30. Epithelial Tumors Flashcards

(48 cards)

1
Q

This is one of the most common skin neoplasms that devo in middle age or older people.

A

Seborrheic Keratoses

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2
Q

Descibe this seborrheic keratoses and where we expect to see it

A

Papules and plaques with ‘stuck on’ warty apperance

Most common on face, trunk, upper extremeties

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3
Q

What is the cause of Seborrheic keratoses?

A

Mutation in FGF 3

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4
Q

What is this?!?

A

Leser-Trelat Sign: multiple SKs are associated with internal maligancies.. espeically stomach cancer

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5
Q

This is indicitative of what? Describe it

A

Seborrheic Keratoses

Acanthotic, HORNCYSTS, see variable hyperkeratosis and you someimes see a monotonous basaloid band

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6
Q

Woman comes in with erythematous yellow/brown lesions on the tops of her hands. She states she spends most days outisde gardening. Dx

A

Actinitc Keratosis

its solar or senile keratosis– usually from chronic sun damage

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7
Q

Does Actinic Keratosis often become maligant?

A

No.. only .1-10% become malignant, most regress or remain stable

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8
Q

Describe what goes on histologically with Actinitc Keratosis

A

See atypia in basal layer of epidermis

(in dif stains, we see blud-gray elastic fibers in dermis d/t so sun exposure)

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9
Q

Common neoplasm in older people d/t UVB radiation that causes DNA damage: also associated with old burn scars, HPV, radiation, arsenic, immunsuppresed people

A

Squamous Cell car.

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10
Q

PRognosis for SCC

A

5% develop invasive component

–30% of them have metestatic potiential

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11
Q

This is SCC—what do we worry about

A

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

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12
Q

Describe features of SCC histology

A

We can see full thickness dysplasia

becomes invasive once it breaks through basement membrane

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13
Q

How can we tell this is invasive SCC

A

Break through the BM

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14
Q

Whats this little tumor?

A

Keratoacanthoma

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15
Q

Solitary flesh colored nodule with central keratin plug

Rapid growth over 2-10 weeks and mostly on sun damaged skin

A

Keratoacanthoma

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16
Q

When do we expect to see multilple keratoacanthomas?

A

Immunosuppresed pts

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17
Q

Why do we do tx for keratoacanthomas?

A

can cause extensive local destrucion.

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18
Q

Describe this lesion and it’s histology

A

Keratoancanthoma

Crate like lesion, proliferating epi is well differentiationed with epithelial palor

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19
Q

Helpful chart on BSC vs SCC

A
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20
Q

What is our MOST common human cancer

A

BSC: secondary to chronic sun exposure

** can be locally destructive

21
Q

Do we worry about metestasis with BSC… and why does it happen

A

SLOW growing, rarely mets–if does, bc pt is immunocompromised

Associated with dysregulation of sonic hedgehog or PTCH pathway

22
Q

Whats this little beauty?

A

BSC with telangectasia…can als be crater like

23
Q

HE of BSC… describe

A

see large nodules blue or purple in color

you can sometimes see clefting between stroma and tumor

24
Q

This guy was present at birth and increases in growth with sun exposure

A

melanocytic nevi

25
What type of Melanocytic nevi is this?
Its junctional... epidermis only
26
Melonocytic nevi are:
Compound nevi; epidermis and dermis
27
Melanocytic nevi that are intradermal are:
in the dermis only
28
What is this?
Congenital Melanocytic Nevi
29
These are larger then aquired nevi \>0.5cm, irregular in shape and uneven discoloration; can occur sporadicaly or in familial form.
Dysplastic Nevi
30
Why do we worry about mulplie dysplastic nevi?
Increased risk of melenoma
31
Describe dysplastic nevi sydrome
familial or sporadic, large in number (more then 80) see increased chance melanoma as well as other maligancies (pancreateic carcinoma)
32
Genetic abnormality in Dysplastic nevus syndrome
Autosomal dominant, mutation in CDKN2a gene 9p21-11 in 40% cases
33
Sporadic vs familial nevi have different or same histology
same
34
represents 3% of all skin cancers 6th most common cancer in US MOre common in white M=F
Melanoma
35
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
36
What clinical features do we look for in melanoma
A: asymmetry B: Borders; notched, uneven, blurred C: color, uneven shades D: diameter; \>6 mm
37
How do we determine how bad melanoma is?
Verticle growth or dermal invasion: this is when we see potential for metastasis
38
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)
39
Depth of invasion is most important predictor of metastatic disease:
called Breslow thickness Tumors \<1mm rarely metastasize \>1.7mm more potential
40
Where does melanoma like to metestasize?
41
Most common type of melanoma and located on the back and extremeties
Superficial spreading type
42
Melenoma with NO raidal growth phase ... directly invades the dermis-- poor prognosis
Nodular type
43
Melenoma mostly commonly located on head and neck area: sun exposed
Lentigo maligna type
44
located on palm, sole, or beneath nail; most common melanoma in AA
Acral Lentiginous type
45
HE of melanoma
early on... only in dermis, then we then progress and have keritinocytes all over and in nests.
46
Older man presents with erythrodermic rash--\> over time progresses to patch--\>plaque--\> nodules
Mycosis fungiodes most common CTCL \*\*becomes aggressive if chronic
47
What is this???
Sezary Syndrome Blood involvement of T cell lymphoma, erythroderma, poor prognosis, survial of 1-3 yrs
48
What is this?
Mycosis Fungoides: infiltration of epidermis and dermis by neoplastic T cells, often have cerebriform nucleus characterized by infolding of nuclear memebrane