091914 neoplasia

Question 1

seborrheic keratosis

Answer 1

benign
one of most common skin neoplasms
papules and plaques with stuck on, warty appearance
some harbor mutations in FGF receptor 3

Question 2

seborrheic keratoses occur in whom

Answer 2

middle age/older pts

Question 3

multiple seborrheic keratoses are associated with?

and what is the term given to it?

Answer 3

internal malignancies (stomach cancer)
called the Leser-Trelat sign

Question 4

verrucous

Answer 4

warty

Question 5

exophytic

Answer 5

growing outward past the surface epithelium

Question 6

acanthotic

Answer 6

epithelial hyperplasia

diffuse

Question 7

hyperkeratosis

Answer 7

thickening of stratum corneum due to keratin

Question 8

histology of seborrheic keratosis

Answer 8

hyperkeratotic (thickening of stratum corneum), papillomatous, and verrucous epidermis

exophytic

HORN and pseudo horn cysts

variable melanin pigmentation

Question 9

actinic keratosis

Answer 9

also known as solar or senile keratoses

resulting from chronic sun damage

dysplastic condition

10% of cases do become malignant, some stabilize or regress

in middle aged, elderly

Question 10

clinical appearance of actinic keratosis

Answer 10

rough, erythematous or yellow/brown, scaly lesions

Question 11

treatment for seborrheic keratosis

Answer 11

not necessary

but cryotherapy can be performed for symptomatic lesions

Question 12

treatment for actinic keratoses

Answer 12

surgical destruction (cryotherapy or biopsy)
medical therapy

Question 13

histology of actinic keratoses

Answer 13

cytologic atypia of basal layer of epidermis
corneal layer is thickened with retained nuclei (parakeratosis)

dermis has thickened, blue-gray elastic fibers (blue-know that has been exposed to sun)

Question 14

squamous cell carcinoma

Answer 14

sun exposed sites
(also other predisposing factors)

SCC in situ is irregular in shape, erythematous, scaly or crusted, plaques.
invasive lesions are nodular, show variable scale, may ulcerate.

5% become invasive

Question 15

treatment for squamous cell carcinoma

Answer 15

can be completely removed with surgery or sometimes with topical med

Question 16

histology of squamous cell carcinoma

Answer 16

full thickness dysplasia

lack of polarity of cells

Question 17

keratoacanthoma

Answer 17

variant of squamous cell carcinoma

often a solitary, pink or flesh colored dome shaped nodule with central keratin plug on sun exposed skin of elderly

tendency to involute spontaneously

Question 18

tx of keratoacanthoma

Answer 18

mostly surgical

Question 19

histology of keratoacanthoma

Answer 19

exophytic lesions with invaginating mass of keratinizing, well differentiated squamous epithelium at the sides and bottom of lesion

central kertain filled crater

Question 20

basal cell carcinoma

Answer 20

most common cutaneous malignant neoplasm
more common in elderly males
PTCH1 mutations in 30% of BCCs

Question 21

clinical appearance of basal cell carcinoma

Answer 21

papule with pearly translucent edge with visible telangiectasia

Question 22

tx of basal cell carcinoma

Answer 22

surgery

Question 23

histology of basal cell carcinoma

Answer 23

several variants
including:
multifocal growths originating from epidermis (superficial type) or
nodular lesions growing downward into dermis (nodular type) of variably basophilic cells with peripheral palisade

Question 24

melanocytic nevi

Answer 24

melanocytes increase w/ stimulation–acquired nevi

also present at birth-congenital nevi

Question 25

histology of melanocytic nevi

Answer 25

3 types: junctional, compound, intradermal

melanocytic nevi are initially made of round to oval cells that grow in nests along dermal-epidermal junction (junctional nevi)

eventually, junctional nevi grow into underlying dermis as nests or cords of cells (compound nevi)

in older lesions, the epidermal nests may be entirely lost to leave pure dermal nevi (intradermal nevi)

Question 26

dysplastic nevus

Answer 26

pts w/ multiple dysplatic nevi have increased risk for melanoma, and dysplatic nevi themselves have some potential for malignant transformation

larger than acquired nevi usually (more than 0.5 cm), irregular in shape, often show uneven color with dark brown centers

Question 27

dysplastic nevus syndrome

Answer 27

familial or sporadic occurrence of multiple dysplastic nevi

sporadic-usually 2 to 10 develop
familial-usually hundreds develop, lifetime risk of melanoma approaches 100%

Question 28

histology of dysplastic nevi

Answer 28

junctional or compound, NEVER intradermal

nevus cell nests may be enlarge and abnormally fuse with adjacent nests (bridging)

nevus cells begin replacing normal basal cel layer, producing “lentiginous hyperplasia”

shoulder phenomenon

Question 29

melanoma

Answer 29

development is multifactorial
risk factors are excessive UV exposure, fair complexion, childhood sunburns, increased number of dysplastic nevi, family history, older age, xeroderma pigmentosum, familial dysplastic nevus syndrome, possibly immunosuppression

radial growth phase-no capacity to metastasize

Question 30

tx for melanoma

Answer 30

superficial lesions are cured surgically
metastatic-poor prognosis

probability for metastasis is predicted by measuring depth of invasion in millimeters of the vertical growth phase nodule (Breslow thickness)–the most important single prognostic indicator

for invasive melanomas greater than 1 mm in Breslow thickness, sentiel lymph node biopsy is recommended

Question 31

types of melanoma

Answer 31

lentigo maligna melanoma
superficial spreading melanoma
nodular melanoma
acral lentiginous melanoma

Question 32

histology of melanoma

Answer 32

melanoma in situ shows asymmetric population of melanocytes within epidermis (single cells and clusters throughout all levels of epidermis). melanoma cells are large with abundant cytoplasm. these atypical melanocytes often show pleomorphic vesicular nuclei with prominent eosinohpilic nucleoli

invasive melanoma (vertical growth phase) shows cells in dermis that grow in poorly formed nests or individual cells as an expansile nodule

Question 33

mycosis fungoides

Answer 33

T cell lymphoma
most common cutaneous lymphoid malignancy
late adulthood, male predominance
patch, plaque, and nodule phases

patch stage: non specific dermatitis, usually patches on the lower trunk and buttocks. ill-defined patches of varying hue. irregular in size and shape and have random distribution. this stage may go on for many years

plaque stage: well demarcated lesions which are often annular. violaceous and occasionally scaly. may develop de novo or from patches.

tumor stage: usually develops in association with pre-exsiting lesions. red in color. tense, shiny surface. ulceration may occur. usually 1 cm or more.

Question 34

course of outcome of mycosis fungoides

Answer 34

quite variable

Question 35

histology of mycosis fungoides

Answer 35

mature CD4 T cells. particular tendency to colonize epidermis.

to a lesser extent in early lesion and more obviously in later stages, the infiltrate has large cells with highly irregular, convoluted nuclei (known as Sezary or mycosis cells)

Pautrier microabscesses

Question 36

Sezary syndrome

Answer 36

rare variant of cutaneous T cell lymphoma

erythroderma, blood involvement, poor prognosis