1M-SKIN Flashcards
(138 cards)
1
Q
Common, benign, pigmented, predominantly basal keratinocytic proliferations
occurring chiefly on the trunk of adults.
A
SEBORRHEIC KERATOSIS
2
Q
Part of Paraneoplastic Syndrome
A
SEBORRHEIC KERATOSIS
3
Q
Sudden appearance or increase in numbers and size + pruritus
A
Lesser Trelat sign
4
Q
What malignancy is seborrheic keratosis assoc with?
A
Malignancy of gastrointestinal tract due to stimulation of TGF-a.
5
Q
Common locations of seborrheic keratosis
A
Trunk, head and neck
*old trans: trunk, head, face, extremities
6
Q
Seborrheic keratosis is assoc with what mutation?
A
FGFR-3
*FGFR3-RAS-mitogen-activated protein kinase
(MAPK) pathway
7
Q
Minute pore openings, crater-like structures filled with keratin
A
Keratinocytic cyst
8
Q
Presence of keratinocytic cysts which are called __
A
Horn cysts
9
Q
The predominant histologic feature in seborrheic keratosis
A
Remarkable
hyperkeratosis
10
Q
Single, benign, heavily pigmented lesion can be
confused with melanoma
A
SEBORRHEIC KERATOSIS
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
12
Q
Elevation of the dermal region covered by skin and fibrovascular stroma surrounding the polyp.
A
ACROCHORDON
13
Q
Other names of ACROCHORDON
A
● Fibroepithelial polyp
● Fibroepithelial/squamous papilloma
● Fibroma molle
● “Skin tag”
14
Q
Main difference of ACROCHORDON with other tumors?
A
Absence of adnexal structures (in the polypoid region) in the underlying dermis
15
Q
An obese, diabetic, pregnant patient complained of flesh colored polypoid lesions in her intertriginous areas
A
ACROCHORDON
16
Q
Common locations of ACROCHORDON
A
Neck, trunk and intertriginous areas
17
Q
Treatment for ACROCHORDON
A
Excision
18
Q
Lesion with brown to dark gray in color, hard to rough/sandpaper-like consistency because of keratin production.
A
ACTINIC KERATOSIS
19
Q
Pre-malignant epidermal tumor common in lightly-pigmented patients
A
ACTINIC KERATOSIS
20
Q
Lesion due to sun-damaged skin - by ionizing radiation and industrial chemicals such as arsenic and hydrocarbons
A
ACTINIC KERATOSIS
21
Q
Common locations of ACTINIC KERATOSIS
A
Face, arms, dorsum of hands
22
Q
Actinic keratosis located in the lips
A
ACTINIC CHEILITIS
23
Q
T or F: Actinic keratosis can regress.
A
TRUE
24
Q
T or F: Actinic keratosis can progress to carcinoma.
A
TRUE
25
Actinic keratosis is assoc with what mutation?
p53 protein accumulation
26
Treatment of Actinic keratosis
- freezing
- superficial curettage
- application of antineoplastic chemotherapeutic agents
- surgical excision
27
Carcinoma-in-situ
BOWEN DISEASE
28
Mutation present in BOWEN DISEASE
p53 mutation
29
Scaly erythematous plaques seen in non-chronically sun-exposed skin
BOWEN DISEASE
30
Squamous cell carcinoma-in-situ in sun exposed areas
Bowenoid actinic keratosis
31
Actinic keratosis and bowen disease are at risk to
| develop into a full blown malignancy called ____?
Squamous cell carcinoma
32
Brown velvety plaques
ACANTHOSIS NIGRICANS
33
Location of ACANTHOSIS NIGRICANS
Axillae, back of
| the neck, and other flexural areas.
34
Mutation involved in ACANTHOSIS NIGRICANS
FGFR-3
35
Malignant condition associated with ACANTHOSIS NIGRICANS
GIT Adenocarcinomas
36
Second most common tumor arising in sun
| exposed areas
SQUAMOUS CELL CA
37
Most common causes of SQUAMOUS CELL CA
```
○ UV exposure
○ Chronic immunosuppression
○ Industrial hazards
○ Chronic ulcers and diseases
○ Tobacco and betel nut chewing
```
38
Mutation involved in SQUAMOUS CELL CA
● Defects in p53
● Mutations leading to increase RAS signaling
● Mutation leading to decrease notch signaling
39
Histologic variants of SQUAMOUS CELL CA
○ Sarcomatoid/Spindle SCCA
○ Adenoid/Pseudoglandular SCCA
○ Verrucous carcinoma
40
Which histologic variant of SQUAMOUS CELL CA?
○ Continuity of tumor to basal layer of epidermis
○ Foci of clear cut squamous change
Sarcomatoid/Spindle SCCA
41
Sarcomatoid/Spindle SCCA variant immunoreactivity
High molecular weight keratin immunoreactivity
42
Histologic variant of SQUAMOUS CELL CA due to defects in desmosomes.
Adenoid/Pseudoglandular SCCA or Acantholytic type
43
Adenoid/Pseudoglandular SCCA variant in sun-exposed areas will require you to rule out ___?
○ Metastatic adenoCA
○ Primary adenoCA
○ Adenoquamous CA
○ Mucoepidermoid CA
44
Adenoid/Pseudoglandular SCCA variant immunoreactivity
Reduction of the cell adhesion molecule (CAM) syndecan-1
45
Which histologic variant of SQUAMOUS CELL CA?
○ Very well differentiated SCC
○ Warty/ cauliflower/ fungating lesion or ulcerated due to crater
○ (+) local/ stromal invasion
Verrucous carcinoma
46
Treatment of SQUAMOUS CELL CA
○ Complete excision - tx of choice
○ Alternative therapies: curettage and
electrodessication, cryotherapy, and radiation
therapy.
47
SCC and BCC staging
T1 = 2 cm
T2 >2 - 5 cm
T3 >5 cm
T4 (+) invasion
48
Most common invasive cancer
BASAL CELL CARCINOMA
49
BASAL CELL CARCINOMA risk factors
○ Sun exposed areas
○ Fair complexion
○ Elderly
○ Immunosuppressed
50
T or F: BASAL CELL CARCINOMA is locally aggressive, fast growing, and frequently metastasizes
FALSE
○ Locally aggressive
○ SLOW growing
○ RARELY metastasizes
51
Mutation involved in BASAL CELL CARCINOMA
Hedgehog signaling pathway
52
Multiple BCC in a young patient
Nevoid basal cell carcinoma syndrome
53
Genetic involvement of NBCCS
○ Autosomal dominant
| ○ Germline loss in PTCH gene
54
Other tumors assoc with NBCCS
○ Medulloblastoma
○ Odontogenic keratocyst
○ Ovarian fibroma
55
BCC histologic features
```
○ Basaloid tumor arising from epidermis
○ Nests of basaloid cells w/ scanty cytoplasm & elongated hyperchromatic nuclei
○ Peripheral palisading
○ Myxoid stroma
○ Peritumoral clefting
```
56
Difference of BCC from SCC histologically
○ Darker/ more bluish
| ○ Not seen in mucosal surfaces
57
BCC growth pattern: originates in epidermis and extend to the skin surface (epidermal region spread)
Multifocal growth
58
BCC growth pattern: downward growth to the dermal region
Nodular growth
59
Immunohistochemical features
○ Positive for
keratin (low-molecular-weight)
○ Negative for EMA, CEA, and involucrin
○ Other markers commonly expressed: CD10, Ber-EP4 and androgen receptors.
60
Tx for BCC
Excision, curettage and desiccation, and
| irradiation
61
Tx for recurrent BCC
Radiation therapy or surgical re-excision.
62
Flesh-colored, solitary or multiple papules and nodules which may be disfiguring when multiple.
SKIN ADNEXA/ Appendage tumors
63
Mutations involved in Appendage tumors
Germline mutations in tumor suppressor genes
64
Appendage tumors: Benign or malignant?
Mostly benign but malignant variants exist
65
_____ are unusual in that
malignant forms appear to be more common than
benign forms.
Apocrine tumors
66
Arises from the meibomian
glands of the eyelid and may follow an aggressive
course replete with systemic metastases.
Sebaceous carcinoma
67
_____ can be confused
| with metastatic adenocarcinoma because of their tendency to form gland-like structures.
Eccrine and apocrine carcinomas
68
Px presented with a nodular lesion in his palms that has a moat and hillock pattern
ECCRINE POROMA
69
Histologic features of ECCRINE POROMA
● Sharp junction of the
neoplastic and non-neoplastic region
● Forms anastomosing cords and nests
70
Origin of ECCRINE POROMA
Eccrine sweat glands
71
Nodular lesions in the papillary dermis with cystic component
HIDRADENOMA/ Eccrine acrosporoma
72
Origin of HIDRADENOMA/ Eccrine acrosporoma
Distal excretory duct
73
Appendage tumor described as a large multicentric lesion with ductal differentiation
CYLINDROMA
74
Common location for CYLINDROMA
Forehead and scalp
Sometimes seen in neck
75
Coalescence of nodules with time may produce
| hat-like growth
Turban tumor
76
Cylindroma can be dominantly inherited; in such cases they appear early in life and are associated with
what mutation?
Inactivating mutations in the tumor suppressor gene
| CYLD
77
Multiple cylindroma
○ Disfiguring
| ○ Assoc w CYLD gene mutation
78
Histologic features of cylindroma
○ 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
Multiple, tan, small (1-3 cm) papulonodular lesions in the face and neck but more commonly in the lower eyelids
Syringoma
80
Origin of Syringoma
Eccrine differentiation
81
Histologic appearance of Syringoma
Cystic ducts lined by two
| cell-layered thick
82
Nodular benign lesion common in children and young adults. Most cases are in the head, neck, and upper extremities.
Pilomatricoma
83
Origin of Pilomatricoma
Hair matrix/ hair follicle differentiation
84
Mutation involved in Pilomatricoma
CTNNB1 (gene encoding B-catenin)
85
Pilomatricoma vs BCC
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
Proliferation of basaloid cells that forms primitive structures resembling hair follicles
TRICHOEPITHELIOMA
87
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.
SEBACEOUS ADENOMA
88
○ Adnexal tumor showing apocrine differentiation with prominent decapitation secretion
○ Most prevalent in axilla and scalp
○ May have an infiltrative growth pattern
APOCRINE CARCINOMA
89
○ Dull lesions
○ Diverse and dynamic
○ Majority are acquired
MELANOCYTIC NEVI
90
Mutation involved in MELANOCYTIC NEVI
Activation of RAS or the
| serine/threonine kinase BRAF
91
T or F: Not all nevi will give rise to melanoma.
TRUE
*Only very few will develop into melanoma.
92
Reason why nevi rarely give rise to melanomas
Oncogene-induced
| senescence
93
There is proliferation of nevus in the rete pegs or in the junction only; considered as the earliest lesions
Junctional nevus
94
Progression of nevi cells proliferation downwards to the papillary dermis
Compound nevus
95
Complete downward progression of cells leaving the junctional region and occupy predominantly the dermal region
Intradermal melanocytic nevus
96
Most nevus seen in clinical practice
Compound and Intradermal
97
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
Neurotization
98
Clinical significance of neurotization
It differentiates benign nevi from melanoma
*Neurotization is absent in melanoma
99
T or F: Junctional nevi are more elevated
FALSE
*Compound and Dermal nevi are more elevated than junctional nevi
100
Superficial vs deeper nevus cells
○ Superficial - larger, produce melanin, grow in nests
| ○ Deep - smaller, produce little or no pigment, appear as cords or single cells
101
○ Nevus present at birth
○ Larger variants have increased risk to develop melanoma
○ Generally benign
○ BRAF and NRAS mutation
Congenital nevus
102
○ Highly dendritic and heavily pigmented nevus cells
○ Confused with melanoma
○ Positive for melanin stains (S-100, HMB-45)
Blue nevus
103
```
○ Large, plump cells with pink-blue cytoplasm
○ Fusiform cells
○ Fascicular growth
○ Common in children
○ Red-pink nodule
○ Confused with hemangioma
```
Spitz nevus
104
○ Lymphocytic infiltration secondary to host immune response
Halo nevus
105
T or F: All melanomas arise from dysplastic nevi
FALSE
* Dysplastic nevi may be direct precursors of melanoma but are not prerequisites
* Increase risk: when multiple
106
T or F: Dysplastic nevi occurs exclusively in sun-exposed surfaces
FALSE
*Occur both in sun-exposed and non-exposed skin
107
First step to the development or progression of dysplastic nevus
Lentiginous hyperplasia
108
Nevus cell hyperplasia -> junctional -> compound with some degree of atypia
Nevus cells coalesce and fuse together and begin to replace the normal basal layer
Lentiginous hyperplasia
109
Release of melanin from dead nevus cells ; melanin is seen within macrophages
Melanin incontinence
110
Histologic features of dysplastic nevi
○ Atypical cells in epidermal and dermal regions (junctional and upper dermis)
○ Sparse lymphocytic infiltrates
○ Lentiginous hyperplasia
○ Linear dermo-epidermal junction fibrosis
○ Melanin incontinence
111
Most deadly of all skin cancers
MELANOMA
112
T or F: UV radiation is a prerequisite in the development of melanoma
FALSE
*UV radiation/ sunlight exposure is an important predisposing factor but not essential
113
T or F: There is no cure for Melanoma
FALSE
*It is curable in the early stages
114
Location of melanoma
```
○ Skin (majority) - cutaneous melanoma
○ Oral
○ Anogenital mucosa
○ Esophagus
○ Meninges
○ Uvea
```
115
Mutations involved in melanoma
○ Disruption in cell cycle control genes --CDKN2A gene
○ Activation of pro growth signaling pathway --RAS & BRAF
○ Activation of telomerase --TERT gene
116
● Horizontal spread within the epidermis and with very
minimal downward spread in the superficial dermis
● Seem to lack the
capacity to metastasize
RADIAL GROWTH PHASE
117
○ Indolent lesion, common to the face
○ May remain in the radial growth phase for
decades
Lentigo maligna
118
○ Most common type of melanoma
○ Seen in sun exposed areas
○ Spread in the epidermal and superficial dermis
Superficial spreading
119
○ Mucosal surfaces
| ○ Unrelated to sun exposure
Acral mucosal lentiginous
120
● Tumor cells invade downward into the deep dermis
● Presence of expansile mass or tumor nodule
● Neurotization is absent
● Capacity to metastasize
VERTICAL GROWTH PHASE
121
Depth of invasion is measured by ____ ?
Breslow thickness
122
Prognostic factors in melanoma
```
● 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
Most powerful predictors for the prognosis of melanoma
● Breslow level
| ● Ulceration
124
Melanoma: High risk sites
scalp, mandibular area, midline trunk, upper medial thighs, hands, feet, fossae, genitalia
125
Prognosis of lentigo malignant melanoma
Better prognosis
126
Prognosis of nodular melanoma
Worse
127
Prognosis of superficial spreading
Intermediate
128
Warning signs of melanoma
```
○ Asymmetry
○ Irregular borders
○ Variegated color
○ Increasing diameter
○ Evolution or change over time
```
129
T or F: Melanoma may be treated medically
TRUE
*success in treating this cancer with drugs
that target the RAS and PI3K/AKT pathways.
130
- Firm, well-defined, nodular/polypoid non-encapsulated mass
| - Common in the extremities
BENIGN FIBROUS HISTIOCYTOMA
131
Dermal tumor microscopic characteristics:
- Cellular: made up of spindle cells
- Fibroblastic proliferation
- Variable collagen deposition
- Delicate fibrovascular stroma
- Cluster of histiocytes
BENIGN FIBROUS HISTIOCYTOMA
132
Well-differentiated, primary fibrosarcoma of the skin
DERMATOFIBROSARCOMA PROTUBERANS
133
- Slow growing
- Locally aggressive
- Can recur
- But rarely metastasize
DERMATOFIBROSARCOMA PROTUBERANS
134
Molecular hallmark of DFSP
Transolation of genes encoding Collagen 1A1 (COL1A1) and platelet derived factor growth factor beta (PDGF B)
135
primary mode of tx for DFSP
Wide local excision
136
Treatment of choice for DFSP cases that are unresectable
Inhibitors of the PDGF B receptor tyrosine kinase
137
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
DERMATOFIBROSARCOMA PROTUBERANS
138
Immunohistochemical stains for DFSP
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
