * primarily in adults; beginning in 3rd decade
- * 90% originates de novo (isolated non-syndromic lesion)
Can arise in or adjacent to a pre-existing melanocytic nevus
- * Aggressive malignancy that metastasizes widely with significant mortality*
— Metastasizes to regional lymph nodes, liver, lungs, and brain

30
Q

Malignant Melanoma: Risk Factors & Mutations

A

Caucasians with * fair skin
- Albinism or genetic syndrome such as xeroderma pigmentosa dramatically increases incidence (50X-100X)

Prolonged MCB * UV exposure

  • 3 episodes of “peeling” or severe
    sunburn before age 20
  • Male gender

Increased telomerase activity from mutated * TERT gene is present in 70% of skin melanomas but not routinely clinically tested

10% to 15% of melanomas are familial

BRAF and NRAS mutations are also present in benign melanocytic nevi and are not sufficient for malignant transformation

31
Q

Mutations seen in both dysplastic nevus and melanoma familial syndromes

A

Proliferation: P16 inhibition is inhibited by CDKN2A mutations; CDK4 mutations block p16 inhibition

32
Q

The ABCD Checklist for Melanoma

A

A = Asymmetry
Melanoma if lesion bisected & halves not identical

B = Border irregularity
Melanoma if the border
is uneven or ragged

C = Color variation
Melanoma if more
than one shade of pigment

D = Diameter- Melanoma if diameter
greater than 6 mm

33
Q

Malignant Melanoma stats

A

Best prognostic indicator on skin biopsy is Breslow level (thickness from epidermal granular layer to deepest dermal penetration)

10 year survival: 92% for melanoma < 1.00 mm thick; 80% if 1.01 to 2.00 mm

Melanoma survival depends on stage: Melanoma metastatic to lymph node(s) represents regional disease (II/III); any distant metastasis is stage IV.

34
Q

Chronic Actinic Skin Damage types

A

solar elastosis
solar lentigo
actinic keratosis

35
Q

Solar elastosis

A

Permanent, incremental damage to reticular collagen (elastosis)
Loss of normal skin texture (leathery and wrinkled)

36
Q

Solar lentigo

A

Focal autonomous overproduction of melanosomes +/- mild melanocyte hyperplasia

37
Q

Actinic keratosis

A

Neoplastic precancerous proliferation of keratinocytes

  • Does not involve full epidermal thickness
  • Size of lesions varies

Erythematous, reddish-brown macules or minimally elevated papules

  • Increased keratin production (scaling)
  • Dermal increase in vascularity (redness)

Middle-aged and elderly individuals
- Face (particularly forehead), neck , dorsum of arms and hands, lips (actinic cheilitis)

Usually asymptomatic, may have mild tenderness

38
Q

other names for actinic keratosis

A

Solar Keratosis, Senile Keratosis & Keratinocytic Intraepidermal Neoplasia

39
Q

Squamous Cell Carcinoma (SCC)

A

Malignant neoplasm of the basal regenerative epithelium of the epidermis

  • Malignant keratinocytes resemble maturing squamous cells
  • The malignant keratinocytes penetrate past the dermal-epidermal junction basement membrane (potential for metastasis)
    • Exception: SCC in situ (e.g. Bowen disease, penile erythroplasia of Queyrat)
  • Epidemiology:
    Second most common cutaneous malignancy (#1 is basal cell carcinoma)
    Incidence increases with increasing age
    M>F
  • Primary etiology in sun exposed skin
    • Long term sun exposure
      Immunosuppression increases incidence of invasive SCC
  • SCC of skin occurs in 40-70% in organ transplant recipient patients
  • Increased incidence with HIV
40
Q

Squamous Cell Carcinoma- Other etiologic agents (can be synergistic with sunlight)

A 
* Human papillomavirus (HPV) 
Chronic skin inflammation, ulcers and draining * fistulous tracts (osteomyelitis)
Some dermatoses
Burns 
Ionizing radiation
Chemical exposures 
- Tars → * scrotal cancer in chimney sweeps
- Arsenic ingestion
- Tobacco and betel nut usage

Genetic syndromes

    • Epidermodysplasia verruciformis (predisposition to HPV infections and HPV subtypes 5 and 8 can lead to SCC)
    • Xeroderma pigmentosa (nucleotide excision repair pathway defects)
  • Other syndromes
41
Q

Squamous Cell Carcinoma: Major Clinical Characteristics

A

Areas of greatest cumulative sun exposure

Early invasive SCC is usually a small, firm, skin-colored or erythematous nodule with indistinct margins

Surface may be smooth, verrucous, ulcerated, papillomatous or granular and may bleed easily

Older SCCs are larger, invasive, and may be ulcerated

Mortality is low for SCC of skin

42
Q

Keratoacanthoma

A

Better term * “Squamous cell carcinoma, Keratoacanthoma type”

Variant of invasive SCC
Occurs on sun-exposed area
M>F

  • Rapidly growing (days-weeks)
  • Often involutes and clears spontaneously within 3 to 4 months
43
Q

Basal Cell Carcinoma

A

Previously known as “basal cell epithelioma”
Malignant neoplasm of the basal regenerative epithelium of the epidermis
Malignant keratinocytes resemble squamous cells of the basalis layer
Almost never metastasizes

Numerous subtypes

  • Nodular and sclerosing types
    • Have local invasion and destruction of adjacent dermis
    • Tend to occur in hair-bearing skin subjected to sun exposure
  • Sclerosing and multifocal superficial spreading types
    • Have difficult to identify margins
    • Have high incidence of post resection recurrences

Etiology

Increased sunlight exposure in childhood and adolescence, and chronic exposure during adulthood

44
Q

Nevoid Basal Cell Carcinoma Syndrome

A

(Gorlin Syndrome)

Multiple basal cell carcinomas before age 20 
Pits of the palms and soles
Odontogenic keratocysts
Medulloblastomas
Ovarian fibromas
  • Autosomal dominant disorder with * PATCH1 * gene mutations
  • SMO is normally inactive via PATCH1 function
  • When hh (sonic, Indian and Desert) proteins bind to PATCH1, SMO is activated leading to production of transcription factors (GLI1) that drive gene activation
  • PATCH1 mutations in Gorlin syndrome bypass the hh protein needed for SMO activation and SMO is active in the absence of hh proteins
45
Q

Basal Cell Carcinoma epidemiology and major clinical characteristics

A

85% occur on head and neck
Remainder predominantly on trunk/limbs
* Clinical appearance related to histologic type
** Rodent Ulcer = advanced presentation

Most common cutaneous neoplasm (but is ignored in cancer data statistics)
98% occur after age 40
After age 50, 1% of population develops BCC each year
M ~ F
Almost all individuals with a significant history of face/neck sun exposure will develop one or more BCCs

46
Q

Nodular BCC

A

Traditional or “classic” appearance of BCC
Dome-shaped, * pearly papule or nodule
Prominent surface * dilated dermal vessels (telangiectasia)
May become quite large if neglected
Easily treated by excision

47
Q

Sclerosing (Morpheaform) BCC

A

Typically waxy yellowish-white or pearly white, indurated plaque that may retract below plane of skin surface
Occurs predominately on face
Poorly defined margins (edge of lesion)
- Difficult to excise, high recurrence rate and may disfigure
- * Mohs surgery can be used during excision to determine complete excision

48
Q

Superficial BCC

A

Multifocal erythematous, scaly plaque; elevated rolled edges
Occurs on * non-sun exposed skin sites on proximal limbs or trunk
Multifocal growth pattern localized to dermal-epidermal junction
- Part of a “field defect” and therefore can recur after excision
Do not become locally invasive or metastasize
If pigmented may be confused clinically with melanoma

49
Q

Dermatofibrosarcoma Protuberans

A

Malignant * superficial fibroblastic neoplasm (fibrosarcoma of skin)
Locally aggressive but rarely metastasizes
* Bednar tumor is pigmented variant

50
Q

Mycosis Fungoides

A

Mycosis Fungoides
CD4+ T-cell lymphoma of the skin (CLA, CCR4 & CCR10)
Aggressive neoplasm with median survival 8-9 years (M>F)
Phases
- * Inflammatory erythrodermic pre-mycotic patch
- * Plaque
- * Tumor

  • Sezary syndrome is variant in which skin involvement is manifest as a * generalized exfoliative erythroderma

Leukemic phase with * Sezary cell (cerebriform nuclei) seen in Sezary syndrome and 25% of plaque and tumor phases with survival <3 years

51
Q

Mastocytosis/Mastocytoma

A

Darier sign – stroking of the skin leads to histamine release which causes swelling, erythema and edema

Mast cell granules can be highlighted with toluidine blue or Wright-Giemsa stains

MSK II Exam I (16 decks)

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