neoplasms Flashcards
leser trelat syndrome
sudden SKs due to chemo drugs, gastric cancer, breast cancer, lymphoma
sk features
white yellow milia cysts, comedo openings, demarcated, hairpin vessels, sulci, gyri
peutz jeghers
lentiges on mucosa and genitalia, due to GI, breast and ovarian cancers
NF 1 Features
> 6 CALM, > 2 plexiform neurofibromas, lisch nodules (pigmented hamartomas of iris), glioma (optic tumor) crowes sign (axillary or inguinal freckling)
NF1 referrals
neuro, opthamology, developmental assessment, scoliosis monitoring
congenital melanocytic nevi sizes
S <1.5cm, M 1.5-19.9cm both after puberty, L >20cm BEFORE puberty
junctional nevi
flat to slightly raised, dermo-epidermal junction, palms, soles, genitalias, mucosa in children
compound nevi
macule with a central raised papule, dermo epidermal junction and dermis, increases in thickness during childhood and adolescence
intradermal nevi
dermis-SC, after adolescence
spitz nevi
spindle shaped melanocytes on scalp and face, legs, before adulthood, worrisome histology so remove them
ATN
clinical dx
dysplastic nevi
histological dx
mild dysplastic nevi
ovoid or ellipsoid shape, hyperchromatic, small nuclei
moderate dysplastic nevi
melanocyte with large, hyperchromatic, ellipsoid or rhomboid shaped with a small nucleus in center of nucleus (2-3mm margin)
severe dysplastic nevi
spidle or ellipsoid shape, hyperchromatic, large nuclei with distal nucleoli (5mm margin)
this gene linked with MM and panc cancer
BRAF
30% of MM patients have these secondary cancers
renal, NMSC, leukemia, prostate, breast, colon
lifetime risk of MM in general population
1.3%
lifetime risk of MM in those with ATN
6%
lifetime risk of MM in those with ATN and FMH MM
15%
risk of MM by age 70 in those with FAMMM
100%
FAMMM
> 50 nevi with FMH of MM
percentage of MM that are hereditary
5-12%
majority of MM have
unknown or no genetic utation, 40% with a genetic mutation have CDKN2A