30. Epithelial Tumors Flashcards
This is one of the most common skin neoplasms that devo in middle age or older people.
Seborrheic Keratoses
Descibe this seborrheic keratoses and where we expect to see it
Papules and plaques with ‘stuck on’ warty apperance
Most common on face, trunk, upper extremeties
What is the cause of Seborrheic keratoses?
Mutation in FGF 3
What is this?!?
Leser-Trelat Sign: multiple SKs are associated with internal maligancies.. espeically stomach cancer
This is indicitative of what? Describe it
Seborrheic Keratoses
Acanthotic, HORNCYSTS, see variable hyperkeratosis and you someimes see a monotonous basaloid band
Woman comes in with erythematous yellow/brown lesions on the tops of her hands. She states she spends most days outisde gardening. Dx
Actinitc Keratosis
its solar or senile keratosis– usually from chronic sun damage
Does Actinic Keratosis often become maligant?
No.. only .1-10% become malignant, most regress or remain stable
Describe what goes on histologically with Actinitc Keratosis
See atypia in basal layer of epidermis
(in dif stains, we see blud-gray elastic fibers in dermis d/t so sun exposure)
Common neoplasm in older people d/t UVB radiation that causes DNA damage: also associated with old burn scars, HPV, radiation, arsenic, immunsuppresed people
Squamous Cell car.
PRognosis for SCC
5% develop invasive component
–30% of them have metestatic potiential
This is SCC—what do we worry about
Invasive SCC tend to be nodular and may ulcerate… likelyhood of metastasis is related to thickness of lesion and degree of invasion into subcutis
Othe image is example of common sharply defined red scaly plaque SCC
Describe features of SCC histology
We can see full thickness dysplasia
becomes invasive once it breaks through basement membrane
How can we tell this is invasive SCC
Break through the BM
Whats this little tumor?
Keratoacanthoma
Solitary flesh colored nodule with central keratin plug
Rapid growth over 2-10 weeks and mostly on sun damaged skin
Keratoacanthoma
When do we expect to see multilple keratoacanthomas?
Immunosuppresed pts
Why do we do tx for keratoacanthomas?
can cause extensive local destrucion.
Describe this lesion and it’s histology
Keratoancanthoma
Crate like lesion, proliferating epi is well differentiationed with epithelial palor
Helpful chart on BSC vs SCC
What is our MOST common human cancer
BSC: secondary to chronic sun exposure
** can be locally destructive
Do we worry about metestasis with BSC… and why does it happen
SLOW growing, rarely mets–if does, bc pt is immunocompromised
Associated with dysregulation of sonic hedgehog or PTCH pathway
Whats this little beauty?
BSC with telangectasia…can als be crater like
HE of BSC… describe
see large nodules blue or purple in color
you can sometimes see clefting between stroma and tumor
This guy was present at birth and increases in growth with sun exposure
melanocytic nevi
What type of Melanocytic nevi is this?
Its junctional… epidermis only
Melonocytic nevi are:
Compound nevi; epidermis and dermis
Melanocytic nevi that are intradermal are:
in the dermis only
What is this?
Congenital Melanocytic Nevi
These are larger then aquired nevi >0.5cm, irregular in shape and uneven discoloration; can occur sporadicaly or in familial form.
Dysplastic Nevi
Why do we worry about mulplie dysplastic nevi?
Increased risk of melenoma
Describe dysplastic nevi sydrome
familial or sporadic, large in number (more then 80) see increased chance melanoma as well as other maligancies (pancreateic carcinoma)
Genetic abnormality in Dysplastic nevus syndrome
Autosomal dominant, mutation in CDKN2a gene 9p21-11 in 40% cases
Sporadic vs familial nevi have different or same histology
same
represents 3% of all skin cancers
6th most common cancer in US
MOre common in white
M=F
Melanoma
Risk factors for melanoma
multifactoral: sun exposure at EARLY AGE (most important risk factor), fair complexion, old age, dysplasic nevi syndrome, hitstory of melanoma and XP
What clinical features do we look for in melanoma
A: asymmetry
B: Borders; notched, uneven, blurred
C: color, uneven shades
D: diameter; >6 mm
How do we determine how bad melanoma is?
Verticle growth or dermal invasion: this is when we see potential for metastasis
Importance of radial growth of melanoma
melanocytes will proliferate within epidermis but NO NO NO metestatic ptoential at this stage: its early to find early on bc easily cured (surgically)
Depth of invasion is most important predictor of metastatic disease:
called Breslow thickness
Tumors <1mm rarely metastasize
>1.7mm more potential
Where does melanoma like to metestasize?
Most common type of melanoma and located on the back and extremeties
Superficial spreading type
Melenoma with NO raidal growth phase … directly invades the dermis– poor prognosis
Nodular type
Melenoma mostly commonly located on head and neck area: sun exposed
Lentigo maligna type
located on palm, sole, or beneath nail; most common melanoma in AA
Acral Lentiginous type
HE of melanoma
early on… only in dermis, then we then progress and have keritinocytes all over and in nests.
Older man presents with erythrodermic rash–> over time progresses to patch–>plaque–> nodules
Mycosis fungiodes
most common CTCL
**becomes aggressive if chronic
What is this???
Sezary Syndrome
Blood involvement of T cell lymphoma, erythroderma, poor prognosis, survial of 1-3 yrs
What is this?
Mycosis Fungoides:
infiltration of epidermis and dermis by neoplastic T cells, often have cerebriform nucleus characterized by infolding of nuclear memebrane
