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ADV PATH > 1M-SKIN > Flashcards

1M-SKIN Flashcards

1
Q

Common, benign, pigmented, predominantly basal keratinocytic proliferations
occurring chiefly on the trunk of adults.

A

SEBORRHEIC KERATOSIS

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2
Q

Part of Paraneoplastic Syndrome

A

SEBORRHEIC KERATOSIS

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3
Q

Sudden appearance or increase in numbers and size + pruritus

A

Lesser Trelat sign

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4
Q

What malignancy is seborrheic keratosis assoc with?

A

Malignancy of gastrointestinal tract due to stimulation of TGF-a.

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5
Q

Common locations of seborrheic keratosis

A

Trunk, head and neck

*old trans: trunk, head, face, extremities

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6
Q

Seborrheic keratosis is assoc with what mutation?

A

FGFR-3

*FGFR3-RAS-mitogen-activated protein kinase
(MAPK) pathway

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7
Q

Minute pore openings, crater-like structures filled with keratin

A

Keratinocytic cyst

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8
Q

Presence of keratinocytic cysts which are called __

A

Horn cysts

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9
Q

The predominant histologic feature in seborrheic keratosis

A

Remarkable

hyperkeratosis

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10
Q

Single, benign, heavily pigmented lesion can be

confused with melanoma

A

SEBORRHEIC KERATOSIS

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11
Q

A 50y/o presented with a dark brown exophytic lesion. It has a waxy plaque appearance with crater-like openings. Px complained of pruritus.

A

SEBORRHEIC KERATOSIS

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12
Q

Elevation of the dermal region covered by skin and fibrovascular stroma surrounding the polyp.

A

ACROCHORDON

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13
Q

Other names of ACROCHORDON

A

● Fibroepithelial polyp
● Fibroepithelial/squamous papilloma
● Fibroma molle
● “Skin tag”

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14
Q

Main difference of ACROCHORDON with other tumors?

A

Absence of adnexal structures (in the polypoid region) in the underlying dermis

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15
Q

An obese, diabetic, pregnant patient complained of flesh colored polypoid lesions in her intertriginous areas

A

ACROCHORDON

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16
Q

Common locations of ACROCHORDON

A

Neck, trunk and intertriginous areas

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17
Q

Treatment for ACROCHORDON

A

Excision

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18
Q

Lesion with brown to dark gray in color, hard to rough/sandpaper-like consistency because of keratin production.

A

ACTINIC KERATOSIS

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19
Q

Pre-malignant epidermal tumor common in lightly-pigmented patients

A

ACTINIC KERATOSIS

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20
Q

Lesion due to sun-damaged skin - by ionizing radiation and industrial chemicals such as arsenic and hydrocarbons

A

ACTINIC KERATOSIS

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21
Q

Common locations of ACTINIC KERATOSIS

A

Face, arms, dorsum of hands

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22
Q

Actinic keratosis located in the lips

A

ACTINIC CHEILITIS

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23
Q

T or F: Actinic keratosis can regress.

A

TRUE

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24
Q

T or F: Actinic keratosis can progress to carcinoma.

A

TRUE

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25
Q

Actinic keratosis is assoc with what mutation?

A

p53 protein accumulation

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26
Q

Treatment of Actinic keratosis

A
  • freezing
  • superficial curettage
  • application of antineoplastic chemotherapeutic agents
  • surgical excision
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27
Q

Carcinoma-in-situ

A

BOWEN DISEASE

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28
Q

Mutation present in BOWEN DISEASE

A

p53 mutation

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29
Q

Scaly erythematous plaques seen in non-chronically sun-exposed skin

A

BOWEN DISEASE

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30
Q

Squamous cell carcinoma-in-situ in sun exposed areas

A

Bowenoid actinic keratosis

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31
Q

Actinic keratosis and bowen disease are at risk to

develop into a full blown malignancy called ____?

A

Squamous cell carcinoma

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32
Q

Brown velvety plaques

A

ACANTHOSIS NIGRICANS

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33
Q

Location of ACANTHOSIS NIGRICANS

A

Axillae, back of

the neck, and other flexural areas.

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34
Q

Mutation involved in ACANTHOSIS NIGRICANS

A

FGFR-3

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35
Q

Malignant condition associated with ACANTHOSIS NIGRICANS

A

GIT Adenocarcinomas

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36
Q

Second most common tumor arising in sun

exposed areas

A

SQUAMOUS CELL CA

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37
Q

Most common causes of SQUAMOUS CELL CA

A 
○ UV exposure 
○ Chronic immunosuppression 
○ Industrial hazards 
○ Chronic ulcers and diseases
○ Tobacco and betel nut chewing
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38
Q

Mutation involved in SQUAMOUS CELL CA

A

● Defects in p53
● Mutations leading to increase RAS signaling
● Mutation leading to decrease notch signaling

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39
Q

Histologic variants of SQUAMOUS CELL CA

A

○ Sarcomatoid/Spindle SCCA
○ Adenoid/Pseudoglandular SCCA
○ Verrucous carcinoma

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40
Q

Which histologic variant of SQUAMOUS CELL CA?

○ Continuity of tumor to basal layer of epidermis
○ Foci of clear cut squamous change

A

Sarcomatoid/Spindle SCCA

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41
Q

Sarcomatoid/Spindle SCCA variant immunoreactivity

A

High molecular weight keratin immunoreactivity

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42
Q

Histologic variant of SQUAMOUS CELL CA due to defects in desmosomes.

A

Adenoid/Pseudoglandular SCCA or Acantholytic type

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43
Q

Adenoid/Pseudoglandular SCCA variant in sun-exposed areas will require you to rule out ___?

A

○ Metastatic adenoCA
○ Primary adenoCA
○ Adenoquamous CA
○ Mucoepidermoid CA

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44
Q

Adenoid/Pseudoglandular SCCA variant immunoreactivity

A

Reduction of the cell adhesion molecule (CAM) syndecan-1

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45
Q

Which histologic variant of SQUAMOUS CELL CA?

○ Very well differentiated SCC
○ Warty/ cauliflower/ fungating lesion or ulcerated due to crater
○ (+) local/ stromal invasion

A

Verrucous carcinoma

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46
Q

Treatment of SQUAMOUS CELL CA

A

○ Complete excision - tx of choice
○ Alternative therapies: curettage and
electrodessication, cryotherapy, and radiation
therapy.

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47
Q

SCC and BCC staging

A

T1 = 2 cm
T2 >2 - 5 cm
T3 >5 cm
T4 (+) invasion

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48
Q

Most common invasive cancer

A

BASAL CELL CARCINOMA

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49
Q

BASAL CELL CARCINOMA risk factors

A

○ Sun exposed areas
○ Fair complexion
○ Elderly
○ Immunosuppressed

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50
Q

T or F: BASAL CELL CARCINOMA is locally aggressive, fast growing, and frequently metastasizes

A

FALSE

○ Locally aggressive
○ SLOW growing
○ RARELY metastasizes

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51
Q

Mutation involved in BASAL CELL CARCINOMA

A

Hedgehog signaling pathway

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52
Q

Multiple BCC in a young patient

A

Nevoid basal cell carcinoma syndrome

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53
Q

Genetic involvement of NBCCS

A

○ Autosomal dominant

○ Germline loss in PTCH gene

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54
Q

Other tumors assoc with NBCCS

A

○ Medulloblastoma
○ Odontogenic keratocyst
○ Ovarian fibroma

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55
Q

BCC histologic features

A 
○ Basaloid tumor arising from epidermis
○ Nests of basaloid cells w/ scanty cytoplasm & elongated hyperchromatic nuclei
○ Peripheral palisading
○ Myxoid stroma
○ Peritumoral clefting
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56
Q

Difference of BCC from SCC histologically

A

○ Darker/ more bluish

○ Not seen in mucosal surfaces

57
Q

BCC growth pattern: originates in epidermis and extend to the skin surface (epidermal region spread)

A

Multifocal growth

58
Q

BCC growth pattern: downward growth to the dermal region

A

Nodular growth

59
Q

Immunohistochemical features

A

○ Positive for
keratin (low-molecular-weight)
○ Negative for EMA, CEA, and involucrin

○ Other markers commonly expressed: CD10, Ber-EP4 and androgen receptors.

60
Q

Tx for BCC

A

Excision, curettage and desiccation, and

irradiation

61
Q

Tx for recurrent BCC

A

Radiation therapy or surgical re-excision.

62
Q

Flesh-colored, solitary or multiple papules and nodules which may be disfiguring when multiple.

A

SKIN ADNEXA/ Appendage tumors

63
Q

Mutations involved in Appendage tumors

A

Germline mutations in tumor suppressor genes

64
Q

Appendage tumors: Benign or malignant?

A

Mostly benign but malignant variants exist

65
Q

_____ are unusual in that
malignant forms appear to be more common than
benign forms.

A

Apocrine tumors

66
Q

Arises from the meibomian
glands of the eyelid and may follow an aggressive
course replete with systemic metastases.

A

Sebaceous carcinoma

67
Q

_____ can be confused

with metastatic adenocarcinoma because of their tendency to form gland-like structures.

A

Eccrine and apocrine carcinomas

68
Q

Px presented with a nodular lesion in his palms that has a moat and hillock pattern

A

ECCRINE POROMA

69
Q

Histologic features of ECCRINE POROMA

A

● Sharp junction of the
neoplastic and non-neoplastic region
● Forms anastomosing cords and nests

70
Q

Origin of ECCRINE POROMA

A

Eccrine sweat glands

71
Q

Nodular lesions in the papillary dermis with cystic component

A

HIDRADENOMA/ Eccrine acrosporoma

72
Q

Origin of HIDRADENOMA/ Eccrine acrosporoma

A

Distal excretory duct

73
Q

Appendage tumor described as a large multicentric lesion with ductal differentiation

A

CYLINDROMA

74
Q

Common location for CYLINDROMA

A

Forehead and scalp

Sometimes seen in neck

75
Q

Coalescence of nodules with time may produce

hat-like growth

A

Turban tumor

76
Q

Cylindroma can be dominantly inherited; in such cases they appear early in life and are associated with
what mutation?

A

Inactivating mutations in the tumor suppressor gene

CYLD

77
Q

Multiple cylindroma

A

○ Disfiguring

○ Assoc w CYLD gene mutation

78
Q

Histologic features of cylindroma

A

○ Heavy accumulation of basement membrane material.
○ Appears to be very pink around and within your
tumor lobules.
○ Composed of islands of cell that fit together like pieces of a jigsaw puzzle
within a fibrous dermal matrix

79
Q

Multiple, tan, small (1-3 cm) papulonodular lesions in the face and neck but more commonly in the lower eyelids

A

Syringoma

80
Q

Origin of Syringoma

A

Eccrine differentiation

81
Q

Histologic appearance of Syringoma

A

Cystic ducts lined by two

cell-layered thick

82
Q

Nodular benign lesion common in children and young adults. Most cases are in the head, neck, and upper extremities.

A

Pilomatricoma

83
Q

Origin of Pilomatricoma

A

Hair matrix/ hair follicle differentiation

84
Q

Mutation involved in Pilomatricoma

A

CTNNB1 (gene encoding B-catenin)

85
Q

Pilomatricoma vs BCC

A

Both are made up of basal cells but…

key feature is that there is abrupt keratinization leading to a shadow or
ghost cells —- Ghost cell lacks nuclei.

86
Q

Proliferation of basaloid cells that forms primitive structures resembling hair follicles

A

TRICHOEPITHELIOMA

87
Q

shows a lobular proliferation of sebocytes with increased peripheral basaloid cells and more mature sebocytes in the central portion that have
frothy or bubbly cytoplasm due to the presence of lipid
vesicles.

A

SEBACEOUS ADENOMA

88
Q

○ Adnexal tumor showing apocrine differentiation with prominent decapitation secretion
○ Most prevalent in axilla and scalp
○ May have an infiltrative growth pattern

A

APOCRINE CARCINOMA

89
Q

○ Dull lesions
○ Diverse and dynamic
○ Majority are acquired

A

MELANOCYTIC NEVI

90
Q

Mutation involved in MELANOCYTIC NEVI

A

Activation of RAS or the

serine/threonine kinase BRAF

91
Q

T or F: Not all nevi will give rise to melanoma.

A

TRUE

*Only very few will develop into melanoma.

92
Q

Reason why nevi rarely give rise to melanomas

A

Oncogene-induced

senescence

93
Q

There is proliferation of nevus in the rete pegs or in the junction only; considered as the earliest lesions

A

Junctional nevus

94
Q

Progression of nevi cells proliferation downwards to the papillary dermis

A

Compound nevus

95
Q

Complete downward progression of cells leaving the junctional region and occupy predominantly the dermal region

A

Intradermal melanocytic nevus

96
Q

Most nevus seen in clinical practice

A

Compound and Intradermal

97
Q

Originally polygonal cells become spindly as they go deeper into the dermis. They mature and lose their melanin pigment. This correlates with progressive loss of tyrosinase activity and acquisition of cholinesterase activity

A

Neurotization

98
Q

Clinical significance of neurotization

A

It differentiates benign nevi from melanoma

*Neurotization is absent in melanoma

99
Q

T or F: Junctional nevi are more elevated

A

FALSE

*Compound and Dermal nevi are more elevated than junctional nevi

100
Q

Superficial vs deeper nevus cells

A

○ Superficial - larger, produce melanin, grow in nests

○ Deep - smaller, produce little or no pigment, appear as cords or single cells

101
Q

○ Nevus present at birth
○ Larger variants have increased risk to develop melanoma
○ Generally benign
○ BRAF and NRAS mutation

A

Congenital nevus

102
Q

○ Highly dendritic and heavily pigmented nevus cells
○ Confused with melanoma
○ Positive for melanin stains (S-100, HMB-45)

A

Blue nevus

103
Q 
○ Large, plump cells with pink-blue cytoplasm
○ Fusiform cells
○ Fascicular growth
○ Common in children
○ Red-pink nodule
○ Confused with hemangioma
A

Spitz nevus

104
Q

○ Lymphocytic infiltration secondary to host immune response

A

Halo nevus

105
Q

T or F: All melanomas arise from dysplastic nevi

A

FALSE

  • Dysplastic nevi may be direct precursors of melanoma but are not prerequisites
  • Increase risk: when multiple
106
Q

T or F: Dysplastic nevi occurs exclusively in sun-exposed surfaces

A

FALSE

*Occur both in sun-exposed and non-exposed skin

107
Q

First step to the development or progression of dysplastic nevus

A

Lentiginous hyperplasia

108
Q

Nevus cell hyperplasia -> junctional -> compound with some degree of atypia

Nevus cells coalesce and fuse together and begin to replace the normal basal layer

A

Lentiginous hyperplasia

109
Q

Release of melanin from dead nevus cells ; melanin is seen within macrophages

A

Melanin incontinence

110
Q

Histologic features of dysplastic nevi

A

○ Atypical cells in epidermal and dermal regions (junctional and upper dermis)
○ Sparse lymphocytic infiltrates
○ Lentiginous hyperplasia
○ Linear dermo-epidermal junction fibrosis
○ Melanin incontinence

111
Q

Most deadly of all skin cancers

A

MELANOMA

112
Q

T or F: UV radiation is a prerequisite in the development of melanoma

A

FALSE

*UV radiation/ sunlight exposure is an important predisposing factor but not essential

113
Q

T or F: There is no cure for Melanoma

A

FALSE

*It is curable in the early stages

114
Q

Location of melanoma

A 
○ Skin (majority) - cutaneous melanoma 
○ Oral
○ Anogenital mucosa
○ Esophagus
○ Meninges
○ Uvea
115
Q

Mutations involved in melanoma

A

○ Disruption in cell cycle control genes –CDKN2A gene
○ Activation of pro growth signaling pathway –RAS & BRAF
○ Activation of telomerase –TERT gene

116
Q

● Horizontal spread within the epidermis and with very
minimal downward spread in the superficial dermis
● Seem to lack the
capacity to metastasize

A

RADIAL GROWTH PHASE

117
Q

○ Indolent lesion, common to the face
○ May remain in the radial growth phase for
decades

A

Lentigo maligna

118
Q

○ Most common type of melanoma
○ Seen in sun exposed areas
○ Spread in the epidermal and superficial dermis

A

Superficial spreading

119
Q

○ Mucosal surfaces

○ Unrelated to sun exposure

A

Acral mucosal lentiginous

120
Q

● Tumor cells invade downward into the deep dermis
● Presence of expansile mass or tumor nodule
● Neurotization is absent
● Capacity to metastasize

A

VERTICAL GROWTH PHASE

121
Q

Depth of invasion is measured by ____ ?

A

Breslow thickness

122
Q

Prognostic factors in melanoma

A 
● Breslow thickness
● Number of mitoses 
● Evidence of tumor progression 
● Ulceration of the skin 
● Presence of tumor infiltrating lymphocytes 
● Gender
● Age
● Location 
● Sentinel lymph node biopsy
123
Q

Most powerful predictors for the prognosis of melanoma

A

● Breslow level

● Ulceration

124
Q

Melanoma: High risk sites

A

scalp, mandibular area, midline trunk, upper medial thighs, hands, feet, fossae, genitalia

125
Q

Prognosis of lentigo malignant melanoma

A

Better prognosis

126
Q

Prognosis of nodular melanoma

A

Worse

127
Q

Prognosis of superficial spreading

A

Intermediate

128
Q

Warning signs of melanoma

A 
○ Asymmetry
○ Irregular borders
○ Variegated color
○ Increasing diameter
○ Evolution or change over time
129
Q

T or F: Melanoma may be treated medically

A

TRUE

*success in treating this cancer with drugs
that target the RAS and PI3K/AKT pathways.

130
Q
  • Firm, well-defined, nodular/polypoid non-encapsulated mass

- Common in the extremities

A

BENIGN FIBROUS HISTIOCYTOMA

131
Q

Dermal tumor microscopic characteristics:

  • Cellular: made up of spindle cells
  • Fibroblastic proliferation
  • Variable collagen deposition
  • Delicate fibrovascular stroma
  • Cluster of histiocytes
A

BENIGN FIBROUS HISTIOCYTOMA

132
Q

Well-differentiated, primary fibrosarcoma of the skin

A

DERMATOFIBROSARCOMA PROTUBERANS

133
Q
  • Slow growing
  • Locally aggressive
  • Can recur
  • But rarely metastasize
A

DERMATOFIBROSARCOMA PROTUBERANS

134
Q

Molecular hallmark of DFSP

A

Transolation of genes encoding Collagen 1A1 (COL1A1) and platelet derived factor growth factor beta (PDGF B)

135
Q

primary mode of tx for DFSP

A

Wide local excision

136
Q

Treatment of choice for DFSP cases that are unresectable

A

Inhibitors of the PDGF B receptor tyrosine kinase

137
Q

Dermal tumor microscopic characteristics:

  • High cellularity
  • Monomorphic appearance of the cells
  • Diffuse infiltration into subcutaneous tissue
  • Closely packed spindle cells in radial whorls -> storiform/cartwheel pattern
A

DERMATOFIBROSARCOMA PROTUBERANS

138
Q

Immunohistochemical stains for DFSP

A

POSITIVE

  • Vimentin
  • Actin
  • CD34 (strongly and consistently)

NEGATIVE

  • S-100 (r/o other soft tissue tumor)
  • HMB 45 (r/o melanoma)
  • Keratin (r/o sarcomatoid type of SCC)
  • Factor XIIIa

ADV PATH (10 decks)

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